Clinical question: What is the epidemiology of bacteremia in one-week to three-month-old infants?

Background: Large studies of bacteremia in infants <90 days of age were largely performed before the era of routine prenatal screening and prophylaxis for Group B Streptococcus (GBS). Additionally, these studies have focused on febrile infants, which might not allow for characterization of the incidence of bacteremia when nonfebrile infants are considered.

Study design: Retrospective review.

Setting: Large HMO database.

Synopsis: Of 160,818 full-term infants born at Kaiser Permanente Northern California from 2005 to 2009, 4,255 blood cultures were obtained from 4,122 infants in outpatient clinics, the ED, or in an inpatient setting within 24 hours of birth. Preterm infants <37 weeks, infants with underlying medical conditions, and infants with cultures drawn within three days of an original culture were excluded.

A total of 8% of the blood cultures were positive, with 2.2% deemed true positives and 5.8% due to contaminants. The incidence rate of true bacteremia was 0.57 per 1,000 full-term births, with gram-negative organisms (predominantly Escherichia coli) representing the majority (63%) of pathogens, followed by GBS (21%), Staphylococcus aureus (8%), and Streptococcus pneumoniae (3%). There were no cases of Listeria monocytogenes or Neisseria meningitidis bacteremia, and there was one case of enterococcal bacteremia. Fever was absent in 7% of cases.

The authors conclude that ampicillin may no longer be necessary for empiric antibiotic coverage in this age group given that 36% of pathogens were resistant to ampicillin, there were no cases of Listeria, and there was only one case of enterococcus. However, these recommendations should be considered in light of the specific study setting, and might not be applicable to all areas.

Bottom line: E. coli, GBS, and S. aureus, in that order, are the most common causes of bacteremia in infants aged one week to three months.

Citation: Greenhow TL, Hung YY, Herz AM. Changing epidemiology of bacteremia in infants aged 1 week to 3 months. Pediatrics. 2012;129(3):e590-e596.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Clinical question: What is the epidemiology of bacteremia in one-week to three-month-old infants?

Background: Large studies of bacteremia in infants <90 days of age were largely performed before the era of routine prenatal screening and prophylaxis for Group B Streptococcus (GBS). Additionally, these studies have focused on febrile infants, which might not allow for characterization of the incidence of bacteremia when nonfebrile infants are considered.

Study design: Retrospective review.

Setting: Large HMO database.

Synopsis: Of 160,818 full-term infants born at Kaiser Permanente Northern California from 2005 to 2009, 4,255 blood cultures were obtained from 4,122 infants in outpatient clinics, the ED, or in an inpatient setting within 24 hours of birth. Preterm infants <37 weeks, infants with underlying medical conditions, and infants with cultures drawn within three days of an original culture were excluded.

A total of 8% of the blood cultures were positive, with 2.2% deemed true positives and 5.8% due to contaminants. The incidence rate of true bacteremia was 0.57 per 1,000 full-term births, with gram-negative organisms (predominantly Escherichia coli) representing the majority (63%) of pathogens, followed by GBS (21%), Staphylococcus aureus (8%), and Streptococcus pneumoniae (3%). There were no cases of Listeria monocytogenes or Neisseria meningitidis bacteremia, and there was one case of enterococcal bacteremia. Fever was absent in 7% of cases.

The authors conclude that ampicillin may no longer be necessary for empiric antibiotic coverage in this age group given that 36% of pathogens were resistant to ampicillin, there were no cases of Listeria, and there was only one case of enterococcus. However, these recommendations should be considered in light of the specific study setting, and might not be applicable to all areas.

Bottom line: E. coli, GBS, and S. aureus, in that order, are the most common causes of bacteremia in infants aged one week to three months.

Citation: Greenhow TL, Hung YY, Herz AM. Changing epidemiology of bacteremia in infants aged 1 week to 3 months. Pediatrics. 2012;129(3):e590-e596.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Clinical question: What is the epidemiology of bacteremia in one-week to three-month-old infants?

Background: Large studies of bacteremia in infants <90 days of age were largely performed before the era of routine prenatal screening and prophylaxis for Group B Streptococcus (GBS). Additionally, these studies have focused on febrile infants, which might not allow for characterization of the incidence of bacteremia when nonfebrile infants are considered.

Study design: Retrospective review.

Setting: Large HMO database.

Synopsis: Of 160,818 full-term infants born at Kaiser Permanente Northern California from 2005 to 2009, 4,255 blood cultures were obtained from 4,122 infants in outpatient clinics, the ED, or in an inpatient setting within 24 hours of birth. Preterm infants <37 weeks, infants with underlying medical conditions, and infants with cultures drawn within three days of an original culture were excluded.

A total of 8% of the blood cultures were positive, with 2.2% deemed true positives and 5.8% due to contaminants. The incidence rate of true bacteremia was 0.57 per 1,000 full-term births, with gram-negative organisms (predominantly Escherichia coli) representing the majority (63%) of pathogens, followed by GBS (21%), Staphylococcus aureus (8%), and Streptococcus pneumoniae (3%). There were no cases of Listeria monocytogenes or Neisseria meningitidis bacteremia, and there was one case of enterococcal bacteremia. Fever was absent in 7% of cases.

The authors conclude that ampicillin may no longer be necessary for empiric antibiotic coverage in this age group given that 36% of pathogens were resistant to ampicillin, there were no cases of Listeria, and there was only one case of enterococcus. However, these recommendations should be considered in light of the specific study setting, and might not be applicable to all areas.

Bottom line: E. coli, GBS, and S. aureus, in that order, are the most common causes of bacteremia in infants aged one week to three months.

Citation: Greenhow TL, Hung YY, Herz AM. Changing epidemiology of bacteremia in infants aged 1 week to 3 months. Pediatrics. 2012;129(3):e590-e596.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Background

have become a ubiquitous feature of modern-day patient care; current estimates suggest that as many as 2 million persons in the U.S. have an intravascular device that is used daily or intermittently.¹ These devices fulfill a variety of clinical needs, including monitoring acutely ill patients and the administration of critical medications, in a variety of settings, including ICUs, medical and surgical units, and the outpatient setting.

This important therapeutic role comes with associated risks, including the possibility of bloodstream infection, which leads to an increase in morbidity, length of stay, and cost. Each year in the ICU alone, 80,000 catheter-related bloodstream infections (CRBSIs) occur. This figure increases to 250,000 to 500,000 infections per year when all hospitalized patients are considered.^1,2

Infections related to intravascular catheters have been targeted by numerous quality-improvement (QI) initiatives, uncovering a number of clinical actions that can impact their rates. Studies have shown that these infections can be avoided and nearly eliminated entirely with close adherence to several evidence-based, infection-control measures.³ Furthermore, these results can be sustained across multiple ICUs over extended periods.⁴

The majority of data that describe the epidemiology of CRBSIs and the interventions needed to prevent these infections have been generated in the ICU. However, the pervasiveness of these devices in other care settings dictates the need for heightened awareness by the entire care team. As such, it is important for hospitalists to understand and be aware of guidelines outlining the standard of care not only in personal practice, but also in order to ensure that all members of the team are playing their part in preventing this serious complication.

Guideline Update

In May 2011, the Society of Critical Care Medicine (SCCM), in collaboration with 14 other professional organizations, published new guidelines for the prevention of intravascular catheter-related infections.⁵ These guidelines are a revision of guidelines published in 2002 and provide recommendations that apply to all intravascular catheters, as well as specific comments based on the type of device in use.⁶

Specific recommendations include:

• Responsible staff should be well-versed and assessed on the proper procedures for the care of all intravascular catheters with designated personnel responsible for central venous catheters (CVCs)
• and peripherally inserted central catheters (PICCs).
• Prior to CVC and arterial catheter insertion and during dressing changes, an antiseptic solution containing more than 0.5% chlorhexidine with alcohol should be used to prepare the skin.
• Nontunneled CVCs should be preferentially placed in a subclavian site rather than a jugular or a femoral site, except in hemodialysis or advanced kidney disease patients, for which this may cause subclavian stenosis, with the understanding that the risks of placing a CVC at a site be weighed against its benefits.
• Skilled personnel should use ultrasound guidance during CVC placement, and the minimal essential number of ports or lumens on the CVC should be present. Avoidance of routine placement of CVCs and prompt removal of any nonessential intravascular catheter is recommended.
• Maximal sterile barrier precautions should be taken during the placement of CVCs and PICCs or guidewire exchange, which includes a sterile full-body drape for the patient and use of cap, mask, sterile gown, and gloves for personnel. After the catheter has been placed, it should be secured with a sutureless securement device. In addition, patients with these intravascular catheters should bathe with 2% chlorhexidine daily.
• If rates of CLABSI remain high despite adherence to education/training, appropriate antisepsis, and maximal sterile barrier precautions, the use of antiseptic- or antibiotic-impregnated, short-term CVCs and chlorhexadine-impregnanted sponge dressings might help to further decrease rates.⁵

No single intervention alone appears to be sufficient to significantly reduce CRBSI rates. Therefore, the guideline recommends “bundling” several of these individual best practices into a streamlined approach—inclusive of feedback to healthcare personnel on infection rates and compliance—thereby promoting quality assurance and performance improvement. This bundling tactic makes best practices a priority and a reality, and offers the largest potential impact on the prevention of intravascular catheter-related infections.⁵

Analysis

Practical recommendations to assist clinicians in preventing CLABSI also were put forth in 2008 guidelines by the Society for Healthcare Epidemiology of America (SHEA) and Infectious Disease Society of America (IDSA).⁷ Compared to the SCCM guidelines, these guidelines are more focused on CVCs and do not directly address other available intravascular devices (PICCs, hemodialysis catheters, etc.). Beyond this, the SCCM guidelines also discuss the microbiology of infection, surveillance measures, and the specifics of the performance improvement measures involved in their implementation, which are not found in the SHEA and IDSA guidelines.

Numerous national initiatives and measures have been established based on these and other clinical practice guidelines. The Joint Commission recently produced the new monograph “Preventing Central Line-Associated Infections: A Global Challenge, A Global Perspective,” listing “Use proven guidelines to prevent infection of the blood from central lines” as one of its National Patient Safety Goals.⁸ The Institute for Healthcare Improvement (IHI) created its Central Line Bundle along with its “How-To Guide: Prevent CLABSI in 2011,” which has been implemented by many hospitals in the U.S. and United Kingdom. The IHI bundle has resulted in dozens of hospitals achieving more than a year of no CLABSIs in their ICU patients, and many have expanded the program to other areas of the hospital.⁹

Giving further impetus toward efforts to prevent these complications, the Centers for Medicare & Medicaid Services (CMS) determined that vascular-catheter-associated infections are hospital-acquired conditions that will no longer be reimbursed, as outlined in 2008 in the Acute Inpatient Prospective Payment System.10 Therefore, hospitals will not receive additional payment for these infections acquired during hospitalization (i.e. was not present on admission), and the case is paid as though the costly infection were not present, thus aligning improved patient care and outcomes with the financial bottom line for hospital reimbursement.

HM Takeaways

Given the significant economic and clinical burden of intravascular-device-related infections, hospital staffs should be aware of and adopt proven interventions to minimize this important complication. No one single intervention can meaningfully impact this infection rate, but a “bundled approach” appears to be the most influential.

Dr. Rohde is a hospitalist and assistant professor of internal medicine and Dr. Hartley is a hospitalist and clinical instructor of internal medicine at the University of Michigan Hospital and Health Systems in Ann Arbor.

Background

have become a ubiquitous feature of modern-day patient care; current estimates suggest that as many as 2 million persons in the U.S. have an intravascular device that is used daily or intermittently.¹ These devices fulfill a variety of clinical needs, including monitoring acutely ill patients and the administration of critical medications, in a variety of settings, including ICUs, medical and surgical units, and the outpatient setting.

This important therapeutic role comes with associated risks, including the possibility of bloodstream infection, which leads to an increase in morbidity, length of stay, and cost. Each year in the ICU alone, 80,000 catheter-related bloodstream infections (CRBSIs) occur. This figure increases to 250,000 to 500,000 infections per year when all hospitalized patients are considered.^1,2

Infections related to intravascular catheters have been targeted by numerous quality-improvement (QI) initiatives, uncovering a number of clinical actions that can impact their rates. Studies have shown that these infections can be avoided and nearly eliminated entirely with close adherence to several evidence-based, infection-control measures.³ Furthermore, these results can be sustained across multiple ICUs over extended periods.⁴

The majority of data that describe the epidemiology of CRBSIs and the interventions needed to prevent these infections have been generated in the ICU. However, the pervasiveness of these devices in other care settings dictates the need for heightened awareness by the entire care team. As such, it is important for hospitalists to understand and be aware of guidelines outlining the standard of care not only in personal practice, but also in order to ensure that all members of the team are playing their part in preventing this serious complication.

Guideline Update

In May 2011, the Society of Critical Care Medicine (SCCM), in collaboration with 14 other professional organizations, published new guidelines for the prevention of intravascular catheter-related infections.⁵ These guidelines are a revision of guidelines published in 2002 and provide recommendations that apply to all intravascular catheters, as well as specific comments based on the type of device in use.⁶

Specific recommendations include:

• Responsible staff should be well-versed and assessed on the proper procedures for the care of all intravascular catheters with designated personnel responsible for central venous catheters (CVCs)
• and peripherally inserted central catheters (PICCs).
• Prior to CVC and arterial catheter insertion and during dressing changes, an antiseptic solution containing more than 0.5% chlorhexidine with alcohol should be used to prepare the skin.
• Nontunneled CVCs should be preferentially placed in a subclavian site rather than a jugular or a femoral site, except in hemodialysis or advanced kidney disease patients, for which this may cause subclavian stenosis, with the understanding that the risks of placing a CVC at a site be weighed against its benefits.
• Skilled personnel should use ultrasound guidance during CVC placement, and the minimal essential number of ports or lumens on the CVC should be present. Avoidance of routine placement of CVCs and prompt removal of any nonessential intravascular catheter is recommended.
• Maximal sterile barrier precautions should be taken during the placement of CVCs and PICCs or guidewire exchange, which includes a sterile full-body drape for the patient and use of cap, mask, sterile gown, and gloves for personnel. After the catheter has been placed, it should be secured with a sutureless securement device. In addition, patients with these intravascular catheters should bathe with 2% chlorhexidine daily.
• If rates of CLABSI remain high despite adherence to education/training, appropriate antisepsis, and maximal sterile barrier precautions, the use of antiseptic- or antibiotic-impregnated, short-term CVCs and chlorhexadine-impregnanted sponge dressings might help to further decrease rates.⁵

No single intervention alone appears to be sufficient to significantly reduce CRBSI rates. Therefore, the guideline recommends “bundling” several of these individual best practices into a streamlined approach—inclusive of feedback to healthcare personnel on infection rates and compliance—thereby promoting quality assurance and performance improvement. This bundling tactic makes best practices a priority and a reality, and offers the largest potential impact on the prevention of intravascular catheter-related infections.⁵

Analysis

Practical recommendations to assist clinicians in preventing CLABSI also were put forth in 2008 guidelines by the Society for Healthcare Epidemiology of America (SHEA) and Infectious Disease Society of America (IDSA).⁷ Compared to the SCCM guidelines, these guidelines are more focused on CVCs and do not directly address other available intravascular devices (PICCs, hemodialysis catheters, etc.). Beyond this, the SCCM guidelines also discuss the microbiology of infection, surveillance measures, and the specifics of the performance improvement measures involved in their implementation, which are not found in the SHEA and IDSA guidelines.

Numerous national initiatives and measures have been established based on these and other clinical practice guidelines. The Joint Commission recently produced the new monograph “Preventing Central Line-Associated Infections: A Global Challenge, A Global Perspective,” listing “Use proven guidelines to prevent infection of the blood from central lines” as one of its National Patient Safety Goals.⁸ The Institute for Healthcare Improvement (IHI) created its Central Line Bundle along with its “How-To Guide: Prevent CLABSI in 2011,” which has been implemented by many hospitals in the U.S. and United Kingdom. The IHI bundle has resulted in dozens of hospitals achieving more than a year of no CLABSIs in their ICU patients, and many have expanded the program to other areas of the hospital.⁹

Giving further impetus toward efforts to prevent these complications, the Centers for Medicare & Medicaid Services (CMS) determined that vascular-catheter-associated infections are hospital-acquired conditions that will no longer be reimbursed, as outlined in 2008 in the Acute Inpatient Prospective Payment System.10 Therefore, hospitals will not receive additional payment for these infections acquired during hospitalization (i.e. was not present on admission), and the case is paid as though the costly infection were not present, thus aligning improved patient care and outcomes with the financial bottom line for hospital reimbursement.

HM Takeaways

Given the significant economic and clinical burden of intravascular-device-related infections, hospital staffs should be aware of and adopt proven interventions to minimize this important complication. No one single intervention can meaningfully impact this infection rate, but a “bundled approach” appears to be the most influential.

Dr. Rohde is a hospitalist and assistant professor of internal medicine and Dr. Hartley is a hospitalist and clinical instructor of internal medicine at the University of Michigan Hospital and Health Systems in Ann Arbor.

Background

have become a ubiquitous feature of modern-day patient care; current estimates suggest that as many as 2 million persons in the U.S. have an intravascular device that is used daily or intermittently.¹ These devices fulfill a variety of clinical needs, including monitoring acutely ill patients and the administration of critical medications, in a variety of settings, including ICUs, medical and surgical units, and the outpatient setting.

This important therapeutic role comes with associated risks, including the possibility of bloodstream infection, which leads to an increase in morbidity, length of stay, and cost. Each year in the ICU alone, 80,000 catheter-related bloodstream infections (CRBSIs) occur. This figure increases to 250,000 to 500,000 infections per year when all hospitalized patients are considered.^1,2

Infections related to intravascular catheters have been targeted by numerous quality-improvement (QI) initiatives, uncovering a number of clinical actions that can impact their rates. Studies have shown that these infections can be avoided and nearly eliminated entirely with close adherence to several evidence-based, infection-control measures.³ Furthermore, these results can be sustained across multiple ICUs over extended periods.⁴

The majority of data that describe the epidemiology of CRBSIs and the interventions needed to prevent these infections have been generated in the ICU. However, the pervasiveness of these devices in other care settings dictates the need for heightened awareness by the entire care team. As such, it is important for hospitalists to understand and be aware of guidelines outlining the standard of care not only in personal practice, but also in order to ensure that all members of the team are playing their part in preventing this serious complication.

Guideline Update

In May 2011, the Society of Critical Care Medicine (SCCM), in collaboration with 14 other professional organizations, published new guidelines for the prevention of intravascular catheter-related infections.⁵ These guidelines are a revision of guidelines published in 2002 and provide recommendations that apply to all intravascular catheters, as well as specific comments based on the type of device in use.⁶

Specific recommendations include:

• Responsible staff should be well-versed and assessed on the proper procedures for the care of all intravascular catheters with designated personnel responsible for central venous catheters (CVCs)
• and peripherally inserted central catheters (PICCs).
• Prior to CVC and arterial catheter insertion and during dressing changes, an antiseptic solution containing more than 0.5% chlorhexidine with alcohol should be used to prepare the skin.
• Nontunneled CVCs should be preferentially placed in a subclavian site rather than a jugular or a femoral site, except in hemodialysis or advanced kidney disease patients, for which this may cause subclavian stenosis, with the understanding that the risks of placing a CVC at a site be weighed against its benefits.
• Skilled personnel should use ultrasound guidance during CVC placement, and the minimal essential number of ports or lumens on the CVC should be present. Avoidance of routine placement of CVCs and prompt removal of any nonessential intravascular catheter is recommended.
• Maximal sterile barrier precautions should be taken during the placement of CVCs and PICCs or guidewire exchange, which includes a sterile full-body drape for the patient and use of cap, mask, sterile gown, and gloves for personnel. After the catheter has been placed, it should be secured with a sutureless securement device. In addition, patients with these intravascular catheters should bathe with 2% chlorhexidine daily.
• If rates of CLABSI remain high despite adherence to education/training, appropriate antisepsis, and maximal sterile barrier precautions, the use of antiseptic- or antibiotic-impregnated, short-term CVCs and chlorhexadine-impregnanted sponge dressings might help to further decrease rates.⁵

No single intervention alone appears to be sufficient to significantly reduce CRBSI rates. Therefore, the guideline recommends “bundling” several of these individual best practices into a streamlined approach—inclusive of feedback to healthcare personnel on infection rates and compliance—thereby promoting quality assurance and performance improvement. This bundling tactic makes best practices a priority and a reality, and offers the largest potential impact on the prevention of intravascular catheter-related infections.⁵

Analysis

Practical recommendations to assist clinicians in preventing CLABSI also were put forth in 2008 guidelines by the Society for Healthcare Epidemiology of America (SHEA) and Infectious Disease Society of America (IDSA).⁷ Compared to the SCCM guidelines, these guidelines are more focused on CVCs and do not directly address other available intravascular devices (PICCs, hemodialysis catheters, etc.). Beyond this, the SCCM guidelines also discuss the microbiology of infection, surveillance measures, and the specifics of the performance improvement measures involved in their implementation, which are not found in the SHEA and IDSA guidelines.

Numerous national initiatives and measures have been established based on these and other clinical practice guidelines. The Joint Commission recently produced the new monograph “Preventing Central Line-Associated Infections: A Global Challenge, A Global Perspective,” listing “Use proven guidelines to prevent infection of the blood from central lines” as one of its National Patient Safety Goals.⁸ The Institute for Healthcare Improvement (IHI) created its Central Line Bundle along with its “How-To Guide: Prevent CLABSI in 2011,” which has been implemented by many hospitals in the U.S. and United Kingdom. The IHI bundle has resulted in dozens of hospitals achieving more than a year of no CLABSIs in their ICU patients, and many have expanded the program to other areas of the hospital.⁹

Giving further impetus toward efforts to prevent these complications, the Centers for Medicare & Medicaid Services (CMS) determined that vascular-catheter-associated infections are hospital-acquired conditions that will no longer be reimbursed, as outlined in 2008 in the Acute Inpatient Prospective Payment System.10 Therefore, hospitals will not receive additional payment for these infections acquired during hospitalization (i.e. was not present on admission), and the case is paid as though the costly infection were not present, thus aligning improved patient care and outcomes with the financial bottom line for hospital reimbursement.

HM Takeaways

Given the significant economic and clinical burden of intravascular-device-related infections, hospital staffs should be aware of and adopt proven interventions to minimize this important complication. No one single intervention can meaningfully impact this infection rate, but a “bundled approach” appears to be the most influential.

Dr. Rohde is a hospitalist and assistant professor of internal medicine and Dr. Hartley is a hospitalist and clinical instructor of internal medicine at the University of Michigan Hospital and Health Systems in Ann Arbor.

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The Case

A 24-year-old white man with no past medical history is admitted after sustaining bilateral, closed femur fractures in a motor vehicle accident. Within hours of the trauma, he is taken to the operating room for open reduction and internal fixation. Of note, preoperatively, his hematocrit is 40%. After surgery, he is easily extubated and transferred to an unmonitored bed for further care. Approximately 30 hours after admission, he develops tachypnea with a respiratory rate of 35 breaths per minute and hypoxia with an oxygen saturation of 86% on room air. He is tachycardic (120 beats per minute) and febrile to 39.0oC. His blood pressure remains stable. He is somnolent, and when awake, he is confused. Notably, his hematocrit is now 22%. An electrocardiogram shows sinus tachycardia, an initial chest X-ray is normal, and a high-resolution CT scan is negative for a pulmonary embolism (PE).

Is this clinical picture consistent with fat embolism syndrome and, if so, how should he be managed?

Overview

“Fat embolism” refers to the presence of fat globules that obstruct the lung parenchyma and peripheral circulation. Fat embolism syndrome, on the other hand, is a more serious manifestation involving multiple organ systems. Specifically, it is a clinical diagnosis presenting with the classic triad of hypoxemia, neurologic abnormalities, and a petechial rash.

Fat embolism syndrome is usually associated with multiple traumas, including long-bone injuries and pelvic fractures. It is more frequently associated with closed fractures than open fractures, possibly due to the higher pressures associated with closed fractures. This syndrome has been less commonly associated with a variety of nontraumatic conditions (Table 1).

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With an increased incidence of long-bone fractures in the younger demographic, fat embolism syndrome is most common in the second or third decade of life. While fat embolism occurs in up to 90% of patients with traumatic skeletal injuries, fat embolism syndrome occurs in 0.5% to 10% of patients following trauma, with a higher incidence in multiple fractures (5% to 10%) than in single long-bone fractures (0.5% to 2%).^1-3

With the increasing role of hospitalists in assisting in the management of orthopedic patients, their knowledge of fat embolism syndrome is important so that it can be included in the differential diagnosis of acute respiratory failure in these orthopedic patients.

Review of the Data

Pathogenesis. Clinical manifestations of fat embolism syndrome have been acknowledged for more than 100 years. Since its first description in the 1860s, there has been speculation about the etiology of this condition. In the 1920s, two theories were proposed to explain the origin of the fat droplets: the mechanical and biochemical theories.^2,4

Mechanical theory suggests that trauma to long bones disturbs fat cells within the bone marrow or adipose tissue, causing fat globules to mobilize.^2,3 There is a rise in marrow pressure above venous pressure, which allows fat particles to enter the circulation through damaged venules surrounding the fracture site. Once lodged in the pulmonary microvasculature, embolized fat causes local ischemia and inflammation. Fat globules may pass into the arterial circulation either by paradoxical embolism through a patent foramen ovale, or by microemboli that pass through the lungs into the arterial circulation. This explains embolization to other organs, including the brain, retina, and skin.

Alternatively, biochemical theory hypothesizes that fat embolism syndrome is contingent on the production of toxic intermediaries from the breakdown of embolized fat.^2,3 This theory suggests that the release of catecholamines after severe trauma can liberate free fatty acids from fat stores, or that acute-phase reactants at the trauma site affect fat solubility, causing agglutination and embolization. This theory helps to explain nontraumatic fat embolism syndrome, as well as the delay in development of the clinical syndrome after acute injury.

Clinical presentation. Most patients have a latent period after trauma of 12 to 72 hours before symptoms of fat embolism syndrome become apparent; however, clinical manifestations might occur immediately or up to one to two weeks following injury.^2,4 As previously mentioned, the classic triad of symptoms includes respiratory compromise, neurological impairment, and a petechial rash.

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The most common and usually earliest manifestation is acute hypoxia, which must be distinguished from other treatable causes of hypoxia, including pneumothorax, hemothorax, PE, and pneumonia. Pulmonary changes might progress to respiratory failure similar to acute respiratory distress syndrome. Neurological manifestations are primarily nonspecific and include headache, irritability, delirium, seizures, and coma. Focal neurological deficits are rare but have been described.⁵ Almost all neurological symptoms are fully reversible. The petechial rash is distinctive and occurs on the chest, axilla, and subconjunctiva. Although the rash occurs in only 20% to 50% of patients and resolves fairly quickly, in the appropriate clinical setting, this rash is considered pathognomonic.^1,2,4

A variety of other nonspecific signs and symptoms might also occur: pyrexia, tachycardia, fat in the urine or sputum, retinal changes, renal insufficiency, myocardial dysfunction, and an otherwise unexplained drop in hematocrit or platelet count.

Diagnosis. Fat embolism syndrome is a clinical diagnosis and a diagnosis of exclusion. There are no specific confirmatory tests. An arterial blood gas will usually reveal a PaO2 of <60 mmHg.3 Laboratory evaluation might also show fat globules in the urine or sputum on Sudan or Oil Red O staining, but these findings are nonspecific.^3,4 Bronchoscopy with bronchial alveolar lavage (BAL) might similarly detect fat droplets in alveolar macrophages in the BAL fluid; however, the sensitivity and specificity for diagnosis of fat embolism syndrome are unknown.⁴ None of these tests can be used solely for the diagnosis of fat embolism syndrome.

Thrombocytopenia and anemia out of proportion to the expected drop from surgery are not uncommon in addition to other nonspecific laboratory findings, including hypocalcemia, elevated serum lipase level, and elevated erythrocyte sedimentation rate.⁴ Several radiological findings have been observed on lung and brain imaging, though the findings are nonspecific and none are diagnostic. A chest X-ray might be normal, but abnormalities are seen in 30% to 50% of cases.² Typically, when abnormal, the chest X-ray shows diffuse interstitial and alveolar densities, as well as patchy perihilar and basilar infiltrates resembling pulmonary edema. These X-ray findings might not be seen for up to 12 to 24 hours following the onset of clinical symptoms.

The most commonly used diagnostic criteria for the diagnosis of fat embolism syndrome are published by Gurd et al.⁶ At least two major criteria or one major criterion and four minor criteria are required for the diagnosis of fat embolism syndrome. The major criteria are based on the three classic signs and symptoms of fat embolism syndrome; the minor criteria include the finding of fat globules in the urine and sputum as well as some of the previously mentioned nonspecific clinical signs and laboratory tests.

Other criteria for diagnosis have been suggested, including those published by Lindeque et al, which focuses primarily on the respiratory characteristics, and a more recent set of semiquantitative diagnostic criteria called the fat embolism index, published by Schonfeld et al.^7,8 Schonfeld’s scoring index accounts for the major signs and symptoms of fat embolism syndrome and weighs them according to relative specificity. A score of 5 or more is required for diagnosis of fat embolism syndrome. Table 2 compares the three sets of criteria used for diagnosis of fat embolism syndrome.

Treatment. The treatment of fat embolism syndrome is supportive. Most often, this requires supplemental oxygen for hypoxia and, possibly, fluid resuscitation in the case of hypovolemia. Occasionally, though, these relatively minor supportive therapies need to be escalated to bipap or even full ventilatory support and vasopressors in the more severe cases.

Based on the premise that steroids will attenuate the inflammatory reaction to free fatty acids within the lung, steroids have been tried in the treatment of fat embolism syndrome. However, there are no studies that clearly show benefit with their use.

Prevention. Most of the methods of prevention involve surgical intervention rather than medical therapy. Because microscopic fat emboli are showered during manipulation of long-bone fragments, early immobilization of fractures is recommended, and operative correction rather than conservative management is the preferred method.^2,3 One report estimates a 70% reduction in pulmonary complications from this intervention alone.⁹

Further, two surgical techniques are debated as possible means of preventing fat embolism syndrome. The first is “venting,” in which a hole is made distal to the site of intramedullary nail placement. This reduces intramedullary pressure elevation and, therefore, extravasation of fat into the circulation.¹⁰ The second technique is the use of a reamer, irrigator, aspirator (RIA) device. A reamer is a tool used to create an accurate-sized hole for an intramedullary nail. Reaming before intramedullary nail placement can release fat deposits into the circulation. The RIA device irrigates and aspirates resident fat deposits as it reams the canal, releasing fewer deposits into the circulation.¹¹ At this time, these two techniques are considered but not used routinely by surgeons.

Corticosteroids remain a debated method of prevention of fat embolism syndrome. A number of smaller studies suggest steroid therapy might reduce the incidence of fat embolism syndrome and hypoxia; a 2009 meta-analysis pooling nearly 400 patients from these smaller studies found such results.12 Unfortunately, the included studies were noted to be of poor quality, and no change in mortality was found. These results, combined with the possibility of poor wound healing or infection as a complication of steroid use, keep steroids from being used routinely to prevent fat embolism syndrome.

Clinical course. The severity of fat embolism syndrome ranges from mild transient hypoxia with confusion to progressively worsening symptoms leading to acute respiratory distress syndrome and coma. Bulger et al found a 7% mortality rate in this population.¹ Less commonly, patients have a fulminant presentation with symptom onset less than 12 hours after injury. With this presentation, patients have a higher rate of mortality—as high as 15%.¹³

Back to the Case

This young man with bilateral long-bone fractures was at high risk of developing fat embolism syndrome. As is recommended, he was quickly taken to the operating room for fracture stabilization with open reduction and internal fixation. In addition, a RIA device was used to decrease intramedullary pressure. Nonetheless, within the first two days of injury, he developed hypoxia and confusion. These clinical changes were associated with an unexpected drop in hematocrit.

Chest X-ray and high-resolution computed tomography did not reveal a cause of his hypoxia. Similarly, laboratory evaluation for a reversible cause of encephalopathy was negative. A Sudan stain of his urine revealed free fat globules. Though he did not develop axillary petechiae, this clinical picture is consistent with fat embolism syndrome based on Gurd’s criteria. He was supported with oxygen therapy, and he stabilized without further complications.

Drs. Smith and Rice are members of the Section of Hospital Medicine at Vanderbilt University in Nashville, Tenn.

References

1. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg. 1997;132:435-439.
2. Levy D. The fat embolism syndrome. Clin Orthop. 1990;261:281-286.
3. Akhtar S. Fat embolism. Anes Clin. 2009;27:533-550.
4. Gupta A, Reilly C. Fat embolism. Anaesth Crit Care Pain. 2007;7:148-151.
5. Thomas JE, Ayyar DR. Systemic fat embolism. Arch Neurol. 1972;26:517-523.
6. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56B:408-416.
7. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. J Bone Joint Surg Br. 1987;69:128-131.
8. Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Ann Intern Med. 1983;99:438-443.
9. Robinson CM. Current concepts of respiratory insufficiency syndromes after fracture. J Bone Joint Surg Br. 2001;83:781-791.
10. Kim YH, Oh SW, Kim JS. Prevalence of fat embolism following bilateral simultaneous and unilateral total hip arthroplasty performed with or without cement: a prospective, randomized clinical study. J Bone Joint Surg Am. 2002;84A:1372-1379.
11. Volgas DA, Burch T, Stannard JP, Ellis T, Bilotta J, Alonso JE. Fat embolus in femur fractures: a comparison of two reaming systems. Injury. 2010;41 Suppl 2:S90-S93.
12. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg. 2009;52:386-393.
13. Bracco D, Favre JB, Joris F, Ravussin A. Fatal fat embolism syndrome: a case report. J Neurosurg Anesthesiol. 2000;12:221-224.

click for large version

The Case

A 24-year-old white man with no past medical history is admitted after sustaining bilateral, closed femur fractures in a motor vehicle accident. Within hours of the trauma, he is taken to the operating room for open reduction and internal fixation. Of note, preoperatively, his hematocrit is 40%. After surgery, he is easily extubated and transferred to an unmonitored bed for further care. Approximately 30 hours after admission, he develops tachypnea with a respiratory rate of 35 breaths per minute and hypoxia with an oxygen saturation of 86% on room air. He is tachycardic (120 beats per minute) and febrile to 39.0oC. His blood pressure remains stable. He is somnolent, and when awake, he is confused. Notably, his hematocrit is now 22%. An electrocardiogram shows sinus tachycardia, an initial chest X-ray is normal, and a high-resolution CT scan is negative for a pulmonary embolism (PE).

Is this clinical picture consistent with fat embolism syndrome and, if so, how should he be managed?

Overview

“Fat embolism” refers to the presence of fat globules that obstruct the lung parenchyma and peripheral circulation. Fat embolism syndrome, on the other hand, is a more serious manifestation involving multiple organ systems. Specifically, it is a clinical diagnosis presenting with the classic triad of hypoxemia, neurologic abnormalities, and a petechial rash.

Fat embolism syndrome is usually associated with multiple traumas, including long-bone injuries and pelvic fractures. It is more frequently associated with closed fractures than open fractures, possibly due to the higher pressures associated with closed fractures. This syndrome has been less commonly associated with a variety of nontraumatic conditions (Table 1).

click for large version

With an increased incidence of long-bone fractures in the younger demographic, fat embolism syndrome is most common in the second or third decade of life. While fat embolism occurs in up to 90% of patients with traumatic skeletal injuries, fat embolism syndrome occurs in 0.5% to 10% of patients following trauma, with a higher incidence in multiple fractures (5% to 10%) than in single long-bone fractures (0.5% to 2%).^1-3

With the increasing role of hospitalists in assisting in the management of orthopedic patients, their knowledge of fat embolism syndrome is important so that it can be included in the differential diagnosis of acute respiratory failure in these orthopedic patients.

Review of the Data

Pathogenesis. Clinical manifestations of fat embolism syndrome have been acknowledged for more than 100 years. Since its first description in the 1860s, there has been speculation about the etiology of this condition. In the 1920s, two theories were proposed to explain the origin of the fat droplets: the mechanical and biochemical theories.^2,4

Mechanical theory suggests that trauma to long bones disturbs fat cells within the bone marrow or adipose tissue, causing fat globules to mobilize.^2,3 There is a rise in marrow pressure above venous pressure, which allows fat particles to enter the circulation through damaged venules surrounding the fracture site. Once lodged in the pulmonary microvasculature, embolized fat causes local ischemia and inflammation. Fat globules may pass into the arterial circulation either by paradoxical embolism through a patent foramen ovale, or by microemboli that pass through the lungs into the arterial circulation. This explains embolization to other organs, including the brain, retina, and skin.

Alternatively, biochemical theory hypothesizes that fat embolism syndrome is contingent on the production of toxic intermediaries from the breakdown of embolized fat.^2,3 This theory suggests that the release of catecholamines after severe trauma can liberate free fatty acids from fat stores, or that acute-phase reactants at the trauma site affect fat solubility, causing agglutination and embolization. This theory helps to explain nontraumatic fat embolism syndrome, as well as the delay in development of the clinical syndrome after acute injury.

Clinical presentation. Most patients have a latent period after trauma of 12 to 72 hours before symptoms of fat embolism syndrome become apparent; however, clinical manifestations might occur immediately or up to one to two weeks following injury.^2,4 As previously mentioned, the classic triad of symptoms includes respiratory compromise, neurological impairment, and a petechial rash.

click for large version

The most common and usually earliest manifestation is acute hypoxia, which must be distinguished from other treatable causes of hypoxia, including pneumothorax, hemothorax, PE, and pneumonia. Pulmonary changes might progress to respiratory failure similar to acute respiratory distress syndrome. Neurological manifestations are primarily nonspecific and include headache, irritability, delirium, seizures, and coma. Focal neurological deficits are rare but have been described.⁵ Almost all neurological symptoms are fully reversible. The petechial rash is distinctive and occurs on the chest, axilla, and subconjunctiva. Although the rash occurs in only 20% to 50% of patients and resolves fairly quickly, in the appropriate clinical setting, this rash is considered pathognomonic.^1,2,4

A variety of other nonspecific signs and symptoms might also occur: pyrexia, tachycardia, fat in the urine or sputum, retinal changes, renal insufficiency, myocardial dysfunction, and an otherwise unexplained drop in hematocrit or platelet count.

Diagnosis. Fat embolism syndrome is a clinical diagnosis and a diagnosis of exclusion. There are no specific confirmatory tests. An arterial blood gas will usually reveal a PaO2 of <60 mmHg.3 Laboratory evaluation might also show fat globules in the urine or sputum on Sudan or Oil Red O staining, but these findings are nonspecific.^3,4 Bronchoscopy with bronchial alveolar lavage (BAL) might similarly detect fat droplets in alveolar macrophages in the BAL fluid; however, the sensitivity and specificity for diagnosis of fat embolism syndrome are unknown.⁴ None of these tests can be used solely for the diagnosis of fat embolism syndrome.

Thrombocytopenia and anemia out of proportion to the expected drop from surgery are not uncommon in addition to other nonspecific laboratory findings, including hypocalcemia, elevated serum lipase level, and elevated erythrocyte sedimentation rate.⁴ Several radiological findings have been observed on lung and brain imaging, though the findings are nonspecific and none are diagnostic. A chest X-ray might be normal, but abnormalities are seen in 30% to 50% of cases.² Typically, when abnormal, the chest X-ray shows diffuse interstitial and alveolar densities, as well as patchy perihilar and basilar infiltrates resembling pulmonary edema. These X-ray findings might not be seen for up to 12 to 24 hours following the onset of clinical symptoms.

The most commonly used diagnostic criteria for the diagnosis of fat embolism syndrome are published by Gurd et al.⁶ At least two major criteria or one major criterion and four minor criteria are required for the diagnosis of fat embolism syndrome. The major criteria are based on the three classic signs and symptoms of fat embolism syndrome; the minor criteria include the finding of fat globules in the urine and sputum as well as some of the previously mentioned nonspecific clinical signs and laboratory tests.

Other criteria for diagnosis have been suggested, including those published by Lindeque et al, which focuses primarily on the respiratory characteristics, and a more recent set of semiquantitative diagnostic criteria called the fat embolism index, published by Schonfeld et al.^7,8 Schonfeld’s scoring index accounts for the major signs and symptoms of fat embolism syndrome and weighs them according to relative specificity. A score of 5 or more is required for diagnosis of fat embolism syndrome. Table 2 compares the three sets of criteria used for diagnosis of fat embolism syndrome.

Treatment. The treatment of fat embolism syndrome is supportive. Most often, this requires supplemental oxygen for hypoxia and, possibly, fluid resuscitation in the case of hypovolemia. Occasionally, though, these relatively minor supportive therapies need to be escalated to bipap or even full ventilatory support and vasopressors in the more severe cases.

Based on the premise that steroids will attenuate the inflammatory reaction to free fatty acids within the lung, steroids have been tried in the treatment of fat embolism syndrome. However, there are no studies that clearly show benefit with their use.

Prevention. Most of the methods of prevention involve surgical intervention rather than medical therapy. Because microscopic fat emboli are showered during manipulation of long-bone fragments, early immobilization of fractures is recommended, and operative correction rather than conservative management is the preferred method.^2,3 One report estimates a 70% reduction in pulmonary complications from this intervention alone.⁹

Further, two surgical techniques are debated as possible means of preventing fat embolism syndrome. The first is “venting,” in which a hole is made distal to the site of intramedullary nail placement. This reduces intramedullary pressure elevation and, therefore, extravasation of fat into the circulation.¹⁰ The second technique is the use of a reamer, irrigator, aspirator (RIA) device. A reamer is a tool used to create an accurate-sized hole for an intramedullary nail. Reaming before intramedullary nail placement can release fat deposits into the circulation. The RIA device irrigates and aspirates resident fat deposits as it reams the canal, releasing fewer deposits into the circulation.¹¹ At this time, these two techniques are considered but not used routinely by surgeons.

Corticosteroids remain a debated method of prevention of fat embolism syndrome. A number of smaller studies suggest steroid therapy might reduce the incidence of fat embolism syndrome and hypoxia; a 2009 meta-analysis pooling nearly 400 patients from these smaller studies found such results.12 Unfortunately, the included studies were noted to be of poor quality, and no change in mortality was found. These results, combined with the possibility of poor wound healing or infection as a complication of steroid use, keep steroids from being used routinely to prevent fat embolism syndrome.

Clinical course. The severity of fat embolism syndrome ranges from mild transient hypoxia with confusion to progressively worsening symptoms leading to acute respiratory distress syndrome and coma. Bulger et al found a 7% mortality rate in this population.¹ Less commonly, patients have a fulminant presentation with symptom onset less than 12 hours after injury. With this presentation, patients have a higher rate of mortality—as high as 15%.¹³

Back to the Case

This young man with bilateral long-bone fractures was at high risk of developing fat embolism syndrome. As is recommended, he was quickly taken to the operating room for fracture stabilization with open reduction and internal fixation. In addition, a RIA device was used to decrease intramedullary pressure. Nonetheless, within the first two days of injury, he developed hypoxia and confusion. These clinical changes were associated with an unexpected drop in hematocrit.

Chest X-ray and high-resolution computed tomography did not reveal a cause of his hypoxia. Similarly, laboratory evaluation for a reversible cause of encephalopathy was negative. A Sudan stain of his urine revealed free fat globules. Though he did not develop axillary petechiae, this clinical picture is consistent with fat embolism syndrome based on Gurd’s criteria. He was supported with oxygen therapy, and he stabilized without further complications.

Drs. Smith and Rice are members of the Section of Hospital Medicine at Vanderbilt University in Nashville, Tenn.

References

1. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg. 1997;132:435-439.
2. Levy D. The fat embolism syndrome. Clin Orthop. 1990;261:281-286.
3. Akhtar S. Fat embolism. Anes Clin. 2009;27:533-550.
4. Gupta A, Reilly C. Fat embolism. Anaesth Crit Care Pain. 2007;7:148-151.
5. Thomas JE, Ayyar DR. Systemic fat embolism. Arch Neurol. 1972;26:517-523.
6. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56B:408-416.
7. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. J Bone Joint Surg Br. 1987;69:128-131.
8. Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Ann Intern Med. 1983;99:438-443.
9. Robinson CM. Current concepts of respiratory insufficiency syndromes after fracture. J Bone Joint Surg Br. 2001;83:781-791.
10. Kim YH, Oh SW, Kim JS. Prevalence of fat embolism following bilateral simultaneous and unilateral total hip arthroplasty performed with or without cement: a prospective, randomized clinical study. J Bone Joint Surg Am. 2002;84A:1372-1379.
11. Volgas DA, Burch T, Stannard JP, Ellis T, Bilotta J, Alonso JE. Fat embolus in femur fractures: a comparison of two reaming systems. Injury. 2010;41 Suppl 2:S90-S93.
12. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg. 2009;52:386-393.
13. Bracco D, Favre JB, Joris F, Ravussin A. Fatal fat embolism syndrome: a case report. J Neurosurg Anesthesiol. 2000;12:221-224.

click for large version

The Case

A 24-year-old white man with no past medical history is admitted after sustaining bilateral, closed femur fractures in a motor vehicle accident. Within hours of the trauma, he is taken to the operating room for open reduction and internal fixation. Of note, preoperatively, his hematocrit is 40%. After surgery, he is easily extubated and transferred to an unmonitored bed for further care. Approximately 30 hours after admission, he develops tachypnea with a respiratory rate of 35 breaths per minute and hypoxia with an oxygen saturation of 86% on room air. He is tachycardic (120 beats per minute) and febrile to 39.0oC. His blood pressure remains stable. He is somnolent, and when awake, he is confused. Notably, his hematocrit is now 22%. An electrocardiogram shows sinus tachycardia, an initial chest X-ray is normal, and a high-resolution CT scan is negative for a pulmonary embolism (PE).

Is this clinical picture consistent with fat embolism syndrome and, if so, how should he be managed?

Overview

“Fat embolism” refers to the presence of fat globules that obstruct the lung parenchyma and peripheral circulation. Fat embolism syndrome, on the other hand, is a more serious manifestation involving multiple organ systems. Specifically, it is a clinical diagnosis presenting with the classic triad of hypoxemia, neurologic abnormalities, and a petechial rash.

Fat embolism syndrome is usually associated with multiple traumas, including long-bone injuries and pelvic fractures. It is more frequently associated with closed fractures than open fractures, possibly due to the higher pressures associated with closed fractures. This syndrome has been less commonly associated with a variety of nontraumatic conditions (Table 1).

click for large version

With an increased incidence of long-bone fractures in the younger demographic, fat embolism syndrome is most common in the second or third decade of life. While fat embolism occurs in up to 90% of patients with traumatic skeletal injuries, fat embolism syndrome occurs in 0.5% to 10% of patients following trauma, with a higher incidence in multiple fractures (5% to 10%) than in single long-bone fractures (0.5% to 2%).^1-3

With the increasing role of hospitalists in assisting in the management of orthopedic patients, their knowledge of fat embolism syndrome is important so that it can be included in the differential diagnosis of acute respiratory failure in these orthopedic patients.

Review of the Data

Pathogenesis. Clinical manifestations of fat embolism syndrome have been acknowledged for more than 100 years. Since its first description in the 1860s, there has been speculation about the etiology of this condition. In the 1920s, two theories were proposed to explain the origin of the fat droplets: the mechanical and biochemical theories.^2,4

Mechanical theory suggests that trauma to long bones disturbs fat cells within the bone marrow or adipose tissue, causing fat globules to mobilize.^2,3 There is a rise in marrow pressure above venous pressure, which allows fat particles to enter the circulation through damaged venules surrounding the fracture site. Once lodged in the pulmonary microvasculature, embolized fat causes local ischemia and inflammation. Fat globules may pass into the arterial circulation either by paradoxical embolism through a patent foramen ovale, or by microemboli that pass through the lungs into the arterial circulation. This explains embolization to other organs, including the brain, retina, and skin.

Alternatively, biochemical theory hypothesizes that fat embolism syndrome is contingent on the production of toxic intermediaries from the breakdown of embolized fat.^2,3 This theory suggests that the release of catecholamines after severe trauma can liberate free fatty acids from fat stores, or that acute-phase reactants at the trauma site affect fat solubility, causing agglutination and embolization. This theory helps to explain nontraumatic fat embolism syndrome, as well as the delay in development of the clinical syndrome after acute injury.

Clinical presentation. Most patients have a latent period after trauma of 12 to 72 hours before symptoms of fat embolism syndrome become apparent; however, clinical manifestations might occur immediately or up to one to two weeks following injury.^2,4 As previously mentioned, the classic triad of symptoms includes respiratory compromise, neurological impairment, and a petechial rash.

click for large version

The most common and usually earliest manifestation is acute hypoxia, which must be distinguished from other treatable causes of hypoxia, including pneumothorax, hemothorax, PE, and pneumonia. Pulmonary changes might progress to respiratory failure similar to acute respiratory distress syndrome. Neurological manifestations are primarily nonspecific and include headache, irritability, delirium, seizures, and coma. Focal neurological deficits are rare but have been described.⁵ Almost all neurological symptoms are fully reversible. The petechial rash is distinctive and occurs on the chest, axilla, and subconjunctiva. Although the rash occurs in only 20% to 50% of patients and resolves fairly quickly, in the appropriate clinical setting, this rash is considered pathognomonic.^1,2,4

A variety of other nonspecific signs and symptoms might also occur: pyrexia, tachycardia, fat in the urine or sputum, retinal changes, renal insufficiency, myocardial dysfunction, and an otherwise unexplained drop in hematocrit or platelet count.

Diagnosis. Fat embolism syndrome is a clinical diagnosis and a diagnosis of exclusion. There are no specific confirmatory tests. An arterial blood gas will usually reveal a PaO2 of <60 mmHg.3 Laboratory evaluation might also show fat globules in the urine or sputum on Sudan or Oil Red O staining, but these findings are nonspecific.^3,4 Bronchoscopy with bronchial alveolar lavage (BAL) might similarly detect fat droplets in alveolar macrophages in the BAL fluid; however, the sensitivity and specificity for diagnosis of fat embolism syndrome are unknown.⁴ None of these tests can be used solely for the diagnosis of fat embolism syndrome.

Thrombocytopenia and anemia out of proportion to the expected drop from surgery are not uncommon in addition to other nonspecific laboratory findings, including hypocalcemia, elevated serum lipase level, and elevated erythrocyte sedimentation rate.⁴ Several radiological findings have been observed on lung and brain imaging, though the findings are nonspecific and none are diagnostic. A chest X-ray might be normal, but abnormalities are seen in 30% to 50% of cases.² Typically, when abnormal, the chest X-ray shows diffuse interstitial and alveolar densities, as well as patchy perihilar and basilar infiltrates resembling pulmonary edema. These X-ray findings might not be seen for up to 12 to 24 hours following the onset of clinical symptoms.

The most commonly used diagnostic criteria for the diagnosis of fat embolism syndrome are published by Gurd et al.⁶ At least two major criteria or one major criterion and four minor criteria are required for the diagnosis of fat embolism syndrome. The major criteria are based on the three classic signs and symptoms of fat embolism syndrome; the minor criteria include the finding of fat globules in the urine and sputum as well as some of the previously mentioned nonspecific clinical signs and laboratory tests.

Other criteria for diagnosis have been suggested, including those published by Lindeque et al, which focuses primarily on the respiratory characteristics, and a more recent set of semiquantitative diagnostic criteria called the fat embolism index, published by Schonfeld et al.^7,8 Schonfeld’s scoring index accounts for the major signs and symptoms of fat embolism syndrome and weighs them according to relative specificity. A score of 5 or more is required for diagnosis of fat embolism syndrome. Table 2 compares the three sets of criteria used for diagnosis of fat embolism syndrome.

Treatment. The treatment of fat embolism syndrome is supportive. Most often, this requires supplemental oxygen for hypoxia and, possibly, fluid resuscitation in the case of hypovolemia. Occasionally, though, these relatively minor supportive therapies need to be escalated to bipap or even full ventilatory support and vasopressors in the more severe cases.

Based on the premise that steroids will attenuate the inflammatory reaction to free fatty acids within the lung, steroids have been tried in the treatment of fat embolism syndrome. However, there are no studies that clearly show benefit with their use.

Prevention. Most of the methods of prevention involve surgical intervention rather than medical therapy. Because microscopic fat emboli are showered during manipulation of long-bone fragments, early immobilization of fractures is recommended, and operative correction rather than conservative management is the preferred method.^2,3 One report estimates a 70% reduction in pulmonary complications from this intervention alone.⁹

Further, two surgical techniques are debated as possible means of preventing fat embolism syndrome. The first is “venting,” in which a hole is made distal to the site of intramedullary nail placement. This reduces intramedullary pressure elevation and, therefore, extravasation of fat into the circulation.¹⁰ The second technique is the use of a reamer, irrigator, aspirator (RIA) device. A reamer is a tool used to create an accurate-sized hole for an intramedullary nail. Reaming before intramedullary nail placement can release fat deposits into the circulation. The RIA device irrigates and aspirates resident fat deposits as it reams the canal, releasing fewer deposits into the circulation.¹¹ At this time, these two techniques are considered but not used routinely by surgeons.

Corticosteroids remain a debated method of prevention of fat embolism syndrome. A number of smaller studies suggest steroid therapy might reduce the incidence of fat embolism syndrome and hypoxia; a 2009 meta-analysis pooling nearly 400 patients from these smaller studies found such results.12 Unfortunately, the included studies were noted to be of poor quality, and no change in mortality was found. These results, combined with the possibility of poor wound healing or infection as a complication of steroid use, keep steroids from being used routinely to prevent fat embolism syndrome.

Clinical course. The severity of fat embolism syndrome ranges from mild transient hypoxia with confusion to progressively worsening symptoms leading to acute respiratory distress syndrome and coma. Bulger et al found a 7% mortality rate in this population.¹ Less commonly, patients have a fulminant presentation with symptom onset less than 12 hours after injury. With this presentation, patients have a higher rate of mortality—as high as 15%.¹³

Back to the Case

This young man with bilateral long-bone fractures was at high risk of developing fat embolism syndrome. As is recommended, he was quickly taken to the operating room for fracture stabilization with open reduction and internal fixation. In addition, a RIA device was used to decrease intramedullary pressure. Nonetheless, within the first two days of injury, he developed hypoxia and confusion. These clinical changes were associated with an unexpected drop in hematocrit.

Chest X-ray and high-resolution computed tomography did not reveal a cause of his hypoxia. Similarly, laboratory evaluation for a reversible cause of encephalopathy was negative. A Sudan stain of his urine revealed free fat globules. Though he did not develop axillary petechiae, this clinical picture is consistent with fat embolism syndrome based on Gurd’s criteria. He was supported with oxygen therapy, and he stabilized without further complications.

Drs. Smith and Rice are members of the Section of Hospital Medicine at Vanderbilt University in Nashville, Tenn.

References

1. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg. 1997;132:435-439.
2. Levy D. The fat embolism syndrome. Clin Orthop. 1990;261:281-286.
3. Akhtar S. Fat embolism. Anes Clin. 2009;27:533-550.
4. Gupta A, Reilly C. Fat embolism. Anaesth Crit Care Pain. 2007;7:148-151.
5. Thomas JE, Ayyar DR. Systemic fat embolism. Arch Neurol. 1972;26:517-523.
6. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56B:408-416.
7. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. J Bone Joint Surg Br. 1987;69:128-131.
8. Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Ann Intern Med. 1983;99:438-443.
9. Robinson CM. Current concepts of respiratory insufficiency syndromes after fracture. J Bone Joint Surg Br. 2001;83:781-791.
10. Kim YH, Oh SW, Kim JS. Prevalence of fat embolism following bilateral simultaneous and unilateral total hip arthroplasty performed with or without cement: a prospective, randomized clinical study. J Bone Joint Surg Am. 2002;84A:1372-1379.
11. Volgas DA, Burch T, Stannard JP, Ellis T, Bilotta J, Alonso JE. Fat embolus in femur fractures: a comparison of two reaming systems. Injury. 2010;41 Suppl 2:S90-S93.
12. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Can J Surg. 2009;52:386-393.
13. Bracco D, Favre JB, Joris F, Ravussin A. Fatal fat embolism syndrome: a case report. J Neurosurg Anesthesiol. 2000;12:221-224.

The Institute of Medicine (IOM) issued the report Health IT and Patient Safety: Building Safer Systems for Better Care in November 2011. SHM considers this a landmark report that serves as a call to action to improve the health information technology (HIT) systems used daily to deliver on the promise of safer, more efficient care. SHM’s IT Committee and IT Policy Committee carefully reviewed this report and have released a letter in support of its findings. SHM encourages its members to read the IOM report (www.iom.edu) or the summary of the report.

In support of the report, SHM highlighted the following:

• SHM specifically supports a call for safety transparency; a mandatory reporting mechanism for vendors; a voluntary reporting mechanism for providers to report unsafe conditions in electronic health records (EHRs) and adverse events; and the elimination of nondisclosure clauses.
• SHM supports the need for additional research to guide the design and implementation of EHR, computerized physician order entry (CPOE) systems, and clinical-decision-support (CDS) systems, including usability and expanded functionality.
• SHM supports the need for HIT education at all levels of the healthcare system from providers to vendors to include quality/safety science and process improvement.
• SHM echoes the need for interoperability, not only for data exchange, but also for CDS tools and for liquidity of data to allow new product incomers into the market and the ability to move between vendors.
• SHM believes in dual accountability between vendors and providers in HIT products to help motivate the industry to more quickly improve the safety and usability of products.
• SHM is moving ahead on these areas independently and believes that hospitalists are well positioned to be involved in achieving these goals. To assist members in their efforts, the IT Education Committee is working on in-person and online HIT educational venues for SHM members. SHM’s Health IT Quality Committee is organizing collaboratives around CDS and quality innovation sharing. The Health Quality and Patient Safety Committee continues to discuss the safety of IT systems and methods to improve them. SHM’s mentored implementation programs are engaging directly with vendors to try to build products and the functionality needed around glycemic control, care transitions, and VTE prophylaxis.
• SHM believes that its members can be involved in the research to answer many of the important questions that are unresolved in HIT. Please contact SHM to ensure that the organization is representing your needs in this important area. The current situation is a long way from the full potential HIT can provide, and SHM is committed to helping its members and the industry in moving to the next level.

The Institute of Medicine (IOM) issued the report Health IT and Patient Safety: Building Safer Systems for Better Care in November 2011. SHM considers this a landmark report that serves as a call to action to improve the health information technology (HIT) systems used daily to deliver on the promise of safer, more efficient care. SHM’s IT Committee and IT Policy Committee carefully reviewed this report and have released a letter in support of its findings. SHM encourages its members to read the IOM report (www.iom.edu) or the summary of the report.

In support of the report, SHM highlighted the following:

• SHM specifically supports a call for safety transparency; a mandatory reporting mechanism for vendors; a voluntary reporting mechanism for providers to report unsafe conditions in electronic health records (EHRs) and adverse events; and the elimination of nondisclosure clauses.
• SHM supports the need for additional research to guide the design and implementation of EHR, computerized physician order entry (CPOE) systems, and clinical-decision-support (CDS) systems, including usability and expanded functionality.
• SHM supports the need for HIT education at all levels of the healthcare system from providers to vendors to include quality/safety science and process improvement.
• SHM echoes the need for interoperability, not only for data exchange, but also for CDS tools and for liquidity of data to allow new product incomers into the market and the ability to move between vendors.
• SHM believes in dual accountability between vendors and providers in HIT products to help motivate the industry to more quickly improve the safety and usability of products.
• SHM is moving ahead on these areas independently and believes that hospitalists are well positioned to be involved in achieving these goals. To assist members in their efforts, the IT Education Committee is working on in-person and online HIT educational venues for SHM members. SHM’s Health IT Quality Committee is organizing collaboratives around CDS and quality innovation sharing. The Health Quality and Patient Safety Committee continues to discuss the safety of IT systems and methods to improve them. SHM’s mentored implementation programs are engaging directly with vendors to try to build products and the functionality needed around glycemic control, care transitions, and VTE prophylaxis.
• SHM believes that its members can be involved in the research to answer many of the important questions that are unresolved in HIT. Please contact SHM to ensure that the organization is representing your needs in this important area. The current situation is a long way from the full potential HIT can provide, and SHM is committed to helping its members and the industry in moving to the next level.

The Institute of Medicine (IOM) issued the report Health IT and Patient Safety: Building Safer Systems for Better Care in November 2011. SHM considers this a landmark report that serves as a call to action to improve the health information technology (HIT) systems used daily to deliver on the promise of safer, more efficient care. SHM’s IT Committee and IT Policy Committee carefully reviewed this report and have released a letter in support of its findings. SHM encourages its members to read the IOM report (www.iom.edu) or the summary of the report.

In support of the report, SHM highlighted the following:

• SHM specifically supports a call for safety transparency; a mandatory reporting mechanism for vendors; a voluntary reporting mechanism for providers to report unsafe conditions in electronic health records (EHRs) and adverse events; and the elimination of nondisclosure clauses.
• SHM supports the need for additional research to guide the design and implementation of EHR, computerized physician order entry (CPOE) systems, and clinical-decision-support (CDS) systems, including usability and expanded functionality.
• SHM supports the need for HIT education at all levels of the healthcare system from providers to vendors to include quality/safety science and process improvement.
• SHM echoes the need for interoperability, not only for data exchange, but also for CDS tools and for liquidity of data to allow new product incomers into the market and the ability to move between vendors.
• SHM believes in dual accountability between vendors and providers in HIT products to help motivate the industry to more quickly improve the safety and usability of products.
• SHM is moving ahead on these areas independently and believes that hospitalists are well positioned to be involved in achieving these goals. To assist members in their efforts, the IT Education Committee is working on in-person and online HIT educational venues for SHM members. SHM’s Health IT Quality Committee is organizing collaboratives around CDS and quality innovation sharing. The Health Quality and Patient Safety Committee continues to discuss the safety of IT systems and methods to improve them. SHM’s mentored implementation programs are engaging directly with vendors to try to build products and the functionality needed around glycemic control, care transitions, and VTE prophylaxis.
• SHM believes that its members can be involved in the research to answer many of the important questions that are unresolved in HIT. Please contact SHM to ensure that the organization is representing your needs in this important area. The current situation is a long way from the full potential HIT can provide, and SHM is committed to helping its members and the industry in moving to the next level.

With last month’s publication of the 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey), we have some fascinating new information about the scheduling choices of HM groups—some of which has never been collected by SHM before.

For example, we learned this year that 42% of respondent groups serving adult patients predominantly utilize a schedule of seven days on followed by seven days off (“seven-on, seven-off”), while another 42% use variable/other scheduling patterns. A small minority of groups utilize other types of rotating block schedules (e.g. five-on/five-off) or Monday-Friday schedules. The type of schedule used varies a lot by area of the country, ownership/employment model, and other group characteristics.

Full-time adult medicine hospitalists working shift-based schedules now work a median of 182 shifts, or work periods, annually, down from 188 the last time SHM asked this question in 2005. For doctors working hybrid schedules, including both shifts and on-call duties, the number of shifts declined to 204 from 215 in 2005. During the same period, hospitalists’ annual encounter volume also has declined, though compensation has continued its inexorable rise.

So if the number of shifts worked and patient encounters both have declined since 2005, why do hospitalists feel so much busier today?

Well, for one thing, we learned in this year’s survey that 75% of adult hospitalist groups schedule day shifts of 12 to 13.9 hours in length, while the other 25% use shorter day shifts. About 85% of night shifts are also 12 to 13.9 hours long, while the preponderance of evening/swing shifts fall into either the 10- to 11.9-hour range (45%) or the eight-hours-or-less range (33%). In 2005, the median shift length for all respondents—both adult and pediatric—was 11 hours for groups using shift-based models, and only eight hours for groups using hybrid or other scheduling models. So although this year’s data is not presented in the same way as it was in 2005, it would appear that the typical shift length might have increased some.

In addition, in 2005, only 51% of groups reported having an on-site provider at night. This year, 55% of groups reported having total on-site nighttime coverage, and an additional 28% reported using a combination of on-site and on-call coverage. And the proportion of groups reporting no responsibility for night coverage at all declined to about 1% from 8%. I’m guessing the need to work more nights also contributes to hospitalists’ feelings of increased workload.

Although encounters have decreased, hospitalist wRVUs have risen dramatically. In part, this is due to adjustments in Medicare wRVU values for typical E&M services, but I believe it also is the result of increased patient complexity and/or improved documentation and coding by hospitalists—both of which require more time.

And finally, hospitalists are being asked to do a lot more nonclinical work these days, such as participating in quality-improvement (QI) and patient-flow initiatives, and championing the implementation of electronic health records (EHRs).

All of these factors, and probably others, have combined to make the typical hospitalist’s job much more complex and demanding today than it was in 2005, despite working a few less shifts and have a few less patient encounters annually.

Leslie Flores is SHM senior advisor, practice management.

With last month’s publication of the 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey), we have some fascinating new information about the scheduling choices of HM groups—some of which has never been collected by SHM before.

For example, we learned this year that 42% of respondent groups serving adult patients predominantly utilize a schedule of seven days on followed by seven days off (“seven-on, seven-off”), while another 42% use variable/other scheduling patterns. A small minority of groups utilize other types of rotating block schedules (e.g. five-on/five-off) or Monday-Friday schedules. The type of schedule used varies a lot by area of the country, ownership/employment model, and other group characteristics.

Full-time adult medicine hospitalists working shift-based schedules now work a median of 182 shifts, or work periods, annually, down from 188 the last time SHM asked this question in 2005. For doctors working hybrid schedules, including both shifts and on-call duties, the number of shifts declined to 204 from 215 in 2005. During the same period, hospitalists’ annual encounter volume also has declined, though compensation has continued its inexorable rise.

So if the number of shifts worked and patient encounters both have declined since 2005, why do hospitalists feel so much busier today?

Well, for one thing, we learned in this year’s survey that 75% of adult hospitalist groups schedule day shifts of 12 to 13.9 hours in length, while the other 25% use shorter day shifts. About 85% of night shifts are also 12 to 13.9 hours long, while the preponderance of evening/swing shifts fall into either the 10- to 11.9-hour range (45%) or the eight-hours-or-less range (33%). In 2005, the median shift length for all respondents—both adult and pediatric—was 11 hours for groups using shift-based models, and only eight hours for groups using hybrid or other scheduling models. So although this year’s data is not presented in the same way as it was in 2005, it would appear that the typical shift length might have increased some.

In addition, in 2005, only 51% of groups reported having an on-site provider at night. This year, 55% of groups reported having total on-site nighttime coverage, and an additional 28% reported using a combination of on-site and on-call coverage. And the proportion of groups reporting no responsibility for night coverage at all declined to about 1% from 8%. I’m guessing the need to work more nights also contributes to hospitalists’ feelings of increased workload.

Although encounters have decreased, hospitalist wRVUs have risen dramatically. In part, this is due to adjustments in Medicare wRVU values for typical E&M services, but I believe it also is the result of increased patient complexity and/or improved documentation and coding by hospitalists—both of which require more time.

And finally, hospitalists are being asked to do a lot more nonclinical work these days, such as participating in quality-improvement (QI) and patient-flow initiatives, and championing the implementation of electronic health records (EHRs).

All of these factors, and probably others, have combined to make the typical hospitalist’s job much more complex and demanding today than it was in 2005, despite working a few less shifts and have a few less patient encounters annually.

Leslie Flores is SHM senior advisor, practice management.

With last month’s publication of the 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey), we have some fascinating new information about the scheduling choices of HM groups—some of which has never been collected by SHM before.

For example, we learned this year that 42% of respondent groups serving adult patients predominantly utilize a schedule of seven days on followed by seven days off (“seven-on, seven-off”), while another 42% use variable/other scheduling patterns. A small minority of groups utilize other types of rotating block schedules (e.g. five-on/five-off) or Monday-Friday schedules. The type of schedule used varies a lot by area of the country, ownership/employment model, and other group characteristics.

Full-time adult medicine hospitalists working shift-based schedules now work a median of 182 shifts, or work periods, annually, down from 188 the last time SHM asked this question in 2005. For doctors working hybrid schedules, including both shifts and on-call duties, the number of shifts declined to 204 from 215 in 2005. During the same period, hospitalists’ annual encounter volume also has declined, though compensation has continued its inexorable rise.

So if the number of shifts worked and patient encounters both have declined since 2005, why do hospitalists feel so much busier today?

Well, for one thing, we learned in this year’s survey that 75% of adult hospitalist groups schedule day shifts of 12 to 13.9 hours in length, while the other 25% use shorter day shifts. About 85% of night shifts are also 12 to 13.9 hours long, while the preponderance of evening/swing shifts fall into either the 10- to 11.9-hour range (45%) or the eight-hours-or-less range (33%). In 2005, the median shift length for all respondents—both adult and pediatric—was 11 hours for groups using shift-based models, and only eight hours for groups using hybrid or other scheduling models. So although this year’s data is not presented in the same way as it was in 2005, it would appear that the typical shift length might have increased some.

In addition, in 2005, only 51% of groups reported having an on-site provider at night. This year, 55% of groups reported having total on-site nighttime coverage, and an additional 28% reported using a combination of on-site and on-call coverage. And the proportion of groups reporting no responsibility for night coverage at all declined to about 1% from 8%. I’m guessing the need to work more nights also contributes to hospitalists’ feelings of increased workload.

Although encounters have decreased, hospitalist wRVUs have risen dramatically. In part, this is due to adjustments in Medicare wRVU values for typical E&M services, but I believe it also is the result of increased patient complexity and/or improved documentation and coding by hospitalists—both of which require more time.

And finally, hospitalists are being asked to do a lot more nonclinical work these days, such as participating in quality-improvement (QI) and patient-flow initiatives, and championing the implementation of electronic health records (EHRs).

All of these factors, and probably others, have combined to make the typical hospitalist’s job much more complex and demanding today than it was in 2005, despite working a few less shifts and have a few less patient encounters annually.

Leslie Flores is SHM senior advisor, practice management.

Fellowship has its privileges. For SHM’s Fellows and Senior Fellows in Hospital Medicine, it means demonstrating leadership and critical experience in a rapidly growing medical specialty. It also means receiving recognition among peers at SHM’s annual meeting and access to the SHM Fellows Lounge.

In addition to being able to use the FHM, SFHM, or MHM designations for professional purposes, Fellows receive an official certificate, listing on the SHM website, and even discounts on products in the SHM online store.

The application process can take time, so plan ahead and apply early. The application deadline for the 2013 class of Fellows is January 18.

For more information, visit www.hospitalmedicine.org/fellows.

Fellowship has its privileges. For SHM’s Fellows and Senior Fellows in Hospital Medicine, it means demonstrating leadership and critical experience in a rapidly growing medical specialty. It also means receiving recognition among peers at SHM’s annual meeting and access to the SHM Fellows Lounge.

In addition to being able to use the FHM, SFHM, or MHM designations for professional purposes, Fellows receive an official certificate, listing on the SHM website, and even discounts on products in the SHM online store.

The application process can take time, so plan ahead and apply early. The application deadline for the 2013 class of Fellows is January 18.

For more information, visit www.hospitalmedicine.org/fellows.

Fellowship has its privileges. For SHM’s Fellows and Senior Fellows in Hospital Medicine, it means demonstrating leadership and critical experience in a rapidly growing medical specialty. It also means receiving recognition among peers at SHM’s annual meeting and access to the SHM Fellows Lounge.

In addition to being able to use the FHM, SFHM, or MHM designations for professional purposes, Fellows receive an official certificate, listing on the SHM website, and even discounts on products in the SHM online store.

The application process can take time, so plan ahead and apply early. The application deadline for the 2013 class of Fellows is January 18.

For more information, visit www.hospitalmedicine.org/fellows.

Business Moves

Spring Valley Hospital Medical Center in Las Vegas has announced that Tacoma, Wash.-based Sound Physicians will provide hospitalist services at the 231-bed acute-care hospital.

Sound Physicians also will offer hospitalist services at Southern Regional Medical Center in Riverdale, Ga., just outside Atlanta.

Summerville (S.C.) Medical Center has teamed up with the Greenville, S.C.-based OB Hospitalist Group to provide obstetrics and gynecology services to inpatients 24 hours a day. Five physicians will provide OB/GYN hospitalist services: Susie Wilson, MD; Tawanna Gilliard, MD; Melissa Pearce, MD; Greg Miller, MD; and Ann Gorman, MD.

Buffalo Medical Group (BMG) has begun providing hospitalist services to inpatients at Sisters of Charity Hospital in Buffalo, N.Y. BMG has been supplying hospitalist services in the Buffalo area since 1999.

Benchmark Hospitalists, based in Manhattan Beach, Calif., has partnered with Methodist Hospital of Southern California in Arcadia to provide hospitalist management services. Benchmark has been helping hospitals improve quality and return on investment in their hospitalist programs since 2009.

Galen Inpatient Physicians will begin providing 24/7 hospitalist services at Memorial Hospital Los Banos in California. Galen has provided HM services to medical centers nationwide since 2000.

—Michael O’Neal

Hospitalist John C. Sorg, MD, recently was appointed medical director of the hospitalist program at North Arkansas Regional Medical Center in Harrison, Ark. Dr. Sorg is board-certified in internal medicine and spent nearly 20 years in private practice in Elkhart, Ind.

Chintu Sharma, MD, is the July Physician of the Month at Carroll Hospital Center in Westminster, Md. Dr. Sharma has been a hospitalist at Carroll for more than two years, and his supervisors say that he leads by example in providing excellent patient care.

Karim Godamunne, MD, is the new chief medical officer of North Fulton Hospital in Roswell, Ga. Dr. Godamunne also serves as the HM group’s medical director at North Fulton.

After working with the HM group at Covenant HealthCare in Saginaw, Mich., since 2003, Iris Mangulabnan, MD, FACP, has been named the group’s medical director. The program employs 27 providers, 18 of whom are hospitalists.

Deborah Puckhaber, MD, has been named medical director of the hospitalist service at North Country Hospital in Newport, Vt. Dr. Puckhaber completed her medical training at the State University of New York Buffalo School of Medicine, and practiced adolescent and internal medicine for 14 years before becoming a hospitalist.

Kenric Maynor, MD, has been named HM director of Geisinger Health System in Pennsylvania. In addition to his duties of overseeing the HM programs at six area hospitals, Dr. Maynor will implement a new program at Geisinger Community Medical Center in Scranton.

Adam Fall, MD, SFHM, has joined TeamHealth’s Hospital Medicine Eastern Division as regional medical director for its eastern Tennessee and Georgia regions.

Jeffrey L. Dryden, DO, is the new medical director of the hospitalist team at Ozarks Medical Center in West Plains, Mo. Dr. Dryden has been practicing medicine for more than 20 years, and currently serves as a member of the American Osteopathic Association, the American College of Osteopathic Internists, and the South Central Ozark Association of Osteopathic Physicians.

Business Moves

Spring Valley Hospital Medical Center in Las Vegas has announced that Tacoma, Wash.-based Sound Physicians will provide hospitalist services at the 231-bed acute-care hospital.

Sound Physicians also will offer hospitalist services at Southern Regional Medical Center in Riverdale, Ga., just outside Atlanta.

Summerville (S.C.) Medical Center has teamed up with the Greenville, S.C.-based OB Hospitalist Group to provide obstetrics and gynecology services to inpatients 24 hours a day. Five physicians will provide OB/GYN hospitalist services: Susie Wilson, MD; Tawanna Gilliard, MD; Melissa Pearce, MD; Greg Miller, MD; and Ann Gorman, MD.

Buffalo Medical Group (BMG) has begun providing hospitalist services to inpatients at Sisters of Charity Hospital in Buffalo, N.Y. BMG has been supplying hospitalist services in the Buffalo area since 1999.

Benchmark Hospitalists, based in Manhattan Beach, Calif., has partnered with Methodist Hospital of Southern California in Arcadia to provide hospitalist management services. Benchmark has been helping hospitals improve quality and return on investment in their hospitalist programs since 2009.

Galen Inpatient Physicians will begin providing 24/7 hospitalist services at Memorial Hospital Los Banos in California. Galen has provided HM services to medical centers nationwide since 2000.

—Michael O’Neal

Hospitalist John C. Sorg, MD, recently was appointed medical director of the hospitalist program at North Arkansas Regional Medical Center in Harrison, Ark. Dr. Sorg is board-certified in internal medicine and spent nearly 20 years in private practice in Elkhart, Ind.

Chintu Sharma, MD, is the July Physician of the Month at Carroll Hospital Center in Westminster, Md. Dr. Sharma has been a hospitalist at Carroll for more than two years, and his supervisors say that he leads by example in providing excellent patient care.

Karim Godamunne, MD, is the new chief medical officer of North Fulton Hospital in Roswell, Ga. Dr. Godamunne also serves as the HM group’s medical director at North Fulton.

After working with the HM group at Covenant HealthCare in Saginaw, Mich., since 2003, Iris Mangulabnan, MD, FACP, has been named the group’s medical director. The program employs 27 providers, 18 of whom are hospitalists.

Deborah Puckhaber, MD, has been named medical director of the hospitalist service at North Country Hospital in Newport, Vt. Dr. Puckhaber completed her medical training at the State University of New York Buffalo School of Medicine, and practiced adolescent and internal medicine for 14 years before becoming a hospitalist.

Kenric Maynor, MD, has been named HM director of Geisinger Health System in Pennsylvania. In addition to his duties of overseeing the HM programs at six area hospitals, Dr. Maynor will implement a new program at Geisinger Community Medical Center in Scranton.

Adam Fall, MD, SFHM, has joined TeamHealth’s Hospital Medicine Eastern Division as regional medical director for its eastern Tennessee and Georgia regions.

Jeffrey L. Dryden, DO, is the new medical director of the hospitalist team at Ozarks Medical Center in West Plains, Mo. Dr. Dryden has been practicing medicine for more than 20 years, and currently serves as a member of the American Osteopathic Association, the American College of Osteopathic Internists, and the South Central Ozark Association of Osteopathic Physicians.

Business Moves

Spring Valley Hospital Medical Center in Las Vegas has announced that Tacoma, Wash.-based Sound Physicians will provide hospitalist services at the 231-bed acute-care hospital.

Sound Physicians also will offer hospitalist services at Southern Regional Medical Center in Riverdale, Ga., just outside Atlanta.

Summerville (S.C.) Medical Center has teamed up with the Greenville, S.C.-based OB Hospitalist Group to provide obstetrics and gynecology services to inpatients 24 hours a day. Five physicians will provide OB/GYN hospitalist services: Susie Wilson, MD; Tawanna Gilliard, MD; Melissa Pearce, MD; Greg Miller, MD; and Ann Gorman, MD.

Buffalo Medical Group (BMG) has begun providing hospitalist services to inpatients at Sisters of Charity Hospital in Buffalo, N.Y. BMG has been supplying hospitalist services in the Buffalo area since 1999.

Benchmark Hospitalists, based in Manhattan Beach, Calif., has partnered with Methodist Hospital of Southern California in Arcadia to provide hospitalist management services. Benchmark has been helping hospitals improve quality and return on investment in their hospitalist programs since 2009.

Galen Inpatient Physicians will begin providing 24/7 hospitalist services at Memorial Hospital Los Banos in California. Galen has provided HM services to medical centers nationwide since 2000.

—Michael O’Neal

Hospitalist John C. Sorg, MD, recently was appointed medical director of the hospitalist program at North Arkansas Regional Medical Center in Harrison, Ark. Dr. Sorg is board-certified in internal medicine and spent nearly 20 years in private practice in Elkhart, Ind.

Chintu Sharma, MD, is the July Physician of the Month at Carroll Hospital Center in Westminster, Md. Dr. Sharma has been a hospitalist at Carroll for more than two years, and his supervisors say that he leads by example in providing excellent patient care.

Karim Godamunne, MD, is the new chief medical officer of North Fulton Hospital in Roswell, Ga. Dr. Godamunne also serves as the HM group’s medical director at North Fulton.

After working with the HM group at Covenant HealthCare in Saginaw, Mich., since 2003, Iris Mangulabnan, MD, FACP, has been named the group’s medical director. The program employs 27 providers, 18 of whom are hospitalists.

Deborah Puckhaber, MD, has been named medical director of the hospitalist service at North Country Hospital in Newport, Vt. Dr. Puckhaber completed her medical training at the State University of New York Buffalo School of Medicine, and practiced adolescent and internal medicine for 14 years before becoming a hospitalist.

Kenric Maynor, MD, has been named HM director of Geisinger Health System in Pennsylvania. In addition to his duties of overseeing the HM programs at six area hospitals, Dr. Maynor will implement a new program at Geisinger Community Medical Center in Scranton.

Adam Fall, MD, SFHM, has joined TeamHealth’s Hospital Medicine Eastern Division as regional medical director for its eastern Tennessee and Georgia regions.

Jeffrey L. Dryden, DO, is the new medical director of the hospitalist team at Ozarks Medical Center in West Plains, Mo. Dr. Dryden has been practicing medicine for more than 20 years, and currently serves as a member of the American Osteopathic Association, the American College of Osteopathic Internists, and the South Central Ozark Association of Osteopathic Physicians.

SHM recently joined more than 135 organizations in opposing legislation that would eliminate funding for the Agency for Health Care Research and Quality (AHRQ), according to a July 30 letter. Language terminating the agency was part of a fiscal-year 2013 spending bill approved July 18 by the Republican-controlled Senate Subcommittee on Labor, Health and Human Services, Education, and Related Agencies.

Organized by the Friends of AHRQ Coalition, the letter calls on members of Congress to oppose any bill that terminates the agency and its important research.

“To ‘terminate’ AHRQ in the current fiscal environment is penny-wise and pound-foolish,” the letter states. “AHRQ-funded research is being used in hospitals, private practices, health departments, and communities across the nation to fuel innovation and improve quality, identify waste, and enhance efficiency of the healthcare system. … This research helps Americans get their money’s worth when it comes to healthcare. We need more of it, not less.”

A longtime supporter of AHRQ and its efforts to improve quality and patient safety, SHM is deeply concerned about efforts to eliminate this important agency and will fight to preserve its funding. A markup by the full committee has been postponed indefinitely.

The spending bill approved by the subcommittee also prohibits any patient-centered-outcomes research and all economic research within the National Institutes of Health (NIH). It freezes funding for NIH and rescinds the $1 billion available in 2013 under the Prevention and Public Health Fund. It also rescinds $1.6 billion for the Center for Medicare & Medicaid Innovation (CMMI) and blocks other funding for and implementation of the Affordable Care Act.

Laura Allendorf, SHM senior advisor, advocacy and government affairs

SHM recently joined more than 135 organizations in opposing legislation that would eliminate funding for the Agency for Health Care Research and Quality (AHRQ), according to a July 30 letter. Language terminating the agency was part of a fiscal-year 2013 spending bill approved July 18 by the Republican-controlled Senate Subcommittee on Labor, Health and Human Services, Education, and Related Agencies.

Organized by the Friends of AHRQ Coalition, the letter calls on members of Congress to oppose any bill that terminates the agency and its important research.

“To ‘terminate’ AHRQ in the current fiscal environment is penny-wise and pound-foolish,” the letter states. “AHRQ-funded research is being used in hospitals, private practices, health departments, and communities across the nation to fuel innovation and improve quality, identify waste, and enhance efficiency of the healthcare system. … This research helps Americans get their money’s worth when it comes to healthcare. We need more of it, not less.”

A longtime supporter of AHRQ and its efforts to improve quality and patient safety, SHM is deeply concerned about efforts to eliminate this important agency and will fight to preserve its funding. A markup by the full committee has been postponed indefinitely.

The spending bill approved by the subcommittee also prohibits any patient-centered-outcomes research and all economic research within the National Institutes of Health (NIH). It freezes funding for NIH and rescinds the $1 billion available in 2013 under the Prevention and Public Health Fund. It also rescinds $1.6 billion for the Center for Medicare & Medicaid Innovation (CMMI) and blocks other funding for and implementation of the Affordable Care Act.

Laura Allendorf, SHM senior advisor, advocacy and government affairs

SHM recently joined more than 135 organizations in opposing legislation that would eliminate funding for the Agency for Health Care Research and Quality (AHRQ), according to a July 30 letter. Language terminating the agency was part of a fiscal-year 2013 spending bill approved July 18 by the Republican-controlled Senate Subcommittee on Labor, Health and Human Services, Education, and Related Agencies.

Organized by the Friends of AHRQ Coalition, the letter calls on members of Congress to oppose any bill that terminates the agency and its important research.

“To ‘terminate’ AHRQ in the current fiscal environment is penny-wise and pound-foolish,” the letter states. “AHRQ-funded research is being used in hospitals, private practices, health departments, and communities across the nation to fuel innovation and improve quality, identify waste, and enhance efficiency of the healthcare system. … This research helps Americans get their money’s worth when it comes to healthcare. We need more of it, not less.”

A longtime supporter of AHRQ and its efforts to improve quality and patient safety, SHM is deeply concerned about efforts to eliminate this important agency and will fight to preserve its funding. A markup by the full committee has been postponed indefinitely.

The spending bill approved by the subcommittee also prohibits any patient-centered-outcomes research and all economic research within the National Institutes of Health (NIH). It freezes funding for NIH and rescinds the $1 billion available in 2013 under the Prevention and Public Health Fund. It also rescinds $1.6 billion for the Center for Medicare & Medicaid Innovation (CMMI) and blocks other funding for and implementation of the Affordable Care Act.

Laura Allendorf, SHM senior advisor, advocacy and government affairs

As elements of the Accountable Care Act are being implemented, improving patient satisfaction has become an important priority for the specialty of hospital medicine. Specifically, under the Hospital Value-Based Purchasing (HVBP) program, a portion of a hospital’s Medicare reimbursement dollars (1% in fiscal-year 2013, growing to 2% in fiscal-year 2017) are at risk. The Centers for Medicare & Medicaid Services (CMS) will use weighted domains to calculate this “at risk” reimbursement, with 30% of the total based on the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey measuring patient experience, or satisfaction.

One of the goals of SHM’s Practice Management Committee in 2011 was to provide additional support to the HM community with regard to patient satisfaction. To that end, the committee came up with a series of questions that address the following high-level topics about patient satisfaction surveys:

• The questionnaire;
• The methodology;
• Reports;
• Vendor support; and
• Organization.

To learn more about how to access information from your hospital’s patient satisfaction survey vendor, visit www.hospitalmedicine.org/pm.

As elements of the Accountable Care Act are being implemented, improving patient satisfaction has become an important priority for the specialty of hospital medicine. Specifically, under the Hospital Value-Based Purchasing (HVBP) program, a portion of a hospital’s Medicare reimbursement dollars (1% in fiscal-year 2013, growing to 2% in fiscal-year 2017) are at risk. The Centers for Medicare & Medicaid Services (CMS) will use weighted domains to calculate this “at risk” reimbursement, with 30% of the total based on the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey measuring patient experience, or satisfaction.

One of the goals of SHM’s Practice Management Committee in 2011 was to provide additional support to the HM community with regard to patient satisfaction. To that end, the committee came up with a series of questions that address the following high-level topics about patient satisfaction surveys:

• The questionnaire;
• The methodology;
• Reports;
• Vendor support; and
• Organization.

To learn more about how to access information from your hospital’s patient satisfaction survey vendor, visit www.hospitalmedicine.org/pm.

As elements of the Accountable Care Act are being implemented, improving patient satisfaction has become an important priority for the specialty of hospital medicine. Specifically, under the Hospital Value-Based Purchasing (HVBP) program, a portion of a hospital’s Medicare reimbursement dollars (1% in fiscal-year 2013, growing to 2% in fiscal-year 2017) are at risk. The Centers for Medicare & Medicaid Services (CMS) will use weighted domains to calculate this “at risk” reimbursement, with 30% of the total based on the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey measuring patient experience, or satisfaction.

One of the goals of SHM’s Practice Management Committee in 2011 was to provide additional support to the HM community with regard to patient satisfaction. To that end, the committee came up with a series of questions that address the following high-level topics about patient satisfaction surveys:

• The questionnaire;
• The methodology;
• Reports;
• Vendor support; and
• Organization.

To learn more about how to access information from your hospital’s patient satisfaction survey vendor, visit www.hospitalmedicine.org/pm.

What’s better than learning from national experts in hospital-based coding? Learning from them, being able to ask them questions, and sharing your own experiences with others, all at the same time.

CODE-H, which will be offered again this fall, is presented via live webinar at SHM’s new online community, Hospital Medicine Exchange, which enables CODE-H users to post messages to other users and the faculty. Using Hospital Medicine Exchange, CODE-H users can also share their own resources and documents.

Each webinar is archived on the CODE-H site, so participants can log in and learn at any time.

Best of all, one subscription is good for up to 10 participants at each hospital or site, so inviting others at your hospital to participate increases the value.

Used first for CODE-H and SHM’s Hospital Value-Based Purchasing toolkit, Hospital Medicine Exchange will soon be available to all hospitalists as a forum for learning and sharing best practices.

To register for CODE-H, visit www.hospitalmedicine.org/codeh.

What’s better than learning from national experts in hospital-based coding? Learning from them, being able to ask them questions, and sharing your own experiences with others, all at the same time.

CODE-H, which will be offered again this fall, is presented via live webinar at SHM’s new online community, Hospital Medicine Exchange, which enables CODE-H users to post messages to other users and the faculty. Using Hospital Medicine Exchange, CODE-H users can also share their own resources and documents.

Each webinar is archived on the CODE-H site, so participants can log in and learn at any time.

Best of all, one subscription is good for up to 10 participants at each hospital or site, so inviting others at your hospital to participate increases the value.

Used first for CODE-H and SHM’s Hospital Value-Based Purchasing toolkit, Hospital Medicine Exchange will soon be available to all hospitalists as a forum for learning and sharing best practices.

To register for CODE-H, visit www.hospitalmedicine.org/codeh.

What’s better than learning from national experts in hospital-based coding? Learning from them, being able to ask them questions, and sharing your own experiences with others, all at the same time.

CODE-H, which will be offered again this fall, is presented via live webinar at SHM’s new online community, Hospital Medicine Exchange, which enables CODE-H users to post messages to other users and the faculty. Using Hospital Medicine Exchange, CODE-H users can also share their own resources and documents.

Each webinar is archived on the CODE-H site, so participants can log in and learn at any time.

Best of all, one subscription is good for up to 10 participants at each hospital or site, so inviting others at your hospital to participate increases the value.

Used first for CODE-H and SHM’s Hospital Value-Based Purchasing toolkit, Hospital Medicine Exchange will soon be available to all hospitalists as a forum for learning and sharing best practices.

To register for CODE-H, visit www.hospitalmedicine.org/codeh.