Healthcare Costs

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The critical role of hospitalists in controlling healthcare costs

Let's think about what we need to do ourselves. We have to acknowledge that orders we write drive up health care costs.1 AMA President, Nancy H. Nielsen, MD, PhD

As the most prominent providers of inpatient care, hospitalists should be aware that, of the total annual expenditures on US healthcare ($2.3 trillion in 2007),2 approximately one‐third goes to hospital‐based medical care, over one‐half of which (57%) is covered by public funds through Medicare and Medicaid3; this high cost of healthcare is increasingly being blamed for unnecessarily burdening our economy and preventing our industries from being globally competitive. I believe that the high proportion of spending on inpatient care places hospitalists firmly in the center of the debate on how to reduce healthcare costs. It is well known that the United States spends about twice as much per capita as other industrialized countries on healthcare,4 without evidence of superior health outcomes.5 However, it is also known that remarkable local and regional variations in healthcare spending also exist within the US, again, without evidence of superior health outcomes in the higher‐spending regions.6 Both of these observations suggest that we are spending many healthcare dollars on things that evidently do not improve the health of our patients. How much of this waste is administrative, operational, or clinical is debatable and remains the focus of growing national healthcare reform efforts.711 However, from the hospitalist perspective, we should be especially wary of providing so‐called flat‐of‐the‐curve medicine, that is, a level of intensity of care that provides no incremental health benefit.12 The purpose of this editorial is to challenge hospitalists to collectively examine how much of our inpatient spending is potentially unnecessary, and how we, as specialists in inpatient medicine, can assume a critical role in controlling healthcare costs.

To illustrate the issue, consider the following clinical scenario, managed in different ways by different hospitalists, with approximate costs itemized in Table 1. The patient is an elderly woman who presents to the emergency room with syncope occurring at church. The first hospitalist takes time to gather history from the patient, family, eyewitnesses, and the primary care physician, and requests a medication list and outside medical records, which reveal several recent and relevant cardiac and imaging studies. He performs a careful examination, discovers orthostatic hypotension, and his final diagnosis is syncope related to volume depletion from a recently added diuretic as well as a mild gastroenteritis. The patient is rehydrated and discharged home from the emergency room in the care of her family, and asked to hold her diuretic until seen by her family physician in 1 or 2 days. The second hospitalist receives the call from the emergency room and tells the staff to get the patient a telemetry bed. He sees the patient 2 hours later when she gets to the floor. The family has gone home and the mildly demented patient does not recall much of the event or her past medical history. The busy hospitalist constructs a broad differential diagnosis and writes some quick orders to evaluate the patient for possible stroke, seizure, pulmonary embolism, and cardiac ischemia or arrhythmia. He also asks cardiology and neurology to give an opinion. The testing is normal, and the patient is discharged with a cardiac event monitor and an outpatient tilt‐table test scheduled.

Comparison of the Approximate Cost of Evaluating Two Patients for Syncope
Mrs. Syncope #1 Cost Mrs. Syncope #2 Cost
  • NOTE: Akron General Medical Center Patient Price Information List. Available at: http://www.akrongeneral.org/portal/page?=pageid=153,10350167&=dad=portal&_schema=PORTAL. Accessed July 2009.

  • Abbreviations: CBC, complete blood count; CMP, comprehensive metabolic panel; CT, computed tomography; EEG, electroencephalogram; EKG, electrocardiogram; MRI, magnetic resonance imaging.

Level 4 emergency room visit $745 Level 4 emergency room visit $745
Level 4 internal medicine consultation $190 Level 3 history and physical $190
Laboratory evaluation: CBC, CMP, cardiac panel, urinalysis, D‐dimer $843
EKG $150
Head CT $1426
Chest CT angiogram $2120
Brain MRI $3388
Echocardiogram $687
Carotid ultrasound $911
Level 4 neurology consult $190
Subsequent visits day 2, day 3 $150
EEG $520
Level 4 cardiology consult $190
Nuclear stress test $1359
Specialist subsequent visits $150
Telemetry bed, 3 days $3453
Discharge, low‐level $90
Cardiac event monitor $421
Tilt‐table test $1766
$935 $18,749

Although the above scenarios purposely demonstrate 2 extremes of care, I suspect most readers would agree that each hospitalist has his or her own style of practice, and that these differences in style inevitably result in significant differences in the total cost of healthcare delivered. This variation in spending among individual physicians is perhaps more easily understood than the striking variations in healthcare spending seen when different states, regions, and hospitals are compared. For example, annual Medicare spending per beneficiary has varied widely from state to state, from $5436 in Iowa to $7995 in New York (in 2004), a 47% difference.13 Specific analysis of inpatient spending variations is presented in the Dartmouth Atlas of Health Care 2008, which reports healthcare spending in the last 2 years of life for patients with at least 1 chronic illness.14 While the average Medicare inpatient spending per capita for these patients was about $25,000, the state‐specific spending varied widely from $37,040 in New Jersey to $17,135 in Idaho. There was also significant variation in spending within individual states (ie, New York: Binghamton, $18,339; Manhattan, $57,000) and between similar types of hospitals (UCLA Medical Center, $63,900; Massachusetts General Hospital, $43,058). Yet there is no evidence that higher‐spending regions produce better health outcomes.6 Interestingly, the observed differences in spending within the US were primarily due to the volume and intensity of care, not the price of care, as has been seen in some comparisons of the US with other industrialized countries.8, 15 In overall Medicare expenditures, higher‐spending locations tended to have a more inpatient‐based and specialist‐oriented pattern of practice, with higher utilization of inpatient consultations, diagnostic testing, and minor procedures.6

Although the wide variation in spending observed is a bit baffling, the encouraging aspect of this data is that some places are apparently doing it right; that is, providing their patients with a much higher value per healthcare dollar. Ultimately, if the higher‐spending locations modeled the lower‐spending locations, we would have the potential to reduce overall healthcare costs by as much as 30% without harming health.9

What are the possible reasons that we are providing unnecessary care? There are both environment‐dependent and physician‐dependent reasons, which I will outline here. The first 3 reasons represent areas that would seem to require system‐wide change, whereas the remaining 7 reasons are perhaps more amenable to local and/or national hospitalist‐directed efforts.

  • Working in a litigious environment promotes unnecessary testing and consultations with the intent of reducing our exposure to malpractice liability, so‐called defensive medicine.16

  • A reimbursement system that is primarily fee‐for‐service encourages physicians to provide more care and involve more physicians in the care of each patient, with little or no incentive to spend less, a core problem that was recently highlighted in a public Society of Hospital Management (SHM) statement.17

  • The lack of integrated medical record systems promotes waste by leading to duplicate testing, simply because we cannot easily obtain old records to confirm whether tests were previously done. Interestingly, data from the Commonwealth Fund conclude that US physicians order duplicate diagnostic tests (a test repeated within 2 years) at more than twice the rate of Canada and the United Kingdom, while the nation with the lowest rate of duplicate testing, The Netherlands, has the highest rate of electronic medical record use (98%).18

  • Working with patients (or families) with high expectations who insist upon aggressive testing, treatment, and referral to specialists inflates spending, especially if associated with futile and expensive end‐of‐life care.

  • The involvement of one or more specialists may subsequently lead to even more aggressive care ordered by each specialist.

  • The availability and promotion of new technology (diagnostic testing, medical devices, etc.) may prompt us to make use of it simply because it is there, with or without evidence of a health benefit. Our natural curiosity or fascination with information, or our desire to do an overly complete evaluation, works against cost containment.

  • Local trends or traditions within our specific work environment, as suggested by the variability data, may have a strong influence on our individual practice. In such a setting, inadequate knowledge of the cost‐effectiveness of various tests and treatment options likely leads to unnecessary health care spending.

  • A hospitalist work environment in which a high patient load is carried will inevitably result in less time to gather a detailed history and obtain old records or other information that could help narrow a differential diagnosis and minimize unnecessary or duplicate testing.

  • Preventable readmissions resulting from inadequate coordination of care add cost,19 a phenomenon highly dependent on efficient information systems and proper physician‐physician communication.20

  • An overestimation of the need for inpatient evaluation and treatment (vs. outpatient) leads to unnecessary admissions and a longer average length‐of‐stay, each of which add dramatically to total healthcare costs. This is not only dependent on our individual threshold for admitting and discharging patients, but also on our efficiency in diagnosing and treating acute conditions. The fact that the average length‐of‐stay for congestive heart failure admissions, for example, ranges in different regions from 4.9 to 6.1 days (with costs of $9143 and $12,528, respectively)21 is enough to show that there is room for progress.

What joint efforts could be made to minimize unnecessary inpatient spending? The following are my personal opinions and suggestions (Table 2). Most importantly, I believe every physician deserves prompt and accurate feedback regarding their spending patterns, accompanied by valid comparisons to national and local standards, to demonstrate where they stand on the spectrum of healthcare spending. We are currently far behind other industries in our ability, as physicians, to evaluate what we are spending money on, how much, and why. If I knew, for example, that my spending was in the 95th percentile of all hospitalists in community hospitals similar to mine, I would be prompted to investigate where the differences were and why. In an informal survey of hospitalist colleagues, I found that the majority do not receive any data on the costs associated with their care, and are largely unaware of the actual cost of the inpatient tests they commonly order. Developing a secure, user‐friendly database of individual physician spending patterns relative to national and local standards could be a preliminary step, and would likely require a unified effort between government agencies, professional societies, hospitals, and the insurance industry. However, once available, the increased transparency and clarity of spending variations would hopefully prompt introspection and change. In the absence of hard data, however, individual self‐assessment on spending patterns could also be offered through the development of an online simulated case‐based examination in which a physician could gain a general idea of how his evaluation and treatment of a case scenario compares to his hospitalist colleagues, and to what degree each of his clinical decisions affects the overall cost of care. There are many excellent quality improvement tools offered through SHM but none that specifically address the cost of care.

Potential Reasons Hospitalists May Order Unnecessary Tests, Treatments, or Consultations, and the Effect of Potential Solutions on Each Area
Spending Data Guidelines Patient Education Advocacy Professional Development
  • Abbreviations: ✓, indirect influence; ✓✓, direct influence or most likely to succeed.

Defensive medicine ✓✓
Patient expectations ✓✓
Specialist consultations ✓✓
Fee‐for‐service environment ✓✓
Availability of technology ✓✓ ✓✓
Poor access to medical records ✓✓
Local medical culture ✓✓ ✓✓
Insufficient knowledge of evidence‐based guidelines ✓✓ ✓✓
Lack of available value‐based data ✓✓
High patient load ✓✓
Preventable readmissions from poor coordination ✓✓
Overestimation of the need for inpatient care ✓✓ ✓✓

Second, hospitalists need quick access to current evidence‐based guidelines regarding the true clinical value, or cost‐effectiveness, of testing and treatment for common inpatient conditions, including specific admission criteria. A single source or clearinghouse of guidelines, sponsored by SHM, may be particularly helpful, especially if it focuses on clarifying areas of highest variability in inpatient spending. In addition, I believe that, given the critically important interface between emergency medicine and hospital medicine, joint guidelines between the 2 groups would potentially be very helpful in controlling costs by limiting unnecessary admissions. Advocacy for comparative effectiveness research to establish validity in these guidelines will be fundamental22, 23; however, I suspect the common sense question: Will this added cost improve my patient's outcome? also needs to be applied more generously, since many individual clinical scenarios will not likely lend themselves to formal study. For discussion, some sample case scenarios are presented (Table 3).

Clinical Cases Designed to Stimulate Discussion Regarding Potentially Unnecessary Healthcare Costs Generated by Hospitalists
  • Abbreviations: CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CT, computed tomography; DVT, deep vein thrombosis; EKG, electrocardiogram; FEV1, forced expiratory volume in 1 second; INR, international normalized ratio; IV, intravenous; IVC, inferior vena cava; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; pCO2, partial pressure of carbon dioxide; PE, phycoerythrin; pO2, partial pressure of oxygen; UTI, urinary tract infection.

An 82‐year‐old nursing home patient limited to a wheelchair due to severe osteoarthritis presents with new‐onset expressive aphasia and mild right‐sided hemiparesis. Head CT is negative for bleed, but shows an acute left middle cerebral artery infarct. Would your stroke workup include an MRI/MRA of the brain, carotid ultrasound, echocardiogram, and neurology consultation?
A 68‐year‐old with known ischemic cardiomyopathy is admitted with a CHF exacerbation clearly due to medication noncompliance. The last echocardiogram was done 18 months ago and showed an ejection fraction of 20% with moderate to severe mitral regurgitation. Would you order a repeat echocardiogram? Would you consult cardiology?
A 35‐year‐old construction worker presents with sharp chest pain that is partially reproducible on examination, and no other physical findings. Vital signs, EKG, and cardiac markers are normal. The patient had a negative stress test last year. However, his D‐dimer is slightly elevated. Would you order a CT angiogram of the chest? If he had a normal one last month for the same symptoms, would you repeat it? In either case, would you admit him to the hospital?
A 42‐year‐old man presents with chest pain associated with recent cocaine use. His chest pain resolves in the emergency room and his repeat troponin is normal at 6 hours. Would you order a nuclear stress test for the patient? Would your management change if a stress test was normal a year ago? Would you admit him?
A 58‐year‐old man admitted with community‐acquired pneumonia of the right lower lobe has improved clinically with empiric treatment. Before discharge, he asks for a repeat radiograph to make sure it is getting better. Would you comply with the patient's request?
A 68‐year‐old woman who underwent left total knee arthroplasty 2 weeks ago presents with a left proximal DVT. She has no other symptoms and vitals are normal. She has no personal or family history of clotting. Would you admit the patient to the hospital? Would you order a CT angiogram of the chest? Would you order a hypercoagulable workup?
A 43‐year‐old is admitted for atypical chest pain. Serial cardiac enzymes and nuclear stress test are negative. However, his transaminases are elevated at twice the normal upper limits. He takes a statin for dyslipidemia. Would you order further laboratory tests or imaging to evaluate for hepatic disorders or discharge the patient?
A 63‐year‐old receiving chemotherapy for colon cancer with multiple liver metastases presents with new‐onset dyspnea and is found to have a large left‐sided pleural effusion on chest radiograph. You perform a thoracentesis and malignant cells are present. Would you order a chest CT? Would you consult pulmonology and/or thoracic surgery (for chest tube and/or pleurodesis)?
A 78‐year‐old with severe oxygen‐dependent obstructive lung disease (FEV1 of 1.0 L) has a new 1‐cm nodule on his chest radiograph when admitted for a COPD exacerbation. Would you order a chest CT? Would you arrange for a biopsy? Would you consult oncology or pulmonology?
A 45‐year‐old woke up with severe low‐back pain with right‐sided radiculitis after shoveling heavy snow yesterday. He is unable to walk due to pain, but no focal neurologic symptoms are identified on exam. Would you order an MRI of the spine? Would you consult orthopedics?
A 68‐year‐old man on coumadin for chronic atrial fibrillation is incidentally found to have an INR of 6.5 in clinic. He is currently asymptomatic without evidence of bleeding and with normal vital signs. His hemoglobin is 10.1 compared to 10.8 last month. Digital rectal exam results in a hemoccult‐positive smear. Would you admit him to the hospital? Would you give fresh frozen plasma? Would you consult gastroenterology?
A 58‐year old truck driver presents with acute PE, identified on CT angiogram. There is no previous history of DVT. The patient's arterial blood gas shows a pH of 7.45, pCO2 of 35 mmHg, and pO2 of 55 mmHg on room air. The heart rate is 75. Would you order a lower extremity duplex to assess for DVT? Would you ask interventional radiology to place an IVC filter if a DVT was present?
A 26‐year‐old presents with fever, headache, and meningismus. Head CT is normal. Would you perform a bedside spinal tap or send the patient for a fluoroscopically‐guided procedure in radiology?
A 68‐year‐old smoker presents with right‐sided pneumonia with a small parapneumonic effusion. He is afebrile after 24 hours of IV antibiotics and clinically feels much better. Would you order a thoracentesis? If so, would you perform it bedside or send the patient to radiology for an ultrasound‐guided procedure? Would you consult a pulmonologist?
An 82‐year‐old severely demented nursing home resident who has required total care for the past few months presents with dehydration and a sodium of 158 after increasingly poor oral intake. No other illness is identified. Would you begin IV fluids immediately and consider gastrostomy tube placement to maintain adequate hydration at the nursing home or would you contact family to discuss end‐of‐life care goals first? Would your management change if a UTI or pneumonia was diagnosed?

Third, hospitalists could potentially benefit from the development of patient education materials, available through SHM, that address the cost‐effectiveness of common inpatient tests and treatments with the goal of decreasing patient demand for unnecessary testing. Education regarding advanced directives and end‐of‐life care decision‐making could be particularly valuable in minimizing futile care, as it is well‐documented that transitioning to palliative care as soon as it is appropriate reduces healthcare spending greatly during the end‐of‐life period.2427 At the same time, we need to be careful to reassure our patients that we are not trying to ration care, but are instead minimizing the risks and costs for them associated with unnecessary care. In my experience, most patients, if given appropriate time, attention, and education, are willing to accept the final recommendation of their physician.

Fourth, intensified federal and state advocacy in several areas could help reduce spending. For example, advocacy for medical liability reform may reduce the atmosphere of defensive medicine, although I suspect that because old habits die hard, it may take a full generation of decreased liability risk to actually change practice patterns. Advocacy for the development of a national, or at least more uniform, electronic medical record, may decrease duplicate testing and improve efficiency. Advocacy for value‐based reimbursement models may help dampen costs resulting from a predominantly fee‐for‐service environment.28

Fifth, and perhaps most fundamental to the future of our specialty, encouraging the broad professional development of hospitalists as a true specialists in inpatient medicine (based on the SHM Core Competencies,)29 could help minimize the unnecessary costs associated with specialist‐oriented care.6 With the desire to create, in the near future, a formal board‐certification in hospital medicine comes an obligation to develop broad knowledge and broad skill sets that are truly unique to our profession, whereas deferring to a specialist‐oriented pattern of care actually shrinks us down to something less than a traditional internist, rather than a unique entity.30 With our 24/7 focus on inpatient care, we should easily be able to demonstrate our superiority in safety, quality, and efficiency, all of which are closely linked to increased value per healthcare dollar. If, however, our focus is blurred by an overly productivity‐based practice, in which patient volume and procedures take precedence, we will not be able to claim any special value to the system.

Last, supporting efforts to improve coordination of care and transitions of care could reduce costs associated with unnecessary readmissions or posthospital complications. A recent policy statement from several professional societies, including SHM, highlights the importance of these transitions,20, 31 and within the past year, SHM has launched the successful Project BOOST (Better Outcomes for Older adults through Safe Transitions) to help in this effort.32

Unfortunately, there is an inherent problem with all of the above proposals: the assumption that physicians actually want to reduce healthcare spending. Since everyone who works in the medical industry benefits financially in some way from the current high levels of spending on healthcare, reducing spending is counterintuitive for many, and the incentives to spend more will likely persist until some form of spending targets or limits are set.33 Moreover, since physicians traditionally do not like to be told how to practice medicine, history would predict that, without attractive incentives, nothing will change. This is the fundamental and unfortunate dilemma that has apparently pushed us to the eleventh hour of a healthcare crisis.

Another concern with an extreme atmosphere of cost cutting is the risk of swinging too far in the opposite direction, focusing so intently on cost that we begin to compromise quality or access to care in order to achieve spending targets. Reassuringly, however, the data suggest that there is plenty of room for us to cut costs without harming health outcomes.

Despite these obstacles, during this historic time in US healthcare, I believe hospitalists have a unique and perhaps transient opportunity to demonstrate their singular commitment to rational healthcare spending and by doing so to gain significant influence in shaping the impending healthcare reforms. If we speak and act with one voice, with transparency, and with the proper data, we could be the first and only professional society to not only demonstrate our current pattern of spending, but also our potential for reducing spending and our plan on how to get there.

Acknowledgements

Judy Knight, MLS, provided valuable research and technical support.

References
  1. Medicare pay overhaul can no longer wait. American Medical News.2009. Available at: http://www.ama‐assn.org/amednews/2009/01/12/edsa0112.htm. Accessed July 2009.
  2. Keehan S,Sisko A,Truffer C, et al.Health spending projections through 2017: the baby‐boom generation is coming to Medicare.Health Aff (Millwood).2008;27(2):w145w155.
  3. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:380.
  4. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:374.
  5. National Scorecard on U.S. Health System Performance, 2008 Chartpack.New York, NY:The Commonwealth Fund;2008:6.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in medicare spending. Part 1: The content, quality, and accessibility of care.Ann Intern Med.2003;138(4):273287.
  7. Bentley TG,Effros RM,Palar K,Keeler EB.Waste in the U.S. health care system: a conceptual framework.Milbank Q.2008;86(4):629659.
  8. Anderson GF,Reinhardt UE,Hussey PS,Petrosyan V.It's the prices, stupid: why the United States is so different from other countries.Health Aff (Millwood).2003;22(3):89105.
  9. Orszag PR. Health Care and the budget: issues and challenges for reform.2007. Available at: http://www.cbo.gov/ftpdocs/82xx/doc8255/06–21‐HealthCareReform.pdf. Accessed July 2009.
  10. Brownlee S.Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.1st ed.New York, NY:Bloomsbury;2007.
  11. Davis K,Schroen C,Guterman S,Shih T. Slowing the growth of U.S. health care expensitures: what are the options?2007. Available at: http://www.commonwealthfund.org/publications/publications_show.htm?doc_id=449510. Accessed July 2009.
  12. Fuchs V.More variation in use of care, more flat‐of‐the‐curve medicine.Health Aff (Millwood).2004;(Suppl Web Exclusives):VAR104VAR107.
  13. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:419.
  14. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:2532.
  15. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:24.
  16. Kessler D,Summerton N,Graham J.Effects of the medical liability system in Australia, the UK, and the USA.Lancet.2006;368(9531):240246.
  17. Comments on the centers for Medicare and Medicaid services plan to transition to a Medicare value‐based purchasing program for physicians and other professional services.2008. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=Issues_in_the_Spotlight12008:62,73.
  18. Jack B,Chetty V,Anthony D, et al.A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.Ann Intern Med.2009;150(3):178187.
  19. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24(8):971976.
  20. Hospitals like mine: 2006 national statistics.2006. Available at: http://www.hcupnet.ahrq.gov. Accessed July 2009.
  21. Brown MM,Brown GC,Sharma S.Evidence‐Based to Value‐Based Medicine.Chicago, IL:AMA Press;2005.
  22. Improved Availability of Comparative Effectiveness Information: An Essential Feature for a High‐Quality and Efficient United States Health Care System.Philadelphia, PA:American College of Physicians;2008.
  23. Morrison R,Meier D.Clinical practice. Palliative care.N Engl J Med.2004;350(25):25822590.
  24. Payne S,Coyne P,Smith T.The health economics of palliative care.Oncology (Williston Park).2002;16(6):801808; discussion 808, 811–802.
  25. Emanuel E.Cost savings at the end of life. What do the data show?JAMA.1996;275(24):19071914.
  26. Morrison R,Penrod J,Cassel J, et al.Cost savings associated with US hospital palliative care consultation programs.Arch Intern Med.2008;168(16):17831790.
  27. Arrow K,Auerbach A,Bertko J, et al.Toward a 21st‐century health care system: recommendations for health care reform.Ann Intern Med.2009;150(7):493495.
  28. Dressler DD,Pistoria MJ,Budnitz TL,McKean SCW,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1(1):4856.
  29. Mitchell DM.The expanding or shrinking universe of the hospitalist.J Hosp Med.2008;3(4):288291.
  30. Kripalani S,Jackson A,Schnipper J,Coleman E.Promoting effective transitions of care at hospital discharge: a review of key issues for hospitalists.J Hosp Med.2007;2(5):314323.
  31. Project BOOST.2009. Available at: http://www.hospitalmedicine.org/ResourceRoomRedesign/RR_CareTransitions/CT_Home.cfm. Accessed Julyyear="2009"2009.
  32. Marmor T,Oberlander J,White J.The Obama administration's options for health care cost control: hope versus reality.Ann Intern Med.2009;150(7):485489.
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Let's think about what we need to do ourselves. We have to acknowledge that orders we write drive up health care costs.1 AMA President, Nancy H. Nielsen, MD, PhD

As the most prominent providers of inpatient care, hospitalists should be aware that, of the total annual expenditures on US healthcare ($2.3 trillion in 2007),2 approximately one‐third goes to hospital‐based medical care, over one‐half of which (57%) is covered by public funds through Medicare and Medicaid3; this high cost of healthcare is increasingly being blamed for unnecessarily burdening our economy and preventing our industries from being globally competitive. I believe that the high proportion of spending on inpatient care places hospitalists firmly in the center of the debate on how to reduce healthcare costs. It is well known that the United States spends about twice as much per capita as other industrialized countries on healthcare,4 without evidence of superior health outcomes.5 However, it is also known that remarkable local and regional variations in healthcare spending also exist within the US, again, without evidence of superior health outcomes in the higher‐spending regions.6 Both of these observations suggest that we are spending many healthcare dollars on things that evidently do not improve the health of our patients. How much of this waste is administrative, operational, or clinical is debatable and remains the focus of growing national healthcare reform efforts.711 However, from the hospitalist perspective, we should be especially wary of providing so‐called flat‐of‐the‐curve medicine, that is, a level of intensity of care that provides no incremental health benefit.12 The purpose of this editorial is to challenge hospitalists to collectively examine how much of our inpatient spending is potentially unnecessary, and how we, as specialists in inpatient medicine, can assume a critical role in controlling healthcare costs.

To illustrate the issue, consider the following clinical scenario, managed in different ways by different hospitalists, with approximate costs itemized in Table 1. The patient is an elderly woman who presents to the emergency room with syncope occurring at church. The first hospitalist takes time to gather history from the patient, family, eyewitnesses, and the primary care physician, and requests a medication list and outside medical records, which reveal several recent and relevant cardiac and imaging studies. He performs a careful examination, discovers orthostatic hypotension, and his final diagnosis is syncope related to volume depletion from a recently added diuretic as well as a mild gastroenteritis. The patient is rehydrated and discharged home from the emergency room in the care of her family, and asked to hold her diuretic until seen by her family physician in 1 or 2 days. The second hospitalist receives the call from the emergency room and tells the staff to get the patient a telemetry bed. He sees the patient 2 hours later when she gets to the floor. The family has gone home and the mildly demented patient does not recall much of the event or her past medical history. The busy hospitalist constructs a broad differential diagnosis and writes some quick orders to evaluate the patient for possible stroke, seizure, pulmonary embolism, and cardiac ischemia or arrhythmia. He also asks cardiology and neurology to give an opinion. The testing is normal, and the patient is discharged with a cardiac event monitor and an outpatient tilt‐table test scheduled.

Comparison of the Approximate Cost of Evaluating Two Patients for Syncope
Mrs. Syncope #1 Cost Mrs. Syncope #2 Cost
  • NOTE: Akron General Medical Center Patient Price Information List. Available at: http://www.akrongeneral.org/portal/page?=pageid=153,10350167&=dad=portal&_schema=PORTAL. Accessed July 2009.

  • Abbreviations: CBC, complete blood count; CMP, comprehensive metabolic panel; CT, computed tomography; EEG, electroencephalogram; EKG, electrocardiogram; MRI, magnetic resonance imaging.

Level 4 emergency room visit $745 Level 4 emergency room visit $745
Level 4 internal medicine consultation $190 Level 3 history and physical $190
Laboratory evaluation: CBC, CMP, cardiac panel, urinalysis, D‐dimer $843
EKG $150
Head CT $1426
Chest CT angiogram $2120
Brain MRI $3388
Echocardiogram $687
Carotid ultrasound $911
Level 4 neurology consult $190
Subsequent visits day 2, day 3 $150
EEG $520
Level 4 cardiology consult $190
Nuclear stress test $1359
Specialist subsequent visits $150
Telemetry bed, 3 days $3453
Discharge, low‐level $90
Cardiac event monitor $421
Tilt‐table test $1766
$935 $18,749

Although the above scenarios purposely demonstrate 2 extremes of care, I suspect most readers would agree that each hospitalist has his or her own style of practice, and that these differences in style inevitably result in significant differences in the total cost of healthcare delivered. This variation in spending among individual physicians is perhaps more easily understood than the striking variations in healthcare spending seen when different states, regions, and hospitals are compared. For example, annual Medicare spending per beneficiary has varied widely from state to state, from $5436 in Iowa to $7995 in New York (in 2004), a 47% difference.13 Specific analysis of inpatient spending variations is presented in the Dartmouth Atlas of Health Care 2008, which reports healthcare spending in the last 2 years of life for patients with at least 1 chronic illness.14 While the average Medicare inpatient spending per capita for these patients was about $25,000, the state‐specific spending varied widely from $37,040 in New Jersey to $17,135 in Idaho. There was also significant variation in spending within individual states (ie, New York: Binghamton, $18,339; Manhattan, $57,000) and between similar types of hospitals (UCLA Medical Center, $63,900; Massachusetts General Hospital, $43,058). Yet there is no evidence that higher‐spending regions produce better health outcomes.6 Interestingly, the observed differences in spending within the US were primarily due to the volume and intensity of care, not the price of care, as has been seen in some comparisons of the US with other industrialized countries.8, 15 In overall Medicare expenditures, higher‐spending locations tended to have a more inpatient‐based and specialist‐oriented pattern of practice, with higher utilization of inpatient consultations, diagnostic testing, and minor procedures.6

Although the wide variation in spending observed is a bit baffling, the encouraging aspect of this data is that some places are apparently doing it right; that is, providing their patients with a much higher value per healthcare dollar. Ultimately, if the higher‐spending locations modeled the lower‐spending locations, we would have the potential to reduce overall healthcare costs by as much as 30% without harming health.9

What are the possible reasons that we are providing unnecessary care? There are both environment‐dependent and physician‐dependent reasons, which I will outline here. The first 3 reasons represent areas that would seem to require system‐wide change, whereas the remaining 7 reasons are perhaps more amenable to local and/or national hospitalist‐directed efforts.

  • Working in a litigious environment promotes unnecessary testing and consultations with the intent of reducing our exposure to malpractice liability, so‐called defensive medicine.16

  • A reimbursement system that is primarily fee‐for‐service encourages physicians to provide more care and involve more physicians in the care of each patient, with little or no incentive to spend less, a core problem that was recently highlighted in a public Society of Hospital Management (SHM) statement.17

  • The lack of integrated medical record systems promotes waste by leading to duplicate testing, simply because we cannot easily obtain old records to confirm whether tests were previously done. Interestingly, data from the Commonwealth Fund conclude that US physicians order duplicate diagnostic tests (a test repeated within 2 years) at more than twice the rate of Canada and the United Kingdom, while the nation with the lowest rate of duplicate testing, The Netherlands, has the highest rate of electronic medical record use (98%).18

  • Working with patients (or families) with high expectations who insist upon aggressive testing, treatment, and referral to specialists inflates spending, especially if associated with futile and expensive end‐of‐life care.

  • The involvement of one or more specialists may subsequently lead to even more aggressive care ordered by each specialist.

  • The availability and promotion of new technology (diagnostic testing, medical devices, etc.) may prompt us to make use of it simply because it is there, with or without evidence of a health benefit. Our natural curiosity or fascination with information, or our desire to do an overly complete evaluation, works against cost containment.

  • Local trends or traditions within our specific work environment, as suggested by the variability data, may have a strong influence on our individual practice. In such a setting, inadequate knowledge of the cost‐effectiveness of various tests and treatment options likely leads to unnecessary health care spending.

  • A hospitalist work environment in which a high patient load is carried will inevitably result in less time to gather a detailed history and obtain old records or other information that could help narrow a differential diagnosis and minimize unnecessary or duplicate testing.

  • Preventable readmissions resulting from inadequate coordination of care add cost,19 a phenomenon highly dependent on efficient information systems and proper physician‐physician communication.20

  • An overestimation of the need for inpatient evaluation and treatment (vs. outpatient) leads to unnecessary admissions and a longer average length‐of‐stay, each of which add dramatically to total healthcare costs. This is not only dependent on our individual threshold for admitting and discharging patients, but also on our efficiency in diagnosing and treating acute conditions. The fact that the average length‐of‐stay for congestive heart failure admissions, for example, ranges in different regions from 4.9 to 6.1 days (with costs of $9143 and $12,528, respectively)21 is enough to show that there is room for progress.

What joint efforts could be made to minimize unnecessary inpatient spending? The following are my personal opinions and suggestions (Table 2). Most importantly, I believe every physician deserves prompt and accurate feedback regarding their spending patterns, accompanied by valid comparisons to national and local standards, to demonstrate where they stand on the spectrum of healthcare spending. We are currently far behind other industries in our ability, as physicians, to evaluate what we are spending money on, how much, and why. If I knew, for example, that my spending was in the 95th percentile of all hospitalists in community hospitals similar to mine, I would be prompted to investigate where the differences were and why. In an informal survey of hospitalist colleagues, I found that the majority do not receive any data on the costs associated with their care, and are largely unaware of the actual cost of the inpatient tests they commonly order. Developing a secure, user‐friendly database of individual physician spending patterns relative to national and local standards could be a preliminary step, and would likely require a unified effort between government agencies, professional societies, hospitals, and the insurance industry. However, once available, the increased transparency and clarity of spending variations would hopefully prompt introspection and change. In the absence of hard data, however, individual self‐assessment on spending patterns could also be offered through the development of an online simulated case‐based examination in which a physician could gain a general idea of how his evaluation and treatment of a case scenario compares to his hospitalist colleagues, and to what degree each of his clinical decisions affects the overall cost of care. There are many excellent quality improvement tools offered through SHM but none that specifically address the cost of care.

Potential Reasons Hospitalists May Order Unnecessary Tests, Treatments, or Consultations, and the Effect of Potential Solutions on Each Area
Spending Data Guidelines Patient Education Advocacy Professional Development
  • Abbreviations: ✓, indirect influence; ✓✓, direct influence or most likely to succeed.

Defensive medicine ✓✓
Patient expectations ✓✓
Specialist consultations ✓✓
Fee‐for‐service environment ✓✓
Availability of technology ✓✓ ✓✓
Poor access to medical records ✓✓
Local medical culture ✓✓ ✓✓
Insufficient knowledge of evidence‐based guidelines ✓✓ ✓✓
Lack of available value‐based data ✓✓
High patient load ✓✓
Preventable readmissions from poor coordination ✓✓
Overestimation of the need for inpatient care ✓✓ ✓✓

Second, hospitalists need quick access to current evidence‐based guidelines regarding the true clinical value, or cost‐effectiveness, of testing and treatment for common inpatient conditions, including specific admission criteria. A single source or clearinghouse of guidelines, sponsored by SHM, may be particularly helpful, especially if it focuses on clarifying areas of highest variability in inpatient spending. In addition, I believe that, given the critically important interface between emergency medicine and hospital medicine, joint guidelines between the 2 groups would potentially be very helpful in controlling costs by limiting unnecessary admissions. Advocacy for comparative effectiveness research to establish validity in these guidelines will be fundamental22, 23; however, I suspect the common sense question: Will this added cost improve my patient's outcome? also needs to be applied more generously, since many individual clinical scenarios will not likely lend themselves to formal study. For discussion, some sample case scenarios are presented (Table 3).

Clinical Cases Designed to Stimulate Discussion Regarding Potentially Unnecessary Healthcare Costs Generated by Hospitalists
  • Abbreviations: CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CT, computed tomography; DVT, deep vein thrombosis; EKG, electrocardiogram; FEV1, forced expiratory volume in 1 second; INR, international normalized ratio; IV, intravenous; IVC, inferior vena cava; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; pCO2, partial pressure of carbon dioxide; PE, phycoerythrin; pO2, partial pressure of oxygen; UTI, urinary tract infection.

An 82‐year‐old nursing home patient limited to a wheelchair due to severe osteoarthritis presents with new‐onset expressive aphasia and mild right‐sided hemiparesis. Head CT is negative for bleed, but shows an acute left middle cerebral artery infarct. Would your stroke workup include an MRI/MRA of the brain, carotid ultrasound, echocardiogram, and neurology consultation?
A 68‐year‐old with known ischemic cardiomyopathy is admitted with a CHF exacerbation clearly due to medication noncompliance. The last echocardiogram was done 18 months ago and showed an ejection fraction of 20% with moderate to severe mitral regurgitation. Would you order a repeat echocardiogram? Would you consult cardiology?
A 35‐year‐old construction worker presents with sharp chest pain that is partially reproducible on examination, and no other physical findings. Vital signs, EKG, and cardiac markers are normal. The patient had a negative stress test last year. However, his D‐dimer is slightly elevated. Would you order a CT angiogram of the chest? If he had a normal one last month for the same symptoms, would you repeat it? In either case, would you admit him to the hospital?
A 42‐year‐old man presents with chest pain associated with recent cocaine use. His chest pain resolves in the emergency room and his repeat troponin is normal at 6 hours. Would you order a nuclear stress test for the patient? Would your management change if a stress test was normal a year ago? Would you admit him?
A 58‐year‐old man admitted with community‐acquired pneumonia of the right lower lobe has improved clinically with empiric treatment. Before discharge, he asks for a repeat radiograph to make sure it is getting better. Would you comply with the patient's request?
A 68‐year‐old woman who underwent left total knee arthroplasty 2 weeks ago presents with a left proximal DVT. She has no other symptoms and vitals are normal. She has no personal or family history of clotting. Would you admit the patient to the hospital? Would you order a CT angiogram of the chest? Would you order a hypercoagulable workup?
A 43‐year‐old is admitted for atypical chest pain. Serial cardiac enzymes and nuclear stress test are negative. However, his transaminases are elevated at twice the normal upper limits. He takes a statin for dyslipidemia. Would you order further laboratory tests or imaging to evaluate for hepatic disorders or discharge the patient?
A 63‐year‐old receiving chemotherapy for colon cancer with multiple liver metastases presents with new‐onset dyspnea and is found to have a large left‐sided pleural effusion on chest radiograph. You perform a thoracentesis and malignant cells are present. Would you order a chest CT? Would you consult pulmonology and/or thoracic surgery (for chest tube and/or pleurodesis)?
A 78‐year‐old with severe oxygen‐dependent obstructive lung disease (FEV1 of 1.0 L) has a new 1‐cm nodule on his chest radiograph when admitted for a COPD exacerbation. Would you order a chest CT? Would you arrange for a biopsy? Would you consult oncology or pulmonology?
A 45‐year‐old woke up with severe low‐back pain with right‐sided radiculitis after shoveling heavy snow yesterday. He is unable to walk due to pain, but no focal neurologic symptoms are identified on exam. Would you order an MRI of the spine? Would you consult orthopedics?
A 68‐year‐old man on coumadin for chronic atrial fibrillation is incidentally found to have an INR of 6.5 in clinic. He is currently asymptomatic without evidence of bleeding and with normal vital signs. His hemoglobin is 10.1 compared to 10.8 last month. Digital rectal exam results in a hemoccult‐positive smear. Would you admit him to the hospital? Would you give fresh frozen plasma? Would you consult gastroenterology?
A 58‐year old truck driver presents with acute PE, identified on CT angiogram. There is no previous history of DVT. The patient's arterial blood gas shows a pH of 7.45, pCO2 of 35 mmHg, and pO2 of 55 mmHg on room air. The heart rate is 75. Would you order a lower extremity duplex to assess for DVT? Would you ask interventional radiology to place an IVC filter if a DVT was present?
A 26‐year‐old presents with fever, headache, and meningismus. Head CT is normal. Would you perform a bedside spinal tap or send the patient for a fluoroscopically‐guided procedure in radiology?
A 68‐year‐old smoker presents with right‐sided pneumonia with a small parapneumonic effusion. He is afebrile after 24 hours of IV antibiotics and clinically feels much better. Would you order a thoracentesis? If so, would you perform it bedside or send the patient to radiology for an ultrasound‐guided procedure? Would you consult a pulmonologist?
An 82‐year‐old severely demented nursing home resident who has required total care for the past few months presents with dehydration and a sodium of 158 after increasingly poor oral intake. No other illness is identified. Would you begin IV fluids immediately and consider gastrostomy tube placement to maintain adequate hydration at the nursing home or would you contact family to discuss end‐of‐life care goals first? Would your management change if a UTI or pneumonia was diagnosed?

Third, hospitalists could potentially benefit from the development of patient education materials, available through SHM, that address the cost‐effectiveness of common inpatient tests and treatments with the goal of decreasing patient demand for unnecessary testing. Education regarding advanced directives and end‐of‐life care decision‐making could be particularly valuable in minimizing futile care, as it is well‐documented that transitioning to palliative care as soon as it is appropriate reduces healthcare spending greatly during the end‐of‐life period.2427 At the same time, we need to be careful to reassure our patients that we are not trying to ration care, but are instead minimizing the risks and costs for them associated with unnecessary care. In my experience, most patients, if given appropriate time, attention, and education, are willing to accept the final recommendation of their physician.

Fourth, intensified federal and state advocacy in several areas could help reduce spending. For example, advocacy for medical liability reform may reduce the atmosphere of defensive medicine, although I suspect that because old habits die hard, it may take a full generation of decreased liability risk to actually change practice patterns. Advocacy for the development of a national, or at least more uniform, electronic medical record, may decrease duplicate testing and improve efficiency. Advocacy for value‐based reimbursement models may help dampen costs resulting from a predominantly fee‐for‐service environment.28

Fifth, and perhaps most fundamental to the future of our specialty, encouraging the broad professional development of hospitalists as a true specialists in inpatient medicine (based on the SHM Core Competencies,)29 could help minimize the unnecessary costs associated with specialist‐oriented care.6 With the desire to create, in the near future, a formal board‐certification in hospital medicine comes an obligation to develop broad knowledge and broad skill sets that are truly unique to our profession, whereas deferring to a specialist‐oriented pattern of care actually shrinks us down to something less than a traditional internist, rather than a unique entity.30 With our 24/7 focus on inpatient care, we should easily be able to demonstrate our superiority in safety, quality, and efficiency, all of which are closely linked to increased value per healthcare dollar. If, however, our focus is blurred by an overly productivity‐based practice, in which patient volume and procedures take precedence, we will not be able to claim any special value to the system.

Last, supporting efforts to improve coordination of care and transitions of care could reduce costs associated with unnecessary readmissions or posthospital complications. A recent policy statement from several professional societies, including SHM, highlights the importance of these transitions,20, 31 and within the past year, SHM has launched the successful Project BOOST (Better Outcomes for Older adults through Safe Transitions) to help in this effort.32

Unfortunately, there is an inherent problem with all of the above proposals: the assumption that physicians actually want to reduce healthcare spending. Since everyone who works in the medical industry benefits financially in some way from the current high levels of spending on healthcare, reducing spending is counterintuitive for many, and the incentives to spend more will likely persist until some form of spending targets or limits are set.33 Moreover, since physicians traditionally do not like to be told how to practice medicine, history would predict that, without attractive incentives, nothing will change. This is the fundamental and unfortunate dilemma that has apparently pushed us to the eleventh hour of a healthcare crisis.

Another concern with an extreme atmosphere of cost cutting is the risk of swinging too far in the opposite direction, focusing so intently on cost that we begin to compromise quality or access to care in order to achieve spending targets. Reassuringly, however, the data suggest that there is plenty of room for us to cut costs without harming health outcomes.

Despite these obstacles, during this historic time in US healthcare, I believe hospitalists have a unique and perhaps transient opportunity to demonstrate their singular commitment to rational healthcare spending and by doing so to gain significant influence in shaping the impending healthcare reforms. If we speak and act with one voice, with transparency, and with the proper data, we could be the first and only professional society to not only demonstrate our current pattern of spending, but also our potential for reducing spending and our plan on how to get there.

Acknowledgements

Judy Knight, MLS, provided valuable research and technical support.

Let's think about what we need to do ourselves. We have to acknowledge that orders we write drive up health care costs.1 AMA President, Nancy H. Nielsen, MD, PhD

As the most prominent providers of inpatient care, hospitalists should be aware that, of the total annual expenditures on US healthcare ($2.3 trillion in 2007),2 approximately one‐third goes to hospital‐based medical care, over one‐half of which (57%) is covered by public funds through Medicare and Medicaid3; this high cost of healthcare is increasingly being blamed for unnecessarily burdening our economy and preventing our industries from being globally competitive. I believe that the high proportion of spending on inpatient care places hospitalists firmly in the center of the debate on how to reduce healthcare costs. It is well known that the United States spends about twice as much per capita as other industrialized countries on healthcare,4 without evidence of superior health outcomes.5 However, it is also known that remarkable local and regional variations in healthcare spending also exist within the US, again, without evidence of superior health outcomes in the higher‐spending regions.6 Both of these observations suggest that we are spending many healthcare dollars on things that evidently do not improve the health of our patients. How much of this waste is administrative, operational, or clinical is debatable and remains the focus of growing national healthcare reform efforts.711 However, from the hospitalist perspective, we should be especially wary of providing so‐called flat‐of‐the‐curve medicine, that is, a level of intensity of care that provides no incremental health benefit.12 The purpose of this editorial is to challenge hospitalists to collectively examine how much of our inpatient spending is potentially unnecessary, and how we, as specialists in inpatient medicine, can assume a critical role in controlling healthcare costs.

To illustrate the issue, consider the following clinical scenario, managed in different ways by different hospitalists, with approximate costs itemized in Table 1. The patient is an elderly woman who presents to the emergency room with syncope occurring at church. The first hospitalist takes time to gather history from the patient, family, eyewitnesses, and the primary care physician, and requests a medication list and outside medical records, which reveal several recent and relevant cardiac and imaging studies. He performs a careful examination, discovers orthostatic hypotension, and his final diagnosis is syncope related to volume depletion from a recently added diuretic as well as a mild gastroenteritis. The patient is rehydrated and discharged home from the emergency room in the care of her family, and asked to hold her diuretic until seen by her family physician in 1 or 2 days. The second hospitalist receives the call from the emergency room and tells the staff to get the patient a telemetry bed. He sees the patient 2 hours later when she gets to the floor. The family has gone home and the mildly demented patient does not recall much of the event or her past medical history. The busy hospitalist constructs a broad differential diagnosis and writes some quick orders to evaluate the patient for possible stroke, seizure, pulmonary embolism, and cardiac ischemia or arrhythmia. He also asks cardiology and neurology to give an opinion. The testing is normal, and the patient is discharged with a cardiac event monitor and an outpatient tilt‐table test scheduled.

Comparison of the Approximate Cost of Evaluating Two Patients for Syncope
Mrs. Syncope #1 Cost Mrs. Syncope #2 Cost
  • NOTE: Akron General Medical Center Patient Price Information List. Available at: http://www.akrongeneral.org/portal/page?=pageid=153,10350167&=dad=portal&_schema=PORTAL. Accessed July 2009.

  • Abbreviations: CBC, complete blood count; CMP, comprehensive metabolic panel; CT, computed tomography; EEG, electroencephalogram; EKG, electrocardiogram; MRI, magnetic resonance imaging.

Level 4 emergency room visit $745 Level 4 emergency room visit $745
Level 4 internal medicine consultation $190 Level 3 history and physical $190
Laboratory evaluation: CBC, CMP, cardiac panel, urinalysis, D‐dimer $843
EKG $150
Head CT $1426
Chest CT angiogram $2120
Brain MRI $3388
Echocardiogram $687
Carotid ultrasound $911
Level 4 neurology consult $190
Subsequent visits day 2, day 3 $150
EEG $520
Level 4 cardiology consult $190
Nuclear stress test $1359
Specialist subsequent visits $150
Telemetry bed, 3 days $3453
Discharge, low‐level $90
Cardiac event monitor $421
Tilt‐table test $1766
$935 $18,749

Although the above scenarios purposely demonstrate 2 extremes of care, I suspect most readers would agree that each hospitalist has his or her own style of practice, and that these differences in style inevitably result in significant differences in the total cost of healthcare delivered. This variation in spending among individual physicians is perhaps more easily understood than the striking variations in healthcare spending seen when different states, regions, and hospitals are compared. For example, annual Medicare spending per beneficiary has varied widely from state to state, from $5436 in Iowa to $7995 in New York (in 2004), a 47% difference.13 Specific analysis of inpatient spending variations is presented in the Dartmouth Atlas of Health Care 2008, which reports healthcare spending in the last 2 years of life for patients with at least 1 chronic illness.14 While the average Medicare inpatient spending per capita for these patients was about $25,000, the state‐specific spending varied widely from $37,040 in New Jersey to $17,135 in Idaho. There was also significant variation in spending within individual states (ie, New York: Binghamton, $18,339; Manhattan, $57,000) and between similar types of hospitals (UCLA Medical Center, $63,900; Massachusetts General Hospital, $43,058). Yet there is no evidence that higher‐spending regions produce better health outcomes.6 Interestingly, the observed differences in spending within the US were primarily due to the volume and intensity of care, not the price of care, as has been seen in some comparisons of the US with other industrialized countries.8, 15 In overall Medicare expenditures, higher‐spending locations tended to have a more inpatient‐based and specialist‐oriented pattern of practice, with higher utilization of inpatient consultations, diagnostic testing, and minor procedures.6

Although the wide variation in spending observed is a bit baffling, the encouraging aspect of this data is that some places are apparently doing it right; that is, providing their patients with a much higher value per healthcare dollar. Ultimately, if the higher‐spending locations modeled the lower‐spending locations, we would have the potential to reduce overall healthcare costs by as much as 30% without harming health.9

What are the possible reasons that we are providing unnecessary care? There are both environment‐dependent and physician‐dependent reasons, which I will outline here. The first 3 reasons represent areas that would seem to require system‐wide change, whereas the remaining 7 reasons are perhaps more amenable to local and/or national hospitalist‐directed efforts.

  • Working in a litigious environment promotes unnecessary testing and consultations with the intent of reducing our exposure to malpractice liability, so‐called defensive medicine.16

  • A reimbursement system that is primarily fee‐for‐service encourages physicians to provide more care and involve more physicians in the care of each patient, with little or no incentive to spend less, a core problem that was recently highlighted in a public Society of Hospital Management (SHM) statement.17

  • The lack of integrated medical record systems promotes waste by leading to duplicate testing, simply because we cannot easily obtain old records to confirm whether tests were previously done. Interestingly, data from the Commonwealth Fund conclude that US physicians order duplicate diagnostic tests (a test repeated within 2 years) at more than twice the rate of Canada and the United Kingdom, while the nation with the lowest rate of duplicate testing, The Netherlands, has the highest rate of electronic medical record use (98%).18

  • Working with patients (or families) with high expectations who insist upon aggressive testing, treatment, and referral to specialists inflates spending, especially if associated with futile and expensive end‐of‐life care.

  • The involvement of one or more specialists may subsequently lead to even more aggressive care ordered by each specialist.

  • The availability and promotion of new technology (diagnostic testing, medical devices, etc.) may prompt us to make use of it simply because it is there, with or without evidence of a health benefit. Our natural curiosity or fascination with information, or our desire to do an overly complete evaluation, works against cost containment.

  • Local trends or traditions within our specific work environment, as suggested by the variability data, may have a strong influence on our individual practice. In such a setting, inadequate knowledge of the cost‐effectiveness of various tests and treatment options likely leads to unnecessary health care spending.

  • A hospitalist work environment in which a high patient load is carried will inevitably result in less time to gather a detailed history and obtain old records or other information that could help narrow a differential diagnosis and minimize unnecessary or duplicate testing.

  • Preventable readmissions resulting from inadequate coordination of care add cost,19 a phenomenon highly dependent on efficient information systems and proper physician‐physician communication.20

  • An overestimation of the need for inpatient evaluation and treatment (vs. outpatient) leads to unnecessary admissions and a longer average length‐of‐stay, each of which add dramatically to total healthcare costs. This is not only dependent on our individual threshold for admitting and discharging patients, but also on our efficiency in diagnosing and treating acute conditions. The fact that the average length‐of‐stay for congestive heart failure admissions, for example, ranges in different regions from 4.9 to 6.1 days (with costs of $9143 and $12,528, respectively)21 is enough to show that there is room for progress.

What joint efforts could be made to minimize unnecessary inpatient spending? The following are my personal opinions and suggestions (Table 2). Most importantly, I believe every physician deserves prompt and accurate feedback regarding their spending patterns, accompanied by valid comparisons to national and local standards, to demonstrate where they stand on the spectrum of healthcare spending. We are currently far behind other industries in our ability, as physicians, to evaluate what we are spending money on, how much, and why. If I knew, for example, that my spending was in the 95th percentile of all hospitalists in community hospitals similar to mine, I would be prompted to investigate where the differences were and why. In an informal survey of hospitalist colleagues, I found that the majority do not receive any data on the costs associated with their care, and are largely unaware of the actual cost of the inpatient tests they commonly order. Developing a secure, user‐friendly database of individual physician spending patterns relative to national and local standards could be a preliminary step, and would likely require a unified effort between government agencies, professional societies, hospitals, and the insurance industry. However, once available, the increased transparency and clarity of spending variations would hopefully prompt introspection and change. In the absence of hard data, however, individual self‐assessment on spending patterns could also be offered through the development of an online simulated case‐based examination in which a physician could gain a general idea of how his evaluation and treatment of a case scenario compares to his hospitalist colleagues, and to what degree each of his clinical decisions affects the overall cost of care. There are many excellent quality improvement tools offered through SHM but none that specifically address the cost of care.

Potential Reasons Hospitalists May Order Unnecessary Tests, Treatments, or Consultations, and the Effect of Potential Solutions on Each Area
Spending Data Guidelines Patient Education Advocacy Professional Development
  • Abbreviations: ✓, indirect influence; ✓✓, direct influence or most likely to succeed.

Defensive medicine ✓✓
Patient expectations ✓✓
Specialist consultations ✓✓
Fee‐for‐service environment ✓✓
Availability of technology ✓✓ ✓✓
Poor access to medical records ✓✓
Local medical culture ✓✓ ✓✓
Insufficient knowledge of evidence‐based guidelines ✓✓ ✓✓
Lack of available value‐based data ✓✓
High patient load ✓✓
Preventable readmissions from poor coordination ✓✓
Overestimation of the need for inpatient care ✓✓ ✓✓

Second, hospitalists need quick access to current evidence‐based guidelines regarding the true clinical value, or cost‐effectiveness, of testing and treatment for common inpatient conditions, including specific admission criteria. A single source or clearinghouse of guidelines, sponsored by SHM, may be particularly helpful, especially if it focuses on clarifying areas of highest variability in inpatient spending. In addition, I believe that, given the critically important interface between emergency medicine and hospital medicine, joint guidelines between the 2 groups would potentially be very helpful in controlling costs by limiting unnecessary admissions. Advocacy for comparative effectiveness research to establish validity in these guidelines will be fundamental22, 23; however, I suspect the common sense question: Will this added cost improve my patient's outcome? also needs to be applied more generously, since many individual clinical scenarios will not likely lend themselves to formal study. For discussion, some sample case scenarios are presented (Table 3).

Clinical Cases Designed to Stimulate Discussion Regarding Potentially Unnecessary Healthcare Costs Generated by Hospitalists
  • Abbreviations: CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CT, computed tomography; DVT, deep vein thrombosis; EKG, electrocardiogram; FEV1, forced expiratory volume in 1 second; INR, international normalized ratio; IV, intravenous; IVC, inferior vena cava; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; pCO2, partial pressure of carbon dioxide; PE, phycoerythrin; pO2, partial pressure of oxygen; UTI, urinary tract infection.

An 82‐year‐old nursing home patient limited to a wheelchair due to severe osteoarthritis presents with new‐onset expressive aphasia and mild right‐sided hemiparesis. Head CT is negative for bleed, but shows an acute left middle cerebral artery infarct. Would your stroke workup include an MRI/MRA of the brain, carotid ultrasound, echocardiogram, and neurology consultation?
A 68‐year‐old with known ischemic cardiomyopathy is admitted with a CHF exacerbation clearly due to medication noncompliance. The last echocardiogram was done 18 months ago and showed an ejection fraction of 20% with moderate to severe mitral regurgitation. Would you order a repeat echocardiogram? Would you consult cardiology?
A 35‐year‐old construction worker presents with sharp chest pain that is partially reproducible on examination, and no other physical findings. Vital signs, EKG, and cardiac markers are normal. The patient had a negative stress test last year. However, his D‐dimer is slightly elevated. Would you order a CT angiogram of the chest? If he had a normal one last month for the same symptoms, would you repeat it? In either case, would you admit him to the hospital?
A 42‐year‐old man presents with chest pain associated with recent cocaine use. His chest pain resolves in the emergency room and his repeat troponin is normal at 6 hours. Would you order a nuclear stress test for the patient? Would your management change if a stress test was normal a year ago? Would you admit him?
A 58‐year‐old man admitted with community‐acquired pneumonia of the right lower lobe has improved clinically with empiric treatment. Before discharge, he asks for a repeat radiograph to make sure it is getting better. Would you comply with the patient's request?
A 68‐year‐old woman who underwent left total knee arthroplasty 2 weeks ago presents with a left proximal DVT. She has no other symptoms and vitals are normal. She has no personal or family history of clotting. Would you admit the patient to the hospital? Would you order a CT angiogram of the chest? Would you order a hypercoagulable workup?
A 43‐year‐old is admitted for atypical chest pain. Serial cardiac enzymes and nuclear stress test are negative. However, his transaminases are elevated at twice the normal upper limits. He takes a statin for dyslipidemia. Would you order further laboratory tests or imaging to evaluate for hepatic disorders or discharge the patient?
A 63‐year‐old receiving chemotherapy for colon cancer with multiple liver metastases presents with new‐onset dyspnea and is found to have a large left‐sided pleural effusion on chest radiograph. You perform a thoracentesis and malignant cells are present. Would you order a chest CT? Would you consult pulmonology and/or thoracic surgery (for chest tube and/or pleurodesis)?
A 78‐year‐old with severe oxygen‐dependent obstructive lung disease (FEV1 of 1.0 L) has a new 1‐cm nodule on his chest radiograph when admitted for a COPD exacerbation. Would you order a chest CT? Would you arrange for a biopsy? Would you consult oncology or pulmonology?
A 45‐year‐old woke up with severe low‐back pain with right‐sided radiculitis after shoveling heavy snow yesterday. He is unable to walk due to pain, but no focal neurologic symptoms are identified on exam. Would you order an MRI of the spine? Would you consult orthopedics?
A 68‐year‐old man on coumadin for chronic atrial fibrillation is incidentally found to have an INR of 6.5 in clinic. He is currently asymptomatic without evidence of bleeding and with normal vital signs. His hemoglobin is 10.1 compared to 10.8 last month. Digital rectal exam results in a hemoccult‐positive smear. Would you admit him to the hospital? Would you give fresh frozen plasma? Would you consult gastroenterology?
A 58‐year old truck driver presents with acute PE, identified on CT angiogram. There is no previous history of DVT. The patient's arterial blood gas shows a pH of 7.45, pCO2 of 35 mmHg, and pO2 of 55 mmHg on room air. The heart rate is 75. Would you order a lower extremity duplex to assess for DVT? Would you ask interventional radiology to place an IVC filter if a DVT was present?
A 26‐year‐old presents with fever, headache, and meningismus. Head CT is normal. Would you perform a bedside spinal tap or send the patient for a fluoroscopically‐guided procedure in radiology?
A 68‐year‐old smoker presents with right‐sided pneumonia with a small parapneumonic effusion. He is afebrile after 24 hours of IV antibiotics and clinically feels much better. Would you order a thoracentesis? If so, would you perform it bedside or send the patient to radiology for an ultrasound‐guided procedure? Would you consult a pulmonologist?
An 82‐year‐old severely demented nursing home resident who has required total care for the past few months presents with dehydration and a sodium of 158 after increasingly poor oral intake. No other illness is identified. Would you begin IV fluids immediately and consider gastrostomy tube placement to maintain adequate hydration at the nursing home or would you contact family to discuss end‐of‐life care goals first? Would your management change if a UTI or pneumonia was diagnosed?

Third, hospitalists could potentially benefit from the development of patient education materials, available through SHM, that address the cost‐effectiveness of common inpatient tests and treatments with the goal of decreasing patient demand for unnecessary testing. Education regarding advanced directives and end‐of‐life care decision‐making could be particularly valuable in minimizing futile care, as it is well‐documented that transitioning to palliative care as soon as it is appropriate reduces healthcare spending greatly during the end‐of‐life period.2427 At the same time, we need to be careful to reassure our patients that we are not trying to ration care, but are instead minimizing the risks and costs for them associated with unnecessary care. In my experience, most patients, if given appropriate time, attention, and education, are willing to accept the final recommendation of their physician.

Fourth, intensified federal and state advocacy in several areas could help reduce spending. For example, advocacy for medical liability reform may reduce the atmosphere of defensive medicine, although I suspect that because old habits die hard, it may take a full generation of decreased liability risk to actually change practice patterns. Advocacy for the development of a national, or at least more uniform, electronic medical record, may decrease duplicate testing and improve efficiency. Advocacy for value‐based reimbursement models may help dampen costs resulting from a predominantly fee‐for‐service environment.28

Fifth, and perhaps most fundamental to the future of our specialty, encouraging the broad professional development of hospitalists as a true specialists in inpatient medicine (based on the SHM Core Competencies,)29 could help minimize the unnecessary costs associated with specialist‐oriented care.6 With the desire to create, in the near future, a formal board‐certification in hospital medicine comes an obligation to develop broad knowledge and broad skill sets that are truly unique to our profession, whereas deferring to a specialist‐oriented pattern of care actually shrinks us down to something less than a traditional internist, rather than a unique entity.30 With our 24/7 focus on inpatient care, we should easily be able to demonstrate our superiority in safety, quality, and efficiency, all of which are closely linked to increased value per healthcare dollar. If, however, our focus is blurred by an overly productivity‐based practice, in which patient volume and procedures take precedence, we will not be able to claim any special value to the system.

Last, supporting efforts to improve coordination of care and transitions of care could reduce costs associated with unnecessary readmissions or posthospital complications. A recent policy statement from several professional societies, including SHM, highlights the importance of these transitions,20, 31 and within the past year, SHM has launched the successful Project BOOST (Better Outcomes for Older adults through Safe Transitions) to help in this effort.32

Unfortunately, there is an inherent problem with all of the above proposals: the assumption that physicians actually want to reduce healthcare spending. Since everyone who works in the medical industry benefits financially in some way from the current high levels of spending on healthcare, reducing spending is counterintuitive for many, and the incentives to spend more will likely persist until some form of spending targets or limits are set.33 Moreover, since physicians traditionally do not like to be told how to practice medicine, history would predict that, without attractive incentives, nothing will change. This is the fundamental and unfortunate dilemma that has apparently pushed us to the eleventh hour of a healthcare crisis.

Another concern with an extreme atmosphere of cost cutting is the risk of swinging too far in the opposite direction, focusing so intently on cost that we begin to compromise quality or access to care in order to achieve spending targets. Reassuringly, however, the data suggest that there is plenty of room for us to cut costs without harming health outcomes.

Despite these obstacles, during this historic time in US healthcare, I believe hospitalists have a unique and perhaps transient opportunity to demonstrate their singular commitment to rational healthcare spending and by doing so to gain significant influence in shaping the impending healthcare reforms. If we speak and act with one voice, with transparency, and with the proper data, we could be the first and only professional society to not only demonstrate our current pattern of spending, but also our potential for reducing spending and our plan on how to get there.

Acknowledgements

Judy Knight, MLS, provided valuable research and technical support.

References
  1. Medicare pay overhaul can no longer wait. American Medical News.2009. Available at: http://www.ama‐assn.org/amednews/2009/01/12/edsa0112.htm. Accessed July 2009.
  2. Keehan S,Sisko A,Truffer C, et al.Health spending projections through 2017: the baby‐boom generation is coming to Medicare.Health Aff (Millwood).2008;27(2):w145w155.
  3. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:380.
  4. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:374.
  5. National Scorecard on U.S. Health System Performance, 2008 Chartpack.New York, NY:The Commonwealth Fund;2008:6.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in medicare spending. Part 1: The content, quality, and accessibility of care.Ann Intern Med.2003;138(4):273287.
  7. Bentley TG,Effros RM,Palar K,Keeler EB.Waste in the U.S. health care system: a conceptual framework.Milbank Q.2008;86(4):629659.
  8. Anderson GF,Reinhardt UE,Hussey PS,Petrosyan V.It's the prices, stupid: why the United States is so different from other countries.Health Aff (Millwood).2003;22(3):89105.
  9. Orszag PR. Health Care and the budget: issues and challenges for reform.2007. Available at: http://www.cbo.gov/ftpdocs/82xx/doc8255/06–21‐HealthCareReform.pdf. Accessed July 2009.
  10. Brownlee S.Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.1st ed.New York, NY:Bloomsbury;2007.
  11. Davis K,Schroen C,Guterman S,Shih T. Slowing the growth of U.S. health care expensitures: what are the options?2007. Available at: http://www.commonwealthfund.org/publications/publications_show.htm?doc_id=449510. Accessed July 2009.
  12. Fuchs V.More variation in use of care, more flat‐of‐the‐curve medicine.Health Aff (Millwood).2004;(Suppl Web Exclusives):VAR104VAR107.
  13. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:419.
  14. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:2532.
  15. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:24.
  16. Kessler D,Summerton N,Graham J.Effects of the medical liability system in Australia, the UK, and the USA.Lancet.2006;368(9531):240246.
  17. Comments on the centers for Medicare and Medicaid services plan to transition to a Medicare value‐based purchasing program for physicians and other professional services.2008. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=Issues_in_the_Spotlight12008:62,73.
  18. Jack B,Chetty V,Anthony D, et al.A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.Ann Intern Med.2009;150(3):178187.
  19. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24(8):971976.
  20. Hospitals like mine: 2006 national statistics.2006. Available at: http://www.hcupnet.ahrq.gov. Accessed July 2009.
  21. Brown MM,Brown GC,Sharma S.Evidence‐Based to Value‐Based Medicine.Chicago, IL:AMA Press;2005.
  22. Improved Availability of Comparative Effectiveness Information: An Essential Feature for a High‐Quality and Efficient United States Health Care System.Philadelphia, PA:American College of Physicians;2008.
  23. Morrison R,Meier D.Clinical practice. Palliative care.N Engl J Med.2004;350(25):25822590.
  24. Payne S,Coyne P,Smith T.The health economics of palliative care.Oncology (Williston Park).2002;16(6):801808; discussion 808, 811–802.
  25. Emanuel E.Cost savings at the end of life. What do the data show?JAMA.1996;275(24):19071914.
  26. Morrison R,Penrod J,Cassel J, et al.Cost savings associated with US hospital palliative care consultation programs.Arch Intern Med.2008;168(16):17831790.
  27. Arrow K,Auerbach A,Bertko J, et al.Toward a 21st‐century health care system: recommendations for health care reform.Ann Intern Med.2009;150(7):493495.
  28. Dressler DD,Pistoria MJ,Budnitz TL,McKean SCW,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1(1):4856.
  29. Mitchell DM.The expanding or shrinking universe of the hospitalist.J Hosp Med.2008;3(4):288291.
  30. Kripalani S,Jackson A,Schnipper J,Coleman E.Promoting effective transitions of care at hospital discharge: a review of key issues for hospitalists.J Hosp Med.2007;2(5):314323.
  31. Project BOOST.2009. Available at: http://www.hospitalmedicine.org/ResourceRoomRedesign/RR_CareTransitions/CT_Home.cfm. Accessed Julyyear="2009"2009.
  32. Marmor T,Oberlander J,White J.The Obama administration's options for health care cost control: hope versus reality.Ann Intern Med.2009;150(7):485489.
References
  1. Medicare pay overhaul can no longer wait. American Medical News.2009. Available at: http://www.ama‐assn.org/amednews/2009/01/12/edsa0112.htm. Accessed July 2009.
  2. Keehan S,Sisko A,Truffer C, et al.Health spending projections through 2017: the baby‐boom generation is coming to Medicare.Health Aff (Millwood).2008;27(2):w145w155.
  3. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:380.
  4. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:374.
  5. National Scorecard on U.S. Health System Performance, 2008 Chartpack.New York, NY:The Commonwealth Fund;2008:6.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in medicare spending. Part 1: The content, quality, and accessibility of care.Ann Intern Med.2003;138(4):273287.
  7. Bentley TG,Effros RM,Palar K,Keeler EB.Waste in the U.S. health care system: a conceptual framework.Milbank Q.2008;86(4):629659.
  8. Anderson GF,Reinhardt UE,Hussey PS,Petrosyan V.It's the prices, stupid: why the United States is so different from other countries.Health Aff (Millwood).2003;22(3):89105.
  9. Orszag PR. Health Care and the budget: issues and challenges for reform.2007. Available at: http://www.cbo.gov/ftpdocs/82xx/doc8255/06–21‐HealthCareReform.pdf. Accessed July 2009.
  10. Brownlee S.Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.1st ed.New York, NY:Bloomsbury;2007.
  11. Davis K,Schroen C,Guterman S,Shih T. Slowing the growth of U.S. health care expensitures: what are the options?2007. Available at: http://www.commonwealthfund.org/publications/publications_show.htm?doc_id=449510. Accessed July 2009.
  12. Fuchs V.More variation in use of care, more flat‐of‐the‐curve medicine.Health Aff (Millwood).2004;(Suppl Web Exclusives):VAR104VAR107.
  13. Health, United States, 2007: Chartbook on Trends in the Health of Americans.Hyattsville, MD:National Center for Health Statistics;2007:419.
  14. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:2532.
  15. Wennberg JE,Fisher ES.Tracking the Care of Patients with Severe Chronic Illness: The Dartmouth Atlas of Health Care 2008.Lebanon, NH:Dartmouth Institute for Health Policy and Clinical Practice, Center for Health Policy Research;2008:24.
  16. Kessler D,Summerton N,Graham J.Effects of the medical liability system in Australia, the UK, and the USA.Lancet.2006;368(9531):240246.
  17. Comments on the centers for Medicare and Medicaid services plan to transition to a Medicare value‐based purchasing program for physicians and other professional services.2008. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=Issues_in_the_Spotlight12008:62,73.
  18. Jack B,Chetty V,Anthony D, et al.A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.Ann Intern Med.2009;150(3):178187.
  19. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24(8):971976.
  20. Hospitals like mine: 2006 national statistics.2006. Available at: http://www.hcupnet.ahrq.gov. Accessed July 2009.
  21. Brown MM,Brown GC,Sharma S.Evidence‐Based to Value‐Based Medicine.Chicago, IL:AMA Press;2005.
  22. Improved Availability of Comparative Effectiveness Information: An Essential Feature for a High‐Quality and Efficient United States Health Care System.Philadelphia, PA:American College of Physicians;2008.
  23. Morrison R,Meier D.Clinical practice. Palliative care.N Engl J Med.2004;350(25):25822590.
  24. Payne S,Coyne P,Smith T.The health economics of palliative care.Oncology (Williston Park).2002;16(6):801808; discussion 808, 811–802.
  25. Emanuel E.Cost savings at the end of life. What do the data show?JAMA.1996;275(24):19071914.
  26. Morrison R,Penrod J,Cassel J, et al.Cost savings associated with US hospital palliative care consultation programs.Arch Intern Med.2008;168(16):17831790.
  27. Arrow K,Auerbach A,Bertko J, et al.Toward a 21st‐century health care system: recommendations for health care reform.Ann Intern Med.2009;150(7):493495.
  28. Dressler DD,Pistoria MJ,Budnitz TL,McKean SCW,Amin AN.Core competencies in hospital medicine: development and methodology.J Hosp Med.2006;1(1):4856.
  29. Mitchell DM.The expanding or shrinking universe of the hospitalist.J Hosp Med.2008;3(4):288291.
  30. Kripalani S,Jackson A,Schnipper J,Coleman E.Promoting effective transitions of care at hospital discharge: a review of key issues for hospitalists.J Hosp Med.2007;2(5):314323.
  31. Project BOOST.2009. Available at: http://www.hospitalmedicine.org/ResourceRoomRedesign/RR_CareTransitions/CT_Home.cfm. Accessed Julyyear="2009"2009.
  32. Marmor T,Oberlander J,White J.The Obama administration's options for health care cost control: hope versus reality.Ann Intern Med.2009;150(7):485489.
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Heart Failure Program Readmissions

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The paradox of readmission: Effect of a quality improvement program in hospitalized patients with heart failure

Congestive heart failure (CHF) is a common disease with high mortality and morbidity.1, 2 Better physiological understanding has led to significant advances in therapy in recent years, with synthesis of this evidence into widely available treatment guidelines.3, 4 However, patients who have had an acute hospitalization with heart failure continue to have a high rate of symptomatic relapse, with up to 25% readmitted within 3 months.2 One of the major challenges in heart failure therapy is to avert these relapses to prevent hospital readmission.

Angiotensin‐converting enzyme (ACE) inhibitors, beta‐blockers, and spironolactone have promised a reduction in hospitalization rates as well as mortality; however, suboptimal prescribing5 and adherence to therapy6, 7 may limit their anticipated benefits. This has led to interest in improved systems of care to reduce hospital utilization. Such approaches have included improved systems for optimizing medications,68 comprehensive discharge planning and postdischarge support,914 and self‐management and case management strategies1517 to enhance patient participation in care.

Combinations of these strategies are known as disease management programs (DMPs), and trials of such combination strategies to improve patient outcomes have been promising.1823 Recognized features4 include skilled multidisciplinary team care; individualized guideline‐based treatment plans that may include dietary and exercise programs as well as optimal pharmacological therapy; patient education and self‐management strategies; improved integration between hospital and community care providers; vigilant follow‐up including prompt review after hospitalization; ready access to expert assessment in the event of deterioration; and regular monitoring with expert titration of therapy, through clinics, home visits, or telemonitoring. Several randomized controlled trials have suggested that DMPs may reduce heart failure‐related9, 1517 and all‐cause9, 10 readmissions. Meta‐analyses12, 1823 have demonstrated reduction in risk of all‐cause readmission of 12% to 25% as well as a reduction in mortality of 14% to 25%.

Trials of DMPs have generally involved careful participant selection, and differences in methods and outcome reporting have led some reviewers to be circumspect in their interpretation of the impact of these programs on readmission rates.23 A large, real‐world quality improvement program conducted as part of the Royal Australasian College of Physicians Clinical Support Systems Project provided an opportunity to measure whether a multifaceted program targeting a representative group of patients with CHF and their healthcare providers could reduce readmission rates. As previously published, this program delivered measurable improvements in processes of care including evidence‐based prescribing, adherence, multidisciplinary involvement, and discharge communication, associated with a reduction in 12‐month mortality.24

Objective

The Brisbane Cardiac Consortium sought to improve processes of care for patients with CHF by using evidence‐based strategies targeting patients and their healthcare providers to optimize uptake of management guidelines, improve discharge processes between hospital and primary care, and increase patient participation in care. We hypothesized that the program would reduce hospital readmissions in the intervention patients in the first 12 months following discharge.

Methods

Setting

The program was conducted in 3 metropolitan public teaching hospitals in Brisbane, Australia (Royal Brisbane, Princess Alexandra, and Queen Elizabeth II Hospitals) and their associated Divisions of General Practice, targeting the hospital and posthospital care of patients with CHF.

Design

The study was a prospective time series study. Consecutive participants were enrolled continuously between October 1, 2000 and August 31, 2002. Interventions were introduced progressively as systems matured. For evaluation purposes, we predefined a baseline cohort (October 1, 2000 to April 17, 2001) who were admitted prior to implementation of any interventions, and an intervention cohort (February 15, 2002 to August 31, 2002) who were admitted after all interventions were mature. The study was approved by the Ethics Committees of all participating institutions.

Participants

All patients with a recorded clinical diagnosis of CHF within 48 hours of hospital presentation, and evidence of at least 2 supporting clinical signs (raised jugular venous pressure, third or fourth heart sounds, bilateral chest crackles, dependent edema, or cardiomegaly and/or pulmonary edema on chest x‐ray) were identified prospectively by trained research nurses. Patients were ineligible for reevaluation if they had already been enrolled in the study. Detailed data were abstracted from the medical record including demographics, illness characteristics, and comorbid conditions.

Interventions

Provider‐directed Interventions

Provider‐directed interventions aimed to improve clinician compliance with agreed management guidelines using decision support tools, reminders, education and academic detailing, and regular performance feedback. These interventions were delivered by project staff and local clinical leaders and were directed toward both hospital clinicians (internists and cardiologists) and general practitioners providing community care.

Patient‐directed Interventions

Patient‐directed interventions included written evidence‐based patient education, pharmacist discharge medication review and inpatient education, and patient diaries. Comprehensive discharge summaries including target‐directed management plans were provided to the general practitioner and community pharmacist.

Participants were considered suitable for more intensive posthospital intervention and follow‐up if they: (1) did not have cognitive impairment or psychiatric illness which would preclude participation in self‐care; (2) did not have a life expectancy due to comorbidities estimated to be less than 6 months; (3) had a stable residence in the community where they could be contacted by telephone; (4) attended a general practitioner within the greater Brisbane area; and (5) consented to more detailed follow‐up. In the baseline phase, this intensive group was contacted by nursing staff at 1, 3, 6, and 12 months for data collection purposes; in the intervention phase, these participants received enhanced predischarge pharmacist education; postdischarge pharmacist telephone follow‐up of medication understanding and adherence; telephone reminders from project nursing staff at 1, 3, 6, and 12 months to attend their general practitioner; and individualized, written, guideline‐based reminders sent to participating general practitioners.

Measures and Analysis

The primary outcome measure was all‐cause hospital readmission over 12 months. Secondary outcomes included 12‐month all‐cause mortality, 12‐month readmissions due to CHF, total hospital days, and the combined endpoint of death or readmission (ie, readmission‐free survival) at 12 months.

Readmission data were obtained from the Queensland Health Information Centre by matching patient data with the Queensland Hospital Admitted Patient Data Collection. Admission to any Queensland hospital is captured in this database. Readmission was defined as due to CHF (same‐cause) if a principal diagnosis code from ICD‐10‐AM code chapter I50 was assigned. Mortality data were obtained from the Australian Institute of Health and Welfare (AIHW) National Death Index.

Processes of inpatient care were collected by trained research nurses using a standardized structured chart abstraction tool. Data items were based on guideline recommendations for patient assessment, investigation, and management.

All analyses were conducted using SAS version for Windows 9.1 (SAS Institute, Cary, NC). Baseline and intervention patient characteristics were compared using independent samples t test for continuous variables and contingency tables with chi‐square tests for proportions.

Logistic regression models adjusted for hospital and posthospital intensity (considered to be significant potential confounders) were used to test the strength of association between the intervention and readmission (or death and readmission); Cox proportional hazards model was used to assess the time to first readmission or death. A Wilcoxon 2‐sample test was used to compare total number of days in hospital over the 12‐month follow‐up period, as these data were highly positively skewed; means rather than medians are reported, as the median was 0 in each group and hence uninformative. Frequency of readmission was compared using Poisson regression adjusted for hospital. A P value of 0.05 was considered significant in all analyses.

Preliminary analysis revealed a number of differences in baseline clinical characteristics between the 2 groups. To account for measured differences other than hospital and intervention intensity, propensity scores (the conditional probability of assignment to a particular treatment group given a vector of observed covariates) were developed using a logistic model with the control or intervention group as the dependent variable and baseline patient characteristic variables with P < 0.2 (as shown in Table 1) as the independent variables. The equation obtained from this model was used to estimate a propensity score for each patient. These scores along with hospital and intervention intensity were then used to provide estimates adjusted for baseline differences between the control and intervention groups.25

Characteristics of Baseline and Intervention Participants
CharacteristicBaseline (n = 197)Intervention (n = 219)P Value
  • Abbreviations: CHF, congestive heart failure; LVEF, left ventricular ejection fraction; NYHA, New York Hospital Association.

Hospital, n (%)  0.001
175 (38)100 (46) 
240 (20)17 (8) 
382 (42)102 (46) 
Age (years), mean (range)75 (24‐100)78 (32‐102)0.059
Female, n (%)103 (52)118 (54)0.74
Hostel resident, n (%)15 (8)38 (17)<0.01
Previous CHF admission, n (%)52 (26)26 (12)<0.01
Contributing factors, n (%)   
Hypertension104 (53)139 (63)0.027
Coronary disease107 (54)118 (54)0.93
Valvular disease20 (10)45 (21)<0.01
Cardiomyopathy29 (15)33 (15)0.92
NYHA class III/IV, n (%)143 (73)155 (71)0.68
Atrial fibrillation, n (%)65 (33)78 (36)0.57
LVEF % (mean)24280.10
Cardiologist care, n (%)42 (21)61 (28)0.12
Comorbidity score2.6 (1,8)2.7 (1,10)0.52

Results

There were 220 patients identified with a clinical diagnosis of CHF during the baseline period, and 235 during the intervention period. Figure 1 shows ascertainment, in‐hospital mortality, and eligibility rates for the 2 cohorts. Eighty‐nine (45%) of baseline patients and 76 (35%) of intervention patients received intensive posthospital follow‐up as described above. Information on readmission was available for 197 baseline patients and 219 intervention patients discharged alive; this is the sample used for all analyses in this report. Table 1 shows the demographic and clinical characteristics of these patients. Table 2 summarizes the previously reported improvements in processes of care.

Figure 1
Flow diagram for participant enrollment. Baseline (control) cohort: consecutive patients with CHF admitted to study hospitals October 1, 2000 to April 17, 2001. Intervention cohort: consecutive patients with CHF admitted to study hospitals February 15, 2002 to August 31, 2002; 7 participants were excluded because they were unable to be matched to readmission datasets.
Processes of Inpatient Care for Baseline and Intervention Cohort
Process indicatorBaseline (n = 220) [n (%)>]Intervention (n = 235) [n (%)]P Value
  • Abbreviations: ACE, angiotensin converting enzyme; DVT, deep vein thrombosis.

  • Denominator is patients discharged alive and not transferred to another facility; n = 191.

  • Denominator is patients discharged alive and not transferred to another facility; n = 219.

Assessment of reversible triggers166 (75)211 (90)<0.001
DVT prophylaxis57 (26)148 (63)<0.001
Imaging of left ventricular function135 (61)164 (70)0.002
Scheduled outpatient visit within 30 days87 (46)*130 (59)0.005
ACE inhibitor prescription at discharge136 (71)*163 (74)0.46
Beta‐blocker prescription at discharge61 (32)*113 (52)<0.001
Avoid deleterious agents at discharge180 (94)*214 (98)0.79

Duing the 12‐month follow‐up, 107 (49%) of intervention patients were readmitted to the hospital compared to 71 (36%) of control patients, representing a 1.7‐fold increase in the adjusted probability of readmission in the intervention group (odds ratio [OR] = 1.71, 95% confidence interval [CI] = 1.14‐2.56; P = 0.009). As shown in Table 3, this was partly balanced by a trend toward reduced post‐hospital mortality, such that no significant difference was seen in readmission‐free survival.

Readmission and Death Rates
 Baseline (%)Intervention (%)OR (95% CI)P Value
  • Abbreviations: CI, confidence interval; OR, odds ratio.

  • Estimates adjusted for hospital and intervention intensity.

  • Estimates adjusted for hospital, intervention intensity, and propensity score.

Readmitted within 12 months71/197 (36)107/219 (49)1.71* (1.14, 2.56); 1.90 (1.24, 2.91)0.009; 0.004
Death within 12 months59/197 (30)53/219 (24)0.68* (0.44, 1.07)0.099
Death or readmission within 12 months104/197 (53)133/219 (61)1.30* (0.87, 1.93); 1.36 (0.89, 2.08)0.20; 0.15

Time‐to‐event analysis (Figures 2 and 3) demonstrated similar findings, with a significant reduction in time to first readmission in the intervention group (adjusted hazard ratio [HR] = 1.43; 95% CI = 1.04‐1.97; P = 0.046) but no difference in time to death or first readmission (adjusted HR = 1.14; 95% CI = 0.86‐1.46; P = 0.36).

Figure 2
Time to first hospital readmission.
Figure 3
Time to death or first hospital readmission.

There was a trend to increased readmissions attributed to heart failure: 47 (21.5%) of intervention patients compared to 33 (16.7%) in the baseline group (OR = 1.30; 95% CI = 0.87‐1.93; P = 0.20). No significant difference was demonstrated in the frequency of readmissions (average 0.75 admission per participant per year in baseline, compared to 0.93 intervention; P = 0.32) nor the mean number of days in hospital in 12 months subsequent to the index admission (5.9 in the baseline group compared to 6.5 in the intervention group; P = 0.1).

Subgroup analysis by intervention intensity showed similar results, with 42 of 76 (55.3%) intensive group participants in the intervention group and 36 of 89 (40.4%) in the baseline group requiring hospital readmission within 12 months. The HR for death or readmission was estimated to be 1.27 (95% CI = 0.85‐1.9).

Discussion

In this study, heart failure patients who received a multidisciplinary intervention (including inpatient education, self‐management support, improved timely medical follow‐up, and better integration between hospital and primary care) showed a trend to improved 1‐year post‐hospital survival, but this appeared to be at the cost of increased readmissions among survivors. This occurred despite our previously reported improved optimization of pharmacological therapy both in‐hospital and posthospital with this program.18

There are a number of potential explanations for this finding, which have important implications for adoption of disease management programs. First, the intervention may not have been of sufficient intensity. Programs primarily aimed at educating providers and patients in evidence‐based guidelines, without structured postdischarge support, have not always improved clinical outcomes.26 In our study, general practitioners were supported to provide improved postdischarge care to their CHF patients, but direct postdischarge patient support was only provided to consenting patients and was limited in scope. There is still some debate about which elements of successful DMPs are most important for efficacy. Most authorities support the central importance of medication optimization, intensive education, and self‐care support. Taylor et al.23 found stronger evidence for programs using individual case management or outreach rather than clinic‐based interventions. Yu et al.27 concluded that outpatient drug titration and ready access to specialist review were factors contributing to success. In our program, even the more intensive intervention did not include regular clinical review by specialist nurses, a system for rapid review in the event of deterioration or supervised drug titration protocols. Furthermore, strategies which prompted more frequent primary care review and improved patient, carer, and general practitioner recognition of disease deterioration may have provided more opportunities to initiate readmission, especially in the absence of an alternative care pathway such as rapid‐access clinics or outreach services.28

Second, this study may reflect the reality of generalizing randomized controlled trial data to an unselected population. Many trials enrolled patients with high anticipated event rates but excluded patients with complex comorbidities, poor life expectancy, and cognitive impairment. Such studies enrolled a high‐risk population (10%‐48% of screened patients randomized) who had a relatively high readmission rate (50%‐60% at 6‐12 months) compared to our unselected population. These studies may overstate the benefits of applying heart failure DMPs in an unselected population. Galbreath et al.29 enrolled a self‐selected community sample of heart failure patients into a disease management program incorporating education, self‐management, telephone support, and advice to primary care providers and home health providers. Like our model, they demonstrated a survival benefit in the intervention group but no reduction in hospital or other healthcare utilization.

Third, only about one‐half of the readmissions were due to heart failure, again reflecting the complexity of this real‐world patient group. Interventions that focus on a single disease in patients with complex comorbidities might be expected to have only limited impact on their subsequent healthcare needs.

Fourth, findings may reflect differences in patient characteristics between the 2 cohorts. While statistical adjustment for measured differences did not have any significant impact on results, unmeasured patient characteristics may have introduced bias. The beforeafter nature of the study also raises the possibility that temporal trends in care practices influenced patient outcomes, such as changing patterns of drug and device therapies. There is conflicting evidence in the literature regarding trends in CHF readmission rates,3032 but it is possible that health system factors external to the study contributed to a higher readmission rate in the later cohort.

Finally, there was a trend toward reduction in mortality within the intervention cohort. These additional survivors might be expected to have more advanced heart failure or other comorbid disease, and therefore may have been more susceptible to deterioration and the need for inpatient care.

Conclusions

We acknowledge the weaknesses inherent in this nonrandomized study design, including convenience sampling, measured and unmeasured confounders and temporal trends in processes and systems of care. Nonetheless, this real world study suggests a note of caution in the widespread enthusiasm for chronic disease management programs. A complex bundle of interventions that resulted in measurable improvements in adherence to evidence‐based guidelines, discharge processes, integration between care providers, and patient education appeared to prolong life expectancy but increase hospital utilization. Mortality reduction in an incurable chronic disease such as heart failure will increase the burden of disease (and therefore treatment costs) unless treatments concurrently reduce disability and the frequency of symptomatic relapse.33 Whether this balance is achieved will depend on patient selection and the intensity and/or components of the intervention. These factors have not been fully defined in the literature to date.

Our study suggests that a widely applied, discharge‐focused intervention which primarily augmented the CHF management knowledge of care providers and patients, and enhanced attendance within the existing care model of primary care and internal medicine/cardiology outpatient services, improved the quality of care and may have reduced mortality at the cost of higher hospital utilization. It raises questions about whether a disease management service can achieve the uncertain promise of reduced readmissions in a cost‐effective manner outside of a high‐risk experimental population.

Acknowledgements

The authors acknowledge the contribution of the advisory and working groups of the Brisbane Cardiac Consortium. The authors appreciate the support of clinicians from the Internal Medicine, Cardiology, and Pharmacy Departments of the participating hospitals as well as staff from the Brisbane North and Brisbane Inner South Divisions of General Practice. The authors are grateful for the efforts of the staff of the PAH Clinical Services Evaluation Unit and the RBWH Internal Medicine Research Unit for data collection and data management; and the Queensland Health Information Centre and Australian Institute of Health and Welfare (AIHW) National Death Index for data matching.

References
  1. Stewart S,MacIntyre K,Hole DJ,Capewell S,McMurray JJ.More ‘malignant’ than cancer? Five‐year survival following a first admission with heart failure.Eur J Heart Fail.2001;3:315322.
  2. Cleland JG,Swedberg K,Follath F, et al.;Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology The EuroHeart Failure survey programme—a survey on the quality of care among patients with heart failure in Europe.Part 1: patient characteristics and diagnosis.Eur Heart J.2003;24(5):442463.
  3. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel.Guidelines for management of patients with chronic heart failure in Australia.Med J Aust.2001;174:459466.
  4. Swedberg K,Cleland J,Dargie H.Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology.Eur Heart J.2005;26(11):11151140.
  5. Scott IA,Denaro CP,Flores JL, et al.Quality of care of patients hospitalized with congestive heart failure.Intern Med J.2003;33(4):140151.
  6. Lappe JM,Muhlestein JB,Lappe DL, et al.Improvements in 1‐year cardiovascular clinical outcomes associated with a hospital‐based discharge medication program.Ann Intern Med.2004;141(6):446453.
  7. Gattis WA,Hasselblad V,Whellan DJ,O'Connor CM.Reduction in heart failure events by the addition of a clinical pharmacist to the heart failure management team.Arch Intern Med.1999;159(16):19391945.
  8. Rainville EC.Impact of pharmacist interventions on hospital readmissions for heart failure.Am J Health Syst Pharm.1999;56:13391342.
  9. Stewart S,Marley JE,Horowitz JD.Effects of a multidisciplinary, home‐based intervention on unplanned readmissions and survival among patients with chronic congestive heart failure: a randomised controlled study.Lancet.1999;354:10771083.
  10. Rich MW,Beckham V,Wittenberg C,Leven C,Freedlane KE,Carney RM.A multidisciplinary intervention to prevent the readmission of elderly patients with congestive heart failure.N Engl J Med.1995;333(18):11901195.
  11. Stewart S,Horowitz JD.Home‐based intervention in congestive heart failure. Long‐term implications on readmission and survival.Circulation.2002;105(24):28612866.
  12. Phillips CO,Wright SM,Kern DE,Singa RM,Shepperd S,Rubin HR.Comprehensive discharge planning with postdischarge support for older patients with congestive heart failure. A meta‐analysis.JAMA.2004;291(11):13581367.
  13. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders. A randomized clinical trial.JAMA.1999;281(7):613620.
  14. Harrison MB,Browne GB,Roberts J,Tugwell P,Gafni A,Graham ID.Quality of life of individuals with heart failure. A randomized trial of the effectiveness of two models of hospital‐to‐home transition.Med Care.2002;40(4):271282.
  15. Blue L,Lang E,McMurray JJV, et al.Randomised controlled trial of specialist nurse intervention in heart failure.BMJ.2001;323(7315):715718.
  16. Riegel B,Carlson B,Kopp Z,LePetrie B,Glaser D,Unger A.Effect of a standardised nurse case‐management telephone intervention on resource use in patients with chronic heart failure.Arch Intern Med.2002;162:705712.
  17. Krumholz H,Amatruda J,Smith G,Mattera JA,Roumanis SA,Radford MJ.Randomized trial of an education and support intervention to prevent readmission of patients with heart failure.J Am Coll Cardiol.2002;39:8389.
  18. McAlister FA,Lawson FME,Teo KK,Armstrong PW.A systematic review of randomized trials of disease management programs in heart failure.Am J Med.2001;2001(110):378384.
  19. McAlister FA,Stewart S,Ferrua S,McMurray JJV.Multidisciplinary strategies for the management of heart failure patients at high risk for admission.J Am Coll Cardiol.2004;44(4):810819.
  20. Roccaforte R,Demers C,Baldassarre F,Teo KK,Yusuf F.Effectiveness of comprehensive disease management programmes in improving clinical outcomes in heart failure patients. A meta‐analysis.Eur J Heart Fail.2005;7:11331144.
  21. Gonseth J,Guallar‐Castillon P,Banegas JR,Rodriguez‐Artalejo F.The effectiveness of disease management programmes in reducing hospital re‐admission in older patients with heart failure: a systematic review and meta‐analysis of published reports.Eur Heart J.2004;25:15701595.
  22. Holland R,Battersby J,Harvey I,Lenaghan E,Smith J,Hay L.Systematic review of multidisciplinary interventions in heart failure.Heart.2005;91:899906.
  23. Taylor S,Bestall J,Cotter S, et al.Clinical service organisation for heart failure.Cochrane Database Syst Rev.2005(2):CD002752.pub2.
  24. Scott IA,Denaro CP,Bennett CJ, et al.Achieving better in‐hospital and after‐hospital care of patients with acute cardiac disease.Med J Aust.2004;180:S83S88.
  25. D'Agostino RB.Propensity score methods for bias reduction in the comparison of a treatment to a non‐randomized control group.Stat Med.1998;17:22652281.
  26. Philbin EF,Rocco TA,Lindenmuth NW,Ulrich K,McCall M,Jenkins P.The results of a randomized trial of a quality improvement intervention in the care of patients with heart failure.Am J Med.2000;109(6):443449.
  27. Yu DSF,Thompson DR,Lee DTF.Disease management programmes for older people with heart failure: crucial characteristics which improve post‐discharge outcomes.Eur Heart J.2006;27:596612.
  28. Weinberger M,Oddone EZ,Henderson WG.Does increased access to primary care reduce hospital readmissions?N Engl J Med.1996;334:14411447.
  29. Galbreath AD,Krasuski RA,Smith B, et al.Long‐term healthcare and cost outcomes of disease management in a large, randomized, community‐based population with heart failure.Circulation.2004;110(23):35183526.
  30. Baker DW,Einstadter D,Husak SS,Cebul R.Trends in postdischarge mortality and readmissions. Has length of stay declined too far?Arch Intern Med.2004;164:538544.
  31. Cleland JG,Gemmell I,Khand A,Boddy A.Is the prognosis of heart failure improving?Eur J Heart Fail.1999;1(3):229241.
  32. Lee DS,Mamdani MM,Austin PC, et al.Trends in heart failure outcomes and pharmacotherapy: 1992 to 2000.Am J Med.2004;116(9):581589.
  33. Zook C,Savickis SF,Moore FD.Repeated hospitalization for the same disease: a multiplier of national health costs.Milbank Mem Fund Q.1908;58(3):454471.
Article PDF
Issue
Journal of Hospital Medicine - 5(3)
Page Number
148-153
Legacy Keywords
congestive heart failure, disease management, patient readmission, quality of health care
Sections
Article PDF
Article PDF

Congestive heart failure (CHF) is a common disease with high mortality and morbidity.1, 2 Better physiological understanding has led to significant advances in therapy in recent years, with synthesis of this evidence into widely available treatment guidelines.3, 4 However, patients who have had an acute hospitalization with heart failure continue to have a high rate of symptomatic relapse, with up to 25% readmitted within 3 months.2 One of the major challenges in heart failure therapy is to avert these relapses to prevent hospital readmission.

Angiotensin‐converting enzyme (ACE) inhibitors, beta‐blockers, and spironolactone have promised a reduction in hospitalization rates as well as mortality; however, suboptimal prescribing5 and adherence to therapy6, 7 may limit their anticipated benefits. This has led to interest in improved systems of care to reduce hospital utilization. Such approaches have included improved systems for optimizing medications,68 comprehensive discharge planning and postdischarge support,914 and self‐management and case management strategies1517 to enhance patient participation in care.

Combinations of these strategies are known as disease management programs (DMPs), and trials of such combination strategies to improve patient outcomes have been promising.1823 Recognized features4 include skilled multidisciplinary team care; individualized guideline‐based treatment plans that may include dietary and exercise programs as well as optimal pharmacological therapy; patient education and self‐management strategies; improved integration between hospital and community care providers; vigilant follow‐up including prompt review after hospitalization; ready access to expert assessment in the event of deterioration; and regular monitoring with expert titration of therapy, through clinics, home visits, or telemonitoring. Several randomized controlled trials have suggested that DMPs may reduce heart failure‐related9, 1517 and all‐cause9, 10 readmissions. Meta‐analyses12, 1823 have demonstrated reduction in risk of all‐cause readmission of 12% to 25% as well as a reduction in mortality of 14% to 25%.

Trials of DMPs have generally involved careful participant selection, and differences in methods and outcome reporting have led some reviewers to be circumspect in their interpretation of the impact of these programs on readmission rates.23 A large, real‐world quality improvement program conducted as part of the Royal Australasian College of Physicians Clinical Support Systems Project provided an opportunity to measure whether a multifaceted program targeting a representative group of patients with CHF and their healthcare providers could reduce readmission rates. As previously published, this program delivered measurable improvements in processes of care including evidence‐based prescribing, adherence, multidisciplinary involvement, and discharge communication, associated with a reduction in 12‐month mortality.24

Objective

The Brisbane Cardiac Consortium sought to improve processes of care for patients with CHF by using evidence‐based strategies targeting patients and their healthcare providers to optimize uptake of management guidelines, improve discharge processes between hospital and primary care, and increase patient participation in care. We hypothesized that the program would reduce hospital readmissions in the intervention patients in the first 12 months following discharge.

Methods

Setting

The program was conducted in 3 metropolitan public teaching hospitals in Brisbane, Australia (Royal Brisbane, Princess Alexandra, and Queen Elizabeth II Hospitals) and their associated Divisions of General Practice, targeting the hospital and posthospital care of patients with CHF.

Design

The study was a prospective time series study. Consecutive participants were enrolled continuously between October 1, 2000 and August 31, 2002. Interventions were introduced progressively as systems matured. For evaluation purposes, we predefined a baseline cohort (October 1, 2000 to April 17, 2001) who were admitted prior to implementation of any interventions, and an intervention cohort (February 15, 2002 to August 31, 2002) who were admitted after all interventions were mature. The study was approved by the Ethics Committees of all participating institutions.

Participants

All patients with a recorded clinical diagnosis of CHF within 48 hours of hospital presentation, and evidence of at least 2 supporting clinical signs (raised jugular venous pressure, third or fourth heart sounds, bilateral chest crackles, dependent edema, or cardiomegaly and/or pulmonary edema on chest x‐ray) were identified prospectively by trained research nurses. Patients were ineligible for reevaluation if they had already been enrolled in the study. Detailed data were abstracted from the medical record including demographics, illness characteristics, and comorbid conditions.

Interventions

Provider‐directed Interventions

Provider‐directed interventions aimed to improve clinician compliance with agreed management guidelines using decision support tools, reminders, education and academic detailing, and regular performance feedback. These interventions were delivered by project staff and local clinical leaders and were directed toward both hospital clinicians (internists and cardiologists) and general practitioners providing community care.

Patient‐directed Interventions

Patient‐directed interventions included written evidence‐based patient education, pharmacist discharge medication review and inpatient education, and patient diaries. Comprehensive discharge summaries including target‐directed management plans were provided to the general practitioner and community pharmacist.

Participants were considered suitable for more intensive posthospital intervention and follow‐up if they: (1) did not have cognitive impairment or psychiatric illness which would preclude participation in self‐care; (2) did not have a life expectancy due to comorbidities estimated to be less than 6 months; (3) had a stable residence in the community where they could be contacted by telephone; (4) attended a general practitioner within the greater Brisbane area; and (5) consented to more detailed follow‐up. In the baseline phase, this intensive group was contacted by nursing staff at 1, 3, 6, and 12 months for data collection purposes; in the intervention phase, these participants received enhanced predischarge pharmacist education; postdischarge pharmacist telephone follow‐up of medication understanding and adherence; telephone reminders from project nursing staff at 1, 3, 6, and 12 months to attend their general practitioner; and individualized, written, guideline‐based reminders sent to participating general practitioners.

Measures and Analysis

The primary outcome measure was all‐cause hospital readmission over 12 months. Secondary outcomes included 12‐month all‐cause mortality, 12‐month readmissions due to CHF, total hospital days, and the combined endpoint of death or readmission (ie, readmission‐free survival) at 12 months.

Readmission data were obtained from the Queensland Health Information Centre by matching patient data with the Queensland Hospital Admitted Patient Data Collection. Admission to any Queensland hospital is captured in this database. Readmission was defined as due to CHF (same‐cause) if a principal diagnosis code from ICD‐10‐AM code chapter I50 was assigned. Mortality data were obtained from the Australian Institute of Health and Welfare (AIHW) National Death Index.

Processes of inpatient care were collected by trained research nurses using a standardized structured chart abstraction tool. Data items were based on guideline recommendations for patient assessment, investigation, and management.

All analyses were conducted using SAS version for Windows 9.1 (SAS Institute, Cary, NC). Baseline and intervention patient characteristics were compared using independent samples t test for continuous variables and contingency tables with chi‐square tests for proportions.

Logistic regression models adjusted for hospital and posthospital intensity (considered to be significant potential confounders) were used to test the strength of association between the intervention and readmission (or death and readmission); Cox proportional hazards model was used to assess the time to first readmission or death. A Wilcoxon 2‐sample test was used to compare total number of days in hospital over the 12‐month follow‐up period, as these data were highly positively skewed; means rather than medians are reported, as the median was 0 in each group and hence uninformative. Frequency of readmission was compared using Poisson regression adjusted for hospital. A P value of 0.05 was considered significant in all analyses.

Preliminary analysis revealed a number of differences in baseline clinical characteristics between the 2 groups. To account for measured differences other than hospital and intervention intensity, propensity scores (the conditional probability of assignment to a particular treatment group given a vector of observed covariates) were developed using a logistic model with the control or intervention group as the dependent variable and baseline patient characteristic variables with P < 0.2 (as shown in Table 1) as the independent variables. The equation obtained from this model was used to estimate a propensity score for each patient. These scores along with hospital and intervention intensity were then used to provide estimates adjusted for baseline differences between the control and intervention groups.25

Characteristics of Baseline and Intervention Participants
CharacteristicBaseline (n = 197)Intervention (n = 219)P Value
  • Abbreviations: CHF, congestive heart failure; LVEF, left ventricular ejection fraction; NYHA, New York Hospital Association.

Hospital, n (%)  0.001
175 (38)100 (46) 
240 (20)17 (8) 
382 (42)102 (46) 
Age (years), mean (range)75 (24‐100)78 (32‐102)0.059
Female, n (%)103 (52)118 (54)0.74
Hostel resident, n (%)15 (8)38 (17)<0.01
Previous CHF admission, n (%)52 (26)26 (12)<0.01
Contributing factors, n (%)   
Hypertension104 (53)139 (63)0.027
Coronary disease107 (54)118 (54)0.93
Valvular disease20 (10)45 (21)<0.01
Cardiomyopathy29 (15)33 (15)0.92
NYHA class III/IV, n (%)143 (73)155 (71)0.68
Atrial fibrillation, n (%)65 (33)78 (36)0.57
LVEF % (mean)24280.10
Cardiologist care, n (%)42 (21)61 (28)0.12
Comorbidity score2.6 (1,8)2.7 (1,10)0.52

Results

There were 220 patients identified with a clinical diagnosis of CHF during the baseline period, and 235 during the intervention period. Figure 1 shows ascertainment, in‐hospital mortality, and eligibility rates for the 2 cohorts. Eighty‐nine (45%) of baseline patients and 76 (35%) of intervention patients received intensive posthospital follow‐up as described above. Information on readmission was available for 197 baseline patients and 219 intervention patients discharged alive; this is the sample used for all analyses in this report. Table 1 shows the demographic and clinical characteristics of these patients. Table 2 summarizes the previously reported improvements in processes of care.

Figure 1
Flow diagram for participant enrollment. Baseline (control) cohort: consecutive patients with CHF admitted to study hospitals October 1, 2000 to April 17, 2001. Intervention cohort: consecutive patients with CHF admitted to study hospitals February 15, 2002 to August 31, 2002; 7 participants were excluded because they were unable to be matched to readmission datasets.
Processes of Inpatient Care for Baseline and Intervention Cohort
Process indicatorBaseline (n = 220) [n (%)>]Intervention (n = 235) [n (%)]P Value
  • Abbreviations: ACE, angiotensin converting enzyme; DVT, deep vein thrombosis.

  • Denominator is patients discharged alive and not transferred to another facility; n = 191.

  • Denominator is patients discharged alive and not transferred to another facility; n = 219.

Assessment of reversible triggers166 (75)211 (90)<0.001
DVT prophylaxis57 (26)148 (63)<0.001
Imaging of left ventricular function135 (61)164 (70)0.002
Scheduled outpatient visit within 30 days87 (46)*130 (59)0.005
ACE inhibitor prescription at discharge136 (71)*163 (74)0.46
Beta‐blocker prescription at discharge61 (32)*113 (52)<0.001
Avoid deleterious agents at discharge180 (94)*214 (98)0.79

Duing the 12‐month follow‐up, 107 (49%) of intervention patients were readmitted to the hospital compared to 71 (36%) of control patients, representing a 1.7‐fold increase in the adjusted probability of readmission in the intervention group (odds ratio [OR] = 1.71, 95% confidence interval [CI] = 1.14‐2.56; P = 0.009). As shown in Table 3, this was partly balanced by a trend toward reduced post‐hospital mortality, such that no significant difference was seen in readmission‐free survival.

Readmission and Death Rates
 Baseline (%)Intervention (%)OR (95% CI)P Value
  • Abbreviations: CI, confidence interval; OR, odds ratio.

  • Estimates adjusted for hospital and intervention intensity.

  • Estimates adjusted for hospital, intervention intensity, and propensity score.

Readmitted within 12 months71/197 (36)107/219 (49)1.71* (1.14, 2.56); 1.90 (1.24, 2.91)0.009; 0.004
Death within 12 months59/197 (30)53/219 (24)0.68* (0.44, 1.07)0.099
Death or readmission within 12 months104/197 (53)133/219 (61)1.30* (0.87, 1.93); 1.36 (0.89, 2.08)0.20; 0.15

Time‐to‐event analysis (Figures 2 and 3) demonstrated similar findings, with a significant reduction in time to first readmission in the intervention group (adjusted hazard ratio [HR] = 1.43; 95% CI = 1.04‐1.97; P = 0.046) but no difference in time to death or first readmission (adjusted HR = 1.14; 95% CI = 0.86‐1.46; P = 0.36).

Figure 2
Time to first hospital readmission.
Figure 3
Time to death or first hospital readmission.

There was a trend to increased readmissions attributed to heart failure: 47 (21.5%) of intervention patients compared to 33 (16.7%) in the baseline group (OR = 1.30; 95% CI = 0.87‐1.93; P = 0.20). No significant difference was demonstrated in the frequency of readmissions (average 0.75 admission per participant per year in baseline, compared to 0.93 intervention; P = 0.32) nor the mean number of days in hospital in 12 months subsequent to the index admission (5.9 in the baseline group compared to 6.5 in the intervention group; P = 0.1).

Subgroup analysis by intervention intensity showed similar results, with 42 of 76 (55.3%) intensive group participants in the intervention group and 36 of 89 (40.4%) in the baseline group requiring hospital readmission within 12 months. The HR for death or readmission was estimated to be 1.27 (95% CI = 0.85‐1.9).

Discussion

In this study, heart failure patients who received a multidisciplinary intervention (including inpatient education, self‐management support, improved timely medical follow‐up, and better integration between hospital and primary care) showed a trend to improved 1‐year post‐hospital survival, but this appeared to be at the cost of increased readmissions among survivors. This occurred despite our previously reported improved optimization of pharmacological therapy both in‐hospital and posthospital with this program.18

There are a number of potential explanations for this finding, which have important implications for adoption of disease management programs. First, the intervention may not have been of sufficient intensity. Programs primarily aimed at educating providers and patients in evidence‐based guidelines, without structured postdischarge support, have not always improved clinical outcomes.26 In our study, general practitioners were supported to provide improved postdischarge care to their CHF patients, but direct postdischarge patient support was only provided to consenting patients and was limited in scope. There is still some debate about which elements of successful DMPs are most important for efficacy. Most authorities support the central importance of medication optimization, intensive education, and self‐care support. Taylor et al.23 found stronger evidence for programs using individual case management or outreach rather than clinic‐based interventions. Yu et al.27 concluded that outpatient drug titration and ready access to specialist review were factors contributing to success. In our program, even the more intensive intervention did not include regular clinical review by specialist nurses, a system for rapid review in the event of deterioration or supervised drug titration protocols. Furthermore, strategies which prompted more frequent primary care review and improved patient, carer, and general practitioner recognition of disease deterioration may have provided more opportunities to initiate readmission, especially in the absence of an alternative care pathway such as rapid‐access clinics or outreach services.28

Second, this study may reflect the reality of generalizing randomized controlled trial data to an unselected population. Many trials enrolled patients with high anticipated event rates but excluded patients with complex comorbidities, poor life expectancy, and cognitive impairment. Such studies enrolled a high‐risk population (10%‐48% of screened patients randomized) who had a relatively high readmission rate (50%‐60% at 6‐12 months) compared to our unselected population. These studies may overstate the benefits of applying heart failure DMPs in an unselected population. Galbreath et al.29 enrolled a self‐selected community sample of heart failure patients into a disease management program incorporating education, self‐management, telephone support, and advice to primary care providers and home health providers. Like our model, they demonstrated a survival benefit in the intervention group but no reduction in hospital or other healthcare utilization.

Third, only about one‐half of the readmissions were due to heart failure, again reflecting the complexity of this real‐world patient group. Interventions that focus on a single disease in patients with complex comorbidities might be expected to have only limited impact on their subsequent healthcare needs.

Fourth, findings may reflect differences in patient characteristics between the 2 cohorts. While statistical adjustment for measured differences did not have any significant impact on results, unmeasured patient characteristics may have introduced bias. The beforeafter nature of the study also raises the possibility that temporal trends in care practices influenced patient outcomes, such as changing patterns of drug and device therapies. There is conflicting evidence in the literature regarding trends in CHF readmission rates,3032 but it is possible that health system factors external to the study contributed to a higher readmission rate in the later cohort.

Finally, there was a trend toward reduction in mortality within the intervention cohort. These additional survivors might be expected to have more advanced heart failure or other comorbid disease, and therefore may have been more susceptible to deterioration and the need for inpatient care.

Conclusions

We acknowledge the weaknesses inherent in this nonrandomized study design, including convenience sampling, measured and unmeasured confounders and temporal trends in processes and systems of care. Nonetheless, this real world study suggests a note of caution in the widespread enthusiasm for chronic disease management programs. A complex bundle of interventions that resulted in measurable improvements in adherence to evidence‐based guidelines, discharge processes, integration between care providers, and patient education appeared to prolong life expectancy but increase hospital utilization. Mortality reduction in an incurable chronic disease such as heart failure will increase the burden of disease (and therefore treatment costs) unless treatments concurrently reduce disability and the frequency of symptomatic relapse.33 Whether this balance is achieved will depend on patient selection and the intensity and/or components of the intervention. These factors have not been fully defined in the literature to date.

Our study suggests that a widely applied, discharge‐focused intervention which primarily augmented the CHF management knowledge of care providers and patients, and enhanced attendance within the existing care model of primary care and internal medicine/cardiology outpatient services, improved the quality of care and may have reduced mortality at the cost of higher hospital utilization. It raises questions about whether a disease management service can achieve the uncertain promise of reduced readmissions in a cost‐effective manner outside of a high‐risk experimental population.

Acknowledgements

The authors acknowledge the contribution of the advisory and working groups of the Brisbane Cardiac Consortium. The authors appreciate the support of clinicians from the Internal Medicine, Cardiology, and Pharmacy Departments of the participating hospitals as well as staff from the Brisbane North and Brisbane Inner South Divisions of General Practice. The authors are grateful for the efforts of the staff of the PAH Clinical Services Evaluation Unit and the RBWH Internal Medicine Research Unit for data collection and data management; and the Queensland Health Information Centre and Australian Institute of Health and Welfare (AIHW) National Death Index for data matching.

Congestive heart failure (CHF) is a common disease with high mortality and morbidity.1, 2 Better physiological understanding has led to significant advances in therapy in recent years, with synthesis of this evidence into widely available treatment guidelines.3, 4 However, patients who have had an acute hospitalization with heart failure continue to have a high rate of symptomatic relapse, with up to 25% readmitted within 3 months.2 One of the major challenges in heart failure therapy is to avert these relapses to prevent hospital readmission.

Angiotensin‐converting enzyme (ACE) inhibitors, beta‐blockers, and spironolactone have promised a reduction in hospitalization rates as well as mortality; however, suboptimal prescribing5 and adherence to therapy6, 7 may limit their anticipated benefits. This has led to interest in improved systems of care to reduce hospital utilization. Such approaches have included improved systems for optimizing medications,68 comprehensive discharge planning and postdischarge support,914 and self‐management and case management strategies1517 to enhance patient participation in care.

Combinations of these strategies are known as disease management programs (DMPs), and trials of such combination strategies to improve patient outcomes have been promising.1823 Recognized features4 include skilled multidisciplinary team care; individualized guideline‐based treatment plans that may include dietary and exercise programs as well as optimal pharmacological therapy; patient education and self‐management strategies; improved integration between hospital and community care providers; vigilant follow‐up including prompt review after hospitalization; ready access to expert assessment in the event of deterioration; and regular monitoring with expert titration of therapy, through clinics, home visits, or telemonitoring. Several randomized controlled trials have suggested that DMPs may reduce heart failure‐related9, 1517 and all‐cause9, 10 readmissions. Meta‐analyses12, 1823 have demonstrated reduction in risk of all‐cause readmission of 12% to 25% as well as a reduction in mortality of 14% to 25%.

Trials of DMPs have generally involved careful participant selection, and differences in methods and outcome reporting have led some reviewers to be circumspect in their interpretation of the impact of these programs on readmission rates.23 A large, real‐world quality improvement program conducted as part of the Royal Australasian College of Physicians Clinical Support Systems Project provided an opportunity to measure whether a multifaceted program targeting a representative group of patients with CHF and their healthcare providers could reduce readmission rates. As previously published, this program delivered measurable improvements in processes of care including evidence‐based prescribing, adherence, multidisciplinary involvement, and discharge communication, associated with a reduction in 12‐month mortality.24

Objective

The Brisbane Cardiac Consortium sought to improve processes of care for patients with CHF by using evidence‐based strategies targeting patients and their healthcare providers to optimize uptake of management guidelines, improve discharge processes between hospital and primary care, and increase patient participation in care. We hypothesized that the program would reduce hospital readmissions in the intervention patients in the first 12 months following discharge.

Methods

Setting

The program was conducted in 3 metropolitan public teaching hospitals in Brisbane, Australia (Royal Brisbane, Princess Alexandra, and Queen Elizabeth II Hospitals) and their associated Divisions of General Practice, targeting the hospital and posthospital care of patients with CHF.

Design

The study was a prospective time series study. Consecutive participants were enrolled continuously between October 1, 2000 and August 31, 2002. Interventions were introduced progressively as systems matured. For evaluation purposes, we predefined a baseline cohort (October 1, 2000 to April 17, 2001) who were admitted prior to implementation of any interventions, and an intervention cohort (February 15, 2002 to August 31, 2002) who were admitted after all interventions were mature. The study was approved by the Ethics Committees of all participating institutions.

Participants

All patients with a recorded clinical diagnosis of CHF within 48 hours of hospital presentation, and evidence of at least 2 supporting clinical signs (raised jugular venous pressure, third or fourth heart sounds, bilateral chest crackles, dependent edema, or cardiomegaly and/or pulmonary edema on chest x‐ray) were identified prospectively by trained research nurses. Patients were ineligible for reevaluation if they had already been enrolled in the study. Detailed data were abstracted from the medical record including demographics, illness characteristics, and comorbid conditions.

Interventions

Provider‐directed Interventions

Provider‐directed interventions aimed to improve clinician compliance with agreed management guidelines using decision support tools, reminders, education and academic detailing, and regular performance feedback. These interventions were delivered by project staff and local clinical leaders and were directed toward both hospital clinicians (internists and cardiologists) and general practitioners providing community care.

Patient‐directed Interventions

Patient‐directed interventions included written evidence‐based patient education, pharmacist discharge medication review and inpatient education, and patient diaries. Comprehensive discharge summaries including target‐directed management plans were provided to the general practitioner and community pharmacist.

Participants were considered suitable for more intensive posthospital intervention and follow‐up if they: (1) did not have cognitive impairment or psychiatric illness which would preclude participation in self‐care; (2) did not have a life expectancy due to comorbidities estimated to be less than 6 months; (3) had a stable residence in the community where they could be contacted by telephone; (4) attended a general practitioner within the greater Brisbane area; and (5) consented to more detailed follow‐up. In the baseline phase, this intensive group was contacted by nursing staff at 1, 3, 6, and 12 months for data collection purposes; in the intervention phase, these participants received enhanced predischarge pharmacist education; postdischarge pharmacist telephone follow‐up of medication understanding and adherence; telephone reminders from project nursing staff at 1, 3, 6, and 12 months to attend their general practitioner; and individualized, written, guideline‐based reminders sent to participating general practitioners.

Measures and Analysis

The primary outcome measure was all‐cause hospital readmission over 12 months. Secondary outcomes included 12‐month all‐cause mortality, 12‐month readmissions due to CHF, total hospital days, and the combined endpoint of death or readmission (ie, readmission‐free survival) at 12 months.

Readmission data were obtained from the Queensland Health Information Centre by matching patient data with the Queensland Hospital Admitted Patient Data Collection. Admission to any Queensland hospital is captured in this database. Readmission was defined as due to CHF (same‐cause) if a principal diagnosis code from ICD‐10‐AM code chapter I50 was assigned. Mortality data were obtained from the Australian Institute of Health and Welfare (AIHW) National Death Index.

Processes of inpatient care were collected by trained research nurses using a standardized structured chart abstraction tool. Data items were based on guideline recommendations for patient assessment, investigation, and management.

All analyses were conducted using SAS version for Windows 9.1 (SAS Institute, Cary, NC). Baseline and intervention patient characteristics were compared using independent samples t test for continuous variables and contingency tables with chi‐square tests for proportions.

Logistic regression models adjusted for hospital and posthospital intensity (considered to be significant potential confounders) were used to test the strength of association between the intervention and readmission (or death and readmission); Cox proportional hazards model was used to assess the time to first readmission or death. A Wilcoxon 2‐sample test was used to compare total number of days in hospital over the 12‐month follow‐up period, as these data were highly positively skewed; means rather than medians are reported, as the median was 0 in each group and hence uninformative. Frequency of readmission was compared using Poisson regression adjusted for hospital. A P value of 0.05 was considered significant in all analyses.

Preliminary analysis revealed a number of differences in baseline clinical characteristics between the 2 groups. To account for measured differences other than hospital and intervention intensity, propensity scores (the conditional probability of assignment to a particular treatment group given a vector of observed covariates) were developed using a logistic model with the control or intervention group as the dependent variable and baseline patient characteristic variables with P < 0.2 (as shown in Table 1) as the independent variables. The equation obtained from this model was used to estimate a propensity score for each patient. These scores along with hospital and intervention intensity were then used to provide estimates adjusted for baseline differences between the control and intervention groups.25

Characteristics of Baseline and Intervention Participants
CharacteristicBaseline (n = 197)Intervention (n = 219)P Value
  • Abbreviations: CHF, congestive heart failure; LVEF, left ventricular ejection fraction; NYHA, New York Hospital Association.

Hospital, n (%)  0.001
175 (38)100 (46) 
240 (20)17 (8) 
382 (42)102 (46) 
Age (years), mean (range)75 (24‐100)78 (32‐102)0.059
Female, n (%)103 (52)118 (54)0.74
Hostel resident, n (%)15 (8)38 (17)<0.01
Previous CHF admission, n (%)52 (26)26 (12)<0.01
Contributing factors, n (%)   
Hypertension104 (53)139 (63)0.027
Coronary disease107 (54)118 (54)0.93
Valvular disease20 (10)45 (21)<0.01
Cardiomyopathy29 (15)33 (15)0.92
NYHA class III/IV, n (%)143 (73)155 (71)0.68
Atrial fibrillation, n (%)65 (33)78 (36)0.57
LVEF % (mean)24280.10
Cardiologist care, n (%)42 (21)61 (28)0.12
Comorbidity score2.6 (1,8)2.7 (1,10)0.52

Results

There were 220 patients identified with a clinical diagnosis of CHF during the baseline period, and 235 during the intervention period. Figure 1 shows ascertainment, in‐hospital mortality, and eligibility rates for the 2 cohorts. Eighty‐nine (45%) of baseline patients and 76 (35%) of intervention patients received intensive posthospital follow‐up as described above. Information on readmission was available for 197 baseline patients and 219 intervention patients discharged alive; this is the sample used for all analyses in this report. Table 1 shows the demographic and clinical characteristics of these patients. Table 2 summarizes the previously reported improvements in processes of care.

Figure 1
Flow diagram for participant enrollment. Baseline (control) cohort: consecutive patients with CHF admitted to study hospitals October 1, 2000 to April 17, 2001. Intervention cohort: consecutive patients with CHF admitted to study hospitals February 15, 2002 to August 31, 2002; 7 participants were excluded because they were unable to be matched to readmission datasets.
Processes of Inpatient Care for Baseline and Intervention Cohort
Process indicatorBaseline (n = 220) [n (%)>]Intervention (n = 235) [n (%)]P Value
  • Abbreviations: ACE, angiotensin converting enzyme; DVT, deep vein thrombosis.

  • Denominator is patients discharged alive and not transferred to another facility; n = 191.

  • Denominator is patients discharged alive and not transferred to another facility; n = 219.

Assessment of reversible triggers166 (75)211 (90)<0.001
DVT prophylaxis57 (26)148 (63)<0.001
Imaging of left ventricular function135 (61)164 (70)0.002
Scheduled outpatient visit within 30 days87 (46)*130 (59)0.005
ACE inhibitor prescription at discharge136 (71)*163 (74)0.46
Beta‐blocker prescription at discharge61 (32)*113 (52)<0.001
Avoid deleterious agents at discharge180 (94)*214 (98)0.79

Duing the 12‐month follow‐up, 107 (49%) of intervention patients were readmitted to the hospital compared to 71 (36%) of control patients, representing a 1.7‐fold increase in the adjusted probability of readmission in the intervention group (odds ratio [OR] = 1.71, 95% confidence interval [CI] = 1.14‐2.56; P = 0.009). As shown in Table 3, this was partly balanced by a trend toward reduced post‐hospital mortality, such that no significant difference was seen in readmission‐free survival.

Readmission and Death Rates
 Baseline (%)Intervention (%)OR (95% CI)P Value
  • Abbreviations: CI, confidence interval; OR, odds ratio.

  • Estimates adjusted for hospital and intervention intensity.

  • Estimates adjusted for hospital, intervention intensity, and propensity score.

Readmitted within 12 months71/197 (36)107/219 (49)1.71* (1.14, 2.56); 1.90 (1.24, 2.91)0.009; 0.004
Death within 12 months59/197 (30)53/219 (24)0.68* (0.44, 1.07)0.099
Death or readmission within 12 months104/197 (53)133/219 (61)1.30* (0.87, 1.93); 1.36 (0.89, 2.08)0.20; 0.15

Time‐to‐event analysis (Figures 2 and 3) demonstrated similar findings, with a significant reduction in time to first readmission in the intervention group (adjusted hazard ratio [HR] = 1.43; 95% CI = 1.04‐1.97; P = 0.046) but no difference in time to death or first readmission (adjusted HR = 1.14; 95% CI = 0.86‐1.46; P = 0.36).

Figure 2
Time to first hospital readmission.
Figure 3
Time to death or first hospital readmission.

There was a trend to increased readmissions attributed to heart failure: 47 (21.5%) of intervention patients compared to 33 (16.7%) in the baseline group (OR = 1.30; 95% CI = 0.87‐1.93; P = 0.20). No significant difference was demonstrated in the frequency of readmissions (average 0.75 admission per participant per year in baseline, compared to 0.93 intervention; P = 0.32) nor the mean number of days in hospital in 12 months subsequent to the index admission (5.9 in the baseline group compared to 6.5 in the intervention group; P = 0.1).

Subgroup analysis by intervention intensity showed similar results, with 42 of 76 (55.3%) intensive group participants in the intervention group and 36 of 89 (40.4%) in the baseline group requiring hospital readmission within 12 months. The HR for death or readmission was estimated to be 1.27 (95% CI = 0.85‐1.9).

Discussion

In this study, heart failure patients who received a multidisciplinary intervention (including inpatient education, self‐management support, improved timely medical follow‐up, and better integration between hospital and primary care) showed a trend to improved 1‐year post‐hospital survival, but this appeared to be at the cost of increased readmissions among survivors. This occurred despite our previously reported improved optimization of pharmacological therapy both in‐hospital and posthospital with this program.18

There are a number of potential explanations for this finding, which have important implications for adoption of disease management programs. First, the intervention may not have been of sufficient intensity. Programs primarily aimed at educating providers and patients in evidence‐based guidelines, without structured postdischarge support, have not always improved clinical outcomes.26 In our study, general practitioners were supported to provide improved postdischarge care to their CHF patients, but direct postdischarge patient support was only provided to consenting patients and was limited in scope. There is still some debate about which elements of successful DMPs are most important for efficacy. Most authorities support the central importance of medication optimization, intensive education, and self‐care support. Taylor et al.23 found stronger evidence for programs using individual case management or outreach rather than clinic‐based interventions. Yu et al.27 concluded that outpatient drug titration and ready access to specialist review were factors contributing to success. In our program, even the more intensive intervention did not include regular clinical review by specialist nurses, a system for rapid review in the event of deterioration or supervised drug titration protocols. Furthermore, strategies which prompted more frequent primary care review and improved patient, carer, and general practitioner recognition of disease deterioration may have provided more opportunities to initiate readmission, especially in the absence of an alternative care pathway such as rapid‐access clinics or outreach services.28

Second, this study may reflect the reality of generalizing randomized controlled trial data to an unselected population. Many trials enrolled patients with high anticipated event rates but excluded patients with complex comorbidities, poor life expectancy, and cognitive impairment. Such studies enrolled a high‐risk population (10%‐48% of screened patients randomized) who had a relatively high readmission rate (50%‐60% at 6‐12 months) compared to our unselected population. These studies may overstate the benefits of applying heart failure DMPs in an unselected population. Galbreath et al.29 enrolled a self‐selected community sample of heart failure patients into a disease management program incorporating education, self‐management, telephone support, and advice to primary care providers and home health providers. Like our model, they demonstrated a survival benefit in the intervention group but no reduction in hospital or other healthcare utilization.

Third, only about one‐half of the readmissions were due to heart failure, again reflecting the complexity of this real‐world patient group. Interventions that focus on a single disease in patients with complex comorbidities might be expected to have only limited impact on their subsequent healthcare needs.

Fourth, findings may reflect differences in patient characteristics between the 2 cohorts. While statistical adjustment for measured differences did not have any significant impact on results, unmeasured patient characteristics may have introduced bias. The beforeafter nature of the study also raises the possibility that temporal trends in care practices influenced patient outcomes, such as changing patterns of drug and device therapies. There is conflicting evidence in the literature regarding trends in CHF readmission rates,3032 but it is possible that health system factors external to the study contributed to a higher readmission rate in the later cohort.

Finally, there was a trend toward reduction in mortality within the intervention cohort. These additional survivors might be expected to have more advanced heart failure or other comorbid disease, and therefore may have been more susceptible to deterioration and the need for inpatient care.

Conclusions

We acknowledge the weaknesses inherent in this nonrandomized study design, including convenience sampling, measured and unmeasured confounders and temporal trends in processes and systems of care. Nonetheless, this real world study suggests a note of caution in the widespread enthusiasm for chronic disease management programs. A complex bundle of interventions that resulted in measurable improvements in adherence to evidence‐based guidelines, discharge processes, integration between care providers, and patient education appeared to prolong life expectancy but increase hospital utilization. Mortality reduction in an incurable chronic disease such as heart failure will increase the burden of disease (and therefore treatment costs) unless treatments concurrently reduce disability and the frequency of symptomatic relapse.33 Whether this balance is achieved will depend on patient selection and the intensity and/or components of the intervention. These factors have not been fully defined in the literature to date.

Our study suggests that a widely applied, discharge‐focused intervention which primarily augmented the CHF management knowledge of care providers and patients, and enhanced attendance within the existing care model of primary care and internal medicine/cardiology outpatient services, improved the quality of care and may have reduced mortality at the cost of higher hospital utilization. It raises questions about whether a disease management service can achieve the uncertain promise of reduced readmissions in a cost‐effective manner outside of a high‐risk experimental population.

Acknowledgements

The authors acknowledge the contribution of the advisory and working groups of the Brisbane Cardiac Consortium. The authors appreciate the support of clinicians from the Internal Medicine, Cardiology, and Pharmacy Departments of the participating hospitals as well as staff from the Brisbane North and Brisbane Inner South Divisions of General Practice. The authors are grateful for the efforts of the staff of the PAH Clinical Services Evaluation Unit and the RBWH Internal Medicine Research Unit for data collection and data management; and the Queensland Health Information Centre and Australian Institute of Health and Welfare (AIHW) National Death Index for data matching.

References
  1. Stewart S,MacIntyre K,Hole DJ,Capewell S,McMurray JJ.More ‘malignant’ than cancer? Five‐year survival following a first admission with heart failure.Eur J Heart Fail.2001;3:315322.
  2. Cleland JG,Swedberg K,Follath F, et al.;Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology The EuroHeart Failure survey programme—a survey on the quality of care among patients with heart failure in Europe.Part 1: patient characteristics and diagnosis.Eur Heart J.2003;24(5):442463.
  3. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel.Guidelines for management of patients with chronic heart failure in Australia.Med J Aust.2001;174:459466.
  4. Swedberg K,Cleland J,Dargie H.Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology.Eur Heart J.2005;26(11):11151140.
  5. Scott IA,Denaro CP,Flores JL, et al.Quality of care of patients hospitalized with congestive heart failure.Intern Med J.2003;33(4):140151.
  6. Lappe JM,Muhlestein JB,Lappe DL, et al.Improvements in 1‐year cardiovascular clinical outcomes associated with a hospital‐based discharge medication program.Ann Intern Med.2004;141(6):446453.
  7. Gattis WA,Hasselblad V,Whellan DJ,O'Connor CM.Reduction in heart failure events by the addition of a clinical pharmacist to the heart failure management team.Arch Intern Med.1999;159(16):19391945.
  8. Rainville EC.Impact of pharmacist interventions on hospital readmissions for heart failure.Am J Health Syst Pharm.1999;56:13391342.
  9. Stewart S,Marley JE,Horowitz JD.Effects of a multidisciplinary, home‐based intervention on unplanned readmissions and survival among patients with chronic congestive heart failure: a randomised controlled study.Lancet.1999;354:10771083.
  10. Rich MW,Beckham V,Wittenberg C,Leven C,Freedlane KE,Carney RM.A multidisciplinary intervention to prevent the readmission of elderly patients with congestive heart failure.N Engl J Med.1995;333(18):11901195.
  11. Stewart S,Horowitz JD.Home‐based intervention in congestive heart failure. Long‐term implications on readmission and survival.Circulation.2002;105(24):28612866.
  12. Phillips CO,Wright SM,Kern DE,Singa RM,Shepperd S,Rubin HR.Comprehensive discharge planning with postdischarge support for older patients with congestive heart failure. A meta‐analysis.JAMA.2004;291(11):13581367.
  13. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders. A randomized clinical trial.JAMA.1999;281(7):613620.
  14. Harrison MB,Browne GB,Roberts J,Tugwell P,Gafni A,Graham ID.Quality of life of individuals with heart failure. A randomized trial of the effectiveness of two models of hospital‐to‐home transition.Med Care.2002;40(4):271282.
  15. Blue L,Lang E,McMurray JJV, et al.Randomised controlled trial of specialist nurse intervention in heart failure.BMJ.2001;323(7315):715718.
  16. Riegel B,Carlson B,Kopp Z,LePetrie B,Glaser D,Unger A.Effect of a standardised nurse case‐management telephone intervention on resource use in patients with chronic heart failure.Arch Intern Med.2002;162:705712.
  17. Krumholz H,Amatruda J,Smith G,Mattera JA,Roumanis SA,Radford MJ.Randomized trial of an education and support intervention to prevent readmission of patients with heart failure.J Am Coll Cardiol.2002;39:8389.
  18. McAlister FA,Lawson FME,Teo KK,Armstrong PW.A systematic review of randomized trials of disease management programs in heart failure.Am J Med.2001;2001(110):378384.
  19. McAlister FA,Stewart S,Ferrua S,McMurray JJV.Multidisciplinary strategies for the management of heart failure patients at high risk for admission.J Am Coll Cardiol.2004;44(4):810819.
  20. Roccaforte R,Demers C,Baldassarre F,Teo KK,Yusuf F.Effectiveness of comprehensive disease management programmes in improving clinical outcomes in heart failure patients. A meta‐analysis.Eur J Heart Fail.2005;7:11331144.
  21. Gonseth J,Guallar‐Castillon P,Banegas JR,Rodriguez‐Artalejo F.The effectiveness of disease management programmes in reducing hospital re‐admission in older patients with heart failure: a systematic review and meta‐analysis of published reports.Eur Heart J.2004;25:15701595.
  22. Holland R,Battersby J,Harvey I,Lenaghan E,Smith J,Hay L.Systematic review of multidisciplinary interventions in heart failure.Heart.2005;91:899906.
  23. Taylor S,Bestall J,Cotter S, et al.Clinical service organisation for heart failure.Cochrane Database Syst Rev.2005(2):CD002752.pub2.
  24. Scott IA,Denaro CP,Bennett CJ, et al.Achieving better in‐hospital and after‐hospital care of patients with acute cardiac disease.Med J Aust.2004;180:S83S88.
  25. D'Agostino RB.Propensity score methods for bias reduction in the comparison of a treatment to a non‐randomized control group.Stat Med.1998;17:22652281.
  26. Philbin EF,Rocco TA,Lindenmuth NW,Ulrich K,McCall M,Jenkins P.The results of a randomized trial of a quality improvement intervention in the care of patients with heart failure.Am J Med.2000;109(6):443449.
  27. Yu DSF,Thompson DR,Lee DTF.Disease management programmes for older people with heart failure: crucial characteristics which improve post‐discharge outcomes.Eur Heart J.2006;27:596612.
  28. Weinberger M,Oddone EZ,Henderson WG.Does increased access to primary care reduce hospital readmissions?N Engl J Med.1996;334:14411447.
  29. Galbreath AD,Krasuski RA,Smith B, et al.Long‐term healthcare and cost outcomes of disease management in a large, randomized, community‐based population with heart failure.Circulation.2004;110(23):35183526.
  30. Baker DW,Einstadter D,Husak SS,Cebul R.Trends in postdischarge mortality and readmissions. Has length of stay declined too far?Arch Intern Med.2004;164:538544.
  31. Cleland JG,Gemmell I,Khand A,Boddy A.Is the prognosis of heart failure improving?Eur J Heart Fail.1999;1(3):229241.
  32. Lee DS,Mamdani MM,Austin PC, et al.Trends in heart failure outcomes and pharmacotherapy: 1992 to 2000.Am J Med.2004;116(9):581589.
  33. Zook C,Savickis SF,Moore FD.Repeated hospitalization for the same disease: a multiplier of national health costs.Milbank Mem Fund Q.1908;58(3):454471.
References
  1. Stewart S,MacIntyre K,Hole DJ,Capewell S,McMurray JJ.More ‘malignant’ than cancer? Five‐year survival following a first admission with heart failure.Eur J Heart Fail.2001;3:315322.
  2. Cleland JG,Swedberg K,Follath F, et al.;Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology The EuroHeart Failure survey programme—a survey on the quality of care among patients with heart failure in Europe.Part 1: patient characteristics and diagnosis.Eur Heart J.2003;24(5):442463.
  3. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel.Guidelines for management of patients with chronic heart failure in Australia.Med J Aust.2001;174:459466.
  4. Swedberg K,Cleland J,Dargie H.Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology.Eur Heart J.2005;26(11):11151140.
  5. Scott IA,Denaro CP,Flores JL, et al.Quality of care of patients hospitalized with congestive heart failure.Intern Med J.2003;33(4):140151.
  6. Lappe JM,Muhlestein JB,Lappe DL, et al.Improvements in 1‐year cardiovascular clinical outcomes associated with a hospital‐based discharge medication program.Ann Intern Med.2004;141(6):446453.
  7. Gattis WA,Hasselblad V,Whellan DJ,O'Connor CM.Reduction in heart failure events by the addition of a clinical pharmacist to the heart failure management team.Arch Intern Med.1999;159(16):19391945.
  8. Rainville EC.Impact of pharmacist interventions on hospital readmissions for heart failure.Am J Health Syst Pharm.1999;56:13391342.
  9. Stewart S,Marley JE,Horowitz JD.Effects of a multidisciplinary, home‐based intervention on unplanned readmissions and survival among patients with chronic congestive heart failure: a randomised controlled study.Lancet.1999;354:10771083.
  10. Rich MW,Beckham V,Wittenberg C,Leven C,Freedlane KE,Carney RM.A multidisciplinary intervention to prevent the readmission of elderly patients with congestive heart failure.N Engl J Med.1995;333(18):11901195.
  11. Stewart S,Horowitz JD.Home‐based intervention in congestive heart failure. Long‐term implications on readmission and survival.Circulation.2002;105(24):28612866.
  12. Phillips CO,Wright SM,Kern DE,Singa RM,Shepperd S,Rubin HR.Comprehensive discharge planning with postdischarge support for older patients with congestive heart failure. A meta‐analysis.JAMA.2004;291(11):13581367.
  13. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders. A randomized clinical trial.JAMA.1999;281(7):613620.
  14. Harrison MB,Browne GB,Roberts J,Tugwell P,Gafni A,Graham ID.Quality of life of individuals with heart failure. A randomized trial of the effectiveness of two models of hospital‐to‐home transition.Med Care.2002;40(4):271282.
  15. Blue L,Lang E,McMurray JJV, et al.Randomised controlled trial of specialist nurse intervention in heart failure.BMJ.2001;323(7315):715718.
  16. Riegel B,Carlson B,Kopp Z,LePetrie B,Glaser D,Unger A.Effect of a standardised nurse case‐management telephone intervention on resource use in patients with chronic heart failure.Arch Intern Med.2002;162:705712.
  17. Krumholz H,Amatruda J,Smith G,Mattera JA,Roumanis SA,Radford MJ.Randomized trial of an education and support intervention to prevent readmission of patients with heart failure.J Am Coll Cardiol.2002;39:8389.
  18. McAlister FA,Lawson FME,Teo KK,Armstrong PW.A systematic review of randomized trials of disease management programs in heart failure.Am J Med.2001;2001(110):378384.
  19. McAlister FA,Stewart S,Ferrua S,McMurray JJV.Multidisciplinary strategies for the management of heart failure patients at high risk for admission.J Am Coll Cardiol.2004;44(4):810819.
  20. Roccaforte R,Demers C,Baldassarre F,Teo KK,Yusuf F.Effectiveness of comprehensive disease management programmes in improving clinical outcomes in heart failure patients. A meta‐analysis.Eur J Heart Fail.2005;7:11331144.
  21. Gonseth J,Guallar‐Castillon P,Banegas JR,Rodriguez‐Artalejo F.The effectiveness of disease management programmes in reducing hospital re‐admission in older patients with heart failure: a systematic review and meta‐analysis of published reports.Eur Heart J.2004;25:15701595.
  22. Holland R,Battersby J,Harvey I,Lenaghan E,Smith J,Hay L.Systematic review of multidisciplinary interventions in heart failure.Heart.2005;91:899906.
  23. Taylor S,Bestall J,Cotter S, et al.Clinical service organisation for heart failure.Cochrane Database Syst Rev.2005(2):CD002752.pub2.
  24. Scott IA,Denaro CP,Bennett CJ, et al.Achieving better in‐hospital and after‐hospital care of patients with acute cardiac disease.Med J Aust.2004;180:S83S88.
  25. D'Agostino RB.Propensity score methods for bias reduction in the comparison of a treatment to a non‐randomized control group.Stat Med.1998;17:22652281.
  26. Philbin EF,Rocco TA,Lindenmuth NW,Ulrich K,McCall M,Jenkins P.The results of a randomized trial of a quality improvement intervention in the care of patients with heart failure.Am J Med.2000;109(6):443449.
  27. Yu DSF,Thompson DR,Lee DTF.Disease management programmes for older people with heart failure: crucial characteristics which improve post‐discharge outcomes.Eur Heart J.2006;27:596612.
  28. Weinberger M,Oddone EZ,Henderson WG.Does increased access to primary care reduce hospital readmissions?N Engl J Med.1996;334:14411447.
  29. Galbreath AD,Krasuski RA,Smith B, et al.Long‐term healthcare and cost outcomes of disease management in a large, randomized, community‐based population with heart failure.Circulation.2004;110(23):35183526.
  30. Baker DW,Einstadter D,Husak SS,Cebul R.Trends in postdischarge mortality and readmissions. Has length of stay declined too far?Arch Intern Med.2004;164:538544.
  31. Cleland JG,Gemmell I,Khand A,Boddy A.Is the prognosis of heart failure improving?Eur J Heart Fail.1999;1(3):229241.
  32. Lee DS,Mamdani MM,Austin PC, et al.Trends in heart failure outcomes and pharmacotherapy: 1992 to 2000.Am J Med.2004;116(9):581589.
  33. Zook C,Savickis SF,Moore FD.Repeated hospitalization for the same disease: a multiplier of national health costs.Milbank Mem Fund Q.1908;58(3):454471.
Issue
Journal of Hospital Medicine - 5(3)
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Journal of Hospital Medicine - 5(3)
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148-153
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148-153
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The paradox of readmission: Effect of a quality improvement program in hospitalized patients with heart failure
Display Headline
The paradox of readmission: Effect of a quality improvement program in hospitalized patients with heart failure
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congestive heart failure, disease management, patient readmission, quality of health care
Legacy Keywords
congestive heart failure, disease management, patient readmission, quality of health care
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UGIB vs. LGIB

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Upper versus lower gastrointestinal bleeding: A direct comparison of clinical presentation, outcomes, and resource utilization

Gastrointestinal bleeding (GIB) is a frequent reason for acute hospitalization, with estimated rates of hospitalization at 375 per 100,000 per year in the United States.1 GIB is not a specific disease but rather a diverse set of conditions that lead to the clinical manifestations associated with bleeding into the gastrointestinal tract. One of the most commonly used organizing frameworks in gastrointestinal bleeding is the differentiation between upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). There are important differences in the etiologies between the 2 sources. For example, acid‐related disease is a common etiology in UGIB but does not occur in LGIB. While some aspects of the acute management are shared between UGIB and LGIB, important differences exist in the management, including initial endoscopy and medication choice. There have been few direct comparisons of rates, resource use, and clinical outcomes between UGIB and LGIB.

Historically, rates of UGIB have been reported to exceed those of LGIB by 2‐fold to 8‐fold.25 Protocols, clinical practice guidelines, and policy decisions reflect this emphasis on UGIB.68 Among 9 guidelines hosted by National Guideline Clearinghouse addressing GIB, 6 were focused on UGIB, 2 on both UGIB and LGIB, and only 1 on LGIB.9 There are several reasons to believe that these relative incidence rates may not be accurate. First, recent advances in therapy and prevention of UGIB, such as the treatment of Helicobacter pylori infection; proton pump inhibitors (PPIs); and selective cyclooxygenase‐2 (COX‐2) inhibitors, may have affected the epidemiology of gastrointestinal bleeding.1016 Among these therapies, only COX‐2 inhibitors may also reduce the incidence of LGIB.14, 1618 Therefore, these advances may result in a disproportionate drop in UGIB relative to LGIB. In addition, known risk factors for both LGIB and UGIB, including advancing age and renal failure, are increasing in the general population.5, 19, 20 Finally, given the recent increased recommendations for aspirin therapy and systemic anticoagulation, exposure to aspirin and warfarin have increased, both risk factors for LGIB and UGIB.2124 Indeed, recent studies in the epidemiology of UGIB do suggest a changing pattern of etiologies of UGIB reflecting these advances.25 One study examining rates of both UGIB and LGIB demonstrate a decrease in hospitalizations overall for GIB driven by a reduction in UGIB while at the same time reporting an increase in the incidence of hospitalization for LGIB.1

In addition to a changing epidemiology, a second reason for a potential underestimation of LGIB incidence is one of methodology. There are well‐recognized limitations with using purely administrative data due to difficulties in accurately identifying patients with LGIB.26

Studies using large administrative databases may not accurately identify LGIB because of the poor sensitivity and specificity of International Classification of Diseases, Ninth revision, Clinical Modification (ICD‐9) codes for LGIB.5 While there are standard methods of identifying patients with UGIB using ICD‐9 codes,19 there is not an accepted standard for LGIB. Thus, estimates using only ICD‐9 codes may overidentify or underidentify patients with LGIB. Prior studies that have most accurately identified patients with LGIB used a 2‐step method to address this issue. The initial ICD‐9 identification included a high sensitivity/low specificity approach. These identified patient charts undergo chart review to confirm the presence of an LGIB.5 This method is labor intensive and cannot be done using administrative databases. No direct comparison of UGIB to LGIB among hospitalized patients using this 2‐step method has been done recently.

The current emphasis on UGIB as seen in the published guidelines could also be supported if patients with UGIB had greater resource utilization or worse clinical outcomes. Limited direct comparisons for these outcomes are available. However, 1 administrative database study reported similar mortality rates for UGIB (2.7%) and LGIB (2.9%) in 2006.1 No direct comparisons of other clinical outcomes or resource use outcomes are available. Therefore, the emphasis on UGIB in publications and guidelines is best supported by the incidence rates that are, as has already been discussed, problematic.

We conducted a retrospective cohort study to examine the incidences of UGIB and LGIB among patients admitted to an academic medical center over 2 years using methods designed to optimally identify patients with either UGIB or LGIB. Our study also examined differences in clinical outcomes and resource utilization between subjects with UGIB and LGIB to examine the relative severity of these 2 clinical entities. These results may be useful in determining the need to reconsider clinical approaches as well as protocols and guidelines among patients with gastrointestinal bleeding.

Patients and Methods

Patients

This retrospective cohort study evaluated all patients who were admitted with GIB to a large urban academic medical center from July 1, 2001 to June 30, 2003 and who consented to a larger study examining the effects of hospitalists on patient care. Subjects unable to provide consent due to death or lack of decisional capacity were consented via proxy. To identify patients with GIB, all patients were screened for a primary or secondary diagnosis of GIB using ICD 9 codes. These codes were selected for a very high sensitivity threshold to assure that all potential subjects with GIB were identified. All subjects identified using these codes underwent chart abstraction to determine if they met criteria for GIB. These inclusion criteria required documentation in any portion of the chart (including emergency department [ED] clinician documentation, admission note, nursing intake note, etc.) of signs or symptoms of GI hemorrhage upon admission, including: hematemesis, coffee ground emesis, gastrooccult‐positive emesis, melena, hematochezia, maroon stools, and hemoccult‐positive stools interpreted by the treating physician team as an acute GIB. Subjects identified using the ICD‐9 codes and confirmed to have an acute GIB by chart review were included in the study and underwent additional chart abstraction and administrative data analysis.

ICD‐9 codes for GIB included: esophageal varices with hemorrhage (456.0, 456.20), Mallory‐Weiss syndrome (530.7), gastric ulcer with hemorrhage (531.00531.61), duodenal ulcer with hemorrhage (532.00532.61), peptic ulcer, site unspecified, with hemorrhage (533.00533.61), gastrojejunal ulcer with hemorrhage (534.00534.61), gastritis with hemorrhage (535.61), angiodysplasia of stomach/duodenum with hemorrhage (537.83), hematemesis (578.0578.9), diverticular disease (562.00562.9), other disorders of the intestine (569.00569.9), congenital anomalies of the digestive system (751.00), proctocolitis (556.00), hemorrhoids (455.00455.6), nondysenteric colitis (006.2), noninfectious gastroenteritis and colitis (558.0558.9), salmonella gastroenteritis (003.3), malignant neoplasm of colon (153), familial adenomatous polyposis (211.3), and gastric varices (456.8).

Data

Trained research assistants performed chart abstraction with validation by the principal investigators (PIs) of the first 15 charts to ensure accuracy. Subsequently, research assistants consulted with PIs with any questions during abstracting with final decisions being made by PIs. Detailed chart abstraction collected admission medication lists as obtained by the admitting physician team, including the use of PPIs, histamine‐2 (H‐2) blockers, COX‐2 inhibitors, and medications known to increase the risk of GIB, such as nonselective NSAIDs (nsNSAIDs), aspirin, and other anticoagulants. Other clinical data including risk factors, comorbid illnesses, laboratory tests, and vital signs were also abstracted from subjects' charts.

The source (UGIB vs. LGIB) and etiology (peptic ulcer disease [PUD], varices, diverticula, etc.) of bleeding were assessed using endoscopic reports as the primary source. When no clear source was identified on endoscopy or no endoscopy was done, the abstracter would review all progress notes, discharge summaries, and other diagnostic test results such as angiography in order to identify the source of bleeding (UGIB vs. LGIB). Endoscopic reports that identified a patient as having a UGIB or LGIB but no confirmed etiology were classified as undetermined etiology unless review of the other clinical documentation provided a specific etiology.

Tachycardia was defined as pulse greater than 100 beats per minute. Orthostasis was defined by either a drop in systolic blood pressure of 20 mmHg or an increase in pulse of 10 beats per minute. Hospital administrative databases were utilized to obtain resource utilization (ie, length of stay [LOS], total cost of care, intensive care transfers), Charlson comorbidity index,27 30‐day readmission rate, and in‐hospital mortality. Hospital costs were determined using TSI cost accounting software (Transition Systems Incorporated [now Eclypsis Corporation], Boston, MA), a validated system to assess actual direct and indirect costs of care.

Statistical Analysis

Descriptive statistics (means and proportions) were calculated by location of GIB for all variables describing patient characteristics, clinical presentation, clinical outcomes, and resource utilization. Differences in age and Charlson comorbidity index by GIB location were evaluated using t tests. Differences in gender, race, and medication use were evaluated using chi‐squared tests of independence.

We fit generalized linear models to investigate differences by location of bleed for those variables measuring clinical outcomes (inpatient mortality, intensive care unit [ICU] transfer, emergency surgery, 30‐day readmission, change in hemoglobin) and those variables measuring resource outcomes (total cost, LOS, number of procedures, number of correct scopes, repeat scope indicator, incorrect scope indicator, number of red blood cell [RBC] transfusions). The repeat scope indicator was used to denote a repeat scope (either esophagogastroduodenoscopy [EGD] or colonoscopy) and the incorrect scope indicator was used to denote when the initial scope was negative and a follow‐up scope from the other direction was positive (negative EGD followed by positive colonoscopy or negative colonoscopy followed by positive EGD). For each variable we fit 2 regression models, the first model (unadjusted effect) only included location of bleed as a covariate. The second model (adjusted effect) included location of bleed, age, gender, race (black/not black) and Charlson comorbidity index as covariates. Binary outcomes were modeled using logistic regressions. For continuous variables, we determined the distribution and link of the outcome variable using residual diagnostics and by comparing the log likelihood and information criteria of competing models. All analyses were performed using STATA SE Version 9.0 (StataCorp, College Station, TX)

This study was approved by the University of Chicago Institutional Review Board.

Results

During the 2 years of observation, a total of 7741 subjects were admitted to the internal medicine service and enrolled in the hospitalist study. Of these, 1014 had a primary or secondary ICD‐9 code that may be consistent with UGIB or LGIB and underwent chart review to determine if they had an acute GIB. Out of 1014 subjects, 647 were determined not to have an acute GI hemorrhage and were excluded from the remaining analyses; 367 of the 1104 subjects identified by ICD‐9 codes were found to have a clinical presentation consistent with GIB and were included in this study. A total of 180 of these 367 had UGIB and 187 had LGIB. The mean age was 62.4 years, 56.7% were female, 82.6% were African American, 12.7% were Caucasian, and the mean Charlson index was 1.5. (Table 1) Among baseline characteristics, both gender and age were statistically associated with a difference in rates of upper vs. lower source bleeding, with LGIB patients more likely to be female (P = 0.01) and older (P < 0.001). Etiologies of UGIB include erosive disease, peptic ulcer disease, variceal bleeding, arteriovenous malformation, and malignancy. Etiologies of LGIB include: diverticulosis, colitis, arteriovenous malformation, cancer, ischemic colitis, polyp, hemorrhoidal bleed, ulcer, inflammatory bowel disease, other, and not determined (Table 2).

Baseline Characteristics Among All Subjects Admitted for GI Hemorrhage
 Upper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

Age (years), mean (SD)62.4 (18.0)58.6 (18.2)66.0 (17.1)<0.001
Female gender (%)56.750.063.10.01
Race (%)    
African American82.685.380.10.43
White12.710.714.5 
Other4.74.05.4 
Charlson comorbidity index, mean (SD)1.5 (1.5)1.6 (1.6)1.4 (1.5)0.44
GI Bleeding Etiologies
Lower GI Bleed (n = 187)Upper GI Bleed (n = 180)
EtiologyFrequencyPercent of Total (%)EtiologyFrequencyPercent of Total (%)
  • NOTE: n = 367. Totals add up to >100% for upper GI bleed as some patients had more than 1 source identified.

  • Abbreviations: AVM, arteriovenous malformation; GI, gastrointestinal; IBD, inflammatory bowel disease; NOS, not otherwise specified.

Diverticulosis7641Erosive disease8648
Not identified3820Peptic ulcer5128
Colitis, NOS147Not identified2614
AVM137Mallory Weiss179
Cancer116Varices84
Ischemic colitis95AVMs53
Polyp95Mass/cancer53
Hemorrhoid84   
Ulcer53   
Other31   
IBD1<1   

Baseline use of medications known to be associated with either increased or decreased risk of GIB was common. Approximately one‐third of subjects with both LGIB and UGIB used aspirin and 10% used warfarin. LGIB subjects were less likely to use an nsNSAID (P < 0.001), but more likely to use a proton pump inhibitor (PPI) (P = 0.06) (Table 3).

Baseline Medication Use Among All Subjects Admitted for Gastrointestinal Hemorrhage
 Upper and Lower GI Bleeding (%) (n = 367)Upper GI Bleeding (%) (n = 180)Lower GI Bleeding (%) (n = 187)P Value*
  • Abbreviations: COX‐2, cyclooxygenase 2; GI, gastrointestinal; nsNSAID, nonselective nonsteroidal antiinflammatory drug; PPI, proton pump inhibitor.

  • P value comparing upper GI bleeding to lower GI bleeding.

Aspirin34.931.837.40.28
nsNSAID12.920.86.4< 0.001
COX‐2 selective inhibitor8.26.59.60.29
Warfarin10.98.412.80.19
PPI24.319.528.30.06
nsNSAID + PPI1.81.32.10.56
COX‐2 + PPI2.91.34.30.11

Key initial clinical presentation findings included vital sign abnormalities and admission hemoglobin levels. While hypotension was not common (4.7%), resting tachycardia (37%) and orthostasis (16%) were seen frequently. Subjects with LGIB were significantly less likely than those with UGIB to present with orthostasis (8.8% vs. 21.0%, respectively; P = 0.006) and resting tachycardia (32.3% vs. 42.5%, respectively; P = 0.04). Subjects with LGIB had a higher admission hemoglobin than those with UGIB (10.7 vs. 9.7, respectively; P < 0.001) (Table 4).

Admission Clinical Findings Among All Subjects Admitted for Gastrointestinal Hemorrhage
Clinical FindingUpper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value*
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • P value comparing upper GI bleeding to lower GI bleeding.

Hypotension (%)4.75.73.80.39
Resting tachycardia (%)37.342.532.30.04
Orthostatic hypotension (%)16.221.08.80.006
Admission hemoglobin (g/dL), mean (SD)10.2 (2.6)9.7 (2.7)10.7 (2.5)<0.001

We also examined several clinical outcomes. When comparing LGIB to UGIB patients for these clinical outcomes using bivariate and multivariate statistics, there was no difference for in‐hospital mortality (1.1% vs. 1.1%), transfer to ICU (16.0% vs. 13.9%), 30‐day readmission (5.9% vs.7.8%), number of red blood cell (RBC) transfusions (2.7 vs. 2.4), or need for GI surgery (1.1% vs. 0.0%). The mean drop in hemoglobin was greater among subjects with LGIB compared to UGIB (1.9 g/dL vs. 1.5 g/dL, respectively) by both bivariate (P = 0.01) and multivariate (P = 0.003) analyses (Table 5).

Comparison of In‐hospital Clinical Outcomes Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; ICU, intensive care unit; OLS, ordinary least squares; RBC, red blood cell; SD, standard deviation.

  • Modeled using logistic regression.

  • Modeled using OLS regression.

In‐hospital mortality (%)*1.11.10.970.74
Transfer to ICU (%)*13.916.00.560.44
Drop in hemoglobin (g/dL), mean (SD)1.5 (1.5)1.9 (1.6)0.010.003
Packed RBC transfusions required (units), mean (SD)*2.4 (2.9)2.7 (3.7)0.360.33
Surgery for GI bleeding (%)0.0%1.1  
30‐day readmission rate (%)*7.85.90.490.45

Mean costs were $11,892 for LGIB and $14,301 for UGIB and median costs were $7,890 for LGIB and $9,548 for UGIB, but were not statistically different. LOS was also similar between subjects with LGIB (5.1 days) and UGIB (5.7 days). In bivariate and multivariate analyses, UGIB subjects had a similar mean number of endoscopic procedures (1.3) compared to LGIB subjects (1.2). Thirteen percent of subjects with UGIB required a second EGD while only 8% of subjects with LGIB required 2 colonoscopies. In addition, 29% of subjects with LGIB received an EGD while only 16% of subjects with an UGIB received a colonoscopy (P = 0.001) (Table 6).

Comparison of Resource Utilization Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; GLM, generalized linear model; OLS, ordinary least squares; SD, standard deviation.

  • Modeled using a GLM with a gamma distribution and log link.

  • Modeled using OLS regression.

Cost ($), mean (SD)*14,301 (17,196)11,892 (13,100)0.130.21
Cost ($), median$9,548$7,890  
Length of stay (days), mean (SD)*5.7 (7.0)5.1 (5.3)0.370.72
Number of endoscopies/ patient, mean (SD)1.3 (0.5)1.2 (0.9)0.180.20

Conclusions

This study represents one of the largest direct comparisons of LGIB to UGIB not based on administrative databases. The most striking finding was the nearly equal rates of LGIB and UGIB. There are 2 likely explanations for this surprising result. First, there may be methodological reasons that we identified a greater proportion of true LGIBs; our study used a highly sensitive search strategy of ICD‐9 coding with confirmatory chart abstraction to ensure that as many LGIB and UGIB cases would be identified as possible while also excluding cases not meeting accepted criteria for GIB. The second possibility is that there is an actual change in epidemiology of GIB. Known risk factors for LGIB are increasing such as advancing age, increased use of chronic aspirin therapy, and renal disease. At the same time, significant advances in the treatment and prevention of UGIB have been made. Recent studies have demonstrated similar trends in admissions for upper and lower GI complications, suggesting that there may be a changing epidemiology due primarily to reductions in upper GI complications.1, 16

Either explanation would have implications for the care of patients with GIB. Clinical decision‐making based on prior literature would support that in ambiguous clinical situations and initial evaluation for an UGIB is appropriate. Most risk stratification literature and clinical guidelines focus on UGIB. If rates of LGIB and UGIB are similar, then existing clinical decision protocols may need to be reevaluated to incorporate the higher likelihood of LGIB. This reevaluation would be less important if the clinical outcomes or resource utilization of UGIB was significantly greater than that for LGIB, but we did not find this was the case. Similarly, if the ability to distinguish between LGIB and UGIB were robust on clinical signs and symptoms, then a reevaluation would be less important. However, we found fairly similar numbers of patients initially receiving evaluation for UGIB then being evaluated for LGIB as we found patients initially receiving evaluation for LGIB then being evaluated for UGIB. This suggests the potential benefit of clinical decision protocols that could better distinguish between UGIB and LGIB and account for the potentially higher incidence of LGIB than previously thought.

In addition to affecting the attention paid to LGIB for acute management, a changed understanding of incidence could also affect the attention paid to prevention of LGIB. Of the recent nonendoscopic advances in the treatment and prevention of GIB, only the use of COX‐2s (when used in place of traditional nsNSAIDs) reduces the risk of both LGIB and UGIB;14, 1618 H .pylori treatment and PPIs only prevent UGIB. Therefore, if the clinical and financial burdens of LGIB are similar to those seen in UGIB, more attention may need to be focused on preventing LGIB.

Baseline medication use was notable primarily for the similarities between UGIB and LGIB. Agents known to affect the rates of GIB were common in both groups. Over one‐third of the population was using aspirin and 10% were taking warfarin. Over 20% of subjects were taking an nsNSAID or a COX‐2 inhibitor. Almost one‐quarter of subjects were taking a PPI, agents known to decrease rates of UGIB and potentially increase LGIB through the risk of C. difficile colitis. Notably, the only statistically significant difference in baseline medication use between subjects with UGIB and LGIB was the more than 3‐fold higher use of nsNSAIDs in patients with UGIB as compared to LGIB. While current guidelines are not clear and consistent about which populations of at‐risk patients should receive GI prophylaxis,2830 these results suggest that patients admitted with GIB are very likely to be taking medications which impact the risk of GIB.

In terms of disease severity, the clinical presentation at admission suggests a greater degree of hemodynamic instability among subjects with UGIB. Rates of orthostatic hypotension and resting tachycardia are higher in UGIB subjects, as well as having a lower mean hemoglobin levels at presentation. However, despite the more severe clinical presentation, clinical outcomes did not differ significantly between the 2 bleeding sources. Thus, the most relevant clinical outcomes suggest that the severity of both LGIB and UGIB are similar. This similarity again suggest that the clinical burden of LGIB is not significantly different than UGIB.

Our results concerning resource utilization demonstrate a similar pattern. While the point estimates for costs and LOS suggest that UGIB may be associated with higher resource utilization, these differences were not significant in either bivariate or multivariate analyses. Those subjects with UGIB did receive more total endoscopic procedures than subjects with LGIB. More interesting though was that 24% of all subjects received an endoscopy of the opposite site (LGIB with EGD and UGIB with colonoscopy). These results suggest that the site of bleeding is not clear in a significant proportion of patients who present with GIB. These additional endoscopies are associated with increased risk, costs, LOS, and discomfort to patients. Improving our ability to accurately predict the source (upper vs. lower) of bleeding would allow us to reduce the number of these excess endoscopies. Additionally, it is interesting that despite the almost universal use of endoscopies, 20% of LGIB and 14% of UGIB subjects could not have a specific etiology identified during endoscopy or subsequent workup.

There are some important limitations to this study. While the sample size is among the largest of its type involving chart abstraction, it may be underpowered to detect some differences. Additionally, our results are from a single urban academic medical center with a patient population that is predominantly African American, which may limit generalizability. This study required consent and therefore only examines a subset of patients admitted to the medical center with GIB, which could potentially introduce bias into the sample. However, it is not clear why there would be systematic differences in subjects who choose to consent vs. those who decide not to consent that would affect the results of this study in substantive ways.

Despite significant efforts at identifying all subjects with GIB admitted during this time period, there were potential methodological reasons that may have resulted in some cases being missed. Only subjects admitted to a medicine service were approached for consent. All subjects in this medical center with GIB are admitted to a medicine service. We captured all subjects who were initially admitted to a medicine service as well as those admitted initially to an ICU and then transferred to the floor at any point prior to discharge. It is possible, though, that a subject would be admitted to an ICU for GIB and die prior to being transferred to the floor. While it is the impression of the director of the ICU that this would be a very unusual event, as most of the patients would be discharged to the floor prior to death (personal communication), given the very low mortality rate seen in this study, small numbers of missed events could have a significant impact on the interpretation of in‐hospital mortality results. It is also important to note that this medical center did not have the ability to perform endoscopy prior to admission for patients with GIB at the time of the study; all patients who presented with GIB would have been admitted and identified for this study. Finally, we were unable to routinely identify the rationale for obtaining an endoscopic exam. We assumed that all endoscopic exams were done for the purpose of evaluating and/or treating the GIB for which the subject was admitted. It is possible that some subjects had additional endoscopies for other reasons, which would have led to our overestimating the rates of additional endoscopies for GIB.

This study highlights the similarities between LGIB and UGIB rather than the differences. There were few significant differences between the 2 bleeding sources in terms of incidence, clinical outcomes, and resource utilization. In fact, the study also suggests that determining the source of bleeding may not be clear, given the high rates of opposite site endoscopies. While this study did reveal several similarities between UGIB and LGIB, it also highlights the need to identify improved strategies to improve the sensitivity and specificity of identification of LGIB compared to UGIB, both for clinical purposes and for research. The value of such improved clinical algorithms have the potential to improve both the cost and outcomes of care, while better algorithms for separating UGIB and LGIB using administrative data might help produce more precise estimates of costs and clinical outcomes, and aid in the development of risk stratification models.

References
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Article PDF
Issue
Journal of Hospital Medicine - 5(3)
Page Number
141-147
Legacy Keywords
cost effectiveness, endoscopy, epidemiology, gastrointestinal hemorrhage
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Gastrointestinal bleeding (GIB) is a frequent reason for acute hospitalization, with estimated rates of hospitalization at 375 per 100,000 per year in the United States.1 GIB is not a specific disease but rather a diverse set of conditions that lead to the clinical manifestations associated with bleeding into the gastrointestinal tract. One of the most commonly used organizing frameworks in gastrointestinal bleeding is the differentiation between upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). There are important differences in the etiologies between the 2 sources. For example, acid‐related disease is a common etiology in UGIB but does not occur in LGIB. While some aspects of the acute management are shared between UGIB and LGIB, important differences exist in the management, including initial endoscopy and medication choice. There have been few direct comparisons of rates, resource use, and clinical outcomes between UGIB and LGIB.

Historically, rates of UGIB have been reported to exceed those of LGIB by 2‐fold to 8‐fold.25 Protocols, clinical practice guidelines, and policy decisions reflect this emphasis on UGIB.68 Among 9 guidelines hosted by National Guideline Clearinghouse addressing GIB, 6 were focused on UGIB, 2 on both UGIB and LGIB, and only 1 on LGIB.9 There are several reasons to believe that these relative incidence rates may not be accurate. First, recent advances in therapy and prevention of UGIB, such as the treatment of Helicobacter pylori infection; proton pump inhibitors (PPIs); and selective cyclooxygenase‐2 (COX‐2) inhibitors, may have affected the epidemiology of gastrointestinal bleeding.1016 Among these therapies, only COX‐2 inhibitors may also reduce the incidence of LGIB.14, 1618 Therefore, these advances may result in a disproportionate drop in UGIB relative to LGIB. In addition, known risk factors for both LGIB and UGIB, including advancing age and renal failure, are increasing in the general population.5, 19, 20 Finally, given the recent increased recommendations for aspirin therapy and systemic anticoagulation, exposure to aspirin and warfarin have increased, both risk factors for LGIB and UGIB.2124 Indeed, recent studies in the epidemiology of UGIB do suggest a changing pattern of etiologies of UGIB reflecting these advances.25 One study examining rates of both UGIB and LGIB demonstrate a decrease in hospitalizations overall for GIB driven by a reduction in UGIB while at the same time reporting an increase in the incidence of hospitalization for LGIB.1

In addition to a changing epidemiology, a second reason for a potential underestimation of LGIB incidence is one of methodology. There are well‐recognized limitations with using purely administrative data due to difficulties in accurately identifying patients with LGIB.26

Studies using large administrative databases may not accurately identify LGIB because of the poor sensitivity and specificity of International Classification of Diseases, Ninth revision, Clinical Modification (ICD‐9) codes for LGIB.5 While there are standard methods of identifying patients with UGIB using ICD‐9 codes,19 there is not an accepted standard for LGIB. Thus, estimates using only ICD‐9 codes may overidentify or underidentify patients with LGIB. Prior studies that have most accurately identified patients with LGIB used a 2‐step method to address this issue. The initial ICD‐9 identification included a high sensitivity/low specificity approach. These identified patient charts undergo chart review to confirm the presence of an LGIB.5 This method is labor intensive and cannot be done using administrative databases. No direct comparison of UGIB to LGIB among hospitalized patients using this 2‐step method has been done recently.

The current emphasis on UGIB as seen in the published guidelines could also be supported if patients with UGIB had greater resource utilization or worse clinical outcomes. Limited direct comparisons for these outcomes are available. However, 1 administrative database study reported similar mortality rates for UGIB (2.7%) and LGIB (2.9%) in 2006.1 No direct comparisons of other clinical outcomes or resource use outcomes are available. Therefore, the emphasis on UGIB in publications and guidelines is best supported by the incidence rates that are, as has already been discussed, problematic.

We conducted a retrospective cohort study to examine the incidences of UGIB and LGIB among patients admitted to an academic medical center over 2 years using methods designed to optimally identify patients with either UGIB or LGIB. Our study also examined differences in clinical outcomes and resource utilization between subjects with UGIB and LGIB to examine the relative severity of these 2 clinical entities. These results may be useful in determining the need to reconsider clinical approaches as well as protocols and guidelines among patients with gastrointestinal bleeding.

Patients and Methods

Patients

This retrospective cohort study evaluated all patients who were admitted with GIB to a large urban academic medical center from July 1, 2001 to June 30, 2003 and who consented to a larger study examining the effects of hospitalists on patient care. Subjects unable to provide consent due to death or lack of decisional capacity were consented via proxy. To identify patients with GIB, all patients were screened for a primary or secondary diagnosis of GIB using ICD 9 codes. These codes were selected for a very high sensitivity threshold to assure that all potential subjects with GIB were identified. All subjects identified using these codes underwent chart abstraction to determine if they met criteria for GIB. These inclusion criteria required documentation in any portion of the chart (including emergency department [ED] clinician documentation, admission note, nursing intake note, etc.) of signs or symptoms of GI hemorrhage upon admission, including: hematemesis, coffee ground emesis, gastrooccult‐positive emesis, melena, hematochezia, maroon stools, and hemoccult‐positive stools interpreted by the treating physician team as an acute GIB. Subjects identified using the ICD‐9 codes and confirmed to have an acute GIB by chart review were included in the study and underwent additional chart abstraction and administrative data analysis.

ICD‐9 codes for GIB included: esophageal varices with hemorrhage (456.0, 456.20), Mallory‐Weiss syndrome (530.7), gastric ulcer with hemorrhage (531.00531.61), duodenal ulcer with hemorrhage (532.00532.61), peptic ulcer, site unspecified, with hemorrhage (533.00533.61), gastrojejunal ulcer with hemorrhage (534.00534.61), gastritis with hemorrhage (535.61), angiodysplasia of stomach/duodenum with hemorrhage (537.83), hematemesis (578.0578.9), diverticular disease (562.00562.9), other disorders of the intestine (569.00569.9), congenital anomalies of the digestive system (751.00), proctocolitis (556.00), hemorrhoids (455.00455.6), nondysenteric colitis (006.2), noninfectious gastroenteritis and colitis (558.0558.9), salmonella gastroenteritis (003.3), malignant neoplasm of colon (153), familial adenomatous polyposis (211.3), and gastric varices (456.8).

Data

Trained research assistants performed chart abstraction with validation by the principal investigators (PIs) of the first 15 charts to ensure accuracy. Subsequently, research assistants consulted with PIs with any questions during abstracting with final decisions being made by PIs. Detailed chart abstraction collected admission medication lists as obtained by the admitting physician team, including the use of PPIs, histamine‐2 (H‐2) blockers, COX‐2 inhibitors, and medications known to increase the risk of GIB, such as nonselective NSAIDs (nsNSAIDs), aspirin, and other anticoagulants. Other clinical data including risk factors, comorbid illnesses, laboratory tests, and vital signs were also abstracted from subjects' charts.

The source (UGIB vs. LGIB) and etiology (peptic ulcer disease [PUD], varices, diverticula, etc.) of bleeding were assessed using endoscopic reports as the primary source. When no clear source was identified on endoscopy or no endoscopy was done, the abstracter would review all progress notes, discharge summaries, and other diagnostic test results such as angiography in order to identify the source of bleeding (UGIB vs. LGIB). Endoscopic reports that identified a patient as having a UGIB or LGIB but no confirmed etiology were classified as undetermined etiology unless review of the other clinical documentation provided a specific etiology.

Tachycardia was defined as pulse greater than 100 beats per minute. Orthostasis was defined by either a drop in systolic blood pressure of 20 mmHg or an increase in pulse of 10 beats per minute. Hospital administrative databases were utilized to obtain resource utilization (ie, length of stay [LOS], total cost of care, intensive care transfers), Charlson comorbidity index,27 30‐day readmission rate, and in‐hospital mortality. Hospital costs were determined using TSI cost accounting software (Transition Systems Incorporated [now Eclypsis Corporation], Boston, MA), a validated system to assess actual direct and indirect costs of care.

Statistical Analysis

Descriptive statistics (means and proportions) were calculated by location of GIB for all variables describing patient characteristics, clinical presentation, clinical outcomes, and resource utilization. Differences in age and Charlson comorbidity index by GIB location were evaluated using t tests. Differences in gender, race, and medication use were evaluated using chi‐squared tests of independence.

We fit generalized linear models to investigate differences by location of bleed for those variables measuring clinical outcomes (inpatient mortality, intensive care unit [ICU] transfer, emergency surgery, 30‐day readmission, change in hemoglobin) and those variables measuring resource outcomes (total cost, LOS, number of procedures, number of correct scopes, repeat scope indicator, incorrect scope indicator, number of red blood cell [RBC] transfusions). The repeat scope indicator was used to denote a repeat scope (either esophagogastroduodenoscopy [EGD] or colonoscopy) and the incorrect scope indicator was used to denote when the initial scope was negative and a follow‐up scope from the other direction was positive (negative EGD followed by positive colonoscopy or negative colonoscopy followed by positive EGD). For each variable we fit 2 regression models, the first model (unadjusted effect) only included location of bleed as a covariate. The second model (adjusted effect) included location of bleed, age, gender, race (black/not black) and Charlson comorbidity index as covariates. Binary outcomes were modeled using logistic regressions. For continuous variables, we determined the distribution and link of the outcome variable using residual diagnostics and by comparing the log likelihood and information criteria of competing models. All analyses were performed using STATA SE Version 9.0 (StataCorp, College Station, TX)

This study was approved by the University of Chicago Institutional Review Board.

Results

During the 2 years of observation, a total of 7741 subjects were admitted to the internal medicine service and enrolled in the hospitalist study. Of these, 1014 had a primary or secondary ICD‐9 code that may be consistent with UGIB or LGIB and underwent chart review to determine if they had an acute GIB. Out of 1014 subjects, 647 were determined not to have an acute GI hemorrhage and were excluded from the remaining analyses; 367 of the 1104 subjects identified by ICD‐9 codes were found to have a clinical presentation consistent with GIB and were included in this study. A total of 180 of these 367 had UGIB and 187 had LGIB. The mean age was 62.4 years, 56.7% were female, 82.6% were African American, 12.7% were Caucasian, and the mean Charlson index was 1.5. (Table 1) Among baseline characteristics, both gender and age were statistically associated with a difference in rates of upper vs. lower source bleeding, with LGIB patients more likely to be female (P = 0.01) and older (P < 0.001). Etiologies of UGIB include erosive disease, peptic ulcer disease, variceal bleeding, arteriovenous malformation, and malignancy. Etiologies of LGIB include: diverticulosis, colitis, arteriovenous malformation, cancer, ischemic colitis, polyp, hemorrhoidal bleed, ulcer, inflammatory bowel disease, other, and not determined (Table 2).

Baseline Characteristics Among All Subjects Admitted for GI Hemorrhage
 Upper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

Age (years), mean (SD)62.4 (18.0)58.6 (18.2)66.0 (17.1)<0.001
Female gender (%)56.750.063.10.01
Race (%)    
African American82.685.380.10.43
White12.710.714.5 
Other4.74.05.4 
Charlson comorbidity index, mean (SD)1.5 (1.5)1.6 (1.6)1.4 (1.5)0.44
GI Bleeding Etiologies
Lower GI Bleed (n = 187)Upper GI Bleed (n = 180)
EtiologyFrequencyPercent of Total (%)EtiologyFrequencyPercent of Total (%)
  • NOTE: n = 367. Totals add up to >100% for upper GI bleed as some patients had more than 1 source identified.

  • Abbreviations: AVM, arteriovenous malformation; GI, gastrointestinal; IBD, inflammatory bowel disease; NOS, not otherwise specified.

Diverticulosis7641Erosive disease8648
Not identified3820Peptic ulcer5128
Colitis, NOS147Not identified2614
AVM137Mallory Weiss179
Cancer116Varices84
Ischemic colitis95AVMs53
Polyp95Mass/cancer53
Hemorrhoid84   
Ulcer53   
Other31   
IBD1<1   

Baseline use of medications known to be associated with either increased or decreased risk of GIB was common. Approximately one‐third of subjects with both LGIB and UGIB used aspirin and 10% used warfarin. LGIB subjects were less likely to use an nsNSAID (P < 0.001), but more likely to use a proton pump inhibitor (PPI) (P = 0.06) (Table 3).

Baseline Medication Use Among All Subjects Admitted for Gastrointestinal Hemorrhage
 Upper and Lower GI Bleeding (%) (n = 367)Upper GI Bleeding (%) (n = 180)Lower GI Bleeding (%) (n = 187)P Value*
  • Abbreviations: COX‐2, cyclooxygenase 2; GI, gastrointestinal; nsNSAID, nonselective nonsteroidal antiinflammatory drug; PPI, proton pump inhibitor.

  • P value comparing upper GI bleeding to lower GI bleeding.

Aspirin34.931.837.40.28
nsNSAID12.920.86.4< 0.001
COX‐2 selective inhibitor8.26.59.60.29
Warfarin10.98.412.80.19
PPI24.319.528.30.06
nsNSAID + PPI1.81.32.10.56
COX‐2 + PPI2.91.34.30.11

Key initial clinical presentation findings included vital sign abnormalities and admission hemoglobin levels. While hypotension was not common (4.7%), resting tachycardia (37%) and orthostasis (16%) were seen frequently. Subjects with LGIB were significantly less likely than those with UGIB to present with orthostasis (8.8% vs. 21.0%, respectively; P = 0.006) and resting tachycardia (32.3% vs. 42.5%, respectively; P = 0.04). Subjects with LGIB had a higher admission hemoglobin than those with UGIB (10.7 vs. 9.7, respectively; P < 0.001) (Table 4).

Admission Clinical Findings Among All Subjects Admitted for Gastrointestinal Hemorrhage
Clinical FindingUpper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value*
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • P value comparing upper GI bleeding to lower GI bleeding.

Hypotension (%)4.75.73.80.39
Resting tachycardia (%)37.342.532.30.04
Orthostatic hypotension (%)16.221.08.80.006
Admission hemoglobin (g/dL), mean (SD)10.2 (2.6)9.7 (2.7)10.7 (2.5)<0.001

We also examined several clinical outcomes. When comparing LGIB to UGIB patients for these clinical outcomes using bivariate and multivariate statistics, there was no difference for in‐hospital mortality (1.1% vs. 1.1%), transfer to ICU (16.0% vs. 13.9%), 30‐day readmission (5.9% vs.7.8%), number of red blood cell (RBC) transfusions (2.7 vs. 2.4), or need for GI surgery (1.1% vs. 0.0%). The mean drop in hemoglobin was greater among subjects with LGIB compared to UGIB (1.9 g/dL vs. 1.5 g/dL, respectively) by both bivariate (P = 0.01) and multivariate (P = 0.003) analyses (Table 5).

Comparison of In‐hospital Clinical Outcomes Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; ICU, intensive care unit; OLS, ordinary least squares; RBC, red blood cell; SD, standard deviation.

  • Modeled using logistic regression.

  • Modeled using OLS regression.

In‐hospital mortality (%)*1.11.10.970.74
Transfer to ICU (%)*13.916.00.560.44
Drop in hemoglobin (g/dL), mean (SD)1.5 (1.5)1.9 (1.6)0.010.003
Packed RBC transfusions required (units), mean (SD)*2.4 (2.9)2.7 (3.7)0.360.33
Surgery for GI bleeding (%)0.0%1.1  
30‐day readmission rate (%)*7.85.90.490.45

Mean costs were $11,892 for LGIB and $14,301 for UGIB and median costs were $7,890 for LGIB and $9,548 for UGIB, but were not statistically different. LOS was also similar between subjects with LGIB (5.1 days) and UGIB (5.7 days). In bivariate and multivariate analyses, UGIB subjects had a similar mean number of endoscopic procedures (1.3) compared to LGIB subjects (1.2). Thirteen percent of subjects with UGIB required a second EGD while only 8% of subjects with LGIB required 2 colonoscopies. In addition, 29% of subjects with LGIB received an EGD while only 16% of subjects with an UGIB received a colonoscopy (P = 0.001) (Table 6).

Comparison of Resource Utilization Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; GLM, generalized linear model; OLS, ordinary least squares; SD, standard deviation.

  • Modeled using a GLM with a gamma distribution and log link.

  • Modeled using OLS regression.

Cost ($), mean (SD)*14,301 (17,196)11,892 (13,100)0.130.21
Cost ($), median$9,548$7,890  
Length of stay (days), mean (SD)*5.7 (7.0)5.1 (5.3)0.370.72
Number of endoscopies/ patient, mean (SD)1.3 (0.5)1.2 (0.9)0.180.20

Conclusions

This study represents one of the largest direct comparisons of LGIB to UGIB not based on administrative databases. The most striking finding was the nearly equal rates of LGIB and UGIB. There are 2 likely explanations for this surprising result. First, there may be methodological reasons that we identified a greater proportion of true LGIBs; our study used a highly sensitive search strategy of ICD‐9 coding with confirmatory chart abstraction to ensure that as many LGIB and UGIB cases would be identified as possible while also excluding cases not meeting accepted criteria for GIB. The second possibility is that there is an actual change in epidemiology of GIB. Known risk factors for LGIB are increasing such as advancing age, increased use of chronic aspirin therapy, and renal disease. At the same time, significant advances in the treatment and prevention of UGIB have been made. Recent studies have demonstrated similar trends in admissions for upper and lower GI complications, suggesting that there may be a changing epidemiology due primarily to reductions in upper GI complications.1, 16

Either explanation would have implications for the care of patients with GIB. Clinical decision‐making based on prior literature would support that in ambiguous clinical situations and initial evaluation for an UGIB is appropriate. Most risk stratification literature and clinical guidelines focus on UGIB. If rates of LGIB and UGIB are similar, then existing clinical decision protocols may need to be reevaluated to incorporate the higher likelihood of LGIB. This reevaluation would be less important if the clinical outcomes or resource utilization of UGIB was significantly greater than that for LGIB, but we did not find this was the case. Similarly, if the ability to distinguish between LGIB and UGIB were robust on clinical signs and symptoms, then a reevaluation would be less important. However, we found fairly similar numbers of patients initially receiving evaluation for UGIB then being evaluated for LGIB as we found patients initially receiving evaluation for LGIB then being evaluated for UGIB. This suggests the potential benefit of clinical decision protocols that could better distinguish between UGIB and LGIB and account for the potentially higher incidence of LGIB than previously thought.

In addition to affecting the attention paid to LGIB for acute management, a changed understanding of incidence could also affect the attention paid to prevention of LGIB. Of the recent nonendoscopic advances in the treatment and prevention of GIB, only the use of COX‐2s (when used in place of traditional nsNSAIDs) reduces the risk of both LGIB and UGIB;14, 1618 H .pylori treatment and PPIs only prevent UGIB. Therefore, if the clinical and financial burdens of LGIB are similar to those seen in UGIB, more attention may need to be focused on preventing LGIB.

Baseline medication use was notable primarily for the similarities between UGIB and LGIB. Agents known to affect the rates of GIB were common in both groups. Over one‐third of the population was using aspirin and 10% were taking warfarin. Over 20% of subjects were taking an nsNSAID or a COX‐2 inhibitor. Almost one‐quarter of subjects were taking a PPI, agents known to decrease rates of UGIB and potentially increase LGIB through the risk of C. difficile colitis. Notably, the only statistically significant difference in baseline medication use between subjects with UGIB and LGIB was the more than 3‐fold higher use of nsNSAIDs in patients with UGIB as compared to LGIB. While current guidelines are not clear and consistent about which populations of at‐risk patients should receive GI prophylaxis,2830 these results suggest that patients admitted with GIB are very likely to be taking medications which impact the risk of GIB.

In terms of disease severity, the clinical presentation at admission suggests a greater degree of hemodynamic instability among subjects with UGIB. Rates of orthostatic hypotension and resting tachycardia are higher in UGIB subjects, as well as having a lower mean hemoglobin levels at presentation. However, despite the more severe clinical presentation, clinical outcomes did not differ significantly between the 2 bleeding sources. Thus, the most relevant clinical outcomes suggest that the severity of both LGIB and UGIB are similar. This similarity again suggest that the clinical burden of LGIB is not significantly different than UGIB.

Our results concerning resource utilization demonstrate a similar pattern. While the point estimates for costs and LOS suggest that UGIB may be associated with higher resource utilization, these differences were not significant in either bivariate or multivariate analyses. Those subjects with UGIB did receive more total endoscopic procedures than subjects with LGIB. More interesting though was that 24% of all subjects received an endoscopy of the opposite site (LGIB with EGD and UGIB with colonoscopy). These results suggest that the site of bleeding is not clear in a significant proportion of patients who present with GIB. These additional endoscopies are associated with increased risk, costs, LOS, and discomfort to patients. Improving our ability to accurately predict the source (upper vs. lower) of bleeding would allow us to reduce the number of these excess endoscopies. Additionally, it is interesting that despite the almost universal use of endoscopies, 20% of LGIB and 14% of UGIB subjects could not have a specific etiology identified during endoscopy or subsequent workup.

There are some important limitations to this study. While the sample size is among the largest of its type involving chart abstraction, it may be underpowered to detect some differences. Additionally, our results are from a single urban academic medical center with a patient population that is predominantly African American, which may limit generalizability. This study required consent and therefore only examines a subset of patients admitted to the medical center with GIB, which could potentially introduce bias into the sample. However, it is not clear why there would be systematic differences in subjects who choose to consent vs. those who decide not to consent that would affect the results of this study in substantive ways.

Despite significant efforts at identifying all subjects with GIB admitted during this time period, there were potential methodological reasons that may have resulted in some cases being missed. Only subjects admitted to a medicine service were approached for consent. All subjects in this medical center with GIB are admitted to a medicine service. We captured all subjects who were initially admitted to a medicine service as well as those admitted initially to an ICU and then transferred to the floor at any point prior to discharge. It is possible, though, that a subject would be admitted to an ICU for GIB and die prior to being transferred to the floor. While it is the impression of the director of the ICU that this would be a very unusual event, as most of the patients would be discharged to the floor prior to death (personal communication), given the very low mortality rate seen in this study, small numbers of missed events could have a significant impact on the interpretation of in‐hospital mortality results. It is also important to note that this medical center did not have the ability to perform endoscopy prior to admission for patients with GIB at the time of the study; all patients who presented with GIB would have been admitted and identified for this study. Finally, we were unable to routinely identify the rationale for obtaining an endoscopic exam. We assumed that all endoscopic exams were done for the purpose of evaluating and/or treating the GIB for which the subject was admitted. It is possible that some subjects had additional endoscopies for other reasons, which would have led to our overestimating the rates of additional endoscopies for GIB.

This study highlights the similarities between LGIB and UGIB rather than the differences. There were few significant differences between the 2 bleeding sources in terms of incidence, clinical outcomes, and resource utilization. In fact, the study also suggests that determining the source of bleeding may not be clear, given the high rates of opposite site endoscopies. While this study did reveal several similarities between UGIB and LGIB, it also highlights the need to identify improved strategies to improve the sensitivity and specificity of identification of LGIB compared to UGIB, both for clinical purposes and for research. The value of such improved clinical algorithms have the potential to improve both the cost and outcomes of care, while better algorithms for separating UGIB and LGIB using administrative data might help produce more precise estimates of costs and clinical outcomes, and aid in the development of risk stratification models.

Gastrointestinal bleeding (GIB) is a frequent reason for acute hospitalization, with estimated rates of hospitalization at 375 per 100,000 per year in the United States.1 GIB is not a specific disease but rather a diverse set of conditions that lead to the clinical manifestations associated with bleeding into the gastrointestinal tract. One of the most commonly used organizing frameworks in gastrointestinal bleeding is the differentiation between upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). There are important differences in the etiologies between the 2 sources. For example, acid‐related disease is a common etiology in UGIB but does not occur in LGIB. While some aspects of the acute management are shared between UGIB and LGIB, important differences exist in the management, including initial endoscopy and medication choice. There have been few direct comparisons of rates, resource use, and clinical outcomes between UGIB and LGIB.

Historically, rates of UGIB have been reported to exceed those of LGIB by 2‐fold to 8‐fold.25 Protocols, clinical practice guidelines, and policy decisions reflect this emphasis on UGIB.68 Among 9 guidelines hosted by National Guideline Clearinghouse addressing GIB, 6 were focused on UGIB, 2 on both UGIB and LGIB, and only 1 on LGIB.9 There are several reasons to believe that these relative incidence rates may not be accurate. First, recent advances in therapy and prevention of UGIB, such as the treatment of Helicobacter pylori infection; proton pump inhibitors (PPIs); and selective cyclooxygenase‐2 (COX‐2) inhibitors, may have affected the epidemiology of gastrointestinal bleeding.1016 Among these therapies, only COX‐2 inhibitors may also reduce the incidence of LGIB.14, 1618 Therefore, these advances may result in a disproportionate drop in UGIB relative to LGIB. In addition, known risk factors for both LGIB and UGIB, including advancing age and renal failure, are increasing in the general population.5, 19, 20 Finally, given the recent increased recommendations for aspirin therapy and systemic anticoagulation, exposure to aspirin and warfarin have increased, both risk factors for LGIB and UGIB.2124 Indeed, recent studies in the epidemiology of UGIB do suggest a changing pattern of etiologies of UGIB reflecting these advances.25 One study examining rates of both UGIB and LGIB demonstrate a decrease in hospitalizations overall for GIB driven by a reduction in UGIB while at the same time reporting an increase in the incidence of hospitalization for LGIB.1

In addition to a changing epidemiology, a second reason for a potential underestimation of LGIB incidence is one of methodology. There are well‐recognized limitations with using purely administrative data due to difficulties in accurately identifying patients with LGIB.26

Studies using large administrative databases may not accurately identify LGIB because of the poor sensitivity and specificity of International Classification of Diseases, Ninth revision, Clinical Modification (ICD‐9) codes for LGIB.5 While there are standard methods of identifying patients with UGIB using ICD‐9 codes,19 there is not an accepted standard for LGIB. Thus, estimates using only ICD‐9 codes may overidentify or underidentify patients with LGIB. Prior studies that have most accurately identified patients with LGIB used a 2‐step method to address this issue. The initial ICD‐9 identification included a high sensitivity/low specificity approach. These identified patient charts undergo chart review to confirm the presence of an LGIB.5 This method is labor intensive and cannot be done using administrative databases. No direct comparison of UGIB to LGIB among hospitalized patients using this 2‐step method has been done recently.

The current emphasis on UGIB as seen in the published guidelines could also be supported if patients with UGIB had greater resource utilization or worse clinical outcomes. Limited direct comparisons for these outcomes are available. However, 1 administrative database study reported similar mortality rates for UGIB (2.7%) and LGIB (2.9%) in 2006.1 No direct comparisons of other clinical outcomes or resource use outcomes are available. Therefore, the emphasis on UGIB in publications and guidelines is best supported by the incidence rates that are, as has already been discussed, problematic.

We conducted a retrospective cohort study to examine the incidences of UGIB and LGIB among patients admitted to an academic medical center over 2 years using methods designed to optimally identify patients with either UGIB or LGIB. Our study also examined differences in clinical outcomes and resource utilization between subjects with UGIB and LGIB to examine the relative severity of these 2 clinical entities. These results may be useful in determining the need to reconsider clinical approaches as well as protocols and guidelines among patients with gastrointestinal bleeding.

Patients and Methods

Patients

This retrospective cohort study evaluated all patients who were admitted with GIB to a large urban academic medical center from July 1, 2001 to June 30, 2003 and who consented to a larger study examining the effects of hospitalists on patient care. Subjects unable to provide consent due to death or lack of decisional capacity were consented via proxy. To identify patients with GIB, all patients were screened for a primary or secondary diagnosis of GIB using ICD 9 codes. These codes were selected for a very high sensitivity threshold to assure that all potential subjects with GIB were identified. All subjects identified using these codes underwent chart abstraction to determine if they met criteria for GIB. These inclusion criteria required documentation in any portion of the chart (including emergency department [ED] clinician documentation, admission note, nursing intake note, etc.) of signs or symptoms of GI hemorrhage upon admission, including: hematemesis, coffee ground emesis, gastrooccult‐positive emesis, melena, hematochezia, maroon stools, and hemoccult‐positive stools interpreted by the treating physician team as an acute GIB. Subjects identified using the ICD‐9 codes and confirmed to have an acute GIB by chart review were included in the study and underwent additional chart abstraction and administrative data analysis.

ICD‐9 codes for GIB included: esophageal varices with hemorrhage (456.0, 456.20), Mallory‐Weiss syndrome (530.7), gastric ulcer with hemorrhage (531.00531.61), duodenal ulcer with hemorrhage (532.00532.61), peptic ulcer, site unspecified, with hemorrhage (533.00533.61), gastrojejunal ulcer with hemorrhage (534.00534.61), gastritis with hemorrhage (535.61), angiodysplasia of stomach/duodenum with hemorrhage (537.83), hematemesis (578.0578.9), diverticular disease (562.00562.9), other disorders of the intestine (569.00569.9), congenital anomalies of the digestive system (751.00), proctocolitis (556.00), hemorrhoids (455.00455.6), nondysenteric colitis (006.2), noninfectious gastroenteritis and colitis (558.0558.9), salmonella gastroenteritis (003.3), malignant neoplasm of colon (153), familial adenomatous polyposis (211.3), and gastric varices (456.8).

Data

Trained research assistants performed chart abstraction with validation by the principal investigators (PIs) of the first 15 charts to ensure accuracy. Subsequently, research assistants consulted with PIs with any questions during abstracting with final decisions being made by PIs. Detailed chart abstraction collected admission medication lists as obtained by the admitting physician team, including the use of PPIs, histamine‐2 (H‐2) blockers, COX‐2 inhibitors, and medications known to increase the risk of GIB, such as nonselective NSAIDs (nsNSAIDs), aspirin, and other anticoagulants. Other clinical data including risk factors, comorbid illnesses, laboratory tests, and vital signs were also abstracted from subjects' charts.

The source (UGIB vs. LGIB) and etiology (peptic ulcer disease [PUD], varices, diverticula, etc.) of bleeding were assessed using endoscopic reports as the primary source. When no clear source was identified on endoscopy or no endoscopy was done, the abstracter would review all progress notes, discharge summaries, and other diagnostic test results such as angiography in order to identify the source of bleeding (UGIB vs. LGIB). Endoscopic reports that identified a patient as having a UGIB or LGIB but no confirmed etiology were classified as undetermined etiology unless review of the other clinical documentation provided a specific etiology.

Tachycardia was defined as pulse greater than 100 beats per minute. Orthostasis was defined by either a drop in systolic blood pressure of 20 mmHg or an increase in pulse of 10 beats per minute. Hospital administrative databases were utilized to obtain resource utilization (ie, length of stay [LOS], total cost of care, intensive care transfers), Charlson comorbidity index,27 30‐day readmission rate, and in‐hospital mortality. Hospital costs were determined using TSI cost accounting software (Transition Systems Incorporated [now Eclypsis Corporation], Boston, MA), a validated system to assess actual direct and indirect costs of care.

Statistical Analysis

Descriptive statistics (means and proportions) were calculated by location of GIB for all variables describing patient characteristics, clinical presentation, clinical outcomes, and resource utilization. Differences in age and Charlson comorbidity index by GIB location were evaluated using t tests. Differences in gender, race, and medication use were evaluated using chi‐squared tests of independence.

We fit generalized linear models to investigate differences by location of bleed for those variables measuring clinical outcomes (inpatient mortality, intensive care unit [ICU] transfer, emergency surgery, 30‐day readmission, change in hemoglobin) and those variables measuring resource outcomes (total cost, LOS, number of procedures, number of correct scopes, repeat scope indicator, incorrect scope indicator, number of red blood cell [RBC] transfusions). The repeat scope indicator was used to denote a repeat scope (either esophagogastroduodenoscopy [EGD] or colonoscopy) and the incorrect scope indicator was used to denote when the initial scope was negative and a follow‐up scope from the other direction was positive (negative EGD followed by positive colonoscopy or negative colonoscopy followed by positive EGD). For each variable we fit 2 regression models, the first model (unadjusted effect) only included location of bleed as a covariate. The second model (adjusted effect) included location of bleed, age, gender, race (black/not black) and Charlson comorbidity index as covariates. Binary outcomes were modeled using logistic regressions. For continuous variables, we determined the distribution and link of the outcome variable using residual diagnostics and by comparing the log likelihood and information criteria of competing models. All analyses were performed using STATA SE Version 9.0 (StataCorp, College Station, TX)

This study was approved by the University of Chicago Institutional Review Board.

Results

During the 2 years of observation, a total of 7741 subjects were admitted to the internal medicine service and enrolled in the hospitalist study. Of these, 1014 had a primary or secondary ICD‐9 code that may be consistent with UGIB or LGIB and underwent chart review to determine if they had an acute GIB. Out of 1014 subjects, 647 were determined not to have an acute GI hemorrhage and were excluded from the remaining analyses; 367 of the 1104 subjects identified by ICD‐9 codes were found to have a clinical presentation consistent with GIB and were included in this study. A total of 180 of these 367 had UGIB and 187 had LGIB. The mean age was 62.4 years, 56.7% were female, 82.6% were African American, 12.7% were Caucasian, and the mean Charlson index was 1.5. (Table 1) Among baseline characteristics, both gender and age were statistically associated with a difference in rates of upper vs. lower source bleeding, with LGIB patients more likely to be female (P = 0.01) and older (P < 0.001). Etiologies of UGIB include erosive disease, peptic ulcer disease, variceal bleeding, arteriovenous malformation, and malignancy. Etiologies of LGIB include: diverticulosis, colitis, arteriovenous malformation, cancer, ischemic colitis, polyp, hemorrhoidal bleed, ulcer, inflammatory bowel disease, other, and not determined (Table 2).

Baseline Characteristics Among All Subjects Admitted for GI Hemorrhage
 Upper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

Age (years), mean (SD)62.4 (18.0)58.6 (18.2)66.0 (17.1)<0.001
Female gender (%)56.750.063.10.01
Race (%)    
African American82.685.380.10.43
White12.710.714.5 
Other4.74.05.4 
Charlson comorbidity index, mean (SD)1.5 (1.5)1.6 (1.6)1.4 (1.5)0.44
GI Bleeding Etiologies
Lower GI Bleed (n = 187)Upper GI Bleed (n = 180)
EtiologyFrequencyPercent of Total (%)EtiologyFrequencyPercent of Total (%)
  • NOTE: n = 367. Totals add up to >100% for upper GI bleed as some patients had more than 1 source identified.

  • Abbreviations: AVM, arteriovenous malformation; GI, gastrointestinal; IBD, inflammatory bowel disease; NOS, not otherwise specified.

Diverticulosis7641Erosive disease8648
Not identified3820Peptic ulcer5128
Colitis, NOS147Not identified2614
AVM137Mallory Weiss179
Cancer116Varices84
Ischemic colitis95AVMs53
Polyp95Mass/cancer53
Hemorrhoid84   
Ulcer53   
Other31   
IBD1<1   

Baseline use of medications known to be associated with either increased or decreased risk of GIB was common. Approximately one‐third of subjects with both LGIB and UGIB used aspirin and 10% used warfarin. LGIB subjects were less likely to use an nsNSAID (P < 0.001), but more likely to use a proton pump inhibitor (PPI) (P = 0.06) (Table 3).

Baseline Medication Use Among All Subjects Admitted for Gastrointestinal Hemorrhage
 Upper and Lower GI Bleeding (%) (n = 367)Upper GI Bleeding (%) (n = 180)Lower GI Bleeding (%) (n = 187)P Value*
  • Abbreviations: COX‐2, cyclooxygenase 2; GI, gastrointestinal; nsNSAID, nonselective nonsteroidal antiinflammatory drug; PPI, proton pump inhibitor.

  • P value comparing upper GI bleeding to lower GI bleeding.

Aspirin34.931.837.40.28
nsNSAID12.920.86.4< 0.001
COX‐2 selective inhibitor8.26.59.60.29
Warfarin10.98.412.80.19
PPI24.319.528.30.06
nsNSAID + PPI1.81.32.10.56
COX‐2 + PPI2.91.34.30.11

Key initial clinical presentation findings included vital sign abnormalities and admission hemoglobin levels. While hypotension was not common (4.7%), resting tachycardia (37%) and orthostasis (16%) were seen frequently. Subjects with LGIB were significantly less likely than those with UGIB to present with orthostasis (8.8% vs. 21.0%, respectively; P = 0.006) and resting tachycardia (32.3% vs. 42.5%, respectively; P = 0.04). Subjects with LGIB had a higher admission hemoglobin than those with UGIB (10.7 vs. 9.7, respectively; P < 0.001) (Table 4).

Admission Clinical Findings Among All Subjects Admitted for Gastrointestinal Hemorrhage
Clinical FindingUpper and Lower GI Bleeding (n = 367)Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)P Value*
  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • P value comparing upper GI bleeding to lower GI bleeding.

Hypotension (%)4.75.73.80.39
Resting tachycardia (%)37.342.532.30.04
Orthostatic hypotension (%)16.221.08.80.006
Admission hemoglobin (g/dL), mean (SD)10.2 (2.6)9.7 (2.7)10.7 (2.5)<0.001

We also examined several clinical outcomes. When comparing LGIB to UGIB patients for these clinical outcomes using bivariate and multivariate statistics, there was no difference for in‐hospital mortality (1.1% vs. 1.1%), transfer to ICU (16.0% vs. 13.9%), 30‐day readmission (5.9% vs.7.8%), number of red blood cell (RBC) transfusions (2.7 vs. 2.4), or need for GI surgery (1.1% vs. 0.0%). The mean drop in hemoglobin was greater among subjects with LGIB compared to UGIB (1.9 g/dL vs. 1.5 g/dL, respectively) by both bivariate (P = 0.01) and multivariate (P = 0.003) analyses (Table 5).

Comparison of In‐hospital Clinical Outcomes Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; ICU, intensive care unit; OLS, ordinary least squares; RBC, red blood cell; SD, standard deviation.

  • Modeled using logistic regression.

  • Modeled using OLS regression.

In‐hospital mortality (%)*1.11.10.970.74
Transfer to ICU (%)*13.916.00.560.44
Drop in hemoglobin (g/dL), mean (SD)1.5 (1.5)1.9 (1.6)0.010.003
Packed RBC transfusions required (units), mean (SD)*2.4 (2.9)2.7 (3.7)0.360.33
Surgery for GI bleeding (%)0.0%1.1  
30‐day readmission rate (%)*7.85.90.490.45

Mean costs were $11,892 for LGIB and $14,301 for UGIB and median costs were $7,890 for LGIB and $9,548 for UGIB, but were not statistically different. LOS was also similar between subjects with LGIB (5.1 days) and UGIB (5.7 days). In bivariate and multivariate analyses, UGIB subjects had a similar mean number of endoscopic procedures (1.3) compared to LGIB subjects (1.2). Thirteen percent of subjects with UGIB required a second EGD while only 8% of subjects with LGIB required 2 colonoscopies. In addition, 29% of subjects with LGIB received an EGD while only 16% of subjects with an UGIB received a colonoscopy (P = 0.001) (Table 6).

Comparison of Resource Utilization Among All Subjects Admitted for GI Hemorrhage Using Bivariate and Multivariate Analyses
 Upper GI Bleeding (n = 180)Lower GI Bleeding (n = 187)Bivariate P ValueMultivariate P Value
  • NOTE: Multivariate analyses control for age, gender, race (black/not black), and Charlson index.

  • Abbreviations: GI, gastrointestinal; GLM, generalized linear model; OLS, ordinary least squares; SD, standard deviation.

  • Modeled using a GLM with a gamma distribution and log link.

  • Modeled using OLS regression.

Cost ($), mean (SD)*14,301 (17,196)11,892 (13,100)0.130.21
Cost ($), median$9,548$7,890  
Length of stay (days), mean (SD)*5.7 (7.0)5.1 (5.3)0.370.72
Number of endoscopies/ patient, mean (SD)1.3 (0.5)1.2 (0.9)0.180.20

Conclusions

This study represents one of the largest direct comparisons of LGIB to UGIB not based on administrative databases. The most striking finding was the nearly equal rates of LGIB and UGIB. There are 2 likely explanations for this surprising result. First, there may be methodological reasons that we identified a greater proportion of true LGIBs; our study used a highly sensitive search strategy of ICD‐9 coding with confirmatory chart abstraction to ensure that as many LGIB and UGIB cases would be identified as possible while also excluding cases not meeting accepted criteria for GIB. The second possibility is that there is an actual change in epidemiology of GIB. Known risk factors for LGIB are increasing such as advancing age, increased use of chronic aspirin therapy, and renal disease. At the same time, significant advances in the treatment and prevention of UGIB have been made. Recent studies have demonstrated similar trends in admissions for upper and lower GI complications, suggesting that there may be a changing epidemiology due primarily to reductions in upper GI complications.1, 16

Either explanation would have implications for the care of patients with GIB. Clinical decision‐making based on prior literature would support that in ambiguous clinical situations and initial evaluation for an UGIB is appropriate. Most risk stratification literature and clinical guidelines focus on UGIB. If rates of LGIB and UGIB are similar, then existing clinical decision protocols may need to be reevaluated to incorporate the higher likelihood of LGIB. This reevaluation would be less important if the clinical outcomes or resource utilization of UGIB was significantly greater than that for LGIB, but we did not find this was the case. Similarly, if the ability to distinguish between LGIB and UGIB were robust on clinical signs and symptoms, then a reevaluation would be less important. However, we found fairly similar numbers of patients initially receiving evaluation for UGIB then being evaluated for LGIB as we found patients initially receiving evaluation for LGIB then being evaluated for UGIB. This suggests the potential benefit of clinical decision protocols that could better distinguish between UGIB and LGIB and account for the potentially higher incidence of LGIB than previously thought.

In addition to affecting the attention paid to LGIB for acute management, a changed understanding of incidence could also affect the attention paid to prevention of LGIB. Of the recent nonendoscopic advances in the treatment and prevention of GIB, only the use of COX‐2s (when used in place of traditional nsNSAIDs) reduces the risk of both LGIB and UGIB;14, 1618 H .pylori treatment and PPIs only prevent UGIB. Therefore, if the clinical and financial burdens of LGIB are similar to those seen in UGIB, more attention may need to be focused on preventing LGIB.

Baseline medication use was notable primarily for the similarities between UGIB and LGIB. Agents known to affect the rates of GIB were common in both groups. Over one‐third of the population was using aspirin and 10% were taking warfarin. Over 20% of subjects were taking an nsNSAID or a COX‐2 inhibitor. Almost one‐quarter of subjects were taking a PPI, agents known to decrease rates of UGIB and potentially increase LGIB through the risk of C. difficile colitis. Notably, the only statistically significant difference in baseline medication use between subjects with UGIB and LGIB was the more than 3‐fold higher use of nsNSAIDs in patients with UGIB as compared to LGIB. While current guidelines are not clear and consistent about which populations of at‐risk patients should receive GI prophylaxis,2830 these results suggest that patients admitted with GIB are very likely to be taking medications which impact the risk of GIB.

In terms of disease severity, the clinical presentation at admission suggests a greater degree of hemodynamic instability among subjects with UGIB. Rates of orthostatic hypotension and resting tachycardia are higher in UGIB subjects, as well as having a lower mean hemoglobin levels at presentation. However, despite the more severe clinical presentation, clinical outcomes did not differ significantly between the 2 bleeding sources. Thus, the most relevant clinical outcomes suggest that the severity of both LGIB and UGIB are similar. This similarity again suggest that the clinical burden of LGIB is not significantly different than UGIB.

Our results concerning resource utilization demonstrate a similar pattern. While the point estimates for costs and LOS suggest that UGIB may be associated with higher resource utilization, these differences were not significant in either bivariate or multivariate analyses. Those subjects with UGIB did receive more total endoscopic procedures than subjects with LGIB. More interesting though was that 24% of all subjects received an endoscopy of the opposite site (LGIB with EGD and UGIB with colonoscopy). These results suggest that the site of bleeding is not clear in a significant proportion of patients who present with GIB. These additional endoscopies are associated with increased risk, costs, LOS, and discomfort to patients. Improving our ability to accurately predict the source (upper vs. lower) of bleeding would allow us to reduce the number of these excess endoscopies. Additionally, it is interesting that despite the almost universal use of endoscopies, 20% of LGIB and 14% of UGIB subjects could not have a specific etiology identified during endoscopy or subsequent workup.

There are some important limitations to this study. While the sample size is among the largest of its type involving chart abstraction, it may be underpowered to detect some differences. Additionally, our results are from a single urban academic medical center with a patient population that is predominantly African American, which may limit generalizability. This study required consent and therefore only examines a subset of patients admitted to the medical center with GIB, which could potentially introduce bias into the sample. However, it is not clear why there would be systematic differences in subjects who choose to consent vs. those who decide not to consent that would affect the results of this study in substantive ways.

Despite significant efforts at identifying all subjects with GIB admitted during this time period, there were potential methodological reasons that may have resulted in some cases being missed. Only subjects admitted to a medicine service were approached for consent. All subjects in this medical center with GIB are admitted to a medicine service. We captured all subjects who were initially admitted to a medicine service as well as those admitted initially to an ICU and then transferred to the floor at any point prior to discharge. It is possible, though, that a subject would be admitted to an ICU for GIB and die prior to being transferred to the floor. While it is the impression of the director of the ICU that this would be a very unusual event, as most of the patients would be discharged to the floor prior to death (personal communication), given the very low mortality rate seen in this study, small numbers of missed events could have a significant impact on the interpretation of in‐hospital mortality results. It is also important to note that this medical center did not have the ability to perform endoscopy prior to admission for patients with GIB at the time of the study; all patients who presented with GIB would have been admitted and identified for this study. Finally, we were unable to routinely identify the rationale for obtaining an endoscopic exam. We assumed that all endoscopic exams were done for the purpose of evaluating and/or treating the GIB for which the subject was admitted. It is possible that some subjects had additional endoscopies for other reasons, which would have led to our overestimating the rates of additional endoscopies for GIB.

This study highlights the similarities between LGIB and UGIB rather than the differences. There were few significant differences between the 2 bleeding sources in terms of incidence, clinical outcomes, and resource utilization. In fact, the study also suggests that determining the source of bleeding may not be clear, given the high rates of opposite site endoscopies. While this study did reveal several similarities between UGIB and LGIB, it also highlights the need to identify improved strategies to improve the sensitivity and specificity of identification of LGIB compared to UGIB, both for clinical purposes and for research. The value of such improved clinical algorithms have the potential to improve both the cost and outcomes of care, while better algorithms for separating UGIB and LGIB using administrative data might help produce more precise estimates of costs and clinical outcomes, and aid in the development of risk stratification models.

References
  1. Zhao Y,Encinosa W.Hospitalizations for Gastrointestinal Bleeding in 1998 and 2006. HCUP Statistical Brief #65, December 2008.Rockville, MD:Agency for Healthcare Research and Quality.
  2. Wilcox CM,Clark WS.Causes and outcome of upper and lower gastrointestinal bleeding: The Grady Hospital Experience.South Med J.1999;92(1):4450.
  3. Blatchford O,Davidson LA,Murray WR, et al.Acute upper gastrointestinal haemorrhage in west of Scotland: case ascertainment study.BMJ.1997;315:510540.
  4. Jiradek GC,Kozarek RA.A cost‐effective approach to the patient with peptic ulcer bleeding.Surg Clin North Am.1996;76:83103.
  5. Longstreth GF.Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population based study.Am J Gastroenterol.1997;92:419424.
  6. Barkun A,Bardou M,Marshall J.Consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding.Ann Int Med.2003;139:843857.
  7. Gralnek IM,Dulai GS.Incremental value of upper endoscopy for triage of patients with acute non‐variceal upper‐GI hemorrhage.Gastrointest Endosc2004;60:914.
  8. Hay JA,Lyubashevsky E,Elashoff J, et al.Upper gastrointestinal hemorrhage clinical guideline‐determining the optimal hospital length of stay.Am J Med.1996;100:313322.
  9. National Guideline Clearinghouse. Available at: http://www.guideline.gov. Accessed August2009.
  10. van der Hulst RW,Rauws EA,Koycu B, et al.Prevention of ulcer recurrence after eradication of Helicobacter pylori: a prospective long‐term follow‐up study.Gastroenterology.1997;113:10821086.
  11. Lai KC,Hui WM,Wong WM, et al.Treatment of Helicobacter pylori in patients with duodenal ulcer hemorrhage‐a long‐term randomized, controlled study.Am J Gastroenterol.2000;95:22252232.
  12. Chan FK,Chung SC,Suen BY, et al.Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low‐dose aspirin or naproxen.N Engl J Med.2001;344:967973.
  13. Lai KC,Lam SK,Chu KM, et al.Lansoprazole for the prevention of recurrences of ulcer complications from long‐term low‐dose aspirin use.N Engl J Med.2002;346:20332038.
  14. Bombardier C,Laine L,Reicin A, et al.Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group.N Engl J Med.2000;343:15201528.
  15. Silverstein FE,Faich G,Goldstein JL, et al.Gastrointestinal toxicity with celecoxib vs nonsteroidal anti‐inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial. Celecoxib Long‐Term Arthritis Safety Study.JAMA.2000;284:12471255.
  16. Lanas A,Garcia‐Rodriguez LA,Rodrigo L, et al.Time trends and clinical impact of upper and lower gastrointestinal complications. Digestive Disease Week National Meeting,2008. San Diego, CA, May 17–22.
  17. Goldstein JL,Eisen GM,Lewis B, et al.Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole, and placebo.Clin Gastroenterol Hepatol.2005;3:133141.
  18. Laine L,Connors LG,Reicin A, et al.Serious lower gastrointestinal clinical events with nonselective NSAID or Coxib use.Gastroenterology.2003;124:288292.
  19. Wasse H,Gillen DL,Ball AM, et al.Risk factors for upper gastrointestinal bleeding among end‐stage renal disease patients.Kidney Int.2003;64:14551461.
  20. Kaplan RC,Heckbert SR,Koepsell TD, et al.Risk factors for hospitalized bleeding among older patients.J Am Geriatr Soc.2001;49:126133.
  21. Institute for Clinical Systems Improvement (ICSI). Preventive services in adults. Bloomington, MN: Institute for Clinical Systems Improvement (ICSI).2005. Available at http://www.isci.org/guidelines_and_more/guidelines_order_sets_protocol/for_patients_families/preventive_services_for_adults_for_patients_families_.html. Accessed Month year.
  22. Cryer B.NSAID‐associated deaths: the rise and fall of NSAID‐associated GI mortality.Am J Gastroenterol.2005;100:16941695.
  23. Cryer B,Feldman M.Effects of very low doses of daily long‐term aspirin therapy on gastric, duodenal, and rectal prostaglandins on mucosal injury in healthy humans.Gastroenterology. 199;117:1725.
  24. Lanas A,Perez‐Asia MA,Feu F, et al.A nationwide study of mortality associated with hospital admission due to severe gastrointestinal events and those associated with nonsteroidal antiinflammatory drug use.Am J Gastroenterol.2005;100:16851693.
  25. van Leerdam ME,Vreeburg EM,Rauws EA, et al.Acute upper GI bleeding: did anything change?Am J Gastroenterol.2003;98:14941499.
  26. Lingenfelser T,Ell C.Lower intestinal bleeding.Best Pract Res Clin Gastroenterol.2001;15:135153.
  27. Charlson ME,Pompei P,Ales KL,MacKenzie CR.A new method of classifying prognostic comorbidity in longitudinal studies: development and validation.J Chronic Dis.1987;40:373383.
  28. AGS Panel on Persistent Pain in Older Persons. The management of persistent pain in older persons.J Am Geriatr Soc.2002;50(6 suppl):S205S224.
  29. Simon LS,Lipman AG,Jacox AK, et al.Pain in Osteoarthritis, Rheumatoid Arthritis and Juvenile Chronic Arthritis.2nd ed.Clinical practice guideline no. 2.Glenview, IL:American Pain Society (APS);2002:179.
  30. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines.Recommendations for the Medical Management of Osteoarthritis of the Hip and Knee.Arthritis Rheum.2000;43:19051915.
References
  1. Zhao Y,Encinosa W.Hospitalizations for Gastrointestinal Bleeding in 1998 and 2006. HCUP Statistical Brief #65, December 2008.Rockville, MD:Agency for Healthcare Research and Quality.
  2. Wilcox CM,Clark WS.Causes and outcome of upper and lower gastrointestinal bleeding: The Grady Hospital Experience.South Med J.1999;92(1):4450.
  3. Blatchford O,Davidson LA,Murray WR, et al.Acute upper gastrointestinal haemorrhage in west of Scotland: case ascertainment study.BMJ.1997;315:510540.
  4. Jiradek GC,Kozarek RA.A cost‐effective approach to the patient with peptic ulcer bleeding.Surg Clin North Am.1996;76:83103.
  5. Longstreth GF.Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population based study.Am J Gastroenterol.1997;92:419424.
  6. Barkun A,Bardou M,Marshall J.Consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding.Ann Int Med.2003;139:843857.
  7. Gralnek IM,Dulai GS.Incremental value of upper endoscopy for triage of patients with acute non‐variceal upper‐GI hemorrhage.Gastrointest Endosc2004;60:914.
  8. Hay JA,Lyubashevsky E,Elashoff J, et al.Upper gastrointestinal hemorrhage clinical guideline‐determining the optimal hospital length of stay.Am J Med.1996;100:313322.
  9. National Guideline Clearinghouse. Available at: http://www.guideline.gov. Accessed August2009.
  10. van der Hulst RW,Rauws EA,Koycu B, et al.Prevention of ulcer recurrence after eradication of Helicobacter pylori: a prospective long‐term follow‐up study.Gastroenterology.1997;113:10821086.
  11. Lai KC,Hui WM,Wong WM, et al.Treatment of Helicobacter pylori in patients with duodenal ulcer hemorrhage‐a long‐term randomized, controlled study.Am J Gastroenterol.2000;95:22252232.
  12. Chan FK,Chung SC,Suen BY, et al.Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low‐dose aspirin or naproxen.N Engl J Med.2001;344:967973.
  13. Lai KC,Lam SK,Chu KM, et al.Lansoprazole for the prevention of recurrences of ulcer complications from long‐term low‐dose aspirin use.N Engl J Med.2002;346:20332038.
  14. Bombardier C,Laine L,Reicin A, et al.Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group.N Engl J Med.2000;343:15201528.
  15. Silverstein FE,Faich G,Goldstein JL, et al.Gastrointestinal toxicity with celecoxib vs nonsteroidal anti‐inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial. Celecoxib Long‐Term Arthritis Safety Study.JAMA.2000;284:12471255.
  16. Lanas A,Garcia‐Rodriguez LA,Rodrigo L, et al.Time trends and clinical impact of upper and lower gastrointestinal complications. Digestive Disease Week National Meeting,2008. San Diego, CA, May 17–22.
  17. Goldstein JL,Eisen GM,Lewis B, et al.Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole, and placebo.Clin Gastroenterol Hepatol.2005;3:133141.
  18. Laine L,Connors LG,Reicin A, et al.Serious lower gastrointestinal clinical events with nonselective NSAID or Coxib use.Gastroenterology.2003;124:288292.
  19. Wasse H,Gillen DL,Ball AM, et al.Risk factors for upper gastrointestinal bleeding among end‐stage renal disease patients.Kidney Int.2003;64:14551461.
  20. Kaplan RC,Heckbert SR,Koepsell TD, et al.Risk factors for hospitalized bleeding among older patients.J Am Geriatr Soc.2001;49:126133.
  21. Institute for Clinical Systems Improvement (ICSI). Preventive services in adults. Bloomington, MN: Institute for Clinical Systems Improvement (ICSI).2005. Available at http://www.isci.org/guidelines_and_more/guidelines_order_sets_protocol/for_patients_families/preventive_services_for_adults_for_patients_families_.html. Accessed Month year.
  22. Cryer B.NSAID‐associated deaths: the rise and fall of NSAID‐associated GI mortality.Am J Gastroenterol.2005;100:16941695.
  23. Cryer B,Feldman M.Effects of very low doses of daily long‐term aspirin therapy on gastric, duodenal, and rectal prostaglandins on mucosal injury in healthy humans.Gastroenterology. 199;117:1725.
  24. Lanas A,Perez‐Asia MA,Feu F, et al.A nationwide study of mortality associated with hospital admission due to severe gastrointestinal events and those associated with nonsteroidal antiinflammatory drug use.Am J Gastroenterol.2005;100:16851693.
  25. van Leerdam ME,Vreeburg EM,Rauws EA, et al.Acute upper GI bleeding: did anything change?Am J Gastroenterol.2003;98:14941499.
  26. Lingenfelser T,Ell C.Lower intestinal bleeding.Best Pract Res Clin Gastroenterol.2001;15:135153.
  27. Charlson ME,Pompei P,Ales KL,MacKenzie CR.A new method of classifying prognostic comorbidity in longitudinal studies: development and validation.J Chronic Dis.1987;40:373383.
  28. AGS Panel on Persistent Pain in Older Persons. The management of persistent pain in older persons.J Am Geriatr Soc.2002;50(6 suppl):S205S224.
  29. Simon LS,Lipman AG,Jacox AK, et al.Pain in Osteoarthritis, Rheumatoid Arthritis and Juvenile Chronic Arthritis.2nd ed.Clinical practice guideline no. 2.Glenview, IL:American Pain Society (APS);2002:179.
  30. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines.Recommendations for the Medical Management of Osteoarthritis of the Hip and Knee.Arthritis Rheum.2000;43:19051915.
Issue
Journal of Hospital Medicine - 5(3)
Issue
Journal of Hospital Medicine - 5(3)
Page Number
141-147
Page Number
141-147
Article Type
Display Headline
Upper versus lower gastrointestinal bleeding: A direct comparison of clinical presentation, outcomes, and resource utilization
Display Headline
Upper versus lower gastrointestinal bleeding: A direct comparison of clinical presentation, outcomes, and resource utilization
Legacy Keywords
cost effectiveness, endoscopy, epidemiology, gastrointestinal hemorrhage
Legacy Keywords
cost effectiveness, endoscopy, epidemiology, gastrointestinal hemorrhage
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Division of Hospital Medicine, Department of Medicine, Loyola University Chicago Stritch School of Medicine, 2160 South First Avenue, Maywood, IL 60153
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Hospitalist Effects on Acute IGIH Patients

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Do hospitalists affect clinical outcomes and efficiency for patients with acute upper gastrointestinal hemorrhage (UGIH)?

Acute upper gastrointestinal hemorrhage (UGIH) is one of the most common hospital admissions for acute care. Estimates indicate that 300,000 patients (100‐150 cases per 100,000 adults) are admitted annually with an associated economic impact of $2.5 billion.15 The current standard management of UGIH requires hospital admission and esophagogastroduodenoscopy (EGD) by a gastroenterologist for diagnosis and/or treatment. This management strategy results in a high consumption of hospital resources and costs.

Simultaneously, hospitalists have dramatically changed the delivery of inpatient care in the United States and are recognized as a location‐driven subspecialty for the care of acute hospitalized patients, similar to emergency medicine. Currently there are 20,000 hospitalists, and more than one‐third of general medicine inpatients are cared for by hospitalists.6, 7

Previous studies have shown that hospitalist care offers better or comparable outcomes, with lower overall length of stay (LOS) and costs compared to traditional providers.810 However, most of these studies were performed in single institutions, had weak designs or little‐to‐no adjustment for severity of illness, or were limited to 7 specific diseases (pneumonia, congestive heart failure [CHF], chest pain, ischemic stroke, urinary tract infection, chronic obstructive lung disease [COPD], and acute myocardial infarction [AMI]).8

Furthermore, less is known about the effect of hospitalists on conditions that may be dependent upon specialist consultation for procedures and/or treatment plans. In this study, gastroenterologists performed diagnostic and/or therapeutic endoscopy work as consultants to the attending physicians in the management of acute inpatient UGIH.

To explore the effects of hospitalists on care of patients with acute UGIH, we examined data from the Multicenter Hospitalist (MCH) trial. The objectives of our study were to compare clinical outcomesin‐hospital mortality and complications (ie, recurrent bleeding, intensive care unit [ICU] transfer, decompensation, transfusion, reendoscopy, 30‐day readmission)and efficiency (LOS and costs) in hospitalized acute UGIH patients cared for by hospitalists and nonhospitalists in 6 academic centers in the United States during a 2‐year period.

Patients and Methods

Study Sites

From July 1, 2001 to June 30, 2003, the MCH trial1113 was a prospective, multicenter, observational trial of the care provided by hospitalists to patients admitted to general medical services at 6 academic medical institutions. There were 31,000 consecutive admissions to the general medical services of these participating sites: University of Chicago (Chicago, IL), University of Wisconsin Hospital (Madison, WI), University of Iowa (Iowa City, IA), University of California at San Francisco (San Francisco, CA), University of New Mexico (Albuquerque, NM), and Brigham and Women's Hospital (Boston, MA). The study was approved by the institutional review boards (IRBs) at each of the 6 participating institutions.

MCH Study Patients

Patients were eligible if they were admitted to the general medical services under the care of a hospitalist or nonhospitalist physician. Regardless of the admitting provider, each medical service was composed of rotating senior and junior resident physicians in all 6 sites. Furthermore, patients were 18 years of age or older, and were able to give consent themselves or had an appropriate proxy. Patients with mini‐mental status score of 17 (out of 22), admitted under their primary care physician or to an inpatient gastroenterology service, or transferred from another hospital, were excluded. The MCH study was designed to study the outcomes and efficiency in patients admitted for CHF, pneumonia, UGIH, and end‐of‐life care.

Acute UGIH Patients

Within the MCH‐eligible patients, we identified those with acute UGIH using the following International Classification of Diseases, 9th edition (ICD‐9) codes assigned at discharge: esophageal varices with hemorrhage (456.0, 456.20); Mallory‐Weiss syndrome (530.7); gastric ulcer with hemorrhage (531.00531.61); duodenal ulcer with hemorrhage (532.00532.61); peptic ulcer, site unspecified, with hemorrhage (533.00533.61); gastrojejunal ulcer with hemorrhage (534.00534.61); gastritis with hemorrhage (535.61); angiodysplasia of stomach/duodenum with hemorrhage (537.83); and hematemesis (578.0, 578.9). We also confirmed the diagnosis of UGIH by reviewing patient medical records for observed hematemesis, nasogastric tube aspirate with gross or hemoccult blood, or clinical history of hematemesis, melena, or hematochezia.14, 15

Data

All data were obtained from the 6 hospitals' administrative records, patient interviews, and medical chart abstractions. Dates of admission and discharge, ICD‐9 diagnosis codes, insurance type, age, race, and gender were obtained from administrative data. One‐month follow‐up telephone interviews assessed whether or not patient had any follow‐up appointment or hospital readmissions. Trained abstractors from each site performed manual chart reviews using a standard data collection sheet. The ICD‐9 code designation and chart abstraction methodology were developed prior to the initiation of the study to ensure consistent data collection and reduce bias.

The following data elements were collected: comorbidities, endoscopic findings, inpatient mortality, clinical evidence of rebleeding, endoscopic treatment or gastrointestinal (GI) surgery to control bleeding, repeat EGD, ICU transfer, decompensated comorbid illness requiring continued hospitalization, and blood transfusion (packed red cells, plasma, platelets). Clinical evidence of rebleeding was defined as either hematemesis or melena with decrease in hemoglobin of 2 g in 24 hours with or without hemodynamic compromise.14, 15 For the purpose of this study, recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery for control of UGIH, or repeat EGD before discharge. Furthermore, a composite endpoint termed total complications encompassed all adverse outcomes related to the UGIH hospitalization. The 30‐day readmission variable was defined using readmission identified in administrative records and a 30‐day follow‐up phone call. To guard against recall bias, self‐report data was only included for nonsite admissions.

We defined efficiency in terms of costs and LOS. Total hospital costs were measured using the TSI cost accounting system (Transition Systems, Inc., Boston, MA; now Eclipsys Corporation)16, 17 at 5 out of the 6 participating sites. TSI is a hospital cost accounting software system that integrates resource utilization and financial data already recorded in other hospital databases (such as the billing system, payroll system, and general ledger system).17 Hospital LOS was defined as the number of days from patient admission to the general medicine service until patient discharge.

Provider Specialization: Hospitalists vs. Nonhospitalists

The study was designed as a natural experiment based on a call cycle. The hospitalist‐led teams at each institution alternated in a 4‐day or 5‐day general medicine call cycle with teams led by traditional academic internal medicine attending physicians. All patients were assigned to teams according to their position in the call cycle without regard to whether the attending physician was a hospitalist or a nonhospitalist. Hospitalists are physicians whose primary professional focus is the general medical care of hospitalized patients.18, 19 As previously reported in a related MCH work,11 a hospitalist was also defined as a provider who spends at least 25% of his or her time on an academic inpatient general medicine service. Nonhospitalist physicians were most often outpatient general internal medicine faculty or subspecialists, who attended 1 month per year. Physicians were classified as hospitalists or nonhospitalists according to the designations provided by each site.

UGIH‐specific Confounders

From chart abstraction, we captured severity of illness, comorbidity, and performance of early EGD, variables that can confound analysis in UGIH. To capture severity of illness, a complete Rockall risk score was calculated for each patient. The complete Rockall uses 3 clinical variables (age, shock, and comorbidity) and 2 endoscopic variables (endoscopic diagnosis and stigmata of recent hemorrhage).5, 20 A complete Rockall score of 2 is considered low‐risk for rebleeding or death following admission.21, 22 The accepted definition of low‐risk is <5% recurrent bleeding and <1% mortality risk. A complete Rockall score of 3 to 5 is considered moderate‐risk while 6 is considered high‐risk. Comorbidity was measured using the Charlson comorbidity index.23 Performance of early endoscopy, usually defined as endoscopy performed within 24 hours from presentation, was previously shown to decrease LOS and need for surgical intervention in patients with acute UGIH.24, 25 Documented times of presentation to the emergency department and time of endoscopy performance were collected to calculate for the rate of early endoscopy in our study population.

Statistical Analysis

All statistical analyses were performed using SAS Version 9.1 for Windows (SAS Institute, Cary, NC).

Differences in baseline demographic characteristics of patients and their endoscopic findings were compared between the 2 types of providers. Univariate analyses were also performed to compare the differences in adverse outcomes, LOS, and costs between patients cared for by hospitalists and nonhospitalists. Chi‐square tests were used for categorical variables; while both Wilcoxon rank sum test and Student's t test were used in the analysis of continuous variables.

Next, we performed multivariable analyses to determine the independent association between hospitalist care and the odds of the patients having certain outcomes. However, to prevent overfitting, we only developed regression models for adverse outcomes that have at least 20% event rate.

Multivariable regression models were developed separately for LOS and costs. In contrast with the models on outcomes, analyses of LOS and costs were restricted to: (1) patients who were discharged alive; and (2) to cases with LOS and costs values within 3 standard deviations (SDs) of the mean because of the skewed nature of these data.

All models were adjusted for age, gender, race, insurance type, complete Rockall risk score, performance of early EGD, Charlson comorbidity index, and study site. Final candidate variables in the models were chosen based on stepwise selection, a method very similar to forward selection except that variables selected for the model do not necessarily remain in the model. Effects were entered into and then removed from the model in such a way that each forward selection step can be followed by 1 or more backward elimination steps. The stepwise selection was terminated if no further effect can be added to the model or if the current model was identical to the previous model. The stepwise selection model was generated using statistical criterion of alpha = 0.05 for entry and elimination from the model. Variables that can be a profound source of variation, such as study site and treating physician, were included in the model irrespective of their statistical significance.

To account for clustering of patients treated by the same physician, we used multilevel modeling with SAS PROC GLIMMIX (with random effects). For outcomes (categorical variables), we utilized models with logit‐link and binomial‐distributed errors. As for efficiency (continuous variables with skewed distribution), the multivariable analyses used a generalized linear model with log‐link and assuming gamma‐distributed errors.

Results

Patient Characteristics and Endoscopic Diagnoses

Out of 31,000 patients, the study identified a total of 566 patients (1.8%) with acute UGIH (Table 1). However, 116 patients transferred from another hospital were excluded as their initial management was provided elsewhere, giving a final study sample of 450 patients. Overall, there are 163 admitting physicians from 6 sites, with 39 (24%) classified as hospitalists and 124 (76%) as nonhospitalists. Forty‐two percent (177/450) of patients were cared for by hospitalists. Compared to nonhospitalists, patients admitted to the hospitalist service were older (62.8 vs. 57.7 years, P < 0.01) and with third‐party payor mix differences (P < 0.01). However, there were no statistical differences between patients attended by hospitalists and nonhospitalists with regard to Complete Rockall risk score, Charlson comorbidity index, performance of early endoscopy, and mean hemoglobin values on admission. Upper endoscopy was performed in all patients with distribution of the 3 most common diagnoses being similar (P > 0.05) between hospitalists and nonhospitalists: erosive disease (49.7% vs. 54.6%), peptic ulcer disease (PUD) (48% vs. 46.9%), and varices (18.6% vs. 14.7%).

Patient Characteristics, Rockall Risk Score, Performance of Early Endoscopy, and Endoscopic Findings by Admitting Service
VariableAdmitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values indicated by bold.

  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • Do not add up to 100% due to dual diagnoses.

  • Data on hemoglobin values on admission were available only for 376 patients (134 patients cared for by hospitalists and 242 cared for by nonhospitalists).

Age, years (meanSD)62.817.457.718.5<0.01
Male sex, n (%)104 (58.8)169 (61.9)0.50
Ethnicity, n (%)  0.13
White83 (46.9)102 (37.4) 
African‐American34 (19.2)75 (27.5) 
Hispanic21 (11.9)40 (14.7) 
Asian/Pacific Islander24 (13.6)29 (10.6) 
Others/unknown15 (8.5)27 (9.9) 
Insurance, n (%)  <0.01
Medicare86 (48.6)104 (38.1) 
Medicaid15 (8.5)33 (12.1) 
No payer18 (10.2)36 (13.2) 
Private46 (26)52 (19.1) 
Unknown12 (6.8)48 (17.5) 
Charlson Comorbidity Index (meanSD)1.91.61.81.70.51
Complete Rockall, n (%)  0.11
Low‐risk (0‐2)82 (46.3)103 (37.7) 
Moderate‐risk (3‐5)71 (40.1)137 (50.2) 
High‐risk (6)24 (14.6)33 (12.1) 
Early endoscopy (<24 hours)82 (46.3)133 (48.7)0.62
Endoscopic diagnosis, n (%)*   
Erosive disease88 (49.7)149 (54.6)0.31
Peptic ulcer disease85 (48.0)128 (46.9)0.81
Varices33 (18.6)40 (14.7)0.26
Mallory‐Weiss tear9 (5.1)21 (7.7)0.28
Angiodysplasia9 (5.1)13 (4.8)0.88
GI mass1 (0.6)4 (1.5)0.65
Normal7 (4.0)8 (2.9)0.55
Admission hemoglobin values (meanSD)10.22.910.22.90.78

Clinical Outcomes

Between hospitalists and nonhospitalists, unadjusted outcomes were similar (P > 0.05) for mortality (2.3% vs. 0.4%), recurrent bleeding (11% vs. 11%), need for endoscopic therapy (24% vs. 22%), ICU‐transfer and decompensation (15% vs. 15%), as well as an overall composite measure of any complication (79% vs. 72%) (Table 2). However, the hospitalist‐led teams performed more blood transfusions (74% vs. 63%, P = 0.02) and readmission rates were higher (7.3% vs. 3.3%, P = 0.05).

Univariate Analyses of Outcomes and Efficiency by Admitting Services
Outcomes, n (%)Admitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values are indicated by bold.

  • Abbreviations: EGD, esophagogastroduodenoscopy; GI, gastrointestinal; ICU, intensive care unit; LOS, length of stay; SD, standard deviation.

  • Recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery and repeat EGD before discharge.

  • Total complications is a composite endpoint of in‐patient mortality, recurrent bleeding, endoscopic treatments to control bleeding, ICU transfer, decompensate comorbid illness requiring continued hospitalization, and blood transfusion.

  • Only 423 patients were used in the resource use (efficiency) analysis. A total of 27 patients were excluded because of inpatient mortality (n = 5) and those with more than 3SD of population mean in terms of costs and LOS (n = 22).

Inpatient mortality4 (2.3)1 (0.4)0.08
Recurrent bleeding*20 (11.3)29 (10.6)0.88
Endoscopic therapy43 (24.3)60 (22.0)0.57
ICU transfers23 (13)24 (8.8)0.20
Decompensated comorbidities that required continued hospitalization26 (14.7)41 (15.0)0.92
Any transfusion131 (74.0)172 (63.0)0.02
Total complications139 (78.5)196 (71.8)0.11
30‐day all‐cause readmissions13 (7.3)9 (3.3)0.05
EfficiencyHospitalist (n = 164)Nonhospitalist (n = 259)P
LOS, days   
MeanSD4.83.54.53.00.30
Median (interquartile range)4 (36)4 (26)0.69
Total costs, U.S. $   
MeanSD10,466.669191.007926.716065.00<0.01
Median (interquartile range)7359.00 (4,698.0012,550.00)6181.00 (3744.0010,344.00)<0.01

Because of the low event rate of certain adverse outcomes (<20%), we were only able to perform adjusted analyses on 4 outcomes: need for endoscopic therapy (odds ratio [OR], 0.82; 95% confidence interval [CI], 0.491.37), ICU transfer and decompensation (OR, 0.82; 95% CI, 0.451.52), blood transfusion (OR, 1.30; 95% CI, 0.822.04), and any complication (OR, 1.18; 95% CI, 0.711.96). Since outcome differences disappeared after controlling for confounders, the data suggest that overall care provided by hospitalists and nonhospitalists might be equivalenteven in certain outcomes that we were unable to substantiate using multivariable methods.

Efficiency

Efficiency, as measured by LOS and costs, are presented both as means and medians in univariate analyses in Table 2. Median LOS was similar for hospitalist‐led and nonhospitalist‐led teams (4 days). Despite having similar LOS, the median costs of acute UGIH in patients cared for by hospitalists were higher ($7,359.00 vs. $6,181.00; P < 0.01).

After adjusting for demographic factors, Rockall risk score, comorbidity, early EGD, and hospital site, LOS remained similar between the 2 groups. On the other hand, the adjusted cost for UGIH patients cared for by hospitalists and nonhospitalists persisted, with hospitalist care costs $1,502.40 more than their nonhospitalist counterparts (Table 3).

Regression Model Estimates for Efficiency by Admitting Service
EfficiencyTreatment ProviderP
Hospitalist (n = 164)Nonhospitalist (n = 259)
  • NOTE: Significant P value indicated by bold. Adjusted means reported in days or dollars. These are antilogs of the mean values for provider type, adjusted for all covariates. Models are adjusted for age, gender, race, insurance, complete Rockall risk score, early EGD, Charlson comorbidity index score, and study site. By utilizing random effects in the regression models, we accounted for the effects of clustering on the physician level.

  • Abbreviations: EGD, esophagogastroduodenoscopy ; SD, standard deviation.

Adjusted length of stay, days (mean SD)5.2 (4.95.6)4.7 (4.55.0)0.15
Adjusted total cost, U.S. $ (mean SD)9006.50 (8366.609693.60)7504.10 (7069.907964.20)0.03

Discussion

This is the first study that has looked at the effect of hospitalists on clinical outcomes and efficiency in patients admitted for acute UGIH, a condition highly dependent upon another specialty for procedures and management. This is also one of only a few studies on UGIH that adjusted for severity of illness (Rockall score), comorbidity, performance of early endoscopypatient‐level confounders usually unaccounted for in prior research.

We show that hospitalists and nonhospitalists caring for acute UGIH patients had overall similar unadjusted outcomes; except for blood transfusion and 30‐day readmission rates. Unfortunately, due to the small number of events for readmissions, we were unable to perform adjusted analysis for readmission. Differences between hospitalists and nonhospitalists on blood transfusion rates were not substantiated on multivariable adjustments.

As for efficiency, univariable and multivariable analyses revealed that LOS was similar between provider types while costs were greater in UGIH patients attended by hospitalists.

Reductions in resource use, particularly costs, may be achieved by increasing throughput (eg, reducing LOS) or by decreasing service intensity (eg, using fewer ancillary services and specialty consultations).26 Specifically in acute UGIH, LOS is significantly affected by performance of early EGD.27, 28 In these studies, gastroenterologist‐led teams, compared to internists and surgeons, have easier access to endoscopy, thus reducing LOS and overall costs.27, 28

Similarly, prior studies have shown that the mechanism by which hospitalists lower costs is by decreasing LOS.810, 29 There are several hypotheses on how hospitalists affect LOS. Hospitalists, by being available all day, are thought to respond quickly to acute symptoms or new test results, are more efficient in navigating the complex hospital environment, or develop greater expertise as a result of added inpatient experience.8 On the downside, although the hospitalist model reduces overall LOS and costs, they also provide higher intensity of care as reflected by greater costs when broken down per hospital day.29 Thus, the cost differential we found may represent higher intensity of care by hospitalists in their management of acute UGIH, as higher intensity care without decreasing LOS can translate to higher costs.

In addition, patients with acute UGIH are unique in several respects. In contrast to diseases like heart failure, COPD, and pneumonia, in which the admitting provider has the option to request a subspecialist consultation, all patients with acute UGIH need a gastroenterologist to perform endoscopy as part of the management. These patients are usually admitted to general medicine wards, aggressively resuscitated with intravenous fluids, with a nonurgent gastroenterology consult or EGD performed on the next available schedule.

Aside from LOS being greatly affected by performance of early EGD and/or delay in consulting gastroenterology, sicker patients require longer hospitalization and drive LOS and healthcare costs up. It was therefore crucial that we accounted for severity of illness, comorbidity, and performance of early EGD in our regression models for LOS and costs. This approach allows us to acquire a more accurate estimate on the effects of hospitalist on LOS and costs in patients admitted with acute UGIH.

Our findings suggest that the academic hospitalist model of care may not have as great of an impact on hospital efficiency in certain patient groups that require nonurgent subspecialty consultations. Future studies should focus on elucidating these relationships.

Limitations

This study has several limitations. First, clinical data were abstracted at 6 sites by different abstractors so it is possible there were variations in how data were collected. To reduce variation, a standardized abstraction form with instructions was developed and the primary investigator (PI) was available for specific questions during the abstraction process. Second, only 5 out of the 6 sites used TSI accounting systems. Although similar, interhospital costs captured by TSI may vary among sites in terms of classifying direct and indirect costs, potentially resulting in misclassification bias in our cost estimates.17 We addressed these issues by including the hospital site variable in our regression models, regardless of its significance. Third, consent rates across sites vary from 70% to 85%. It is possible that patients who refused enrollment in the MCH trial are systematically different and may introduce bias in our analysis.

Furthermore, the study was designed as a natural experiment based on a rotational call cycle between hospitalist‐led and nonhospitalist‐led teams. It is possible that the order of patient assignment might not be completely naturally random as we intended. However, the study period was for 2 years and we expect the effect of order would have averaged out in time.

There are many hospitalist models of care. In terms of generalizability, the study pertains only to academic hospitalists and may not be applicable to hospitalists practicing in community hospitals. For example, the nonhospitalist comparison group is likely different in the community and academic settings. Community nonhospitalists (traditional practitioners) are usually internists covering both inpatient and outpatient responsibilities at the same time. In contrast, academic nonhospitalists are internists or subspecialists serving as ward attendings for a limited period (usually 1 month) with considerable variation in their nonattending responsibilities (eg, research, clinic, administration). Furthermore, academic nonhospitalist providers might be a self‐selected group by their willingness to serve as a ward attending, making them more hospitalist‐like. Changes and variability of inpatient attendings may also affect our findings when compared to prior work. Finally, it is also possible that having residents at academic medical centers may attenuate the effect of hospitalists more than in community‐based models.

Conclusions/Implications

Compared to nonhospitalists, academic hospitalist care of acute UGIH patients had similar overall clinical outcomes. However, our finding of similar LOS yet higher costs for patients cared for by hospitalists support 1 proposed mechanism in which hospitalists decrease healthcare costs: providing higher intensity of care per day of hospitalization. However, in academic hospitalist models, this higher intensity hypothesis should be revisited, especially in certain patient groups in which timing and involvement of subspecialists may influence discharge decisions, affecting LOS and overall costs.

Due to inherent limitations in this observational study, future studies should focus on verifying and elucidating these relationships further. Lastly, understanding which patient groups receive the greatest potential benefit from this model will help guide both organizational efforts and quality improvement strategies.

References
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  3. Rockall TA,Logan RF,Devlin HB, et al.Variation in outcome after acute upper gastrointestinal haemorrhage. the national audit of acute upper gastrointestinal haemorrhage.Lancet.1995;346(8971):346350.
  4. Rockall TA,Logan RF,Devlin HB, et al.Influencing the practice and outcome in acute upper gastrointestinal haemorrhage. Steering committee of the National Audit of Acute Upper Gastrointestinal Haemorrhage.Gut.1997;41(5):606611.
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  6. Lurie JD,Miller DP,Lindenauer PK, et al.The potential size of the hospitalist workforce in the united states.Am J Med.1999;106(4):441445.
  7. Society of Hospital Medicine. About SHM. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=General_Information357(25):25892600.
  8. Meltzer D,Manning WG,Morrison J, et al.Effects of physician experience on costs and outcomes on an academic general medicine service: results of a trial of hospitalists.Ann Intern Med.2002;137(11):866874.
  9. Peterson MC.A systematic review of outcomes and quality measures in adult patients cared for by hospitalists vs nonhospitalists.Mayo Clin Proc.2009;84(3):248254.
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Article PDF
Issue
Journal of Hospital Medicine - 5(3)
Page Number
133-139
Legacy Keywords
costs, gastrointestinal hemorrhage, hospitalists, length of stay, outcomes
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Acute upper gastrointestinal hemorrhage (UGIH) is one of the most common hospital admissions for acute care. Estimates indicate that 300,000 patients (100‐150 cases per 100,000 adults) are admitted annually with an associated economic impact of $2.5 billion.15 The current standard management of UGIH requires hospital admission and esophagogastroduodenoscopy (EGD) by a gastroenterologist for diagnosis and/or treatment. This management strategy results in a high consumption of hospital resources and costs.

Simultaneously, hospitalists have dramatically changed the delivery of inpatient care in the United States and are recognized as a location‐driven subspecialty for the care of acute hospitalized patients, similar to emergency medicine. Currently there are 20,000 hospitalists, and more than one‐third of general medicine inpatients are cared for by hospitalists.6, 7

Previous studies have shown that hospitalist care offers better or comparable outcomes, with lower overall length of stay (LOS) and costs compared to traditional providers.810 However, most of these studies were performed in single institutions, had weak designs or little‐to‐no adjustment for severity of illness, or were limited to 7 specific diseases (pneumonia, congestive heart failure [CHF], chest pain, ischemic stroke, urinary tract infection, chronic obstructive lung disease [COPD], and acute myocardial infarction [AMI]).8

Furthermore, less is known about the effect of hospitalists on conditions that may be dependent upon specialist consultation for procedures and/or treatment plans. In this study, gastroenterologists performed diagnostic and/or therapeutic endoscopy work as consultants to the attending physicians in the management of acute inpatient UGIH.

To explore the effects of hospitalists on care of patients with acute UGIH, we examined data from the Multicenter Hospitalist (MCH) trial. The objectives of our study were to compare clinical outcomesin‐hospital mortality and complications (ie, recurrent bleeding, intensive care unit [ICU] transfer, decompensation, transfusion, reendoscopy, 30‐day readmission)and efficiency (LOS and costs) in hospitalized acute UGIH patients cared for by hospitalists and nonhospitalists in 6 academic centers in the United States during a 2‐year period.

Patients and Methods

Study Sites

From July 1, 2001 to June 30, 2003, the MCH trial1113 was a prospective, multicenter, observational trial of the care provided by hospitalists to patients admitted to general medical services at 6 academic medical institutions. There were 31,000 consecutive admissions to the general medical services of these participating sites: University of Chicago (Chicago, IL), University of Wisconsin Hospital (Madison, WI), University of Iowa (Iowa City, IA), University of California at San Francisco (San Francisco, CA), University of New Mexico (Albuquerque, NM), and Brigham and Women's Hospital (Boston, MA). The study was approved by the institutional review boards (IRBs) at each of the 6 participating institutions.

MCH Study Patients

Patients were eligible if they were admitted to the general medical services under the care of a hospitalist or nonhospitalist physician. Regardless of the admitting provider, each medical service was composed of rotating senior and junior resident physicians in all 6 sites. Furthermore, patients were 18 years of age or older, and were able to give consent themselves or had an appropriate proxy. Patients with mini‐mental status score of 17 (out of 22), admitted under their primary care physician or to an inpatient gastroenterology service, or transferred from another hospital, were excluded. The MCH study was designed to study the outcomes and efficiency in patients admitted for CHF, pneumonia, UGIH, and end‐of‐life care.

Acute UGIH Patients

Within the MCH‐eligible patients, we identified those with acute UGIH using the following International Classification of Diseases, 9th edition (ICD‐9) codes assigned at discharge: esophageal varices with hemorrhage (456.0, 456.20); Mallory‐Weiss syndrome (530.7); gastric ulcer with hemorrhage (531.00531.61); duodenal ulcer with hemorrhage (532.00532.61); peptic ulcer, site unspecified, with hemorrhage (533.00533.61); gastrojejunal ulcer with hemorrhage (534.00534.61); gastritis with hemorrhage (535.61); angiodysplasia of stomach/duodenum with hemorrhage (537.83); and hematemesis (578.0, 578.9). We also confirmed the diagnosis of UGIH by reviewing patient medical records for observed hematemesis, nasogastric tube aspirate with gross or hemoccult blood, or clinical history of hematemesis, melena, or hematochezia.14, 15

Data

All data were obtained from the 6 hospitals' administrative records, patient interviews, and medical chart abstractions. Dates of admission and discharge, ICD‐9 diagnosis codes, insurance type, age, race, and gender were obtained from administrative data. One‐month follow‐up telephone interviews assessed whether or not patient had any follow‐up appointment or hospital readmissions. Trained abstractors from each site performed manual chart reviews using a standard data collection sheet. The ICD‐9 code designation and chart abstraction methodology were developed prior to the initiation of the study to ensure consistent data collection and reduce bias.

The following data elements were collected: comorbidities, endoscopic findings, inpatient mortality, clinical evidence of rebleeding, endoscopic treatment or gastrointestinal (GI) surgery to control bleeding, repeat EGD, ICU transfer, decompensated comorbid illness requiring continued hospitalization, and blood transfusion (packed red cells, plasma, platelets). Clinical evidence of rebleeding was defined as either hematemesis or melena with decrease in hemoglobin of 2 g in 24 hours with or without hemodynamic compromise.14, 15 For the purpose of this study, recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery for control of UGIH, or repeat EGD before discharge. Furthermore, a composite endpoint termed total complications encompassed all adverse outcomes related to the UGIH hospitalization. The 30‐day readmission variable was defined using readmission identified in administrative records and a 30‐day follow‐up phone call. To guard against recall bias, self‐report data was only included for nonsite admissions.

We defined efficiency in terms of costs and LOS. Total hospital costs were measured using the TSI cost accounting system (Transition Systems, Inc., Boston, MA; now Eclipsys Corporation)16, 17 at 5 out of the 6 participating sites. TSI is a hospital cost accounting software system that integrates resource utilization and financial data already recorded in other hospital databases (such as the billing system, payroll system, and general ledger system).17 Hospital LOS was defined as the number of days from patient admission to the general medicine service until patient discharge.

Provider Specialization: Hospitalists vs. Nonhospitalists

The study was designed as a natural experiment based on a call cycle. The hospitalist‐led teams at each institution alternated in a 4‐day or 5‐day general medicine call cycle with teams led by traditional academic internal medicine attending physicians. All patients were assigned to teams according to their position in the call cycle without regard to whether the attending physician was a hospitalist or a nonhospitalist. Hospitalists are physicians whose primary professional focus is the general medical care of hospitalized patients.18, 19 As previously reported in a related MCH work,11 a hospitalist was also defined as a provider who spends at least 25% of his or her time on an academic inpatient general medicine service. Nonhospitalist physicians were most often outpatient general internal medicine faculty or subspecialists, who attended 1 month per year. Physicians were classified as hospitalists or nonhospitalists according to the designations provided by each site.

UGIH‐specific Confounders

From chart abstraction, we captured severity of illness, comorbidity, and performance of early EGD, variables that can confound analysis in UGIH. To capture severity of illness, a complete Rockall risk score was calculated for each patient. The complete Rockall uses 3 clinical variables (age, shock, and comorbidity) and 2 endoscopic variables (endoscopic diagnosis and stigmata of recent hemorrhage).5, 20 A complete Rockall score of 2 is considered low‐risk for rebleeding or death following admission.21, 22 The accepted definition of low‐risk is <5% recurrent bleeding and <1% mortality risk. A complete Rockall score of 3 to 5 is considered moderate‐risk while 6 is considered high‐risk. Comorbidity was measured using the Charlson comorbidity index.23 Performance of early endoscopy, usually defined as endoscopy performed within 24 hours from presentation, was previously shown to decrease LOS and need for surgical intervention in patients with acute UGIH.24, 25 Documented times of presentation to the emergency department and time of endoscopy performance were collected to calculate for the rate of early endoscopy in our study population.

Statistical Analysis

All statistical analyses were performed using SAS Version 9.1 for Windows (SAS Institute, Cary, NC).

Differences in baseline demographic characteristics of patients and their endoscopic findings were compared between the 2 types of providers. Univariate analyses were also performed to compare the differences in adverse outcomes, LOS, and costs between patients cared for by hospitalists and nonhospitalists. Chi‐square tests were used for categorical variables; while both Wilcoxon rank sum test and Student's t test were used in the analysis of continuous variables.

Next, we performed multivariable analyses to determine the independent association between hospitalist care and the odds of the patients having certain outcomes. However, to prevent overfitting, we only developed regression models for adverse outcomes that have at least 20% event rate.

Multivariable regression models were developed separately for LOS and costs. In contrast with the models on outcomes, analyses of LOS and costs were restricted to: (1) patients who were discharged alive; and (2) to cases with LOS and costs values within 3 standard deviations (SDs) of the mean because of the skewed nature of these data.

All models were adjusted for age, gender, race, insurance type, complete Rockall risk score, performance of early EGD, Charlson comorbidity index, and study site. Final candidate variables in the models were chosen based on stepwise selection, a method very similar to forward selection except that variables selected for the model do not necessarily remain in the model. Effects were entered into and then removed from the model in such a way that each forward selection step can be followed by 1 or more backward elimination steps. The stepwise selection was terminated if no further effect can be added to the model or if the current model was identical to the previous model. The stepwise selection model was generated using statistical criterion of alpha = 0.05 for entry and elimination from the model. Variables that can be a profound source of variation, such as study site and treating physician, were included in the model irrespective of their statistical significance.

To account for clustering of patients treated by the same physician, we used multilevel modeling with SAS PROC GLIMMIX (with random effects). For outcomes (categorical variables), we utilized models with logit‐link and binomial‐distributed errors. As for efficiency (continuous variables with skewed distribution), the multivariable analyses used a generalized linear model with log‐link and assuming gamma‐distributed errors.

Results

Patient Characteristics and Endoscopic Diagnoses

Out of 31,000 patients, the study identified a total of 566 patients (1.8%) with acute UGIH (Table 1). However, 116 patients transferred from another hospital were excluded as their initial management was provided elsewhere, giving a final study sample of 450 patients. Overall, there are 163 admitting physicians from 6 sites, with 39 (24%) classified as hospitalists and 124 (76%) as nonhospitalists. Forty‐two percent (177/450) of patients were cared for by hospitalists. Compared to nonhospitalists, patients admitted to the hospitalist service were older (62.8 vs. 57.7 years, P < 0.01) and with third‐party payor mix differences (P < 0.01). However, there were no statistical differences between patients attended by hospitalists and nonhospitalists with regard to Complete Rockall risk score, Charlson comorbidity index, performance of early endoscopy, and mean hemoglobin values on admission. Upper endoscopy was performed in all patients with distribution of the 3 most common diagnoses being similar (P > 0.05) between hospitalists and nonhospitalists: erosive disease (49.7% vs. 54.6%), peptic ulcer disease (PUD) (48% vs. 46.9%), and varices (18.6% vs. 14.7%).

Patient Characteristics, Rockall Risk Score, Performance of Early Endoscopy, and Endoscopic Findings by Admitting Service
VariableAdmitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values indicated by bold.

  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • Do not add up to 100% due to dual diagnoses.

  • Data on hemoglobin values on admission were available only for 376 patients (134 patients cared for by hospitalists and 242 cared for by nonhospitalists).

Age, years (meanSD)62.817.457.718.5<0.01
Male sex, n (%)104 (58.8)169 (61.9)0.50
Ethnicity, n (%)  0.13
White83 (46.9)102 (37.4) 
African‐American34 (19.2)75 (27.5) 
Hispanic21 (11.9)40 (14.7) 
Asian/Pacific Islander24 (13.6)29 (10.6) 
Others/unknown15 (8.5)27 (9.9) 
Insurance, n (%)  <0.01
Medicare86 (48.6)104 (38.1) 
Medicaid15 (8.5)33 (12.1) 
No payer18 (10.2)36 (13.2) 
Private46 (26)52 (19.1) 
Unknown12 (6.8)48 (17.5) 
Charlson Comorbidity Index (meanSD)1.91.61.81.70.51
Complete Rockall, n (%)  0.11
Low‐risk (0‐2)82 (46.3)103 (37.7) 
Moderate‐risk (3‐5)71 (40.1)137 (50.2) 
High‐risk (6)24 (14.6)33 (12.1) 
Early endoscopy (<24 hours)82 (46.3)133 (48.7)0.62
Endoscopic diagnosis, n (%)*   
Erosive disease88 (49.7)149 (54.6)0.31
Peptic ulcer disease85 (48.0)128 (46.9)0.81
Varices33 (18.6)40 (14.7)0.26
Mallory‐Weiss tear9 (5.1)21 (7.7)0.28
Angiodysplasia9 (5.1)13 (4.8)0.88
GI mass1 (0.6)4 (1.5)0.65
Normal7 (4.0)8 (2.9)0.55
Admission hemoglobin values (meanSD)10.22.910.22.90.78

Clinical Outcomes

Between hospitalists and nonhospitalists, unadjusted outcomes were similar (P > 0.05) for mortality (2.3% vs. 0.4%), recurrent bleeding (11% vs. 11%), need for endoscopic therapy (24% vs. 22%), ICU‐transfer and decompensation (15% vs. 15%), as well as an overall composite measure of any complication (79% vs. 72%) (Table 2). However, the hospitalist‐led teams performed more blood transfusions (74% vs. 63%, P = 0.02) and readmission rates were higher (7.3% vs. 3.3%, P = 0.05).

Univariate Analyses of Outcomes and Efficiency by Admitting Services
Outcomes, n (%)Admitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values are indicated by bold.

  • Abbreviations: EGD, esophagogastroduodenoscopy; GI, gastrointestinal; ICU, intensive care unit; LOS, length of stay; SD, standard deviation.

  • Recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery and repeat EGD before discharge.

  • Total complications is a composite endpoint of in‐patient mortality, recurrent bleeding, endoscopic treatments to control bleeding, ICU transfer, decompensate comorbid illness requiring continued hospitalization, and blood transfusion.

  • Only 423 patients were used in the resource use (efficiency) analysis. A total of 27 patients were excluded because of inpatient mortality (n = 5) and those with more than 3SD of population mean in terms of costs and LOS (n = 22).

Inpatient mortality4 (2.3)1 (0.4)0.08
Recurrent bleeding*20 (11.3)29 (10.6)0.88
Endoscopic therapy43 (24.3)60 (22.0)0.57
ICU transfers23 (13)24 (8.8)0.20
Decompensated comorbidities that required continued hospitalization26 (14.7)41 (15.0)0.92
Any transfusion131 (74.0)172 (63.0)0.02
Total complications139 (78.5)196 (71.8)0.11
30‐day all‐cause readmissions13 (7.3)9 (3.3)0.05
EfficiencyHospitalist (n = 164)Nonhospitalist (n = 259)P
LOS, days   
MeanSD4.83.54.53.00.30
Median (interquartile range)4 (36)4 (26)0.69
Total costs, U.S. $   
MeanSD10,466.669191.007926.716065.00<0.01
Median (interquartile range)7359.00 (4,698.0012,550.00)6181.00 (3744.0010,344.00)<0.01

Because of the low event rate of certain adverse outcomes (<20%), we were only able to perform adjusted analyses on 4 outcomes: need for endoscopic therapy (odds ratio [OR], 0.82; 95% confidence interval [CI], 0.491.37), ICU transfer and decompensation (OR, 0.82; 95% CI, 0.451.52), blood transfusion (OR, 1.30; 95% CI, 0.822.04), and any complication (OR, 1.18; 95% CI, 0.711.96). Since outcome differences disappeared after controlling for confounders, the data suggest that overall care provided by hospitalists and nonhospitalists might be equivalenteven in certain outcomes that we were unable to substantiate using multivariable methods.

Efficiency

Efficiency, as measured by LOS and costs, are presented both as means and medians in univariate analyses in Table 2. Median LOS was similar for hospitalist‐led and nonhospitalist‐led teams (4 days). Despite having similar LOS, the median costs of acute UGIH in patients cared for by hospitalists were higher ($7,359.00 vs. $6,181.00; P < 0.01).

After adjusting for demographic factors, Rockall risk score, comorbidity, early EGD, and hospital site, LOS remained similar between the 2 groups. On the other hand, the adjusted cost for UGIH patients cared for by hospitalists and nonhospitalists persisted, with hospitalist care costs $1,502.40 more than their nonhospitalist counterparts (Table 3).

Regression Model Estimates for Efficiency by Admitting Service
EfficiencyTreatment ProviderP
Hospitalist (n = 164)Nonhospitalist (n = 259)
  • NOTE: Significant P value indicated by bold. Adjusted means reported in days or dollars. These are antilogs of the mean values for provider type, adjusted for all covariates. Models are adjusted for age, gender, race, insurance, complete Rockall risk score, early EGD, Charlson comorbidity index score, and study site. By utilizing random effects in the regression models, we accounted for the effects of clustering on the physician level.

  • Abbreviations: EGD, esophagogastroduodenoscopy ; SD, standard deviation.

Adjusted length of stay, days (mean SD)5.2 (4.95.6)4.7 (4.55.0)0.15
Adjusted total cost, U.S. $ (mean SD)9006.50 (8366.609693.60)7504.10 (7069.907964.20)0.03

Discussion

This is the first study that has looked at the effect of hospitalists on clinical outcomes and efficiency in patients admitted for acute UGIH, a condition highly dependent upon another specialty for procedures and management. This is also one of only a few studies on UGIH that adjusted for severity of illness (Rockall score), comorbidity, performance of early endoscopypatient‐level confounders usually unaccounted for in prior research.

We show that hospitalists and nonhospitalists caring for acute UGIH patients had overall similar unadjusted outcomes; except for blood transfusion and 30‐day readmission rates. Unfortunately, due to the small number of events for readmissions, we were unable to perform adjusted analysis for readmission. Differences between hospitalists and nonhospitalists on blood transfusion rates were not substantiated on multivariable adjustments.

As for efficiency, univariable and multivariable analyses revealed that LOS was similar between provider types while costs were greater in UGIH patients attended by hospitalists.

Reductions in resource use, particularly costs, may be achieved by increasing throughput (eg, reducing LOS) or by decreasing service intensity (eg, using fewer ancillary services and specialty consultations).26 Specifically in acute UGIH, LOS is significantly affected by performance of early EGD.27, 28 In these studies, gastroenterologist‐led teams, compared to internists and surgeons, have easier access to endoscopy, thus reducing LOS and overall costs.27, 28

Similarly, prior studies have shown that the mechanism by which hospitalists lower costs is by decreasing LOS.810, 29 There are several hypotheses on how hospitalists affect LOS. Hospitalists, by being available all day, are thought to respond quickly to acute symptoms or new test results, are more efficient in navigating the complex hospital environment, or develop greater expertise as a result of added inpatient experience.8 On the downside, although the hospitalist model reduces overall LOS and costs, they also provide higher intensity of care as reflected by greater costs when broken down per hospital day.29 Thus, the cost differential we found may represent higher intensity of care by hospitalists in their management of acute UGIH, as higher intensity care without decreasing LOS can translate to higher costs.

In addition, patients with acute UGIH are unique in several respects. In contrast to diseases like heart failure, COPD, and pneumonia, in which the admitting provider has the option to request a subspecialist consultation, all patients with acute UGIH need a gastroenterologist to perform endoscopy as part of the management. These patients are usually admitted to general medicine wards, aggressively resuscitated with intravenous fluids, with a nonurgent gastroenterology consult or EGD performed on the next available schedule.

Aside from LOS being greatly affected by performance of early EGD and/or delay in consulting gastroenterology, sicker patients require longer hospitalization and drive LOS and healthcare costs up. It was therefore crucial that we accounted for severity of illness, comorbidity, and performance of early EGD in our regression models for LOS and costs. This approach allows us to acquire a more accurate estimate on the effects of hospitalist on LOS and costs in patients admitted with acute UGIH.

Our findings suggest that the academic hospitalist model of care may not have as great of an impact on hospital efficiency in certain patient groups that require nonurgent subspecialty consultations. Future studies should focus on elucidating these relationships.

Limitations

This study has several limitations. First, clinical data were abstracted at 6 sites by different abstractors so it is possible there were variations in how data were collected. To reduce variation, a standardized abstraction form with instructions was developed and the primary investigator (PI) was available for specific questions during the abstraction process. Second, only 5 out of the 6 sites used TSI accounting systems. Although similar, interhospital costs captured by TSI may vary among sites in terms of classifying direct and indirect costs, potentially resulting in misclassification bias in our cost estimates.17 We addressed these issues by including the hospital site variable in our regression models, regardless of its significance. Third, consent rates across sites vary from 70% to 85%. It is possible that patients who refused enrollment in the MCH trial are systematically different and may introduce bias in our analysis.

Furthermore, the study was designed as a natural experiment based on a rotational call cycle between hospitalist‐led and nonhospitalist‐led teams. It is possible that the order of patient assignment might not be completely naturally random as we intended. However, the study period was for 2 years and we expect the effect of order would have averaged out in time.

There are many hospitalist models of care. In terms of generalizability, the study pertains only to academic hospitalists and may not be applicable to hospitalists practicing in community hospitals. For example, the nonhospitalist comparison group is likely different in the community and academic settings. Community nonhospitalists (traditional practitioners) are usually internists covering both inpatient and outpatient responsibilities at the same time. In contrast, academic nonhospitalists are internists or subspecialists serving as ward attendings for a limited period (usually 1 month) with considerable variation in their nonattending responsibilities (eg, research, clinic, administration). Furthermore, academic nonhospitalist providers might be a self‐selected group by their willingness to serve as a ward attending, making them more hospitalist‐like. Changes and variability of inpatient attendings may also affect our findings when compared to prior work. Finally, it is also possible that having residents at academic medical centers may attenuate the effect of hospitalists more than in community‐based models.

Conclusions/Implications

Compared to nonhospitalists, academic hospitalist care of acute UGIH patients had similar overall clinical outcomes. However, our finding of similar LOS yet higher costs for patients cared for by hospitalists support 1 proposed mechanism in which hospitalists decrease healthcare costs: providing higher intensity of care per day of hospitalization. However, in academic hospitalist models, this higher intensity hypothesis should be revisited, especially in certain patient groups in which timing and involvement of subspecialists may influence discharge decisions, affecting LOS and overall costs.

Due to inherent limitations in this observational study, future studies should focus on verifying and elucidating these relationships further. Lastly, understanding which patient groups receive the greatest potential benefit from this model will help guide both organizational efforts and quality improvement strategies.

Acute upper gastrointestinal hemorrhage (UGIH) is one of the most common hospital admissions for acute care. Estimates indicate that 300,000 patients (100‐150 cases per 100,000 adults) are admitted annually with an associated economic impact of $2.5 billion.15 The current standard management of UGIH requires hospital admission and esophagogastroduodenoscopy (EGD) by a gastroenterologist for diagnosis and/or treatment. This management strategy results in a high consumption of hospital resources and costs.

Simultaneously, hospitalists have dramatically changed the delivery of inpatient care in the United States and are recognized as a location‐driven subspecialty for the care of acute hospitalized patients, similar to emergency medicine. Currently there are 20,000 hospitalists, and more than one‐third of general medicine inpatients are cared for by hospitalists.6, 7

Previous studies have shown that hospitalist care offers better or comparable outcomes, with lower overall length of stay (LOS) and costs compared to traditional providers.810 However, most of these studies were performed in single institutions, had weak designs or little‐to‐no adjustment for severity of illness, or were limited to 7 specific diseases (pneumonia, congestive heart failure [CHF], chest pain, ischemic stroke, urinary tract infection, chronic obstructive lung disease [COPD], and acute myocardial infarction [AMI]).8

Furthermore, less is known about the effect of hospitalists on conditions that may be dependent upon specialist consultation for procedures and/or treatment plans. In this study, gastroenterologists performed diagnostic and/or therapeutic endoscopy work as consultants to the attending physicians in the management of acute inpatient UGIH.

To explore the effects of hospitalists on care of patients with acute UGIH, we examined data from the Multicenter Hospitalist (MCH) trial. The objectives of our study were to compare clinical outcomesin‐hospital mortality and complications (ie, recurrent bleeding, intensive care unit [ICU] transfer, decompensation, transfusion, reendoscopy, 30‐day readmission)and efficiency (LOS and costs) in hospitalized acute UGIH patients cared for by hospitalists and nonhospitalists in 6 academic centers in the United States during a 2‐year period.

Patients and Methods

Study Sites

From July 1, 2001 to June 30, 2003, the MCH trial1113 was a prospective, multicenter, observational trial of the care provided by hospitalists to patients admitted to general medical services at 6 academic medical institutions. There were 31,000 consecutive admissions to the general medical services of these participating sites: University of Chicago (Chicago, IL), University of Wisconsin Hospital (Madison, WI), University of Iowa (Iowa City, IA), University of California at San Francisco (San Francisco, CA), University of New Mexico (Albuquerque, NM), and Brigham and Women's Hospital (Boston, MA). The study was approved by the institutional review boards (IRBs) at each of the 6 participating institutions.

MCH Study Patients

Patients were eligible if they were admitted to the general medical services under the care of a hospitalist or nonhospitalist physician. Regardless of the admitting provider, each medical service was composed of rotating senior and junior resident physicians in all 6 sites. Furthermore, patients were 18 years of age or older, and were able to give consent themselves or had an appropriate proxy. Patients with mini‐mental status score of 17 (out of 22), admitted under their primary care physician or to an inpatient gastroenterology service, or transferred from another hospital, were excluded. The MCH study was designed to study the outcomes and efficiency in patients admitted for CHF, pneumonia, UGIH, and end‐of‐life care.

Acute UGIH Patients

Within the MCH‐eligible patients, we identified those with acute UGIH using the following International Classification of Diseases, 9th edition (ICD‐9) codes assigned at discharge: esophageal varices with hemorrhage (456.0, 456.20); Mallory‐Weiss syndrome (530.7); gastric ulcer with hemorrhage (531.00531.61); duodenal ulcer with hemorrhage (532.00532.61); peptic ulcer, site unspecified, with hemorrhage (533.00533.61); gastrojejunal ulcer with hemorrhage (534.00534.61); gastritis with hemorrhage (535.61); angiodysplasia of stomach/duodenum with hemorrhage (537.83); and hematemesis (578.0, 578.9). We also confirmed the diagnosis of UGIH by reviewing patient medical records for observed hematemesis, nasogastric tube aspirate with gross or hemoccult blood, or clinical history of hematemesis, melena, or hematochezia.14, 15

Data

All data were obtained from the 6 hospitals' administrative records, patient interviews, and medical chart abstractions. Dates of admission and discharge, ICD‐9 diagnosis codes, insurance type, age, race, and gender were obtained from administrative data. One‐month follow‐up telephone interviews assessed whether or not patient had any follow‐up appointment or hospital readmissions. Trained abstractors from each site performed manual chart reviews using a standard data collection sheet. The ICD‐9 code designation and chart abstraction methodology were developed prior to the initiation of the study to ensure consistent data collection and reduce bias.

The following data elements were collected: comorbidities, endoscopic findings, inpatient mortality, clinical evidence of rebleeding, endoscopic treatment or gastrointestinal (GI) surgery to control bleeding, repeat EGD, ICU transfer, decompensated comorbid illness requiring continued hospitalization, and blood transfusion (packed red cells, plasma, platelets). Clinical evidence of rebleeding was defined as either hematemesis or melena with decrease in hemoglobin of 2 g in 24 hours with or without hemodynamic compromise.14, 15 For the purpose of this study, recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery for control of UGIH, or repeat EGD before discharge. Furthermore, a composite endpoint termed total complications encompassed all adverse outcomes related to the UGIH hospitalization. The 30‐day readmission variable was defined using readmission identified in administrative records and a 30‐day follow‐up phone call. To guard against recall bias, self‐report data was only included for nonsite admissions.

We defined efficiency in terms of costs and LOS. Total hospital costs were measured using the TSI cost accounting system (Transition Systems, Inc., Boston, MA; now Eclipsys Corporation)16, 17 at 5 out of the 6 participating sites. TSI is a hospital cost accounting software system that integrates resource utilization and financial data already recorded in other hospital databases (such as the billing system, payroll system, and general ledger system).17 Hospital LOS was defined as the number of days from patient admission to the general medicine service until patient discharge.

Provider Specialization: Hospitalists vs. Nonhospitalists

The study was designed as a natural experiment based on a call cycle. The hospitalist‐led teams at each institution alternated in a 4‐day or 5‐day general medicine call cycle with teams led by traditional academic internal medicine attending physicians. All patients were assigned to teams according to their position in the call cycle without regard to whether the attending physician was a hospitalist or a nonhospitalist. Hospitalists are physicians whose primary professional focus is the general medical care of hospitalized patients.18, 19 As previously reported in a related MCH work,11 a hospitalist was also defined as a provider who spends at least 25% of his or her time on an academic inpatient general medicine service. Nonhospitalist physicians were most often outpatient general internal medicine faculty or subspecialists, who attended 1 month per year. Physicians were classified as hospitalists or nonhospitalists according to the designations provided by each site.

UGIH‐specific Confounders

From chart abstraction, we captured severity of illness, comorbidity, and performance of early EGD, variables that can confound analysis in UGIH. To capture severity of illness, a complete Rockall risk score was calculated for each patient. The complete Rockall uses 3 clinical variables (age, shock, and comorbidity) and 2 endoscopic variables (endoscopic diagnosis and stigmata of recent hemorrhage).5, 20 A complete Rockall score of 2 is considered low‐risk for rebleeding or death following admission.21, 22 The accepted definition of low‐risk is <5% recurrent bleeding and <1% mortality risk. A complete Rockall score of 3 to 5 is considered moderate‐risk while 6 is considered high‐risk. Comorbidity was measured using the Charlson comorbidity index.23 Performance of early endoscopy, usually defined as endoscopy performed within 24 hours from presentation, was previously shown to decrease LOS and need for surgical intervention in patients with acute UGIH.24, 25 Documented times of presentation to the emergency department and time of endoscopy performance were collected to calculate for the rate of early endoscopy in our study population.

Statistical Analysis

All statistical analyses were performed using SAS Version 9.1 for Windows (SAS Institute, Cary, NC).

Differences in baseline demographic characteristics of patients and their endoscopic findings were compared between the 2 types of providers. Univariate analyses were also performed to compare the differences in adverse outcomes, LOS, and costs between patients cared for by hospitalists and nonhospitalists. Chi‐square tests were used for categorical variables; while both Wilcoxon rank sum test and Student's t test were used in the analysis of continuous variables.

Next, we performed multivariable analyses to determine the independent association between hospitalist care and the odds of the patients having certain outcomes. However, to prevent overfitting, we only developed regression models for adverse outcomes that have at least 20% event rate.

Multivariable regression models were developed separately for LOS and costs. In contrast with the models on outcomes, analyses of LOS and costs were restricted to: (1) patients who were discharged alive; and (2) to cases with LOS and costs values within 3 standard deviations (SDs) of the mean because of the skewed nature of these data.

All models were adjusted for age, gender, race, insurance type, complete Rockall risk score, performance of early EGD, Charlson comorbidity index, and study site. Final candidate variables in the models were chosen based on stepwise selection, a method very similar to forward selection except that variables selected for the model do not necessarily remain in the model. Effects were entered into and then removed from the model in such a way that each forward selection step can be followed by 1 or more backward elimination steps. The stepwise selection was terminated if no further effect can be added to the model or if the current model was identical to the previous model. The stepwise selection model was generated using statistical criterion of alpha = 0.05 for entry and elimination from the model. Variables that can be a profound source of variation, such as study site and treating physician, were included in the model irrespective of their statistical significance.

To account for clustering of patients treated by the same physician, we used multilevel modeling with SAS PROC GLIMMIX (with random effects). For outcomes (categorical variables), we utilized models with logit‐link and binomial‐distributed errors. As for efficiency (continuous variables with skewed distribution), the multivariable analyses used a generalized linear model with log‐link and assuming gamma‐distributed errors.

Results

Patient Characteristics and Endoscopic Diagnoses

Out of 31,000 patients, the study identified a total of 566 patients (1.8%) with acute UGIH (Table 1). However, 116 patients transferred from another hospital were excluded as their initial management was provided elsewhere, giving a final study sample of 450 patients. Overall, there are 163 admitting physicians from 6 sites, with 39 (24%) classified as hospitalists and 124 (76%) as nonhospitalists. Forty‐two percent (177/450) of patients were cared for by hospitalists. Compared to nonhospitalists, patients admitted to the hospitalist service were older (62.8 vs. 57.7 years, P < 0.01) and with third‐party payor mix differences (P < 0.01). However, there were no statistical differences between patients attended by hospitalists and nonhospitalists with regard to Complete Rockall risk score, Charlson comorbidity index, performance of early endoscopy, and mean hemoglobin values on admission. Upper endoscopy was performed in all patients with distribution of the 3 most common diagnoses being similar (P > 0.05) between hospitalists and nonhospitalists: erosive disease (49.7% vs. 54.6%), peptic ulcer disease (PUD) (48% vs. 46.9%), and varices (18.6% vs. 14.7%).

Patient Characteristics, Rockall Risk Score, Performance of Early Endoscopy, and Endoscopic Findings by Admitting Service
VariableAdmitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values indicated by bold.

  • Abbreviations: GI, gastrointestinal; SD, standard deviation.

  • Do not add up to 100% due to dual diagnoses.

  • Data on hemoglobin values on admission were available only for 376 patients (134 patients cared for by hospitalists and 242 cared for by nonhospitalists).

Age, years (meanSD)62.817.457.718.5<0.01
Male sex, n (%)104 (58.8)169 (61.9)0.50
Ethnicity, n (%)  0.13
White83 (46.9)102 (37.4) 
African‐American34 (19.2)75 (27.5) 
Hispanic21 (11.9)40 (14.7) 
Asian/Pacific Islander24 (13.6)29 (10.6) 
Others/unknown15 (8.5)27 (9.9) 
Insurance, n (%)  <0.01
Medicare86 (48.6)104 (38.1) 
Medicaid15 (8.5)33 (12.1) 
No payer18 (10.2)36 (13.2) 
Private46 (26)52 (19.1) 
Unknown12 (6.8)48 (17.5) 
Charlson Comorbidity Index (meanSD)1.91.61.81.70.51
Complete Rockall, n (%)  0.11
Low‐risk (0‐2)82 (46.3)103 (37.7) 
Moderate‐risk (3‐5)71 (40.1)137 (50.2) 
High‐risk (6)24 (14.6)33 (12.1) 
Early endoscopy (<24 hours)82 (46.3)133 (48.7)0.62
Endoscopic diagnosis, n (%)*   
Erosive disease88 (49.7)149 (54.6)0.31
Peptic ulcer disease85 (48.0)128 (46.9)0.81
Varices33 (18.6)40 (14.7)0.26
Mallory‐Weiss tear9 (5.1)21 (7.7)0.28
Angiodysplasia9 (5.1)13 (4.8)0.88
GI mass1 (0.6)4 (1.5)0.65
Normal7 (4.0)8 (2.9)0.55
Admission hemoglobin values (meanSD)10.22.910.22.90.78

Clinical Outcomes

Between hospitalists and nonhospitalists, unadjusted outcomes were similar (P > 0.05) for mortality (2.3% vs. 0.4%), recurrent bleeding (11% vs. 11%), need for endoscopic therapy (24% vs. 22%), ICU‐transfer and decompensation (15% vs. 15%), as well as an overall composite measure of any complication (79% vs. 72%) (Table 2). However, the hospitalist‐led teams performed more blood transfusions (74% vs. 63%, P = 0.02) and readmission rates were higher (7.3% vs. 3.3%, P = 0.05).

Univariate Analyses of Outcomes and Efficiency by Admitting Services
Outcomes, n (%)Admitting ServiceP
Hospitalist (n = 177)Nonhospitalist (n = 273)
  • NOTE: Significant P values are indicated by bold.

  • Abbreviations: EGD, esophagogastroduodenoscopy; GI, gastrointestinal; ICU, intensive care unit; LOS, length of stay; SD, standard deviation.

  • Recurrent bleeding was defined as clinical evidence of rebleeding, emergency GI surgery and repeat EGD before discharge.

  • Total complications is a composite endpoint of in‐patient mortality, recurrent bleeding, endoscopic treatments to control bleeding, ICU transfer, decompensate comorbid illness requiring continued hospitalization, and blood transfusion.

  • Only 423 patients were used in the resource use (efficiency) analysis. A total of 27 patients were excluded because of inpatient mortality (n = 5) and those with more than 3SD of population mean in terms of costs and LOS (n = 22).

Inpatient mortality4 (2.3)1 (0.4)0.08
Recurrent bleeding*20 (11.3)29 (10.6)0.88
Endoscopic therapy43 (24.3)60 (22.0)0.57
ICU transfers23 (13)24 (8.8)0.20
Decompensated comorbidities that required continued hospitalization26 (14.7)41 (15.0)0.92
Any transfusion131 (74.0)172 (63.0)0.02
Total complications139 (78.5)196 (71.8)0.11
30‐day all‐cause readmissions13 (7.3)9 (3.3)0.05
EfficiencyHospitalist (n = 164)Nonhospitalist (n = 259)P
LOS, days   
MeanSD4.83.54.53.00.30
Median (interquartile range)4 (36)4 (26)0.69
Total costs, U.S. $   
MeanSD10,466.669191.007926.716065.00<0.01
Median (interquartile range)7359.00 (4,698.0012,550.00)6181.00 (3744.0010,344.00)<0.01

Because of the low event rate of certain adverse outcomes (<20%), we were only able to perform adjusted analyses on 4 outcomes: need for endoscopic therapy (odds ratio [OR], 0.82; 95% confidence interval [CI], 0.491.37), ICU transfer and decompensation (OR, 0.82; 95% CI, 0.451.52), blood transfusion (OR, 1.30; 95% CI, 0.822.04), and any complication (OR, 1.18; 95% CI, 0.711.96). Since outcome differences disappeared after controlling for confounders, the data suggest that overall care provided by hospitalists and nonhospitalists might be equivalenteven in certain outcomes that we were unable to substantiate using multivariable methods.

Efficiency

Efficiency, as measured by LOS and costs, are presented both as means and medians in univariate analyses in Table 2. Median LOS was similar for hospitalist‐led and nonhospitalist‐led teams (4 days). Despite having similar LOS, the median costs of acute UGIH in patients cared for by hospitalists were higher ($7,359.00 vs. $6,181.00; P < 0.01).

After adjusting for demographic factors, Rockall risk score, comorbidity, early EGD, and hospital site, LOS remained similar between the 2 groups. On the other hand, the adjusted cost for UGIH patients cared for by hospitalists and nonhospitalists persisted, with hospitalist care costs $1,502.40 more than their nonhospitalist counterparts (Table 3).

Regression Model Estimates for Efficiency by Admitting Service
EfficiencyTreatment ProviderP
Hospitalist (n = 164)Nonhospitalist (n = 259)
  • NOTE: Significant P value indicated by bold. Adjusted means reported in days or dollars. These are antilogs of the mean values for provider type, adjusted for all covariates. Models are adjusted for age, gender, race, insurance, complete Rockall risk score, early EGD, Charlson comorbidity index score, and study site. By utilizing random effects in the regression models, we accounted for the effects of clustering on the physician level.

  • Abbreviations: EGD, esophagogastroduodenoscopy ; SD, standard deviation.

Adjusted length of stay, days (mean SD)5.2 (4.95.6)4.7 (4.55.0)0.15
Adjusted total cost, U.S. $ (mean SD)9006.50 (8366.609693.60)7504.10 (7069.907964.20)0.03

Discussion

This is the first study that has looked at the effect of hospitalists on clinical outcomes and efficiency in patients admitted for acute UGIH, a condition highly dependent upon another specialty for procedures and management. This is also one of only a few studies on UGIH that adjusted for severity of illness (Rockall score), comorbidity, performance of early endoscopypatient‐level confounders usually unaccounted for in prior research.

We show that hospitalists and nonhospitalists caring for acute UGIH patients had overall similar unadjusted outcomes; except for blood transfusion and 30‐day readmission rates. Unfortunately, due to the small number of events for readmissions, we were unable to perform adjusted analysis for readmission. Differences between hospitalists and nonhospitalists on blood transfusion rates were not substantiated on multivariable adjustments.

As for efficiency, univariable and multivariable analyses revealed that LOS was similar between provider types while costs were greater in UGIH patients attended by hospitalists.

Reductions in resource use, particularly costs, may be achieved by increasing throughput (eg, reducing LOS) or by decreasing service intensity (eg, using fewer ancillary services and specialty consultations).26 Specifically in acute UGIH, LOS is significantly affected by performance of early EGD.27, 28 In these studies, gastroenterologist‐led teams, compared to internists and surgeons, have easier access to endoscopy, thus reducing LOS and overall costs.27, 28

Similarly, prior studies have shown that the mechanism by which hospitalists lower costs is by decreasing LOS.810, 29 There are several hypotheses on how hospitalists affect LOS. Hospitalists, by being available all day, are thought to respond quickly to acute symptoms or new test results, are more efficient in navigating the complex hospital environment, or develop greater expertise as a result of added inpatient experience.8 On the downside, although the hospitalist model reduces overall LOS and costs, they also provide higher intensity of care as reflected by greater costs when broken down per hospital day.29 Thus, the cost differential we found may represent higher intensity of care by hospitalists in their management of acute UGIH, as higher intensity care without decreasing LOS can translate to higher costs.

In addition, patients with acute UGIH are unique in several respects. In contrast to diseases like heart failure, COPD, and pneumonia, in which the admitting provider has the option to request a subspecialist consultation, all patients with acute UGIH need a gastroenterologist to perform endoscopy as part of the management. These patients are usually admitted to general medicine wards, aggressively resuscitated with intravenous fluids, with a nonurgent gastroenterology consult or EGD performed on the next available schedule.

Aside from LOS being greatly affected by performance of early EGD and/or delay in consulting gastroenterology, sicker patients require longer hospitalization and drive LOS and healthcare costs up. It was therefore crucial that we accounted for severity of illness, comorbidity, and performance of early EGD in our regression models for LOS and costs. This approach allows us to acquire a more accurate estimate on the effects of hospitalist on LOS and costs in patients admitted with acute UGIH.

Our findings suggest that the academic hospitalist model of care may not have as great of an impact on hospital efficiency in certain patient groups that require nonurgent subspecialty consultations. Future studies should focus on elucidating these relationships.

Limitations

This study has several limitations. First, clinical data were abstracted at 6 sites by different abstractors so it is possible there were variations in how data were collected. To reduce variation, a standardized abstraction form with instructions was developed and the primary investigator (PI) was available for specific questions during the abstraction process. Second, only 5 out of the 6 sites used TSI accounting systems. Although similar, interhospital costs captured by TSI may vary among sites in terms of classifying direct and indirect costs, potentially resulting in misclassification bias in our cost estimates.17 We addressed these issues by including the hospital site variable in our regression models, regardless of its significance. Third, consent rates across sites vary from 70% to 85%. It is possible that patients who refused enrollment in the MCH trial are systematically different and may introduce bias in our analysis.

Furthermore, the study was designed as a natural experiment based on a rotational call cycle between hospitalist‐led and nonhospitalist‐led teams. It is possible that the order of patient assignment might not be completely naturally random as we intended. However, the study period was for 2 years and we expect the effect of order would have averaged out in time.

There are many hospitalist models of care. In terms of generalizability, the study pertains only to academic hospitalists and may not be applicable to hospitalists practicing in community hospitals. For example, the nonhospitalist comparison group is likely different in the community and academic settings. Community nonhospitalists (traditional practitioners) are usually internists covering both inpatient and outpatient responsibilities at the same time. In contrast, academic nonhospitalists are internists or subspecialists serving as ward attendings for a limited period (usually 1 month) with considerable variation in their nonattending responsibilities (eg, research, clinic, administration). Furthermore, academic nonhospitalist providers might be a self‐selected group by their willingness to serve as a ward attending, making them more hospitalist‐like. Changes and variability of inpatient attendings may also affect our findings when compared to prior work. Finally, it is also possible that having residents at academic medical centers may attenuate the effect of hospitalists more than in community‐based models.

Conclusions/Implications

Compared to nonhospitalists, academic hospitalist care of acute UGIH patients had similar overall clinical outcomes. However, our finding of similar LOS yet higher costs for patients cared for by hospitalists support 1 proposed mechanism in which hospitalists decrease healthcare costs: providing higher intensity of care per day of hospitalization. However, in academic hospitalist models, this higher intensity hypothesis should be revisited, especially in certain patient groups in which timing and involvement of subspecialists may influence discharge decisions, affecting LOS and overall costs.

Due to inherent limitations in this observational study, future studies should focus on verifying and elucidating these relationships further. Lastly, understanding which patient groups receive the greatest potential benefit from this model will help guide both organizational efforts and quality improvement strategies.

References
  1. Laine L,Peterson WL.Bleeding peptic ulcer.N Engl J Med.1994;331(11):717727.
  2. Longstreth GF.Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: a population‐based study.Am J Gastroenterol.1995;90(2):206210.
  3. Rockall TA,Logan RF,Devlin HB, et al.Variation in outcome after acute upper gastrointestinal haemorrhage. the national audit of acute upper gastrointestinal haemorrhage.Lancet.1995;346(8971):346350.
  4. Rockall TA,Logan RF,Devlin HB, et al.Influencing the practice and outcome in acute upper gastrointestinal haemorrhage. Steering committee of the National Audit of Acute Upper Gastrointestinal Haemorrhage.Gut.1997;41(5):606611.
  5. Rockall TA,Logan RF,Devlin HB, et al.Risk assessment after acute upper gastrointestinal haemorrhage.Gut.1996;38(3):316321.
  6. Lurie JD,Miller DP,Lindenauer PK, et al.The potential size of the hospitalist workforce in the united states.Am J Med.1999;106(4):441445.
  7. Society of Hospital Medicine. About SHM. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=General_Information357(25):25892600.
  8. Meltzer D,Manning WG,Morrison J, et al.Effects of physician experience on costs and outcomes on an academic general medicine service: results of a trial of hospitalists.Ann Intern Med.2002;137(11):866874.
  9. Peterson MC.A systematic review of outcomes and quality measures in adult patients cared for by hospitalists vs nonhospitalists.Mayo Clin Proc.2009;84(3):248254.
  10. Schneider JA,Zhang Q,Auerbach A, et al.Do hospitalists or physicians with greater inpatient HIV experience improve HIV care in the era of highly active antiretroviral therapy? Results from a multicenter trial of academic hospitalists.Clin Infect Dis.2008;46(7):10851092.
  11. Vasilevskis EE,Meltzer D,Schnipper J, et al.Quality of care for decompensated heart failure: comparable performance between academic hospitalists and non‐hospitalists. J Gen Intern Med.2008;23(9):13991406.
  12. Auerbach AD,Katz R,Pantilat SZ, et al.Factors associated with discussion of care plans and code status at the time of hospital admission: results from the Multicenter Hospitalist Study.J Hosp Med.2008;3(6):437445.
  13. Hay JA,Lyubashevsky E,Elashoff J, et al.Upper gastrointestinal hemorrhage clinical guideline determining the optimal hospital length of stay.Am J Med.1996;100(3):313322.
  14. Hay JA,Maldonado L,Weingarten SR, et al.Prospective evaluation of a clinical guideline recommending hospital length of stay in upper gastrointestinal tract hemorrhage.JAMA.1997;278(24):21512156.
  15. Brox AC,Filion KB,Zhang X, et al.In‐hospital cost of abdominal aortic aneurysm repair in Canada and the United States.Arch Intern Med.2003;163(20):25002504.
  16. Azoulay A,Doris NM,Filion KB, et al.The use of transition cost accounting system in health services research.Cost Eff Resour Alloc.2007;5:11.
  17. Society of Hospital Medicine. Definition of a Hospitalist. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=General_Information335(7):514517.
  18. Rockall TA,Logan RF,Devlin HB, et al.Selection of patients for early discharge or outpatient care after acute upper gastrointestinal haemorrhage. National Audit of Acute Upper Gastrointestinal Haemorrhage.Lancet.1996;347(9009):11381140.
  19. Dulai GS,Gralnek IM,Oei TT, et al.Utilization of health care resources for low‐risk patients with acute, nonvariceal upper GI hemorrhage: an historical cohort study.Gastrointest Endosc.2002;55(3):321327.
  20. Gralnek IM,Dulai GS.Incremental value of upper endoscopy for triage of patients with acute non‐variceal upper‐GI hemorrhage.Gastrointest Endosc.2004;60(1):914.
  21. Charlson ME,Charlson RE,Peterson JC, et al.The Charlson comorbidity index is adapted to predict costs of chronic disease in primary care patients.J Clin Epidemiol.2008;61(12):12341240.
  22. Cooper GS,Chak A,Connors AF, et al.The effectiveness of early endoscopy for upper gastrointestinal hemorrhage: a community‐based analysis.Med Care.1998;36(4):462474.
  23. Cooper GS,Chak A,Way LE, et al.Early endoscopy in upper gastrointestinal hemorrhage: associations with recurrent bleeding, surgery, and length of hospital stay.Gastrointest Endosc.1999;49(2):145152.
  24. Coffman J,Rundall TG.The impact of hospitalists on the cost and quality of inpatient care in the united states: a research synthesis.Med Care Res Rev.2005;62(4):379406.
  25. Quirk DM,Barry MJ,Aserkoff B, et al.Physician specialty and variations in the cost of treating patients with acute upper gastrointestinal bleeding.Gastroenterology.1997;113(5):14431448.
  26. Pardo A,Durandez R,Hernandez M, et al.Impact of physician specialty on the cost of nonvariceal upper GI bleeding care.Am J Gastroenterol.2002;97(6):15351542.
  27. Kaboli PJ,Barnett MJ,Rosenthal GE.Associations with reduced length of stay and costs on an academic hospitalist service.Am J Manag Care.2004;10(8):561568.
References
  1. Laine L,Peterson WL.Bleeding peptic ulcer.N Engl J Med.1994;331(11):717727.
  2. Longstreth GF.Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: a population‐based study.Am J Gastroenterol.1995;90(2):206210.
  3. Rockall TA,Logan RF,Devlin HB, et al.Variation in outcome after acute upper gastrointestinal haemorrhage. the national audit of acute upper gastrointestinal haemorrhage.Lancet.1995;346(8971):346350.
  4. Rockall TA,Logan RF,Devlin HB, et al.Influencing the practice and outcome in acute upper gastrointestinal haemorrhage. Steering committee of the National Audit of Acute Upper Gastrointestinal Haemorrhage.Gut.1997;41(5):606611.
  5. Rockall TA,Logan RF,Devlin HB, et al.Risk assessment after acute upper gastrointestinal haemorrhage.Gut.1996;38(3):316321.
  6. Lurie JD,Miller DP,Lindenauer PK, et al.The potential size of the hospitalist workforce in the united states.Am J Med.1999;106(4):441445.
  7. Society of Hospital Medicine. About SHM. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=General_Information357(25):25892600.
  8. Meltzer D,Manning WG,Morrison J, et al.Effects of physician experience on costs and outcomes on an academic general medicine service: results of a trial of hospitalists.Ann Intern Med.2002;137(11):866874.
  9. Peterson MC.A systematic review of outcomes and quality measures in adult patients cared for by hospitalists vs nonhospitalists.Mayo Clin Proc.2009;84(3):248254.
  10. Schneider JA,Zhang Q,Auerbach A, et al.Do hospitalists or physicians with greater inpatient HIV experience improve HIV care in the era of highly active antiretroviral therapy? Results from a multicenter trial of academic hospitalists.Clin Infect Dis.2008;46(7):10851092.
  11. Vasilevskis EE,Meltzer D,Schnipper J, et al.Quality of care for decompensated heart failure: comparable performance between academic hospitalists and non‐hospitalists. J Gen Intern Med.2008;23(9):13991406.
  12. Auerbach AD,Katz R,Pantilat SZ, et al.Factors associated with discussion of care plans and code status at the time of hospital admission: results from the Multicenter Hospitalist Study.J Hosp Med.2008;3(6):437445.
  13. Hay JA,Lyubashevsky E,Elashoff J, et al.Upper gastrointestinal hemorrhage clinical guideline determining the optimal hospital length of stay.Am J Med.1996;100(3):313322.
  14. Hay JA,Maldonado L,Weingarten SR, et al.Prospective evaluation of a clinical guideline recommending hospital length of stay in upper gastrointestinal tract hemorrhage.JAMA.1997;278(24):21512156.
  15. Brox AC,Filion KB,Zhang X, et al.In‐hospital cost of abdominal aortic aneurysm repair in Canada and the United States.Arch Intern Med.2003;163(20):25002504.
  16. Azoulay A,Doris NM,Filion KB, et al.The use of transition cost accounting system in health services research.Cost Eff Resour Alloc.2007;5:11.
  17. Society of Hospital Medicine. Definition of a Hospitalist. Available at: http://www.hospitalmedicine.org/AM/Template.cfm?Section=General_Information335(7):514517.
  18. Rockall TA,Logan RF,Devlin HB, et al.Selection of patients for early discharge or outpatient care after acute upper gastrointestinal haemorrhage. National Audit of Acute Upper Gastrointestinal Haemorrhage.Lancet.1996;347(9009):11381140.
  19. Dulai GS,Gralnek IM,Oei TT, et al.Utilization of health care resources for low‐risk patients with acute, nonvariceal upper GI hemorrhage: an historical cohort study.Gastrointest Endosc.2002;55(3):321327.
  20. Gralnek IM,Dulai GS.Incremental value of upper endoscopy for triage of patients with acute non‐variceal upper‐GI hemorrhage.Gastrointest Endosc.2004;60(1):914.
  21. Charlson ME,Charlson RE,Peterson JC, et al.The Charlson comorbidity index is adapted to predict costs of chronic disease in primary care patients.J Clin Epidemiol.2008;61(12):12341240.
  22. Cooper GS,Chak A,Connors AF, et al.The effectiveness of early endoscopy for upper gastrointestinal hemorrhage: a community‐based analysis.Med Care.1998;36(4):462474.
  23. Cooper GS,Chak A,Way LE, et al.Early endoscopy in upper gastrointestinal hemorrhage: associations with recurrent bleeding, surgery, and length of hospital stay.Gastrointest Endosc.1999;49(2):145152.
  24. Coffman J,Rundall TG.The impact of hospitalists on the cost and quality of inpatient care in the united states: a research synthesis.Med Care Res Rev.2005;62(4):379406.
  25. Quirk DM,Barry MJ,Aserkoff B, et al.Physician specialty and variations in the cost of treating patients with acute upper gastrointestinal bleeding.Gastroenterology.1997;113(5):14431448.
  26. Pardo A,Durandez R,Hernandez M, et al.Impact of physician specialty on the cost of nonvariceal upper GI bleeding care.Am J Gastroenterol.2002;97(6):15351542.
  27. Kaboli PJ,Barnett MJ,Rosenthal GE.Associations with reduced length of stay and costs on an academic hospitalist service.Am J Manag Care.2004;10(8):561568.
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Do hospitalists affect clinical outcomes and efficiency for patients with acute upper gastrointestinal hemorrhage (UGIH)?
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Do hospitalists affect clinical outcomes and efficiency for patients with acute upper gastrointestinal hemorrhage (UGIH)?
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A Painful Rash

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A painful rash

A 40‐year‐old man presented to the emergency department with a 5‐day history of fever, productive cough, and a painful rash. The rash was composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting (Figure 1). The patient had a history of prior tuberculosis infection, illicit drug use, and human immunodeficiency virus (HIV). On initial physical examination, oral temperature was 98.5F, pulse was 110 beats/minute, respiratory rate was 22 breaths/minute, blood pressure was 151/79 mm Hg, and oxygen saturation (SpO2) was 94%. Laboratory test results at admission were as follows: hemoglobin 10.6 g/dL; platelets 364,000 cells/L; white blood cell count 8,300 cells/L; CD4 count 132 cells/L; total serum protein 9.1 g/dL; albumin 2.0 g/dL; and lactate dehydrogenase (LDH) 158 IU/L. Chest radiograph showed diffuse pulmonary infiltrates bilaterally (Figure 2). Sputum cultures showed regular respiratory flora and no acid fast bacilli. Viral cultures of the vesicular lesions were positive for varicella zoster virus (VZV). The patient was started on acyclovir for VZV. After 2 days the patient's symptoms improved and he was subsequently discharged.

Figure 1
Rash composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting.
Figure 2
Chest radiograph showing diffuse bilateral pulmonary infiltrates.

Herpes zoster is caused by the reactivation of a latent VZV infection in the dorsal root ganglion or cranial nerve ganglion. Zoster is characterized by an erythematous, vesicular, pustular rash in a unilateral dermatomal distribution. Immunosuppression is a risk factor for zoster; however, 92% of cases are in immunocompetent patients.1 Further, immunocompromised patients are more likely to develop disseminated zoster infection, including pneumonia, hepatitis, and encephalitis. These patients are also more likely to have secondary bacterial superinfections of cutaneous lesions and respiratory tracts.2 While zoster is often self‐limiting, it can lead to significant morbidity and mortality in immunocompromised patients. Intravenous acyclovir should be considered in patients with disseminated disease or visceral involvement, with advanced HIV, and in transplant patients being treated for rejection.2 Unilateral erythematous, vesicular rashes in a dermatomal distribution should yield a high clinical suspicion for herpes zoster, especially in immunocompromised patients.

References
  1. Yawn BP.A population‐based study of the incidence and complication rates of herpes zoster before zoster vaccine introduction.Mayo Clin Proc.2007;82(11):13411349.
  2. Krause RS. Herpes zoster. http://www.emedicine.com/emerg/TOPIC823. HTM. Accessed May2009.
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A 40‐year‐old man presented to the emergency department with a 5‐day history of fever, productive cough, and a painful rash. The rash was composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting (Figure 1). The patient had a history of prior tuberculosis infection, illicit drug use, and human immunodeficiency virus (HIV). On initial physical examination, oral temperature was 98.5F, pulse was 110 beats/minute, respiratory rate was 22 breaths/minute, blood pressure was 151/79 mm Hg, and oxygen saturation (SpO2) was 94%. Laboratory test results at admission were as follows: hemoglobin 10.6 g/dL; platelets 364,000 cells/L; white blood cell count 8,300 cells/L; CD4 count 132 cells/L; total serum protein 9.1 g/dL; albumin 2.0 g/dL; and lactate dehydrogenase (LDH) 158 IU/L. Chest radiograph showed diffuse pulmonary infiltrates bilaterally (Figure 2). Sputum cultures showed regular respiratory flora and no acid fast bacilli. Viral cultures of the vesicular lesions were positive for varicella zoster virus (VZV). The patient was started on acyclovir for VZV. After 2 days the patient's symptoms improved and he was subsequently discharged.

Figure 1
Rash composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting.
Figure 2
Chest radiograph showing diffuse bilateral pulmonary infiltrates.

Herpes zoster is caused by the reactivation of a latent VZV infection in the dorsal root ganglion or cranial nerve ganglion. Zoster is characterized by an erythematous, vesicular, pustular rash in a unilateral dermatomal distribution. Immunosuppression is a risk factor for zoster; however, 92% of cases are in immunocompetent patients.1 Further, immunocompromised patients are more likely to develop disseminated zoster infection, including pneumonia, hepatitis, and encephalitis. These patients are also more likely to have secondary bacterial superinfections of cutaneous lesions and respiratory tracts.2 While zoster is often self‐limiting, it can lead to significant morbidity and mortality in immunocompromised patients. Intravenous acyclovir should be considered in patients with disseminated disease or visceral involvement, with advanced HIV, and in transplant patients being treated for rejection.2 Unilateral erythematous, vesicular rashes in a dermatomal distribution should yield a high clinical suspicion for herpes zoster, especially in immunocompromised patients.

A 40‐year‐old man presented to the emergency department with a 5‐day history of fever, productive cough, and a painful rash. The rash was composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting (Figure 1). The patient had a history of prior tuberculosis infection, illicit drug use, and human immunodeficiency virus (HIV). On initial physical examination, oral temperature was 98.5F, pulse was 110 beats/minute, respiratory rate was 22 breaths/minute, blood pressure was 151/79 mm Hg, and oxygen saturation (SpO2) was 94%. Laboratory test results at admission were as follows: hemoglobin 10.6 g/dL; platelets 364,000 cells/L; white blood cell count 8,300 cells/L; CD4 count 132 cells/L; total serum protein 9.1 g/dL; albumin 2.0 g/dL; and lactate dehydrogenase (LDH) 158 IU/L. Chest radiograph showed diffuse pulmonary infiltrates bilaterally (Figure 2). Sputum cultures showed regular respiratory flora and no acid fast bacilli. Viral cultures of the vesicular lesions were positive for varicella zoster virus (VZV). The patient was started on acyclovir for VZV. After 2 days the patient's symptoms improved and he was subsequently discharged.

Figure 1
Rash composed of grouped, raised, fluid‐filled vesicles with an erythematous base and honey‐colored crusting.
Figure 2
Chest radiograph showing diffuse bilateral pulmonary infiltrates.

Herpes zoster is caused by the reactivation of a latent VZV infection in the dorsal root ganglion or cranial nerve ganglion. Zoster is characterized by an erythematous, vesicular, pustular rash in a unilateral dermatomal distribution. Immunosuppression is a risk factor for zoster; however, 92% of cases are in immunocompetent patients.1 Further, immunocompromised patients are more likely to develop disseminated zoster infection, including pneumonia, hepatitis, and encephalitis. These patients are also more likely to have secondary bacterial superinfections of cutaneous lesions and respiratory tracts.2 While zoster is often self‐limiting, it can lead to significant morbidity and mortality in immunocompromised patients. Intravenous acyclovir should be considered in patients with disseminated disease or visceral involvement, with advanced HIV, and in transplant patients being treated for rejection.2 Unilateral erythematous, vesicular rashes in a dermatomal distribution should yield a high clinical suspicion for herpes zoster, especially in immunocompromised patients.

References
  1. Yawn BP.A population‐based study of the incidence and complication rates of herpes zoster before zoster vaccine introduction.Mayo Clin Proc.2007;82(11):13411349.
  2. Krause RS. Herpes zoster. http://www.emedicine.com/emerg/TOPIC823. HTM. Accessed May2009.
References
  1. Yawn BP.A population‐based study of the incidence and complication rates of herpes zoster before zoster vaccine introduction.Mayo Clin Proc.2007;82(11):13411349.
  2. Krause RS. Herpes zoster. http://www.emedicine.com/emerg/TOPIC823. HTM. Accessed May2009.
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Journal of Hospital Medicine - 5(3)
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Journal of Hospital Medicine - 5(3)
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A painful rash
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A painful rash
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Fatal HIT

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A fatal case of heparin‐induced thrombocytopenia and thrombosis

Heparin induced thrombocytopenia (HIT) is a significant, potentially life‐threatening immune‐mediated adverse event that occurs several days after commencement of therapy with unfractionated or low‐molecular weight heparin. There are several potential sequelae of HIT, the most frequent of these is thrombosis, including but not limited to deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction, limb arterial occlusion, and disseminated intravascular coagulation. The prothrombotic state induced by HIT can be very significant, generating a thrombosis risk 30 times that of the general population and a mortality risk of 17% to 30% in those patients who develop thrombosis.1, 2

Case Report

A 51‐year‐old female was transferred to our institution for further management of a prothrombotic state. Six days prior to transfer, she presented to an outside hospital with significant edema and discomfort of her left lower extremity. She was found to have bilateral pulmonary emboli and a left lower extremity DVT. She was anticoagulated with unfractionated heparin and transitioned to coumadin. Upon preparation for discharge she developed drastically increased edema of her left lower extremity. Coumadin was discontinued and she was transferred to our institution for alternate anticoagulation and potential interventional vascular treatments.

On examination, the patient reported pain in her legs bilaterally but was in no distress. She had marked edema of the left lower extremity with tender erythematous skin over the anterior thigh with mild cyanosis and pallor of the left toes. Pulses were not palpable but could be identified by handheld Doppler scan. Urgent bilateral lower extremity venous and arterial duplex studies were completed, revealing extensive thrombosis involving the entire deep and superficial venous system on the left and the superficial femoral, popliteal, and peroneal veins on the right.

She was treated with an argatroban drip and a complete thrombophilia evaluation commenced. The following day she was mildly obtunded and slow to mentate. A noninfused computed tomography (CT) scan of the head revealed multiple acute left middle cerebral artery ischemic infarctions (Figure 1). CT scans of the chest, abdomen, and pelvis were done to assess for further thrombosis; bilateral renal infarcts were discovered.

Figure 1
Noncontrast computed tomography scan revealing multiple acute areas of ischemia (arrow) in the distribution of the left middle cerebral artery.

The hypercoagulable workup revealed prothrombin and Factor V Leiden gene mutations and anticardiolipin immunoglobulin (Ig)G, IgA and IgM that were all negative; however, heparin‐dependent antibody platelet factor 4 (PF4) enzyme‐linked immunosorbent assay (ELISA) was positive. Her preheparin platelet count was 149,000/L, 185,000/L at the time of her transfer and thrombosis extension, and 117,000/L at its nadir, 11 days after initial heparin exposure.

Despite lower extremity thrombectomy, right common femoral endarterectomy, and therapeutic anticoagulation, the patient continued to develop massive thrombosis and she expired. The patient underwent autopsy, which confirmed her extensive thrombosis and cited multisystem organ failure as the cause of death. Additionally, this examination revealed an occult high‐grade cervical cancer with lymphatic invasion.

Discussion

This case is an example of multiorgan failure as a result of the prothrombotic state induced by HIT. The thrombocytopenia of HIT is defined as either a platelet count of less than 150,000/L or a decrease of greater than 50% from baseline.3, 4 Despite the eventual confirmation of the diagnosis by PF4 ELISA (sensitivity 80%‐90%), the patient was not thrombocytopenic by definition at the time of extension of her thrombosis.5

Greinacher et al.3 retrospectively evaluated 408 patients with thrombosis associated with HIT and found that at the time of their thrombosis 40.2% became thrombocytopenic (>50% decrease in their platelet count) 1 or more days prior to their initial thrombosis, 26% became thrombocytopenic on the day of their initial thrombosis, and 33.5% had thrombosis that preceded their thrombocytopenia with a 3‐day median delay between thrombosis and thrombocytopenia. Our patient fell in the latter category, developing her thrombocytopenia 5 days after the extension of her thrombosis. The time course of this presentation places emphasis on the need for clinicians to be aware of this pattern and to have a suspicion for HIT in patients on heparin who develop thrombosis regardless of their platelet count at the time of the thrombotic event.

In addition, our patient had the occult diagnosis of cervical cancer. In a retrospective review, Opatrny and Warner6 found that thrombotic complications associated with HIT, venous thrombosis, and PE specifically, occurred more frequently in patients with malignancy than those without malignant disease. They evaluated 64 patients with the diagnosis of HIT, made by heparin‐PF4 ELISA, and discovered the incidence of thrombosis to be 73% in the patients with malignancy compared to 30% in the patients without malignancy. However, since our patient's cancer diagnosis was unknown at the time of the case events, it could not be considered.

There have been rare case reports published describing patients who develop thrombosis secondary to heparin‐dependent antibodies (HDA) without meeting the above definition of thrombocytopenia in HIT. Bream‐Rouwenhorst and Hobbs7 recently reported a similar case in which a 35‐year‐old woman with bilateral lower extremity arterial thrombosis had additional thrombotic events after reexposure to heparin; the patient had a positive heparin‐PF4 ELISA with a platelet count that remained consistently above 200,000/L and never fell below 75% of her baseline. They cite only 22 additional cases of patients with HDA without thrombocytopenia reported in the literature since 1965 and suggest that the term heparin‐associated thrombosis without HIT may be a more appropriate terminology to describe similar cases.

Conclusions

Early recognition and initiation of alternate anticoagulation are essential to the effective management of HIT and prevention of its sequelae. The possible diagnosis of HIT is important for clinicians to keep in mind for all patients that are receiving any form of heparin, not only those patients who present with thrombocytopenia but also those with otherwise unexplainable thrombosis regardless of the platelet count.

References
  1. Girolami B,Pradoni P,Stefani PM, et. al.The incidence of heparin‐induced thrombocytopenia in hospitalized medical patients treated with subcutaneous unfractionated heparin: a prospective cohort study.Blood.2003;101(8):29552959.
  2. Levy J,Hursting MJ.Heparin‐induced thrombocytopenia, a prothrombotic disease.Hematol Oncol Clin North Am.2007;21:6588.
  3. Greinacher A,Farner B,Kroll H,Kohlmann T,Warkentin TE,Eichler P.Clinical features of heparin‐induced thrombocytopenia including risk factors for thrombosis: a retrospective analysis of 408 patients.Thromb Haemost.2005;94(1):132135.
  4. Warkentin T,Roberts RS,Hirsh J,Kelton JG.An improved definition of immune heparin‐induced thrombocytopenia in postoperative orthopedic patients.Arch Intern Med.2003;163:25182524.
  5. Chong BHEisbacher M.Pathophysiology and laboratory testing of heparin‐induced thrombocytopenia.Semin Hematol.1998;35(suppl 5):38.
  6. Opatrny L,Warner MN.Risk of thrombosis in patients with malignancy and heparin‐induced thrombocytopenia.Am J Hematol.2004;76:240244.
  7. Bream‐Rouwenhorst HR,Hobbs RA.Heparin‐dependent antibodies and thrombosis with out heparin‐induced thrombocytopenia.Pharmacotherapy.2008;28(11):14011407.
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Journal of Hospital Medicine - 5(3)
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heparin, thrombocytopenia, thrombosis
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Heparin induced thrombocytopenia (HIT) is a significant, potentially life‐threatening immune‐mediated adverse event that occurs several days after commencement of therapy with unfractionated or low‐molecular weight heparin. There are several potential sequelae of HIT, the most frequent of these is thrombosis, including but not limited to deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction, limb arterial occlusion, and disseminated intravascular coagulation. The prothrombotic state induced by HIT can be very significant, generating a thrombosis risk 30 times that of the general population and a mortality risk of 17% to 30% in those patients who develop thrombosis.1, 2

Case Report

A 51‐year‐old female was transferred to our institution for further management of a prothrombotic state. Six days prior to transfer, she presented to an outside hospital with significant edema and discomfort of her left lower extremity. She was found to have bilateral pulmonary emboli and a left lower extremity DVT. She was anticoagulated with unfractionated heparin and transitioned to coumadin. Upon preparation for discharge she developed drastically increased edema of her left lower extremity. Coumadin was discontinued and she was transferred to our institution for alternate anticoagulation and potential interventional vascular treatments.

On examination, the patient reported pain in her legs bilaterally but was in no distress. She had marked edema of the left lower extremity with tender erythematous skin over the anterior thigh with mild cyanosis and pallor of the left toes. Pulses were not palpable but could be identified by handheld Doppler scan. Urgent bilateral lower extremity venous and arterial duplex studies were completed, revealing extensive thrombosis involving the entire deep and superficial venous system on the left and the superficial femoral, popliteal, and peroneal veins on the right.

She was treated with an argatroban drip and a complete thrombophilia evaluation commenced. The following day she was mildly obtunded and slow to mentate. A noninfused computed tomography (CT) scan of the head revealed multiple acute left middle cerebral artery ischemic infarctions (Figure 1). CT scans of the chest, abdomen, and pelvis were done to assess for further thrombosis; bilateral renal infarcts were discovered.

Figure 1
Noncontrast computed tomography scan revealing multiple acute areas of ischemia (arrow) in the distribution of the left middle cerebral artery.

The hypercoagulable workup revealed prothrombin and Factor V Leiden gene mutations and anticardiolipin immunoglobulin (Ig)G, IgA and IgM that were all negative; however, heparin‐dependent antibody platelet factor 4 (PF4) enzyme‐linked immunosorbent assay (ELISA) was positive. Her preheparin platelet count was 149,000/L, 185,000/L at the time of her transfer and thrombosis extension, and 117,000/L at its nadir, 11 days after initial heparin exposure.

Despite lower extremity thrombectomy, right common femoral endarterectomy, and therapeutic anticoagulation, the patient continued to develop massive thrombosis and she expired. The patient underwent autopsy, which confirmed her extensive thrombosis and cited multisystem organ failure as the cause of death. Additionally, this examination revealed an occult high‐grade cervical cancer with lymphatic invasion.

Discussion

This case is an example of multiorgan failure as a result of the prothrombotic state induced by HIT. The thrombocytopenia of HIT is defined as either a platelet count of less than 150,000/L or a decrease of greater than 50% from baseline.3, 4 Despite the eventual confirmation of the diagnosis by PF4 ELISA (sensitivity 80%‐90%), the patient was not thrombocytopenic by definition at the time of extension of her thrombosis.5

Greinacher et al.3 retrospectively evaluated 408 patients with thrombosis associated with HIT and found that at the time of their thrombosis 40.2% became thrombocytopenic (>50% decrease in their platelet count) 1 or more days prior to their initial thrombosis, 26% became thrombocytopenic on the day of their initial thrombosis, and 33.5% had thrombosis that preceded their thrombocytopenia with a 3‐day median delay between thrombosis and thrombocytopenia. Our patient fell in the latter category, developing her thrombocytopenia 5 days after the extension of her thrombosis. The time course of this presentation places emphasis on the need for clinicians to be aware of this pattern and to have a suspicion for HIT in patients on heparin who develop thrombosis regardless of their platelet count at the time of the thrombotic event.

In addition, our patient had the occult diagnosis of cervical cancer. In a retrospective review, Opatrny and Warner6 found that thrombotic complications associated with HIT, venous thrombosis, and PE specifically, occurred more frequently in patients with malignancy than those without malignant disease. They evaluated 64 patients with the diagnosis of HIT, made by heparin‐PF4 ELISA, and discovered the incidence of thrombosis to be 73% in the patients with malignancy compared to 30% in the patients without malignancy. However, since our patient's cancer diagnosis was unknown at the time of the case events, it could not be considered.

There have been rare case reports published describing patients who develop thrombosis secondary to heparin‐dependent antibodies (HDA) without meeting the above definition of thrombocytopenia in HIT. Bream‐Rouwenhorst and Hobbs7 recently reported a similar case in which a 35‐year‐old woman with bilateral lower extremity arterial thrombosis had additional thrombotic events after reexposure to heparin; the patient had a positive heparin‐PF4 ELISA with a platelet count that remained consistently above 200,000/L and never fell below 75% of her baseline. They cite only 22 additional cases of patients with HDA without thrombocytopenia reported in the literature since 1965 and suggest that the term heparin‐associated thrombosis without HIT may be a more appropriate terminology to describe similar cases.

Conclusions

Early recognition and initiation of alternate anticoagulation are essential to the effective management of HIT and prevention of its sequelae. The possible diagnosis of HIT is important for clinicians to keep in mind for all patients that are receiving any form of heparin, not only those patients who present with thrombocytopenia but also those with otherwise unexplainable thrombosis regardless of the platelet count.

Heparin induced thrombocytopenia (HIT) is a significant, potentially life‐threatening immune‐mediated adverse event that occurs several days after commencement of therapy with unfractionated or low‐molecular weight heparin. There are several potential sequelae of HIT, the most frequent of these is thrombosis, including but not limited to deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction, limb arterial occlusion, and disseminated intravascular coagulation. The prothrombotic state induced by HIT can be very significant, generating a thrombosis risk 30 times that of the general population and a mortality risk of 17% to 30% in those patients who develop thrombosis.1, 2

Case Report

A 51‐year‐old female was transferred to our institution for further management of a prothrombotic state. Six days prior to transfer, she presented to an outside hospital with significant edema and discomfort of her left lower extremity. She was found to have bilateral pulmonary emboli and a left lower extremity DVT. She was anticoagulated with unfractionated heparin and transitioned to coumadin. Upon preparation for discharge she developed drastically increased edema of her left lower extremity. Coumadin was discontinued and she was transferred to our institution for alternate anticoagulation and potential interventional vascular treatments.

On examination, the patient reported pain in her legs bilaterally but was in no distress. She had marked edema of the left lower extremity with tender erythematous skin over the anterior thigh with mild cyanosis and pallor of the left toes. Pulses were not palpable but could be identified by handheld Doppler scan. Urgent bilateral lower extremity venous and arterial duplex studies were completed, revealing extensive thrombosis involving the entire deep and superficial venous system on the left and the superficial femoral, popliteal, and peroneal veins on the right.

She was treated with an argatroban drip and a complete thrombophilia evaluation commenced. The following day she was mildly obtunded and slow to mentate. A noninfused computed tomography (CT) scan of the head revealed multiple acute left middle cerebral artery ischemic infarctions (Figure 1). CT scans of the chest, abdomen, and pelvis were done to assess for further thrombosis; bilateral renal infarcts were discovered.

Figure 1
Noncontrast computed tomography scan revealing multiple acute areas of ischemia (arrow) in the distribution of the left middle cerebral artery.

The hypercoagulable workup revealed prothrombin and Factor V Leiden gene mutations and anticardiolipin immunoglobulin (Ig)G, IgA and IgM that were all negative; however, heparin‐dependent antibody platelet factor 4 (PF4) enzyme‐linked immunosorbent assay (ELISA) was positive. Her preheparin platelet count was 149,000/L, 185,000/L at the time of her transfer and thrombosis extension, and 117,000/L at its nadir, 11 days after initial heparin exposure.

Despite lower extremity thrombectomy, right common femoral endarterectomy, and therapeutic anticoagulation, the patient continued to develop massive thrombosis and she expired. The patient underwent autopsy, which confirmed her extensive thrombosis and cited multisystem organ failure as the cause of death. Additionally, this examination revealed an occult high‐grade cervical cancer with lymphatic invasion.

Discussion

This case is an example of multiorgan failure as a result of the prothrombotic state induced by HIT. The thrombocytopenia of HIT is defined as either a platelet count of less than 150,000/L or a decrease of greater than 50% from baseline.3, 4 Despite the eventual confirmation of the diagnosis by PF4 ELISA (sensitivity 80%‐90%), the patient was not thrombocytopenic by definition at the time of extension of her thrombosis.5

Greinacher et al.3 retrospectively evaluated 408 patients with thrombosis associated with HIT and found that at the time of their thrombosis 40.2% became thrombocytopenic (>50% decrease in their platelet count) 1 or more days prior to their initial thrombosis, 26% became thrombocytopenic on the day of their initial thrombosis, and 33.5% had thrombosis that preceded their thrombocytopenia with a 3‐day median delay between thrombosis and thrombocytopenia. Our patient fell in the latter category, developing her thrombocytopenia 5 days after the extension of her thrombosis. The time course of this presentation places emphasis on the need for clinicians to be aware of this pattern and to have a suspicion for HIT in patients on heparin who develop thrombosis regardless of their platelet count at the time of the thrombotic event.

In addition, our patient had the occult diagnosis of cervical cancer. In a retrospective review, Opatrny and Warner6 found that thrombotic complications associated with HIT, venous thrombosis, and PE specifically, occurred more frequently in patients with malignancy than those without malignant disease. They evaluated 64 patients with the diagnosis of HIT, made by heparin‐PF4 ELISA, and discovered the incidence of thrombosis to be 73% in the patients with malignancy compared to 30% in the patients without malignancy. However, since our patient's cancer diagnosis was unknown at the time of the case events, it could not be considered.

There have been rare case reports published describing patients who develop thrombosis secondary to heparin‐dependent antibodies (HDA) without meeting the above definition of thrombocytopenia in HIT. Bream‐Rouwenhorst and Hobbs7 recently reported a similar case in which a 35‐year‐old woman with bilateral lower extremity arterial thrombosis had additional thrombotic events after reexposure to heparin; the patient had a positive heparin‐PF4 ELISA with a platelet count that remained consistently above 200,000/L and never fell below 75% of her baseline. They cite only 22 additional cases of patients with HDA without thrombocytopenia reported in the literature since 1965 and suggest that the term heparin‐associated thrombosis without HIT may be a more appropriate terminology to describe similar cases.

Conclusions

Early recognition and initiation of alternate anticoagulation are essential to the effective management of HIT and prevention of its sequelae. The possible diagnosis of HIT is important for clinicians to keep in mind for all patients that are receiving any form of heparin, not only those patients who present with thrombocytopenia but also those with otherwise unexplainable thrombosis regardless of the platelet count.

References
  1. Girolami B,Pradoni P,Stefani PM, et. al.The incidence of heparin‐induced thrombocytopenia in hospitalized medical patients treated with subcutaneous unfractionated heparin: a prospective cohort study.Blood.2003;101(8):29552959.
  2. Levy J,Hursting MJ.Heparin‐induced thrombocytopenia, a prothrombotic disease.Hematol Oncol Clin North Am.2007;21:6588.
  3. Greinacher A,Farner B,Kroll H,Kohlmann T,Warkentin TE,Eichler P.Clinical features of heparin‐induced thrombocytopenia including risk factors for thrombosis: a retrospective analysis of 408 patients.Thromb Haemost.2005;94(1):132135.
  4. Warkentin T,Roberts RS,Hirsh J,Kelton JG.An improved definition of immune heparin‐induced thrombocytopenia in postoperative orthopedic patients.Arch Intern Med.2003;163:25182524.
  5. Chong BHEisbacher M.Pathophysiology and laboratory testing of heparin‐induced thrombocytopenia.Semin Hematol.1998;35(suppl 5):38.
  6. Opatrny L,Warner MN.Risk of thrombosis in patients with malignancy and heparin‐induced thrombocytopenia.Am J Hematol.2004;76:240244.
  7. Bream‐Rouwenhorst HR,Hobbs RA.Heparin‐dependent antibodies and thrombosis with out heparin‐induced thrombocytopenia.Pharmacotherapy.2008;28(11):14011407.
References
  1. Girolami B,Pradoni P,Stefani PM, et. al.The incidence of heparin‐induced thrombocytopenia in hospitalized medical patients treated with subcutaneous unfractionated heparin: a prospective cohort study.Blood.2003;101(8):29552959.
  2. Levy J,Hursting MJ.Heparin‐induced thrombocytopenia, a prothrombotic disease.Hematol Oncol Clin North Am.2007;21:6588.
  3. Greinacher A,Farner B,Kroll H,Kohlmann T,Warkentin TE,Eichler P.Clinical features of heparin‐induced thrombocytopenia including risk factors for thrombosis: a retrospective analysis of 408 patients.Thromb Haemost.2005;94(1):132135.
  4. Warkentin T,Roberts RS,Hirsh J,Kelton JG.An improved definition of immune heparin‐induced thrombocytopenia in postoperative orthopedic patients.Arch Intern Med.2003;163:25182524.
  5. Chong BHEisbacher M.Pathophysiology and laboratory testing of heparin‐induced thrombocytopenia.Semin Hematol.1998;35(suppl 5):38.
  6. Opatrny L,Warner MN.Risk of thrombosis in patients with malignancy and heparin‐induced thrombocytopenia.Am J Hematol.2004;76:240244.
  7. Bream‐Rouwenhorst HR,Hobbs RA.Heparin‐dependent antibodies and thrombosis with out heparin‐induced thrombocytopenia.Pharmacotherapy.2008;28(11):14011407.
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Journal of Hospital Medicine - 5(3)
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A fatal case of heparin‐induced thrombocytopenia and thrombosis
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A fatal case of heparin‐induced thrombocytopenia and thrombosis
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ESIR and Peripheral Insulin Resistance

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A case of extreme subcutaneous and peripheral insulin resistance

A 34‐year‐old man was admitted for evaluation of elevated blood glucose despite extremely high subcutaneous (SQ) insulin requirements. He had a 12‐year history of Type 2 diabetes mellitus (T2DM) without episodes of ketoacidosis, managed initially with oral medications (metformin with various sulfonylureas and thiazolidinediones). Three months prior to admission, he was transitioned to SQ insulin and thereafter his requirements escalated rapidly. By the time of his admission, his blood glucose measurements were consistently above 300 mg/dL despite injecting more than 4100 units of insulin daily. His regimen included 300 units of insulin glargine (Lantus) 2 times per day (BID) and 1.75 mL of Humilin U‐500 Insulin (875 units) 4 times per day (QID). Past medical history included metabolic syndrome, nonalcoholic steatohepatitis, and diabetic neuropathy. Physical exam was remarkable for centripetal obesity (body mass index [BMI] = 38.9 kg/m2), acanthosis nigricans, and necrobiosis lipoidica diabeticorum (NLD) (Figure 1).

Figure 1
Necrobiosis lipoidica diabeticorum.

We undertook an investigation to characterize this extreme insulin resistance. After 24 hours without insulin supplementation, and 12 hours of nothing by mouth (NPO), his blood glucose level was 280 mg/dL and his serum insulin was 133.5 IU/mL. We injected 12 units of insulin Aspart and subsequently measured his serum glucose and insulin once more. His blood glucose level had risen to 289 mg/dL and his serum insulin fell to 110.7 IU/mL. We then transitioned the patient to intravenous (IV) insulin. After a series of boluses totaling 400 units, his blood glucose normalized (90 mg/dL) and was maintained in normal range on a rate of 48 units per hour. Over 24 hours, we had infused over 1400 units.

During this time, we also drew several labs. Serum antiinsulin antibodies were undetectable (ARUP Laboratories, Salt Lake City, UT). A full rheumatologic workup was negative for systemic lupus erythematosus (SLE), rheumatoid factor, Sjgren's syndrome (SS)‐A and SS‐B. Androgen levels were normal, as were 24‐hour urine collections for cortisol and metanephrines. The patient was discharged on a regimen of U‐500 without glargine.

By 5 months after discharge, his blood glucose remained uncontrolled despite increasing doses of U‐500 (with or without metformin and thiazolidinediones). The patient was offered a gastric bypass operation. Now, 4 months postoperative, his blood glucose is controlled, no greater than 90 mg/dL in the morning and 125 mg/dL in the evening. He is off insulin, taking 30 mg pioglitazone (Actos) daily and 500 mg metformin 3 times per day (TID).

Discussion

Extreme insulin resistance (EIR), defined by daily insulin requirements in excess of 200 U, is a rare and frustrating condition.1 Rarer still is extreme subcutaneous insulin resistance (ESIR). A systematic Medline review revealed only 29 reported cases of ESIR, all of which involved patients that maintained IV sensitivity to insulin. Classic diagnostic criteria for ESIR include preserved sensitivity to IV insulin, failure to increase serum insulin with subcutaneous injection, and insulin degrading activity of subcutaneous tissue.2, 3 However, there are, at present, no laboratory tests that can test the final criterion. Indeed, very few of the published reports of ESIR satisfy it, with most studies considering as diagnostic of ESIR the constellation of EIR with failure to raise serum insulin after injection and preserved intravenous insulin sensitivity.

As was evident in the high doses of IV insulin required for blood glucose normalization, our patient also had a proven receptor‐level peripheral resistance. Beyond the common, multifactorial insulin resistance of T2DM, the published reports of patients with extreme peripheral resistance are of 2 types: (A) genetic (eg, Leprechaunism) and (B) acquired autoimmune (Table 1).4 This patient fits neither category. Patients with Type A are very sick, with a syndromic disease that sharply curtails their life expectancy. Patients with Type B acquire antibodies directed against their insulin receptors and are almost invariably elderly African‐American women with severe rheumatological disease, namely SLE. We could not test our patient for an insulin‐receptor antibody secondary to prohibitive cost. This is probably moot, given that his autoimmune workup was negative and, as above, patients with such antibodies are vastly different compared to our patients.

Types of Insulin Resistance
Class of Insulin Resistance Mechanism Incidence Treatment
  • Abbreviation: SQ, subcutaneous.

Type 2 diabetes mellitus Multifactorial 3% of total population Many
Type A receptor‐level insulin resistance Congenital receptor defect 86 cases U‐500, insulin‐like growth factor‐1
Type B receptor‐level insulin resistance Antiinsulin receptor antibody 50 cases U‐500, immune modulation
Subcutaneous insulin resistance Unknown; SQ protease? 30 cases U‐500, intraperitoneal insulin delivery, other

Based on SQ insulin requirements, our patient had EIR. As his insulin levels failed to rise following an insulin injection, his EIR is thus subcutaneous in nature. However, among patients with this condition his failure to respond to IV insulin is unique. He does not fit criteria for types A or B insulin resistance; his condition is likely also due to an extreme version of the more common, multifactorial peripheral insulin resistance. This is supported by his successful response to the gastric bypass operation.5

The standard treatments for ESIR include: (1) concentrated regular insulin (U‐500) and (2) implantable intraperitoneal delivery; our patient received the former.6 U‐500 use in EIR has been shown to be more cost‐effective.1 Several reports have suggested success with protease inhibitors (aprotinin, nafamostat ointment), plasmapheresis, and intravenous immunoglobulin for extreme SQ resistance. Our case also represents the first treated successfully with a gastric bypass operation.

CONCLUSIONS

EIR can present a significant challenge for both the patient and hospitalist. The approach to this condition should begin with the determination of 24‐hour IV insulin requirement utilizing an insulin drip; serum insulin antibody evaluation; and endocrinology consultation. Our case also highlights a few important points about the broader management of diabetes mellitus. First, there are dermatological manifestations of diabetes that serve as potential markers for disease (namely acanthosis nigricans and NLD). Second, for patients with extreme insulin requirements, an extensive workup should be initiated and the patient should be transitioned to a concentrated regular insulin or intraperitoneal delivery. Third, our experience suggests a role for other measures such as gastric bypass that ought to be studied further.

References
  1. Cochan E,Musso C,Gorden P.The use of U‐500 in patients with extreme insulin resistance.Diabetes Care.2005;28:12401244.
  2. Schneider AJ,Bennett RH.Impaired absorption of insulin as a cause insulin resistance.Diabetes.1975;24:443.
  3. Paulsen EP,Courtney JW,Duckworth WC.Insulin resistance caused by massive degradation of subcutaneous insulin.Diabetes.1979;28:640645.
  4. Musso C,Cochran E,Moran SA, et al.Clinical course of genetic diseases of the insulin receptor: a 30‐year prospective.Medicine.2004;83:209222.
  5. Pories WJ,Swanson MJ,MacDonald KG, et al.Who would have thought it? An operation proves to be the most effective therapy for adult‐onset diabetes mellitus.Ann Surg.1995;222:339352.
  6. Soudan B,Girardot C,Fermon C,Verlet E,Pattou F,Vantyghem MC.Extreme subcutaneous insulin resistance: a misunderstood syndrome.Diabetes Metab.2003;29:539546.
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A 34‐year‐old man was admitted for evaluation of elevated blood glucose despite extremely high subcutaneous (SQ) insulin requirements. He had a 12‐year history of Type 2 diabetes mellitus (T2DM) without episodes of ketoacidosis, managed initially with oral medications (metformin with various sulfonylureas and thiazolidinediones). Three months prior to admission, he was transitioned to SQ insulin and thereafter his requirements escalated rapidly. By the time of his admission, his blood glucose measurements were consistently above 300 mg/dL despite injecting more than 4100 units of insulin daily. His regimen included 300 units of insulin glargine (Lantus) 2 times per day (BID) and 1.75 mL of Humilin U‐500 Insulin (875 units) 4 times per day (QID). Past medical history included metabolic syndrome, nonalcoholic steatohepatitis, and diabetic neuropathy. Physical exam was remarkable for centripetal obesity (body mass index [BMI] = 38.9 kg/m2), acanthosis nigricans, and necrobiosis lipoidica diabeticorum (NLD) (Figure 1).

Figure 1
Necrobiosis lipoidica diabeticorum.

We undertook an investigation to characterize this extreme insulin resistance. After 24 hours without insulin supplementation, and 12 hours of nothing by mouth (NPO), his blood glucose level was 280 mg/dL and his serum insulin was 133.5 IU/mL. We injected 12 units of insulin Aspart and subsequently measured his serum glucose and insulin once more. His blood glucose level had risen to 289 mg/dL and his serum insulin fell to 110.7 IU/mL. We then transitioned the patient to intravenous (IV) insulin. After a series of boluses totaling 400 units, his blood glucose normalized (90 mg/dL) and was maintained in normal range on a rate of 48 units per hour. Over 24 hours, we had infused over 1400 units.

During this time, we also drew several labs. Serum antiinsulin antibodies were undetectable (ARUP Laboratories, Salt Lake City, UT). A full rheumatologic workup was negative for systemic lupus erythematosus (SLE), rheumatoid factor, Sjgren's syndrome (SS)‐A and SS‐B. Androgen levels were normal, as were 24‐hour urine collections for cortisol and metanephrines. The patient was discharged on a regimen of U‐500 without glargine.

By 5 months after discharge, his blood glucose remained uncontrolled despite increasing doses of U‐500 (with or without metformin and thiazolidinediones). The patient was offered a gastric bypass operation. Now, 4 months postoperative, his blood glucose is controlled, no greater than 90 mg/dL in the morning and 125 mg/dL in the evening. He is off insulin, taking 30 mg pioglitazone (Actos) daily and 500 mg metformin 3 times per day (TID).

Discussion

Extreme insulin resistance (EIR), defined by daily insulin requirements in excess of 200 U, is a rare and frustrating condition.1 Rarer still is extreme subcutaneous insulin resistance (ESIR). A systematic Medline review revealed only 29 reported cases of ESIR, all of which involved patients that maintained IV sensitivity to insulin. Classic diagnostic criteria for ESIR include preserved sensitivity to IV insulin, failure to increase serum insulin with subcutaneous injection, and insulin degrading activity of subcutaneous tissue.2, 3 However, there are, at present, no laboratory tests that can test the final criterion. Indeed, very few of the published reports of ESIR satisfy it, with most studies considering as diagnostic of ESIR the constellation of EIR with failure to raise serum insulin after injection and preserved intravenous insulin sensitivity.

As was evident in the high doses of IV insulin required for blood glucose normalization, our patient also had a proven receptor‐level peripheral resistance. Beyond the common, multifactorial insulin resistance of T2DM, the published reports of patients with extreme peripheral resistance are of 2 types: (A) genetic (eg, Leprechaunism) and (B) acquired autoimmune (Table 1).4 This patient fits neither category. Patients with Type A are very sick, with a syndromic disease that sharply curtails their life expectancy. Patients with Type B acquire antibodies directed against their insulin receptors and are almost invariably elderly African‐American women with severe rheumatological disease, namely SLE. We could not test our patient for an insulin‐receptor antibody secondary to prohibitive cost. This is probably moot, given that his autoimmune workup was negative and, as above, patients with such antibodies are vastly different compared to our patients.

Types of Insulin Resistance
Class of Insulin Resistance Mechanism Incidence Treatment
  • Abbreviation: SQ, subcutaneous.

Type 2 diabetes mellitus Multifactorial 3% of total population Many
Type A receptor‐level insulin resistance Congenital receptor defect 86 cases U‐500, insulin‐like growth factor‐1
Type B receptor‐level insulin resistance Antiinsulin receptor antibody 50 cases U‐500, immune modulation
Subcutaneous insulin resistance Unknown; SQ protease? 30 cases U‐500, intraperitoneal insulin delivery, other

Based on SQ insulin requirements, our patient had EIR. As his insulin levels failed to rise following an insulin injection, his EIR is thus subcutaneous in nature. However, among patients with this condition his failure to respond to IV insulin is unique. He does not fit criteria for types A or B insulin resistance; his condition is likely also due to an extreme version of the more common, multifactorial peripheral insulin resistance. This is supported by his successful response to the gastric bypass operation.5

The standard treatments for ESIR include: (1) concentrated regular insulin (U‐500) and (2) implantable intraperitoneal delivery; our patient received the former.6 U‐500 use in EIR has been shown to be more cost‐effective.1 Several reports have suggested success with protease inhibitors (aprotinin, nafamostat ointment), plasmapheresis, and intravenous immunoglobulin for extreme SQ resistance. Our case also represents the first treated successfully with a gastric bypass operation.

CONCLUSIONS

EIR can present a significant challenge for both the patient and hospitalist. The approach to this condition should begin with the determination of 24‐hour IV insulin requirement utilizing an insulin drip; serum insulin antibody evaluation; and endocrinology consultation. Our case also highlights a few important points about the broader management of diabetes mellitus. First, there are dermatological manifestations of diabetes that serve as potential markers for disease (namely acanthosis nigricans and NLD). Second, for patients with extreme insulin requirements, an extensive workup should be initiated and the patient should be transitioned to a concentrated regular insulin or intraperitoneal delivery. Third, our experience suggests a role for other measures such as gastric bypass that ought to be studied further.

A 34‐year‐old man was admitted for evaluation of elevated blood glucose despite extremely high subcutaneous (SQ) insulin requirements. He had a 12‐year history of Type 2 diabetes mellitus (T2DM) without episodes of ketoacidosis, managed initially with oral medications (metformin with various sulfonylureas and thiazolidinediones). Three months prior to admission, he was transitioned to SQ insulin and thereafter his requirements escalated rapidly. By the time of his admission, his blood glucose measurements were consistently above 300 mg/dL despite injecting more than 4100 units of insulin daily. His regimen included 300 units of insulin glargine (Lantus) 2 times per day (BID) and 1.75 mL of Humilin U‐500 Insulin (875 units) 4 times per day (QID). Past medical history included metabolic syndrome, nonalcoholic steatohepatitis, and diabetic neuropathy. Physical exam was remarkable for centripetal obesity (body mass index [BMI] = 38.9 kg/m2), acanthosis nigricans, and necrobiosis lipoidica diabeticorum (NLD) (Figure 1).

Figure 1
Necrobiosis lipoidica diabeticorum.

We undertook an investigation to characterize this extreme insulin resistance. After 24 hours without insulin supplementation, and 12 hours of nothing by mouth (NPO), his blood glucose level was 280 mg/dL and his serum insulin was 133.5 IU/mL. We injected 12 units of insulin Aspart and subsequently measured his serum glucose and insulin once more. His blood glucose level had risen to 289 mg/dL and his serum insulin fell to 110.7 IU/mL. We then transitioned the patient to intravenous (IV) insulin. After a series of boluses totaling 400 units, his blood glucose normalized (90 mg/dL) and was maintained in normal range on a rate of 48 units per hour. Over 24 hours, we had infused over 1400 units.

During this time, we also drew several labs. Serum antiinsulin antibodies were undetectable (ARUP Laboratories, Salt Lake City, UT). A full rheumatologic workup was negative for systemic lupus erythematosus (SLE), rheumatoid factor, Sjgren's syndrome (SS)‐A and SS‐B. Androgen levels were normal, as were 24‐hour urine collections for cortisol and metanephrines. The patient was discharged on a regimen of U‐500 without glargine.

By 5 months after discharge, his blood glucose remained uncontrolled despite increasing doses of U‐500 (with or without metformin and thiazolidinediones). The patient was offered a gastric bypass operation. Now, 4 months postoperative, his blood glucose is controlled, no greater than 90 mg/dL in the morning and 125 mg/dL in the evening. He is off insulin, taking 30 mg pioglitazone (Actos) daily and 500 mg metformin 3 times per day (TID).

Discussion

Extreme insulin resistance (EIR), defined by daily insulin requirements in excess of 200 U, is a rare and frustrating condition.1 Rarer still is extreme subcutaneous insulin resistance (ESIR). A systematic Medline review revealed only 29 reported cases of ESIR, all of which involved patients that maintained IV sensitivity to insulin. Classic diagnostic criteria for ESIR include preserved sensitivity to IV insulin, failure to increase serum insulin with subcutaneous injection, and insulin degrading activity of subcutaneous tissue.2, 3 However, there are, at present, no laboratory tests that can test the final criterion. Indeed, very few of the published reports of ESIR satisfy it, with most studies considering as diagnostic of ESIR the constellation of EIR with failure to raise serum insulin after injection and preserved intravenous insulin sensitivity.

As was evident in the high doses of IV insulin required for blood glucose normalization, our patient also had a proven receptor‐level peripheral resistance. Beyond the common, multifactorial insulin resistance of T2DM, the published reports of patients with extreme peripheral resistance are of 2 types: (A) genetic (eg, Leprechaunism) and (B) acquired autoimmune (Table 1).4 This patient fits neither category. Patients with Type A are very sick, with a syndromic disease that sharply curtails their life expectancy. Patients with Type B acquire antibodies directed against their insulin receptors and are almost invariably elderly African‐American women with severe rheumatological disease, namely SLE. We could not test our patient for an insulin‐receptor antibody secondary to prohibitive cost. This is probably moot, given that his autoimmune workup was negative and, as above, patients with such antibodies are vastly different compared to our patients.

Types of Insulin Resistance
Class of Insulin Resistance Mechanism Incidence Treatment
  • Abbreviation: SQ, subcutaneous.

Type 2 diabetes mellitus Multifactorial 3% of total population Many
Type A receptor‐level insulin resistance Congenital receptor defect 86 cases U‐500, insulin‐like growth factor‐1
Type B receptor‐level insulin resistance Antiinsulin receptor antibody 50 cases U‐500, immune modulation
Subcutaneous insulin resistance Unknown; SQ protease? 30 cases U‐500, intraperitoneal insulin delivery, other

Based on SQ insulin requirements, our patient had EIR. As his insulin levels failed to rise following an insulin injection, his EIR is thus subcutaneous in nature. However, among patients with this condition his failure to respond to IV insulin is unique. He does not fit criteria for types A or B insulin resistance; his condition is likely also due to an extreme version of the more common, multifactorial peripheral insulin resistance. This is supported by his successful response to the gastric bypass operation.5

The standard treatments for ESIR include: (1) concentrated regular insulin (U‐500) and (2) implantable intraperitoneal delivery; our patient received the former.6 U‐500 use in EIR has been shown to be more cost‐effective.1 Several reports have suggested success with protease inhibitors (aprotinin, nafamostat ointment), plasmapheresis, and intravenous immunoglobulin for extreme SQ resistance. Our case also represents the first treated successfully with a gastric bypass operation.

CONCLUSIONS

EIR can present a significant challenge for both the patient and hospitalist. The approach to this condition should begin with the determination of 24‐hour IV insulin requirement utilizing an insulin drip; serum insulin antibody evaluation; and endocrinology consultation. Our case also highlights a few important points about the broader management of diabetes mellitus. First, there are dermatological manifestations of diabetes that serve as potential markers for disease (namely acanthosis nigricans and NLD). Second, for patients with extreme insulin requirements, an extensive workup should be initiated and the patient should be transitioned to a concentrated regular insulin or intraperitoneal delivery. Third, our experience suggests a role for other measures such as gastric bypass that ought to be studied further.

References
  1. Cochan E,Musso C,Gorden P.The use of U‐500 in patients with extreme insulin resistance.Diabetes Care.2005;28:12401244.
  2. Schneider AJ,Bennett RH.Impaired absorption of insulin as a cause insulin resistance.Diabetes.1975;24:443.
  3. Paulsen EP,Courtney JW,Duckworth WC.Insulin resistance caused by massive degradation of subcutaneous insulin.Diabetes.1979;28:640645.
  4. Musso C,Cochran E,Moran SA, et al.Clinical course of genetic diseases of the insulin receptor: a 30‐year prospective.Medicine.2004;83:209222.
  5. Pories WJ,Swanson MJ,MacDonald KG, et al.Who would have thought it? An operation proves to be the most effective therapy for adult‐onset diabetes mellitus.Ann Surg.1995;222:339352.
  6. Soudan B,Girardot C,Fermon C,Verlet E,Pattou F,Vantyghem MC.Extreme subcutaneous insulin resistance: a misunderstood syndrome.Diabetes Metab.2003;29:539546.
References
  1. Cochan E,Musso C,Gorden P.The use of U‐500 in patients with extreme insulin resistance.Diabetes Care.2005;28:12401244.
  2. Schneider AJ,Bennett RH.Impaired absorption of insulin as a cause insulin resistance.Diabetes.1975;24:443.
  3. Paulsen EP,Courtney JW,Duckworth WC.Insulin resistance caused by massive degradation of subcutaneous insulin.Diabetes.1979;28:640645.
  4. Musso C,Cochran E,Moran SA, et al.Clinical course of genetic diseases of the insulin receptor: a 30‐year prospective.Medicine.2004;83:209222.
  5. Pories WJ,Swanson MJ,MacDonald KG, et al.Who would have thought it? An operation proves to be the most effective therapy for adult‐onset diabetes mellitus.Ann Surg.1995;222:339352.
  6. Soudan B,Girardot C,Fermon C,Verlet E,Pattou F,Vantyghem MC.Extreme subcutaneous insulin resistance: a misunderstood syndrome.Diabetes Metab.2003;29:539546.
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A case of extreme subcutaneous and peripheral insulin resistance
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Hand‐Carried Ultrasound Use

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“On the other hand …”: The evidence does not support the use of hand‐carried ultrasound by hospitalists

Ultrasound, one of the most reliable diagnostic technologies in medicine, has a unique long‐term safety profile across a wide spectrum of applications. In line with the trend toward the miniaturization of many other technologies, increasingly sophisticated hand‐held or hand‐carried ultrasound (HCU) devices have become widely available. To date, the U.S. Food and Drug Administration (FDA) has approved more than 10 new‐generation portable (1.0‐4.5 kg) ultrasound devices, and a recent industry report projected that the HCU market will see revenues in excess of $1 billion by 2011.1

Although cardiovascular assessment remains its primary use, hospitalist physicians are increasingly turning to this technology for the localization of fluid and other abnormalities prior to paracentesis and thoracentesis. While there are other potential uses (eg, managing acute scrotal pain, diagnosing meniscal tears, measuring carotid intimal thickness), the higher‐quality studies of hospitalist‐physicians' use of HCU have focused on cardiovascular assessment. HCU confers a number of potential workflow‐related advantages, including coordinated point‐of‐care evaluation at short notice when formal ultrasound may be unavailable, as well as circumvention of the need to call on radiology or cardiology specialists.2 Even for experienced cardiologists, heart failure can be difficult to identify using any modality, and the clinical diagnosis of cardiovascular disease by hospital physicians has been documented as poor.3, 4 Thus, the addition of HCU to the palette of diagnostic and teaching tools available to frontline physicians potentially offers improvements over stethoscope‐assisted physical examination alone (including visual inspection, palpation, and auscultation), which has remained essentially unaltered for 150 years.57

Evidence Base for HCU Use by Hospitalists

The few primary studies on HCU use by hospitalists have focused on the potential utility of this technology as a valuable adjunct to the physical exam for the detection of cardiovascular disease (eg, asymptomatic left ventricular [LV] dysfunction, cardiomegaly, pericardial effusion) in the ambulatory or acute care setting.8, 9 Operation of HCU by hospitalists is not clearly indicated for the evaluation of valvular disease (eg, aortic and mitral regurgitation), in part due to the limited Doppler capabilities of the smaller devices.911 The risk of a gradual erosion of physical exam skills accompanying expansion of HCU use by hospitalists could itself become a potential disadvantage of a premature replacement of the stethoscope, since the results obtained by hospitalists performing a standard physical exam have been shown to be better than those obtained with HCU.8, 9

The lack of large, multicenter studies of HCU use by hospitalists leaves many questions unanswered, including whether or not the relatively low initial cost of an HCU device ($9,000‐$50,000) vs. that of a full‐sized hospital ultrasound system ($250,000) will eventually translate into overall cost‐effectiveness or actual patient‐centered benefit.10 While cautious advocates have insisted that HCU provides additive information in conjunction with the physical exam, this approach is not meant to serve as a substitute for standard echocardiography in patients requiring full evaluation in inpatient settings relevant for hospitalists.1114 Referral for additional testing or specialist opinionsand the associated costs incurredcannot necessarily be circumvented by hospitalist‐operated HCU.

A major problem with the HCU literature in general is its lack of standardization betweenand withinstudies, which renders it nearly impossible to generalize findings about important clinical outcomes, patient satisfaction, quality‐of‐life, symptoms, physical functioning, and morbidity and mortality. There are a preponderance of underpowered, methodologically inconsistent, single‐center case series that do not evaluate diagnostic accuracy in terms of patient outcomes. For example, although one study did find a modest (22‐29%) reduction in department workload with HCU, the authors omitted important information regarding blinding, and no power calculations were reported; thus, it was not possible to ascertain whether or not the reported results were due to the intervention or to chance.15 There clearly remains a need to convincingly demonstrate that patient care, shortening of length of stay, long‐term prognosis, or potential financial savings could occur with use of these devices by hospitalists.5 The process of device acquisition and resource allocation is, at least in part, based on accumulated evidence from studies that have ill‐defined relevant outcomes (eg, left ventricular function). However, even if such outcomes were to be more closely examined, medical decision‐making would still suffer from discrepant findings due to numerous differences in study design, including parameters involving patient population and selection, setting (eg, echocardiography laboratory vs. critical care unit), provider background, and specific device(s) used.

Training Issues

Hospitalist proficiency across HCU imaging skills (ie, acquisition, measurement, interpretation) has been found to be inconsistent.9 Endorsement and expansion of hospitalist use of HCU may to some extent reflect an overgeneralization from disparate comparative studies showing moderate success obtained with HCU (vs. physical exam) by other practitioner groups such as medical students and fellows with limited experience.16, 17 Whereas in 2005, Hellmann et al.18 concluded that medical residents with minimal training can learn to perform some of the basic functions of HCU with reasonable accuracy, Martin et al.8, 9 (in 2007 and 2009) reported conflicting results from a study of hospitalists trained at the same institution.

Concern about switching from standard to nonstandard HCU operators is raised by studies in which specialized operators (eg, echocardiography technicians) obtained better results than hospitalists using these devices.8, 9 In 2004, Borges et al.19 reported the results of 315 patients referred to specialists at a cardiology clinic for preoperative assessment prior to noncardiac surgery; the results (94.8% and 96.7% agreement with standard echocardiography on the main echocardiographic finding and detection of valve disease, respectively) were attributed to the fact that experienced cardiologists were working under ideal conditions using only the most advanced HCU devices with Doppler as well as harmonic imaging capabilities. Likewise, in 2004, Tsutsui et al.20 studied 44 consecutive hospitalized patients who underwent comprehensive echocardiography and bedside HCU. They reported that hemodynamic assessment by HCU was poor, even when performed by practitioners with relatively high levels of training.20 In 2003, DeCara et al.12 performed standard echocardiography on 300 adult inpatients referred for imaging, and concluded that standardized training, competency testing, and quality assurance guidelines need to be established before these devices can be utilized for clinical decision‐making by physicians without formal training in echocardiography. Although there have been numerous calls for training guidelines, it has not yet been determined how much training would be optimalor even necessaryfor professionals of each subspecialty to achieve levels of accuracy that are acceptable. Furthermore, it is well known that skill level declines unless a technique is regularly reinforced with practice, and therefore, recertification or procedure volume standards should be established.

The issue of potential harm needs to be raised, if hospitalists with access to HCU are indeed less accurate in their diagnoses than trained cardiologists interpreting images acquired by an established alternative such as echocardiography. False negatives can lead to delayed treatment, and false positives to unwarranted treatment. Given that the treatment effects of HCU use by hospitalists have not been closely scrutinized, the expansion of such use appears unwarranted, at least until further randomized studies with well‐defined outcomes have been conducted. Although the HCU devices themselves have a good safety profile, their potential benefits and harms (eg, possibility of increased nosocomial infection) will ultimately reflect operator skill and their impact on patient management relative to the gold‐standard diagnostic modalities for which there is abundant evidence of safety and efficacy.21

Premarketing and Postmarketing Concerns

The controversy regarding hospitalist use of HCU exposes gaps in the FDA approval process for medical devices, which are subjected to much less rigorous scrutiny during the premarketing approval process than pharmaceuticals.22 Moreover, the aggressive marketing of newly approved devices (and drugs) can drive medically unwarranted overuse, or indication creep, which justifies calls for the establishment of rigorous standards of clinical relevance and practice.23, 24 While the available literature on HCU operation by hospitalists is focused on cardiovascular indications for the technology, hospital medicine physicians are increasingly using HCU to guide paracentesis and thoracentesis. Given how commonplace the expansion of such practices has become, it is noteworthy that HCU operation by hospitalists has not yet been evaluated and endorsed in larger, controlled trials demonstrating appropriate outcomes.25

Across all fields of medicine, the transition from traditional to newer modalities remains a slippery slope in terms of demonstration of persuasive evidence of patient‐centered benefit.26 Fascination with emerging technologies (so‐called gizmo idolatry) and increased reimbursement potential threaten to distract patients and their providers from legitimate concerns about how medical device manufacturers and for‐profit corporations increasingly influence device acquisition and clinical practice.2731 While we lack strong evidence demonstrating that diagnostic tests such as HCU are beneficial when performed by hospitalists, the expanded use of these handy new devices by hospitalists is simultaneously generating increased incidental and equivocal findings, which in turn render it necessary to go back and perform secondary verification studies by specialists using older, gold‐standard modalities. This vicious cycle, coupled with the current lack of evidence, will continue to degrade confidence in the initiation of either acute or chronic treatment on the basis of HCU results obtained by hospitalist physicians.

Eventually, the increased use of HCU by hospitalists might lead to demonstrations of improved hospital workflow management, but it may just as easily represent another new coupling of technology and practitioner that prematurely becomes the standard of care in the absence of any demonstration of added value. The initially enthusiastic application of pulmonary artery catheters (PACs) serves as a cautionary tale in which the acquisition of additional clinical data did not necessarily lead to improved clinical outcomes: whereas PACs did enhance the clinical understanding of hemodynamics, they were not associated with an overall advantage in terms of mortality, length of hospital stay, or cost.3235 Ultimately, more information is not necessarily better information. Although new medical technologies can produce extremely useful diagnostic results that aid in the management of critically ill patients, poor data interpretation resulting from lack of targeted training and experience can nullify point‐of‐care advantages, and perhaps lead to excess morbidity and mortality.14 In clinical practice, it is generally best to avoid reliance on assumptions of added value in lieu of demonstrations of the same.

Conclusions

Hospital practitioners should not yet put away their stethoscopes. New technologies such as HCU need to be embraced in parallel with accumulating evidence of benefit. In the hands of hospitalists, the smaller HCU devices may very well prove handy, but at present, the literature simply does not support the use of HCU by hospitalist physicians.

References
  1. Hand‐Carried Ultrasound—Reshaping the ultrasound marketplace. Available at: http://www.sonoworld.com/NewsStories/NewsStories.aspx?ID= 450. Accessed August2009.
  2. Young A,Schleyer A,Nelson J.A new narrative for hospitalists.J Hosp Med.2009;4(4):207208.
  3. Hobbs R.Can heart failure be diagnosed in primary care?BMJ.2000;321(7255):188189.
  4. Clarke KW,Gray D,Hampton JR.Evidence of inadequate investigation and treatment of patients with heart failure.Br Heart J.1994;71(6):584587.
  5. Gorcsan J.Utility of hand‐carried ultrasound for consultative cardiology.Echocardiography.2003;20(5):463469.
  6. Bryan CS.Tomorrow's stethoscope: the hand‐held ultrasound device?J S C Med Assoc.2006;102(10):345.
  7. DeCara JM,Lang RM,Spencer KT.The hand‐carried echocardiographic device as an aid to the physical examination.Echocardiography.2003;20(5):477485.
  8. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  9. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalists: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  10. Alpert JS,Mladenovic J,Hellmann DB.Should a hand‐carried ultrasound machine become standard equipment for every internist?Am J Med.2009;122(1):13.
  11. Goodkin GM,Spevack DM,Tunick PA,Kronzon I.How useful is hand‐carried bedside echocardiography in critically ill patients?J Am Coll Cardiol.2001;37(8):20192022.
  12. DeCara JM,Lang RM,Koch R,Bala R,Penzotti J,Spencer KT.The use of small personal ultrasound devices by internists without formal training in echocardiography.Eur J Echocardiogr.2003;4(2):141147.
  13. Duvall WL,Croft LB,Goldman ME.Can hand‐carried ultrasound devices be extended for use by the noncardiology medical community?Echocardiography.2003;20(5):471476.
  14. Beaulieu Y.Specific skill set and goals of focused echocardiography for critical care clinicians.Crit Care Med.2007;35(5 suppl):S144S149.
  15. Greaves K,Jeetley P,Hickman M, et al.The use of hand‐carried ultrasound in the hospital setting—a cost‐effective analysis.J Am Soc Echocardiogr.2005;18(6):620625.
  16. Brennan JM,Blair JE,Goonewardena S, et al.A comparison by medicine residents of physical examination versus hand‐carried ultrasound for estimation of right atrial pressure.Am J Cardiol.2007;99(11):16141616.
  17. Brennan JM,Blair JE,Hampole C, et al.Radial artery pulse pressure variation correlates with brachial artery peak velocity variation in ventilated subjects when measured by internal medicine residents using hand‐carried ultrasound devices.Chest.2007;131(5):13011307.
  18. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  19. Borges AC,Knebel F,Walde T,Sanad W,Baumann G.Diagnostic accuracy of new handheld echocardiography with Doppler and harmonic imaging properties.J Am Soc Echocardiogr.2004;17(3):234238.
  20. Tsutsui JM,Maciel RR,Costa JM,Andrade JL,Ramires JF,Mathias W.Hand‐carried ultrasound performed at bedside in cardiology inpatient setting ‐ a comparative study with comprehensive echocardiography.Cardiovasc Ultrasound.2004;2:24.
  21. Gorcsan J,Pandey P,Sade LE. Influence of hand‐carried ultrasound on bedside patient treatment decisions for consultative cardiology.J Am Soc Echocardiogr.2004;17(1):5055.
  22. Feldman MD,Petersen AJ,Karliner LS,Tice JA.Who is responsible for evaluating the safety and effectiveness of medical devices? The role of independent technology assessment.J Gen Intern Med.2008;23(suppl 1):5763.
  23. Anderson GM,Juurlink D,Detsky AS.Newly approved does not always mean new and improved.JAMA.2008;299(13):15981600.
  24. Hébert PC,Stanbrook M.Indication creep: physician beware.CMAJ.2007;177(7):697,699.
  25. Nicolaou S,Talsky A,Khashoggi K,Venu V.Ultrasound‐guided interventional radiology in critical care.Crit Care Med.2007;35(5 suppl):S186S197.
  26. Redberg RF,Walsh J.Pay now, benefits may follow—the case of cardiac computed tomographic angiography.N Engl J Med.2008;359(22):23092311.
  27. Leff B,Finucane TE.Gizmo idolatry.JAMA.2008;299(15):18301832.
  28. Siegal EM.Just because you can, doesn't mean that you should: a call for the rational application of hospitalist comanagement.J Hosp Med.2008;3(5):398402.
  29. DeAngelis CD,Fontanarosa PB.Impugning the integrity of medical science: the adverse effects of industry influence.JAMA.2008;299(15):18331835.
  30. Bozic KJ,Smith AR,Hariri S, et al.The 2007 ABJS Marshall Urist Award: the impact of direct‐to‐consumer advertising in orthopaedics.Clin Orthop Relat Res.2007;458:202219.
  31. Adeoye S,Bozic KJ.Direct to consumer advertising in healthcare: history, benefits, and concerns.Clin Orthop Relat Res.2007;457:96104.
  32. ConnorsAF Jr,Speroff T,Dawson NV, et al.The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators.JAMA.1996;276(11):889897.
  33. Harvey S,Harrison DA,Singer M, et al.Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC‐Man): a randomised controlled trial.Lancet.2005;366(9484):472477.
  34. Binanay C,Califf RM,Hasselblad V, et al.Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial.JAMA.2005;294(13):16251633.
  35. Richard C,Warszawski J,Anguel N, et al.Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial.JAMA.2003;290(20):27132720.
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Ultrasound, one of the most reliable diagnostic technologies in medicine, has a unique long‐term safety profile across a wide spectrum of applications. In line with the trend toward the miniaturization of many other technologies, increasingly sophisticated hand‐held or hand‐carried ultrasound (HCU) devices have become widely available. To date, the U.S. Food and Drug Administration (FDA) has approved more than 10 new‐generation portable (1.0‐4.5 kg) ultrasound devices, and a recent industry report projected that the HCU market will see revenues in excess of $1 billion by 2011.1

Although cardiovascular assessment remains its primary use, hospitalist physicians are increasingly turning to this technology for the localization of fluid and other abnormalities prior to paracentesis and thoracentesis. While there are other potential uses (eg, managing acute scrotal pain, diagnosing meniscal tears, measuring carotid intimal thickness), the higher‐quality studies of hospitalist‐physicians' use of HCU have focused on cardiovascular assessment. HCU confers a number of potential workflow‐related advantages, including coordinated point‐of‐care evaluation at short notice when formal ultrasound may be unavailable, as well as circumvention of the need to call on radiology or cardiology specialists.2 Even for experienced cardiologists, heart failure can be difficult to identify using any modality, and the clinical diagnosis of cardiovascular disease by hospital physicians has been documented as poor.3, 4 Thus, the addition of HCU to the palette of diagnostic and teaching tools available to frontline physicians potentially offers improvements over stethoscope‐assisted physical examination alone (including visual inspection, palpation, and auscultation), which has remained essentially unaltered for 150 years.57

Evidence Base for HCU Use by Hospitalists

The few primary studies on HCU use by hospitalists have focused on the potential utility of this technology as a valuable adjunct to the physical exam for the detection of cardiovascular disease (eg, asymptomatic left ventricular [LV] dysfunction, cardiomegaly, pericardial effusion) in the ambulatory or acute care setting.8, 9 Operation of HCU by hospitalists is not clearly indicated for the evaluation of valvular disease (eg, aortic and mitral regurgitation), in part due to the limited Doppler capabilities of the smaller devices.911 The risk of a gradual erosion of physical exam skills accompanying expansion of HCU use by hospitalists could itself become a potential disadvantage of a premature replacement of the stethoscope, since the results obtained by hospitalists performing a standard physical exam have been shown to be better than those obtained with HCU.8, 9

The lack of large, multicenter studies of HCU use by hospitalists leaves many questions unanswered, including whether or not the relatively low initial cost of an HCU device ($9,000‐$50,000) vs. that of a full‐sized hospital ultrasound system ($250,000) will eventually translate into overall cost‐effectiveness or actual patient‐centered benefit.10 While cautious advocates have insisted that HCU provides additive information in conjunction with the physical exam, this approach is not meant to serve as a substitute for standard echocardiography in patients requiring full evaluation in inpatient settings relevant for hospitalists.1114 Referral for additional testing or specialist opinionsand the associated costs incurredcannot necessarily be circumvented by hospitalist‐operated HCU.

A major problem with the HCU literature in general is its lack of standardization betweenand withinstudies, which renders it nearly impossible to generalize findings about important clinical outcomes, patient satisfaction, quality‐of‐life, symptoms, physical functioning, and morbidity and mortality. There are a preponderance of underpowered, methodologically inconsistent, single‐center case series that do not evaluate diagnostic accuracy in terms of patient outcomes. For example, although one study did find a modest (22‐29%) reduction in department workload with HCU, the authors omitted important information regarding blinding, and no power calculations were reported; thus, it was not possible to ascertain whether or not the reported results were due to the intervention or to chance.15 There clearly remains a need to convincingly demonstrate that patient care, shortening of length of stay, long‐term prognosis, or potential financial savings could occur with use of these devices by hospitalists.5 The process of device acquisition and resource allocation is, at least in part, based on accumulated evidence from studies that have ill‐defined relevant outcomes (eg, left ventricular function). However, even if such outcomes were to be more closely examined, medical decision‐making would still suffer from discrepant findings due to numerous differences in study design, including parameters involving patient population and selection, setting (eg, echocardiography laboratory vs. critical care unit), provider background, and specific device(s) used.

Training Issues

Hospitalist proficiency across HCU imaging skills (ie, acquisition, measurement, interpretation) has been found to be inconsistent.9 Endorsement and expansion of hospitalist use of HCU may to some extent reflect an overgeneralization from disparate comparative studies showing moderate success obtained with HCU (vs. physical exam) by other practitioner groups such as medical students and fellows with limited experience.16, 17 Whereas in 2005, Hellmann et al.18 concluded that medical residents with minimal training can learn to perform some of the basic functions of HCU with reasonable accuracy, Martin et al.8, 9 (in 2007 and 2009) reported conflicting results from a study of hospitalists trained at the same institution.

Concern about switching from standard to nonstandard HCU operators is raised by studies in which specialized operators (eg, echocardiography technicians) obtained better results than hospitalists using these devices.8, 9 In 2004, Borges et al.19 reported the results of 315 patients referred to specialists at a cardiology clinic for preoperative assessment prior to noncardiac surgery; the results (94.8% and 96.7% agreement with standard echocardiography on the main echocardiographic finding and detection of valve disease, respectively) were attributed to the fact that experienced cardiologists were working under ideal conditions using only the most advanced HCU devices with Doppler as well as harmonic imaging capabilities. Likewise, in 2004, Tsutsui et al.20 studied 44 consecutive hospitalized patients who underwent comprehensive echocardiography and bedside HCU. They reported that hemodynamic assessment by HCU was poor, even when performed by practitioners with relatively high levels of training.20 In 2003, DeCara et al.12 performed standard echocardiography on 300 adult inpatients referred for imaging, and concluded that standardized training, competency testing, and quality assurance guidelines need to be established before these devices can be utilized for clinical decision‐making by physicians without formal training in echocardiography. Although there have been numerous calls for training guidelines, it has not yet been determined how much training would be optimalor even necessaryfor professionals of each subspecialty to achieve levels of accuracy that are acceptable. Furthermore, it is well known that skill level declines unless a technique is regularly reinforced with practice, and therefore, recertification or procedure volume standards should be established.

The issue of potential harm needs to be raised, if hospitalists with access to HCU are indeed less accurate in their diagnoses than trained cardiologists interpreting images acquired by an established alternative such as echocardiography. False negatives can lead to delayed treatment, and false positives to unwarranted treatment. Given that the treatment effects of HCU use by hospitalists have not been closely scrutinized, the expansion of such use appears unwarranted, at least until further randomized studies with well‐defined outcomes have been conducted. Although the HCU devices themselves have a good safety profile, their potential benefits and harms (eg, possibility of increased nosocomial infection) will ultimately reflect operator skill and their impact on patient management relative to the gold‐standard diagnostic modalities for which there is abundant evidence of safety and efficacy.21

Premarketing and Postmarketing Concerns

The controversy regarding hospitalist use of HCU exposes gaps in the FDA approval process for medical devices, which are subjected to much less rigorous scrutiny during the premarketing approval process than pharmaceuticals.22 Moreover, the aggressive marketing of newly approved devices (and drugs) can drive medically unwarranted overuse, or indication creep, which justifies calls for the establishment of rigorous standards of clinical relevance and practice.23, 24 While the available literature on HCU operation by hospitalists is focused on cardiovascular indications for the technology, hospital medicine physicians are increasingly using HCU to guide paracentesis and thoracentesis. Given how commonplace the expansion of such practices has become, it is noteworthy that HCU operation by hospitalists has not yet been evaluated and endorsed in larger, controlled trials demonstrating appropriate outcomes.25

Across all fields of medicine, the transition from traditional to newer modalities remains a slippery slope in terms of demonstration of persuasive evidence of patient‐centered benefit.26 Fascination with emerging technologies (so‐called gizmo idolatry) and increased reimbursement potential threaten to distract patients and their providers from legitimate concerns about how medical device manufacturers and for‐profit corporations increasingly influence device acquisition and clinical practice.2731 While we lack strong evidence demonstrating that diagnostic tests such as HCU are beneficial when performed by hospitalists, the expanded use of these handy new devices by hospitalists is simultaneously generating increased incidental and equivocal findings, which in turn render it necessary to go back and perform secondary verification studies by specialists using older, gold‐standard modalities. This vicious cycle, coupled with the current lack of evidence, will continue to degrade confidence in the initiation of either acute or chronic treatment on the basis of HCU results obtained by hospitalist physicians.

Eventually, the increased use of HCU by hospitalists might lead to demonstrations of improved hospital workflow management, but it may just as easily represent another new coupling of technology and practitioner that prematurely becomes the standard of care in the absence of any demonstration of added value. The initially enthusiastic application of pulmonary artery catheters (PACs) serves as a cautionary tale in which the acquisition of additional clinical data did not necessarily lead to improved clinical outcomes: whereas PACs did enhance the clinical understanding of hemodynamics, they were not associated with an overall advantage in terms of mortality, length of hospital stay, or cost.3235 Ultimately, more information is not necessarily better information. Although new medical technologies can produce extremely useful diagnostic results that aid in the management of critically ill patients, poor data interpretation resulting from lack of targeted training and experience can nullify point‐of‐care advantages, and perhaps lead to excess morbidity and mortality.14 In clinical practice, it is generally best to avoid reliance on assumptions of added value in lieu of demonstrations of the same.

Conclusions

Hospital practitioners should not yet put away their stethoscopes. New technologies such as HCU need to be embraced in parallel with accumulating evidence of benefit. In the hands of hospitalists, the smaller HCU devices may very well prove handy, but at present, the literature simply does not support the use of HCU by hospitalist physicians.

Ultrasound, one of the most reliable diagnostic technologies in medicine, has a unique long‐term safety profile across a wide spectrum of applications. In line with the trend toward the miniaturization of many other technologies, increasingly sophisticated hand‐held or hand‐carried ultrasound (HCU) devices have become widely available. To date, the U.S. Food and Drug Administration (FDA) has approved more than 10 new‐generation portable (1.0‐4.5 kg) ultrasound devices, and a recent industry report projected that the HCU market will see revenues in excess of $1 billion by 2011.1

Although cardiovascular assessment remains its primary use, hospitalist physicians are increasingly turning to this technology for the localization of fluid and other abnormalities prior to paracentesis and thoracentesis. While there are other potential uses (eg, managing acute scrotal pain, diagnosing meniscal tears, measuring carotid intimal thickness), the higher‐quality studies of hospitalist‐physicians' use of HCU have focused on cardiovascular assessment. HCU confers a number of potential workflow‐related advantages, including coordinated point‐of‐care evaluation at short notice when formal ultrasound may be unavailable, as well as circumvention of the need to call on radiology or cardiology specialists.2 Even for experienced cardiologists, heart failure can be difficult to identify using any modality, and the clinical diagnosis of cardiovascular disease by hospital physicians has been documented as poor.3, 4 Thus, the addition of HCU to the palette of diagnostic and teaching tools available to frontline physicians potentially offers improvements over stethoscope‐assisted physical examination alone (including visual inspection, palpation, and auscultation), which has remained essentially unaltered for 150 years.57

Evidence Base for HCU Use by Hospitalists

The few primary studies on HCU use by hospitalists have focused on the potential utility of this technology as a valuable adjunct to the physical exam for the detection of cardiovascular disease (eg, asymptomatic left ventricular [LV] dysfunction, cardiomegaly, pericardial effusion) in the ambulatory or acute care setting.8, 9 Operation of HCU by hospitalists is not clearly indicated for the evaluation of valvular disease (eg, aortic and mitral regurgitation), in part due to the limited Doppler capabilities of the smaller devices.911 The risk of a gradual erosion of physical exam skills accompanying expansion of HCU use by hospitalists could itself become a potential disadvantage of a premature replacement of the stethoscope, since the results obtained by hospitalists performing a standard physical exam have been shown to be better than those obtained with HCU.8, 9

The lack of large, multicenter studies of HCU use by hospitalists leaves many questions unanswered, including whether or not the relatively low initial cost of an HCU device ($9,000‐$50,000) vs. that of a full‐sized hospital ultrasound system ($250,000) will eventually translate into overall cost‐effectiveness or actual patient‐centered benefit.10 While cautious advocates have insisted that HCU provides additive information in conjunction with the physical exam, this approach is not meant to serve as a substitute for standard echocardiography in patients requiring full evaluation in inpatient settings relevant for hospitalists.1114 Referral for additional testing or specialist opinionsand the associated costs incurredcannot necessarily be circumvented by hospitalist‐operated HCU.

A major problem with the HCU literature in general is its lack of standardization betweenand withinstudies, which renders it nearly impossible to generalize findings about important clinical outcomes, patient satisfaction, quality‐of‐life, symptoms, physical functioning, and morbidity and mortality. There are a preponderance of underpowered, methodologically inconsistent, single‐center case series that do not evaluate diagnostic accuracy in terms of patient outcomes. For example, although one study did find a modest (22‐29%) reduction in department workload with HCU, the authors omitted important information regarding blinding, and no power calculations were reported; thus, it was not possible to ascertain whether or not the reported results were due to the intervention or to chance.15 There clearly remains a need to convincingly demonstrate that patient care, shortening of length of stay, long‐term prognosis, or potential financial savings could occur with use of these devices by hospitalists.5 The process of device acquisition and resource allocation is, at least in part, based on accumulated evidence from studies that have ill‐defined relevant outcomes (eg, left ventricular function). However, even if such outcomes were to be more closely examined, medical decision‐making would still suffer from discrepant findings due to numerous differences in study design, including parameters involving patient population and selection, setting (eg, echocardiography laboratory vs. critical care unit), provider background, and specific device(s) used.

Training Issues

Hospitalist proficiency across HCU imaging skills (ie, acquisition, measurement, interpretation) has been found to be inconsistent.9 Endorsement and expansion of hospitalist use of HCU may to some extent reflect an overgeneralization from disparate comparative studies showing moderate success obtained with HCU (vs. physical exam) by other practitioner groups such as medical students and fellows with limited experience.16, 17 Whereas in 2005, Hellmann et al.18 concluded that medical residents with minimal training can learn to perform some of the basic functions of HCU with reasonable accuracy, Martin et al.8, 9 (in 2007 and 2009) reported conflicting results from a study of hospitalists trained at the same institution.

Concern about switching from standard to nonstandard HCU operators is raised by studies in which specialized operators (eg, echocardiography technicians) obtained better results than hospitalists using these devices.8, 9 In 2004, Borges et al.19 reported the results of 315 patients referred to specialists at a cardiology clinic for preoperative assessment prior to noncardiac surgery; the results (94.8% and 96.7% agreement with standard echocardiography on the main echocardiographic finding and detection of valve disease, respectively) were attributed to the fact that experienced cardiologists were working under ideal conditions using only the most advanced HCU devices with Doppler as well as harmonic imaging capabilities. Likewise, in 2004, Tsutsui et al.20 studied 44 consecutive hospitalized patients who underwent comprehensive echocardiography and bedside HCU. They reported that hemodynamic assessment by HCU was poor, even when performed by practitioners with relatively high levels of training.20 In 2003, DeCara et al.12 performed standard echocardiography on 300 adult inpatients referred for imaging, and concluded that standardized training, competency testing, and quality assurance guidelines need to be established before these devices can be utilized for clinical decision‐making by physicians without formal training in echocardiography. Although there have been numerous calls for training guidelines, it has not yet been determined how much training would be optimalor even necessaryfor professionals of each subspecialty to achieve levels of accuracy that are acceptable. Furthermore, it is well known that skill level declines unless a technique is regularly reinforced with practice, and therefore, recertification or procedure volume standards should be established.

The issue of potential harm needs to be raised, if hospitalists with access to HCU are indeed less accurate in their diagnoses than trained cardiologists interpreting images acquired by an established alternative such as echocardiography. False negatives can lead to delayed treatment, and false positives to unwarranted treatment. Given that the treatment effects of HCU use by hospitalists have not been closely scrutinized, the expansion of such use appears unwarranted, at least until further randomized studies with well‐defined outcomes have been conducted. Although the HCU devices themselves have a good safety profile, their potential benefits and harms (eg, possibility of increased nosocomial infection) will ultimately reflect operator skill and their impact on patient management relative to the gold‐standard diagnostic modalities for which there is abundant evidence of safety and efficacy.21

Premarketing and Postmarketing Concerns

The controversy regarding hospitalist use of HCU exposes gaps in the FDA approval process for medical devices, which are subjected to much less rigorous scrutiny during the premarketing approval process than pharmaceuticals.22 Moreover, the aggressive marketing of newly approved devices (and drugs) can drive medically unwarranted overuse, or indication creep, which justifies calls for the establishment of rigorous standards of clinical relevance and practice.23, 24 While the available literature on HCU operation by hospitalists is focused on cardiovascular indications for the technology, hospital medicine physicians are increasingly using HCU to guide paracentesis and thoracentesis. Given how commonplace the expansion of such practices has become, it is noteworthy that HCU operation by hospitalists has not yet been evaluated and endorsed in larger, controlled trials demonstrating appropriate outcomes.25

Across all fields of medicine, the transition from traditional to newer modalities remains a slippery slope in terms of demonstration of persuasive evidence of patient‐centered benefit.26 Fascination with emerging technologies (so‐called gizmo idolatry) and increased reimbursement potential threaten to distract patients and their providers from legitimate concerns about how medical device manufacturers and for‐profit corporations increasingly influence device acquisition and clinical practice.2731 While we lack strong evidence demonstrating that diagnostic tests such as HCU are beneficial when performed by hospitalists, the expanded use of these handy new devices by hospitalists is simultaneously generating increased incidental and equivocal findings, which in turn render it necessary to go back and perform secondary verification studies by specialists using older, gold‐standard modalities. This vicious cycle, coupled with the current lack of evidence, will continue to degrade confidence in the initiation of either acute or chronic treatment on the basis of HCU results obtained by hospitalist physicians.

Eventually, the increased use of HCU by hospitalists might lead to demonstrations of improved hospital workflow management, but it may just as easily represent another new coupling of technology and practitioner that prematurely becomes the standard of care in the absence of any demonstration of added value. The initially enthusiastic application of pulmonary artery catheters (PACs) serves as a cautionary tale in which the acquisition of additional clinical data did not necessarily lead to improved clinical outcomes: whereas PACs did enhance the clinical understanding of hemodynamics, they were not associated with an overall advantage in terms of mortality, length of hospital stay, or cost.3235 Ultimately, more information is not necessarily better information. Although new medical technologies can produce extremely useful diagnostic results that aid in the management of critically ill patients, poor data interpretation resulting from lack of targeted training and experience can nullify point‐of‐care advantages, and perhaps lead to excess morbidity and mortality.14 In clinical practice, it is generally best to avoid reliance on assumptions of added value in lieu of demonstrations of the same.

Conclusions

Hospital practitioners should not yet put away their stethoscopes. New technologies such as HCU need to be embraced in parallel with accumulating evidence of benefit. In the hands of hospitalists, the smaller HCU devices may very well prove handy, but at present, the literature simply does not support the use of HCU by hospitalist physicians.

References
  1. Hand‐Carried Ultrasound—Reshaping the ultrasound marketplace. Available at: http://www.sonoworld.com/NewsStories/NewsStories.aspx?ID= 450. Accessed August2009.
  2. Young A,Schleyer A,Nelson J.A new narrative for hospitalists.J Hosp Med.2009;4(4):207208.
  3. Hobbs R.Can heart failure be diagnosed in primary care?BMJ.2000;321(7255):188189.
  4. Clarke KW,Gray D,Hampton JR.Evidence of inadequate investigation and treatment of patients with heart failure.Br Heart J.1994;71(6):584587.
  5. Gorcsan J.Utility of hand‐carried ultrasound for consultative cardiology.Echocardiography.2003;20(5):463469.
  6. Bryan CS.Tomorrow's stethoscope: the hand‐held ultrasound device?J S C Med Assoc.2006;102(10):345.
  7. DeCara JM,Lang RM,Spencer KT.The hand‐carried echocardiographic device as an aid to the physical examination.Echocardiography.2003;20(5):477485.
  8. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  9. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalists: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  10. Alpert JS,Mladenovic J,Hellmann DB.Should a hand‐carried ultrasound machine become standard equipment for every internist?Am J Med.2009;122(1):13.
  11. Goodkin GM,Spevack DM,Tunick PA,Kronzon I.How useful is hand‐carried bedside echocardiography in critically ill patients?J Am Coll Cardiol.2001;37(8):20192022.
  12. DeCara JM,Lang RM,Koch R,Bala R,Penzotti J,Spencer KT.The use of small personal ultrasound devices by internists without formal training in echocardiography.Eur J Echocardiogr.2003;4(2):141147.
  13. Duvall WL,Croft LB,Goldman ME.Can hand‐carried ultrasound devices be extended for use by the noncardiology medical community?Echocardiography.2003;20(5):471476.
  14. Beaulieu Y.Specific skill set and goals of focused echocardiography for critical care clinicians.Crit Care Med.2007;35(5 suppl):S144S149.
  15. Greaves K,Jeetley P,Hickman M, et al.The use of hand‐carried ultrasound in the hospital setting—a cost‐effective analysis.J Am Soc Echocardiogr.2005;18(6):620625.
  16. Brennan JM,Blair JE,Goonewardena S, et al.A comparison by medicine residents of physical examination versus hand‐carried ultrasound for estimation of right atrial pressure.Am J Cardiol.2007;99(11):16141616.
  17. Brennan JM,Blair JE,Hampole C, et al.Radial artery pulse pressure variation correlates with brachial artery peak velocity variation in ventilated subjects when measured by internal medicine residents using hand‐carried ultrasound devices.Chest.2007;131(5):13011307.
  18. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  19. Borges AC,Knebel F,Walde T,Sanad W,Baumann G.Diagnostic accuracy of new handheld echocardiography with Doppler and harmonic imaging properties.J Am Soc Echocardiogr.2004;17(3):234238.
  20. Tsutsui JM,Maciel RR,Costa JM,Andrade JL,Ramires JF,Mathias W.Hand‐carried ultrasound performed at bedside in cardiology inpatient setting ‐ a comparative study with comprehensive echocardiography.Cardiovasc Ultrasound.2004;2:24.
  21. Gorcsan J,Pandey P,Sade LE. Influence of hand‐carried ultrasound on bedside patient treatment decisions for consultative cardiology.J Am Soc Echocardiogr.2004;17(1):5055.
  22. Feldman MD,Petersen AJ,Karliner LS,Tice JA.Who is responsible for evaluating the safety and effectiveness of medical devices? The role of independent technology assessment.J Gen Intern Med.2008;23(suppl 1):5763.
  23. Anderson GM,Juurlink D,Detsky AS.Newly approved does not always mean new and improved.JAMA.2008;299(13):15981600.
  24. Hébert PC,Stanbrook M.Indication creep: physician beware.CMAJ.2007;177(7):697,699.
  25. Nicolaou S,Talsky A,Khashoggi K,Venu V.Ultrasound‐guided interventional radiology in critical care.Crit Care Med.2007;35(5 suppl):S186S197.
  26. Redberg RF,Walsh J.Pay now, benefits may follow—the case of cardiac computed tomographic angiography.N Engl J Med.2008;359(22):23092311.
  27. Leff B,Finucane TE.Gizmo idolatry.JAMA.2008;299(15):18301832.
  28. Siegal EM.Just because you can, doesn't mean that you should: a call for the rational application of hospitalist comanagement.J Hosp Med.2008;3(5):398402.
  29. DeAngelis CD,Fontanarosa PB.Impugning the integrity of medical science: the adverse effects of industry influence.JAMA.2008;299(15):18331835.
  30. Bozic KJ,Smith AR,Hariri S, et al.The 2007 ABJS Marshall Urist Award: the impact of direct‐to‐consumer advertising in orthopaedics.Clin Orthop Relat Res.2007;458:202219.
  31. Adeoye S,Bozic KJ.Direct to consumer advertising in healthcare: history, benefits, and concerns.Clin Orthop Relat Res.2007;457:96104.
  32. ConnorsAF Jr,Speroff T,Dawson NV, et al.The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators.JAMA.1996;276(11):889897.
  33. Harvey S,Harrison DA,Singer M, et al.Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC‐Man): a randomised controlled trial.Lancet.2005;366(9484):472477.
  34. Binanay C,Califf RM,Hasselblad V, et al.Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial.JAMA.2005;294(13):16251633.
  35. Richard C,Warszawski J,Anguel N, et al.Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial.JAMA.2003;290(20):27132720.
References
  1. Hand‐Carried Ultrasound—Reshaping the ultrasound marketplace. Available at: http://www.sonoworld.com/NewsStories/NewsStories.aspx?ID= 450. Accessed August2009.
  2. Young A,Schleyer A,Nelson J.A new narrative for hospitalists.J Hosp Med.2009;4(4):207208.
  3. Hobbs R.Can heart failure be diagnosed in primary care?BMJ.2000;321(7255):188189.
  4. Clarke KW,Gray D,Hampton JR.Evidence of inadequate investigation and treatment of patients with heart failure.Br Heart J.1994;71(6):584587.
  5. Gorcsan J.Utility of hand‐carried ultrasound for consultative cardiology.Echocardiography.2003;20(5):463469.
  6. Bryan CS.Tomorrow's stethoscope: the hand‐held ultrasound device?J S C Med Assoc.2006;102(10):345.
  7. DeCara JM,Lang RM,Spencer KT.The hand‐carried echocardiographic device as an aid to the physical examination.Echocardiography.2003;20(5):477485.
  8. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  9. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalists: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  10. Alpert JS,Mladenovic J,Hellmann DB.Should a hand‐carried ultrasound machine become standard equipment for every internist?Am J Med.2009;122(1):13.
  11. Goodkin GM,Spevack DM,Tunick PA,Kronzon I.How useful is hand‐carried bedside echocardiography in critically ill patients?J Am Coll Cardiol.2001;37(8):20192022.
  12. DeCara JM,Lang RM,Koch R,Bala R,Penzotti J,Spencer KT.The use of small personal ultrasound devices by internists without formal training in echocardiography.Eur J Echocardiogr.2003;4(2):141147.
  13. Duvall WL,Croft LB,Goldman ME.Can hand‐carried ultrasound devices be extended for use by the noncardiology medical community?Echocardiography.2003;20(5):471476.
  14. Beaulieu Y.Specific skill set and goals of focused echocardiography for critical care clinicians.Crit Care Med.2007;35(5 suppl):S144S149.
  15. Greaves K,Jeetley P,Hickman M, et al.The use of hand‐carried ultrasound in the hospital setting—a cost‐effective analysis.J Am Soc Echocardiogr.2005;18(6):620625.
  16. Brennan JM,Blair JE,Goonewardena S, et al.A comparison by medicine residents of physical examination versus hand‐carried ultrasound for estimation of right atrial pressure.Am J Cardiol.2007;99(11):16141616.
  17. Brennan JM,Blair JE,Hampole C, et al.Radial artery pulse pressure variation correlates with brachial artery peak velocity variation in ventilated subjects when measured by internal medicine residents using hand‐carried ultrasound devices.Chest.2007;131(5):13011307.
  18. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  19. Borges AC,Knebel F,Walde T,Sanad W,Baumann G.Diagnostic accuracy of new handheld echocardiography with Doppler and harmonic imaging properties.J Am Soc Echocardiogr.2004;17(3):234238.
  20. Tsutsui JM,Maciel RR,Costa JM,Andrade JL,Ramires JF,Mathias W.Hand‐carried ultrasound performed at bedside in cardiology inpatient setting ‐ a comparative study with comprehensive echocardiography.Cardiovasc Ultrasound.2004;2:24.
  21. Gorcsan J,Pandey P,Sade LE. Influence of hand‐carried ultrasound on bedside patient treatment decisions for consultative cardiology.J Am Soc Echocardiogr.2004;17(1):5055.
  22. Feldman MD,Petersen AJ,Karliner LS,Tice JA.Who is responsible for evaluating the safety and effectiveness of medical devices? The role of independent technology assessment.J Gen Intern Med.2008;23(suppl 1):5763.
  23. Anderson GM,Juurlink D,Detsky AS.Newly approved does not always mean new and improved.JAMA.2008;299(13):15981600.
  24. Hébert PC,Stanbrook M.Indication creep: physician beware.CMAJ.2007;177(7):697,699.
  25. Nicolaou S,Talsky A,Khashoggi K,Venu V.Ultrasound‐guided interventional radiology in critical care.Crit Care Med.2007;35(5 suppl):S186S197.
  26. Redberg RF,Walsh J.Pay now, benefits may follow—the case of cardiac computed tomographic angiography.N Engl J Med.2008;359(22):23092311.
  27. Leff B,Finucane TE.Gizmo idolatry.JAMA.2008;299(15):18301832.
  28. Siegal EM.Just because you can, doesn't mean that you should: a call for the rational application of hospitalist comanagement.J Hosp Med.2008;3(5):398402.
  29. DeAngelis CD,Fontanarosa PB.Impugning the integrity of medical science: the adverse effects of industry influence.JAMA.2008;299(15):18331835.
  30. Bozic KJ,Smith AR,Hariri S, et al.The 2007 ABJS Marshall Urist Award: the impact of direct‐to‐consumer advertising in orthopaedics.Clin Orthop Relat Res.2007;458:202219.
  31. Adeoye S,Bozic KJ.Direct to consumer advertising in healthcare: history, benefits, and concerns.Clin Orthop Relat Res.2007;457:96104.
  32. ConnorsAF Jr,Speroff T,Dawson NV, et al.The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators.JAMA.1996;276(11):889897.
  33. Harvey S,Harrison DA,Singer M, et al.Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC‐Man): a randomised controlled trial.Lancet.2005;366(9484):472477.
  34. Binanay C,Califf RM,Hasselblad V, et al.Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial.JAMA.2005;294(13):16251633.
  35. Richard C,Warszawski J,Anguel N, et al.Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial.JAMA.2003;290(20):27132720.
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Journal of Hospital Medicine - 5(3)
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Journal of Hospital Medicine - 5(3)
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“On the other hand …”: The evidence does not support the use of hand‐carried ultrasound by hospitalists
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“On the other hand …”: The evidence does not support the use of hand‐carried ultrasound by hospitalists
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Hospitalist Physician Leadership Skills

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Hospitalist physician leadership skills: Perspectives from participants of a leadership conference

Physicians assume myriad leadership roles within medical institutions. Clinically‐oriented leadership roles can range from managing a small group of providers, to leading entire health systems, to heading up national quality improvement initiatives. While often competent in the practice of medicine, many physicians have not pursued structured management or administrative training. In a survey of Medicine Department Chairs at academic medical centers, none had advanced management degrees despite spending an average of 55% of their time on administrative duties. It is not uncommon for physicians to attend leadership development programs or management seminars, as evidenced by the increasing demand for education.1 Various methods for skill enhancement have been described24; however, the most effective approaches have yet to be determined.

Miller and Dollard5 and Bandura6, 7 have explained that behavioral contracts have evolved from social cognitive theory principles. These contracts are formal written agreements, often negotiated between 2 individuals, to facilitate behavior change. Typically, they involve a clear definition of expected behaviors with specific consequences (usually positive reinforcement).810 Their use in modifying physician behavior, particularly those related to leadership, has not been studied.

Hospitalist physicians represent the fastest growing specialty in the United States.11, 12 Among other responsibilities, they have taken on roles as leaders in hospital administration, education, quality improvement, and public health.1315 The Society of Hospital Medicine (SHM), the largest US organization committed to the practice of hospital medicine,16 has established Leadership Academies to prepare hospitalists for these duties. The goal of this study was to assess how hospitalist physicians' commitment to grow as leaders was expressed using behavioral contacts as a vehicle to clarify their intentions and whether behavioral change occurred over time.

Methods

Study Design

A qualitative study design was selected to explore how current and future hospitalist leaders planned to modify their behaviors after participating in a hospitalist leadership training course. Participants were encouraged to complete a behavioral contract highlighting their personal goals.

Approximately 12 months later, follow‐up data were collected. Participants were sent copies of their behavioral contracts and surveyed about the extent to which they have realized their personal goals.

Subjects

Hospitalist leaders participating in the 4‐day level I or II leadership courses of the SHM Leadership Academy were studied.

Data Collection

In the final sessions of the 2007‐2008 Leadership Academy courses, participants completed an optional behavioral contract exercise in which they partnered with a colleague and were asked to identify 4 action plans they intended to implement upon their return home. These were written down and signed. Selected demographic information was also collected.

Follow‐up surveys were sent by mail and electronically to a subset of participants with completed behavioral contracts. A 5‐point Likert scale (strongly agree . . . strongly disagree) was used to assess the extent of adherence to the goals listed in the behavioral contracts.

Data Analysis

Transcripts were analyzed using an editing organizing style, a qualitative analysis technique to find meaningful units or segments of text that both stand on their own and relate to the purpose of the study.12 With this method, the coding template emerges from the data. Two investigators independently analyzed the transcripts and created a coding template based on common themes identified among the participants. In cases of discrepant coding, the 2 investigators had discussions to reach consensus. The authors agreed on representative quotes for each theme. Triangulation was established through sharing results of the analysis with a subset of participants.

Follow‐up survey data was summarized descriptively showing proportion data.

Results

Response Rate and Participant Demographics

Out of 264 people who completed the course, 120 decided to participate in the optional behavioral contract exercise. The median age of participants was 38 years (Table 1). The majority were male (84; 70.0%), and hospitalist leaders (76; 63.3%). The median time in practice as a hospitalist was 4 years. Fewer than one‐half held an academic appointment (40; 33.3%) with most being at the rank of Assistant Professor (14; 11.7%). Most of the participants worked in a private hospital (80; 66.7%).

Demographic Characteristics of the 120 Participants of the Society of Hospital Medicine Leadership Academy 2007‐2008 Who Took Part in the Behavioral Contract Exercise
Characteristic 
  • Abbreviation: SD, standard deviation.

Age in years [median (SD)]38 (8)
Male [n (%)]84 (70.0)
Years in practice as hospitalist [median (SD)]4 (13)
Leader of hospitalist program [n (%)]76 (63.3)
Academic affiliation [n (%)]40 (33.3)
Academic rank [n (%)] 
Instructor9 (7.5)
Assistant professor14 (11.7)
Associate professor13 (10.8)
Hospital type [n (%)] 
Private80 (66.7)
University15 (12.5)
Government2 (1.7)
Veterans administration0 (0.0)
Other1 (0.1)

Results of Qualitative Analysis of Behavioral Contracts

From the analyses of the behavioral contracts, themes emerged related to ways in which participants hoped to develop and improve. The themes and the frequencies with which they were recorded in the behavioral contracts are shown in Table 2.

Total Number of Times and Numbers of Respondents Referring to the Major Themes Related to Physician Leadership Development From the Behavioral Contracts of 120 Hospitalist Leaders and Practitioners
ThemeTotal Number of Times Theme Mentioned in All Behavioral ContractsNumber of Respondents Referring to Theme [n (%)]
  • NOTE: Respondents were not queried specifically about these themes and these counts represent spontaneous and unsolicited responses in each subcategory.

Improving communication and interpersonal skills13270 (58.3)
Refinement of vision, goals, and strategic planning11562 (51.7)
Improve intrapersonal development6536 (30.0)
Enhance negotiation skills6544 (36.7)
Commit to organizational change5332 (26.7)
Understanding business drivers3828 (23.3)
Setting performance and clinical metrics3426 (21.7)
Strengthen interdepartmental relations3226 (21.7)

Improving Communication and Interpersonal Skills

A desire to improve communication and listening skills, particularly in the context of conflict resolution, was mentioned repeatedly. Heightened awareness about different personality types to allow for improved interpersonal relationships was another concept that was emphasized.

One female Instructor from an academic medical center described her intentions:

  • I will try to do a better job at assessing the behavioral tendencies of my partners and adjust my own style for more effective communication.

 

Refinement of Vision, Goals, and Strategic Planning

Physicians were committed to returning to their home institutions and embarking on initiatives to advance vision and goals of their groups within the context of strategic planning. Participants were interested in creating hospitalist‐specific mission statements, developing specific goals that take advantage of strengths and opportunities while minimizing internal weaknesses and considering external threats. They described wanting to align the interests of members of their hospitalist groups around a common goal.

A female hospitalist leader in private practice wished to:

  • Clearly define a group vision and commit to re‐evaluation on a regular basis to ensure we are on track . . . and conduct a SWOT (Strengths, Weaknesses, Opportunities, Threats) analysis to set future goals.

 

Improve Intrapersonal Development

Participants expressed desire to improve their leadership skills. Proposed goals included: (1) recognizing their weaknesses and soliciting feedback from colleagues, (2) minimizing emotional response to stress, (3) sharing their knowledge and skills for the benefit of peers, (4) delegating work more effectively to others, (5) reading suggested books on leadership, (6) serving as a positive role model and mentor, and (7) managing meetings and difficult coworkers more skillfully.

One female Assistant Professor from an academic medical center outlined:

  • I want to be able to: (1) manage up better and effectively negotiate with the administration on behalf of my group; (2) become better at leadership skills by using the tools offered at the Academy; and (3) effectively support my group members to develop their skills to become successful in their chosen niches. I will . . . improve the poor morale in my group.

 

Enhance Negotiation Skills

Many physician leaders identified negotiation principles and techniques as foundations for improvement for interactions within their own groups, as well as with the hospital administration.

A male private hospitalist leader working for 4 years as a hospitalist described plans to utilize negotiation skills within and outside the group:

  • Negotiate with my team of hospitalists to make them more compliant with the rules and regulations of the group, and negotiate an excellent contract with hospital administration. . . .

 

Commit to Organizational Change

The hospitalist respondents described their ability to influence organizational change given their unique position at the interface between patient care delivery and hospital administration. To realize organizational change, commonly cited ideas included recruitment and retention of clinically excellent practitioners, and developing standard protocols to facilitate quality improvement initiatives.

A male Instructor of Medicine listed select areas in which to become more involved:

  • Participation with the Chief Executive Officer of the company in quality improvement projects, calls to the primary care practitioners upon discharge, and the handoff process.

 

Other Themes

The final 3 themes included are: understanding business drivers; the establishment of better metrics to assess performance; and the strengthening of interdepartmental relations.

Follow‐up Data About Adherence to Plans Delineated in Behavioral Contracts

Out of 65 completed behavioral contracts from the 2007 Level I participants, 32 returned a follow‐up survey (response rate 49.3%). Figure 1 shows the extent to which respondents believed that they were compliant with their proposed plans for change or improvement. Degree of adherence was displayed as a proportion of total goals. Out of those who returned a follow‐up survey, all but 1 respondent either strongly agreed or agreed that they adhered to at least one of their goals (96.9%).

Figure 1
Self‐assessed compliance with respect to achievement of the 112 personal goals delineated in the behavioral contracts among the 32 participants who completed the follow‐up survey.

Select representative comments that illustrate the physicians' appreciation of using behavioral contracts include:

  • my approach to problems is a bit more analytical.

  • simple changes in how I approach people and interact with them has greatly improved my skills as a leader and allowed me to accomplish my goals with much less effort.

 

Discussion

Through the qualitative analysis of the behavioral contracts completed by participants of a Leadership Academy for hospitalists, we characterized the ways that hospitalist practitioners hoped to evolve as leaders. The major themes that emerged relate not only to their own growth and development but also their pledge to advance the success of the group or division. The level of commitment and impact of the behavioral contracts appear to be reinforced by an overwhelmingly positive response to adherence to personal goals one year after course participation. Communication and interpersonal development were most frequently cited in the behavioral contracts as areas for which the hospitalist leaders acknowledged a desire to grow. In a study of academic department of medicine chairs, communication skills were identified as being vital for effective leadership.3 The Chairs also recognized other proficiencies required for leading that were consistent with those outlined in the behavioral contracts: strategic planning, change management, team building, personnel management, and systems thinking. McDade et al.17 examined the effects of participation in an executive leadership program developed for female academic faculty in medical and dental schools in the United States and Canada. They noted increased self‐assessed leadership capabilities at 18 months after attending the program, across 10 leadership constructs taught in the classes. These leadership constructs resonate with the themes found in the plans for change described by our informants.

Hospitalists are assuming leadership roles in an increasing number and with greater scope; however, until now their perspectives on what skill sets are required to be successful have not been well documented. Significant time, effort, and money are invested into the development of hospitalists as leaders.4 The behavioral contract appears to be a tool acceptable to hospitalist physicians; perhaps it can be used as part annual reviews with hospitalists aspiring to be leaders.

Several limitations of the study shall be considered. First, not all participants attending the Leadership Academy opted to fill out the behavioral contracts. Second, this qualitative study is limited to those practitioners who are genuinely interested in growing as leaders as evidenced by their willingness to invest in going to the course. Third, follow‐up surveys relied on self‐assessment and it is not known whether actual realization of these goals occurred or the extent to which behavioral contracts were responsible. Further, follow‐up data were only completed by 49% percent of those targeted. However, hospitalists may be fairly resistant to being surveyed as evidenced by the fact that SHM's 2005‐2006 membership survey yielded a response rate of only 26%.18 Finally, many of the thematic goals were described by fewer than 50% of informants. However, it is important to note that the elements included on each person's behavioral contract emerged spontaneously. If subjects were specifically asked about each theme, the number of comments related to each would certainly be much higher. Qualitative analysis does not really allow us to know whether one theme is more important than another merely because it was mentioned more frequently.

Hospitalist leaders appear to be committed to professional growth and they have reported realization of goals delineated in their behavioral contracts. While varied methods are being used as part of physician leadership training programs, behavioral contracts may enhance promise for change.

Acknowledgements

The authors thank Regina Hess for assistance in data preparation and Laurence Wellikson, MD, FHM, Russell Holman, MD and Erica Pearson (all from the SHM) for data collection.

Article PDF
Issue
Journal of Hospital Medicine - 5(3)
Page Number
E1-E4
Legacy Keywords
behavior, hospitalist, leadership, physician executives
Sections
Article PDF
Article PDF

Physicians assume myriad leadership roles within medical institutions. Clinically‐oriented leadership roles can range from managing a small group of providers, to leading entire health systems, to heading up national quality improvement initiatives. While often competent in the practice of medicine, many physicians have not pursued structured management or administrative training. In a survey of Medicine Department Chairs at academic medical centers, none had advanced management degrees despite spending an average of 55% of their time on administrative duties. It is not uncommon for physicians to attend leadership development programs or management seminars, as evidenced by the increasing demand for education.1 Various methods for skill enhancement have been described24; however, the most effective approaches have yet to be determined.

Miller and Dollard5 and Bandura6, 7 have explained that behavioral contracts have evolved from social cognitive theory principles. These contracts are formal written agreements, often negotiated between 2 individuals, to facilitate behavior change. Typically, they involve a clear definition of expected behaviors with specific consequences (usually positive reinforcement).810 Their use in modifying physician behavior, particularly those related to leadership, has not been studied.

Hospitalist physicians represent the fastest growing specialty in the United States.11, 12 Among other responsibilities, they have taken on roles as leaders in hospital administration, education, quality improvement, and public health.1315 The Society of Hospital Medicine (SHM), the largest US organization committed to the practice of hospital medicine,16 has established Leadership Academies to prepare hospitalists for these duties. The goal of this study was to assess how hospitalist physicians' commitment to grow as leaders was expressed using behavioral contacts as a vehicle to clarify their intentions and whether behavioral change occurred over time.

Methods

Study Design

A qualitative study design was selected to explore how current and future hospitalist leaders planned to modify their behaviors after participating in a hospitalist leadership training course. Participants were encouraged to complete a behavioral contract highlighting their personal goals.

Approximately 12 months later, follow‐up data were collected. Participants were sent copies of their behavioral contracts and surveyed about the extent to which they have realized their personal goals.

Subjects

Hospitalist leaders participating in the 4‐day level I or II leadership courses of the SHM Leadership Academy were studied.

Data Collection

In the final sessions of the 2007‐2008 Leadership Academy courses, participants completed an optional behavioral contract exercise in which they partnered with a colleague and were asked to identify 4 action plans they intended to implement upon their return home. These were written down and signed. Selected demographic information was also collected.

Follow‐up surveys were sent by mail and electronically to a subset of participants with completed behavioral contracts. A 5‐point Likert scale (strongly agree . . . strongly disagree) was used to assess the extent of adherence to the goals listed in the behavioral contracts.

Data Analysis

Transcripts were analyzed using an editing organizing style, a qualitative analysis technique to find meaningful units or segments of text that both stand on their own and relate to the purpose of the study.12 With this method, the coding template emerges from the data. Two investigators independently analyzed the transcripts and created a coding template based on common themes identified among the participants. In cases of discrepant coding, the 2 investigators had discussions to reach consensus. The authors agreed on representative quotes for each theme. Triangulation was established through sharing results of the analysis with a subset of participants.

Follow‐up survey data was summarized descriptively showing proportion data.

Results

Response Rate and Participant Demographics

Out of 264 people who completed the course, 120 decided to participate in the optional behavioral contract exercise. The median age of participants was 38 years (Table 1). The majority were male (84; 70.0%), and hospitalist leaders (76; 63.3%). The median time in practice as a hospitalist was 4 years. Fewer than one‐half held an academic appointment (40; 33.3%) with most being at the rank of Assistant Professor (14; 11.7%). Most of the participants worked in a private hospital (80; 66.7%).

Demographic Characteristics of the 120 Participants of the Society of Hospital Medicine Leadership Academy 2007‐2008 Who Took Part in the Behavioral Contract Exercise
Characteristic 
  • Abbreviation: SD, standard deviation.

Age in years [median (SD)]38 (8)
Male [n (%)]84 (70.0)
Years in practice as hospitalist [median (SD)]4 (13)
Leader of hospitalist program [n (%)]76 (63.3)
Academic affiliation [n (%)]40 (33.3)
Academic rank [n (%)] 
Instructor9 (7.5)
Assistant professor14 (11.7)
Associate professor13 (10.8)
Hospital type [n (%)] 
Private80 (66.7)
University15 (12.5)
Government2 (1.7)
Veterans administration0 (0.0)
Other1 (0.1)

Results of Qualitative Analysis of Behavioral Contracts

From the analyses of the behavioral contracts, themes emerged related to ways in which participants hoped to develop and improve. The themes and the frequencies with which they were recorded in the behavioral contracts are shown in Table 2.

Total Number of Times and Numbers of Respondents Referring to the Major Themes Related to Physician Leadership Development From the Behavioral Contracts of 120 Hospitalist Leaders and Practitioners
ThemeTotal Number of Times Theme Mentioned in All Behavioral ContractsNumber of Respondents Referring to Theme [n (%)]
  • NOTE: Respondents were not queried specifically about these themes and these counts represent spontaneous and unsolicited responses in each subcategory.

Improving communication and interpersonal skills13270 (58.3)
Refinement of vision, goals, and strategic planning11562 (51.7)
Improve intrapersonal development6536 (30.0)
Enhance negotiation skills6544 (36.7)
Commit to organizational change5332 (26.7)
Understanding business drivers3828 (23.3)
Setting performance and clinical metrics3426 (21.7)
Strengthen interdepartmental relations3226 (21.7)

Improving Communication and Interpersonal Skills

A desire to improve communication and listening skills, particularly in the context of conflict resolution, was mentioned repeatedly. Heightened awareness about different personality types to allow for improved interpersonal relationships was another concept that was emphasized.

One female Instructor from an academic medical center described her intentions:

  • I will try to do a better job at assessing the behavioral tendencies of my partners and adjust my own style for more effective communication.

 

Refinement of Vision, Goals, and Strategic Planning

Physicians were committed to returning to their home institutions and embarking on initiatives to advance vision and goals of their groups within the context of strategic planning. Participants were interested in creating hospitalist‐specific mission statements, developing specific goals that take advantage of strengths and opportunities while minimizing internal weaknesses and considering external threats. They described wanting to align the interests of members of their hospitalist groups around a common goal.

A female hospitalist leader in private practice wished to:

  • Clearly define a group vision and commit to re‐evaluation on a regular basis to ensure we are on track . . . and conduct a SWOT (Strengths, Weaknesses, Opportunities, Threats) analysis to set future goals.

 

Improve Intrapersonal Development

Participants expressed desire to improve their leadership skills. Proposed goals included: (1) recognizing their weaknesses and soliciting feedback from colleagues, (2) minimizing emotional response to stress, (3) sharing their knowledge and skills for the benefit of peers, (4) delegating work more effectively to others, (5) reading suggested books on leadership, (6) serving as a positive role model and mentor, and (7) managing meetings and difficult coworkers more skillfully.

One female Assistant Professor from an academic medical center outlined:

  • I want to be able to: (1) manage up better and effectively negotiate with the administration on behalf of my group; (2) become better at leadership skills by using the tools offered at the Academy; and (3) effectively support my group members to develop their skills to become successful in their chosen niches. I will . . . improve the poor morale in my group.

 

Enhance Negotiation Skills

Many physician leaders identified negotiation principles and techniques as foundations for improvement for interactions within their own groups, as well as with the hospital administration.

A male private hospitalist leader working for 4 years as a hospitalist described plans to utilize negotiation skills within and outside the group:

  • Negotiate with my team of hospitalists to make them more compliant with the rules and regulations of the group, and negotiate an excellent contract with hospital administration. . . .

 

Commit to Organizational Change

The hospitalist respondents described their ability to influence organizational change given their unique position at the interface between patient care delivery and hospital administration. To realize organizational change, commonly cited ideas included recruitment and retention of clinically excellent practitioners, and developing standard protocols to facilitate quality improvement initiatives.

A male Instructor of Medicine listed select areas in which to become more involved:

  • Participation with the Chief Executive Officer of the company in quality improvement projects, calls to the primary care practitioners upon discharge, and the handoff process.

 

Other Themes

The final 3 themes included are: understanding business drivers; the establishment of better metrics to assess performance; and the strengthening of interdepartmental relations.

Follow‐up Data About Adherence to Plans Delineated in Behavioral Contracts

Out of 65 completed behavioral contracts from the 2007 Level I participants, 32 returned a follow‐up survey (response rate 49.3%). Figure 1 shows the extent to which respondents believed that they were compliant with their proposed plans for change or improvement. Degree of adherence was displayed as a proportion of total goals. Out of those who returned a follow‐up survey, all but 1 respondent either strongly agreed or agreed that they adhered to at least one of their goals (96.9%).

Figure 1
Self‐assessed compliance with respect to achievement of the 112 personal goals delineated in the behavioral contracts among the 32 participants who completed the follow‐up survey.

Select representative comments that illustrate the physicians' appreciation of using behavioral contracts include:

  • my approach to problems is a bit more analytical.

  • simple changes in how I approach people and interact with them has greatly improved my skills as a leader and allowed me to accomplish my goals with much less effort.

 

Discussion

Through the qualitative analysis of the behavioral contracts completed by participants of a Leadership Academy for hospitalists, we characterized the ways that hospitalist practitioners hoped to evolve as leaders. The major themes that emerged relate not only to their own growth and development but also their pledge to advance the success of the group or division. The level of commitment and impact of the behavioral contracts appear to be reinforced by an overwhelmingly positive response to adherence to personal goals one year after course participation. Communication and interpersonal development were most frequently cited in the behavioral contracts as areas for which the hospitalist leaders acknowledged a desire to grow. In a study of academic department of medicine chairs, communication skills were identified as being vital for effective leadership.3 The Chairs also recognized other proficiencies required for leading that were consistent with those outlined in the behavioral contracts: strategic planning, change management, team building, personnel management, and systems thinking. McDade et al.17 examined the effects of participation in an executive leadership program developed for female academic faculty in medical and dental schools in the United States and Canada. They noted increased self‐assessed leadership capabilities at 18 months after attending the program, across 10 leadership constructs taught in the classes. These leadership constructs resonate with the themes found in the plans for change described by our informants.

Hospitalists are assuming leadership roles in an increasing number and with greater scope; however, until now their perspectives on what skill sets are required to be successful have not been well documented. Significant time, effort, and money are invested into the development of hospitalists as leaders.4 The behavioral contract appears to be a tool acceptable to hospitalist physicians; perhaps it can be used as part annual reviews with hospitalists aspiring to be leaders.

Several limitations of the study shall be considered. First, not all participants attending the Leadership Academy opted to fill out the behavioral contracts. Second, this qualitative study is limited to those practitioners who are genuinely interested in growing as leaders as evidenced by their willingness to invest in going to the course. Third, follow‐up surveys relied on self‐assessment and it is not known whether actual realization of these goals occurred or the extent to which behavioral contracts were responsible. Further, follow‐up data were only completed by 49% percent of those targeted. However, hospitalists may be fairly resistant to being surveyed as evidenced by the fact that SHM's 2005‐2006 membership survey yielded a response rate of only 26%.18 Finally, many of the thematic goals were described by fewer than 50% of informants. However, it is important to note that the elements included on each person's behavioral contract emerged spontaneously. If subjects were specifically asked about each theme, the number of comments related to each would certainly be much higher. Qualitative analysis does not really allow us to know whether one theme is more important than another merely because it was mentioned more frequently.

Hospitalist leaders appear to be committed to professional growth and they have reported realization of goals delineated in their behavioral contracts. While varied methods are being used as part of physician leadership training programs, behavioral contracts may enhance promise for change.

Acknowledgements

The authors thank Regina Hess for assistance in data preparation and Laurence Wellikson, MD, FHM, Russell Holman, MD and Erica Pearson (all from the SHM) for data collection.

Physicians assume myriad leadership roles within medical institutions. Clinically‐oriented leadership roles can range from managing a small group of providers, to leading entire health systems, to heading up national quality improvement initiatives. While often competent in the practice of medicine, many physicians have not pursued structured management or administrative training. In a survey of Medicine Department Chairs at academic medical centers, none had advanced management degrees despite spending an average of 55% of their time on administrative duties. It is not uncommon for physicians to attend leadership development programs or management seminars, as evidenced by the increasing demand for education.1 Various methods for skill enhancement have been described24; however, the most effective approaches have yet to be determined.

Miller and Dollard5 and Bandura6, 7 have explained that behavioral contracts have evolved from social cognitive theory principles. These contracts are formal written agreements, often negotiated between 2 individuals, to facilitate behavior change. Typically, they involve a clear definition of expected behaviors with specific consequences (usually positive reinforcement).810 Their use in modifying physician behavior, particularly those related to leadership, has not been studied.

Hospitalist physicians represent the fastest growing specialty in the United States.11, 12 Among other responsibilities, they have taken on roles as leaders in hospital administration, education, quality improvement, and public health.1315 The Society of Hospital Medicine (SHM), the largest US organization committed to the practice of hospital medicine,16 has established Leadership Academies to prepare hospitalists for these duties. The goal of this study was to assess how hospitalist physicians' commitment to grow as leaders was expressed using behavioral contacts as a vehicle to clarify their intentions and whether behavioral change occurred over time.

Methods

Study Design

A qualitative study design was selected to explore how current and future hospitalist leaders planned to modify their behaviors after participating in a hospitalist leadership training course. Participants were encouraged to complete a behavioral contract highlighting their personal goals.

Approximately 12 months later, follow‐up data were collected. Participants were sent copies of their behavioral contracts and surveyed about the extent to which they have realized their personal goals.

Subjects

Hospitalist leaders participating in the 4‐day level I or II leadership courses of the SHM Leadership Academy were studied.

Data Collection

In the final sessions of the 2007‐2008 Leadership Academy courses, participants completed an optional behavioral contract exercise in which they partnered with a colleague and were asked to identify 4 action plans they intended to implement upon their return home. These were written down and signed. Selected demographic information was also collected.

Follow‐up surveys were sent by mail and electronically to a subset of participants with completed behavioral contracts. A 5‐point Likert scale (strongly agree . . . strongly disagree) was used to assess the extent of adherence to the goals listed in the behavioral contracts.

Data Analysis

Transcripts were analyzed using an editing organizing style, a qualitative analysis technique to find meaningful units or segments of text that both stand on their own and relate to the purpose of the study.12 With this method, the coding template emerges from the data. Two investigators independently analyzed the transcripts and created a coding template based on common themes identified among the participants. In cases of discrepant coding, the 2 investigators had discussions to reach consensus. The authors agreed on representative quotes for each theme. Triangulation was established through sharing results of the analysis with a subset of participants.

Follow‐up survey data was summarized descriptively showing proportion data.

Results

Response Rate and Participant Demographics

Out of 264 people who completed the course, 120 decided to participate in the optional behavioral contract exercise. The median age of participants was 38 years (Table 1). The majority were male (84; 70.0%), and hospitalist leaders (76; 63.3%). The median time in practice as a hospitalist was 4 years. Fewer than one‐half held an academic appointment (40; 33.3%) with most being at the rank of Assistant Professor (14; 11.7%). Most of the participants worked in a private hospital (80; 66.7%).

Demographic Characteristics of the 120 Participants of the Society of Hospital Medicine Leadership Academy 2007‐2008 Who Took Part in the Behavioral Contract Exercise
Characteristic 
  • Abbreviation: SD, standard deviation.

Age in years [median (SD)]38 (8)
Male [n (%)]84 (70.0)
Years in practice as hospitalist [median (SD)]4 (13)
Leader of hospitalist program [n (%)]76 (63.3)
Academic affiliation [n (%)]40 (33.3)
Academic rank [n (%)] 
Instructor9 (7.5)
Assistant professor14 (11.7)
Associate professor13 (10.8)
Hospital type [n (%)] 
Private80 (66.7)
University15 (12.5)
Government2 (1.7)
Veterans administration0 (0.0)
Other1 (0.1)

Results of Qualitative Analysis of Behavioral Contracts

From the analyses of the behavioral contracts, themes emerged related to ways in which participants hoped to develop and improve. The themes and the frequencies with which they were recorded in the behavioral contracts are shown in Table 2.

Total Number of Times and Numbers of Respondents Referring to the Major Themes Related to Physician Leadership Development From the Behavioral Contracts of 120 Hospitalist Leaders and Practitioners
ThemeTotal Number of Times Theme Mentioned in All Behavioral ContractsNumber of Respondents Referring to Theme [n (%)]
  • NOTE: Respondents were not queried specifically about these themes and these counts represent spontaneous and unsolicited responses in each subcategory.

Improving communication and interpersonal skills13270 (58.3)
Refinement of vision, goals, and strategic planning11562 (51.7)
Improve intrapersonal development6536 (30.0)
Enhance negotiation skills6544 (36.7)
Commit to organizational change5332 (26.7)
Understanding business drivers3828 (23.3)
Setting performance and clinical metrics3426 (21.7)
Strengthen interdepartmental relations3226 (21.7)

Improving Communication and Interpersonal Skills

A desire to improve communication and listening skills, particularly in the context of conflict resolution, was mentioned repeatedly. Heightened awareness about different personality types to allow for improved interpersonal relationships was another concept that was emphasized.

One female Instructor from an academic medical center described her intentions:

  • I will try to do a better job at assessing the behavioral tendencies of my partners and adjust my own style for more effective communication.

 

Refinement of Vision, Goals, and Strategic Planning

Physicians were committed to returning to their home institutions and embarking on initiatives to advance vision and goals of their groups within the context of strategic planning. Participants were interested in creating hospitalist‐specific mission statements, developing specific goals that take advantage of strengths and opportunities while minimizing internal weaknesses and considering external threats. They described wanting to align the interests of members of their hospitalist groups around a common goal.

A female hospitalist leader in private practice wished to:

  • Clearly define a group vision and commit to re‐evaluation on a regular basis to ensure we are on track . . . and conduct a SWOT (Strengths, Weaknesses, Opportunities, Threats) analysis to set future goals.

 

Improve Intrapersonal Development

Participants expressed desire to improve their leadership skills. Proposed goals included: (1) recognizing their weaknesses and soliciting feedback from colleagues, (2) minimizing emotional response to stress, (3) sharing their knowledge and skills for the benefit of peers, (4) delegating work more effectively to others, (5) reading suggested books on leadership, (6) serving as a positive role model and mentor, and (7) managing meetings and difficult coworkers more skillfully.

One female Assistant Professor from an academic medical center outlined:

  • I want to be able to: (1) manage up better and effectively negotiate with the administration on behalf of my group; (2) become better at leadership skills by using the tools offered at the Academy; and (3) effectively support my group members to develop their skills to become successful in their chosen niches. I will . . . improve the poor morale in my group.

 

Enhance Negotiation Skills

Many physician leaders identified negotiation principles and techniques as foundations for improvement for interactions within their own groups, as well as with the hospital administration.

A male private hospitalist leader working for 4 years as a hospitalist described plans to utilize negotiation skills within and outside the group:

  • Negotiate with my team of hospitalists to make them more compliant with the rules and regulations of the group, and negotiate an excellent contract with hospital administration. . . .

 

Commit to Organizational Change

The hospitalist respondents described their ability to influence organizational change given their unique position at the interface between patient care delivery and hospital administration. To realize organizational change, commonly cited ideas included recruitment and retention of clinically excellent practitioners, and developing standard protocols to facilitate quality improvement initiatives.

A male Instructor of Medicine listed select areas in which to become more involved:

  • Participation with the Chief Executive Officer of the company in quality improvement projects, calls to the primary care practitioners upon discharge, and the handoff process.

 

Other Themes

The final 3 themes included are: understanding business drivers; the establishment of better metrics to assess performance; and the strengthening of interdepartmental relations.

Follow‐up Data About Adherence to Plans Delineated in Behavioral Contracts

Out of 65 completed behavioral contracts from the 2007 Level I participants, 32 returned a follow‐up survey (response rate 49.3%). Figure 1 shows the extent to which respondents believed that they were compliant with their proposed plans for change or improvement. Degree of adherence was displayed as a proportion of total goals. Out of those who returned a follow‐up survey, all but 1 respondent either strongly agreed or agreed that they adhered to at least one of their goals (96.9%).

Figure 1
Self‐assessed compliance with respect to achievement of the 112 personal goals delineated in the behavioral contracts among the 32 participants who completed the follow‐up survey.

Select representative comments that illustrate the physicians' appreciation of using behavioral contracts include:

  • my approach to problems is a bit more analytical.

  • simple changes in how I approach people and interact with them has greatly improved my skills as a leader and allowed me to accomplish my goals with much less effort.

 

Discussion

Through the qualitative analysis of the behavioral contracts completed by participants of a Leadership Academy for hospitalists, we characterized the ways that hospitalist practitioners hoped to evolve as leaders. The major themes that emerged relate not only to their own growth and development but also their pledge to advance the success of the group or division. The level of commitment and impact of the behavioral contracts appear to be reinforced by an overwhelmingly positive response to adherence to personal goals one year after course participation. Communication and interpersonal development were most frequently cited in the behavioral contracts as areas for which the hospitalist leaders acknowledged a desire to grow. In a study of academic department of medicine chairs, communication skills were identified as being vital for effective leadership.3 The Chairs also recognized other proficiencies required for leading that were consistent with those outlined in the behavioral contracts: strategic planning, change management, team building, personnel management, and systems thinking. McDade et al.17 examined the effects of participation in an executive leadership program developed for female academic faculty in medical and dental schools in the United States and Canada. They noted increased self‐assessed leadership capabilities at 18 months after attending the program, across 10 leadership constructs taught in the classes. These leadership constructs resonate with the themes found in the plans for change described by our informants.

Hospitalists are assuming leadership roles in an increasing number and with greater scope; however, until now their perspectives on what skill sets are required to be successful have not been well documented. Significant time, effort, and money are invested into the development of hospitalists as leaders.4 The behavioral contract appears to be a tool acceptable to hospitalist physicians; perhaps it can be used as part annual reviews with hospitalists aspiring to be leaders.

Several limitations of the study shall be considered. First, not all participants attending the Leadership Academy opted to fill out the behavioral contracts. Second, this qualitative study is limited to those practitioners who are genuinely interested in growing as leaders as evidenced by their willingness to invest in going to the course. Third, follow‐up surveys relied on self‐assessment and it is not known whether actual realization of these goals occurred or the extent to which behavioral contracts were responsible. Further, follow‐up data were only completed by 49% percent of those targeted. However, hospitalists may be fairly resistant to being surveyed as evidenced by the fact that SHM's 2005‐2006 membership survey yielded a response rate of only 26%.18 Finally, many of the thematic goals were described by fewer than 50% of informants. However, it is important to note that the elements included on each person's behavioral contract emerged spontaneously. If subjects were specifically asked about each theme, the number of comments related to each would certainly be much higher. Qualitative analysis does not really allow us to know whether one theme is more important than another merely because it was mentioned more frequently.

Hospitalist leaders appear to be committed to professional growth and they have reported realization of goals delineated in their behavioral contracts. While varied methods are being used as part of physician leadership training programs, behavioral contracts may enhance promise for change.

Acknowledgements

The authors thank Regina Hess for assistance in data preparation and Laurence Wellikson, MD, FHM, Russell Holman, MD and Erica Pearson (all from the SHM) for data collection.

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Hospitalist Use of HCU

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Hospitalist use of hand‐carried ultrasound: Preparing for battle

Hand‐carried ultrasound (HCU) is a field technique. Originally intended for military triage, the advent of small, portable, ultrasound devices has brought ultrasound imaging to the patient's bedside to guide procedures and evaluate life‐threatening conditions. Although many recently‐trained physicians in emergency or critical care medicine now routinely use HCU to place central lines1 and tap effusions,2, 3 the capability of this technique to augment physical examination by all physicians has far greater potential value in medicine. When applied in acute critical scenarios, HCU techniques can quickly demonstrate findings regarding abdominal aortic aneurysm,4 deep vein thrombosis,5 pericardial fluid, or hemoperitoneum6 in patients with unexplained hypotension, and examine inferior vena cava collapsibility7 or brachial artery velocity variation8 to help determine the need for volume resuscitation in sepsis. In patients with unexplained dyspnea, HCU can search for ultrasound lung comet‐tail artifacts as a sign of pulmonary edema,9 or use the presence of pleural sliding to exclude pneumothorax.10 In addition, numerous less urgent applications for HCU imaging are emerging such as cardiac, lung, vascular, musculoskeletal, nerve, thyroid, gallbladder, liver, spleen, renal, testicular, and bladder imaging.

Medical or surgical subspecialties familiar with ultrasound have developed limited HCU examinations that serve specific purposes within the relatively narrow clinical indications encountered by these specialties. As a consequence, overall expertise in bedside HCU currently requires the mastery of multiple unrelated ultrasound views and diagnostic criteria. Without central leadership within this burgeoning field, HCU has found no consensus on its use or development within general medical practice. No one has yet validated a single ultrasound imaging protocol for augmenting the physical examination on all patients akin to the use of the stethoscope. This review discusses the importance of the internisthospitalist at this critical point in the early development of bedside HCU examination, focusing on the cardiopulmonary component as a prototype that has universal application across medical practice. Involvement by hospitalists in pioneering the overall technique will direct research in clinical outcome, restructure internal medicine education, change perception of the physical examination, and spur industry in device development specific for general medicine.

The role of the hospitalist as the leading in‐house diagnostician is unique in medicine, requiring breadth in medical knowledge and unprecedented communication skills in the seamless care of the most medically ill patients in the community.11 Ideally, the hospitalist quickly recognizes disease, discriminately uses consultation or expensive diagnostic testing, chooses cost‐effective therapies, and shortens length of hospital stay. Early accurate diagnosis afforded by HCU imaging has the potential to improve efficiency of medical care across a wide spectrum of clinical presentations. Although to date there are no outcome studies using a mortality endpoint, small individual studies have demonstrated that specific HCU findings improve diagnostic accuracy and relate to hospital stay length12 and readmission.13 The hospitalist position is in theory well‐suited for learning and applying bedside ultrasound, having both expert resources in the hospital to guide training and a clinical objective to reduce unnecessary hospital costs.

Saving the Bedside Examination: The Laying‐on of Ultrasound

Bedside examination is a vital component of the initial hospitalist‐patient interaction, adding objective data to the patient's history. In this era of physician surrogates and telemedicine, physical examination remains a nonnegotiable reason why physicians must appear in person at the patient's bedside to lay on hands. However, bedside cardiovascular examination skills have greatly diminished over the past decade for a variety of reasons.14 In particular, physical examination is impaired in the environment in which the hospitalist must practice. The admitting physician must oftentimes hurriedly examine the patient on the gurney in the noisy emergency department or in bed in an alarm‐filled intensive care unit (ICU) or hospital room. Ambient noise levels often preclude auscultation of acute aortic and mitral valve regurgitation, splitting of valve sounds, low diastolic rumbles, soft gallops, and fine rales. Patient positioning is limited in ventilated patients or those in respiratory or circulatory distress. Although medical education still honors the value of teaching the traditional cardiac examination, no outcome data exist to justify the application of the various maneuvers and techniques learned in medical school to contemporary, commonly encountered inpatient care scenarios. For example, few physical examination data exist on how to evaluate central venous pressures of an obese patient on the ventilator or assess the severity of aortic stenosis in the elderly hypertensive patient. Furthermore, many important cardiopulmonary abnormalities that are easily detected by ultrasound, such as pericardial fluid, well‐compensated left ventricular systolic dysfunction, small pleural effusion, and left atrial enlargement, make no characteristic sound for auscultation. The effect of undiagnosed cardiac abnormalities on the patient's immediate hospital course is unknown, but is likely related to the clinical presentation and long‐term outcome. Today, the hospitalist's suspicion of cardiovascular abnormalities is more often generated from elements in the patient's initial history, serum biomarkers, chest radiography, or electrocardiogram, and less from auscultation. Accordingly, cardiac physical examination is only adjunctively used in determining the general direction of the ensuing evaluation and when abnormal, often generates additional diagnostic testing for confirmation.

The optimal role of HCU for the internist‐hospitalist is in augmentation of bedside physical diagnosis.15, 16 Unlike x‐ray or even rapid serum biomarkers, ultrasound is a safe, immediate, noninvasive modality and has been particularly effective in delineating cardiac structure and physiology. Accurate HCU estimation of a patient's central venous pressure,17 left atrial size,18 or left ventricular ejection fraction19, 20 is of particular value in those with unexplained respiratory distress or circulatory collapse, or in those in whom referral for echocardiography or cardiac consultation is not obvious. Asymptomatic left ventricular systolic dysfunction has an estimated prevalence of 5% in adult populations,21 and its detection would have immediate implications in regard to etiology, volume management, and drug therapy. Multiple studies have shown the prognostic importance of left atrial enlargement in ischemic cardiac disease, congestive heart failure, atrial arrhythmias, and stroke.22 The inferior vena cava diameter has been related to central venous pressure and prognosis in congestive heart failure. A recent study13 using medical residents employing HCU demonstrated that persistent dilatation of the inferior vena cava at discharge related to a higher readmission rate in patients with congestive heart failure. The potential exists to follow and guide a patient's response to therapy with HCU during daily rounds. Comparative studies2325 confirm that HCU examinations are better than expert auscultation and improve overall exam accuracy when added to traditional physical exam techniques. Entering into the modern‐day emergency room with a pocket‐sized ultrasound device that provides the immediate capability of detecting left ventricular dysfunction, left atrial enlargement, pericardial effusion, or abnormalities in volume status, provides an additional sense of being prepared for battle.

Deriving Limited Ultrasound Applications: Time Well Spent

However, in order for a hospitalist to use HCU, easily applied limited imaging protocols must be derived from standard ultrasound examination techniques for each organ. For the heart, studies from our laboratory have shown that it is feasible to distill the comprehensive echocardiogram down to simple cardiac screening examinations for rapid bedside HCU use.2628 We found that a limited cardiac ultrasound study consisting of a single parasternal long‐axis (PLAX) view (Figure 1) requires only seconds to perform and can identify those patients who have significant cardiac abnormalities. In an outpatient population (n = 196) followed in an internal medicine clinic, the PLAX component of an HCU cardiac screening protocol uncovered left atrial enlargement in 4 patients and left ventricular systolic dysfunction in 4 patients that had not been suspected by the patients' primary physicians.29 In a study of 124 patients in the emergency department with suspected cardiac disease,12 abnormal cardiac findings were noted 3 times more frequently by PLAX than by clinical evaluation, and an abnormal PLAX was significantly associated with a longer hospital length of stay. In other preliminary studies using cardiologists, limited imaging has been shown to reduce costs of unnecessary echo referral.28, 3032 Cost analysis has yet to be performed in nonexpert HCU users, but benefit is likely related to the difference between the user's own accuracy with the stethoscope and the HCU device.

Figure 1
PLAX in diastole using an HCU device demonstrates depressed LVEF, left atrial enlargement, right ventricular enlargement, normal aortic and mitral valves, and no pericardial effusion. This patient should be referred for standard echocardiography to characterize these findings. Abbreviations: HCU, hand‐carried ultrasound; LVEF, left ventricular ejection fraction; PLAX, parasternal long‐axis view.

Although experts in ultrasound exist in radiology and cardiology, it is unlikely these subspecialists will spontaneously create and optimize a full‐body HCU imaging protocol for hospitalists. Similar to the use of ultrasound in emergency medicine, anesthesiology, and critical care medicine, the derivation of a bedside ultrasound exam appropriate for the in‐hospital physical examination should be developed within the specialty itself, by those acquainted with the clinical scenarios in which HCU would be deployed. For example, the question of whether the gallbladder should be routinely imaged by a quick HCU exam in the evaluation of chest pain is similar to the question of whether the Valsalva maneuver should be performed in the evaluation of every murmurboth require Bayesian knowledge of disease prevalence, exam difficulty, and test accuracy. With the collaboration of experts in ultrasound, internists can derive brief, easily learned, limited ultrasound exams for left ventricular dysfunction, left atrial enlargement, carotid atherosclerosis, interstitial lung disease, hepatosplenomegaly, cholelithiasis, hydronephrosis, renal atrophy, pleural or pericardial effusion, ascites, deep vein thrombosis, and abdominal aortic aneurysm. The discovery of these disease states has clinical value for long‐term care, even if incidental to the patient's acute presentation. The lasting implications of a more comprehensive general examination will likely differentiate the use of HCU in internal medicine practice from that of emergency medicine.

Basic Training in HCU

A significant challenge to medical education will be in physician training in HCU. Over 15 studies12, 13, 15, 1720, 22, 23, 3343 have now shown the ability of briefly trained medical students, residents, and physicians in internal medicine to perform a limited cardiovascular ultrasound examination. Not surprisingly, these studies show variable degrees of training proficiency, apparently dependent upon the complexity of the imaging protocol. In a recent pair of studies from 1 institution,42, 43 10 hospitalists were trained to perform an extensive HCU echocardiogram including 4 views, color and spectral Doppler, and interpret severity of valvular disease, ventricular function, pericardial effusion. In 345 patients already referred for formal echocardiography, which later served as the gold standard, HCU improved the hospitalists' physical examination for left ventricular dysfunction, cardiomegaly, and pericardial effusion, but not for valvular disease. Notably, despite a focused training program including didactic teaching, self‐study cases, 5 training studies, and the imaging of 35 patients with assistance as needed, image acquisition was inferior to standard examination and image interpretation was inferior to that of cardiology fellows. Such data reemphasize the fact that the scope of each body‐system imaging protocol must be narrow in order to make the learning of a full‐body HCU exam feasible and to incorporate training into time already allocated to the bedside physical examination curriculum or continuing medical education activities.

At our institution, internal medical residents are trained in bedside cardiovascular ultrasound to blend results with their auscultative findings during bedside examination. We have developed 2 cardiovascular limited ultrasound examinations (CLUEs) that can be performed in 5 minutes and have evidence‐basis for their clinical use through pilot training studies.18, 19, 29, 35 Our basic CLUE, designed for general cardiovascular examination, includes screening the carotid bulb for subclinical atherosclerosis, PLAX imaging for left atrial enlargement and systolic dysfunction of the left ventricle, and abdominal scanning for abdominal aortic aneurysm. In this imaging protocol consisting of only 4 targets, atherosclerotic risk increases from top to bottom (cephalad to caudal), making the exam easy to remember. The CLUEparasternal, lung, and subcostal (CLUE‐PLUS), designed for the urgent evaluation of unexplained dyspnea or hypotension, uses a work backward imaging format (from left ventricle to right atrium) and a single cardiac transducer for simplicity. The PLAX view screens for left ventricular systolic dysfunction and then left atrial enlargement. Next, a brief 4‐point lung exam screens for ultrasonic lung comets and pleural effusion. A subcostal view of the heart is used to evaluate right ventricular size and pericardial effusion, and finally the inferior vena cava is evaluated for central venous pressures. CLUEs are taught in bedside and didactic formats over the 3 years of residency with formal competency testing after lecture attendance, practice imaging in our echo‐vascular laboratories, participation in rounds, and completion of at least 30 supervised examinations.

Reaffirming the Role of the Internist

Although emergency44 and critical care45 medical subspecialties have begun to train their constituencies in HCU, general diagnostic techniques that have wide‐ranging application in medical illness should be the evidence‐based tools of the internist. The rejuvenation of bedside examination using HCU on multiple organ systems should be orchestrated within internal medicine and not simply evolve as an unedited collection of all subspecialty organ ultrasound examinations. Device development can then be customized and made affordable for use in general internal medicine, perhaps limiting the unnecessary production costs and training requirements for advanced Doppler or multiple transducers.

Concern has been raised about the medical and economic impact of training internists in HCU. Although training costs can be incorporated in residency or hospital‐based continuing medical education, discussions regarding reimbursement for cardiac imaging require a distinction between the brief application of ultrasound using a small device by a nontraditional user and a limited echocardiogram as defined by payers and professional societies.46 To date, no procedural code or reimbursement has yet been approved for ultrasound‐assisted physical examination using HCU devices and likely awaits outcome data. There is also concern about the possibility of errors being made by HCU use by briefly trained physicians. Patient care and cost‐savings depend on HCU accuracy, being liable both for unnecessary referrals due to false‐positive screening HCU exams and delays in diagnosis due to false‐negative examinations. However, such errors are commonplace and accepted with standard physical examination techniques and the current use of the stethoscope, both of which lack sensitivity when compared to HCU.

HCU is a disruptive technology.47 However, unlike the successful disruption that small desktop computers had on their mainframe counterparts, HCU devices appeared before the operating system of their clinical application had been formulated, making dissemination to new users nearly impossible. Furthermore, placing ultrasound transducers into the hands of nontraditional users often alienates or displaces established users of ultrasound as well as established untrained members within the profession. Competency requirements will have to be derived, preferably from studies performed within the profession for specific uses in internal medicine. Perhaps championed by hospitalists and driven by hospital‐based outcome studies, the use of HCU by internists as a physical exam technique will require advocacy by internists themselves. The alternative, having the hospitalist ask the emergency department physician for help in examining the patient, is difficult to imagine. The answer to whether the hospitalist should use HCU should be a resounding yesbased upon the benefit of earlier, more accurate examination and the value of preserving the diagnostic role of the internist at the bedside. In regard to the latter, it is a concept worth fighting for.

References
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  19. Kimura BJ,Amundson SA,Willis CL,Gilpin EA,DeMaria AN.Usefulness of a hand‐held ultrasound device for the bedside examination of left ventricular function.Am J Cardiol.2002;90(9):10381039.
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  21. Goldberg LR,Jessup M.Stage B heart failure: management of asymptomatic left ventricular systolic dysfunction.Circulation.2006;113:28512860.
  22. Douglas PS.The left atrium. A biomarker of chronic diastolic dysfunction and cardiovascular disease risk.J Am Coll Cardiol.2003;42:12061207.
  23. Spencer KT,Anderson AS,Bhargava A, et al.Physician‐performed point‐of‐care echocardiography using a laptop platform compared with physical examination in the cardiovascular patient.J Am Coll Cardiol.2001;3(8):20132018.
  24. DeCara JM,Lang RM,Spencer KT.The hand‐carried echocardiographic device as an aid to the physical examination.Echocardiography.2003;20(5):477485.
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  27. Kimura BJ,DeMaria AN.Indications for limited echocardiographic imaging: a mathematical model.J Am Soc Echocardiogr.2000;13(9):855861.
  28. Kimura BJ,Willis CL,Blanchard DG,DeMaria AN.Limited cardiac ultrasound examination for cost‐effective echo referral.J Am Soc Echocardiogr.2002;15:640646.
  29. Kimura BJ,Shaw DJ,Agan DL,Amundson SA,Ping AC,DeMaria AN.Value of a cardiovascular limited ultrasound examination using a hand‐carried ultrasound device on clinical management in an outpatient medical clinic.Am J Cardiol.2007;100(2):321325.
  30. Kimura BJ,Scott R,Willis CL,DeMaria AN.Diagnostic accuracy and cost‐effective implications of an ultrasound screening strategy in suspected mitral valve prolapse.Am J Medicine.2000;108:331333.
  31. Greaves K,Jeetly P,Hickman M, et al.The use of hand‐carried ultrasound in the hospital setting—a cost‐effective analysis.J Am Soc Echocardiogr.2005;18(6):620625.
  32. Trambaiolo P,Papetti F,Posteraro A, et al.A hand‐carried cardiac ultrasound device in the outpatient cardiology clinic reduces the need for standard echocardiography.Heart.2007;93(4):470475.
  33. Wittich CM,Montgomery SC,Neben MA, et al.Teaching cardiovascular anatomy to medical students by using a handheld ultrasound device.JAMA.2002;288(9):10621063.
  34. DeCara JM,Lang RM,Bala R,Penzotti J,Spencer KT.The use of small personal ultrasound devices by internists without formal training in echocardiography.Eur J Echocardiogr.2003;4:141147.
  35. Kimura BJ,Fowler SJ,Nguyen DT,Amundson SA,DeMaria AN.Briefly‐trained physicians can screen for early atherosclerosis at the bedside using hand‐held ultrasound.Am J Cardiol.2003;92:239240.
  36. Alexander JH,Peterson ED,Chen AY,Harding TM,Adams DB,Kisslo JA.Feasibility of point‐of‐care echocardiography by internal medicine house staff.Am Heart J.2004;147(3):476481.
  37. Kirkpatrick JN,Davis A,DeCara JM, et al.Hand‐carried cardiac ultrasound as a tool to screen for important cardiovascular disease in an underserved minority health care clinic.J Am Soc Echocardiogr.2004;17(5):339403.
  38. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  39. DeCara JM,Kirkpatrick JN,Spencer KT, et al.Use of hand‐carried ultrasound devices to augment the accuracy of medical student bedside cardiac diagnoses.J Am Soc Echocardiogr.2005;18(3):257263.
  40. Vignon P,Dugard A,Abraham J, et al.Focused training for goal‐oriented hand‐held echocardiography performed by noncardiologist residents in the intensive care unit.Intensive Care Med.2007;33(10):17951799.
  41. Croft LB,Duvall WL,Goldman ME.A pilot study of the clinical impact of hand‐carried cardiac ultrasound in the medical clinic.Echocardiography.2006;23(6):439446.
  42. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  43. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalist: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  44. Lapostolle F,Petrovic T,Lenoir G, et al.Usefulness of hand‐held ultrasound devices in out‐of‐hospital diagnosis performed by emergency physicians.Am J Emerg Med.2006;24(2):237242.
  45. Manasia AR,Nagaraj HM,Kodali RB, et al.Feasibility and potential clinical utility of goal‐directed transthoracic echocardiography performed by noncardiologist intensivists using a small hand‐carried device (SonoHeart) in critically ill patients.J Cardiothorac Vasc Anesth.2005;19(2):155159.
  46. Seward JB,Douglas PS,Erbel R, et al.Hand‐carried cardiac ultrasound (HCU) device: recommendations regarding new technology. A report from the Echocardiography Task Force on New Technology of the Nomenclature and Standards Committee of the American Society of Echocardiography.J Am Soc of Echocardiogr.2002;15(4):369373.
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Hand‐carried ultrasound (HCU) is a field technique. Originally intended for military triage, the advent of small, portable, ultrasound devices has brought ultrasound imaging to the patient's bedside to guide procedures and evaluate life‐threatening conditions. Although many recently‐trained physicians in emergency or critical care medicine now routinely use HCU to place central lines1 and tap effusions,2, 3 the capability of this technique to augment physical examination by all physicians has far greater potential value in medicine. When applied in acute critical scenarios, HCU techniques can quickly demonstrate findings regarding abdominal aortic aneurysm,4 deep vein thrombosis,5 pericardial fluid, or hemoperitoneum6 in patients with unexplained hypotension, and examine inferior vena cava collapsibility7 or brachial artery velocity variation8 to help determine the need for volume resuscitation in sepsis. In patients with unexplained dyspnea, HCU can search for ultrasound lung comet‐tail artifacts as a sign of pulmonary edema,9 or use the presence of pleural sliding to exclude pneumothorax.10 In addition, numerous less urgent applications for HCU imaging are emerging such as cardiac, lung, vascular, musculoskeletal, nerve, thyroid, gallbladder, liver, spleen, renal, testicular, and bladder imaging.

Medical or surgical subspecialties familiar with ultrasound have developed limited HCU examinations that serve specific purposes within the relatively narrow clinical indications encountered by these specialties. As a consequence, overall expertise in bedside HCU currently requires the mastery of multiple unrelated ultrasound views and diagnostic criteria. Without central leadership within this burgeoning field, HCU has found no consensus on its use or development within general medical practice. No one has yet validated a single ultrasound imaging protocol for augmenting the physical examination on all patients akin to the use of the stethoscope. This review discusses the importance of the internisthospitalist at this critical point in the early development of bedside HCU examination, focusing on the cardiopulmonary component as a prototype that has universal application across medical practice. Involvement by hospitalists in pioneering the overall technique will direct research in clinical outcome, restructure internal medicine education, change perception of the physical examination, and spur industry in device development specific for general medicine.

The role of the hospitalist as the leading in‐house diagnostician is unique in medicine, requiring breadth in medical knowledge and unprecedented communication skills in the seamless care of the most medically ill patients in the community.11 Ideally, the hospitalist quickly recognizes disease, discriminately uses consultation or expensive diagnostic testing, chooses cost‐effective therapies, and shortens length of hospital stay. Early accurate diagnosis afforded by HCU imaging has the potential to improve efficiency of medical care across a wide spectrum of clinical presentations. Although to date there are no outcome studies using a mortality endpoint, small individual studies have demonstrated that specific HCU findings improve diagnostic accuracy and relate to hospital stay length12 and readmission.13 The hospitalist position is in theory well‐suited for learning and applying bedside ultrasound, having both expert resources in the hospital to guide training and a clinical objective to reduce unnecessary hospital costs.

Saving the Bedside Examination: The Laying‐on of Ultrasound

Bedside examination is a vital component of the initial hospitalist‐patient interaction, adding objective data to the patient's history. In this era of physician surrogates and telemedicine, physical examination remains a nonnegotiable reason why physicians must appear in person at the patient's bedside to lay on hands. However, bedside cardiovascular examination skills have greatly diminished over the past decade for a variety of reasons.14 In particular, physical examination is impaired in the environment in which the hospitalist must practice. The admitting physician must oftentimes hurriedly examine the patient on the gurney in the noisy emergency department or in bed in an alarm‐filled intensive care unit (ICU) or hospital room. Ambient noise levels often preclude auscultation of acute aortic and mitral valve regurgitation, splitting of valve sounds, low diastolic rumbles, soft gallops, and fine rales. Patient positioning is limited in ventilated patients or those in respiratory or circulatory distress. Although medical education still honors the value of teaching the traditional cardiac examination, no outcome data exist to justify the application of the various maneuvers and techniques learned in medical school to contemporary, commonly encountered inpatient care scenarios. For example, few physical examination data exist on how to evaluate central venous pressures of an obese patient on the ventilator or assess the severity of aortic stenosis in the elderly hypertensive patient. Furthermore, many important cardiopulmonary abnormalities that are easily detected by ultrasound, such as pericardial fluid, well‐compensated left ventricular systolic dysfunction, small pleural effusion, and left atrial enlargement, make no characteristic sound for auscultation. The effect of undiagnosed cardiac abnormalities on the patient's immediate hospital course is unknown, but is likely related to the clinical presentation and long‐term outcome. Today, the hospitalist's suspicion of cardiovascular abnormalities is more often generated from elements in the patient's initial history, serum biomarkers, chest radiography, or electrocardiogram, and less from auscultation. Accordingly, cardiac physical examination is only adjunctively used in determining the general direction of the ensuing evaluation and when abnormal, often generates additional diagnostic testing for confirmation.

The optimal role of HCU for the internist‐hospitalist is in augmentation of bedside physical diagnosis.15, 16 Unlike x‐ray or even rapid serum biomarkers, ultrasound is a safe, immediate, noninvasive modality and has been particularly effective in delineating cardiac structure and physiology. Accurate HCU estimation of a patient's central venous pressure,17 left atrial size,18 or left ventricular ejection fraction19, 20 is of particular value in those with unexplained respiratory distress or circulatory collapse, or in those in whom referral for echocardiography or cardiac consultation is not obvious. Asymptomatic left ventricular systolic dysfunction has an estimated prevalence of 5% in adult populations,21 and its detection would have immediate implications in regard to etiology, volume management, and drug therapy. Multiple studies have shown the prognostic importance of left atrial enlargement in ischemic cardiac disease, congestive heart failure, atrial arrhythmias, and stroke.22 The inferior vena cava diameter has been related to central venous pressure and prognosis in congestive heart failure. A recent study13 using medical residents employing HCU demonstrated that persistent dilatation of the inferior vena cava at discharge related to a higher readmission rate in patients with congestive heart failure. The potential exists to follow and guide a patient's response to therapy with HCU during daily rounds. Comparative studies2325 confirm that HCU examinations are better than expert auscultation and improve overall exam accuracy when added to traditional physical exam techniques. Entering into the modern‐day emergency room with a pocket‐sized ultrasound device that provides the immediate capability of detecting left ventricular dysfunction, left atrial enlargement, pericardial effusion, or abnormalities in volume status, provides an additional sense of being prepared for battle.

Deriving Limited Ultrasound Applications: Time Well Spent

However, in order for a hospitalist to use HCU, easily applied limited imaging protocols must be derived from standard ultrasound examination techniques for each organ. For the heart, studies from our laboratory have shown that it is feasible to distill the comprehensive echocardiogram down to simple cardiac screening examinations for rapid bedside HCU use.2628 We found that a limited cardiac ultrasound study consisting of a single parasternal long‐axis (PLAX) view (Figure 1) requires only seconds to perform and can identify those patients who have significant cardiac abnormalities. In an outpatient population (n = 196) followed in an internal medicine clinic, the PLAX component of an HCU cardiac screening protocol uncovered left atrial enlargement in 4 patients and left ventricular systolic dysfunction in 4 patients that had not been suspected by the patients' primary physicians.29 In a study of 124 patients in the emergency department with suspected cardiac disease,12 abnormal cardiac findings were noted 3 times more frequently by PLAX than by clinical evaluation, and an abnormal PLAX was significantly associated with a longer hospital length of stay. In other preliminary studies using cardiologists, limited imaging has been shown to reduce costs of unnecessary echo referral.28, 3032 Cost analysis has yet to be performed in nonexpert HCU users, but benefit is likely related to the difference between the user's own accuracy with the stethoscope and the HCU device.

Figure 1
PLAX in diastole using an HCU device demonstrates depressed LVEF, left atrial enlargement, right ventricular enlargement, normal aortic and mitral valves, and no pericardial effusion. This patient should be referred for standard echocardiography to characterize these findings. Abbreviations: HCU, hand‐carried ultrasound; LVEF, left ventricular ejection fraction; PLAX, parasternal long‐axis view.

Although experts in ultrasound exist in radiology and cardiology, it is unlikely these subspecialists will spontaneously create and optimize a full‐body HCU imaging protocol for hospitalists. Similar to the use of ultrasound in emergency medicine, anesthesiology, and critical care medicine, the derivation of a bedside ultrasound exam appropriate for the in‐hospital physical examination should be developed within the specialty itself, by those acquainted with the clinical scenarios in which HCU would be deployed. For example, the question of whether the gallbladder should be routinely imaged by a quick HCU exam in the evaluation of chest pain is similar to the question of whether the Valsalva maneuver should be performed in the evaluation of every murmurboth require Bayesian knowledge of disease prevalence, exam difficulty, and test accuracy. With the collaboration of experts in ultrasound, internists can derive brief, easily learned, limited ultrasound exams for left ventricular dysfunction, left atrial enlargement, carotid atherosclerosis, interstitial lung disease, hepatosplenomegaly, cholelithiasis, hydronephrosis, renal atrophy, pleural or pericardial effusion, ascites, deep vein thrombosis, and abdominal aortic aneurysm. The discovery of these disease states has clinical value for long‐term care, even if incidental to the patient's acute presentation. The lasting implications of a more comprehensive general examination will likely differentiate the use of HCU in internal medicine practice from that of emergency medicine.

Basic Training in HCU

A significant challenge to medical education will be in physician training in HCU. Over 15 studies12, 13, 15, 1720, 22, 23, 3343 have now shown the ability of briefly trained medical students, residents, and physicians in internal medicine to perform a limited cardiovascular ultrasound examination. Not surprisingly, these studies show variable degrees of training proficiency, apparently dependent upon the complexity of the imaging protocol. In a recent pair of studies from 1 institution,42, 43 10 hospitalists were trained to perform an extensive HCU echocardiogram including 4 views, color and spectral Doppler, and interpret severity of valvular disease, ventricular function, pericardial effusion. In 345 patients already referred for formal echocardiography, which later served as the gold standard, HCU improved the hospitalists' physical examination for left ventricular dysfunction, cardiomegaly, and pericardial effusion, but not for valvular disease. Notably, despite a focused training program including didactic teaching, self‐study cases, 5 training studies, and the imaging of 35 patients with assistance as needed, image acquisition was inferior to standard examination and image interpretation was inferior to that of cardiology fellows. Such data reemphasize the fact that the scope of each body‐system imaging protocol must be narrow in order to make the learning of a full‐body HCU exam feasible and to incorporate training into time already allocated to the bedside physical examination curriculum or continuing medical education activities.

At our institution, internal medical residents are trained in bedside cardiovascular ultrasound to blend results with their auscultative findings during bedside examination. We have developed 2 cardiovascular limited ultrasound examinations (CLUEs) that can be performed in 5 minutes and have evidence‐basis for their clinical use through pilot training studies.18, 19, 29, 35 Our basic CLUE, designed for general cardiovascular examination, includes screening the carotid bulb for subclinical atherosclerosis, PLAX imaging for left atrial enlargement and systolic dysfunction of the left ventricle, and abdominal scanning for abdominal aortic aneurysm. In this imaging protocol consisting of only 4 targets, atherosclerotic risk increases from top to bottom (cephalad to caudal), making the exam easy to remember. The CLUEparasternal, lung, and subcostal (CLUE‐PLUS), designed for the urgent evaluation of unexplained dyspnea or hypotension, uses a work backward imaging format (from left ventricle to right atrium) and a single cardiac transducer for simplicity. The PLAX view screens for left ventricular systolic dysfunction and then left atrial enlargement. Next, a brief 4‐point lung exam screens for ultrasonic lung comets and pleural effusion. A subcostal view of the heart is used to evaluate right ventricular size and pericardial effusion, and finally the inferior vena cava is evaluated for central venous pressures. CLUEs are taught in bedside and didactic formats over the 3 years of residency with formal competency testing after lecture attendance, practice imaging in our echo‐vascular laboratories, participation in rounds, and completion of at least 30 supervised examinations.

Reaffirming the Role of the Internist

Although emergency44 and critical care45 medical subspecialties have begun to train their constituencies in HCU, general diagnostic techniques that have wide‐ranging application in medical illness should be the evidence‐based tools of the internist. The rejuvenation of bedside examination using HCU on multiple organ systems should be orchestrated within internal medicine and not simply evolve as an unedited collection of all subspecialty organ ultrasound examinations. Device development can then be customized and made affordable for use in general internal medicine, perhaps limiting the unnecessary production costs and training requirements for advanced Doppler or multiple transducers.

Concern has been raised about the medical and economic impact of training internists in HCU. Although training costs can be incorporated in residency or hospital‐based continuing medical education, discussions regarding reimbursement for cardiac imaging require a distinction between the brief application of ultrasound using a small device by a nontraditional user and a limited echocardiogram as defined by payers and professional societies.46 To date, no procedural code or reimbursement has yet been approved for ultrasound‐assisted physical examination using HCU devices and likely awaits outcome data. There is also concern about the possibility of errors being made by HCU use by briefly trained physicians. Patient care and cost‐savings depend on HCU accuracy, being liable both for unnecessary referrals due to false‐positive screening HCU exams and delays in diagnosis due to false‐negative examinations. However, such errors are commonplace and accepted with standard physical examination techniques and the current use of the stethoscope, both of which lack sensitivity when compared to HCU.

HCU is a disruptive technology.47 However, unlike the successful disruption that small desktop computers had on their mainframe counterparts, HCU devices appeared before the operating system of their clinical application had been formulated, making dissemination to new users nearly impossible. Furthermore, placing ultrasound transducers into the hands of nontraditional users often alienates or displaces established users of ultrasound as well as established untrained members within the profession. Competency requirements will have to be derived, preferably from studies performed within the profession for specific uses in internal medicine. Perhaps championed by hospitalists and driven by hospital‐based outcome studies, the use of HCU by internists as a physical exam technique will require advocacy by internists themselves. The alternative, having the hospitalist ask the emergency department physician for help in examining the patient, is difficult to imagine. The answer to whether the hospitalist should use HCU should be a resounding yesbased upon the benefit of earlier, more accurate examination and the value of preserving the diagnostic role of the internist at the bedside. In regard to the latter, it is a concept worth fighting for.

Hand‐carried ultrasound (HCU) is a field technique. Originally intended for military triage, the advent of small, portable, ultrasound devices has brought ultrasound imaging to the patient's bedside to guide procedures and evaluate life‐threatening conditions. Although many recently‐trained physicians in emergency or critical care medicine now routinely use HCU to place central lines1 and tap effusions,2, 3 the capability of this technique to augment physical examination by all physicians has far greater potential value in medicine. When applied in acute critical scenarios, HCU techniques can quickly demonstrate findings regarding abdominal aortic aneurysm,4 deep vein thrombosis,5 pericardial fluid, or hemoperitoneum6 in patients with unexplained hypotension, and examine inferior vena cava collapsibility7 or brachial artery velocity variation8 to help determine the need for volume resuscitation in sepsis. In patients with unexplained dyspnea, HCU can search for ultrasound lung comet‐tail artifacts as a sign of pulmonary edema,9 or use the presence of pleural sliding to exclude pneumothorax.10 In addition, numerous less urgent applications for HCU imaging are emerging such as cardiac, lung, vascular, musculoskeletal, nerve, thyroid, gallbladder, liver, spleen, renal, testicular, and bladder imaging.

Medical or surgical subspecialties familiar with ultrasound have developed limited HCU examinations that serve specific purposes within the relatively narrow clinical indications encountered by these specialties. As a consequence, overall expertise in bedside HCU currently requires the mastery of multiple unrelated ultrasound views and diagnostic criteria. Without central leadership within this burgeoning field, HCU has found no consensus on its use or development within general medical practice. No one has yet validated a single ultrasound imaging protocol for augmenting the physical examination on all patients akin to the use of the stethoscope. This review discusses the importance of the internisthospitalist at this critical point in the early development of bedside HCU examination, focusing on the cardiopulmonary component as a prototype that has universal application across medical practice. Involvement by hospitalists in pioneering the overall technique will direct research in clinical outcome, restructure internal medicine education, change perception of the physical examination, and spur industry in device development specific for general medicine.

The role of the hospitalist as the leading in‐house diagnostician is unique in medicine, requiring breadth in medical knowledge and unprecedented communication skills in the seamless care of the most medically ill patients in the community.11 Ideally, the hospitalist quickly recognizes disease, discriminately uses consultation or expensive diagnostic testing, chooses cost‐effective therapies, and shortens length of hospital stay. Early accurate diagnosis afforded by HCU imaging has the potential to improve efficiency of medical care across a wide spectrum of clinical presentations. Although to date there are no outcome studies using a mortality endpoint, small individual studies have demonstrated that specific HCU findings improve diagnostic accuracy and relate to hospital stay length12 and readmission.13 The hospitalist position is in theory well‐suited for learning and applying bedside ultrasound, having both expert resources in the hospital to guide training and a clinical objective to reduce unnecessary hospital costs.

Saving the Bedside Examination: The Laying‐on of Ultrasound

Bedside examination is a vital component of the initial hospitalist‐patient interaction, adding objective data to the patient's history. In this era of physician surrogates and telemedicine, physical examination remains a nonnegotiable reason why physicians must appear in person at the patient's bedside to lay on hands. However, bedside cardiovascular examination skills have greatly diminished over the past decade for a variety of reasons.14 In particular, physical examination is impaired in the environment in which the hospitalist must practice. The admitting physician must oftentimes hurriedly examine the patient on the gurney in the noisy emergency department or in bed in an alarm‐filled intensive care unit (ICU) or hospital room. Ambient noise levels often preclude auscultation of acute aortic and mitral valve regurgitation, splitting of valve sounds, low diastolic rumbles, soft gallops, and fine rales. Patient positioning is limited in ventilated patients or those in respiratory or circulatory distress. Although medical education still honors the value of teaching the traditional cardiac examination, no outcome data exist to justify the application of the various maneuvers and techniques learned in medical school to contemporary, commonly encountered inpatient care scenarios. For example, few physical examination data exist on how to evaluate central venous pressures of an obese patient on the ventilator or assess the severity of aortic stenosis in the elderly hypertensive patient. Furthermore, many important cardiopulmonary abnormalities that are easily detected by ultrasound, such as pericardial fluid, well‐compensated left ventricular systolic dysfunction, small pleural effusion, and left atrial enlargement, make no characteristic sound for auscultation. The effect of undiagnosed cardiac abnormalities on the patient's immediate hospital course is unknown, but is likely related to the clinical presentation and long‐term outcome. Today, the hospitalist's suspicion of cardiovascular abnormalities is more often generated from elements in the patient's initial history, serum biomarkers, chest radiography, or electrocardiogram, and less from auscultation. Accordingly, cardiac physical examination is only adjunctively used in determining the general direction of the ensuing evaluation and when abnormal, often generates additional diagnostic testing for confirmation.

The optimal role of HCU for the internist‐hospitalist is in augmentation of bedside physical diagnosis.15, 16 Unlike x‐ray or even rapid serum biomarkers, ultrasound is a safe, immediate, noninvasive modality and has been particularly effective in delineating cardiac structure and physiology. Accurate HCU estimation of a patient's central venous pressure,17 left atrial size,18 or left ventricular ejection fraction19, 20 is of particular value in those with unexplained respiratory distress or circulatory collapse, or in those in whom referral for echocardiography or cardiac consultation is not obvious. Asymptomatic left ventricular systolic dysfunction has an estimated prevalence of 5% in adult populations,21 and its detection would have immediate implications in regard to etiology, volume management, and drug therapy. Multiple studies have shown the prognostic importance of left atrial enlargement in ischemic cardiac disease, congestive heart failure, atrial arrhythmias, and stroke.22 The inferior vena cava diameter has been related to central venous pressure and prognosis in congestive heart failure. A recent study13 using medical residents employing HCU demonstrated that persistent dilatation of the inferior vena cava at discharge related to a higher readmission rate in patients with congestive heart failure. The potential exists to follow and guide a patient's response to therapy with HCU during daily rounds. Comparative studies2325 confirm that HCU examinations are better than expert auscultation and improve overall exam accuracy when added to traditional physical exam techniques. Entering into the modern‐day emergency room with a pocket‐sized ultrasound device that provides the immediate capability of detecting left ventricular dysfunction, left atrial enlargement, pericardial effusion, or abnormalities in volume status, provides an additional sense of being prepared for battle.

Deriving Limited Ultrasound Applications: Time Well Spent

However, in order for a hospitalist to use HCU, easily applied limited imaging protocols must be derived from standard ultrasound examination techniques for each organ. For the heart, studies from our laboratory have shown that it is feasible to distill the comprehensive echocardiogram down to simple cardiac screening examinations for rapid bedside HCU use.2628 We found that a limited cardiac ultrasound study consisting of a single parasternal long‐axis (PLAX) view (Figure 1) requires only seconds to perform and can identify those patients who have significant cardiac abnormalities. In an outpatient population (n = 196) followed in an internal medicine clinic, the PLAX component of an HCU cardiac screening protocol uncovered left atrial enlargement in 4 patients and left ventricular systolic dysfunction in 4 patients that had not been suspected by the patients' primary physicians.29 In a study of 124 patients in the emergency department with suspected cardiac disease,12 abnormal cardiac findings were noted 3 times more frequently by PLAX than by clinical evaluation, and an abnormal PLAX was significantly associated with a longer hospital length of stay. In other preliminary studies using cardiologists, limited imaging has been shown to reduce costs of unnecessary echo referral.28, 3032 Cost analysis has yet to be performed in nonexpert HCU users, but benefit is likely related to the difference between the user's own accuracy with the stethoscope and the HCU device.

Figure 1
PLAX in diastole using an HCU device demonstrates depressed LVEF, left atrial enlargement, right ventricular enlargement, normal aortic and mitral valves, and no pericardial effusion. This patient should be referred for standard echocardiography to characterize these findings. Abbreviations: HCU, hand‐carried ultrasound; LVEF, left ventricular ejection fraction; PLAX, parasternal long‐axis view.

Although experts in ultrasound exist in radiology and cardiology, it is unlikely these subspecialists will spontaneously create and optimize a full‐body HCU imaging protocol for hospitalists. Similar to the use of ultrasound in emergency medicine, anesthesiology, and critical care medicine, the derivation of a bedside ultrasound exam appropriate for the in‐hospital physical examination should be developed within the specialty itself, by those acquainted with the clinical scenarios in which HCU would be deployed. For example, the question of whether the gallbladder should be routinely imaged by a quick HCU exam in the evaluation of chest pain is similar to the question of whether the Valsalva maneuver should be performed in the evaluation of every murmurboth require Bayesian knowledge of disease prevalence, exam difficulty, and test accuracy. With the collaboration of experts in ultrasound, internists can derive brief, easily learned, limited ultrasound exams for left ventricular dysfunction, left atrial enlargement, carotid atherosclerosis, interstitial lung disease, hepatosplenomegaly, cholelithiasis, hydronephrosis, renal atrophy, pleural or pericardial effusion, ascites, deep vein thrombosis, and abdominal aortic aneurysm. The discovery of these disease states has clinical value for long‐term care, even if incidental to the patient's acute presentation. The lasting implications of a more comprehensive general examination will likely differentiate the use of HCU in internal medicine practice from that of emergency medicine.

Basic Training in HCU

A significant challenge to medical education will be in physician training in HCU. Over 15 studies12, 13, 15, 1720, 22, 23, 3343 have now shown the ability of briefly trained medical students, residents, and physicians in internal medicine to perform a limited cardiovascular ultrasound examination. Not surprisingly, these studies show variable degrees of training proficiency, apparently dependent upon the complexity of the imaging protocol. In a recent pair of studies from 1 institution,42, 43 10 hospitalists were trained to perform an extensive HCU echocardiogram including 4 views, color and spectral Doppler, and interpret severity of valvular disease, ventricular function, pericardial effusion. In 345 patients already referred for formal echocardiography, which later served as the gold standard, HCU improved the hospitalists' physical examination for left ventricular dysfunction, cardiomegaly, and pericardial effusion, but not for valvular disease. Notably, despite a focused training program including didactic teaching, self‐study cases, 5 training studies, and the imaging of 35 patients with assistance as needed, image acquisition was inferior to standard examination and image interpretation was inferior to that of cardiology fellows. Such data reemphasize the fact that the scope of each body‐system imaging protocol must be narrow in order to make the learning of a full‐body HCU exam feasible and to incorporate training into time already allocated to the bedside physical examination curriculum or continuing medical education activities.

At our institution, internal medical residents are trained in bedside cardiovascular ultrasound to blend results with their auscultative findings during bedside examination. We have developed 2 cardiovascular limited ultrasound examinations (CLUEs) that can be performed in 5 minutes and have evidence‐basis for their clinical use through pilot training studies.18, 19, 29, 35 Our basic CLUE, designed for general cardiovascular examination, includes screening the carotid bulb for subclinical atherosclerosis, PLAX imaging for left atrial enlargement and systolic dysfunction of the left ventricle, and abdominal scanning for abdominal aortic aneurysm. In this imaging protocol consisting of only 4 targets, atherosclerotic risk increases from top to bottom (cephalad to caudal), making the exam easy to remember. The CLUEparasternal, lung, and subcostal (CLUE‐PLUS), designed for the urgent evaluation of unexplained dyspnea or hypotension, uses a work backward imaging format (from left ventricle to right atrium) and a single cardiac transducer for simplicity. The PLAX view screens for left ventricular systolic dysfunction and then left atrial enlargement. Next, a brief 4‐point lung exam screens for ultrasonic lung comets and pleural effusion. A subcostal view of the heart is used to evaluate right ventricular size and pericardial effusion, and finally the inferior vena cava is evaluated for central venous pressures. CLUEs are taught in bedside and didactic formats over the 3 years of residency with formal competency testing after lecture attendance, practice imaging in our echo‐vascular laboratories, participation in rounds, and completion of at least 30 supervised examinations.

Reaffirming the Role of the Internist

Although emergency44 and critical care45 medical subspecialties have begun to train their constituencies in HCU, general diagnostic techniques that have wide‐ranging application in medical illness should be the evidence‐based tools of the internist. The rejuvenation of bedside examination using HCU on multiple organ systems should be orchestrated within internal medicine and not simply evolve as an unedited collection of all subspecialty organ ultrasound examinations. Device development can then be customized and made affordable for use in general internal medicine, perhaps limiting the unnecessary production costs and training requirements for advanced Doppler or multiple transducers.

Concern has been raised about the medical and economic impact of training internists in HCU. Although training costs can be incorporated in residency or hospital‐based continuing medical education, discussions regarding reimbursement for cardiac imaging require a distinction between the brief application of ultrasound using a small device by a nontraditional user and a limited echocardiogram as defined by payers and professional societies.46 To date, no procedural code or reimbursement has yet been approved for ultrasound‐assisted physical examination using HCU devices and likely awaits outcome data. There is also concern about the possibility of errors being made by HCU use by briefly trained physicians. Patient care and cost‐savings depend on HCU accuracy, being liable both for unnecessary referrals due to false‐positive screening HCU exams and delays in diagnosis due to false‐negative examinations. However, such errors are commonplace and accepted with standard physical examination techniques and the current use of the stethoscope, both of which lack sensitivity when compared to HCU.

HCU is a disruptive technology.47 However, unlike the successful disruption that small desktop computers had on their mainframe counterparts, HCU devices appeared before the operating system of their clinical application had been formulated, making dissemination to new users nearly impossible. Furthermore, placing ultrasound transducers into the hands of nontraditional users often alienates or displaces established users of ultrasound as well as established untrained members within the profession. Competency requirements will have to be derived, preferably from studies performed within the profession for specific uses in internal medicine. Perhaps championed by hospitalists and driven by hospital‐based outcome studies, the use of HCU by internists as a physical exam technique will require advocacy by internists themselves. The alternative, having the hospitalist ask the emergency department physician for help in examining the patient, is difficult to imagine. The answer to whether the hospitalist should use HCU should be a resounding yesbased upon the benefit of earlier, more accurate examination and the value of preserving the diagnostic role of the internist at the bedside. In regard to the latter, it is a concept worth fighting for.

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  37. Kirkpatrick JN,Davis A,DeCara JM, et al.Hand‐carried cardiac ultrasound as a tool to screen for important cardiovascular disease in an underserved minority health care clinic.J Am Soc Echocardiogr.2004;17(5):339403.
  38. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  39. DeCara JM,Kirkpatrick JN,Spencer KT, et al.Use of hand‐carried ultrasound devices to augment the accuracy of medical student bedside cardiac diagnoses.J Am Soc Echocardiogr.2005;18(3):257263.
  40. Vignon P,Dugard A,Abraham J, et al.Focused training for goal‐oriented hand‐held echocardiography performed by noncardiologist residents in the intensive care unit.Intensive Care Med.2007;33(10):17951799.
  41. Croft LB,Duvall WL,Goldman ME.A pilot study of the clinical impact of hand‐carried cardiac ultrasound in the medical clinic.Echocardiography.2006;23(6):439446.
  42. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  43. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalist: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  44. Lapostolle F,Petrovic T,Lenoir G, et al.Usefulness of hand‐held ultrasound devices in out‐of‐hospital diagnosis performed by emergency physicians.Am J Emerg Med.2006;24(2):237242.
  45. Manasia AR,Nagaraj HM,Kodali RB, et al.Feasibility and potential clinical utility of goal‐directed transthoracic echocardiography performed by noncardiologist intensivists using a small hand‐carried device (SonoHeart) in critically ill patients.J Cardiothorac Vasc Anesth.2005;19(2):155159.
  46. Seward JB,Douglas PS,Erbel R, et al.Hand‐carried cardiac ultrasound (HCU) device: recommendations regarding new technology. A report from the Echocardiography Task Force on New Technology of the Nomenclature and Standards Committee of the American Society of Echocardiography.J Am Soc of Echocardiogr.2002;15(4):369373.
  47. Christensen CM,Bohmer R,Kenagy J.Will disruptive innovations cure health care?Harv Bus Rev.2000;78(5):102112,199.
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  38. Hellmann DB,Whiting‐O'Keefe Q,Shapiro EP,Martin LD,Martire C,Ziegelstein RC.The rate at which residents learn to use hand‐held echocardiography at the bedside.Am J Med.2005;118(9):10101018.
  39. DeCara JM,Kirkpatrick JN,Spencer KT, et al.Use of hand‐carried ultrasound devices to augment the accuracy of medical student bedside cardiac diagnoses.J Am Soc Echocardiogr.2005;18(3):257263.
  40. Vignon P,Dugard A,Abraham J, et al.Focused training for goal‐oriented hand‐held echocardiography performed by noncardiologist residents in the intensive care unit.Intensive Care Med.2007;33(10):17951799.
  41. Croft LB,Duvall WL,Goldman ME.A pilot study of the clinical impact of hand‐carried cardiac ultrasound in the medical clinic.Echocardiography.2006;23(6):439446.
  42. Martin LD,Howell EE,Ziegelstein RC,Martire C,Shapiro EP,Hellmann DB.Hospitalist performance of cardiac hand‐carried ultrasound after focused training.Am J Med.2007;120(11):10001004.
  43. Martin LD,Howell EE,Ziegelstein RC, et al.Hand‐carried ultrasound performed by hospitalist: does it improve the cardiac physical examination?Am J Med.2009;122(1):3541.
  44. Lapostolle F,Petrovic T,Lenoir G, et al.Usefulness of hand‐held ultrasound devices in out‐of‐hospital diagnosis performed by emergency physicians.Am J Emerg Med.2006;24(2):237242.
  45. Manasia AR,Nagaraj HM,Kodali RB, et al.Feasibility and potential clinical utility of goal‐directed transthoracic echocardiography performed by noncardiologist intensivists using a small hand‐carried device (SonoHeart) in critically ill patients.J Cardiothorac Vasc Anesth.2005;19(2):155159.
  46. Seward JB,Douglas PS,Erbel R, et al.Hand‐carried cardiac ultrasound (HCU) device: recommendations regarding new technology. A report from the Echocardiography Task Force on New Technology of the Nomenclature and Standards Committee of the American Society of Echocardiography.J Am Soc of Echocardiogr.2002;15(4):369373.
  47. Christensen CM,Bohmer R,Kenagy J.Will disruptive innovations cure health care?Harv Bus Rev.2000;78(5):102112,199.
Issue
Journal of Hospital Medicine - 5(3)
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Journal of Hospital Medicine - 5(3)
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163-167
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163-167
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Hospitalist use of hand‐carried ultrasound: Preparing for battle
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Hospitalist use of hand‐carried ultrasound: Preparing for battle
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hand‐carried ultrasound, hospitalist, physical diagnosis, physical examination
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hand‐carried ultrasound, hospitalist, physical diagnosis, physical examination
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University of California, Medical Director, Cardiovascular Ultrasound, Scripps Mercy Hospital, 4060 Fourth Ave #206, San Diego, CA
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