Clinical Conundrum

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A distinguishing feature

56‐year‐old man with a history of chronic liver disease of unknown etiology was referred for evaluation of intermittent low‐grade fevers, constipation, and an unintentional weight loss of 20‐kg during the previous 9 months. Three weeks prior to presentation, he was admitted to his local hospital for these symptoms and was treated empirically with cefotaxime for 6 days, but his symptoms persisted.

The patient's age and sex make him statistically at risk for vascular disease as well as malignancy. The history of chronic liver disease of unknown etiology is intriguing. In evaluating a patient with chronic liver disease, I want to know about alcohol consumption, intravenous drug use, family history, viral hepatitis serology, and antinuclear antibody testing. Chronic liver disease places this patient at increased risk for infection because portal hypertension causes blood to bypass a large part of the reticuloendothelial system (liver and spleen), therefore increasing the risk of sustained bacteremia.

Regarding his chronic low‐grade fever, I would like to know about his country of origin, travel history, occupational history, risk factors for human immunodeficiency virus (HIV) and tuberculosis, and any symptoms or signs of rheumatologic disease. Constipation and weight loss can be a result of malignancy (eg, hepatocellular carcinoma, colorectal cancer), vascular disease (eg, mesenteric thrombosis), or metabolic derangement (eg, hypercalcemia).

The patient had a history of recurrent episodes of ascites and low‐grade fevers. He first developed ascites, abdominal pain, low‐grade fevers, and pedal edema 20 years ago. These signs and symptoms resolved spontaneously, but similar episodes have recurred every 46 years since. Each time, diagnostic evaluation failed to reveal a specific etiology.

Twelve years prior to presentation, the patient was evaluated for chronic liver disease. Diagnostic tests at that time included viral hepatitis serology, ceruloplasmin, ferritin, alpha‐1‐antitrypsin, antimitochondrial antibody, and antinuclear antibody testing, all the results of which were within the normal range. The patient denied consumption of alcohol, medications, or toxic substances. Percutaneous liver biopsy demonstrated focal parenchymal scarring interspersed with areas of normal parenchyma, consistent with focal ischemic injury (Fig. 1).

Figure 1
Liver biopsy specimen showing extensive scarring (arrow) interspersed with areas of completely normal liver parenchyma (hematoxylin and eosin, ×400).

The duration of the patient's symptoms is striking. A unifying diagnosis for this patient must explain his chronic liver disease, periodic fevers, ascites, and abdominal pain that started at a relatively young age. Conditions to consider include hepatitis B or C, hemochromatosis, Wilson's disease, primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, alpha‐1‐antitrypsin deficiency, and drug or toxin exposure. Venoocclusive disease of the liver and chronic congestive hepatopathy (from heart failure or constrictive pericarditis) are especially attractive possibilities, given the findings of focal ischemic injury on liver biopsy.

Recurrent fever and abdominal pain can occur because of familial Mediterranean fever, which results from a genetic abnormality and causes recurrent peritoneal inflammation associated with fever and ascites. Although unlikely in this case, familial Mediterranean fever can cause secondary amyloidosis with liver involvement.

The patient reported episodic, vague abdominal pain, nausea, anorexia, night sweats, hair thinning, extreme fatigue, and lightheadedness. He had no known allergies, and his medications included propranolol, lactulose, docusate, and omeprazole. He was white, born in the United States, and a lawyer, but he had not worked during the previous 4 months. He was married and monogamous, and an HIV antibody test 4 months prior was negative. He had a remote history of tobacco and alcohol use between the 1960s and the 1980s. He denied intravenous drug use. His family history was only remarkable for a father with coronary artery disease.

With fever, the hypothalamic set point for temperature increases. Night sweats usually indicate an exaggeration of the normal diurnal drop in the hypothalamic set point for temperature, with dissipation of increased heat (caused by fever) through evaporation of perspiration. Unfortunately, night sweats are not specific to any particular cause of fever. Fatigue is equally nonspecific but could result from anemia, hypothyroidism, or adrenal insufficiency or could be a side effect of the propranolol. The lack of a family history makes hereditary periodic fevers unlikely.

The patient appeared chronically ill. His temperature was 35.2C, blood pressure 71/53 mm Hg, heart rate 84 beats per minute, respiratory rate 14 breaths per minute, and oxygen saturation 99% while breathing room air. His weight was 47 kg. Examination of the patient's head and neck revealed bitemporal wasting but no scleral icterus, and the oropharynx was clear. There was no thyromegaly or lymphadenopathy. The findings of the cardiopulmonary examination was normal. The abdomen was soft with mild diffuse tenderness. There was no organomegaly or obvious ascites. His extremities were warm and without edema or cyanosis. He was dark‐skinned and had rare spider angiomas. The results of his neurological examination were normal.

Sepsis, drug ingestion (particularly vasodilators), environmental exposure, and endocrine abnormalities such as adrenal insufficiency and hypothyroidism can all cause both hypothermia and hypotension. Adrenal insufficiency is especially intriguing becauase it is also associated with malaise, abdominal pain, and hyperpigmentation. Explaining both adrenal insufficiency and chronic liver disease is more difficult. Hemochromatosis can cause cirrhotic liver disease, adrenal and thyroid insufficiency, and dark skin, but the patient's normal ferritin and liver biopsy findings make this disease unlikely.

The results of the laboratory studies were: white‐cell count, 4900/mm3, with a normal differential count; hemoglobin, 11.0 g/dL; platelet count, 52,000/mm3; mean corpuscular volume, 89 m3; sodium, 131 mmol/L; potassium, 5.0 mmol/L; chloride, 101 mmol/L; bicarbonate, 21 mmol/L; blood urea nitrogen, 31 mg/dL; creatinine, 1.8 mg/dL; aspartate aminotransferase, 45 U/L (normal range 1641 U/L); alanine aminotransferase, 30 U/L (normal range 1259 U/L); alkaline phosphatase, 587 U/L (normal range 29111 U/L); total bilirubin, 1.1 mg/dL (normal range 0.31.3 mg/dL); gamma‐glutamyl transferase, 169 U/L (normal range 771 U/L); lactate dehydrogenase, 127 IU/L (normal range 91185 IU/L); thyroid‐stimulating hormone, 3.1 mIU/L (normal range 0.54.7 mIU/L). Coagulation studies revealed a prothrombin time of 12 seconds (international normalized ratio [INR] 1.1) and an activated partial thromboplastin time (aPTT) of greater than 100 seconds. Urinalysis and chest radiography were unremarkable.

The low sodium, high potassium, and relatively low bicarbonate levels are all compatible with adrenal insufficiency. When present, the combination of hyponatremia (primarily from glucocorticoid deficiency) and hyperkalemia (from mineralocorticoid deficiency) suggests the adrenal insufficiency is primary, rather than from the pituitary. The differential diagnosis of primary adrenal insufficiency includes autoimmune disease, granulomatous disease, and tumor.

Most interesting is the isolated prolongation of the aPTT, making adrenal hemorrhage another possibility as a cause of the adrenal insufficiency. Isolated elevation of the aPTT suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which would interfere with the test. Heparin administration (which may not be immediately obvious, as in the case of a heparin lock of an intravenous line) and von Willebrand disease (from loss of the normal von Willebrand factorassociated prevention of factor VIII proteolysis) can also cause isolated prolongation of the aPTT.

Tumor, perhaps hepatocellular cancer, remains a possible explanation for the elevated alkaline phosphatase, with possible adrenal involvement. Amyloidosis and diffuse granulomatous disease (either infectious or noninfectious, such as sarcoidosis) can cause elevation in alkaline phosphatase. At this time, I would rule out adrenal insufficiency, further evaluate the elevated aPTT, and image the liver and adrenal glands.

The patient was hospitalized and given intravenous fluids. His blood pressure increased to 90/54 mm Hg. Further testing revealed an alpha‐fetoprotein of 1.5 g/dL (normal range < 6.4 g/dL), an erythrocyte sedimentation rate of greater than 100 mm/s, and normal results of an antinuclear antibody test. Serum cortisol, drawn at 6 a.m., was 3 ng/dL; 60 minutes after cosyntropin stimulation, serum cortisol was 1 ng/dL. An ultrasound of the liver revealed chronic hepatic vein thrombosis.

The low absolute values and the failure of serum cortisol to respond to cosyntropin confirm the diagnosis of adrenal glucocorticoid deficiency. Hepatic vein thrombosis (Budd‐Chiari syndrome) is an unusual occurrence, often associated with a hypercoagulable state or tumor. How can we put these new findings together with the rest of the patient's abnormalities?

Primary antiphospholipid antibody syndrome is the most attractive unifying diagnosis because it appears to explain the most abnormalities with the fewest diagnoses. This syndrome includes arterial and venous thrombosis, thrombocytopenia, and isolated elevation of the aPTT and has been associated with hepatic vein thrombosis (acute and chronic) and adrenal insufficiency (from adrenal hemorrhage as a result of adrenal vein thrombosis). The histological findings of focal ischemic injury, seen on the patient's liver biopsy, are likely explained by hepatic venoocclusive disease.

Magnetic resonance imaging (MRI) of the abdomen (Fig. 2) demonstrated adrenal hemorrhage in the right adrenal gland. The patient's aPTT remained elevated even after his serum was mixed with normal serum, thereby excluding a factor deficiency. The results of a dilute Russell's viper venom time test (which tests the phospholipid‐dependent portion of the coagulation cascade) also showed elevation. The addition of phospholipids to the patient's serum corrected the aPTT, and a screen for factor inhibitors was negative. An anticardiolipin antibody (IgG) test was positive at 59.0 U (normal 0.42.3 U). These findings confirmed the presence of antiphospholipid antibodies.

Figure 2
Magnetic resonance imaging of the abdomen showing right adrenal hemorrhage (arrow) adjacent to the inferior vena cava (arrowhead).

The findings of a bone marrow biopsy, performed to exclude infiltrative diseases, were normal. The patient was diagnosed with primary antiphospholipid syndrome. Hydrocortisone and fludrocortisone were initiated, with the intention to continue them indefinitely. The patient was also started on intravenous heparin, which continued until he achieved a goal INR of 2.03.0 on warfarin. The patient was counseled on the importance of lifelong warfarin therapy given his diagnosis of antiphospholipid syndrome with hepatic vein and adrenal vein thromboses. On follow‐up 6 months after discharge, the patient's hypotension and fatigue had resolved, his alkaline phosphatase level had decreased substantially, and he had returned to work as a lawyer.

COMMENTARY

The diagnosis of a complex case with numerous clinical and laboratory abnormalities can be very difficult. The discussant successfully came to the correct diagnosis because he carefully evaluated each piece of evidence and did not fall prey to faulty triggering, the generation of diagnostic hypotheses based on selected pieces of clinical data.1 In the diagnostic process, physicians trigger new diagnostic possibilities and discard initial hypotheses as new findings emerge. Often, because of heuristic (analytic) biases, physicians fall victim to faulty triggering when evaluating patients.2 When confronted with a trigger feature such as night sweats, many physicians increase their consideration of tuberculosis or lymphoma at the expense of more common diagnoses, even though, as the discussant pointed out, any patient with fever can have this symptom.3 Whereas faulty use of trigger features may make physicians inappropriately consider uncommon diseases, a distinguishing feature limits the number of diagnostic possibilities and significantly changesincreases or decreasesthe likelihood of there being a rare disease.4 By correctly using the distinguishing feature of an elevated aPTT in the context of the patient's diverse clinical features, the discussant was able to arrive at a single, unifying diagnosis of antiphospholipid syndrome.

Antiphospholipid syndrome is arterial or venous thrombosis associated with significantly elevated antiphospholipid antibodies. Isolated prolongation of the aPTT is often the first clue to the presence of antiphospholipid antibodies, which interfere with phospholipid‐dependent coagulation assays.5 Antiphospholipid syndrome is considered primary if it is not associated with a known underlying disease or medication. Antiphospholipid syndrome is secondary if it is associated with certain diseases such as systemic lupus erythematosus and malignancy or with an adverse effect of medication. Although the prevalence of antiphospholipid antibodies is 1%5% in young, apparently healthy control subjects, it is higher in elderly patients with chronic diseases.6 It remains unclear why only certain patients with antiphospholipid antibodies manifest the syndrome, though having vascular risk factors may increase the risk of developing thrombosis in the presence of antiphospholipid antibodies.7

Three types of antiphospholipid antibody tests are currently in clinical use: lupus anticoagulants (measured by prolonged clotting time in a phospholipid‐dependent clotting test, such as the aPTT), anticardiolipin antibodies, and anti‐2‐glycoprotein I antibodies. All 3 tests are plagued by not being standardized between hospitals and laboratories and have limited sensitivity and specificity.8, 9 Lupus anticoagulants are most closely associated with thrombosis. Although a prolonged aPTT in the presence of thrombosis is often the first clue to the presence of lupus anticoagulants, only 30%40% of patients with the syndrome have this laboratory abnormality.10 Therefore, a normal aPTT result does not rule out the presence of antiphospholipid antibodies, and other tests of lupus anticoagulants, such as the dilute Russell viper venom time, should be performed.8, 9 There are many types of anticardiolipin antibodies of varying immunoglobulin isotypes, which all share the ability to bind cardiolipin in vitro. The IgG isotypes (as in our patient) are thought to be most closely associated with thrombosis, and it is known that high titers of anticardiolipin antibodies have much better discriminatory value than low titers.810 There is little data on the anti‐2‐glycoprotein I antibodies, but preliminary data suggest these antibodies may be more specific for the antiphospholipid syndrome.11

The antiphospholipid syndrome has classically been associated with lower‐extremity deep venous thrombosis, recurrent fetal loss, thrombocytopenia, and livedo reticularis.10 However, depending on the size and distribution of the vasculature involved and the extent and chronicity of involvement, antiphospholipid syndrome can result in manifestation of a wide range of diseases. Acute presentations such as thrombotic disease of the gastrointestinal, cardiac, and central nervous systems can be rapid and catastrophic. A more chronic and indolent course can lead to progressive organ dysfunction, as in this patient, with chronic liver disease resulting from recurrent episodes of hepatic venoocclusive disease and chronic hepatic vein thrombosis, a rare but well‐described complication of antiphospholipid syndrome.12, 13 It is unclear why the course of our patient's hepatic vein thrombosis waxed and waned so much. We hypothesized that he had episodes of microvascular hepatic venous thrombosis that led to transient hepatic dysfunction, with subsequent recovery upon spontaneous recanalization of hepatic veins or with healing and regeneration of liver tissue.

Treatment of antiphospholipid syndrome is controversial. Although prior reports suggested that patients with this syndrome were at higher risk for recurrent thrombosis when treated with the usual dose of warfarin (target INR 2.03.0), 2 randomized trial showed there was no difference in the recurrence of thrombosis between moderate‐intensity treatment with warfarin and high‐intensity treatment with warfarin.14, 15 Our patient was treated with warfarin to a moderate‐intensity target INR of 2.03.0 because he had liver disease and adrenal hemorrhage. Although he has done well, it is important that he be continuously reassessed, as should all patients with similar conditions, for the risk and recurrence of thrombosis weighed against the risk of bleeding.

Adrenal insufficiency is another rare complication of antiphospholipid syndrome. It was first described as such in 198016 and has since been reported in both children and adults.1719 Abdominal pain and hypotension were the most common findings (55% and 54%, respectively) in one case series of 86 patients with adrenal insufficiency from antiphospholipid syndrome.20 Fever, nausea, vomiting, weakness, fatigue, lethargy, and altered mental status were also variably present. Loss of adrenal function is most often a result of adrenal hemorrhage, which is best detected by MRI of the adrenal glands.21

The vascular anatomy of the adrenal gland is unusual. Multiple arteries supply the gland, but only one central vein provides drainage, making the gland relatively vulnerable to hemorrhagic infarction.22 Most cases of adrenal insufficiency from antiphospholipid syndrome are thought to be a result of adrenal vein thrombosis. The MRI showed that only the right adrenal gland of our patient had evidence of hemorrhage. Because both adrenal glands must be damaged before adrenal insufficiency results, it is probable that the left adrenal gland was damaged because of prior episodes of infarction and/or hemorrhage, but remote damage could not be detected by MRI. Of note, antiphospholipid antibodies directed against cholesterol‐rich proteins in the adrenal gland can also cause a locally active procoagulant state with microvascular venous thrombosis and subsequent postinfarction hemorrhage, which is another way in which the left adrenal gland could have been damaged without showing up radiographically.23

As for other types of adrenal insufficiency, the primary treatment for adrenal insufficiency from antiphospholipid syndrome is rapid corticosteroid replacement, with the addition of anticoagulants to treat the hypercoagulable state of the antiphospholipid syndrome. Adrenal insufficiency is temporary in some cases.24 Mortality from adrenal insufficiency due to antiphospholipid syndrome may be higher than that from other forms of adrenal insufficiency.22 Therefore, screening for adrenal insufficiency is critical for any patient with suspected or documented antiphospholipid syndrome who presents with abdominal pain, weakness, electrolyte abnormalities, or unexplained hypotension.

This case illustrates the importance, as the key to diagnosis, of determining a distinguishing feature such as a prolonged aPTT from among the multitude of abnormalities that could have led the diagnostic process astray. Occasionally, a single clinical or laboratory abnormality, such as the elevated aPTT in our patient, is so valuable in the assessment of a difficult case that it significantly increases the likelihood of an uncommon condition and leads to the correct final diagnosis, thereby becoming the pivotal distinguishing feature.

Key Points

  • Hypercoagulability can lead to adrenal insufficiency by causing adrenal vein thrombosis and adrenal infarction. Therefore, hypercoagulable states, such as antiphospholipid syndrome, should be considered for patients who present with symptoms or signs of unexplained adrenal insufficiency.

  • Isolated elevation of activated partial thromboplastin time (aPTT) suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which interferes with this test. Heparin administration and von Willebrand disease can also cause isolated prolongation of the aPTT.

  • Treatment of the antiphospholipid syndrome is controversial, but according to the results of 2 recent randomized, controlled trials, patients with this syndrome who have had their first episode of thrombosis should be treated with warfarin, with a goal INR of 2.03.0.

  • When interpreted incorrectly, trigger features such as night sweats cause clinicians to inappropriately consider a rare diagnosis, even though common diagnoses may be more likely. On the other hand, distinguishing features, such as the prolonged aPTT in this patient, truly do increase or decrease the probability of a rare diagnosis.

References
  1. Kassirer JP.Diagnostic reasoning.Ann Intern Med.1989;110:893900.
  2. Kassirer JP,Kopelman RI.Cognitive errors in diagnosis: instantiation, classification, and consequences.Am J Med.1989;86:433441.
  3. Viera AJ,Bond MM,Yates SW.Diagnosing night sweats.Am Fam Physician.2003;67:10191024.
  4. Smith CS,Paauw DS.When you hear hoof beats: four principles for separating zebras from horses.J Am Board Fam Pract.2000;13:424429.
  5. Levine JS,Branch DW,Rauch J.The antiphospholipid syndrome.N Engl J Med.2002;346:752763.
  6. Petri M.Epidemiology of the antiphospholipid antibody syndrome.J Autoimmun.2000;15:145151.
  7. Giron‐Gonzalez JA,Garcia del Rio E,Rodriguez C,Rodriguez‐Martorell J,Serrano A.Antiphospholipid syndrome and asymptomatic carriers of antiphospholipid antibody: prospective analysis of 404 individuals.J Rheumatol.2004;31:15601567.
  8. Lim W,Crowther MA,Eikelboom JW.Management of antiphospholipid antibody syndrome: a systematic review.JAMA2006;295:10507.
  9. Miyakis S,Lockshin MD,Atsumi T, et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost.2006;4:295306.
  10. Gezer S.Antiphospholipid syndrome.Dis Mon.2003;49:696741.
  11. Audrain MA,El‐Kouri D,Hamidou MA, et al.Value of autoantibodies to beta(2)‐glycoprotein 1 in the diagnosis of antiphospholipid syndrome.Rheumatology (Oxford).2002;41:550553.
  12. Espinosa G,Font J,Garcia‐Pagan JC, et al.Budd‐Chiari syndrome secondary to antiphospholipid syndrome: clinical and immunologic characteristics of 43 patients.Medicine (Baltimore).2001;80:345354.
  13. Menon KV,Shah V,Kamath PS.The Budd‐Chiari syndrome.N Engl J Med.2004;350:578585.
  14. Finazzi G,Marchioli R,Brancaccio V, et al.A randomized clinical trial of high‐intensity warfarin vs. conventional antithrombotic therapy for the prevention of recurrent thrombosis in patients with the antiphospholipid syndrome (WAPS).J Thromb Haemost.2005;3:848853.
  15. Crowther MA,Ginsberg JS,Julian J, et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med.2003;349:11331138.
  16. Mueh JR,Herbst KD,Rapaport SI.Thrombosis in patients with the lupus anticoagulant.Ann Intern Med.1980;92:156159.
  17. Purandare A,Godil MA,Prakash D,Parker R,Zerah M,Wilson TA.Spontaneous adrenal hemorrhage associated with transient antiphospholipid antibody in a child.Clin Pediatr (Phila).2001;40:347350.
  18. Gonzalez G,Gutierrez M,Ortiz M,Tellez R,Figueroa F,Jacobelli S.Association of primary antiphospholipid syndrome with primary adrenal insufficiency.J Rheumatol.1996;23:12861287.
  19. Arnason JA,Graziano FM.Adrenal insufficiency in the antiphospholipid antibody syndrome.Semin Arthritis Rheum.1995;25:109116.
  20. Espinosa G,Santos E,Cervera R, et al.Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients.Medicine (Baltimore).2003;82:106118.
  21. Provenzale JM,Ortel TL,Nelson RC.Adrenal hemorrhage in patients with primary antiphospholipid syndrome: imaging findings.AJR Am J Roentgenol.1995;165:361364.
  22. Vella A,Nippoldt TB,Morris JC.Adrenal hemorrhage: a 25‐year experience at the Mayo Clinic.Mayo Clin Proc.2001;76:161168.
  23. Berneis K,Buitrago‐Tellez C,Muller B,Keller U,Tsakiris DA.Antiphospholipid syndrome and endocrine damage: why bilateral adrenal thrombosis?Eur J Haematol.2003;71:299302.
  24. Boccarossa GN,Boccarossa SG.Reversible adrenal insufficiency after adrenal hemorrhage.Ann Intern Med.1993;119:439440.
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56‐year‐old man with a history of chronic liver disease of unknown etiology was referred for evaluation of intermittent low‐grade fevers, constipation, and an unintentional weight loss of 20‐kg during the previous 9 months. Three weeks prior to presentation, he was admitted to his local hospital for these symptoms and was treated empirically with cefotaxime for 6 days, but his symptoms persisted.

The patient's age and sex make him statistically at risk for vascular disease as well as malignancy. The history of chronic liver disease of unknown etiology is intriguing. In evaluating a patient with chronic liver disease, I want to know about alcohol consumption, intravenous drug use, family history, viral hepatitis serology, and antinuclear antibody testing. Chronic liver disease places this patient at increased risk for infection because portal hypertension causes blood to bypass a large part of the reticuloendothelial system (liver and spleen), therefore increasing the risk of sustained bacteremia.

Regarding his chronic low‐grade fever, I would like to know about his country of origin, travel history, occupational history, risk factors for human immunodeficiency virus (HIV) and tuberculosis, and any symptoms or signs of rheumatologic disease. Constipation and weight loss can be a result of malignancy (eg, hepatocellular carcinoma, colorectal cancer), vascular disease (eg, mesenteric thrombosis), or metabolic derangement (eg, hypercalcemia).

The patient had a history of recurrent episodes of ascites and low‐grade fevers. He first developed ascites, abdominal pain, low‐grade fevers, and pedal edema 20 years ago. These signs and symptoms resolved spontaneously, but similar episodes have recurred every 46 years since. Each time, diagnostic evaluation failed to reveal a specific etiology.

Twelve years prior to presentation, the patient was evaluated for chronic liver disease. Diagnostic tests at that time included viral hepatitis serology, ceruloplasmin, ferritin, alpha‐1‐antitrypsin, antimitochondrial antibody, and antinuclear antibody testing, all the results of which were within the normal range. The patient denied consumption of alcohol, medications, or toxic substances. Percutaneous liver biopsy demonstrated focal parenchymal scarring interspersed with areas of normal parenchyma, consistent with focal ischemic injury (Fig. 1).

Figure 1
Liver biopsy specimen showing extensive scarring (arrow) interspersed with areas of completely normal liver parenchyma (hematoxylin and eosin, ×400).

The duration of the patient's symptoms is striking. A unifying diagnosis for this patient must explain his chronic liver disease, periodic fevers, ascites, and abdominal pain that started at a relatively young age. Conditions to consider include hepatitis B or C, hemochromatosis, Wilson's disease, primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, alpha‐1‐antitrypsin deficiency, and drug or toxin exposure. Venoocclusive disease of the liver and chronic congestive hepatopathy (from heart failure or constrictive pericarditis) are especially attractive possibilities, given the findings of focal ischemic injury on liver biopsy.

Recurrent fever and abdominal pain can occur because of familial Mediterranean fever, which results from a genetic abnormality and causes recurrent peritoneal inflammation associated with fever and ascites. Although unlikely in this case, familial Mediterranean fever can cause secondary amyloidosis with liver involvement.

The patient reported episodic, vague abdominal pain, nausea, anorexia, night sweats, hair thinning, extreme fatigue, and lightheadedness. He had no known allergies, and his medications included propranolol, lactulose, docusate, and omeprazole. He was white, born in the United States, and a lawyer, but he had not worked during the previous 4 months. He was married and monogamous, and an HIV antibody test 4 months prior was negative. He had a remote history of tobacco and alcohol use between the 1960s and the 1980s. He denied intravenous drug use. His family history was only remarkable for a father with coronary artery disease.

With fever, the hypothalamic set point for temperature increases. Night sweats usually indicate an exaggeration of the normal diurnal drop in the hypothalamic set point for temperature, with dissipation of increased heat (caused by fever) through evaporation of perspiration. Unfortunately, night sweats are not specific to any particular cause of fever. Fatigue is equally nonspecific but could result from anemia, hypothyroidism, or adrenal insufficiency or could be a side effect of the propranolol. The lack of a family history makes hereditary periodic fevers unlikely.

The patient appeared chronically ill. His temperature was 35.2C, blood pressure 71/53 mm Hg, heart rate 84 beats per minute, respiratory rate 14 breaths per minute, and oxygen saturation 99% while breathing room air. His weight was 47 kg. Examination of the patient's head and neck revealed bitemporal wasting but no scleral icterus, and the oropharynx was clear. There was no thyromegaly or lymphadenopathy. The findings of the cardiopulmonary examination was normal. The abdomen was soft with mild diffuse tenderness. There was no organomegaly or obvious ascites. His extremities were warm and without edema or cyanosis. He was dark‐skinned and had rare spider angiomas. The results of his neurological examination were normal.

Sepsis, drug ingestion (particularly vasodilators), environmental exposure, and endocrine abnormalities such as adrenal insufficiency and hypothyroidism can all cause both hypothermia and hypotension. Adrenal insufficiency is especially intriguing becauase it is also associated with malaise, abdominal pain, and hyperpigmentation. Explaining both adrenal insufficiency and chronic liver disease is more difficult. Hemochromatosis can cause cirrhotic liver disease, adrenal and thyroid insufficiency, and dark skin, but the patient's normal ferritin and liver biopsy findings make this disease unlikely.

The results of the laboratory studies were: white‐cell count, 4900/mm3, with a normal differential count; hemoglobin, 11.0 g/dL; platelet count, 52,000/mm3; mean corpuscular volume, 89 m3; sodium, 131 mmol/L; potassium, 5.0 mmol/L; chloride, 101 mmol/L; bicarbonate, 21 mmol/L; blood urea nitrogen, 31 mg/dL; creatinine, 1.8 mg/dL; aspartate aminotransferase, 45 U/L (normal range 1641 U/L); alanine aminotransferase, 30 U/L (normal range 1259 U/L); alkaline phosphatase, 587 U/L (normal range 29111 U/L); total bilirubin, 1.1 mg/dL (normal range 0.31.3 mg/dL); gamma‐glutamyl transferase, 169 U/L (normal range 771 U/L); lactate dehydrogenase, 127 IU/L (normal range 91185 IU/L); thyroid‐stimulating hormone, 3.1 mIU/L (normal range 0.54.7 mIU/L). Coagulation studies revealed a prothrombin time of 12 seconds (international normalized ratio [INR] 1.1) and an activated partial thromboplastin time (aPTT) of greater than 100 seconds. Urinalysis and chest radiography were unremarkable.

The low sodium, high potassium, and relatively low bicarbonate levels are all compatible with adrenal insufficiency. When present, the combination of hyponatremia (primarily from glucocorticoid deficiency) and hyperkalemia (from mineralocorticoid deficiency) suggests the adrenal insufficiency is primary, rather than from the pituitary. The differential diagnosis of primary adrenal insufficiency includes autoimmune disease, granulomatous disease, and tumor.

Most interesting is the isolated prolongation of the aPTT, making adrenal hemorrhage another possibility as a cause of the adrenal insufficiency. Isolated elevation of the aPTT suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which would interfere with the test. Heparin administration (which may not be immediately obvious, as in the case of a heparin lock of an intravenous line) and von Willebrand disease (from loss of the normal von Willebrand factorassociated prevention of factor VIII proteolysis) can also cause isolated prolongation of the aPTT.

Tumor, perhaps hepatocellular cancer, remains a possible explanation for the elevated alkaline phosphatase, with possible adrenal involvement. Amyloidosis and diffuse granulomatous disease (either infectious or noninfectious, such as sarcoidosis) can cause elevation in alkaline phosphatase. At this time, I would rule out adrenal insufficiency, further evaluate the elevated aPTT, and image the liver and adrenal glands.

The patient was hospitalized and given intravenous fluids. His blood pressure increased to 90/54 mm Hg. Further testing revealed an alpha‐fetoprotein of 1.5 g/dL (normal range < 6.4 g/dL), an erythrocyte sedimentation rate of greater than 100 mm/s, and normal results of an antinuclear antibody test. Serum cortisol, drawn at 6 a.m., was 3 ng/dL; 60 minutes after cosyntropin stimulation, serum cortisol was 1 ng/dL. An ultrasound of the liver revealed chronic hepatic vein thrombosis.

The low absolute values and the failure of serum cortisol to respond to cosyntropin confirm the diagnosis of adrenal glucocorticoid deficiency. Hepatic vein thrombosis (Budd‐Chiari syndrome) is an unusual occurrence, often associated with a hypercoagulable state or tumor. How can we put these new findings together with the rest of the patient's abnormalities?

Primary antiphospholipid antibody syndrome is the most attractive unifying diagnosis because it appears to explain the most abnormalities with the fewest diagnoses. This syndrome includes arterial and venous thrombosis, thrombocytopenia, and isolated elevation of the aPTT and has been associated with hepatic vein thrombosis (acute and chronic) and adrenal insufficiency (from adrenal hemorrhage as a result of adrenal vein thrombosis). The histological findings of focal ischemic injury, seen on the patient's liver biopsy, are likely explained by hepatic venoocclusive disease.

Magnetic resonance imaging (MRI) of the abdomen (Fig. 2) demonstrated adrenal hemorrhage in the right adrenal gland. The patient's aPTT remained elevated even after his serum was mixed with normal serum, thereby excluding a factor deficiency. The results of a dilute Russell's viper venom time test (which tests the phospholipid‐dependent portion of the coagulation cascade) also showed elevation. The addition of phospholipids to the patient's serum corrected the aPTT, and a screen for factor inhibitors was negative. An anticardiolipin antibody (IgG) test was positive at 59.0 U (normal 0.42.3 U). These findings confirmed the presence of antiphospholipid antibodies.

Figure 2
Magnetic resonance imaging of the abdomen showing right adrenal hemorrhage (arrow) adjacent to the inferior vena cava (arrowhead).

The findings of a bone marrow biopsy, performed to exclude infiltrative diseases, were normal. The patient was diagnosed with primary antiphospholipid syndrome. Hydrocortisone and fludrocortisone were initiated, with the intention to continue them indefinitely. The patient was also started on intravenous heparin, which continued until he achieved a goal INR of 2.03.0 on warfarin. The patient was counseled on the importance of lifelong warfarin therapy given his diagnosis of antiphospholipid syndrome with hepatic vein and adrenal vein thromboses. On follow‐up 6 months after discharge, the patient's hypotension and fatigue had resolved, his alkaline phosphatase level had decreased substantially, and he had returned to work as a lawyer.

COMMENTARY

The diagnosis of a complex case with numerous clinical and laboratory abnormalities can be very difficult. The discussant successfully came to the correct diagnosis because he carefully evaluated each piece of evidence and did not fall prey to faulty triggering, the generation of diagnostic hypotheses based on selected pieces of clinical data.1 In the diagnostic process, physicians trigger new diagnostic possibilities and discard initial hypotheses as new findings emerge. Often, because of heuristic (analytic) biases, physicians fall victim to faulty triggering when evaluating patients.2 When confronted with a trigger feature such as night sweats, many physicians increase their consideration of tuberculosis or lymphoma at the expense of more common diagnoses, even though, as the discussant pointed out, any patient with fever can have this symptom.3 Whereas faulty use of trigger features may make physicians inappropriately consider uncommon diseases, a distinguishing feature limits the number of diagnostic possibilities and significantly changesincreases or decreasesthe likelihood of there being a rare disease.4 By correctly using the distinguishing feature of an elevated aPTT in the context of the patient's diverse clinical features, the discussant was able to arrive at a single, unifying diagnosis of antiphospholipid syndrome.

Antiphospholipid syndrome is arterial or venous thrombosis associated with significantly elevated antiphospholipid antibodies. Isolated prolongation of the aPTT is often the first clue to the presence of antiphospholipid antibodies, which interfere with phospholipid‐dependent coagulation assays.5 Antiphospholipid syndrome is considered primary if it is not associated with a known underlying disease or medication. Antiphospholipid syndrome is secondary if it is associated with certain diseases such as systemic lupus erythematosus and malignancy or with an adverse effect of medication. Although the prevalence of antiphospholipid antibodies is 1%5% in young, apparently healthy control subjects, it is higher in elderly patients with chronic diseases.6 It remains unclear why only certain patients with antiphospholipid antibodies manifest the syndrome, though having vascular risk factors may increase the risk of developing thrombosis in the presence of antiphospholipid antibodies.7

Three types of antiphospholipid antibody tests are currently in clinical use: lupus anticoagulants (measured by prolonged clotting time in a phospholipid‐dependent clotting test, such as the aPTT), anticardiolipin antibodies, and anti‐2‐glycoprotein I antibodies. All 3 tests are plagued by not being standardized between hospitals and laboratories and have limited sensitivity and specificity.8, 9 Lupus anticoagulants are most closely associated with thrombosis. Although a prolonged aPTT in the presence of thrombosis is often the first clue to the presence of lupus anticoagulants, only 30%40% of patients with the syndrome have this laboratory abnormality.10 Therefore, a normal aPTT result does not rule out the presence of antiphospholipid antibodies, and other tests of lupus anticoagulants, such as the dilute Russell viper venom time, should be performed.8, 9 There are many types of anticardiolipin antibodies of varying immunoglobulin isotypes, which all share the ability to bind cardiolipin in vitro. The IgG isotypes (as in our patient) are thought to be most closely associated with thrombosis, and it is known that high titers of anticardiolipin antibodies have much better discriminatory value than low titers.810 There is little data on the anti‐2‐glycoprotein I antibodies, but preliminary data suggest these antibodies may be more specific for the antiphospholipid syndrome.11

The antiphospholipid syndrome has classically been associated with lower‐extremity deep venous thrombosis, recurrent fetal loss, thrombocytopenia, and livedo reticularis.10 However, depending on the size and distribution of the vasculature involved and the extent and chronicity of involvement, antiphospholipid syndrome can result in manifestation of a wide range of diseases. Acute presentations such as thrombotic disease of the gastrointestinal, cardiac, and central nervous systems can be rapid and catastrophic. A more chronic and indolent course can lead to progressive organ dysfunction, as in this patient, with chronic liver disease resulting from recurrent episodes of hepatic venoocclusive disease and chronic hepatic vein thrombosis, a rare but well‐described complication of antiphospholipid syndrome.12, 13 It is unclear why the course of our patient's hepatic vein thrombosis waxed and waned so much. We hypothesized that he had episodes of microvascular hepatic venous thrombosis that led to transient hepatic dysfunction, with subsequent recovery upon spontaneous recanalization of hepatic veins or with healing and regeneration of liver tissue.

Treatment of antiphospholipid syndrome is controversial. Although prior reports suggested that patients with this syndrome were at higher risk for recurrent thrombosis when treated with the usual dose of warfarin (target INR 2.03.0), 2 randomized trial showed there was no difference in the recurrence of thrombosis between moderate‐intensity treatment with warfarin and high‐intensity treatment with warfarin.14, 15 Our patient was treated with warfarin to a moderate‐intensity target INR of 2.03.0 because he had liver disease and adrenal hemorrhage. Although he has done well, it is important that he be continuously reassessed, as should all patients with similar conditions, for the risk and recurrence of thrombosis weighed against the risk of bleeding.

Adrenal insufficiency is another rare complication of antiphospholipid syndrome. It was first described as such in 198016 and has since been reported in both children and adults.1719 Abdominal pain and hypotension were the most common findings (55% and 54%, respectively) in one case series of 86 patients with adrenal insufficiency from antiphospholipid syndrome.20 Fever, nausea, vomiting, weakness, fatigue, lethargy, and altered mental status were also variably present. Loss of adrenal function is most often a result of adrenal hemorrhage, which is best detected by MRI of the adrenal glands.21

The vascular anatomy of the adrenal gland is unusual. Multiple arteries supply the gland, but only one central vein provides drainage, making the gland relatively vulnerable to hemorrhagic infarction.22 Most cases of adrenal insufficiency from antiphospholipid syndrome are thought to be a result of adrenal vein thrombosis. The MRI showed that only the right adrenal gland of our patient had evidence of hemorrhage. Because both adrenal glands must be damaged before adrenal insufficiency results, it is probable that the left adrenal gland was damaged because of prior episodes of infarction and/or hemorrhage, but remote damage could not be detected by MRI. Of note, antiphospholipid antibodies directed against cholesterol‐rich proteins in the adrenal gland can also cause a locally active procoagulant state with microvascular venous thrombosis and subsequent postinfarction hemorrhage, which is another way in which the left adrenal gland could have been damaged without showing up radiographically.23

As for other types of adrenal insufficiency, the primary treatment for adrenal insufficiency from antiphospholipid syndrome is rapid corticosteroid replacement, with the addition of anticoagulants to treat the hypercoagulable state of the antiphospholipid syndrome. Adrenal insufficiency is temporary in some cases.24 Mortality from adrenal insufficiency due to antiphospholipid syndrome may be higher than that from other forms of adrenal insufficiency.22 Therefore, screening for adrenal insufficiency is critical for any patient with suspected or documented antiphospholipid syndrome who presents with abdominal pain, weakness, electrolyte abnormalities, or unexplained hypotension.

This case illustrates the importance, as the key to diagnosis, of determining a distinguishing feature such as a prolonged aPTT from among the multitude of abnormalities that could have led the diagnostic process astray. Occasionally, a single clinical or laboratory abnormality, such as the elevated aPTT in our patient, is so valuable in the assessment of a difficult case that it significantly increases the likelihood of an uncommon condition and leads to the correct final diagnosis, thereby becoming the pivotal distinguishing feature.

Key Points

  • Hypercoagulability can lead to adrenal insufficiency by causing adrenal vein thrombosis and adrenal infarction. Therefore, hypercoagulable states, such as antiphospholipid syndrome, should be considered for patients who present with symptoms or signs of unexplained adrenal insufficiency.

  • Isolated elevation of activated partial thromboplastin time (aPTT) suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which interferes with this test. Heparin administration and von Willebrand disease can also cause isolated prolongation of the aPTT.

  • Treatment of the antiphospholipid syndrome is controversial, but according to the results of 2 recent randomized, controlled trials, patients with this syndrome who have had their first episode of thrombosis should be treated with warfarin, with a goal INR of 2.03.0.

  • When interpreted incorrectly, trigger features such as night sweats cause clinicians to inappropriately consider a rare diagnosis, even though common diagnoses may be more likely. On the other hand, distinguishing features, such as the prolonged aPTT in this patient, truly do increase or decrease the probability of a rare diagnosis.

56‐year‐old man with a history of chronic liver disease of unknown etiology was referred for evaluation of intermittent low‐grade fevers, constipation, and an unintentional weight loss of 20‐kg during the previous 9 months. Three weeks prior to presentation, he was admitted to his local hospital for these symptoms and was treated empirically with cefotaxime for 6 days, but his symptoms persisted.

The patient's age and sex make him statistically at risk for vascular disease as well as malignancy. The history of chronic liver disease of unknown etiology is intriguing. In evaluating a patient with chronic liver disease, I want to know about alcohol consumption, intravenous drug use, family history, viral hepatitis serology, and antinuclear antibody testing. Chronic liver disease places this patient at increased risk for infection because portal hypertension causes blood to bypass a large part of the reticuloendothelial system (liver and spleen), therefore increasing the risk of sustained bacteremia.

Regarding his chronic low‐grade fever, I would like to know about his country of origin, travel history, occupational history, risk factors for human immunodeficiency virus (HIV) and tuberculosis, and any symptoms or signs of rheumatologic disease. Constipation and weight loss can be a result of malignancy (eg, hepatocellular carcinoma, colorectal cancer), vascular disease (eg, mesenteric thrombosis), or metabolic derangement (eg, hypercalcemia).

The patient had a history of recurrent episodes of ascites and low‐grade fevers. He first developed ascites, abdominal pain, low‐grade fevers, and pedal edema 20 years ago. These signs and symptoms resolved spontaneously, but similar episodes have recurred every 46 years since. Each time, diagnostic evaluation failed to reveal a specific etiology.

Twelve years prior to presentation, the patient was evaluated for chronic liver disease. Diagnostic tests at that time included viral hepatitis serology, ceruloplasmin, ferritin, alpha‐1‐antitrypsin, antimitochondrial antibody, and antinuclear antibody testing, all the results of which were within the normal range. The patient denied consumption of alcohol, medications, or toxic substances. Percutaneous liver biopsy demonstrated focal parenchymal scarring interspersed with areas of normal parenchyma, consistent with focal ischemic injury (Fig. 1).

Figure 1
Liver biopsy specimen showing extensive scarring (arrow) interspersed with areas of completely normal liver parenchyma (hematoxylin and eosin, ×400).

The duration of the patient's symptoms is striking. A unifying diagnosis for this patient must explain his chronic liver disease, periodic fevers, ascites, and abdominal pain that started at a relatively young age. Conditions to consider include hepatitis B or C, hemochromatosis, Wilson's disease, primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, alpha‐1‐antitrypsin deficiency, and drug or toxin exposure. Venoocclusive disease of the liver and chronic congestive hepatopathy (from heart failure or constrictive pericarditis) are especially attractive possibilities, given the findings of focal ischemic injury on liver biopsy.

Recurrent fever and abdominal pain can occur because of familial Mediterranean fever, which results from a genetic abnormality and causes recurrent peritoneal inflammation associated with fever and ascites. Although unlikely in this case, familial Mediterranean fever can cause secondary amyloidosis with liver involvement.

The patient reported episodic, vague abdominal pain, nausea, anorexia, night sweats, hair thinning, extreme fatigue, and lightheadedness. He had no known allergies, and his medications included propranolol, lactulose, docusate, and omeprazole. He was white, born in the United States, and a lawyer, but he had not worked during the previous 4 months. He was married and monogamous, and an HIV antibody test 4 months prior was negative. He had a remote history of tobacco and alcohol use between the 1960s and the 1980s. He denied intravenous drug use. His family history was only remarkable for a father with coronary artery disease.

With fever, the hypothalamic set point for temperature increases. Night sweats usually indicate an exaggeration of the normal diurnal drop in the hypothalamic set point for temperature, with dissipation of increased heat (caused by fever) through evaporation of perspiration. Unfortunately, night sweats are not specific to any particular cause of fever. Fatigue is equally nonspecific but could result from anemia, hypothyroidism, or adrenal insufficiency or could be a side effect of the propranolol. The lack of a family history makes hereditary periodic fevers unlikely.

The patient appeared chronically ill. His temperature was 35.2C, blood pressure 71/53 mm Hg, heart rate 84 beats per minute, respiratory rate 14 breaths per minute, and oxygen saturation 99% while breathing room air. His weight was 47 kg. Examination of the patient's head and neck revealed bitemporal wasting but no scleral icterus, and the oropharynx was clear. There was no thyromegaly or lymphadenopathy. The findings of the cardiopulmonary examination was normal. The abdomen was soft with mild diffuse tenderness. There was no organomegaly or obvious ascites. His extremities were warm and without edema or cyanosis. He was dark‐skinned and had rare spider angiomas. The results of his neurological examination were normal.

Sepsis, drug ingestion (particularly vasodilators), environmental exposure, and endocrine abnormalities such as adrenal insufficiency and hypothyroidism can all cause both hypothermia and hypotension. Adrenal insufficiency is especially intriguing becauase it is also associated with malaise, abdominal pain, and hyperpigmentation. Explaining both adrenal insufficiency and chronic liver disease is more difficult. Hemochromatosis can cause cirrhotic liver disease, adrenal and thyroid insufficiency, and dark skin, but the patient's normal ferritin and liver biopsy findings make this disease unlikely.

The results of the laboratory studies were: white‐cell count, 4900/mm3, with a normal differential count; hemoglobin, 11.0 g/dL; platelet count, 52,000/mm3; mean corpuscular volume, 89 m3; sodium, 131 mmol/L; potassium, 5.0 mmol/L; chloride, 101 mmol/L; bicarbonate, 21 mmol/L; blood urea nitrogen, 31 mg/dL; creatinine, 1.8 mg/dL; aspartate aminotransferase, 45 U/L (normal range 1641 U/L); alanine aminotransferase, 30 U/L (normal range 1259 U/L); alkaline phosphatase, 587 U/L (normal range 29111 U/L); total bilirubin, 1.1 mg/dL (normal range 0.31.3 mg/dL); gamma‐glutamyl transferase, 169 U/L (normal range 771 U/L); lactate dehydrogenase, 127 IU/L (normal range 91185 IU/L); thyroid‐stimulating hormone, 3.1 mIU/L (normal range 0.54.7 mIU/L). Coagulation studies revealed a prothrombin time of 12 seconds (international normalized ratio [INR] 1.1) and an activated partial thromboplastin time (aPTT) of greater than 100 seconds. Urinalysis and chest radiography were unremarkable.

The low sodium, high potassium, and relatively low bicarbonate levels are all compatible with adrenal insufficiency. When present, the combination of hyponatremia (primarily from glucocorticoid deficiency) and hyperkalemia (from mineralocorticoid deficiency) suggests the adrenal insufficiency is primary, rather than from the pituitary. The differential diagnosis of primary adrenal insufficiency includes autoimmune disease, granulomatous disease, and tumor.

Most interesting is the isolated prolongation of the aPTT, making adrenal hemorrhage another possibility as a cause of the adrenal insufficiency. Isolated elevation of the aPTT suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which would interfere with the test. Heparin administration (which may not be immediately obvious, as in the case of a heparin lock of an intravenous line) and von Willebrand disease (from loss of the normal von Willebrand factorassociated prevention of factor VIII proteolysis) can also cause isolated prolongation of the aPTT.

Tumor, perhaps hepatocellular cancer, remains a possible explanation for the elevated alkaline phosphatase, with possible adrenal involvement. Amyloidosis and diffuse granulomatous disease (either infectious or noninfectious, such as sarcoidosis) can cause elevation in alkaline phosphatase. At this time, I would rule out adrenal insufficiency, further evaluate the elevated aPTT, and image the liver and adrenal glands.

The patient was hospitalized and given intravenous fluids. His blood pressure increased to 90/54 mm Hg. Further testing revealed an alpha‐fetoprotein of 1.5 g/dL (normal range < 6.4 g/dL), an erythrocyte sedimentation rate of greater than 100 mm/s, and normal results of an antinuclear antibody test. Serum cortisol, drawn at 6 a.m., was 3 ng/dL; 60 minutes after cosyntropin stimulation, serum cortisol was 1 ng/dL. An ultrasound of the liver revealed chronic hepatic vein thrombosis.

The low absolute values and the failure of serum cortisol to respond to cosyntropin confirm the diagnosis of adrenal glucocorticoid deficiency. Hepatic vein thrombosis (Budd‐Chiari syndrome) is an unusual occurrence, often associated with a hypercoagulable state or tumor. How can we put these new findings together with the rest of the patient's abnormalities?

Primary antiphospholipid antibody syndrome is the most attractive unifying diagnosis because it appears to explain the most abnormalities with the fewest diagnoses. This syndrome includes arterial and venous thrombosis, thrombocytopenia, and isolated elevation of the aPTT and has been associated with hepatic vein thrombosis (acute and chronic) and adrenal insufficiency (from adrenal hemorrhage as a result of adrenal vein thrombosis). The histological findings of focal ischemic injury, seen on the patient's liver biopsy, are likely explained by hepatic venoocclusive disease.

Magnetic resonance imaging (MRI) of the abdomen (Fig. 2) demonstrated adrenal hemorrhage in the right adrenal gland. The patient's aPTT remained elevated even after his serum was mixed with normal serum, thereby excluding a factor deficiency. The results of a dilute Russell's viper venom time test (which tests the phospholipid‐dependent portion of the coagulation cascade) also showed elevation. The addition of phospholipids to the patient's serum corrected the aPTT, and a screen for factor inhibitors was negative. An anticardiolipin antibody (IgG) test was positive at 59.0 U (normal 0.42.3 U). These findings confirmed the presence of antiphospholipid antibodies.

Figure 2
Magnetic resonance imaging of the abdomen showing right adrenal hemorrhage (arrow) adjacent to the inferior vena cava (arrowhead).

The findings of a bone marrow biopsy, performed to exclude infiltrative diseases, were normal. The patient was diagnosed with primary antiphospholipid syndrome. Hydrocortisone and fludrocortisone were initiated, with the intention to continue them indefinitely. The patient was also started on intravenous heparin, which continued until he achieved a goal INR of 2.03.0 on warfarin. The patient was counseled on the importance of lifelong warfarin therapy given his diagnosis of antiphospholipid syndrome with hepatic vein and adrenal vein thromboses. On follow‐up 6 months after discharge, the patient's hypotension and fatigue had resolved, his alkaline phosphatase level had decreased substantially, and he had returned to work as a lawyer.

COMMENTARY

The diagnosis of a complex case with numerous clinical and laboratory abnormalities can be very difficult. The discussant successfully came to the correct diagnosis because he carefully evaluated each piece of evidence and did not fall prey to faulty triggering, the generation of diagnostic hypotheses based on selected pieces of clinical data.1 In the diagnostic process, physicians trigger new diagnostic possibilities and discard initial hypotheses as new findings emerge. Often, because of heuristic (analytic) biases, physicians fall victim to faulty triggering when evaluating patients.2 When confronted with a trigger feature such as night sweats, many physicians increase their consideration of tuberculosis or lymphoma at the expense of more common diagnoses, even though, as the discussant pointed out, any patient with fever can have this symptom.3 Whereas faulty use of trigger features may make physicians inappropriately consider uncommon diseases, a distinguishing feature limits the number of diagnostic possibilities and significantly changesincreases or decreasesthe likelihood of there being a rare disease.4 By correctly using the distinguishing feature of an elevated aPTT in the context of the patient's diverse clinical features, the discussant was able to arrive at a single, unifying diagnosis of antiphospholipid syndrome.

Antiphospholipid syndrome is arterial or venous thrombosis associated with significantly elevated antiphospholipid antibodies. Isolated prolongation of the aPTT is often the first clue to the presence of antiphospholipid antibodies, which interfere with phospholipid‐dependent coagulation assays.5 Antiphospholipid syndrome is considered primary if it is not associated with a known underlying disease or medication. Antiphospholipid syndrome is secondary if it is associated with certain diseases such as systemic lupus erythematosus and malignancy or with an adverse effect of medication. Although the prevalence of antiphospholipid antibodies is 1%5% in young, apparently healthy control subjects, it is higher in elderly patients with chronic diseases.6 It remains unclear why only certain patients with antiphospholipid antibodies manifest the syndrome, though having vascular risk factors may increase the risk of developing thrombosis in the presence of antiphospholipid antibodies.7

Three types of antiphospholipid antibody tests are currently in clinical use: lupus anticoagulants (measured by prolonged clotting time in a phospholipid‐dependent clotting test, such as the aPTT), anticardiolipin antibodies, and anti‐2‐glycoprotein I antibodies. All 3 tests are plagued by not being standardized between hospitals and laboratories and have limited sensitivity and specificity.8, 9 Lupus anticoagulants are most closely associated with thrombosis. Although a prolonged aPTT in the presence of thrombosis is often the first clue to the presence of lupus anticoagulants, only 30%40% of patients with the syndrome have this laboratory abnormality.10 Therefore, a normal aPTT result does not rule out the presence of antiphospholipid antibodies, and other tests of lupus anticoagulants, such as the dilute Russell viper venom time, should be performed.8, 9 There are many types of anticardiolipin antibodies of varying immunoglobulin isotypes, which all share the ability to bind cardiolipin in vitro. The IgG isotypes (as in our patient) are thought to be most closely associated with thrombosis, and it is known that high titers of anticardiolipin antibodies have much better discriminatory value than low titers.810 There is little data on the anti‐2‐glycoprotein I antibodies, but preliminary data suggest these antibodies may be more specific for the antiphospholipid syndrome.11

The antiphospholipid syndrome has classically been associated with lower‐extremity deep venous thrombosis, recurrent fetal loss, thrombocytopenia, and livedo reticularis.10 However, depending on the size and distribution of the vasculature involved and the extent and chronicity of involvement, antiphospholipid syndrome can result in manifestation of a wide range of diseases. Acute presentations such as thrombotic disease of the gastrointestinal, cardiac, and central nervous systems can be rapid and catastrophic. A more chronic and indolent course can lead to progressive organ dysfunction, as in this patient, with chronic liver disease resulting from recurrent episodes of hepatic venoocclusive disease and chronic hepatic vein thrombosis, a rare but well‐described complication of antiphospholipid syndrome.12, 13 It is unclear why the course of our patient's hepatic vein thrombosis waxed and waned so much. We hypothesized that he had episodes of microvascular hepatic venous thrombosis that led to transient hepatic dysfunction, with subsequent recovery upon spontaneous recanalization of hepatic veins or with healing and regeneration of liver tissue.

Treatment of antiphospholipid syndrome is controversial. Although prior reports suggested that patients with this syndrome were at higher risk for recurrent thrombosis when treated with the usual dose of warfarin (target INR 2.03.0), 2 randomized trial showed there was no difference in the recurrence of thrombosis between moderate‐intensity treatment with warfarin and high‐intensity treatment with warfarin.14, 15 Our patient was treated with warfarin to a moderate‐intensity target INR of 2.03.0 because he had liver disease and adrenal hemorrhage. Although he has done well, it is important that he be continuously reassessed, as should all patients with similar conditions, for the risk and recurrence of thrombosis weighed against the risk of bleeding.

Adrenal insufficiency is another rare complication of antiphospholipid syndrome. It was first described as such in 198016 and has since been reported in both children and adults.1719 Abdominal pain and hypotension were the most common findings (55% and 54%, respectively) in one case series of 86 patients with adrenal insufficiency from antiphospholipid syndrome.20 Fever, nausea, vomiting, weakness, fatigue, lethargy, and altered mental status were also variably present. Loss of adrenal function is most often a result of adrenal hemorrhage, which is best detected by MRI of the adrenal glands.21

The vascular anatomy of the adrenal gland is unusual. Multiple arteries supply the gland, but only one central vein provides drainage, making the gland relatively vulnerable to hemorrhagic infarction.22 Most cases of adrenal insufficiency from antiphospholipid syndrome are thought to be a result of adrenal vein thrombosis. The MRI showed that only the right adrenal gland of our patient had evidence of hemorrhage. Because both adrenal glands must be damaged before adrenal insufficiency results, it is probable that the left adrenal gland was damaged because of prior episodes of infarction and/or hemorrhage, but remote damage could not be detected by MRI. Of note, antiphospholipid antibodies directed against cholesterol‐rich proteins in the adrenal gland can also cause a locally active procoagulant state with microvascular venous thrombosis and subsequent postinfarction hemorrhage, which is another way in which the left adrenal gland could have been damaged without showing up radiographically.23

As for other types of adrenal insufficiency, the primary treatment for adrenal insufficiency from antiphospholipid syndrome is rapid corticosteroid replacement, with the addition of anticoagulants to treat the hypercoagulable state of the antiphospholipid syndrome. Adrenal insufficiency is temporary in some cases.24 Mortality from adrenal insufficiency due to antiphospholipid syndrome may be higher than that from other forms of adrenal insufficiency.22 Therefore, screening for adrenal insufficiency is critical for any patient with suspected or documented antiphospholipid syndrome who presents with abdominal pain, weakness, electrolyte abnormalities, or unexplained hypotension.

This case illustrates the importance, as the key to diagnosis, of determining a distinguishing feature such as a prolonged aPTT from among the multitude of abnormalities that could have led the diagnostic process astray. Occasionally, a single clinical or laboratory abnormality, such as the elevated aPTT in our patient, is so valuable in the assessment of a difficult case that it significantly increases the likelihood of an uncommon condition and leads to the correct final diagnosis, thereby becoming the pivotal distinguishing feature.

Key Points

  • Hypercoagulability can lead to adrenal insufficiency by causing adrenal vein thrombosis and adrenal infarction. Therefore, hypercoagulable states, such as antiphospholipid syndrome, should be considered for patients who present with symptoms or signs of unexplained adrenal insufficiency.

  • Isolated elevation of activated partial thromboplastin time (aPTT) suggests deficiency or inhibition of the factors involved in the intrinsic pathway (factors VIII, IX, XI, and XII) or the presence of an antiphospholipid antibody, which interferes with this test. Heparin administration and von Willebrand disease can also cause isolated prolongation of the aPTT.

  • Treatment of the antiphospholipid syndrome is controversial, but according to the results of 2 recent randomized, controlled trials, patients with this syndrome who have had their first episode of thrombosis should be treated with warfarin, with a goal INR of 2.03.0.

  • When interpreted incorrectly, trigger features such as night sweats cause clinicians to inappropriately consider a rare diagnosis, even though common diagnoses may be more likely. On the other hand, distinguishing features, such as the prolonged aPTT in this patient, truly do increase or decrease the probability of a rare diagnosis.

References
  1. Kassirer JP.Diagnostic reasoning.Ann Intern Med.1989;110:893900.
  2. Kassirer JP,Kopelman RI.Cognitive errors in diagnosis: instantiation, classification, and consequences.Am J Med.1989;86:433441.
  3. Viera AJ,Bond MM,Yates SW.Diagnosing night sweats.Am Fam Physician.2003;67:10191024.
  4. Smith CS,Paauw DS.When you hear hoof beats: four principles for separating zebras from horses.J Am Board Fam Pract.2000;13:424429.
  5. Levine JS,Branch DW,Rauch J.The antiphospholipid syndrome.N Engl J Med.2002;346:752763.
  6. Petri M.Epidemiology of the antiphospholipid antibody syndrome.J Autoimmun.2000;15:145151.
  7. Giron‐Gonzalez JA,Garcia del Rio E,Rodriguez C,Rodriguez‐Martorell J,Serrano A.Antiphospholipid syndrome and asymptomatic carriers of antiphospholipid antibody: prospective analysis of 404 individuals.J Rheumatol.2004;31:15601567.
  8. Lim W,Crowther MA,Eikelboom JW.Management of antiphospholipid antibody syndrome: a systematic review.JAMA2006;295:10507.
  9. Miyakis S,Lockshin MD,Atsumi T, et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost.2006;4:295306.
  10. Gezer S.Antiphospholipid syndrome.Dis Mon.2003;49:696741.
  11. Audrain MA,El‐Kouri D,Hamidou MA, et al.Value of autoantibodies to beta(2)‐glycoprotein 1 in the diagnosis of antiphospholipid syndrome.Rheumatology (Oxford).2002;41:550553.
  12. Espinosa G,Font J,Garcia‐Pagan JC, et al.Budd‐Chiari syndrome secondary to antiphospholipid syndrome: clinical and immunologic characteristics of 43 patients.Medicine (Baltimore).2001;80:345354.
  13. Menon KV,Shah V,Kamath PS.The Budd‐Chiari syndrome.N Engl J Med.2004;350:578585.
  14. Finazzi G,Marchioli R,Brancaccio V, et al.A randomized clinical trial of high‐intensity warfarin vs. conventional antithrombotic therapy for the prevention of recurrent thrombosis in patients with the antiphospholipid syndrome (WAPS).J Thromb Haemost.2005;3:848853.
  15. Crowther MA,Ginsberg JS,Julian J, et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med.2003;349:11331138.
  16. Mueh JR,Herbst KD,Rapaport SI.Thrombosis in patients with the lupus anticoagulant.Ann Intern Med.1980;92:156159.
  17. Purandare A,Godil MA,Prakash D,Parker R,Zerah M,Wilson TA.Spontaneous adrenal hemorrhage associated with transient antiphospholipid antibody in a child.Clin Pediatr (Phila).2001;40:347350.
  18. Gonzalez G,Gutierrez M,Ortiz M,Tellez R,Figueroa F,Jacobelli S.Association of primary antiphospholipid syndrome with primary adrenal insufficiency.J Rheumatol.1996;23:12861287.
  19. Arnason JA,Graziano FM.Adrenal insufficiency in the antiphospholipid antibody syndrome.Semin Arthritis Rheum.1995;25:109116.
  20. Espinosa G,Santos E,Cervera R, et al.Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients.Medicine (Baltimore).2003;82:106118.
  21. Provenzale JM,Ortel TL,Nelson RC.Adrenal hemorrhage in patients with primary antiphospholipid syndrome: imaging findings.AJR Am J Roentgenol.1995;165:361364.
  22. Vella A,Nippoldt TB,Morris JC.Adrenal hemorrhage: a 25‐year experience at the Mayo Clinic.Mayo Clin Proc.2001;76:161168.
  23. Berneis K,Buitrago‐Tellez C,Muller B,Keller U,Tsakiris DA.Antiphospholipid syndrome and endocrine damage: why bilateral adrenal thrombosis?Eur J Haematol.2003;71:299302.
  24. Boccarossa GN,Boccarossa SG.Reversible adrenal insufficiency after adrenal hemorrhage.Ann Intern Med.1993;119:439440.
References
  1. Kassirer JP.Diagnostic reasoning.Ann Intern Med.1989;110:893900.
  2. Kassirer JP,Kopelman RI.Cognitive errors in diagnosis: instantiation, classification, and consequences.Am J Med.1989;86:433441.
  3. Viera AJ,Bond MM,Yates SW.Diagnosing night sweats.Am Fam Physician.2003;67:10191024.
  4. Smith CS,Paauw DS.When you hear hoof beats: four principles for separating zebras from horses.J Am Board Fam Pract.2000;13:424429.
  5. Levine JS,Branch DW,Rauch J.The antiphospholipid syndrome.N Engl J Med.2002;346:752763.
  6. Petri M.Epidemiology of the antiphospholipid antibody syndrome.J Autoimmun.2000;15:145151.
  7. Giron‐Gonzalez JA,Garcia del Rio E,Rodriguez C,Rodriguez‐Martorell J,Serrano A.Antiphospholipid syndrome and asymptomatic carriers of antiphospholipid antibody: prospective analysis of 404 individuals.J Rheumatol.2004;31:15601567.
  8. Lim W,Crowther MA,Eikelboom JW.Management of antiphospholipid antibody syndrome: a systematic review.JAMA2006;295:10507.
  9. Miyakis S,Lockshin MD,Atsumi T, et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost.2006;4:295306.
  10. Gezer S.Antiphospholipid syndrome.Dis Mon.2003;49:696741.
  11. Audrain MA,El‐Kouri D,Hamidou MA, et al.Value of autoantibodies to beta(2)‐glycoprotein 1 in the diagnosis of antiphospholipid syndrome.Rheumatology (Oxford).2002;41:550553.
  12. Espinosa G,Font J,Garcia‐Pagan JC, et al.Budd‐Chiari syndrome secondary to antiphospholipid syndrome: clinical and immunologic characteristics of 43 patients.Medicine (Baltimore).2001;80:345354.
  13. Menon KV,Shah V,Kamath PS.The Budd‐Chiari syndrome.N Engl J Med.2004;350:578585.
  14. Finazzi G,Marchioli R,Brancaccio V, et al.A randomized clinical trial of high‐intensity warfarin vs. conventional antithrombotic therapy for the prevention of recurrent thrombosis in patients with the antiphospholipid syndrome (WAPS).J Thromb Haemost.2005;3:848853.
  15. Crowther MA,Ginsberg JS,Julian J, et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med.2003;349:11331138.
  16. Mueh JR,Herbst KD,Rapaport SI.Thrombosis in patients with the lupus anticoagulant.Ann Intern Med.1980;92:156159.
  17. Purandare A,Godil MA,Prakash D,Parker R,Zerah M,Wilson TA.Spontaneous adrenal hemorrhage associated with transient antiphospholipid antibody in a child.Clin Pediatr (Phila).2001;40:347350.
  18. Gonzalez G,Gutierrez M,Ortiz M,Tellez R,Figueroa F,Jacobelli S.Association of primary antiphospholipid syndrome with primary adrenal insufficiency.J Rheumatol.1996;23:12861287.
  19. Arnason JA,Graziano FM.Adrenal insufficiency in the antiphospholipid antibody syndrome.Semin Arthritis Rheum.1995;25:109116.
  20. Espinosa G,Santos E,Cervera R, et al.Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients.Medicine (Baltimore).2003;82:106118.
  21. Provenzale JM,Ortel TL,Nelson RC.Adrenal hemorrhage in patients with primary antiphospholipid syndrome: imaging findings.AJR Am J Roentgenol.1995;165:361364.
  22. Vella A,Nippoldt TB,Morris JC.Adrenal hemorrhage: a 25‐year experience at the Mayo Clinic.Mayo Clin Proc.2001;76:161168.
  23. Berneis K,Buitrago‐Tellez C,Muller B,Keller U,Tsakiris DA.Antiphospholipid syndrome and endocrine damage: why bilateral adrenal thrombosis?Eur J Haematol.2003;71:299302.
  24. Boccarossa GN,Boccarossa SG.Reversible adrenal insufficiency after adrenal hemorrhage.Ann Intern Med.1993;119:439440.
Issue
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Annual reviewers list

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We deeply appreciate the involvement of our reviewers who made the Journal of Hospital Medicine so successful in its first year. Listed below are the many reviewers and volume of their contributions. They have our sincere gratitude.

Reviewed 4 or More Articles

Eric Alper (6)

David Anthony (4)

Vineet Arora (4)

Thomas E. Baudendistel (11)

Daniel J. Brotman (7)

Vincent W. Chiang (5)

Eugene Shu‐Sen Chu (5)

Gurpreet Dhaliwal (7)

Lorenzo Di Francesco (4)

Andras Fenyves (4)

Stacy Fischer (5)

Kathlyn Fletcher (5)

Philip H. Goodman (4)

Carolyn Gould (4)

Jeffrey L. Greenwald (6)

Lakshmi Halasyamani (4)

Brian Harte (13)

Christopher P. Landrigan (5)

Peter K. Lindenauer (4)

Greg Maynard (7)

Sylvia Cheney McKean (4)

Thomas Aquinas Murphy (4)

James C. Pile (9)

Thomas Price (4)

Sumant Ranji (8)

Bradley Allen Sharpe (4)

Jason Stein (7)

Robin Tricoles (9)

Guillermo E. Umpierrez (5)

Arpana Vidyarthi (6)

Heidi Wald (7)

David Wesorick (4)

Reviewed 3 Articles

Ron G. Angus

Paul Aronowitz

Vanitha Bala

Jennifer Best

Cynthia Jean Brown

Gregory Bump

Hugo Quinny Cheng

Eva Chittenden

Eric Coleman

Curtiss B. Cook

Edward Etchells

Alan John Forster

Roma Y. Gianchandani

Leslie W. Hall

Jennifer Hanrahan

Amir K. Jaffer

Peter John Kaboli

Jennifer Kapo

Dennis Manning

Constantine Manthous

Janet Nagamine

Kevin J. O'Leary

Brian Michael Pate

Robert C. Pendleton

Jeffrey Lawrence Schnipper

Hasan Shabbir

James Edwin Stone

Chad Whelan

Audrey Young

Reviewed 2 Articles

Drew Abernathy

Stephen J. Bekanich

Paul Cantey

Kerry Cho

Patrick Conway

Jasminka Criley

Catherine Curley

Jennifer Daru

Catherine F. Decker

Andrew Paul DeFilippis

Daniel J. DiBona

Mark Earnest

Douglas Einstadter

Margaret Fang

Jonathan M. Flacker

Bradley Evan Flansbaum

Michael Frankel

Jeffrey Glasheen

Amir H. Hamrahian

Karen E. Hauer

Eric Edwin Howell

Carlos Manuel Isada

Christopher Seoung Kim

Sunil Kripalani

Jean S. Kutner

Cindy Lai

Janet Larson

David Likosky

David Ling

Michelle Magee

Navneet Majhail

Michael Matheny

George Mathew

Govardhanan Nagaiah

James Newman

Christopher Ohl

Shawn Ralston

Daniel A. Rauch

John James Ross

Joel Rubenstein

David Schulman

Kaveh G. Shojania

Gregory Randall Smith Jr.

Peter Youngers Watson

Chad T. Whelan

Neil Winawer

Scott Wright

Reviewed 1 Article

Adebola Adesanya

Nasim Afsarmanesh

Richard Keith Albert

Mel L. Anderson, III

Wendy Artrong

Thomas W. Barrett

David Bar‐Shain

Marc Baskin

Brent Beasley

Thomas Bookwalter

Susan S. Braithwaite

Beril Caker

Douglas Carlson

Alison Chantal Caviness

Steven L. Cohn

Yvette Marie Cua

Russ Cucina

Ethan Ulysses Cumbler

Mellar Davis

Allan S. Detsky

Jeffrey Randolph Dichter

Thomas Donner

Daniel David Dressler

Erin Egan

Matthew Eisen

Kenneth Richard Epstein

Leslie Fall

Shaun Uiglas Frost

Michael Sebastian Galin

Matthew Garber

Rajesh Garg

Raminder Singh Gill

Jackie Glover

Adrienne Green

Paul Hain

Braden Hale

Sajeev Handa

Julie Hauer

Michael Heisler

Jeanne M. Huddleston

Alan J. Hunter

Kevin Hwang

Brian Jack

Ian Harold Jenkins

Kurien John

Daniel Johnson

Todd Joyner

Deepa Kabirdas

Allen Kachalia

Abel Ngo Kho

Steven Jay Kravet

Marco Aurelio Ladino

Robert Lash

Joshua Lee

Sei Lee

Arthur Jefferson Lesesne

Marcia Levetown

Luci Leykum

Joshua David Liberman

Jonathan Mansbach

Brian Markoff

David Meltzer

Anna Leco Merca

Barbara Messinger‐Rapport

Gregory Misky

William Moran

Brahmajee Nallamothu

Theore Elliott Nash

Heather Nye

Timothy O'Brien

Bruce Ovbiagele

Thomas Andrew Owens

Mary Pak

Steven Zvi Pantilat

Vikas Parekh

Kimberly Rask

Michael Rothberg

Hilary F. Ryder

Wael Saber

Sanjay Saint

Rene Salazar

Kaycee Sink

N. Smith

Malathi Srinivasin

Raj Srivastava

Erin Stucky

Alexander Turchin

Bobbak Vahid

Robert Wachter

Robert L. Wears

Howard Weitz

Winthrop Whitcomb

Mark V. Williams

Sherrie Williams

David Woods

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We deeply appreciate the involvement of our reviewers who made the Journal of Hospital Medicine so successful in its first year. Listed below are the many reviewers and volume of their contributions. They have our sincere gratitude.

Reviewed 4 or More Articles

Eric Alper (6)

David Anthony (4)

Vineet Arora (4)

Thomas E. Baudendistel (11)

Daniel J. Brotman (7)

Vincent W. Chiang (5)

Eugene Shu‐Sen Chu (5)

Gurpreet Dhaliwal (7)

Lorenzo Di Francesco (4)

Andras Fenyves (4)

Stacy Fischer (5)

Kathlyn Fletcher (5)

Philip H. Goodman (4)

Carolyn Gould (4)

Jeffrey L. Greenwald (6)

Lakshmi Halasyamani (4)

Brian Harte (13)

Christopher P. Landrigan (5)

Peter K. Lindenauer (4)

Greg Maynard (7)

Sylvia Cheney McKean (4)

Thomas Aquinas Murphy (4)

James C. Pile (9)

Thomas Price (4)

Sumant Ranji (8)

Bradley Allen Sharpe (4)

Jason Stein (7)

Robin Tricoles (9)

Guillermo E. Umpierrez (5)

Arpana Vidyarthi (6)

Heidi Wald (7)

David Wesorick (4)

Reviewed 3 Articles

Ron G. Angus

Paul Aronowitz

Vanitha Bala

Jennifer Best

Cynthia Jean Brown

Gregory Bump

Hugo Quinny Cheng

Eva Chittenden

Eric Coleman

Curtiss B. Cook

Edward Etchells

Alan John Forster

Roma Y. Gianchandani

Leslie W. Hall

Jennifer Hanrahan

Amir K. Jaffer

Peter John Kaboli

Jennifer Kapo

Dennis Manning

Constantine Manthous

Janet Nagamine

Kevin J. O'Leary

Brian Michael Pate

Robert C. Pendleton

Jeffrey Lawrence Schnipper

Hasan Shabbir

James Edwin Stone

Chad Whelan

Audrey Young

Reviewed 2 Articles

Drew Abernathy

Stephen J. Bekanich

Paul Cantey

Kerry Cho

Patrick Conway

Jasminka Criley

Catherine Curley

Jennifer Daru

Catherine F. Decker

Andrew Paul DeFilippis

Daniel J. DiBona

Mark Earnest

Douglas Einstadter

Margaret Fang

Jonathan M. Flacker

Bradley Evan Flansbaum

Michael Frankel

Jeffrey Glasheen

Amir H. Hamrahian

Karen E. Hauer

Eric Edwin Howell

Carlos Manuel Isada

Christopher Seoung Kim

Sunil Kripalani

Jean S. Kutner

Cindy Lai

Janet Larson

David Likosky

David Ling

Michelle Magee

Navneet Majhail

Michael Matheny

George Mathew

Govardhanan Nagaiah

James Newman

Christopher Ohl

Shawn Ralston

Daniel A. Rauch

John James Ross

Joel Rubenstein

David Schulman

Kaveh G. Shojania

Gregory Randall Smith Jr.

Peter Youngers Watson

Chad T. Whelan

Neil Winawer

Scott Wright

Reviewed 1 Article

Adebola Adesanya

Nasim Afsarmanesh

Richard Keith Albert

Mel L. Anderson, III

Wendy Artrong

Thomas W. Barrett

David Bar‐Shain

Marc Baskin

Brent Beasley

Thomas Bookwalter

Susan S. Braithwaite

Beril Caker

Douglas Carlson

Alison Chantal Caviness

Steven L. Cohn

Yvette Marie Cua

Russ Cucina

Ethan Ulysses Cumbler

Mellar Davis

Allan S. Detsky

Jeffrey Randolph Dichter

Thomas Donner

Daniel David Dressler

Erin Egan

Matthew Eisen

Kenneth Richard Epstein

Leslie Fall

Shaun Uiglas Frost

Michael Sebastian Galin

Matthew Garber

Rajesh Garg

Raminder Singh Gill

Jackie Glover

Adrienne Green

Paul Hain

Braden Hale

Sajeev Handa

Julie Hauer

Michael Heisler

Jeanne M. Huddleston

Alan J. Hunter

Kevin Hwang

Brian Jack

Ian Harold Jenkins

Kurien John

Daniel Johnson

Todd Joyner

Deepa Kabirdas

Allen Kachalia

Abel Ngo Kho

Steven Jay Kravet

Marco Aurelio Ladino

Robert Lash

Joshua Lee

Sei Lee

Arthur Jefferson Lesesne

Marcia Levetown

Luci Leykum

Joshua David Liberman

Jonathan Mansbach

Brian Markoff

David Meltzer

Anna Leco Merca

Barbara Messinger‐Rapport

Gregory Misky

William Moran

Brahmajee Nallamothu

Theore Elliott Nash

Heather Nye

Timothy O'Brien

Bruce Ovbiagele

Thomas Andrew Owens

Mary Pak

Steven Zvi Pantilat

Vikas Parekh

Kimberly Rask

Michael Rothberg

Hilary F. Ryder

Wael Saber

Sanjay Saint

Rene Salazar

Kaycee Sink

N. Smith

Malathi Srinivasin

Raj Srivastava

Erin Stucky

Alexander Turchin

Bobbak Vahid

Robert Wachter

Robert L. Wears

Howard Weitz

Winthrop Whitcomb

Mark V. Williams

Sherrie Williams

David Woods

We deeply appreciate the involvement of our reviewers who made the Journal of Hospital Medicine so successful in its first year. Listed below are the many reviewers and volume of their contributions. They have our sincere gratitude.

Reviewed 4 or More Articles

Eric Alper (6)

David Anthony (4)

Vineet Arora (4)

Thomas E. Baudendistel (11)

Daniel J. Brotman (7)

Vincent W. Chiang (5)

Eugene Shu‐Sen Chu (5)

Gurpreet Dhaliwal (7)

Lorenzo Di Francesco (4)

Andras Fenyves (4)

Stacy Fischer (5)

Kathlyn Fletcher (5)

Philip H. Goodman (4)

Carolyn Gould (4)

Jeffrey L. Greenwald (6)

Lakshmi Halasyamani (4)

Brian Harte (13)

Christopher P. Landrigan (5)

Peter K. Lindenauer (4)

Greg Maynard (7)

Sylvia Cheney McKean (4)

Thomas Aquinas Murphy (4)

James C. Pile (9)

Thomas Price (4)

Sumant Ranji (8)

Bradley Allen Sharpe (4)

Jason Stein (7)

Robin Tricoles (9)

Guillermo E. Umpierrez (5)

Arpana Vidyarthi (6)

Heidi Wald (7)

David Wesorick (4)

Reviewed 3 Articles

Ron G. Angus

Paul Aronowitz

Vanitha Bala

Jennifer Best

Cynthia Jean Brown

Gregory Bump

Hugo Quinny Cheng

Eva Chittenden

Eric Coleman

Curtiss B. Cook

Edward Etchells

Alan John Forster

Roma Y. Gianchandani

Leslie W. Hall

Jennifer Hanrahan

Amir K. Jaffer

Peter John Kaboli

Jennifer Kapo

Dennis Manning

Constantine Manthous

Janet Nagamine

Kevin J. O'Leary

Brian Michael Pate

Robert C. Pendleton

Jeffrey Lawrence Schnipper

Hasan Shabbir

James Edwin Stone

Chad Whelan

Audrey Young

Reviewed 2 Articles

Drew Abernathy

Stephen J. Bekanich

Paul Cantey

Kerry Cho

Patrick Conway

Jasminka Criley

Catherine Curley

Jennifer Daru

Catherine F. Decker

Andrew Paul DeFilippis

Daniel J. DiBona

Mark Earnest

Douglas Einstadter

Margaret Fang

Jonathan M. Flacker

Bradley Evan Flansbaum

Michael Frankel

Jeffrey Glasheen

Amir H. Hamrahian

Karen E. Hauer

Eric Edwin Howell

Carlos Manuel Isada

Christopher Seoung Kim

Sunil Kripalani

Jean S. Kutner

Cindy Lai

Janet Larson

David Likosky

David Ling

Michelle Magee

Navneet Majhail

Michael Matheny

George Mathew

Govardhanan Nagaiah

James Newman

Christopher Ohl

Shawn Ralston

Daniel A. Rauch

John James Ross

Joel Rubenstein

David Schulman

Kaveh G. Shojania

Gregory Randall Smith Jr.

Peter Youngers Watson

Chad T. Whelan

Neil Winawer

Scott Wright

Reviewed 1 Article

Adebola Adesanya

Nasim Afsarmanesh

Richard Keith Albert

Mel L. Anderson, III

Wendy Artrong

Thomas W. Barrett

David Bar‐Shain

Marc Baskin

Brent Beasley

Thomas Bookwalter

Susan S. Braithwaite

Beril Caker

Douglas Carlson

Alison Chantal Caviness

Steven L. Cohn

Yvette Marie Cua

Russ Cucina

Ethan Ulysses Cumbler

Mellar Davis

Allan S. Detsky

Jeffrey Randolph Dichter

Thomas Donner

Daniel David Dressler

Erin Egan

Matthew Eisen

Kenneth Richard Epstein

Leslie Fall

Shaun Uiglas Frost

Michael Sebastian Galin

Matthew Garber

Rajesh Garg

Raminder Singh Gill

Jackie Glover

Adrienne Green

Paul Hain

Braden Hale

Sajeev Handa

Julie Hauer

Michael Heisler

Jeanne M. Huddleston

Alan J. Hunter

Kevin Hwang

Brian Jack

Ian Harold Jenkins

Kurien John

Daniel Johnson

Todd Joyner

Deepa Kabirdas

Allen Kachalia

Abel Ngo Kho

Steven Jay Kravet

Marco Aurelio Ladino

Robert Lash

Joshua Lee

Sei Lee

Arthur Jefferson Lesesne

Marcia Levetown

Luci Leykum

Joshua David Liberman

Jonathan Mansbach

Brian Markoff

David Meltzer

Anna Leco Merca

Barbara Messinger‐Rapport

Gregory Misky

William Moran

Brahmajee Nallamothu

Theore Elliott Nash

Heather Nye

Timothy O'Brien

Bruce Ovbiagele

Thomas Andrew Owens

Mary Pak

Steven Zvi Pantilat

Vikas Parekh

Kimberly Rask

Michael Rothberg

Hilary F. Ryder

Wael Saber

Sanjay Saint

Rene Salazar

Kaycee Sink

N. Smith

Malathi Srinivasin

Raj Srivastava

Erin Stucky

Alexander Turchin

Bobbak Vahid

Robert Wachter

Robert L. Wears

Howard Weitz

Winthrop Whitcomb

Mark V. Williams

Sherrie Williams

David Woods

Issue
Journal of Hospital Medicine - 2(1)
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Journal of Hospital Medicine - 2(1)
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Fixed‐dose, subcutaneous, unfractionated heparin effective for VTE

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Fixed‐dose, subcutaneous, unfractionated heparin effective for VTE

  • CLINICAL QUESTION: How safe and effective is fixed‐dose subcutaneous unfractionated heparin in the treatment of venous thromboembolism?

  • BOTTOM LINE: In this study, fixed‐dose weight‐adjusted unfractionated heparin (UFH) administered subcutaneously was as safe and effective as low‐molecular‐weight heparin (LMWH) in the treatment of venous thromboembolism (VTE). Estimated drug costs for a 6‐day course are $712 for LMWH and $37 for UFH. Most clinicians will want to see similar results from at least 1 additional well‐done clinical trial, including more patients with symptomatic pulmonary embolism, before routinely treating VTE with subcutaneous UFH. (LOE = 1b)

  • REFERENCE: Kearon C, Ginsberg JS, Julian JA, et al, for the Fixed‐Dose Heparin (FIDO) Investigators. Comparison of fixed‐dose weight‐adjusted unfractionated heparin and low‐molecular‐weight heparin for acute treatment of venous thromboembolism. JAMA 2006;296:935‐942.

  • STUDY DESIGN: Randomized controlled trial (single‐blinded)

  • FUNDING: Foundation

  • SETTING: Outpatient (any)

  • ALLOCATION: Concealed

  • SYNOPSIS: These investigators randomly assigned (concealed allocation assignment) 708 patients, 18 years or older, with acute VTE to subcutaneous UFH (initial dose of 333 U/kg, followed by a fixed dose of 250 U/kg every 12 hours) or LMWH (dalteparin or enoxaparin, 100 IU/kg every 12 hours). The dose of subcutaneous UFH remained fixed for individual patients and was not changed during treatment as a result of anticoagulation profiles. The diagnosis of VTE included patients with acute deep vein thrombosis of the legs (81%) or symptomatic pulmonary embolism (19%). Oral warfarin was usually started on the same day as heparin in both groups and continued for a minimum of 3 months with doses adjusted to achieve an international normalized ratio (INR) of between 2.0 and 3.0. Heparin was continued for at least 5 days and until the INR was 2.0 or higher for 2 consecutive days. Individuals unaware of treatment group assignment assessed all outcomes, including study eligibility criteria. Follow‐up occurred for more than 98% of subjects for 3 months. All eligible and consenting patients underwent final data analysis. The risk of recurrent VTE in the first 3 months after treatment was not significantly different between patients in the UFH group (3.8%) and those in the LMWH group (3.4%). The risk of major bleeding during the first 10 days of treatment was also similar between the UFH group (1.1%) and LMWH group (1.4%). Approximately 70% of patients in both groups received treatment entirely out of hospital. Overall, there were 18 deaths in the UFH group and 22 deaths in the LMWH group (difference not significant). Adverse events were unrelated to whether subjects were subtherapeutic or supratherapeutic.

Article PDF
Issue
Journal of Hospital Medicine - 2(1)
Page Number
54-54
Sections
Article PDF
Article PDF

  • CLINICAL QUESTION: How safe and effective is fixed‐dose subcutaneous unfractionated heparin in the treatment of venous thromboembolism?

  • BOTTOM LINE: In this study, fixed‐dose weight‐adjusted unfractionated heparin (UFH) administered subcutaneously was as safe and effective as low‐molecular‐weight heparin (LMWH) in the treatment of venous thromboembolism (VTE). Estimated drug costs for a 6‐day course are $712 for LMWH and $37 for UFH. Most clinicians will want to see similar results from at least 1 additional well‐done clinical trial, including more patients with symptomatic pulmonary embolism, before routinely treating VTE with subcutaneous UFH. (LOE = 1b)

  • REFERENCE: Kearon C, Ginsberg JS, Julian JA, et al, for the Fixed‐Dose Heparin (FIDO) Investigators. Comparison of fixed‐dose weight‐adjusted unfractionated heparin and low‐molecular‐weight heparin for acute treatment of venous thromboembolism. JAMA 2006;296:935‐942.

  • STUDY DESIGN: Randomized controlled trial (single‐blinded)

  • FUNDING: Foundation

  • SETTING: Outpatient (any)

  • ALLOCATION: Concealed

  • SYNOPSIS: These investigators randomly assigned (concealed allocation assignment) 708 patients, 18 years or older, with acute VTE to subcutaneous UFH (initial dose of 333 U/kg, followed by a fixed dose of 250 U/kg every 12 hours) or LMWH (dalteparin or enoxaparin, 100 IU/kg every 12 hours). The dose of subcutaneous UFH remained fixed for individual patients and was not changed during treatment as a result of anticoagulation profiles. The diagnosis of VTE included patients with acute deep vein thrombosis of the legs (81%) or symptomatic pulmonary embolism (19%). Oral warfarin was usually started on the same day as heparin in both groups and continued for a minimum of 3 months with doses adjusted to achieve an international normalized ratio (INR) of between 2.0 and 3.0. Heparin was continued for at least 5 days and until the INR was 2.0 or higher for 2 consecutive days. Individuals unaware of treatment group assignment assessed all outcomes, including study eligibility criteria. Follow‐up occurred for more than 98% of subjects for 3 months. All eligible and consenting patients underwent final data analysis. The risk of recurrent VTE in the first 3 months after treatment was not significantly different between patients in the UFH group (3.8%) and those in the LMWH group (3.4%). The risk of major bleeding during the first 10 days of treatment was also similar between the UFH group (1.1%) and LMWH group (1.4%). Approximately 70% of patients in both groups received treatment entirely out of hospital. Overall, there were 18 deaths in the UFH group and 22 deaths in the LMWH group (difference not significant). Adverse events were unrelated to whether subjects were subtherapeutic or supratherapeutic.

  • CLINICAL QUESTION: How safe and effective is fixed‐dose subcutaneous unfractionated heparin in the treatment of venous thromboembolism?

  • BOTTOM LINE: In this study, fixed‐dose weight‐adjusted unfractionated heparin (UFH) administered subcutaneously was as safe and effective as low‐molecular‐weight heparin (LMWH) in the treatment of venous thromboembolism (VTE). Estimated drug costs for a 6‐day course are $712 for LMWH and $37 for UFH. Most clinicians will want to see similar results from at least 1 additional well‐done clinical trial, including more patients with symptomatic pulmonary embolism, before routinely treating VTE with subcutaneous UFH. (LOE = 1b)

  • REFERENCE: Kearon C, Ginsberg JS, Julian JA, et al, for the Fixed‐Dose Heparin (FIDO) Investigators. Comparison of fixed‐dose weight‐adjusted unfractionated heparin and low‐molecular‐weight heparin for acute treatment of venous thromboembolism. JAMA 2006;296:935‐942.

  • STUDY DESIGN: Randomized controlled trial (single‐blinded)

  • FUNDING: Foundation

  • SETTING: Outpatient (any)

  • ALLOCATION: Concealed

  • SYNOPSIS: These investigators randomly assigned (concealed allocation assignment) 708 patients, 18 years or older, with acute VTE to subcutaneous UFH (initial dose of 333 U/kg, followed by a fixed dose of 250 U/kg every 12 hours) or LMWH (dalteparin or enoxaparin, 100 IU/kg every 12 hours). The dose of subcutaneous UFH remained fixed for individual patients and was not changed during treatment as a result of anticoagulation profiles. The diagnosis of VTE included patients with acute deep vein thrombosis of the legs (81%) or symptomatic pulmonary embolism (19%). Oral warfarin was usually started on the same day as heparin in both groups and continued for a minimum of 3 months with doses adjusted to achieve an international normalized ratio (INR) of between 2.0 and 3.0. Heparin was continued for at least 5 days and until the INR was 2.0 or higher for 2 consecutive days. Individuals unaware of treatment group assignment assessed all outcomes, including study eligibility criteria. Follow‐up occurred for more than 98% of subjects for 3 months. All eligible and consenting patients underwent final data analysis. The risk of recurrent VTE in the first 3 months after treatment was not significantly different between patients in the UFH group (3.8%) and those in the LMWH group (3.4%). The risk of major bleeding during the first 10 days of treatment was also similar between the UFH group (1.1%) and LMWH group (1.4%). Approximately 70% of patients in both groups received treatment entirely out of hospital. Overall, there were 18 deaths in the UFH group and 22 deaths in the LMWH group (difference not significant). Adverse events were unrelated to whether subjects were subtherapeutic or supratherapeutic.

Issue
Journal of Hospital Medicine - 2(1)
Issue
Journal of Hospital Medicine - 2(1)
Page Number
54-54
Page Number
54-54
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Fixed‐dose, subcutaneous, unfractionated heparin effective for VTE
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Fixed‐dose, subcutaneous, unfractionated heparin effective for VTE
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Disseminated histoplasmosis

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Disseminated histoplasmosis

A previously healthy 27‐year‐old El Salvadoran immigrant presented with a 2‐week history of cough, fever, rigors, prostration, anorexia, weight loss, and scant hemoptysis. Physical examination revealed a thin, febrile, toxic‐appearing man in respiratory distress with bibasilar rales and scattered wheezes. Laboratory data showed a sodium of 126 mEq/L, lactate dehydrogenase of 617 U/L, ferritin of 3570 ng/mL, and liver test abnormalities suggestive of cholestasis. Chest film (Fig. 1) and computed tomography (Fig. 2) demonstrated a diffuse miliary air space pattern. Sputum smears for mycobacterium tuberculosis were negative. A urine histoplasmosis antigen level was markedly positive (7.6 EIA units), and bone marrow cultures eventually grew Histoplasma capsulatum. The HIV test result was positive, and his CD4 count was 34 cells/mm3. He was successfully treated with liposomal amphotericin B followed by itraconazole.

Figure 1
Chest radiograph.
Figure 2
Thoracic CT.

Histoplasmosis is the most prevalent endemic mycosis in Latin America. Most infections are asymptomatic or self‐limited, but immunodeficient individuals may develop acute pulmonary or severe, progressive disseminated infection, usually from reactivation of latent disease. Although nonspecific, the serum lactate dehydrogenase and ferritin levels are often markedly elevated. Chest imaging may be normal or show a diffuse reticulonodular pattern (with nodules less than 3 mm in diameter), indistinguishable from miliary tuberculosis. In HIV‐infected individuals, disseminated histoplasmosis usually develops when the CD4 count is less than 75 cells/mm3. Treatment is generally lifelong.

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Journal of Hospital Medicine - 2(1)
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A previously healthy 27‐year‐old El Salvadoran immigrant presented with a 2‐week history of cough, fever, rigors, prostration, anorexia, weight loss, and scant hemoptysis. Physical examination revealed a thin, febrile, toxic‐appearing man in respiratory distress with bibasilar rales and scattered wheezes. Laboratory data showed a sodium of 126 mEq/L, lactate dehydrogenase of 617 U/L, ferritin of 3570 ng/mL, and liver test abnormalities suggestive of cholestasis. Chest film (Fig. 1) and computed tomography (Fig. 2) demonstrated a diffuse miliary air space pattern. Sputum smears for mycobacterium tuberculosis were negative. A urine histoplasmosis antigen level was markedly positive (7.6 EIA units), and bone marrow cultures eventually grew Histoplasma capsulatum. The HIV test result was positive, and his CD4 count was 34 cells/mm3. He was successfully treated with liposomal amphotericin B followed by itraconazole.

Figure 1
Chest radiograph.
Figure 2
Thoracic CT.

Histoplasmosis is the most prevalent endemic mycosis in Latin America. Most infections are asymptomatic or self‐limited, but immunodeficient individuals may develop acute pulmonary or severe, progressive disseminated infection, usually from reactivation of latent disease. Although nonspecific, the serum lactate dehydrogenase and ferritin levels are often markedly elevated. Chest imaging may be normal or show a diffuse reticulonodular pattern (with nodules less than 3 mm in diameter), indistinguishable from miliary tuberculosis. In HIV‐infected individuals, disseminated histoplasmosis usually develops when the CD4 count is less than 75 cells/mm3. Treatment is generally lifelong.

A previously healthy 27‐year‐old El Salvadoran immigrant presented with a 2‐week history of cough, fever, rigors, prostration, anorexia, weight loss, and scant hemoptysis. Physical examination revealed a thin, febrile, toxic‐appearing man in respiratory distress with bibasilar rales and scattered wheezes. Laboratory data showed a sodium of 126 mEq/L, lactate dehydrogenase of 617 U/L, ferritin of 3570 ng/mL, and liver test abnormalities suggestive of cholestasis. Chest film (Fig. 1) and computed tomography (Fig. 2) demonstrated a diffuse miliary air space pattern. Sputum smears for mycobacterium tuberculosis were negative. A urine histoplasmosis antigen level was markedly positive (7.6 EIA units), and bone marrow cultures eventually grew Histoplasma capsulatum. The HIV test result was positive, and his CD4 count was 34 cells/mm3. He was successfully treated with liposomal amphotericin B followed by itraconazole.

Figure 1
Chest radiograph.
Figure 2
Thoracic CT.

Histoplasmosis is the most prevalent endemic mycosis in Latin America. Most infections are asymptomatic or self‐limited, but immunodeficient individuals may develop acute pulmonary or severe, progressive disseminated infection, usually from reactivation of latent disease. Although nonspecific, the serum lactate dehydrogenase and ferritin levels are often markedly elevated. Chest imaging may be normal or show a diffuse reticulonodular pattern (with nodules less than 3 mm in diameter), indistinguishable from miliary tuberculosis. In HIV‐infected individuals, disseminated histoplasmosis usually develops when the CD4 count is less than 75 cells/mm3. Treatment is generally lifelong.

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It was 8 p.m. on a cold Minnesota night, and my vision was obscured by flurries of snow and decomposing wiper blades. I was late for home. When I arrived, 11 sets of eyes turned toward me. (Twelve, really, counting my boxer Chocky Locky). They were sitting in the dining room, and the evening meal had just started. I washed quickly and took my seat at the table.

We have a large dining table that seats 12, but our current dish service—due to an unforeseen disaster—has only 11 settings. Thus, our service was at its maximum capacity. Tonight’s crowd included my wife and me, a grandmother, four offspring of various genders and a female teenager of unknown origin, a male preteen well-known to the household, and two young females who had sat at the table before.

It was unclear whose turn it was to clear the table. The schedule was not available, and several offspring cited work limits they would hate to see abused.

As per standard operating procedure, each person at the table began to speak at the same time. Eventually order was established, though this was at best a transitory phenomenon. We received reports on each participant’s day, with highlights of lunch hour mayhem, recess riots, and general curricular boredom.

I began to question the unknown teen: name, age, place of origin, habits, and so on, but my history taking was interrupted. My younger son wanted to relay the results of an important test he had taken. He had passed and was now certified to use punctuation. I turned to resume my history taking, but made the important physical exam observation of intense eye rolling on the part of my daughter and her friend. This is a well-known physical finding in this age group and one that generally signals a pre-seizure threshold that I did not want to further induce.

After an intense nutritional session that included all major food groups and several minor ones, there were several short, unscheduled presentations. The grandmother gave a long and interesting family history with highlights of a great-great grandfather, who had been a freelance horse thief for both the Polish and Russian armies, and his son, who had been—alternatively—a gambler, a rabbi, a communist, and a union organizer.

After this history lesson, we received a fascinating report from one of my male offspring entitled, “proper placement of the hand and axillae, combined with repetitive flapping movements of the arm, to elicit an auditory stimulus similar to flatulence.” Much hilarity ensued.

Dr. Newman’s staff performs rounds at a Chinese restaurant

It was unclear whose turn it was to clear the table. The schedule was not available, and several of the offspring cited work limits they would hate to see abused. Eventually the job was done with only minimal threats of withdrawal of privileges. As I prepared to resume my reading, a call went out for transportation services. It was time to discharge one of the visiting children to her abode. I was happy to decrease the numbers in house, though I would have been happier to see our numbers go even lower. Our length of stay seemed to be rising daily. As I attempted to initiate the transportation home, I realized we had to go through the checklist. Do you have your scarf, your gloves, and your shoes? Did you have a good time? I considered a policy of no readmission in 30 days, but it was voted down in a team meeting.

I returned from transportation duties, and I sat quietly for a moment and looked at the Times and the Post-Bulletin. These were papers I had been waiting to review—especially the comics. But something always seems to come up when one has papers to review. My youngest daughter and her friends needed my guidance on an art project. I had hoped they would see one, do one, teach one, but I had to repeatedly sketch the face outlines for them to color.

 

 

As I sat down again to the papers, the doorbell rang. Nobody else appeared to be on doorbell duty, so I went to the front of the house. There was a young man in a white shirt and black tie. He was proselytizing for a religious group. I informed him that our house had adopted a “no religious rep policy.” This helps us to avoid being unduly influenced by reps, though I must admit I still use my Taoist pen. It’s a Zen-Pen: one side writes, the other doesn’t.

Finally, I returned to my seat. At that point, the room plunged into darkness. A moment of panic. Quickly, I took my own pulse, a technique I had learned from the medical literature. Once calmed, I went through the differential. The power might be out for the whole city or just the house. Perhaps a fuse had blown from one too many electronic entertainment devices. Or maybe mice had chewed through a power cable. As I pondered my next course of diagnostic action and reviewed my alternatives in an evidence-based and allorhythmic approach, I auscultated a series of breath sounds that might be interpreted as gasps or giggles.

I intuitively realized that it was a severe case of “little girls playing a joke on Dad by switching off the light.” I had two choices. The first was to be crabby and bellow for them to quit playing with the switch. I felt this to be a harsh choice with bad potential side effects. Instead, I ducked under the table and silently hid. When proper lighting was restored, they were amazed to see I had vanished, and when they came to investigate, I revealed myself and uttered the key phrase: “Boo!” A riotous wrestling match ensued, which led to the injury of a family heirloom and my spine.

It was time for bed, despite my elder son’s complaint of a type of chronic insomnia only remediable by late-night cartoon observation. Evening reading began. Such important journals as Click Clack Moo, P.J. Funnybunny Camps Out, and the Stinky Cheese Man and Other Fairly Stupid Tales were on the agenda.

As I drifted off to sleep, the phone rang. It was a wrong number. Several hours later, an emergency call for supplemental H2O was answered. Two hours after that, I awoke to a hideous scream; it was a nightmare. My alarm rang at 6:15, and I jumped from bed refreshed. No, that’s a lie. I stumbled from bed after hitting the snooze button four times. Morning nutrition rounds were a stale toaster pastry and coffee. Team Newman noted that there were last-minute reports not finished for school and preparation for a day of testing.

I drove to work exhausted after a night of Home. TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

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It was 8 p.m. on a cold Minnesota night, and my vision was obscured by flurries of snow and decomposing wiper blades. I was late for home. When I arrived, 11 sets of eyes turned toward me. (Twelve, really, counting my boxer Chocky Locky). They were sitting in the dining room, and the evening meal had just started. I washed quickly and took my seat at the table.

We have a large dining table that seats 12, but our current dish service—due to an unforeseen disaster—has only 11 settings. Thus, our service was at its maximum capacity. Tonight’s crowd included my wife and me, a grandmother, four offspring of various genders and a female teenager of unknown origin, a male preteen well-known to the household, and two young females who had sat at the table before.

It was unclear whose turn it was to clear the table. The schedule was not available, and several offspring cited work limits they would hate to see abused.

As per standard operating procedure, each person at the table began to speak at the same time. Eventually order was established, though this was at best a transitory phenomenon. We received reports on each participant’s day, with highlights of lunch hour mayhem, recess riots, and general curricular boredom.

I began to question the unknown teen: name, age, place of origin, habits, and so on, but my history taking was interrupted. My younger son wanted to relay the results of an important test he had taken. He had passed and was now certified to use punctuation. I turned to resume my history taking, but made the important physical exam observation of intense eye rolling on the part of my daughter and her friend. This is a well-known physical finding in this age group and one that generally signals a pre-seizure threshold that I did not want to further induce.

After an intense nutritional session that included all major food groups and several minor ones, there were several short, unscheduled presentations. The grandmother gave a long and interesting family history with highlights of a great-great grandfather, who had been a freelance horse thief for both the Polish and Russian armies, and his son, who had been—alternatively—a gambler, a rabbi, a communist, and a union organizer.

After this history lesson, we received a fascinating report from one of my male offspring entitled, “proper placement of the hand and axillae, combined with repetitive flapping movements of the arm, to elicit an auditory stimulus similar to flatulence.” Much hilarity ensued.

Dr. Newman’s staff performs rounds at a Chinese restaurant

It was unclear whose turn it was to clear the table. The schedule was not available, and several of the offspring cited work limits they would hate to see abused. Eventually the job was done with only minimal threats of withdrawal of privileges. As I prepared to resume my reading, a call went out for transportation services. It was time to discharge one of the visiting children to her abode. I was happy to decrease the numbers in house, though I would have been happier to see our numbers go even lower. Our length of stay seemed to be rising daily. As I attempted to initiate the transportation home, I realized we had to go through the checklist. Do you have your scarf, your gloves, and your shoes? Did you have a good time? I considered a policy of no readmission in 30 days, but it was voted down in a team meeting.

I returned from transportation duties, and I sat quietly for a moment and looked at the Times and the Post-Bulletin. These were papers I had been waiting to review—especially the comics. But something always seems to come up when one has papers to review. My youngest daughter and her friends needed my guidance on an art project. I had hoped they would see one, do one, teach one, but I had to repeatedly sketch the face outlines for them to color.

 

 

As I sat down again to the papers, the doorbell rang. Nobody else appeared to be on doorbell duty, so I went to the front of the house. There was a young man in a white shirt and black tie. He was proselytizing for a religious group. I informed him that our house had adopted a “no religious rep policy.” This helps us to avoid being unduly influenced by reps, though I must admit I still use my Taoist pen. It’s a Zen-Pen: one side writes, the other doesn’t.

Finally, I returned to my seat. At that point, the room plunged into darkness. A moment of panic. Quickly, I took my own pulse, a technique I had learned from the medical literature. Once calmed, I went through the differential. The power might be out for the whole city or just the house. Perhaps a fuse had blown from one too many electronic entertainment devices. Or maybe mice had chewed through a power cable. As I pondered my next course of diagnostic action and reviewed my alternatives in an evidence-based and allorhythmic approach, I auscultated a series of breath sounds that might be interpreted as gasps or giggles.

I intuitively realized that it was a severe case of “little girls playing a joke on Dad by switching off the light.” I had two choices. The first was to be crabby and bellow for them to quit playing with the switch. I felt this to be a harsh choice with bad potential side effects. Instead, I ducked under the table and silently hid. When proper lighting was restored, they were amazed to see I had vanished, and when they came to investigate, I revealed myself and uttered the key phrase: “Boo!” A riotous wrestling match ensued, which led to the injury of a family heirloom and my spine.

It was time for bed, despite my elder son’s complaint of a type of chronic insomnia only remediable by late-night cartoon observation. Evening reading began. Such important journals as Click Clack Moo, P.J. Funnybunny Camps Out, and the Stinky Cheese Man and Other Fairly Stupid Tales were on the agenda.

As I drifted off to sleep, the phone rang. It was a wrong number. Several hours later, an emergency call for supplemental H2O was answered. Two hours after that, I awoke to a hideous scream; it was a nightmare. My alarm rang at 6:15, and I jumped from bed refreshed. No, that’s a lie. I stumbled from bed after hitting the snooze button four times. Morning nutrition rounds were a stale toaster pastry and coffee. Team Newman noted that there were last-minute reports not finished for school and preparation for a day of testing.

I drove to work exhausted after a night of Home. TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

It was 8 p.m. on a cold Minnesota night, and my vision was obscured by flurries of snow and decomposing wiper blades. I was late for home. When I arrived, 11 sets of eyes turned toward me. (Twelve, really, counting my boxer Chocky Locky). They were sitting in the dining room, and the evening meal had just started. I washed quickly and took my seat at the table.

We have a large dining table that seats 12, but our current dish service—due to an unforeseen disaster—has only 11 settings. Thus, our service was at its maximum capacity. Tonight’s crowd included my wife and me, a grandmother, four offspring of various genders and a female teenager of unknown origin, a male preteen well-known to the household, and two young females who had sat at the table before.

It was unclear whose turn it was to clear the table. The schedule was not available, and several offspring cited work limits they would hate to see abused.

As per standard operating procedure, each person at the table began to speak at the same time. Eventually order was established, though this was at best a transitory phenomenon. We received reports on each participant’s day, with highlights of lunch hour mayhem, recess riots, and general curricular boredom.

I began to question the unknown teen: name, age, place of origin, habits, and so on, but my history taking was interrupted. My younger son wanted to relay the results of an important test he had taken. He had passed and was now certified to use punctuation. I turned to resume my history taking, but made the important physical exam observation of intense eye rolling on the part of my daughter and her friend. This is a well-known physical finding in this age group and one that generally signals a pre-seizure threshold that I did not want to further induce.

After an intense nutritional session that included all major food groups and several minor ones, there were several short, unscheduled presentations. The grandmother gave a long and interesting family history with highlights of a great-great grandfather, who had been a freelance horse thief for both the Polish and Russian armies, and his son, who had been—alternatively—a gambler, a rabbi, a communist, and a union organizer.

After this history lesson, we received a fascinating report from one of my male offspring entitled, “proper placement of the hand and axillae, combined with repetitive flapping movements of the arm, to elicit an auditory stimulus similar to flatulence.” Much hilarity ensued.

Dr. Newman’s staff performs rounds at a Chinese restaurant

It was unclear whose turn it was to clear the table. The schedule was not available, and several of the offspring cited work limits they would hate to see abused. Eventually the job was done with only minimal threats of withdrawal of privileges. As I prepared to resume my reading, a call went out for transportation services. It was time to discharge one of the visiting children to her abode. I was happy to decrease the numbers in house, though I would have been happier to see our numbers go even lower. Our length of stay seemed to be rising daily. As I attempted to initiate the transportation home, I realized we had to go through the checklist. Do you have your scarf, your gloves, and your shoes? Did you have a good time? I considered a policy of no readmission in 30 days, but it was voted down in a team meeting.

I returned from transportation duties, and I sat quietly for a moment and looked at the Times and the Post-Bulletin. These were papers I had been waiting to review—especially the comics. But something always seems to come up when one has papers to review. My youngest daughter and her friends needed my guidance on an art project. I had hoped they would see one, do one, teach one, but I had to repeatedly sketch the face outlines for them to color.

 

 

As I sat down again to the papers, the doorbell rang. Nobody else appeared to be on doorbell duty, so I went to the front of the house. There was a young man in a white shirt and black tie. He was proselytizing for a religious group. I informed him that our house had adopted a “no religious rep policy.” This helps us to avoid being unduly influenced by reps, though I must admit I still use my Taoist pen. It’s a Zen-Pen: one side writes, the other doesn’t.

Finally, I returned to my seat. At that point, the room plunged into darkness. A moment of panic. Quickly, I took my own pulse, a technique I had learned from the medical literature. Once calmed, I went through the differential. The power might be out for the whole city or just the house. Perhaps a fuse had blown from one too many electronic entertainment devices. Or maybe mice had chewed through a power cable. As I pondered my next course of diagnostic action and reviewed my alternatives in an evidence-based and allorhythmic approach, I auscultated a series of breath sounds that might be interpreted as gasps or giggles.

I intuitively realized that it was a severe case of “little girls playing a joke on Dad by switching off the light.” I had two choices. The first was to be crabby and bellow for them to quit playing with the switch. I felt this to be a harsh choice with bad potential side effects. Instead, I ducked under the table and silently hid. When proper lighting was restored, they were amazed to see I had vanished, and when they came to investigate, I revealed myself and uttered the key phrase: “Boo!” A riotous wrestling match ensued, which led to the injury of a family heirloom and my spine.

It was time for bed, despite my elder son’s complaint of a type of chronic insomnia only remediable by late-night cartoon observation. Evening reading began. Such important journals as Click Clack Moo, P.J. Funnybunny Camps Out, and the Stinky Cheese Man and Other Fairly Stupid Tales were on the agenda.

As I drifted off to sleep, the phone rang. It was a wrong number. Several hours later, an emergency call for supplemental H2O was answered. Two hours after that, I awoke to a hideous scream; it was a nightmare. My alarm rang at 6:15, and I jumped from bed refreshed. No, that’s a lie. I stumbled from bed after hitting the snooze button four times. Morning nutrition rounds were a stale toaster pastry and coffee. Team Newman noted that there were last-minute reports not finished for school and preparation for a day of testing.

I drove to work exhausted after a night of Home. TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

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The Hospitalist-Patient Conundrum

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The Hospitalist-Patient Conundrum

Hospitalist-patient continuity is primarily a function of the number of consecutive days worked by a hospitalist, but the way new referrals are distributed can also affect continuity. This month, I will discuss both.

For my first few years as a hospitalist in the late 1980s and early 1990s, my one partner and I generally worked a schedule of 21 days on and seven days off. While I wouldn’t recommend that anyone try that today, it wasn’t as bad as you might think, because our patient volumes weren’t terribly high and, on about a third of the worked days, I was done shortly after lunch.

While working that schedule, I became aware of its benefit to hospitalist-patient continuity. I can remember many patients with hospital stays of more than two weeks whom I saw every day myself. As you might imagine, my partner and I talked periodically about working fewer than 21 days at a stretch and handing a service over to one another more frequently. But we were concerned that this would make us inefficient because more of our worked days would involve getting to know a new list of patients. In effect, we’d work more hours without an increase in income or patient volume.

While still working the 21-day schedule, I came to know another practice and was stunned that these doctors had taken essentially the opposite approach to scheduling. They worked 24-hour shifts on site and never worked more than one shift at a time. (If your shifts are 24-hours long, you probably can’t or shouldn’t work more than one at a time.) This schedule meant that a patient would see a different hospitalist each day. I couldn’t believe that either the patients or the hospitalists would think this was a reasonable thing to do, but the doctors were convinced it worked well. Later I learned that this group had been started by an emergency medicine practice, and it seems they had made the mistake of inserting an emergency department (ED) physician schedule into a hospitalist practice—and 24-hour shifts for ED doctors were more common then than now.

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an impact.

So, early in my career, the first two schedules I became acquainted with sat on opposite ends of a continuum that has since been filled in by many other options. Both the practice I was part of and the 24-hour-shift practice abandoned their original schedules within a few years and moved on to other alternatives. In fact, I have since worked nearly every schedule you can imagine, including the seven-on/seven-off schedule, which I think is a suboptimal choice for most groups. (See August 2006 “Career Management,” p. 9.) With each variation in my work schedule, I’ve thought a lot about its effect on continuity.

While there isn’t a great deal of research to prove it, improved continuity is probably associated with improvements in things like:

  • Quality care and safety;
  • Patient satisfaction (and probably hospitalist satisfaction also);
  • Hospital resource utilization; and
  • Hospitalist efficiency.

When hospitalists design a schedule, I recommend that the doctors think first about what will allow them a sustainable lifestyle while ensuring the necessary coverage—for some practices, this means keeping a doctor in the hospital around the clock. Ideally, they will come up with several options that satisfy these two metrics. In many cases, the option that results in the best continuity is the one they should choose.

 

 

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an effect. If a hospitalist doesn’t take on any new referrals on the day before starting a series of days off, there will be fewer patients to hand over to the doctor who takes over the next day. If every member of the practice is exempted from taking on new patients on the day before rotating off, then fewer patients will have a new hospitalist, which means continuity is better. Another way to think of this is that new referrals are “frontloaded” into the earlier days a hospitalist works in each series, and no new patients are assigned on the last day—or maybe more—of a hospitalist’s consecutive days of work.

In my experience, most groups try to distribute patients equally to each doctor each day. This means that a doctor who will be off starting tomorrow takes the standard portion of new referrals to the practice today. The fact that all of those patients will be turned over to a new hospitalist tomorrow, however, adversely affects continuity.

Note that exempting a group member from taking on new patients on the last day of a rotation means that the doctors can’t all rotate on and off on the same day. For example, if a group has four doctors working each day, and all rotate off on the same day—a common practice—then of course it is impossible to exempt all the doctors from new referrals on the day before going off. Instead, it will work best if only one doctor rotates on or off at a time. That leaves all the other doctors available to accept new referrals, while exempting the one about to rotate off.

You can see how adjusting the number of consecutive days worked affects continuity by using this formula:

Continuity = [days — (LOS — 1)]/days x 100

Continuity = the percent of patients who have the same hospitalist for every day of their stay

Days = number of consecutive days worked by an individual hospitalist

LOS = length of stay (best to use median LOS, but mean LOS still allows a reasonable estimate)

Note: The continuity that is derived using this formula can be improved if doctors in the practice are exempted from accepting new referrals on the day before rotating off.

This approach has benefits that go beyond improving continuity. It means a hospitalist’s workload the day before rotating off will be lighter than on other days. This provides extra time to “tee the patient up” for the next hospitalist—maybe write a more detailed note or dictate a discharge summary in anticipation of the patient leaving the next day—and/or it means a shorter day of work, assuming the doctors can leave the hospital when their work is done and aren’t required to stay around until the end of a pre-defined shift. This shorter day can mean an opportunity to do things like scheduling a flight to vacation late on the last day of work rather than the next morning, which might mean an extra day out of town.

And if a doctor isn’t assigned any new patients on the day prior to rotating off, there will be fewer patients to get to know for the doctor coming in the next day. The first day back on service will be less stressful and, arguably, more efficient.

A principle benefit of having all hospitalists switch on the same day is that the system quickly becomes transparent to the hospital staff. They learn that every Monday—or whatever day is decided upon—all of the hospitalists are getting to know patients for the first time and will probably round much more slowly. Many important processes, such as discharges, may be delayed until later in the day. If only one hospitalist switches at a time, hospital staff will have a hard time keeping up. Any inefficiencies caused by the switch will be spread over many days, however, and this may make it easier to handle. And if patients are teed up better for the new hospitalist and there are fewer patients on the list, the inefficiency that is caused by a new doctor getting to know the patients can be offset by the smaller number of patients. That means, for example, that discharges are much less likely to be delayed because of the smaller patient load on the doctor’s first day on service.

 

 

Up to this point I’ve been discussing continuity during a single admission. What about continuity from one admission to the next? Nearly all groups assign patients based on when they are admitted, and the hospitalist who cared for the patient during a prior admission may have little influence on which hospitalist admits them this time. If a patient is readmitted within a week or two, and the previous attending hospitalist is working, some groups will try to pair them once again through a bounce-back system.

It’s worth thinking about whether your group could make an effort to always have the same hospitalist care for a patient unless that physician is off—even if the admissions are months apart. This system would mean that on first admission to the practice a patient would be assigned to the hospitalist who is up next. In this way, each hospitalist in the group would develop his or her own panel of patients. This would be particularly valuable for patients who are admitted frequently; however, it would be difficult for a doctor to control how labor-intensive his patient panel might become. One person might have the bad luck to collect far more medically and socially complex patients than others in the group, and workloads might become unbalanced, making the whole group less efficient. I’m hopeful that a group will come up with a way to overcome these problems and create a workable system of good continuity from one admission to the next, but, as far as I’m aware, no group is doing this now. If you have a workable system, please let me know.

One group I worked with years ago addressed continuity from one admission to the next by using a system that matched each hospitalist with a panel of referring doctors. For example, the same hospitalist would always admit the patients “belonging to” a cadre of primary care physicians (PCPs), and another hospitalist in the group would always admit patients from another set of PCPs. The patient would see the same hospitalist each admission, and the hospitalist could develop a close working relationship with the panel of PCPs. The hospitalist and the PCP became familiar with each other’s practice styles, schedules, and days off, and memorized one another’s phone and fax numbers, the names of office and support staff, and so on, making for a very smooth working relationship that could benefit patient care. If the assigned hospitalist was off when a particular PCP’s patient needed admission, then a partner would provide interim care and turn the patient over when that hospitalist returned.

As you can imagine, this can be a difficult system to implement because there are many days on which a patient might be hospitalized when the assigned hospitalist is not around. Additionally, it is nearly impossible to divide PCPs and their patients equitably so that each hospitalist has a reasonable workload and patient complexity. I can imagine this group meeting periodically to match hospitalists and PCPs in a fashion similar to a fantasy football draft: “I’ll take PCP Smith and Williams from you, if you take PCP Wilson off my hands.”

I’m interested in hearing any additional ideas groups have developed to facilitate good continuity. The number of consecutive days worked by each hospitalist and the way new patients are assigned are significant ways to influence continuity, but there may be others that we should all keep in mind. And remember, maximizing continuity is not only good for patients; it enables the hospitalist practice to function more efficiently because it minimizes the number of new patients each hospitalist will have to get to know. TH

 

 

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

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Hospitalist-patient continuity is primarily a function of the number of consecutive days worked by a hospitalist, but the way new referrals are distributed can also affect continuity. This month, I will discuss both.

For my first few years as a hospitalist in the late 1980s and early 1990s, my one partner and I generally worked a schedule of 21 days on and seven days off. While I wouldn’t recommend that anyone try that today, it wasn’t as bad as you might think, because our patient volumes weren’t terribly high and, on about a third of the worked days, I was done shortly after lunch.

While working that schedule, I became aware of its benefit to hospitalist-patient continuity. I can remember many patients with hospital stays of more than two weeks whom I saw every day myself. As you might imagine, my partner and I talked periodically about working fewer than 21 days at a stretch and handing a service over to one another more frequently. But we were concerned that this would make us inefficient because more of our worked days would involve getting to know a new list of patients. In effect, we’d work more hours without an increase in income or patient volume.

While still working the 21-day schedule, I came to know another practice and was stunned that these doctors had taken essentially the opposite approach to scheduling. They worked 24-hour shifts on site and never worked more than one shift at a time. (If your shifts are 24-hours long, you probably can’t or shouldn’t work more than one at a time.) This schedule meant that a patient would see a different hospitalist each day. I couldn’t believe that either the patients or the hospitalists would think this was a reasonable thing to do, but the doctors were convinced it worked well. Later I learned that this group had been started by an emergency medicine practice, and it seems they had made the mistake of inserting an emergency department (ED) physician schedule into a hospitalist practice—and 24-hour shifts for ED doctors were more common then than now.

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an impact.

So, early in my career, the first two schedules I became acquainted with sat on opposite ends of a continuum that has since been filled in by many other options. Both the practice I was part of and the 24-hour-shift practice abandoned their original schedules within a few years and moved on to other alternatives. In fact, I have since worked nearly every schedule you can imagine, including the seven-on/seven-off schedule, which I think is a suboptimal choice for most groups. (See August 2006 “Career Management,” p. 9.) With each variation in my work schedule, I’ve thought a lot about its effect on continuity.

While there isn’t a great deal of research to prove it, improved continuity is probably associated with improvements in things like:

  • Quality care and safety;
  • Patient satisfaction (and probably hospitalist satisfaction also);
  • Hospital resource utilization; and
  • Hospitalist efficiency.

When hospitalists design a schedule, I recommend that the doctors think first about what will allow them a sustainable lifestyle while ensuring the necessary coverage—for some practices, this means keeping a doctor in the hospital around the clock. Ideally, they will come up with several options that satisfy these two metrics. In many cases, the option that results in the best continuity is the one they should choose.

 

 

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an effect. If a hospitalist doesn’t take on any new referrals on the day before starting a series of days off, there will be fewer patients to hand over to the doctor who takes over the next day. If every member of the practice is exempted from taking on new patients on the day before rotating off, then fewer patients will have a new hospitalist, which means continuity is better. Another way to think of this is that new referrals are “frontloaded” into the earlier days a hospitalist works in each series, and no new patients are assigned on the last day—or maybe more—of a hospitalist’s consecutive days of work.

In my experience, most groups try to distribute patients equally to each doctor each day. This means that a doctor who will be off starting tomorrow takes the standard portion of new referrals to the practice today. The fact that all of those patients will be turned over to a new hospitalist tomorrow, however, adversely affects continuity.

Note that exempting a group member from taking on new patients on the last day of a rotation means that the doctors can’t all rotate on and off on the same day. For example, if a group has four doctors working each day, and all rotate off on the same day—a common practice—then of course it is impossible to exempt all the doctors from new referrals on the day before going off. Instead, it will work best if only one doctor rotates on or off at a time. That leaves all the other doctors available to accept new referrals, while exempting the one about to rotate off.

You can see how adjusting the number of consecutive days worked affects continuity by using this formula:

Continuity = [days — (LOS — 1)]/days x 100

Continuity = the percent of patients who have the same hospitalist for every day of their stay

Days = number of consecutive days worked by an individual hospitalist

LOS = length of stay (best to use median LOS, but mean LOS still allows a reasonable estimate)

Note: The continuity that is derived using this formula can be improved if doctors in the practice are exempted from accepting new referrals on the day before rotating off.

This approach has benefits that go beyond improving continuity. It means a hospitalist’s workload the day before rotating off will be lighter than on other days. This provides extra time to “tee the patient up” for the next hospitalist—maybe write a more detailed note or dictate a discharge summary in anticipation of the patient leaving the next day—and/or it means a shorter day of work, assuming the doctors can leave the hospital when their work is done and aren’t required to stay around until the end of a pre-defined shift. This shorter day can mean an opportunity to do things like scheduling a flight to vacation late on the last day of work rather than the next morning, which might mean an extra day out of town.

And if a doctor isn’t assigned any new patients on the day prior to rotating off, there will be fewer patients to get to know for the doctor coming in the next day. The first day back on service will be less stressful and, arguably, more efficient.

A principle benefit of having all hospitalists switch on the same day is that the system quickly becomes transparent to the hospital staff. They learn that every Monday—or whatever day is decided upon—all of the hospitalists are getting to know patients for the first time and will probably round much more slowly. Many important processes, such as discharges, may be delayed until later in the day. If only one hospitalist switches at a time, hospital staff will have a hard time keeping up. Any inefficiencies caused by the switch will be spread over many days, however, and this may make it easier to handle. And if patients are teed up better for the new hospitalist and there are fewer patients on the list, the inefficiency that is caused by a new doctor getting to know the patients can be offset by the smaller number of patients. That means, for example, that discharges are much less likely to be delayed because of the smaller patient load on the doctor’s first day on service.

 

 

Up to this point I’ve been discussing continuity during a single admission. What about continuity from one admission to the next? Nearly all groups assign patients based on when they are admitted, and the hospitalist who cared for the patient during a prior admission may have little influence on which hospitalist admits them this time. If a patient is readmitted within a week or two, and the previous attending hospitalist is working, some groups will try to pair them once again through a bounce-back system.

It’s worth thinking about whether your group could make an effort to always have the same hospitalist care for a patient unless that physician is off—even if the admissions are months apart. This system would mean that on first admission to the practice a patient would be assigned to the hospitalist who is up next. In this way, each hospitalist in the group would develop his or her own panel of patients. This would be particularly valuable for patients who are admitted frequently; however, it would be difficult for a doctor to control how labor-intensive his patient panel might become. One person might have the bad luck to collect far more medically and socially complex patients than others in the group, and workloads might become unbalanced, making the whole group less efficient. I’m hopeful that a group will come up with a way to overcome these problems and create a workable system of good continuity from one admission to the next, but, as far as I’m aware, no group is doing this now. If you have a workable system, please let me know.

One group I worked with years ago addressed continuity from one admission to the next by using a system that matched each hospitalist with a panel of referring doctors. For example, the same hospitalist would always admit the patients “belonging to” a cadre of primary care physicians (PCPs), and another hospitalist in the group would always admit patients from another set of PCPs. The patient would see the same hospitalist each admission, and the hospitalist could develop a close working relationship with the panel of PCPs. The hospitalist and the PCP became familiar with each other’s practice styles, schedules, and days off, and memorized one another’s phone and fax numbers, the names of office and support staff, and so on, making for a very smooth working relationship that could benefit patient care. If the assigned hospitalist was off when a particular PCP’s patient needed admission, then a partner would provide interim care and turn the patient over when that hospitalist returned.

As you can imagine, this can be a difficult system to implement because there are many days on which a patient might be hospitalized when the assigned hospitalist is not around. Additionally, it is nearly impossible to divide PCPs and their patients equitably so that each hospitalist has a reasonable workload and patient complexity. I can imagine this group meeting periodically to match hospitalists and PCPs in a fashion similar to a fantasy football draft: “I’ll take PCP Smith and Williams from you, if you take PCP Wilson off my hands.”

I’m interested in hearing any additional ideas groups have developed to facilitate good continuity. The number of consecutive days worked by each hospitalist and the way new patients are assigned are significant ways to influence continuity, but there may be others that we should all keep in mind. And remember, maximizing continuity is not only good for patients; it enables the hospitalist practice to function more efficiently because it minimizes the number of new patients each hospitalist will have to get to know. TH

 

 

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

Hospitalist-patient continuity is primarily a function of the number of consecutive days worked by a hospitalist, but the way new referrals are distributed can also affect continuity. This month, I will discuss both.

For my first few years as a hospitalist in the late 1980s and early 1990s, my one partner and I generally worked a schedule of 21 days on and seven days off. While I wouldn’t recommend that anyone try that today, it wasn’t as bad as you might think, because our patient volumes weren’t terribly high and, on about a third of the worked days, I was done shortly after lunch.

While working that schedule, I became aware of its benefit to hospitalist-patient continuity. I can remember many patients with hospital stays of more than two weeks whom I saw every day myself. As you might imagine, my partner and I talked periodically about working fewer than 21 days at a stretch and handing a service over to one another more frequently. But we were concerned that this would make us inefficient because more of our worked days would involve getting to know a new list of patients. In effect, we’d work more hours without an increase in income or patient volume.

While still working the 21-day schedule, I came to know another practice and was stunned that these doctors had taken essentially the opposite approach to scheduling. They worked 24-hour shifts on site and never worked more than one shift at a time. (If your shifts are 24-hours long, you probably can’t or shouldn’t work more than one at a time.) This schedule meant that a patient would see a different hospitalist each day. I couldn’t believe that either the patients or the hospitalists would think this was a reasonable thing to do, but the doctors were convinced it worked well. Later I learned that this group had been started by an emergency medicine practice, and it seems they had made the mistake of inserting an emergency department (ED) physician schedule into a hospitalist practice—and 24-hour shifts for ED doctors were more common then than now.

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an impact.

So, early in my career, the first two schedules I became acquainted with sat on opposite ends of a continuum that has since been filled in by many other options. Both the practice I was part of and the 24-hour-shift practice abandoned their original schedules within a few years and moved on to other alternatives. In fact, I have since worked nearly every schedule you can imagine, including the seven-on/seven-off schedule, which I think is a suboptimal choice for most groups. (See August 2006 “Career Management,” p. 9.) With each variation in my work schedule, I’ve thought a lot about its effect on continuity.

While there isn’t a great deal of research to prove it, improved continuity is probably associated with improvements in things like:

  • Quality care and safety;
  • Patient satisfaction (and probably hospitalist satisfaction also);
  • Hospital resource utilization; and
  • Hospitalist efficiency.

When hospitalists design a schedule, I recommend that the doctors think first about what will allow them a sustainable lifestyle while ensuring the necessary coverage—for some practices, this means keeping a doctor in the hospital around the clock. Ideally, they will come up with several options that satisfy these two metrics. In many cases, the option that results in the best continuity is the one they should choose.

 

 

While the number of consecutive days of work is the most important variable in determining continuity, the way a group distributes new referrals can also have an effect. If a hospitalist doesn’t take on any new referrals on the day before starting a series of days off, there will be fewer patients to hand over to the doctor who takes over the next day. If every member of the practice is exempted from taking on new patients on the day before rotating off, then fewer patients will have a new hospitalist, which means continuity is better. Another way to think of this is that new referrals are “frontloaded” into the earlier days a hospitalist works in each series, and no new patients are assigned on the last day—or maybe more—of a hospitalist’s consecutive days of work.

In my experience, most groups try to distribute patients equally to each doctor each day. This means that a doctor who will be off starting tomorrow takes the standard portion of new referrals to the practice today. The fact that all of those patients will be turned over to a new hospitalist tomorrow, however, adversely affects continuity.

Note that exempting a group member from taking on new patients on the last day of a rotation means that the doctors can’t all rotate on and off on the same day. For example, if a group has four doctors working each day, and all rotate off on the same day—a common practice—then of course it is impossible to exempt all the doctors from new referrals on the day before going off. Instead, it will work best if only one doctor rotates on or off at a time. That leaves all the other doctors available to accept new referrals, while exempting the one about to rotate off.

You can see how adjusting the number of consecutive days worked affects continuity by using this formula:

Continuity = [days — (LOS — 1)]/days x 100

Continuity = the percent of patients who have the same hospitalist for every day of their stay

Days = number of consecutive days worked by an individual hospitalist

LOS = length of stay (best to use median LOS, but mean LOS still allows a reasonable estimate)

Note: The continuity that is derived using this formula can be improved if doctors in the practice are exempted from accepting new referrals on the day before rotating off.

This approach has benefits that go beyond improving continuity. It means a hospitalist’s workload the day before rotating off will be lighter than on other days. This provides extra time to “tee the patient up” for the next hospitalist—maybe write a more detailed note or dictate a discharge summary in anticipation of the patient leaving the next day—and/or it means a shorter day of work, assuming the doctors can leave the hospital when their work is done and aren’t required to stay around until the end of a pre-defined shift. This shorter day can mean an opportunity to do things like scheduling a flight to vacation late on the last day of work rather than the next morning, which might mean an extra day out of town.

And if a doctor isn’t assigned any new patients on the day prior to rotating off, there will be fewer patients to get to know for the doctor coming in the next day. The first day back on service will be less stressful and, arguably, more efficient.

A principle benefit of having all hospitalists switch on the same day is that the system quickly becomes transparent to the hospital staff. They learn that every Monday—or whatever day is decided upon—all of the hospitalists are getting to know patients for the first time and will probably round much more slowly. Many important processes, such as discharges, may be delayed until later in the day. If only one hospitalist switches at a time, hospital staff will have a hard time keeping up. Any inefficiencies caused by the switch will be spread over many days, however, and this may make it easier to handle. And if patients are teed up better for the new hospitalist and there are fewer patients on the list, the inefficiency that is caused by a new doctor getting to know the patients can be offset by the smaller number of patients. That means, for example, that discharges are much less likely to be delayed because of the smaller patient load on the doctor’s first day on service.

 

 

Up to this point I’ve been discussing continuity during a single admission. What about continuity from one admission to the next? Nearly all groups assign patients based on when they are admitted, and the hospitalist who cared for the patient during a prior admission may have little influence on which hospitalist admits them this time. If a patient is readmitted within a week or two, and the previous attending hospitalist is working, some groups will try to pair them once again through a bounce-back system.

It’s worth thinking about whether your group could make an effort to always have the same hospitalist care for a patient unless that physician is off—even if the admissions are months apart. This system would mean that on first admission to the practice a patient would be assigned to the hospitalist who is up next. In this way, each hospitalist in the group would develop his or her own panel of patients. This would be particularly valuable for patients who are admitted frequently; however, it would be difficult for a doctor to control how labor-intensive his patient panel might become. One person might have the bad luck to collect far more medically and socially complex patients than others in the group, and workloads might become unbalanced, making the whole group less efficient. I’m hopeful that a group will come up with a way to overcome these problems and create a workable system of good continuity from one admission to the next, but, as far as I’m aware, no group is doing this now. If you have a workable system, please let me know.

One group I worked with years ago addressed continuity from one admission to the next by using a system that matched each hospitalist with a panel of referring doctors. For example, the same hospitalist would always admit the patients “belonging to” a cadre of primary care physicians (PCPs), and another hospitalist in the group would always admit patients from another set of PCPs. The patient would see the same hospitalist each admission, and the hospitalist could develop a close working relationship with the panel of PCPs. The hospitalist and the PCP became familiar with each other’s practice styles, schedules, and days off, and memorized one another’s phone and fax numbers, the names of office and support staff, and so on, making for a very smooth working relationship that could benefit patient care. If the assigned hospitalist was off when a particular PCP’s patient needed admission, then a partner would provide interim care and turn the patient over when that hospitalist returned.

As you can imagine, this can be a difficult system to implement because there are many days on which a patient might be hospitalized when the assigned hospitalist is not around. Additionally, it is nearly impossible to divide PCPs and their patients equitably so that each hospitalist has a reasonable workload and patient complexity. I can imagine this group meeting periodically to match hospitalists and PCPs in a fashion similar to a fantasy football draft: “I’ll take PCP Smith and Williams from you, if you take PCP Wilson off my hands.”

I’m interested in hearing any additional ideas groups have developed to facilitate good continuity. The number of consecutive days worked by each hospitalist and the way new patients are assigned are significant ways to influence continuity, but there may be others that we should all keep in mind. And remember, maximizing continuity is not only good for patients; it enables the hospitalist practice to function more efficiently because it minimizes the number of new patients each hospitalist will have to get to know. TH

 

 

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

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The Business of Hospitalists

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In March 2005, the Association of American Medical Colleges announced that America will face a shortage of between 85,000 and 200,000 physicians by 2020. The U.S. population is growing faster than the number of new physicians entering the workforce. How big the shortfall will be has been argued since last year, but most pundits expect there to be too few physicians—in total—to take care of the burgeoning population, especially the elderly.

If a shortage of physicians is to be anticipated, what effect might this have on hospitals and hospitalists?

Where Does the Number Come From?

The debate about the range of the projected shortfall of 85,000 to 200,000 physicians reflects several differing assumptions. All estimates are based on the ratio of physicians to the overall population. Different estimates are based on distinctive models for the necessary staffing of the medical enterprise. For example, prepaid medical groups that serve large populations of patients (e.g., Kaiser Permanente) have physician-per-capita ratios of up to 20% less than fee-for-service environments. A larger elderly population will likely demand more medical services per capita. So, the estimate of a shortfall depends on the model of medical care for 2020 anticipated to be predominant in 2020 and a calculation of usage rate per capita for services—again, especially among the elderly.

Work/life balance choices that recent medical school graduates make also add to the uncertainty of predictions concerning the relative size of the shortage in total and by specialty. Young men and women graduating today increasingly express a preference for reduced or more manageable hours of work per week, sometimes opting for shift work or other forms of more predictable workload. There is also an understanding that women physicians tend to work part-time in some stages of their career—especially when they are trying to balance the demands of starting and raising a young family. Many of their male spouses are making similar choices.

The Specialty Nature of the Shortfall

A relative shortfall in available physicians relates to the specialty choice of new residency graduates. From 1996 to 2002, for example, certain specialties experienced increases in the number of applicants to residency programs, such as anesthesiology, dermatology, and radiology; whereas, other specialties saw reduced demand for training slots, such as in family practice and general surgery. For example, U.S. medical school seniors filled 89% of the general surgery residency slots available in 1996, but only 75% of the available slots in 2002.

The relative number of physicians in certain geographies will also be affected by the attractiveness of that particular area of the country or practice location and style, such as rural versus urban or suburban.

Physicians’ retirement rates generate different estimates, too. Currently, 18% of physicians in the United States are older than 65—compared with 12.6% of the overall population. In certain states, the percentage of physicians older than 65 is substantially higher, in some cases more than 20%. Different analysts generate different expectations about how many physicians over age 65 will leave the workforce. The number of hours that doctors practice and their decisions about when they will retire, based on their personal financial circumstances, are quite varied. This makes calculations of the shortfall to be anticipated subject to a variety of interpretations

Substitution

There is a debate also over the question of substitution. If there are too few physicians in the United States, will a shortfall in supply be made up by increasing numbers of foreign medical graduates or by other non-physician practitioners?

New foreign medical graduates may make up perhaps as many as 6,000 positions nationally. This will not make up for the shortfall of between 3,000 and 10,000 per year of additional physicians who need to graduate and enter the workforce.

 

 

Substitution by non-physician practitioners will mitigate some of the effects of the shortfall. We can anticipate that the use of nurse practitioners, physician assistants, nurses, and health educators will increase in situations where they can substitute for lower intensity medical care—especially in primary care settings, outpatient environments, and as adjuncts to care delivered by proceduralists and surgeons of many types. This will make some difference in the overall expectation for reduced availability of physicians.

Given all of these inputs, all projections point to a shortage of physicians, but none of the analyses agree on the absolute size.

The Effects of the Shortage

In any event, the projected shortage will affect how hospitals support their various service lines and, thus, will impact on the work performed by hospitalists, intensivists, and other physicians who support that work in hospitals. Hospitals anticipate this effect at the intersection of the shortage with increasing demands for rapid throughput, thorough and safe care for patients, and accountability for clearly specified clinical outcomes. Hospitals are already worrying about how to staff neurosurgery, cardiology, and general surgery positions. Changes in how primary care is delivered will affect where patient referrals come from and hospitals’ relationship with their specialist physicians.

How Will a Shortage Affect Hospitalists?

Increasing demand for services: With fewer physicians choosing general or primary care practice, hospitalists will find increasing demand for their services as coverage for acute care. Fewer primary care physicians will be able to afford the luxury of inpatient practice and gravitate toward highly efficient outpatient office-based practice while referring acute care to their hospitalist colleagues and specialists to pick up the slack for specific procedures, hospital follow-up care and return on discharge.

Hospitalists will be responsible then for a larger population of inpatients, providing for comprehensive care management in coordinating the services for all the care needs of many different types of diagnoses.

Increasing span of influence: In addition, there will be increasing demand by procedure-oriented physicians for hospitalist coverage to improve their efficiency in providing acute specialty care. Some of this demand may spill into single-specialty outpatient and focused freestanding hospital environments. Hospitalists will be pulled to cover specialists, who find their efficiency and the volume of work required prohibits them from providing comprehensive inpatient care for complex patients. They will prefer to focus on procedural interventions. Orthopedic surgery, cardiac surgery, neurosurgery, and cardiology, in particular, are likely to be new clients for hospitalist services.

Increasing emphasis on multidisciplinary care: Given the demand for evidence-based outcomes, hospitalists will provide physician input into clinical care design for a greater variety of patients in an increasing span of clinical service lines. This will put a demand on hospitalists for skills related to teamwork, leadership, and management in group environments. It will also require hospitalists to become broadly knowledgeable about the skills and contributions of all other potential care providers.

The New Medical Staff

The looming physician shortage in the United States will significantly affect the demand for and the variety and scope of work that hospitalists perform. The number of medical specialties dependent on hospitalist services will broaden. And hospitals will turn to hospitalists as their primary medical staff partners, responsible for the majority of medical staff functions and responsibilities. TH

Mike Guthrie, MD, is executive in residence at the University of Colorado (Denver) School of Business, Program in Health Administration, and a faculty member of SHM’s Leadership Academy.

What about the Nurses?

Healthcare Workforce Data shows medical training not keeping pace with population growth

By Larry Beresford

California has more employed registered nurses—211,068—than any other state, but it has the fewest RNs per capita (588 per 100,000 population). That is one of the key findings in a new report, The United States Health Workforce Profile, released last November by the Center for Health Workforce Studies at the University of Albany, N.Y. The highest concentration of America’s 2.4 million RNs employed in nursing is in New Hampshire, with 1,283 per 100,000 people, followed by South Dakota, North Dakota, Massachusetts, and Maine. Arkansas employs the most licensed practical nurses per capita—461 per 100,000 people or 63 for every 100 employed RNs.

The survey also found that Massachusetts has the highest concentration of physicians—303 for every 100,000 people—followed by Maryland, Vermont, Rhode Island, Connecticut, and New York; Mississippi has the lowest. Vermont, Massachusetts, and Maine have the most primary care doctors per capita.

The workforce study used 2004 data from the U.S. Department of Labor’s Bureau of Labor Statistics, the Area Resource File of physician data produced by QRS, Inc., for the U.S. Health Resources and Services Administration, the Division of Nursing’s 2004 National Sample Survey of RNs, and other sources to capture state, regional, and national workforce trends for physicians, nurses, and about two dozen other categories of health providers.

The report tallied 8.5 million health professionals working in health service settings—including hospitals, nursing homes, home health agencies, offices, and clinics—and another 4.1 million working in non-healthcare settings such as schools and insurance offices. Add 4.4 million non-health professionals working in health service settings, and the U.S. health workforce exceeds 17 million—12% of the country’s civilian labor force.

The success of the healthcare system in the United States depends on having sufficient, qualified personnel to provide needed services, and this report offers an array of data to help planners and policymakers understand and address workforce trends, explains Jean Moore, director of the workforce center and one of the report’s authors.

“This report is the view from 30,000 feet,” she says. “It gives you a starting point for drilling down into issues of supply and demand.”

It will be up to state policymakers and health professional groups to interpret the results. “You should do employer demand surveys—who are they having the most trouble recruiting and retaining?” adds Moore.

Although the report does not break out individual medical specialties, focusing only on primary care as a whole the potential for future shortages of physicians in some categories and locales is an important concern. “Understanding physician supply and looking down the road to potential shortages suggests the need to think smart,” says Moore. “If you can’t find enough physicians, can you consider physician extenders? Looking at demographics as our population ages, I think the nature of healthcare will change—with a lot more focus on chronic disease management. But to what extent are we preparing future physicians for this role?”

John Nelson, MD, a hospitalist and consultant in Bellevue, Wash., and a columnist for The Hospitalist, agrees that the role of hospitalists is likely to evolve. “We’ve always said that hospitalists will have to adapt our scope of practice according to the changing demands of the systems we’re part of,” he says. “Workforce shortages in different categories will affect what we do.”

In some facilities, hospitalists would never admit neurosurgery patients, while in other places they do.

Hospital medicine could be considered the fastest growing medical field in history, adds Robert Wachter, MD, head of the hospital medicine service at the University of California-San Francisco. But even if hospital medicine remains a popular career choice for young physicians, overall shortages of primary care physicians could heighten competition with other care settings that need these doctors.

The physician workforce is aging, and medical training is not keeping up with the aging population, Dr. Wachter notes. Variations in geographic distribution are state by state but also occur in urban, suburban, and rural areas within a state. There is not enough organized manpower planning to ameliorate these inequities.

Other results of the workforce study:

  • The average age of working physicians is 50, while 18% are over 65;
  • Currently, 26% of physicians are female, but 49% of today’s medical school graduates are women;
  • Blacks and Hispanics/Latinos are substantially under-represented in both medicine and nursing;
  • Medical schools had 79,000 students enroll in 2004, up slightly from 73,000 in 1987, although most of this growth was in osteopathic medical schools. Graduation rates are not keeping up with population growth;
  • Advanced practice nurses were found in the highest concentration in Alaska, Washington, New Hampshire, and Delaware; and
  • The number of physician assistant degrees awarded grew 1,700% in the past decade to approximately 50,000, with the heaviest concentrations in the Northeast, Alaska, and South Dakota.

View a full copy of the 164-page report at: www.albany.edu/news/pdf_files/U.S._Health_Workforce_Profile_October2006_11-09.pdf.

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In March 2005, the Association of American Medical Colleges announced that America will face a shortage of between 85,000 and 200,000 physicians by 2020. The U.S. population is growing faster than the number of new physicians entering the workforce. How big the shortfall will be has been argued since last year, but most pundits expect there to be too few physicians—in total—to take care of the burgeoning population, especially the elderly.

If a shortage of physicians is to be anticipated, what effect might this have on hospitals and hospitalists?

Where Does the Number Come From?

The debate about the range of the projected shortfall of 85,000 to 200,000 physicians reflects several differing assumptions. All estimates are based on the ratio of physicians to the overall population. Different estimates are based on distinctive models for the necessary staffing of the medical enterprise. For example, prepaid medical groups that serve large populations of patients (e.g., Kaiser Permanente) have physician-per-capita ratios of up to 20% less than fee-for-service environments. A larger elderly population will likely demand more medical services per capita. So, the estimate of a shortfall depends on the model of medical care for 2020 anticipated to be predominant in 2020 and a calculation of usage rate per capita for services—again, especially among the elderly.

Work/life balance choices that recent medical school graduates make also add to the uncertainty of predictions concerning the relative size of the shortage in total and by specialty. Young men and women graduating today increasingly express a preference for reduced or more manageable hours of work per week, sometimes opting for shift work or other forms of more predictable workload. There is also an understanding that women physicians tend to work part-time in some stages of their career—especially when they are trying to balance the demands of starting and raising a young family. Many of their male spouses are making similar choices.

The Specialty Nature of the Shortfall

A relative shortfall in available physicians relates to the specialty choice of new residency graduates. From 1996 to 2002, for example, certain specialties experienced increases in the number of applicants to residency programs, such as anesthesiology, dermatology, and radiology; whereas, other specialties saw reduced demand for training slots, such as in family practice and general surgery. For example, U.S. medical school seniors filled 89% of the general surgery residency slots available in 1996, but only 75% of the available slots in 2002.

The relative number of physicians in certain geographies will also be affected by the attractiveness of that particular area of the country or practice location and style, such as rural versus urban or suburban.

Physicians’ retirement rates generate different estimates, too. Currently, 18% of physicians in the United States are older than 65—compared with 12.6% of the overall population. In certain states, the percentage of physicians older than 65 is substantially higher, in some cases more than 20%. Different analysts generate different expectations about how many physicians over age 65 will leave the workforce. The number of hours that doctors practice and their decisions about when they will retire, based on their personal financial circumstances, are quite varied. This makes calculations of the shortfall to be anticipated subject to a variety of interpretations

Substitution

There is a debate also over the question of substitution. If there are too few physicians in the United States, will a shortfall in supply be made up by increasing numbers of foreign medical graduates or by other non-physician practitioners?

New foreign medical graduates may make up perhaps as many as 6,000 positions nationally. This will not make up for the shortfall of between 3,000 and 10,000 per year of additional physicians who need to graduate and enter the workforce.

 

 

Substitution by non-physician practitioners will mitigate some of the effects of the shortfall. We can anticipate that the use of nurse practitioners, physician assistants, nurses, and health educators will increase in situations where they can substitute for lower intensity medical care—especially in primary care settings, outpatient environments, and as adjuncts to care delivered by proceduralists and surgeons of many types. This will make some difference in the overall expectation for reduced availability of physicians.

Given all of these inputs, all projections point to a shortage of physicians, but none of the analyses agree on the absolute size.

The Effects of the Shortage

In any event, the projected shortage will affect how hospitals support their various service lines and, thus, will impact on the work performed by hospitalists, intensivists, and other physicians who support that work in hospitals. Hospitals anticipate this effect at the intersection of the shortage with increasing demands for rapid throughput, thorough and safe care for patients, and accountability for clearly specified clinical outcomes. Hospitals are already worrying about how to staff neurosurgery, cardiology, and general surgery positions. Changes in how primary care is delivered will affect where patient referrals come from and hospitals’ relationship with their specialist physicians.

How Will a Shortage Affect Hospitalists?

Increasing demand for services: With fewer physicians choosing general or primary care practice, hospitalists will find increasing demand for their services as coverage for acute care. Fewer primary care physicians will be able to afford the luxury of inpatient practice and gravitate toward highly efficient outpatient office-based practice while referring acute care to their hospitalist colleagues and specialists to pick up the slack for specific procedures, hospital follow-up care and return on discharge.

Hospitalists will be responsible then for a larger population of inpatients, providing for comprehensive care management in coordinating the services for all the care needs of many different types of diagnoses.

Increasing span of influence: In addition, there will be increasing demand by procedure-oriented physicians for hospitalist coverage to improve their efficiency in providing acute specialty care. Some of this demand may spill into single-specialty outpatient and focused freestanding hospital environments. Hospitalists will be pulled to cover specialists, who find their efficiency and the volume of work required prohibits them from providing comprehensive inpatient care for complex patients. They will prefer to focus on procedural interventions. Orthopedic surgery, cardiac surgery, neurosurgery, and cardiology, in particular, are likely to be new clients for hospitalist services.

Increasing emphasis on multidisciplinary care: Given the demand for evidence-based outcomes, hospitalists will provide physician input into clinical care design for a greater variety of patients in an increasing span of clinical service lines. This will put a demand on hospitalists for skills related to teamwork, leadership, and management in group environments. It will also require hospitalists to become broadly knowledgeable about the skills and contributions of all other potential care providers.

The New Medical Staff

The looming physician shortage in the United States will significantly affect the demand for and the variety and scope of work that hospitalists perform. The number of medical specialties dependent on hospitalist services will broaden. And hospitals will turn to hospitalists as their primary medical staff partners, responsible for the majority of medical staff functions and responsibilities. TH

Mike Guthrie, MD, is executive in residence at the University of Colorado (Denver) School of Business, Program in Health Administration, and a faculty member of SHM’s Leadership Academy.

What about the Nurses?

Healthcare Workforce Data shows medical training not keeping pace with population growth

By Larry Beresford

California has more employed registered nurses—211,068—than any other state, but it has the fewest RNs per capita (588 per 100,000 population). That is one of the key findings in a new report, The United States Health Workforce Profile, released last November by the Center for Health Workforce Studies at the University of Albany, N.Y. The highest concentration of America’s 2.4 million RNs employed in nursing is in New Hampshire, with 1,283 per 100,000 people, followed by South Dakota, North Dakota, Massachusetts, and Maine. Arkansas employs the most licensed practical nurses per capita—461 per 100,000 people or 63 for every 100 employed RNs.

The survey also found that Massachusetts has the highest concentration of physicians—303 for every 100,000 people—followed by Maryland, Vermont, Rhode Island, Connecticut, and New York; Mississippi has the lowest. Vermont, Massachusetts, and Maine have the most primary care doctors per capita.

The workforce study used 2004 data from the U.S. Department of Labor’s Bureau of Labor Statistics, the Area Resource File of physician data produced by QRS, Inc., for the U.S. Health Resources and Services Administration, the Division of Nursing’s 2004 National Sample Survey of RNs, and other sources to capture state, regional, and national workforce trends for physicians, nurses, and about two dozen other categories of health providers.

The report tallied 8.5 million health professionals working in health service settings—including hospitals, nursing homes, home health agencies, offices, and clinics—and another 4.1 million working in non-healthcare settings such as schools and insurance offices. Add 4.4 million non-health professionals working in health service settings, and the U.S. health workforce exceeds 17 million—12% of the country’s civilian labor force.

The success of the healthcare system in the United States depends on having sufficient, qualified personnel to provide needed services, and this report offers an array of data to help planners and policymakers understand and address workforce trends, explains Jean Moore, director of the workforce center and one of the report’s authors.

“This report is the view from 30,000 feet,” she says. “It gives you a starting point for drilling down into issues of supply and demand.”

It will be up to state policymakers and health professional groups to interpret the results. “You should do employer demand surveys—who are they having the most trouble recruiting and retaining?” adds Moore.

Although the report does not break out individual medical specialties, focusing only on primary care as a whole the potential for future shortages of physicians in some categories and locales is an important concern. “Understanding physician supply and looking down the road to potential shortages suggests the need to think smart,” says Moore. “If you can’t find enough physicians, can you consider physician extenders? Looking at demographics as our population ages, I think the nature of healthcare will change—with a lot more focus on chronic disease management. But to what extent are we preparing future physicians for this role?”

John Nelson, MD, a hospitalist and consultant in Bellevue, Wash., and a columnist for The Hospitalist, agrees that the role of hospitalists is likely to evolve. “We’ve always said that hospitalists will have to adapt our scope of practice according to the changing demands of the systems we’re part of,” he says. “Workforce shortages in different categories will affect what we do.”

In some facilities, hospitalists would never admit neurosurgery patients, while in other places they do.

Hospital medicine could be considered the fastest growing medical field in history, adds Robert Wachter, MD, head of the hospital medicine service at the University of California-San Francisco. But even if hospital medicine remains a popular career choice for young physicians, overall shortages of primary care physicians could heighten competition with other care settings that need these doctors.

The physician workforce is aging, and medical training is not keeping up with the aging population, Dr. Wachter notes. Variations in geographic distribution are state by state but also occur in urban, suburban, and rural areas within a state. There is not enough organized manpower planning to ameliorate these inequities.

Other results of the workforce study:

  • The average age of working physicians is 50, while 18% are over 65;
  • Currently, 26% of physicians are female, but 49% of today’s medical school graduates are women;
  • Blacks and Hispanics/Latinos are substantially under-represented in both medicine and nursing;
  • Medical schools had 79,000 students enroll in 2004, up slightly from 73,000 in 1987, although most of this growth was in osteopathic medical schools. Graduation rates are not keeping up with population growth;
  • Advanced practice nurses were found in the highest concentration in Alaska, Washington, New Hampshire, and Delaware; and
  • The number of physician assistant degrees awarded grew 1,700% in the past decade to approximately 50,000, with the heaviest concentrations in the Northeast, Alaska, and South Dakota.

View a full copy of the 164-page report at: www.albany.edu/news/pdf_files/U.S._Health_Workforce_Profile_October2006_11-09.pdf.

In March 2005, the Association of American Medical Colleges announced that America will face a shortage of between 85,000 and 200,000 physicians by 2020. The U.S. population is growing faster than the number of new physicians entering the workforce. How big the shortfall will be has been argued since last year, but most pundits expect there to be too few physicians—in total—to take care of the burgeoning population, especially the elderly.

If a shortage of physicians is to be anticipated, what effect might this have on hospitals and hospitalists?

Where Does the Number Come From?

The debate about the range of the projected shortfall of 85,000 to 200,000 physicians reflects several differing assumptions. All estimates are based on the ratio of physicians to the overall population. Different estimates are based on distinctive models for the necessary staffing of the medical enterprise. For example, prepaid medical groups that serve large populations of patients (e.g., Kaiser Permanente) have physician-per-capita ratios of up to 20% less than fee-for-service environments. A larger elderly population will likely demand more medical services per capita. So, the estimate of a shortfall depends on the model of medical care for 2020 anticipated to be predominant in 2020 and a calculation of usage rate per capita for services—again, especially among the elderly.

Work/life balance choices that recent medical school graduates make also add to the uncertainty of predictions concerning the relative size of the shortage in total and by specialty. Young men and women graduating today increasingly express a preference for reduced or more manageable hours of work per week, sometimes opting for shift work or other forms of more predictable workload. There is also an understanding that women physicians tend to work part-time in some stages of their career—especially when they are trying to balance the demands of starting and raising a young family. Many of their male spouses are making similar choices.

The Specialty Nature of the Shortfall

A relative shortfall in available physicians relates to the specialty choice of new residency graduates. From 1996 to 2002, for example, certain specialties experienced increases in the number of applicants to residency programs, such as anesthesiology, dermatology, and radiology; whereas, other specialties saw reduced demand for training slots, such as in family practice and general surgery. For example, U.S. medical school seniors filled 89% of the general surgery residency slots available in 1996, but only 75% of the available slots in 2002.

The relative number of physicians in certain geographies will also be affected by the attractiveness of that particular area of the country or practice location and style, such as rural versus urban or suburban.

Physicians’ retirement rates generate different estimates, too. Currently, 18% of physicians in the United States are older than 65—compared with 12.6% of the overall population. In certain states, the percentage of physicians older than 65 is substantially higher, in some cases more than 20%. Different analysts generate different expectations about how many physicians over age 65 will leave the workforce. The number of hours that doctors practice and their decisions about when they will retire, based on their personal financial circumstances, are quite varied. This makes calculations of the shortfall to be anticipated subject to a variety of interpretations

Substitution

There is a debate also over the question of substitution. If there are too few physicians in the United States, will a shortfall in supply be made up by increasing numbers of foreign medical graduates or by other non-physician practitioners?

New foreign medical graduates may make up perhaps as many as 6,000 positions nationally. This will not make up for the shortfall of between 3,000 and 10,000 per year of additional physicians who need to graduate and enter the workforce.

 

 

Substitution by non-physician practitioners will mitigate some of the effects of the shortfall. We can anticipate that the use of nurse practitioners, physician assistants, nurses, and health educators will increase in situations where they can substitute for lower intensity medical care—especially in primary care settings, outpatient environments, and as adjuncts to care delivered by proceduralists and surgeons of many types. This will make some difference in the overall expectation for reduced availability of physicians.

Given all of these inputs, all projections point to a shortage of physicians, but none of the analyses agree on the absolute size.

The Effects of the Shortage

In any event, the projected shortage will affect how hospitals support their various service lines and, thus, will impact on the work performed by hospitalists, intensivists, and other physicians who support that work in hospitals. Hospitals anticipate this effect at the intersection of the shortage with increasing demands for rapid throughput, thorough and safe care for patients, and accountability for clearly specified clinical outcomes. Hospitals are already worrying about how to staff neurosurgery, cardiology, and general surgery positions. Changes in how primary care is delivered will affect where patient referrals come from and hospitals’ relationship with their specialist physicians.

How Will a Shortage Affect Hospitalists?

Increasing demand for services: With fewer physicians choosing general or primary care practice, hospitalists will find increasing demand for their services as coverage for acute care. Fewer primary care physicians will be able to afford the luxury of inpatient practice and gravitate toward highly efficient outpatient office-based practice while referring acute care to their hospitalist colleagues and specialists to pick up the slack for specific procedures, hospital follow-up care and return on discharge.

Hospitalists will be responsible then for a larger population of inpatients, providing for comprehensive care management in coordinating the services for all the care needs of many different types of diagnoses.

Increasing span of influence: In addition, there will be increasing demand by procedure-oriented physicians for hospitalist coverage to improve their efficiency in providing acute specialty care. Some of this demand may spill into single-specialty outpatient and focused freestanding hospital environments. Hospitalists will be pulled to cover specialists, who find their efficiency and the volume of work required prohibits them from providing comprehensive inpatient care for complex patients. They will prefer to focus on procedural interventions. Orthopedic surgery, cardiac surgery, neurosurgery, and cardiology, in particular, are likely to be new clients for hospitalist services.

Increasing emphasis on multidisciplinary care: Given the demand for evidence-based outcomes, hospitalists will provide physician input into clinical care design for a greater variety of patients in an increasing span of clinical service lines. This will put a demand on hospitalists for skills related to teamwork, leadership, and management in group environments. It will also require hospitalists to become broadly knowledgeable about the skills and contributions of all other potential care providers.

The New Medical Staff

The looming physician shortage in the United States will significantly affect the demand for and the variety and scope of work that hospitalists perform. The number of medical specialties dependent on hospitalist services will broaden. And hospitals will turn to hospitalists as their primary medical staff partners, responsible for the majority of medical staff functions and responsibilities. TH

Mike Guthrie, MD, is executive in residence at the University of Colorado (Denver) School of Business, Program in Health Administration, and a faculty member of SHM’s Leadership Academy.

What about the Nurses?

Healthcare Workforce Data shows medical training not keeping pace with population growth

By Larry Beresford

California has more employed registered nurses—211,068—than any other state, but it has the fewest RNs per capita (588 per 100,000 population). That is one of the key findings in a new report, The United States Health Workforce Profile, released last November by the Center for Health Workforce Studies at the University of Albany, N.Y. The highest concentration of America’s 2.4 million RNs employed in nursing is in New Hampshire, with 1,283 per 100,000 people, followed by South Dakota, North Dakota, Massachusetts, and Maine. Arkansas employs the most licensed practical nurses per capita—461 per 100,000 people or 63 for every 100 employed RNs.

The survey also found that Massachusetts has the highest concentration of physicians—303 for every 100,000 people—followed by Maryland, Vermont, Rhode Island, Connecticut, and New York; Mississippi has the lowest. Vermont, Massachusetts, and Maine have the most primary care doctors per capita.

The workforce study used 2004 data from the U.S. Department of Labor’s Bureau of Labor Statistics, the Area Resource File of physician data produced by QRS, Inc., for the U.S. Health Resources and Services Administration, the Division of Nursing’s 2004 National Sample Survey of RNs, and other sources to capture state, regional, and national workforce trends for physicians, nurses, and about two dozen other categories of health providers.

The report tallied 8.5 million health professionals working in health service settings—including hospitals, nursing homes, home health agencies, offices, and clinics—and another 4.1 million working in non-healthcare settings such as schools and insurance offices. Add 4.4 million non-health professionals working in health service settings, and the U.S. health workforce exceeds 17 million—12% of the country’s civilian labor force.

The success of the healthcare system in the United States depends on having sufficient, qualified personnel to provide needed services, and this report offers an array of data to help planners and policymakers understand and address workforce trends, explains Jean Moore, director of the workforce center and one of the report’s authors.

“This report is the view from 30,000 feet,” she says. “It gives you a starting point for drilling down into issues of supply and demand.”

It will be up to state policymakers and health professional groups to interpret the results. “You should do employer demand surveys—who are they having the most trouble recruiting and retaining?” adds Moore.

Although the report does not break out individual medical specialties, focusing only on primary care as a whole the potential for future shortages of physicians in some categories and locales is an important concern. “Understanding physician supply and looking down the road to potential shortages suggests the need to think smart,” says Moore. “If you can’t find enough physicians, can you consider physician extenders? Looking at demographics as our population ages, I think the nature of healthcare will change—with a lot more focus on chronic disease management. But to what extent are we preparing future physicians for this role?”

John Nelson, MD, a hospitalist and consultant in Bellevue, Wash., and a columnist for The Hospitalist, agrees that the role of hospitalists is likely to evolve. “We’ve always said that hospitalists will have to adapt our scope of practice according to the changing demands of the systems we’re part of,” he says. “Workforce shortages in different categories will affect what we do.”

In some facilities, hospitalists would never admit neurosurgery patients, while in other places they do.

Hospital medicine could be considered the fastest growing medical field in history, adds Robert Wachter, MD, head of the hospital medicine service at the University of California-San Francisco. But even if hospital medicine remains a popular career choice for young physicians, overall shortages of primary care physicians could heighten competition with other care settings that need these doctors.

The physician workforce is aging, and medical training is not keeping up with the aging population, Dr. Wachter notes. Variations in geographic distribution are state by state but also occur in urban, suburban, and rural areas within a state. There is not enough organized manpower planning to ameliorate these inequities.

Other results of the workforce study:

  • The average age of working physicians is 50, while 18% are over 65;
  • Currently, 26% of physicians are female, but 49% of today’s medical school graduates are women;
  • Blacks and Hispanics/Latinos are substantially under-represented in both medicine and nursing;
  • Medical schools had 79,000 students enroll in 2004, up slightly from 73,000 in 1987, although most of this growth was in osteopathic medical schools. Graduation rates are not keeping up with population growth;
  • Advanced practice nurses were found in the highest concentration in Alaska, Washington, New Hampshire, and Delaware; and
  • The number of physician assistant degrees awarded grew 1,700% in the past decade to approximately 50,000, with the heaviest concentrations in the Northeast, Alaska, and South Dakota.

View a full copy of the 164-page report at: www.albany.edu/news/pdf_files/U.S._Health_Workforce_Profile_October2006_11-09.pdf.

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Hospital Quality for AMI: Process Measures and Their Relationship with Short-term Mortality

Bradley EH, Herrin J, Elbel B, et al. Hospital quality for acute myocardial infarction: correlation among process measures and relationship with short-term mortality. JAMA. 2006 Jul 5;296(1):72-78.

Background

The Centers for Medicare and Medicaid Services (CMS) and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) monitor and publicly report hospital performance in the treatment of acute myocardial infarction (AMI). Core process measures are considered an indicator of quality of care, but little is known about how these measures affect outcomes (mortality). Five of the seven core measures for AMI assess medication prescription practices; the other two measures are counseling on smoking cessation and timely reperfusion therapy.

Inferences about a hospital’s quality of care for AMI are created by measuring the hospital’s success at performing these measures. No previous study had evaluated a possible correlation between performance on these measures and short-term mortality. The authors of this study used National Registry of Myocardial Infarction (NRMI) and CMS databases to determine the association between hospital performance on AMI process measures and hospital-specific, risk-standardized, 30-day mortality rates.

There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Methods

A cross-sectional study was performed using hospitals that reported AMI discharges to the NRMI from January 2002 through March 2003. Hospitals had to report a minimum of 10 eligible patients. Hospital performance on core measures was recorded: beta-blocker on admission, beta-blocker on dismissal, aspirin on admission, aspirin on dismissal, angiotensin-converting enzyme inhibitor (ACE) prescription on dismissal, smoking cessation counseling for smokers during admission, and time to reperfusion therapy. Risk-standardized, 30-day, all-cause mortality rates were calculated for each hospital using CMS Medicare claims for patients ages 66 and older with AMI. The primary analysis determined the association of hospital-specific, risk-standardized, 30-day mortality rates with hospital performance on the core process measures.

Results

The most successfully completed core process measure for AMI was aspirin on admission. A mean of 86.4% of participating hospitals completed this measure. The core process measure for AMI that was the least frequently documented was smoking cessation counseling; a mean of 13.9% of participating hospitals completed this measure. Notably, timely reperfusion therapy for AMI—fibrinolytic therapy within 30 minutes of arrival or percutaneous intervention within 120 minutes of arrival—was completed by only 54.5% (mean) of participating hospitals.

Each core process measure had a statistically significant but small correlation with the risk-standardized, 30-day mortality rate (explaining between 0.1% and 3.3% of variance in mortality). Of the 180 hospitals in the top quintile of risk-standardized, 30-day mortality rates, only 31% were in the top quintile of the core process measures. A composite model of all seven core process measures determined that these measures could only explain 6% of the hospital-level variation in risk-standardized, 30-day mortality rates. Secondary analyses did not differ substantially.

Conclusions

In this study, each core process measure for AMI showed a modest correlation with 30-day mortality, but accounted for only 6% of 30-day mortality. This finding highlights the fact that continued measurement of these processes is valuable, but a hospital’s short-term mortality rates for AMI cannot be reliably inferred from performance on publicly reported process measures. These measures are weighted more toward long-term outcome measures. There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Clopidogrel and Aspirin versus Aspirin Alone for the Prevention of Atherothrombotic Events

 

 

Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006 Apr 20;354(16):1706-1717.

Background

Atherothrombotic disorders of the circulatory system are the leading cause of death and disability in the world. Low-dose aspirin has been shown to reduce ischemic event in populations above a certain risk threshold; however, aspirin alone may be insufficient treatment to prevent ischemic events in high-risk patients. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce ischemic events in patients with unstable angina, non-ST segment elevation and ST segment elevation myocardial infarction, as well as in those undergoing angioplasty and stenting.

The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group.

Methods

This was a prospective, multicenter, randomized, double-blind, placebo-controlled study of the efficacy and safety of aspirin plus clopidogrel in comparison with aspirin plus placebo in patients at high risk for a cardiovascular event. Patients included in the study were 45 or older and had one of the following: multiple atherothrombotic risk factors, documented coronary artery disease, documented cerebrovascular disease, or documented symptomatic peripheral vascular disease. The primary efficacy endpoint was the first occurrence of myocardial infarction (MI), stroke, or death from cardiovascular causes. The primary safety endpoint was severe bleeding.

Results

A total of 15,603 patients were enrolled in the study. Treatment was permanently discontinued by 20.4% in the clopidogrel group as compared with 18.2% in the placebo group (P<0.001). A total of 4.8% of patients in the clopidogrel group and 4.9% in the placebo group discontinued treatment because of an adverse event (P=0.67). Other than the treatment medications, concomitant medication use was similar in both groups. A median follow-up of 28 months revealed that the rates of primary efficacy events in the clopidogrel and placebo group were similar (6.8% versus 7.3%, P=0.22, respectively). The rate of primary safety events was 1.7% in the clopidogrel group and 1.3% in the placebo group, P=0.09.

Conclusions

This trial enrolled patients who either had established atherothrombotic disease or were at high risk for such disease and found that there was no significant benefit associated with the use of clopidogrel plus aspirin compared to aspirin alone in reducing myocardial infarction, stroke, or cardiovascular death. The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group. Overall, these findings do not support the use of dual antiplatelet therapy across this broad patient population.

D-Dimer in the Diagnosis of Pulmonary Embolism

Kearon C, Ginsberg JS, Douketis J, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med. 2006 Jun 6;144(11):812-821.

Background

The clinical usefulness of the D-dimer test in the diagnosis of pulmonary embolism (PE) has been previously studied. In patients with suspected PE, it may be safe to omit additional diagnostic testing if a patient has a negative D-dimer test; however, this approach has never been evaluated in a randomized, controlled trial.

The investigators in this trial studied two subgroups of patients with suspected PE and a negative D-dimer: patients with a low clinical probability of PE and those with a moderate or high clinical probability of PE who had a non-diagnostic ventilation perfusion scan (VQ scan) and no proximal deep vein thrombosis on venous ultrasonography. The hypothesis was that patients with a negative D-dimer who do not have further testing for PE won’t have a higher frequency of venous thromboembolism during follow-up than patients who undergo routine diagnostic testing.

 

 

Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up.

Methods

Before any diagnostic testing, patients were assigned a probability score, using the Wells Criteria, to categorize the probability of PE as low or moderate to high.

Patients with low probability Wells scores: D-dimer testing was done on all patients with a low clinical probability of PE. Patients with a negative D-dimer were randomly assigned either to no additional diagnostic testing and no anticoagulation treatment or to additional diagnostic testing with an initial VQ scan. If the VQ scan was negative, then PE was excluded. If the VQ scan showed one or more segmental perfusion defects that were normally ventilated, then the scan was considered diagnostic for PE. If there were perfusion defects that did not meet the criteria for a high probability scan, then the scan was considered non-diagnostic. Patients with non-diagnostic scans underwent ultrasonography of the proximal veins of the legs. If deep vein thrombosis was present, PE was diagnosed. If ultrasonography was normal, the test was repeated after seven and 14 days. In all patients with a positive D-dimer, a VQ scan was performed.

Patients with moderate to high probability Wells scores: A VQ scan was performed on all patients with a moderate to high probability for PE. Patients with high probability scans were treated; patients with normal scans were not treated. Patients with non-diagnostic scans and normal venous ultrasonography were randomly assigned to receive either no additional testing or serial ultrasonography.

Outcomes: All patients were followed for six months for the development of venous thromboembolism after initial diagnostic testing.

Results

The study enrolled 1,126 patients. Overall, 160 patients (14.2%) had PE diagnosed at initial presentation or by venous ultrasonography. Of 952 patients who did not receive an initial diagnosis of PE, 11 (1.2%) had PE diagnosed at follow-up.

Patients with low probability Wells scores: Low clinical probability was present in 670 patients (60%). In patients with low clinical probability of PE, 373 (56%) had negative D-dimer tests and 297 (44%) had positive D-dimer tests. Of the 373 patients with low probability and negative D-dimer results, 187 were randomized to no additional testing and 186 received a VQ scan. The frequency of venous thromboembolism at six-month follow-up was similar in these two groups (-0.5% [CI, -3.0% to 1.6%]). Three patients with negative D-dimer tests were diagnosed with PE by VQ scan. Results were fairly complete (five patients without a six-month follow-up in the no additional testing group and one without a follow-up in the VQ scan group).

Twenty-four patients with low clinical probability and positive D-dimer results (n=297) were diagnosed with PE. Three patients did not complete the six-month follow-up. Of the remaining 294 patients, five patients had venous thromboembolism at six months.

Patients with moderate to high probability Wells scores: There were 456 patients (40%) had moderate or high clinical probability for PE. Each of these patients had a VQ scan. Non-diagnostic VQ scans and normal venous ultrasonography were performed on 226 patients. Of these 226 patients, 86 had a negative D-dimer and 140 had a positive D-dimer. Of the 86 patients with negative VQ scans, normal venous ultrasonography, and a negative D-dimer, 83 were randomly assigned to no additional testing or serial venous ultrasonography (42 and 41 respectively). At six months follow-up, one patient assigned to no additional testing had venous thromboembolism, and no patients in the additional testing group had venous thromboembolism.

 

 

Conclusions

The results of this trial suggest that it is safe to withhold additional diagnostic testing in patients with suspected PE, low pretest clinical probability, and a negative D-dimer test. Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up. The assay used for this study was an erythrocyte agglutination SimpliRED assay. Reported sensitivity is approximately 90%, and specificity is approximately 75%. To the readers, it should be noted that the authors defined a low probability Wells score as 4 rather than 1.5 or lower.

Efficacy and Safety of Inhaled Insulin Therapy in Adults with Diabetes Mellitus

Ceglia L, Lau J, Pittas AG. Meta-analysis: efficacy and safety of inhaled insulin therapy in adults with diabetes mellitus. Ann Intern Med. 2006 Nov 7;145(9):665-675.

Background

Despite its effectiveness in attaining glycemic control, there is considerable resistance to insulin use by patients and healthcare providers, primarily because of the need for subcutaneous injection. In January 2006, the U.S. Food and Drug Administration (FDA) approved the first formulation of inhaled insulin for clinical use in nonsmoking adults with type 1 or type 2 diabetes and no pulmonary disease. The authors of this paper present a systematic review to examine the efficacy, safety, and patient acceptability of inhaled insulin.

All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin.

Methods

The authors conducted a search of MEDLINE to find English-language, randomized, controlled trials of inhaled insulin in nonpregnant adults with diabetes. To find unpublished studies, the authors reviewed the briefing document on Exubera powder for oral inhalation (Pfizer Inc., New York). An abstract was included if it reported original data from controlled trials in patients with type 1 or 2 diabetes and hemoglobin A1C outcomes for patients receiving inhaled insulin versus outcomes for a comparison group (subcutaneous insulin or oral hypoglycemics). Studies with less than 12 weeks duration were excluded because no comparison could be made regarding glycemic efficacy. For glycemic efficacy, the primary outcome was the treatment group difference in hemoglobin A1C from baseline. Secondary outcome was the proportion of patients with hemoglobin A1C levels less than 7%. To evaluate safety, the primary outcomes were severe hypoglycemia (glucose ≤36 mg/dL), cough, and treatment group difference in pulmonary function variables.

Results

Sixteen trials involving a total of 4,023 patients met inclusion criteria. Seven trials compared inhaled insulin with various subcutaneous insulin regimens in patients with type 1 diabetes. Nine trials compared inhaled insulin with subcutaneous insulin or oral hypoglycemic agents in patients with type 2 diabetes. Inhaled insulin was given with meals and titrated according to study-specific glucose goals. Subcutaneous insulin was titrated to the same specific goals. Doses of oral hypoglycemic agents were adjusted for glycemic targets in only two of the nine trials. The combined data from the studies demonstrated a small but statistically significant decrease in the levels of baseline hemoglobin A1C levels in favor of subcutaneous insulin (weighted mean difference 0.08%, [CI 0.03% to 0.14%]) in patients with type 1 or type 2 diabetes. The greatest advantage of subcutaneous insulin was noted in the study with the longest duration (104 weeks). There was no difference between the study groups in studies with duration of 24 weeks or less. Patients with type 1 or type 2 diabetes taking inhaled insulin were no more likely to achieve hemoglobin A1C levels less than 7% than those using subcutaneous insulin.

The combined data from studies comparing inhaled insulin to oral hypoglycemic agents in patients with type 2 diabetes showed that inhaled insulin lowered hemoglobin A1C levels more effectively (weighted mean difference -1.04%, [CI -1.59% to -0.49%]). In studies in which the oral hypoglycemic agents were titrated, inhaled insulin still lowered baseline hemoglobin A1C levels but to a lesser degree (weighted mean difference -0.20%, [CI - 0.34% to -0.07%]). Patients with type 2 diabetes taking inhaled insulin were more likely to achieve hemoglobin A1C levels less than 7% than those taking oral agents.

 

 

There was no difference in episodes of severe hypoglycemia in patients using inhaled insulin compared to those using subcutaneous insulin. A higher proportion of patients using inhaled insulin reported at least one episode of severe hypoglycemia compared to those using oral agents (risk ratio, 3.06 [CI 1.03 to 9.07]; 9.4% versus 3.5%, respectively).

With respect to pulmonary safety, all trials selected patients without histories of pulmonary problems and with at least six months of nonsmoking status. Pulmonary safety was assessed by self-reported symptoms and by pulmonary function tests. The most common pulmonary symptom associated with inhaled insulin was nonproductive cough. This symptom was reported more frequently compared to patients using subcutaneous insulin or oral agents (risk ratio, 3.52 [CI 2.23 to 5.56]; 16.9% versus 5.0%). Cough was noted early in the treatment course and diminished in frequency over time. Patients receiving inhaled insulin had a greater decrease in FEV1 (forced expiratory volume in the first second) from baseline than the comparator group (weighted mean difference, -0.031 L [CI-0.043 L to -0.020 L]). This decrease progressed slowly over the first six months but stabilized in studies of up to two years’ duration.

Only four trials reported data on overall patient satisfaction for inhaled insulin versus subcutaneous insulin. All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin. Patients randomly assigned to inhaled insulin were more likely to continue taking inhaled insulin than to switch back to subcutaneous insulin.

Conclusions

This meta-analysis showed that inhaled insulin is comparable to subcutaneous insulin in lowering hemoglobin A1C levels in patients with type 1 or type 2 diabetes. The proportion of patients reaching a target hemoglobin A1C of less than 7% was much lower in the studies in this meta-analysis as compared to levels in trials of intensive subcutaneous insulin therapy.

It’s more difficult to compare inhaled insulin with oral hypoglycemic agents because most studies involving oral agents used fixed dosing with different types of oral agents. There was a three-fold risk of severe hypoglycemia in patients using inhaled insulin compared to those using oral hypoglycemic agents. This is probably due to overall improved glycemic control in the inhaled insulin group. Cough was more common in the inhaled insulin groups, and there were small decreases in FEV1, but these did not progress over two years. The potential for pulmonary toxicity with long-term administration has not been evaluated and deserves further study.

Classic Literature

A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care

Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999 Feb 11;340(6):409-417.

Background

There are important risks and benefits of red cell transfusion in critically ill patients. One concern is that anemia may not be tolerated well in this group. Because red cell transfusions are used to augment the delivery of oxygen to avoid the harmful effects of oxygen debt, transfusing patients to keep their hemoglobin levels higher than 10.0 g per deciliter has become a routine practice. There is concern, however, that critically ill patients may be at increased risk of immunosuppressive and microcirculatory complications of red cell transfusions. Also, concern about the safety and supply of red cell transfusions has encouraged a more conservative approach to transfusion strategies.

The authors of this study conducted a randomized, controlled, clinical trial involving critically ill patients with euvolemia to determine whether a restrictive transfusion strategy that maintains hemoglobin concentrations between 7.0 and 9.0 g per deciliter was equivalent to a liberal strategy of maintaining hemoglobin concentrations between 10.0 and 12.0 g per deciliter.

Methods

Enrolled patients were admitted to 25 different intensive care units in Canada between 1994 and 1997. Included patients were expected to have an intensive care unit stay longer than 24 hours and a hemoglobin concentration of 9.0 g per deciliter or less within 72 hours after admission and were considered euvolemic after initial treatment by physicians. Critically ill patients with euvolemia were randomized to either the restrictive or the liberal strategy. Patients were given one unit at a time, and the hemoglobin concentration was measured after each unit transfused. Transfusion was stopped when the patient’s hemoglobin concentration was in the target range. The primary outcome was death from all causes within 30 days of randomization.

Results

A total of 838 patients were enrolled in the study; 418 in the restrictive group and 420 in the liberal group. The average daily hemoglobin concentrations were 8.5 g per deciliter in the restrictive group and 10.7 g per deciliter in the liberal group (P<0.01). An average of 2.6 red cell units per patient was transfused in the restrictive group, as compared to an average of 5.6 red cell units in the liberal group (P<0.01). Thirty-three percent of patients in the restrictive group did not receive any transfusion; every patient in the liberal group received at least one red cell unit.

The rate of death from all causes in the 30 days after admission was 18.7% in the restrictive group and 23.3% in the liberal group (-0.84% to 10.2%, P=0.11). The inpatient mortality rates were lower in the restrictive group (22.2% versus 28.1%, P=0.05). More patients in the liberal group had some type of cardiac complication (21.0% versus 13.2% respectively, P<0.01). Subgroup analyses demonstrated that patients with lower APACHE II scores (20 or less) and patients younger than 55 had improved survival in the restrictive strategy group. There were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5% in the restrictive group and 22.9% in the liberal group, P=0.69).

Conclusions

The findings in this study indicate that the use of a restrictive red cell transfusion strategy to hemoglobin levels as low as 7.0 g per deciliter, combined with the maintenance of hemoglobin concentrations between 7.0 and 9.0 g per deciliter, was at least as effective as a more liberal strategy in critically ill patients with euvolemia. All-cause 30-day mortality was no different between the groups but favored the restrictive strategy. The rates of inpatient deaths were lower in the restrictive group. There were more cardiac complications in the liberal group. An important subgroup of patients, those with a history of cardiac disease, had no differences in mortality. The use of this strategy decreased the average number of red cell transfusions by 54%. TH

Issue
The Hospitalist - 2007(02)
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Hospital Quality for AMI: Process Measures and Their Relationship with Short-term Mortality

Bradley EH, Herrin J, Elbel B, et al. Hospital quality for acute myocardial infarction: correlation among process measures and relationship with short-term mortality. JAMA. 2006 Jul 5;296(1):72-78.

Background

The Centers for Medicare and Medicaid Services (CMS) and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) monitor and publicly report hospital performance in the treatment of acute myocardial infarction (AMI). Core process measures are considered an indicator of quality of care, but little is known about how these measures affect outcomes (mortality). Five of the seven core measures for AMI assess medication prescription practices; the other two measures are counseling on smoking cessation and timely reperfusion therapy.

Inferences about a hospital’s quality of care for AMI are created by measuring the hospital’s success at performing these measures. No previous study had evaluated a possible correlation between performance on these measures and short-term mortality. The authors of this study used National Registry of Myocardial Infarction (NRMI) and CMS databases to determine the association between hospital performance on AMI process measures and hospital-specific, risk-standardized, 30-day mortality rates.

There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Methods

A cross-sectional study was performed using hospitals that reported AMI discharges to the NRMI from January 2002 through March 2003. Hospitals had to report a minimum of 10 eligible patients. Hospital performance on core measures was recorded: beta-blocker on admission, beta-blocker on dismissal, aspirin on admission, aspirin on dismissal, angiotensin-converting enzyme inhibitor (ACE) prescription on dismissal, smoking cessation counseling for smokers during admission, and time to reperfusion therapy. Risk-standardized, 30-day, all-cause mortality rates were calculated for each hospital using CMS Medicare claims for patients ages 66 and older with AMI. The primary analysis determined the association of hospital-specific, risk-standardized, 30-day mortality rates with hospital performance on the core process measures.

Results

The most successfully completed core process measure for AMI was aspirin on admission. A mean of 86.4% of participating hospitals completed this measure. The core process measure for AMI that was the least frequently documented was smoking cessation counseling; a mean of 13.9% of participating hospitals completed this measure. Notably, timely reperfusion therapy for AMI—fibrinolytic therapy within 30 minutes of arrival or percutaneous intervention within 120 minutes of arrival—was completed by only 54.5% (mean) of participating hospitals.

Each core process measure had a statistically significant but small correlation with the risk-standardized, 30-day mortality rate (explaining between 0.1% and 3.3% of variance in mortality). Of the 180 hospitals in the top quintile of risk-standardized, 30-day mortality rates, only 31% were in the top quintile of the core process measures. A composite model of all seven core process measures determined that these measures could only explain 6% of the hospital-level variation in risk-standardized, 30-day mortality rates. Secondary analyses did not differ substantially.

Conclusions

In this study, each core process measure for AMI showed a modest correlation with 30-day mortality, but accounted for only 6% of 30-day mortality. This finding highlights the fact that continued measurement of these processes is valuable, but a hospital’s short-term mortality rates for AMI cannot be reliably inferred from performance on publicly reported process measures. These measures are weighted more toward long-term outcome measures. There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Clopidogrel and Aspirin versus Aspirin Alone for the Prevention of Atherothrombotic Events

 

 

Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006 Apr 20;354(16):1706-1717.

Background

Atherothrombotic disorders of the circulatory system are the leading cause of death and disability in the world. Low-dose aspirin has been shown to reduce ischemic event in populations above a certain risk threshold; however, aspirin alone may be insufficient treatment to prevent ischemic events in high-risk patients. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce ischemic events in patients with unstable angina, non-ST segment elevation and ST segment elevation myocardial infarction, as well as in those undergoing angioplasty and stenting.

The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group.

Methods

This was a prospective, multicenter, randomized, double-blind, placebo-controlled study of the efficacy and safety of aspirin plus clopidogrel in comparison with aspirin plus placebo in patients at high risk for a cardiovascular event. Patients included in the study were 45 or older and had one of the following: multiple atherothrombotic risk factors, documented coronary artery disease, documented cerebrovascular disease, or documented symptomatic peripheral vascular disease. The primary efficacy endpoint was the first occurrence of myocardial infarction (MI), stroke, or death from cardiovascular causes. The primary safety endpoint was severe bleeding.

Results

A total of 15,603 patients were enrolled in the study. Treatment was permanently discontinued by 20.4% in the clopidogrel group as compared with 18.2% in the placebo group (P<0.001). A total of 4.8% of patients in the clopidogrel group and 4.9% in the placebo group discontinued treatment because of an adverse event (P=0.67). Other than the treatment medications, concomitant medication use was similar in both groups. A median follow-up of 28 months revealed that the rates of primary efficacy events in the clopidogrel and placebo group were similar (6.8% versus 7.3%, P=0.22, respectively). The rate of primary safety events was 1.7% in the clopidogrel group and 1.3% in the placebo group, P=0.09.

Conclusions

This trial enrolled patients who either had established atherothrombotic disease or were at high risk for such disease and found that there was no significant benefit associated with the use of clopidogrel plus aspirin compared to aspirin alone in reducing myocardial infarction, stroke, or cardiovascular death. The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group. Overall, these findings do not support the use of dual antiplatelet therapy across this broad patient population.

D-Dimer in the Diagnosis of Pulmonary Embolism

Kearon C, Ginsberg JS, Douketis J, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med. 2006 Jun 6;144(11):812-821.

Background

The clinical usefulness of the D-dimer test in the diagnosis of pulmonary embolism (PE) has been previously studied. In patients with suspected PE, it may be safe to omit additional diagnostic testing if a patient has a negative D-dimer test; however, this approach has never been evaluated in a randomized, controlled trial.

The investigators in this trial studied two subgroups of patients with suspected PE and a negative D-dimer: patients with a low clinical probability of PE and those with a moderate or high clinical probability of PE who had a non-diagnostic ventilation perfusion scan (VQ scan) and no proximal deep vein thrombosis on venous ultrasonography. The hypothesis was that patients with a negative D-dimer who do not have further testing for PE won’t have a higher frequency of venous thromboembolism during follow-up than patients who undergo routine diagnostic testing.

 

 

Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up.

Methods

Before any diagnostic testing, patients were assigned a probability score, using the Wells Criteria, to categorize the probability of PE as low or moderate to high.

Patients with low probability Wells scores: D-dimer testing was done on all patients with a low clinical probability of PE. Patients with a negative D-dimer were randomly assigned either to no additional diagnostic testing and no anticoagulation treatment or to additional diagnostic testing with an initial VQ scan. If the VQ scan was negative, then PE was excluded. If the VQ scan showed one or more segmental perfusion defects that were normally ventilated, then the scan was considered diagnostic for PE. If there were perfusion defects that did not meet the criteria for a high probability scan, then the scan was considered non-diagnostic. Patients with non-diagnostic scans underwent ultrasonography of the proximal veins of the legs. If deep vein thrombosis was present, PE was diagnosed. If ultrasonography was normal, the test was repeated after seven and 14 days. In all patients with a positive D-dimer, a VQ scan was performed.

Patients with moderate to high probability Wells scores: A VQ scan was performed on all patients with a moderate to high probability for PE. Patients with high probability scans were treated; patients with normal scans were not treated. Patients with non-diagnostic scans and normal venous ultrasonography were randomly assigned to receive either no additional testing or serial ultrasonography.

Outcomes: All patients were followed for six months for the development of venous thromboembolism after initial diagnostic testing.

Results

The study enrolled 1,126 patients. Overall, 160 patients (14.2%) had PE diagnosed at initial presentation or by venous ultrasonography. Of 952 patients who did not receive an initial diagnosis of PE, 11 (1.2%) had PE diagnosed at follow-up.

Patients with low probability Wells scores: Low clinical probability was present in 670 patients (60%). In patients with low clinical probability of PE, 373 (56%) had negative D-dimer tests and 297 (44%) had positive D-dimer tests. Of the 373 patients with low probability and negative D-dimer results, 187 were randomized to no additional testing and 186 received a VQ scan. The frequency of venous thromboembolism at six-month follow-up was similar in these two groups (-0.5% [CI, -3.0% to 1.6%]). Three patients with negative D-dimer tests were diagnosed with PE by VQ scan. Results were fairly complete (five patients without a six-month follow-up in the no additional testing group and one without a follow-up in the VQ scan group).

Twenty-four patients with low clinical probability and positive D-dimer results (n=297) were diagnosed with PE. Three patients did not complete the six-month follow-up. Of the remaining 294 patients, five patients had venous thromboembolism at six months.

Patients with moderate to high probability Wells scores: There were 456 patients (40%) had moderate or high clinical probability for PE. Each of these patients had a VQ scan. Non-diagnostic VQ scans and normal venous ultrasonography were performed on 226 patients. Of these 226 patients, 86 had a negative D-dimer and 140 had a positive D-dimer. Of the 86 patients with negative VQ scans, normal venous ultrasonography, and a negative D-dimer, 83 were randomly assigned to no additional testing or serial venous ultrasonography (42 and 41 respectively). At six months follow-up, one patient assigned to no additional testing had venous thromboembolism, and no patients in the additional testing group had venous thromboembolism.

 

 

Conclusions

The results of this trial suggest that it is safe to withhold additional diagnostic testing in patients with suspected PE, low pretest clinical probability, and a negative D-dimer test. Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up. The assay used for this study was an erythrocyte agglutination SimpliRED assay. Reported sensitivity is approximately 90%, and specificity is approximately 75%. To the readers, it should be noted that the authors defined a low probability Wells score as 4 rather than 1.5 or lower.

Efficacy and Safety of Inhaled Insulin Therapy in Adults with Diabetes Mellitus

Ceglia L, Lau J, Pittas AG. Meta-analysis: efficacy and safety of inhaled insulin therapy in adults with diabetes mellitus. Ann Intern Med. 2006 Nov 7;145(9):665-675.

Background

Despite its effectiveness in attaining glycemic control, there is considerable resistance to insulin use by patients and healthcare providers, primarily because of the need for subcutaneous injection. In January 2006, the U.S. Food and Drug Administration (FDA) approved the first formulation of inhaled insulin for clinical use in nonsmoking adults with type 1 or type 2 diabetes and no pulmonary disease. The authors of this paper present a systematic review to examine the efficacy, safety, and patient acceptability of inhaled insulin.

All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin.

Methods

The authors conducted a search of MEDLINE to find English-language, randomized, controlled trials of inhaled insulin in nonpregnant adults with diabetes. To find unpublished studies, the authors reviewed the briefing document on Exubera powder for oral inhalation (Pfizer Inc., New York). An abstract was included if it reported original data from controlled trials in patients with type 1 or 2 diabetes and hemoglobin A1C outcomes for patients receiving inhaled insulin versus outcomes for a comparison group (subcutaneous insulin or oral hypoglycemics). Studies with less than 12 weeks duration were excluded because no comparison could be made regarding glycemic efficacy. For glycemic efficacy, the primary outcome was the treatment group difference in hemoglobin A1C from baseline. Secondary outcome was the proportion of patients with hemoglobin A1C levels less than 7%. To evaluate safety, the primary outcomes were severe hypoglycemia (glucose ≤36 mg/dL), cough, and treatment group difference in pulmonary function variables.

Results

Sixteen trials involving a total of 4,023 patients met inclusion criteria. Seven trials compared inhaled insulin with various subcutaneous insulin regimens in patients with type 1 diabetes. Nine trials compared inhaled insulin with subcutaneous insulin or oral hypoglycemic agents in patients with type 2 diabetes. Inhaled insulin was given with meals and titrated according to study-specific glucose goals. Subcutaneous insulin was titrated to the same specific goals. Doses of oral hypoglycemic agents were adjusted for glycemic targets in only two of the nine trials. The combined data from the studies demonstrated a small but statistically significant decrease in the levels of baseline hemoglobin A1C levels in favor of subcutaneous insulin (weighted mean difference 0.08%, [CI 0.03% to 0.14%]) in patients with type 1 or type 2 diabetes. The greatest advantage of subcutaneous insulin was noted in the study with the longest duration (104 weeks). There was no difference between the study groups in studies with duration of 24 weeks or less. Patients with type 1 or type 2 diabetes taking inhaled insulin were no more likely to achieve hemoglobin A1C levels less than 7% than those using subcutaneous insulin.

The combined data from studies comparing inhaled insulin to oral hypoglycemic agents in patients with type 2 diabetes showed that inhaled insulin lowered hemoglobin A1C levels more effectively (weighted mean difference -1.04%, [CI -1.59% to -0.49%]). In studies in which the oral hypoglycemic agents were titrated, inhaled insulin still lowered baseline hemoglobin A1C levels but to a lesser degree (weighted mean difference -0.20%, [CI - 0.34% to -0.07%]). Patients with type 2 diabetes taking inhaled insulin were more likely to achieve hemoglobin A1C levels less than 7% than those taking oral agents.

 

 

There was no difference in episodes of severe hypoglycemia in patients using inhaled insulin compared to those using subcutaneous insulin. A higher proportion of patients using inhaled insulin reported at least one episode of severe hypoglycemia compared to those using oral agents (risk ratio, 3.06 [CI 1.03 to 9.07]; 9.4% versus 3.5%, respectively).

With respect to pulmonary safety, all trials selected patients without histories of pulmonary problems and with at least six months of nonsmoking status. Pulmonary safety was assessed by self-reported symptoms and by pulmonary function tests. The most common pulmonary symptom associated with inhaled insulin was nonproductive cough. This symptom was reported more frequently compared to patients using subcutaneous insulin or oral agents (risk ratio, 3.52 [CI 2.23 to 5.56]; 16.9% versus 5.0%). Cough was noted early in the treatment course and diminished in frequency over time. Patients receiving inhaled insulin had a greater decrease in FEV1 (forced expiratory volume in the first second) from baseline than the comparator group (weighted mean difference, -0.031 L [CI-0.043 L to -0.020 L]). This decrease progressed slowly over the first six months but stabilized in studies of up to two years’ duration.

Only four trials reported data on overall patient satisfaction for inhaled insulin versus subcutaneous insulin. All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin. Patients randomly assigned to inhaled insulin were more likely to continue taking inhaled insulin than to switch back to subcutaneous insulin.

Conclusions

This meta-analysis showed that inhaled insulin is comparable to subcutaneous insulin in lowering hemoglobin A1C levels in patients with type 1 or type 2 diabetes. The proportion of patients reaching a target hemoglobin A1C of less than 7% was much lower in the studies in this meta-analysis as compared to levels in trials of intensive subcutaneous insulin therapy.

It’s more difficult to compare inhaled insulin with oral hypoglycemic agents because most studies involving oral agents used fixed dosing with different types of oral agents. There was a three-fold risk of severe hypoglycemia in patients using inhaled insulin compared to those using oral hypoglycemic agents. This is probably due to overall improved glycemic control in the inhaled insulin group. Cough was more common in the inhaled insulin groups, and there were small decreases in FEV1, but these did not progress over two years. The potential for pulmonary toxicity with long-term administration has not been evaluated and deserves further study.

Classic Literature

A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care

Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999 Feb 11;340(6):409-417.

Background

There are important risks and benefits of red cell transfusion in critically ill patients. One concern is that anemia may not be tolerated well in this group. Because red cell transfusions are used to augment the delivery of oxygen to avoid the harmful effects of oxygen debt, transfusing patients to keep their hemoglobin levels higher than 10.0 g per deciliter has become a routine practice. There is concern, however, that critically ill patients may be at increased risk of immunosuppressive and microcirculatory complications of red cell transfusions. Also, concern about the safety and supply of red cell transfusions has encouraged a more conservative approach to transfusion strategies.

The authors of this study conducted a randomized, controlled, clinical trial involving critically ill patients with euvolemia to determine whether a restrictive transfusion strategy that maintains hemoglobin concentrations between 7.0 and 9.0 g per deciliter was equivalent to a liberal strategy of maintaining hemoglobin concentrations between 10.0 and 12.0 g per deciliter.

Methods

Enrolled patients were admitted to 25 different intensive care units in Canada between 1994 and 1997. Included patients were expected to have an intensive care unit stay longer than 24 hours and a hemoglobin concentration of 9.0 g per deciliter or less within 72 hours after admission and were considered euvolemic after initial treatment by physicians. Critically ill patients with euvolemia were randomized to either the restrictive or the liberal strategy. Patients were given one unit at a time, and the hemoglobin concentration was measured after each unit transfused. Transfusion was stopped when the patient’s hemoglobin concentration was in the target range. The primary outcome was death from all causes within 30 days of randomization.

Results

A total of 838 patients were enrolled in the study; 418 in the restrictive group and 420 in the liberal group. The average daily hemoglobin concentrations were 8.5 g per deciliter in the restrictive group and 10.7 g per deciliter in the liberal group (P<0.01). An average of 2.6 red cell units per patient was transfused in the restrictive group, as compared to an average of 5.6 red cell units in the liberal group (P<0.01). Thirty-three percent of patients in the restrictive group did not receive any transfusion; every patient in the liberal group received at least one red cell unit.

The rate of death from all causes in the 30 days after admission was 18.7% in the restrictive group and 23.3% in the liberal group (-0.84% to 10.2%, P=0.11). The inpatient mortality rates were lower in the restrictive group (22.2% versus 28.1%, P=0.05). More patients in the liberal group had some type of cardiac complication (21.0% versus 13.2% respectively, P<0.01). Subgroup analyses demonstrated that patients with lower APACHE II scores (20 or less) and patients younger than 55 had improved survival in the restrictive strategy group. There were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5% in the restrictive group and 22.9% in the liberal group, P=0.69).

Conclusions

The findings in this study indicate that the use of a restrictive red cell transfusion strategy to hemoglobin levels as low as 7.0 g per deciliter, combined with the maintenance of hemoglobin concentrations between 7.0 and 9.0 g per deciliter, was at least as effective as a more liberal strategy in critically ill patients with euvolemia. All-cause 30-day mortality was no different between the groups but favored the restrictive strategy. The rates of inpatient deaths were lower in the restrictive group. There were more cardiac complications in the liberal group. An important subgroup of patients, those with a history of cardiac disease, had no differences in mortality. The use of this strategy decreased the average number of red cell transfusions by 54%. TH

Hospital Quality for AMI: Process Measures and Their Relationship with Short-term Mortality

Bradley EH, Herrin J, Elbel B, et al. Hospital quality for acute myocardial infarction: correlation among process measures and relationship with short-term mortality. JAMA. 2006 Jul 5;296(1):72-78.

Background

The Centers for Medicare and Medicaid Services (CMS) and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) monitor and publicly report hospital performance in the treatment of acute myocardial infarction (AMI). Core process measures are considered an indicator of quality of care, but little is known about how these measures affect outcomes (mortality). Five of the seven core measures for AMI assess medication prescription practices; the other two measures are counseling on smoking cessation and timely reperfusion therapy.

Inferences about a hospital’s quality of care for AMI are created by measuring the hospital’s success at performing these measures. No previous study had evaluated a possible correlation between performance on these measures and short-term mortality. The authors of this study used National Registry of Myocardial Infarction (NRMI) and CMS databases to determine the association between hospital performance on AMI process measures and hospital-specific, risk-standardized, 30-day mortality rates.

There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Methods

A cross-sectional study was performed using hospitals that reported AMI discharges to the NRMI from January 2002 through March 2003. Hospitals had to report a minimum of 10 eligible patients. Hospital performance on core measures was recorded: beta-blocker on admission, beta-blocker on dismissal, aspirin on admission, aspirin on dismissal, angiotensin-converting enzyme inhibitor (ACE) prescription on dismissal, smoking cessation counseling for smokers during admission, and time to reperfusion therapy. Risk-standardized, 30-day, all-cause mortality rates were calculated for each hospital using CMS Medicare claims for patients ages 66 and older with AMI. The primary analysis determined the association of hospital-specific, risk-standardized, 30-day mortality rates with hospital performance on the core process measures.

Results

The most successfully completed core process measure for AMI was aspirin on admission. A mean of 86.4% of participating hospitals completed this measure. The core process measure for AMI that was the least frequently documented was smoking cessation counseling; a mean of 13.9% of participating hospitals completed this measure. Notably, timely reperfusion therapy for AMI—fibrinolytic therapy within 30 minutes of arrival or percutaneous intervention within 120 minutes of arrival—was completed by only 54.5% (mean) of participating hospitals.

Each core process measure had a statistically significant but small correlation with the risk-standardized, 30-day mortality rate (explaining between 0.1% and 3.3% of variance in mortality). Of the 180 hospitals in the top quintile of risk-standardized, 30-day mortality rates, only 31% were in the top quintile of the core process measures. A composite model of all seven core process measures determined that these measures could only explain 6% of the hospital-level variation in risk-standardized, 30-day mortality rates. Secondary analyses did not differ substantially.

Conclusions

In this study, each core process measure for AMI showed a modest correlation with 30-day mortality, but accounted for only 6% of 30-day mortality. This finding highlights the fact that continued measurement of these processes is valuable, but a hospital’s short-term mortality rates for AMI cannot be reliably inferred from performance on publicly reported process measures. These measures are weighted more toward long-term outcome measures. There is a need for new research to define and study new AMI process measures that can explain more of the variance in both short- and long-term outcomes.

Clopidogrel and Aspirin versus Aspirin Alone for the Prevention of Atherothrombotic Events

 

 

Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006 Apr 20;354(16):1706-1717.

Background

Atherothrombotic disorders of the circulatory system are the leading cause of death and disability in the world. Low-dose aspirin has been shown to reduce ischemic event in populations above a certain risk threshold; however, aspirin alone may be insufficient treatment to prevent ischemic events in high-risk patients. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce ischemic events in patients with unstable angina, non-ST segment elevation and ST segment elevation myocardial infarction, as well as in those undergoing angioplasty and stenting.

The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group.

Methods

This was a prospective, multicenter, randomized, double-blind, placebo-controlled study of the efficacy and safety of aspirin plus clopidogrel in comparison with aspirin plus placebo in patients at high risk for a cardiovascular event. Patients included in the study were 45 or older and had one of the following: multiple atherothrombotic risk factors, documented coronary artery disease, documented cerebrovascular disease, or documented symptomatic peripheral vascular disease. The primary efficacy endpoint was the first occurrence of myocardial infarction (MI), stroke, or death from cardiovascular causes. The primary safety endpoint was severe bleeding.

Results

A total of 15,603 patients were enrolled in the study. Treatment was permanently discontinued by 20.4% in the clopidogrel group as compared with 18.2% in the placebo group (P<0.001). A total of 4.8% of patients in the clopidogrel group and 4.9% in the placebo group discontinued treatment because of an adverse event (P=0.67). Other than the treatment medications, concomitant medication use was similar in both groups. A median follow-up of 28 months revealed that the rates of primary efficacy events in the clopidogrel and placebo group were similar (6.8% versus 7.3%, P=0.22, respectively). The rate of primary safety events was 1.7% in the clopidogrel group and 1.3% in the placebo group, P=0.09.

Conclusions

This trial enrolled patients who either had established atherothrombotic disease or were at high risk for such disease and found that there was no significant benefit associated with the use of clopidogrel plus aspirin compared to aspirin alone in reducing myocardial infarction, stroke, or cardiovascular death. The risk of moderate or severe bleeding in symptomatic patients was higher in the clopidogrel plus aspirin group than in the aspirin plus placebo group. Overall, these findings do not support the use of dual antiplatelet therapy across this broad patient population.

D-Dimer in the Diagnosis of Pulmonary Embolism

Kearon C, Ginsberg JS, Douketis J, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med. 2006 Jun 6;144(11):812-821.

Background

The clinical usefulness of the D-dimer test in the diagnosis of pulmonary embolism (PE) has been previously studied. In patients with suspected PE, it may be safe to omit additional diagnostic testing if a patient has a negative D-dimer test; however, this approach has never been evaluated in a randomized, controlled trial.

The investigators in this trial studied two subgroups of patients with suspected PE and a negative D-dimer: patients with a low clinical probability of PE and those with a moderate or high clinical probability of PE who had a non-diagnostic ventilation perfusion scan (VQ scan) and no proximal deep vein thrombosis on venous ultrasonography. The hypothesis was that patients with a negative D-dimer who do not have further testing for PE won’t have a higher frequency of venous thromboembolism during follow-up than patients who undergo routine diagnostic testing.

 

 

Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up.

Methods

Before any diagnostic testing, patients were assigned a probability score, using the Wells Criteria, to categorize the probability of PE as low or moderate to high.

Patients with low probability Wells scores: D-dimer testing was done on all patients with a low clinical probability of PE. Patients with a negative D-dimer were randomly assigned either to no additional diagnostic testing and no anticoagulation treatment or to additional diagnostic testing with an initial VQ scan. If the VQ scan was negative, then PE was excluded. If the VQ scan showed one or more segmental perfusion defects that were normally ventilated, then the scan was considered diagnostic for PE. If there were perfusion defects that did not meet the criteria for a high probability scan, then the scan was considered non-diagnostic. Patients with non-diagnostic scans underwent ultrasonography of the proximal veins of the legs. If deep vein thrombosis was present, PE was diagnosed. If ultrasonography was normal, the test was repeated after seven and 14 days. In all patients with a positive D-dimer, a VQ scan was performed.

Patients with moderate to high probability Wells scores: A VQ scan was performed on all patients with a moderate to high probability for PE. Patients with high probability scans were treated; patients with normal scans were not treated. Patients with non-diagnostic scans and normal venous ultrasonography were randomly assigned to receive either no additional testing or serial ultrasonography.

Outcomes: All patients were followed for six months for the development of venous thromboembolism after initial diagnostic testing.

Results

The study enrolled 1,126 patients. Overall, 160 patients (14.2%) had PE diagnosed at initial presentation or by venous ultrasonography. Of 952 patients who did not receive an initial diagnosis of PE, 11 (1.2%) had PE diagnosed at follow-up.

Patients with low probability Wells scores: Low clinical probability was present in 670 patients (60%). In patients with low clinical probability of PE, 373 (56%) had negative D-dimer tests and 297 (44%) had positive D-dimer tests. Of the 373 patients with low probability and negative D-dimer results, 187 were randomized to no additional testing and 186 received a VQ scan. The frequency of venous thromboembolism at six-month follow-up was similar in these two groups (-0.5% [CI, -3.0% to 1.6%]). Three patients with negative D-dimer tests were diagnosed with PE by VQ scan. Results were fairly complete (five patients without a six-month follow-up in the no additional testing group and one without a follow-up in the VQ scan group).

Twenty-four patients with low clinical probability and positive D-dimer results (n=297) were diagnosed with PE. Three patients did not complete the six-month follow-up. Of the remaining 294 patients, five patients had venous thromboembolism at six months.

Patients with moderate to high probability Wells scores: There were 456 patients (40%) had moderate or high clinical probability for PE. Each of these patients had a VQ scan. Non-diagnostic VQ scans and normal venous ultrasonography were performed on 226 patients. Of these 226 patients, 86 had a negative D-dimer and 140 had a positive D-dimer. Of the 86 patients with negative VQ scans, normal venous ultrasonography, and a negative D-dimer, 83 were randomly assigned to no additional testing or serial venous ultrasonography (42 and 41 respectively). At six months follow-up, one patient assigned to no additional testing had venous thromboembolism, and no patients in the additional testing group had venous thromboembolism.

 

 

Conclusions

The results of this trial suggest that it is safe to withhold additional diagnostic testing in patients with suspected PE, low pretest clinical probability, and a negative D-dimer test. Even in patients with moderate to high pretest clinical probability, a non-diagnostic VQ scan, and normal venous ultrasonography, only one patient with a negative D-dimer had a venous thromboembolic event at six months follow-up. The assay used for this study was an erythrocyte agglutination SimpliRED assay. Reported sensitivity is approximately 90%, and specificity is approximately 75%. To the readers, it should be noted that the authors defined a low probability Wells score as 4 rather than 1.5 or lower.

Efficacy and Safety of Inhaled Insulin Therapy in Adults with Diabetes Mellitus

Ceglia L, Lau J, Pittas AG. Meta-analysis: efficacy and safety of inhaled insulin therapy in adults with diabetes mellitus. Ann Intern Med. 2006 Nov 7;145(9):665-675.

Background

Despite its effectiveness in attaining glycemic control, there is considerable resistance to insulin use by patients and healthcare providers, primarily because of the need for subcutaneous injection. In January 2006, the U.S. Food and Drug Administration (FDA) approved the first formulation of inhaled insulin for clinical use in nonsmoking adults with type 1 or type 2 diabetes and no pulmonary disease. The authors of this paper present a systematic review to examine the efficacy, safety, and patient acceptability of inhaled insulin.

All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin.

Methods

The authors conducted a search of MEDLINE to find English-language, randomized, controlled trials of inhaled insulin in nonpregnant adults with diabetes. To find unpublished studies, the authors reviewed the briefing document on Exubera powder for oral inhalation (Pfizer Inc., New York). An abstract was included if it reported original data from controlled trials in patients with type 1 or 2 diabetes and hemoglobin A1C outcomes for patients receiving inhaled insulin versus outcomes for a comparison group (subcutaneous insulin or oral hypoglycemics). Studies with less than 12 weeks duration were excluded because no comparison could be made regarding glycemic efficacy. For glycemic efficacy, the primary outcome was the treatment group difference in hemoglobin A1C from baseline. Secondary outcome was the proportion of patients with hemoglobin A1C levels less than 7%. To evaluate safety, the primary outcomes were severe hypoglycemia (glucose ≤36 mg/dL), cough, and treatment group difference in pulmonary function variables.

Results

Sixteen trials involving a total of 4,023 patients met inclusion criteria. Seven trials compared inhaled insulin with various subcutaneous insulin regimens in patients with type 1 diabetes. Nine trials compared inhaled insulin with subcutaneous insulin or oral hypoglycemic agents in patients with type 2 diabetes. Inhaled insulin was given with meals and titrated according to study-specific glucose goals. Subcutaneous insulin was titrated to the same specific goals. Doses of oral hypoglycemic agents were adjusted for glycemic targets in only two of the nine trials. The combined data from the studies demonstrated a small but statistically significant decrease in the levels of baseline hemoglobin A1C levels in favor of subcutaneous insulin (weighted mean difference 0.08%, [CI 0.03% to 0.14%]) in patients with type 1 or type 2 diabetes. The greatest advantage of subcutaneous insulin was noted in the study with the longest duration (104 weeks). There was no difference between the study groups in studies with duration of 24 weeks or less. Patients with type 1 or type 2 diabetes taking inhaled insulin were no more likely to achieve hemoglobin A1C levels less than 7% than those using subcutaneous insulin.

The combined data from studies comparing inhaled insulin to oral hypoglycemic agents in patients with type 2 diabetes showed that inhaled insulin lowered hemoglobin A1C levels more effectively (weighted mean difference -1.04%, [CI -1.59% to -0.49%]). In studies in which the oral hypoglycemic agents were titrated, inhaled insulin still lowered baseline hemoglobin A1C levels but to a lesser degree (weighted mean difference -0.20%, [CI - 0.34% to -0.07%]). Patients with type 2 diabetes taking inhaled insulin were more likely to achieve hemoglobin A1C levels less than 7% than those taking oral agents.

 

 

There was no difference in episodes of severe hypoglycemia in patients using inhaled insulin compared to those using subcutaneous insulin. A higher proportion of patients using inhaled insulin reported at least one episode of severe hypoglycemia compared to those using oral agents (risk ratio, 3.06 [CI 1.03 to 9.07]; 9.4% versus 3.5%, respectively).

With respect to pulmonary safety, all trials selected patients without histories of pulmonary problems and with at least six months of nonsmoking status. Pulmonary safety was assessed by self-reported symptoms and by pulmonary function tests. The most common pulmonary symptom associated with inhaled insulin was nonproductive cough. This symptom was reported more frequently compared to patients using subcutaneous insulin or oral agents (risk ratio, 3.52 [CI 2.23 to 5.56]; 16.9% versus 5.0%). Cough was noted early in the treatment course and diminished in frequency over time. Patients receiving inhaled insulin had a greater decrease in FEV1 (forced expiratory volume in the first second) from baseline than the comparator group (weighted mean difference, -0.031 L [CI-0.043 L to -0.020 L]). This decrease progressed slowly over the first six months but stabilized in studies of up to two years’ duration.

Only four trials reported data on overall patient satisfaction for inhaled insulin versus subcutaneous insulin. All trials reported a statistically significant increase in overall patient satisfaction with inhaled insulin over subcutaneous insulin. Patients randomly assigned to inhaled insulin were more likely to continue taking inhaled insulin than to switch back to subcutaneous insulin.

Conclusions

This meta-analysis showed that inhaled insulin is comparable to subcutaneous insulin in lowering hemoglobin A1C levels in patients with type 1 or type 2 diabetes. The proportion of patients reaching a target hemoglobin A1C of less than 7% was much lower in the studies in this meta-analysis as compared to levels in trials of intensive subcutaneous insulin therapy.

It’s more difficult to compare inhaled insulin with oral hypoglycemic agents because most studies involving oral agents used fixed dosing with different types of oral agents. There was a three-fold risk of severe hypoglycemia in patients using inhaled insulin compared to those using oral hypoglycemic agents. This is probably due to overall improved glycemic control in the inhaled insulin group. Cough was more common in the inhaled insulin groups, and there were small decreases in FEV1, but these did not progress over two years. The potential for pulmonary toxicity with long-term administration has not been evaluated and deserves further study.

Classic Literature

A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care

Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999 Feb 11;340(6):409-417.

Background

There are important risks and benefits of red cell transfusion in critically ill patients. One concern is that anemia may not be tolerated well in this group. Because red cell transfusions are used to augment the delivery of oxygen to avoid the harmful effects of oxygen debt, transfusing patients to keep their hemoglobin levels higher than 10.0 g per deciliter has become a routine practice. There is concern, however, that critically ill patients may be at increased risk of immunosuppressive and microcirculatory complications of red cell transfusions. Also, concern about the safety and supply of red cell transfusions has encouraged a more conservative approach to transfusion strategies.

The authors of this study conducted a randomized, controlled, clinical trial involving critically ill patients with euvolemia to determine whether a restrictive transfusion strategy that maintains hemoglobin concentrations between 7.0 and 9.0 g per deciliter was equivalent to a liberal strategy of maintaining hemoglobin concentrations between 10.0 and 12.0 g per deciliter.

Methods

Enrolled patients were admitted to 25 different intensive care units in Canada between 1994 and 1997. Included patients were expected to have an intensive care unit stay longer than 24 hours and a hemoglobin concentration of 9.0 g per deciliter or less within 72 hours after admission and were considered euvolemic after initial treatment by physicians. Critically ill patients with euvolemia were randomized to either the restrictive or the liberal strategy. Patients were given one unit at a time, and the hemoglobin concentration was measured after each unit transfused. Transfusion was stopped when the patient’s hemoglobin concentration was in the target range. The primary outcome was death from all causes within 30 days of randomization.

Results

A total of 838 patients were enrolled in the study; 418 in the restrictive group and 420 in the liberal group. The average daily hemoglobin concentrations were 8.5 g per deciliter in the restrictive group and 10.7 g per deciliter in the liberal group (P<0.01). An average of 2.6 red cell units per patient was transfused in the restrictive group, as compared to an average of 5.6 red cell units in the liberal group (P<0.01). Thirty-three percent of patients in the restrictive group did not receive any transfusion; every patient in the liberal group received at least one red cell unit.

The rate of death from all causes in the 30 days after admission was 18.7% in the restrictive group and 23.3% in the liberal group (-0.84% to 10.2%, P=0.11). The inpatient mortality rates were lower in the restrictive group (22.2% versus 28.1%, P=0.05). More patients in the liberal group had some type of cardiac complication (21.0% versus 13.2% respectively, P<0.01). Subgroup analyses demonstrated that patients with lower APACHE II scores (20 or less) and patients younger than 55 had improved survival in the restrictive strategy group. There were no significant differences in 30-day mortality between treatment groups in the subgroup of patients with a primary or secondary diagnosis of cardiac disease (20.5% in the restrictive group and 22.9% in the liberal group, P=0.69).

Conclusions

The findings in this study indicate that the use of a restrictive red cell transfusion strategy to hemoglobin levels as low as 7.0 g per deciliter, combined with the maintenance of hemoglobin concentrations between 7.0 and 9.0 g per deciliter, was at least as effective as a more liberal strategy in critically ill patients with euvolemia. All-cause 30-day mortality was no different between the groups but favored the restrictive strategy. The rates of inpatient deaths were lower in the restrictive group. There were more cardiac complications in the liberal group. An important subgroup of patients, those with a history of cardiac disease, had no differences in mortality. The use of this strategy decreased the average number of red cell transfusions by 54%. TH

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Read Your Patients

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Translate the following statement into plain English:*

“It is fruitless to become lachrymose over precipitately departed lacteal fluid.”1

If these words made you pause—even for a moment—you now have an inkling of what people of limited literacy confront when they deal with the healthcare system.

Health literacy is best defined as a patient’s ability to read, comprehend, and act on medical instructions and to make appropriate health-related decisions.2,3 It is closely related to, although not absolutely dependent upon, one’s overall level of literacy—and literacy problems are surprisingly widespread. According to the National Assessment of Adult Literacy (NAAL), a survey of more than 19,000 adults conducted in 2003 by the National Center for Educational Statistics and published in 2006, 36% of American adults have nothing more than basic or below basic literacy. People in these two categories might be able to sign their names, decipher a bus schedule, or read very simple instructions telling them what they can and cannot eat before a medical test, but they cannot read a juror information pamphlet, much less an informed consent form. Another recent survey suggested that about one-third of adults in public hospitals read at or below a sixth-grade level.4

Components of Health Literacy

Several components figure into a person’s ability to manage his health and engage the healthcare system. Literacy limitations can impair any or all of these factors, which include:

  • Health promotion: reading and understanding product labels or articles in newspapers;
  • Health protection: reading and understanding applications for insurance or following sanitary precautions in the workplace;
  • Disease prevention and screening: obtaining information about flu shots and blood pressure maintenance;
  • Ability to access care and navigate the system: determining the most appropriate healthcare provider to call when a problem arises or filling out forms correctly; and
  • Routine care and maintenance: testing blood glucose and getting regular checkups.1

Health literacy is further complicated by the fact that it can fluctuate in the same individual at different times and under different circumstances. For example, you might have no trouble deciphering the sentence at the beginning of this article if you feel well and are reading it in your office, living room, study, or some other familiar and comfortable environment. Now imagine that you’re ill and sitting in a noisy, chaotic emergency department, with a sheaf of other forms and papers to plow through. Suddenly the statement above may not be as easy to interpret.

“We must leave behind the notion of ‘illiterates,’ ” says Lakshmi Halasyamani, MD, chair of the Hospital Quality and Patient Safety Committee for SHM. “A person may not normally have a literacy problem, but they may be overwhelmed by the medical terminology, or they simply may not feel well enough to comprehend immediately everything the doctor says to them.”

The changing nature of healthcare may exacerbate the problem. Thirty years ago, only 650 drugs were available, and the average hospital stay for a myocardial infarction was four to six weeks. Today, there are more than 10,000 prescription drugs alone, and the typical stay for a heart attack is two to four days. As healthcare grows increasingly fragmented and complex, doctors have less time than ever to explain things and answer questions for their patients. Nevertheless, patients are expected to shoulder an ever-greater portion of the responsibility for their care and to live with conditions like diabetes or congestive heart failure, which require aggressive and detailed management.5 This is a challenge for even the most highly educated person; for someone whose literacy skills are fragile, the task can seem hopeless.

 

 

In addition to its medical and emotional consequences, limited health literacy is estimated to cost U.S. society $50 to $73 billion per year.6

Ask Me 3

To address the problem of low health literacy in vulnerable populations, a coalition of 19 organizations and individuals, backed by several experts in health literacy, formed the nonprofit Partnership for Clear Health Communications in 2002. The partnership’s mission is to increase awareness of the problem among clinicians, and to offer solutions to patients and healthcare providers alike.

The cornerstone of the partnership’s efforts is the “Ask Me 3” campaign, consisting of nothing more than three simple questions that all patients should ask their doctors:

  • What is my main problem?
  • What do I need to do?
  • Why is it important for me to do this?

Brochures written in elementary English and Spanish about the campaign are available from the partnership free for distribution in office and hospital waiting rooms, seniors’ centers, and the like. Doctors are encouraged to adorn their office walls with “Ask Me 3” posters, also in an effort to encourage better physician-patient communication.

More information for patients and physicians is available on the partnership’s Web site: www.p4chc.org.—NM

Who Is Most Likely to Have Literacy Problems?

In general, “the likelihood of low literacy increases in racial and ethnic minority groups, patients with language barriers, and those with low educational achievement,” says Benjamin Powers, MD, associate professor of general internal medicine at Duke University and a physician at the Durham Veterans Affairs Medical Center in North Carolina.

It’s no surprise that literacy overall, and health literacy specifically, correlate so closely with education and especially with the lack of a high school degree. What is perhaps more surprising is that educational achievement alone does not necessarily guarantee good health literacy.

“Even high school graduates may have trouble,” says Mark Williams, MD. In addition to being a professor of medicine and director of the hospital medicine unit at Emory University School of Medicine in Atlanta, Dr. Williams is the editor of the Journal of Hospital Medicine and has studied health literacy problems for years. “Some highly literate people may have problems reading or absorbing health-related information if they’re sick and not feeling well.”

These people are not illiterate in the conventional sense, but they may have inadequate functional health literacy skills, at least in certain settings.

Age is another risk factor. In one survey of Medicare enrollees, at least one-third of people age 65 or older had some degree of health illiteracy, Dr. Williams says. As with so many other skills, proficient reading requires regular practice, and people tend to read less as they age, so their literacy skills may decline. “It’s especially a problem for the ‘oldest old,’ people who are 75 years old or more,” he explains.

Language and cultural differences also enter into the equation. A patient may be well educated and able to articulate in her own language (perhaps even able to converse well in English under normal circumstances), but may be unfamiliar with medical terminology. Put her in a situation in which she feels ill, flustered, and disoriented, and her communication skills may deteriorate even more, says Dr. Halasyamani.

In short, health literacy consists of many components, including “an emotional overlay, information overload, and cultural overload. All of these factor into the patients’ ability to understand what we tell them,” says Barbara DeBuono, MD, MPH, senior medical advisor on U.S. Public Health and Policy at Pfizer Pharmaceuticals.

Issues Unique to Hospitalists

There are also a few issues unique to hospitalists and their patients, warns Dr. DeBuono, who is also on the board of the Partnership for Clear Health Communication (See “Ask Me 3,” at right.) “Hospitalists don’t necessarily have a long-term relationship with these patients, so they have to make a quick assessment of the patient’s ability to understand and absorb information. Then they have to determine the best way to communicate that information, and, when necessary, change their communication strategy to fit the circumstances.”

 

 

In addition, she says, “hospital patients usually are more complicated than patients seen in an office practice. They may have chronic conditions and several comorbidities, and the information and discharge instructions the physicians give them can be pretty complex.”

Indeed, “a patient may come in thinking she had no issues and leave the hospital with four or five complaints. We’ve rocked her world, and that can be overwhelming for even the most motivated person,” says Dr. Halasyamani, who cautions that any chronic illness that requires a significant amount of ongoing self-care, such as diabetes or heart failure, can tax a patient’s ability to completely understand her situation and coordinate her care effectively.

Fragmented Care

Patients with multiple and complex morbidities also are likely to be cared for by several physicians, who prescribe numerous drugs, tests, and procedures, and who don’t necessarily know what the other members of the care team are doing. Even highly sophisticated people can get the feeling that they’re caught in an ever-changing kaleidoscope of medical visits and jargon, in which the various fragments never coalesce into a comprehensible whole. As Dr. Powers and coauthor Hayden Bosworth, PhD, wrote in a recent editorial: “ … there may be specific physician and health system organizational factors that exacerbate or mitigate the impact of low literacy. Literacy may matter more for patients who are cared for in a chaotic and discontinuous system that is not organized around delivering high quality care in a multidisciplinary setting.”7

This is more than a subjective impression: There is evidence supporting the importance of coordinated care for people of limited literacy skills. Dr. Powers and Bosworth recently compared the impact of low literacy on blood pressure control in patients in the Veterans Affairs (VA) system and those who attended local community clinics.

“Although the prevalence of low literacy was high in both populations, there was a significant association with low literacy and poor blood pressure control in the community clinics but not the VA,” Dr. Powers tells The Hospitalist. “In other words, literacy seemed to be an important predictor of good blood pressure control in one healthcare setting but not in another.”

In hospitals, “the frequency of handoffs among doctors, nurses, caseworkers, and social workers may all contribute to the fragmented nature of a patient’s care,” warns Dr. Halasyamani. This may be exacerbated even further should the patient have the misfortune to be admitted during a transitional period, such as a weekend or the end of the month when staff members rotate.

Red Flags

Literacy limitations are easy to miss: Patients rarely announce that they can’t read forms or comprehend a clinician’s instructions. “Just asking, ‘Do you understand?’ rarely works, because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively,” says Dr. Williams.

Usually, the clues are subtle. “Most physicians do encounter such patients, but we’re not trained to detect literacy problems and respond appropriately,” says Sunil Kripalani, MD, MSc, who, like Dr. Williams, is an Emory University hospitalist with a special interest in patient literacy issues. Dr. Kripalani suggests looking for red flags, including:

  • Vague or evasive answers to questions. For example, “the patient who is taking a host of medications but can’t name them or tell you what time of day he’s supposed to take them;”
  • Few, if any, questions or discussions of concerns: “Patients with limited literacy are less prone to ask questions, and the questions they do ask may not be as deep as those asked by a patient with greater literacy skills. The patient may use very simple terminology and not integrate any of the concepts discussed during the appointment;” and
  • Missed appointments and repeated crises and hospitalizations resulting from the patient’s inability to read appointment cards or manage his illness. “Limited literacy skills may be a contributor to the exacerbations that put the patient in the hospital,” says Dr. Kripalani.
 

 

A patient with few family or social connections is also cause for concern, adds Dr. Halasyamani: “Lack of social support means there’s not another set of eyes and ears taking in the information.” Yet another red flag to her is the patient who cannot describe his plans for pursuing his care at home.

When patients have their medications with them, Dr. Williams asks how they take them. Those who can read simply look at the label, but a patient with literacy problems must open the bottle and look at the pills to identify them.

Solutions

How can physicians ensure that these patients understand and can follow instructions? Perhaps the easiest and most effective way is the “teach-back” approach, in which you ask the patient to repeat or teach back to you what you’ve just explained to him. For example, you might have him show you how to use an asthma inhaler or how to measure his blood glucose. In this way, you can rapidly assess and correct any deficiencies in the patient’s understanding.

“I’ve seen it take less than 90 seconds for physicians to confirm patient understanding in the context of a clinical visit,” says Dr. Kripalani.

A related technique that might help save time is to resist the temptation to tell the patient too much in a single visit. “Don’t try to give the patient too much information,” he advises. “People can process and retain maybe three nuggets of information at a time, so tell the patient the three most important things and then confirm their understanding of those three things.”

Dr. DeBuono suggests using visual aids like pictures or cartoons to help get important points across. If written material is necessary, have it printed in large type, which might appear less daunting than a page covered in dense, tiny print.

Above all, never embarrass a patient by bluntly asking him if he can read. “Explore the issue sensitively and respectfully,” Dr. Williams says. “Ask if they ever struggle with written materials or what the best way is for them to learn.” Adds Dr. DeBuono, “just by being sensitive to the fact that the patient may not understand is half the game.” TH

Norra MacReady is a medical journalist based in Southern California.

*“There’s no use crying over spilt milk.”

References

  1. Rudd RE. Literacy and implications for navigating health care. Harvard School of Public Health: Health Literacy Website. Slide 20. 2002. Available at www.hsph.harvard.edu/healthliteracy/slides/2002/2002_01.html. Last accessed December 1, 2006.
  2. Schillinger D, Grumbach K, Piette J, et al. Association of health literacy with diabetes outcomes. JAMA. 2002 Jul 24;288(4):475-482.
  3. Paasche-Orlow MK, Schillinger D, Greene SM, et al. How health care systems can begin to address the challenge of limited literacy. J Gen Intern Med. 2006 Aug;21(8):884-887.
  4. Marcus EN. The silent epidemic—the health effects of illiteracy. N Engl J Med. 2006 Jul 27;355(4):339-341. Erratum in N Engl J Med. 2006 Sept 7;355(10):1076.
  5. Williams MV. Recognizing and overcoming inadequate health literacy, a barrier to care. Cleve Clin J Med. 2002 May;69(5):415-418.
  6. Weiss BD. Health literacy: a manual for clinicians [American Medical Association Web site]. American Medical Association Foundation and the American Medical Association, 2003. Available at: www.ama-assn.org/ama1/pub/upload/mm/367/healthlitclinicians.pdf. Last accessed December 16, 2006.
  7. Powers BJ, Bosworth HB. Revisiting literacy and adherence: future clinical and research directions. J Gen Intern Med. 2006;21:1341-1342.

Just asking, “Do you understand?” rarely works because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively.—Mark Williams, MD, professor of medicine and director of the hospital medicine unit at Emory University School of Medicine, Atlanta.

Issue
The Hospitalist - 2007(02)
Publications
Sections

Translate the following statement into plain English:*

“It is fruitless to become lachrymose over precipitately departed lacteal fluid.”1

If these words made you pause—even for a moment—you now have an inkling of what people of limited literacy confront when they deal with the healthcare system.

Health literacy is best defined as a patient’s ability to read, comprehend, and act on medical instructions and to make appropriate health-related decisions.2,3 It is closely related to, although not absolutely dependent upon, one’s overall level of literacy—and literacy problems are surprisingly widespread. According to the National Assessment of Adult Literacy (NAAL), a survey of more than 19,000 adults conducted in 2003 by the National Center for Educational Statistics and published in 2006, 36% of American adults have nothing more than basic or below basic literacy. People in these two categories might be able to sign their names, decipher a bus schedule, or read very simple instructions telling them what they can and cannot eat before a medical test, but they cannot read a juror information pamphlet, much less an informed consent form. Another recent survey suggested that about one-third of adults in public hospitals read at or below a sixth-grade level.4

Components of Health Literacy

Several components figure into a person’s ability to manage his health and engage the healthcare system. Literacy limitations can impair any or all of these factors, which include:

  • Health promotion: reading and understanding product labels or articles in newspapers;
  • Health protection: reading and understanding applications for insurance or following sanitary precautions in the workplace;
  • Disease prevention and screening: obtaining information about flu shots and blood pressure maintenance;
  • Ability to access care and navigate the system: determining the most appropriate healthcare provider to call when a problem arises or filling out forms correctly; and
  • Routine care and maintenance: testing blood glucose and getting regular checkups.1

Health literacy is further complicated by the fact that it can fluctuate in the same individual at different times and under different circumstances. For example, you might have no trouble deciphering the sentence at the beginning of this article if you feel well and are reading it in your office, living room, study, or some other familiar and comfortable environment. Now imagine that you’re ill and sitting in a noisy, chaotic emergency department, with a sheaf of other forms and papers to plow through. Suddenly the statement above may not be as easy to interpret.

“We must leave behind the notion of ‘illiterates,’ ” says Lakshmi Halasyamani, MD, chair of the Hospital Quality and Patient Safety Committee for SHM. “A person may not normally have a literacy problem, but they may be overwhelmed by the medical terminology, or they simply may not feel well enough to comprehend immediately everything the doctor says to them.”

The changing nature of healthcare may exacerbate the problem. Thirty years ago, only 650 drugs were available, and the average hospital stay for a myocardial infarction was four to six weeks. Today, there are more than 10,000 prescription drugs alone, and the typical stay for a heart attack is two to four days. As healthcare grows increasingly fragmented and complex, doctors have less time than ever to explain things and answer questions for their patients. Nevertheless, patients are expected to shoulder an ever-greater portion of the responsibility for their care and to live with conditions like diabetes or congestive heart failure, which require aggressive and detailed management.5 This is a challenge for even the most highly educated person; for someone whose literacy skills are fragile, the task can seem hopeless.

 

 

In addition to its medical and emotional consequences, limited health literacy is estimated to cost U.S. society $50 to $73 billion per year.6

Ask Me 3

To address the problem of low health literacy in vulnerable populations, a coalition of 19 organizations and individuals, backed by several experts in health literacy, formed the nonprofit Partnership for Clear Health Communications in 2002. The partnership’s mission is to increase awareness of the problem among clinicians, and to offer solutions to patients and healthcare providers alike.

The cornerstone of the partnership’s efforts is the “Ask Me 3” campaign, consisting of nothing more than three simple questions that all patients should ask their doctors:

  • What is my main problem?
  • What do I need to do?
  • Why is it important for me to do this?

Brochures written in elementary English and Spanish about the campaign are available from the partnership free for distribution in office and hospital waiting rooms, seniors’ centers, and the like. Doctors are encouraged to adorn their office walls with “Ask Me 3” posters, also in an effort to encourage better physician-patient communication.

More information for patients and physicians is available on the partnership’s Web site: www.p4chc.org.—NM

Who Is Most Likely to Have Literacy Problems?

In general, “the likelihood of low literacy increases in racial and ethnic minority groups, patients with language barriers, and those with low educational achievement,” says Benjamin Powers, MD, associate professor of general internal medicine at Duke University and a physician at the Durham Veterans Affairs Medical Center in North Carolina.

It’s no surprise that literacy overall, and health literacy specifically, correlate so closely with education and especially with the lack of a high school degree. What is perhaps more surprising is that educational achievement alone does not necessarily guarantee good health literacy.

“Even high school graduates may have trouble,” says Mark Williams, MD. In addition to being a professor of medicine and director of the hospital medicine unit at Emory University School of Medicine in Atlanta, Dr. Williams is the editor of the Journal of Hospital Medicine and has studied health literacy problems for years. “Some highly literate people may have problems reading or absorbing health-related information if they’re sick and not feeling well.”

These people are not illiterate in the conventional sense, but they may have inadequate functional health literacy skills, at least in certain settings.

Age is another risk factor. In one survey of Medicare enrollees, at least one-third of people age 65 or older had some degree of health illiteracy, Dr. Williams says. As with so many other skills, proficient reading requires regular practice, and people tend to read less as they age, so their literacy skills may decline. “It’s especially a problem for the ‘oldest old,’ people who are 75 years old or more,” he explains.

Language and cultural differences also enter into the equation. A patient may be well educated and able to articulate in her own language (perhaps even able to converse well in English under normal circumstances), but may be unfamiliar with medical terminology. Put her in a situation in which she feels ill, flustered, and disoriented, and her communication skills may deteriorate even more, says Dr. Halasyamani.

In short, health literacy consists of many components, including “an emotional overlay, information overload, and cultural overload. All of these factor into the patients’ ability to understand what we tell them,” says Barbara DeBuono, MD, MPH, senior medical advisor on U.S. Public Health and Policy at Pfizer Pharmaceuticals.

Issues Unique to Hospitalists

There are also a few issues unique to hospitalists and their patients, warns Dr. DeBuono, who is also on the board of the Partnership for Clear Health Communication (See “Ask Me 3,” at right.) “Hospitalists don’t necessarily have a long-term relationship with these patients, so they have to make a quick assessment of the patient’s ability to understand and absorb information. Then they have to determine the best way to communicate that information, and, when necessary, change their communication strategy to fit the circumstances.”

 

 

In addition, she says, “hospital patients usually are more complicated than patients seen in an office practice. They may have chronic conditions and several comorbidities, and the information and discharge instructions the physicians give them can be pretty complex.”

Indeed, “a patient may come in thinking she had no issues and leave the hospital with four or five complaints. We’ve rocked her world, and that can be overwhelming for even the most motivated person,” says Dr. Halasyamani, who cautions that any chronic illness that requires a significant amount of ongoing self-care, such as diabetes or heart failure, can tax a patient’s ability to completely understand her situation and coordinate her care effectively.

Fragmented Care

Patients with multiple and complex morbidities also are likely to be cared for by several physicians, who prescribe numerous drugs, tests, and procedures, and who don’t necessarily know what the other members of the care team are doing. Even highly sophisticated people can get the feeling that they’re caught in an ever-changing kaleidoscope of medical visits and jargon, in which the various fragments never coalesce into a comprehensible whole. As Dr. Powers and coauthor Hayden Bosworth, PhD, wrote in a recent editorial: “ … there may be specific physician and health system organizational factors that exacerbate or mitigate the impact of low literacy. Literacy may matter more for patients who are cared for in a chaotic and discontinuous system that is not organized around delivering high quality care in a multidisciplinary setting.”7

This is more than a subjective impression: There is evidence supporting the importance of coordinated care for people of limited literacy skills. Dr. Powers and Bosworth recently compared the impact of low literacy on blood pressure control in patients in the Veterans Affairs (VA) system and those who attended local community clinics.

“Although the prevalence of low literacy was high in both populations, there was a significant association with low literacy and poor blood pressure control in the community clinics but not the VA,” Dr. Powers tells The Hospitalist. “In other words, literacy seemed to be an important predictor of good blood pressure control in one healthcare setting but not in another.”

In hospitals, “the frequency of handoffs among doctors, nurses, caseworkers, and social workers may all contribute to the fragmented nature of a patient’s care,” warns Dr. Halasyamani. This may be exacerbated even further should the patient have the misfortune to be admitted during a transitional period, such as a weekend or the end of the month when staff members rotate.

Red Flags

Literacy limitations are easy to miss: Patients rarely announce that they can’t read forms or comprehend a clinician’s instructions. “Just asking, ‘Do you understand?’ rarely works, because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively,” says Dr. Williams.

Usually, the clues are subtle. “Most physicians do encounter such patients, but we’re not trained to detect literacy problems and respond appropriately,” says Sunil Kripalani, MD, MSc, who, like Dr. Williams, is an Emory University hospitalist with a special interest in patient literacy issues. Dr. Kripalani suggests looking for red flags, including:

  • Vague or evasive answers to questions. For example, “the patient who is taking a host of medications but can’t name them or tell you what time of day he’s supposed to take them;”
  • Few, if any, questions or discussions of concerns: “Patients with limited literacy are less prone to ask questions, and the questions they do ask may not be as deep as those asked by a patient with greater literacy skills. The patient may use very simple terminology and not integrate any of the concepts discussed during the appointment;” and
  • Missed appointments and repeated crises and hospitalizations resulting from the patient’s inability to read appointment cards or manage his illness. “Limited literacy skills may be a contributor to the exacerbations that put the patient in the hospital,” says Dr. Kripalani.
 

 

A patient with few family or social connections is also cause for concern, adds Dr. Halasyamani: “Lack of social support means there’s not another set of eyes and ears taking in the information.” Yet another red flag to her is the patient who cannot describe his plans for pursuing his care at home.

When patients have their medications with them, Dr. Williams asks how they take them. Those who can read simply look at the label, but a patient with literacy problems must open the bottle and look at the pills to identify them.

Solutions

How can physicians ensure that these patients understand and can follow instructions? Perhaps the easiest and most effective way is the “teach-back” approach, in which you ask the patient to repeat or teach back to you what you’ve just explained to him. For example, you might have him show you how to use an asthma inhaler or how to measure his blood glucose. In this way, you can rapidly assess and correct any deficiencies in the patient’s understanding.

“I’ve seen it take less than 90 seconds for physicians to confirm patient understanding in the context of a clinical visit,” says Dr. Kripalani.

A related technique that might help save time is to resist the temptation to tell the patient too much in a single visit. “Don’t try to give the patient too much information,” he advises. “People can process and retain maybe three nuggets of information at a time, so tell the patient the three most important things and then confirm their understanding of those three things.”

Dr. DeBuono suggests using visual aids like pictures or cartoons to help get important points across. If written material is necessary, have it printed in large type, which might appear less daunting than a page covered in dense, tiny print.

Above all, never embarrass a patient by bluntly asking him if he can read. “Explore the issue sensitively and respectfully,” Dr. Williams says. “Ask if they ever struggle with written materials or what the best way is for them to learn.” Adds Dr. DeBuono, “just by being sensitive to the fact that the patient may not understand is half the game.” TH

Norra MacReady is a medical journalist based in Southern California.

*“There’s no use crying over spilt milk.”

References

  1. Rudd RE. Literacy and implications for navigating health care. Harvard School of Public Health: Health Literacy Website. Slide 20. 2002. Available at www.hsph.harvard.edu/healthliteracy/slides/2002/2002_01.html. Last accessed December 1, 2006.
  2. Schillinger D, Grumbach K, Piette J, et al. Association of health literacy with diabetes outcomes. JAMA. 2002 Jul 24;288(4):475-482.
  3. Paasche-Orlow MK, Schillinger D, Greene SM, et al. How health care systems can begin to address the challenge of limited literacy. J Gen Intern Med. 2006 Aug;21(8):884-887.
  4. Marcus EN. The silent epidemic—the health effects of illiteracy. N Engl J Med. 2006 Jul 27;355(4):339-341. Erratum in N Engl J Med. 2006 Sept 7;355(10):1076.
  5. Williams MV. Recognizing and overcoming inadequate health literacy, a barrier to care. Cleve Clin J Med. 2002 May;69(5):415-418.
  6. Weiss BD. Health literacy: a manual for clinicians [American Medical Association Web site]. American Medical Association Foundation and the American Medical Association, 2003. Available at: www.ama-assn.org/ama1/pub/upload/mm/367/healthlitclinicians.pdf. Last accessed December 16, 2006.
  7. Powers BJ, Bosworth HB. Revisiting literacy and adherence: future clinical and research directions. J Gen Intern Med. 2006;21:1341-1342.

Just asking, “Do you understand?” rarely works because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively.—Mark Williams, MD, professor of medicine and director of the hospital medicine unit at Emory University School of Medicine, Atlanta.

Translate the following statement into plain English:*

“It is fruitless to become lachrymose over precipitately departed lacteal fluid.”1

If these words made you pause—even for a moment—you now have an inkling of what people of limited literacy confront when they deal with the healthcare system.

Health literacy is best defined as a patient’s ability to read, comprehend, and act on medical instructions and to make appropriate health-related decisions.2,3 It is closely related to, although not absolutely dependent upon, one’s overall level of literacy—and literacy problems are surprisingly widespread. According to the National Assessment of Adult Literacy (NAAL), a survey of more than 19,000 adults conducted in 2003 by the National Center for Educational Statistics and published in 2006, 36% of American adults have nothing more than basic or below basic literacy. People in these two categories might be able to sign their names, decipher a bus schedule, or read very simple instructions telling them what they can and cannot eat before a medical test, but they cannot read a juror information pamphlet, much less an informed consent form. Another recent survey suggested that about one-third of adults in public hospitals read at or below a sixth-grade level.4

Components of Health Literacy

Several components figure into a person’s ability to manage his health and engage the healthcare system. Literacy limitations can impair any or all of these factors, which include:

  • Health promotion: reading and understanding product labels or articles in newspapers;
  • Health protection: reading and understanding applications for insurance or following sanitary precautions in the workplace;
  • Disease prevention and screening: obtaining information about flu shots and blood pressure maintenance;
  • Ability to access care and navigate the system: determining the most appropriate healthcare provider to call when a problem arises or filling out forms correctly; and
  • Routine care and maintenance: testing blood glucose and getting regular checkups.1

Health literacy is further complicated by the fact that it can fluctuate in the same individual at different times and under different circumstances. For example, you might have no trouble deciphering the sentence at the beginning of this article if you feel well and are reading it in your office, living room, study, or some other familiar and comfortable environment. Now imagine that you’re ill and sitting in a noisy, chaotic emergency department, with a sheaf of other forms and papers to plow through. Suddenly the statement above may not be as easy to interpret.

“We must leave behind the notion of ‘illiterates,’ ” says Lakshmi Halasyamani, MD, chair of the Hospital Quality and Patient Safety Committee for SHM. “A person may not normally have a literacy problem, but they may be overwhelmed by the medical terminology, or they simply may not feel well enough to comprehend immediately everything the doctor says to them.”

The changing nature of healthcare may exacerbate the problem. Thirty years ago, only 650 drugs were available, and the average hospital stay for a myocardial infarction was four to six weeks. Today, there are more than 10,000 prescription drugs alone, and the typical stay for a heart attack is two to four days. As healthcare grows increasingly fragmented and complex, doctors have less time than ever to explain things and answer questions for their patients. Nevertheless, patients are expected to shoulder an ever-greater portion of the responsibility for their care and to live with conditions like diabetes or congestive heart failure, which require aggressive and detailed management.5 This is a challenge for even the most highly educated person; for someone whose literacy skills are fragile, the task can seem hopeless.

 

 

In addition to its medical and emotional consequences, limited health literacy is estimated to cost U.S. society $50 to $73 billion per year.6

Ask Me 3

To address the problem of low health literacy in vulnerable populations, a coalition of 19 organizations and individuals, backed by several experts in health literacy, formed the nonprofit Partnership for Clear Health Communications in 2002. The partnership’s mission is to increase awareness of the problem among clinicians, and to offer solutions to patients and healthcare providers alike.

The cornerstone of the partnership’s efforts is the “Ask Me 3” campaign, consisting of nothing more than three simple questions that all patients should ask their doctors:

  • What is my main problem?
  • What do I need to do?
  • Why is it important for me to do this?

Brochures written in elementary English and Spanish about the campaign are available from the partnership free for distribution in office and hospital waiting rooms, seniors’ centers, and the like. Doctors are encouraged to adorn their office walls with “Ask Me 3” posters, also in an effort to encourage better physician-patient communication.

More information for patients and physicians is available on the partnership’s Web site: www.p4chc.org.—NM

Who Is Most Likely to Have Literacy Problems?

In general, “the likelihood of low literacy increases in racial and ethnic minority groups, patients with language barriers, and those with low educational achievement,” says Benjamin Powers, MD, associate professor of general internal medicine at Duke University and a physician at the Durham Veterans Affairs Medical Center in North Carolina.

It’s no surprise that literacy overall, and health literacy specifically, correlate so closely with education and especially with the lack of a high school degree. What is perhaps more surprising is that educational achievement alone does not necessarily guarantee good health literacy.

“Even high school graduates may have trouble,” says Mark Williams, MD. In addition to being a professor of medicine and director of the hospital medicine unit at Emory University School of Medicine in Atlanta, Dr. Williams is the editor of the Journal of Hospital Medicine and has studied health literacy problems for years. “Some highly literate people may have problems reading or absorbing health-related information if they’re sick and not feeling well.”

These people are not illiterate in the conventional sense, but they may have inadequate functional health literacy skills, at least in certain settings.

Age is another risk factor. In one survey of Medicare enrollees, at least one-third of people age 65 or older had some degree of health illiteracy, Dr. Williams says. As with so many other skills, proficient reading requires regular practice, and people tend to read less as they age, so their literacy skills may decline. “It’s especially a problem for the ‘oldest old,’ people who are 75 years old or more,” he explains.

Language and cultural differences also enter into the equation. A patient may be well educated and able to articulate in her own language (perhaps even able to converse well in English under normal circumstances), but may be unfamiliar with medical terminology. Put her in a situation in which she feels ill, flustered, and disoriented, and her communication skills may deteriorate even more, says Dr. Halasyamani.

In short, health literacy consists of many components, including “an emotional overlay, information overload, and cultural overload. All of these factor into the patients’ ability to understand what we tell them,” says Barbara DeBuono, MD, MPH, senior medical advisor on U.S. Public Health and Policy at Pfizer Pharmaceuticals.

Issues Unique to Hospitalists

There are also a few issues unique to hospitalists and their patients, warns Dr. DeBuono, who is also on the board of the Partnership for Clear Health Communication (See “Ask Me 3,” at right.) “Hospitalists don’t necessarily have a long-term relationship with these patients, so they have to make a quick assessment of the patient’s ability to understand and absorb information. Then they have to determine the best way to communicate that information, and, when necessary, change their communication strategy to fit the circumstances.”

 

 

In addition, she says, “hospital patients usually are more complicated than patients seen in an office practice. They may have chronic conditions and several comorbidities, and the information and discharge instructions the physicians give them can be pretty complex.”

Indeed, “a patient may come in thinking she had no issues and leave the hospital with four or five complaints. We’ve rocked her world, and that can be overwhelming for even the most motivated person,” says Dr. Halasyamani, who cautions that any chronic illness that requires a significant amount of ongoing self-care, such as diabetes or heart failure, can tax a patient’s ability to completely understand her situation and coordinate her care effectively.

Fragmented Care

Patients with multiple and complex morbidities also are likely to be cared for by several physicians, who prescribe numerous drugs, tests, and procedures, and who don’t necessarily know what the other members of the care team are doing. Even highly sophisticated people can get the feeling that they’re caught in an ever-changing kaleidoscope of medical visits and jargon, in which the various fragments never coalesce into a comprehensible whole. As Dr. Powers and coauthor Hayden Bosworth, PhD, wrote in a recent editorial: “ … there may be specific physician and health system organizational factors that exacerbate or mitigate the impact of low literacy. Literacy may matter more for patients who are cared for in a chaotic and discontinuous system that is not organized around delivering high quality care in a multidisciplinary setting.”7

This is more than a subjective impression: There is evidence supporting the importance of coordinated care for people of limited literacy skills. Dr. Powers and Bosworth recently compared the impact of low literacy on blood pressure control in patients in the Veterans Affairs (VA) system and those who attended local community clinics.

“Although the prevalence of low literacy was high in both populations, there was a significant association with low literacy and poor blood pressure control in the community clinics but not the VA,” Dr. Powers tells The Hospitalist. “In other words, literacy seemed to be an important predictor of good blood pressure control in one healthcare setting but not in another.”

In hospitals, “the frequency of handoffs among doctors, nurses, caseworkers, and social workers may all contribute to the fragmented nature of a patient’s care,” warns Dr. Halasyamani. This may be exacerbated even further should the patient have the misfortune to be admitted during a transitional period, such as a weekend or the end of the month when staff members rotate.

Red Flags

Literacy limitations are easy to miss: Patients rarely announce that they can’t read forms or comprehend a clinician’s instructions. “Just asking, ‘Do you understand?’ rarely works, because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively,” says Dr. Williams.

Usually, the clues are subtle. “Most physicians do encounter such patients, but we’re not trained to detect literacy problems and respond appropriately,” says Sunil Kripalani, MD, MSc, who, like Dr. Williams, is an Emory University hospitalist with a special interest in patient literacy issues. Dr. Kripalani suggests looking for red flags, including:

  • Vague or evasive answers to questions. For example, “the patient who is taking a host of medications but can’t name them or tell you what time of day he’s supposed to take them;”
  • Few, if any, questions or discussions of concerns: “Patients with limited literacy are less prone to ask questions, and the questions they do ask may not be as deep as those asked by a patient with greater literacy skills. The patient may use very simple terminology and not integrate any of the concepts discussed during the appointment;” and
  • Missed appointments and repeated crises and hospitalizations resulting from the patient’s inability to read appointment cards or manage his illness. “Limited literacy skills may be a contributor to the exacerbations that put the patient in the hospital,” says Dr. Kripalani.
 

 

A patient with few family or social connections is also cause for concern, adds Dr. Halasyamani: “Lack of social support means there’s not another set of eyes and ears taking in the information.” Yet another red flag to her is the patient who cannot describe his plans for pursuing his care at home.

When patients have their medications with them, Dr. Williams asks how they take them. Those who can read simply look at the label, but a patient with literacy problems must open the bottle and look at the pills to identify them.

Solutions

How can physicians ensure that these patients understand and can follow instructions? Perhaps the easiest and most effective way is the “teach-back” approach, in which you ask the patient to repeat or teach back to you what you’ve just explained to him. For example, you might have him show you how to use an asthma inhaler or how to measure his blood glucose. In this way, you can rapidly assess and correct any deficiencies in the patient’s understanding.

“I’ve seen it take less than 90 seconds for physicians to confirm patient understanding in the context of a clinical visit,” says Dr. Kripalani.

A related technique that might help save time is to resist the temptation to tell the patient too much in a single visit. “Don’t try to give the patient too much information,” he advises. “People can process and retain maybe three nuggets of information at a time, so tell the patient the three most important things and then confirm their understanding of those three things.”

Dr. DeBuono suggests using visual aids like pictures or cartoons to help get important points across. If written material is necessary, have it printed in large type, which might appear less daunting than a page covered in dense, tiny print.

Above all, never embarrass a patient by bluntly asking him if he can read. “Explore the issue sensitively and respectfully,” Dr. Williams says. “Ask if they ever struggle with written materials or what the best way is for them to learn.” Adds Dr. DeBuono, “just by being sensitive to the fact that the patient may not understand is half the game.” TH

Norra MacReady is a medical journalist based in Southern California.

*“There’s no use crying over spilt milk.”

References

  1. Rudd RE. Literacy and implications for navigating health care. Harvard School of Public Health: Health Literacy Website. Slide 20. 2002. Available at www.hsph.harvard.edu/healthliteracy/slides/2002/2002_01.html. Last accessed December 1, 2006.
  2. Schillinger D, Grumbach K, Piette J, et al. Association of health literacy with diabetes outcomes. JAMA. 2002 Jul 24;288(4):475-482.
  3. Paasche-Orlow MK, Schillinger D, Greene SM, et al. How health care systems can begin to address the challenge of limited literacy. J Gen Intern Med. 2006 Aug;21(8):884-887.
  4. Marcus EN. The silent epidemic—the health effects of illiteracy. N Engl J Med. 2006 Jul 27;355(4):339-341. Erratum in N Engl J Med. 2006 Sept 7;355(10):1076.
  5. Williams MV. Recognizing and overcoming inadequate health literacy, a barrier to care. Cleve Clin J Med. 2002 May;69(5):415-418.
  6. Weiss BD. Health literacy: a manual for clinicians [American Medical Association Web site]. American Medical Association Foundation and the American Medical Association, 2003. Available at: www.ama-assn.org/ama1/pub/upload/mm/367/healthlitclinicians.pdf. Last accessed December 16, 2006.
  7. Powers BJ, Bosworth HB. Revisiting literacy and adherence: future clinical and research directions. J Gen Intern Med. 2006;21:1341-1342.

Just asking, “Do you understand?” rarely works because the patient may just nod yes. Physicians need to assess the patient’s comprehension proactively.—Mark Williams, MD, professor of medicine and director of the hospital medicine unit at Emory University School of Medicine, Atlanta.

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In YOU: The Smart Patient: An Insider's Handbook for Getting the Best Treatment, authors Michael F. Roizen, MD, and Mehmet C. Oz, MD, well-credentialed celebrity physicians, tell the reader that being a smart patient may make the difference between good and poor care and may even save your life. Everyone can be a “medical detective,” they suggest, seeking and supplying the facts that providers and administrators need in order to avoid errors or mix-ups.

The Joint Commission Resources, a collaborator on this publication, announces on its Web site that this book “empowers patients” (www.jcrinc.com/generic.asp?durki=11727&site=11&return=405.). Dr. Oz, in a Web post to customers who might purchase the book, puts it this way: “[T]he Joint Commission, our nation’s healthcare safety advocate, approached us to help with a big problem. Medical errors cost us 98,000 lives per year, and the Joint Commission could not squash this crazily large number without pulling in the biggest ally of all, the Smart Patient.” It’s a “scary statistic,” but true, he writes, “You have a two in five chance of being affected by a major medical complication in your life.” (For more information on the book, visit www.amazon.com/YOU-Insiders-Handbook-Getting-Treatment/dp/0743293010.)

The Hospitalist asked some hospitalists what they would recommend to a friend or relative headed for a hospital stay. Do they have any tips that only an insider would know? As might be expected, some of their advice echoes that already available in print, in broadcasts, and on the Web. And some things that were mentioned in these publications were also on our hospitalists’ list, including bringing along statistics, dates, and other healthcare specifics that might be crucial to providers. In fact, Drs. Roizen and Oz recommend assembling a thorough health history and bringing two copies of it to hospital admission—one especially for “the admitting nurse who welcomes you to your bed.”

Assume Nothing

In their book chapter on hospital stays, Drs. Oz and Roizen emphasize that patients and their visitors should keep an eye out to make certain hospital staff wash their hands and give the patient the right treatments, tests, and medications. “It’s astounding the amount of diligence you and your family will have to exercise during a hospital stay,” a reader-reviewer writes on the book’s Web page on the Amazon.com site. Some of the warnings posted in a book excerpt at the Joint Commission on Accreditation of Healthcare Organizations (JCAHO)’s site include “Don’t touch that remote!” and “wear rubber gloves” if you do want to watch TV. Readers are told that “a study found that the TV remote control is one of the most germ-infested things in a hospital room.”

Patients are also cautioned to “insist on being scanned,” to “insist on a clean stethoscope,” and to keep “an industrial-sized jug of alcohol hand-sanitizing gel” by the bed. In fact, the authors write: “Stethoscopes are filthy from being used on several patients an hour. Most doc[tor]s now wash their stethoscopes with alcohol between patients, but we’d always ask.” Our hospitalists agreed.

Ian Jenkins, MD, a hospitalist with the University of California at San Diego, would tell his friends and family to remind providers to wash their hands. “Don’t let anyone touch you unless you’ve seen them wash or gel their hands correctly—and their stethoscopes, too.”

Drs. Oz and Roizen say, “You might even post a sign that reads ‘Thank You for Washing Your Hands’ as a gentle reminder.”

Trust your intuition, one hospitalist tells people facing hospitalization. “If you sense that something is awry, it probably is,” says Jeanne Farnan, MD, a hospitalist scholar at The University of Chicago Hospitals. “Discuss concerns with physicians/nurses. Write down your questions in case they come to you spontaneously.”

 

 

On the other hand, she tells friends and relatives, “Patients, when asked questions, will often respond, ‘it’s in my chart.’ We often don't have access to a primary MD’s notes/chart, and not all documentation is pristine. When we are asking questions regarding your medical history, it is only to provide you with the best care—not to be a nuisance.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital … someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?

Be Selective about Your Providers and Hospital

One recommendation from JCAHO’s patient education Web pages is a section entitled “Finding Dr. Right.” “Choose wisely and you could rest easy for many years to come,” it says.

Sandeep Sachdeva, MD, lead hospitalist at Swedish Medical Center’s Stroke Program and clinical instructor at the University of Washington at Seattle, says this may apply even to a patient’s relationship with a hospitalist.

“Sometimes patients come in and tell us their stories [about how providers treat them]. It’s just amazing; I think patients who have family members providing close supervision seem to get better care than somebody [who] is not asking questions,” he says. “And some care providers find questions intimidating, but the patient should not get discouraged by that. … If they feel that the care provider is not listening to them or not being attentive to them, they can always have a recourse: They can talk to the supervisor of that provider or somebody else [to get] a different provider. Patients sometimes have the fear that if they speak up against somebody that their care might be jeopardized.”

Dr. Sachdeva advises friends and relatives that they talk to the nursing supervisor or ask for the physician supervisor or an administrative person or social worker so that they get the attention they need.

Dr. Jenkins agrees. “Informed consent” is one of his tips for friends and family: “If your doctor won't talk to you about the risks and benefits of your treatments, and alternatives to them, you need a new doctor.”

Our hospitalists suggest being discriminating, savvy, and proactive:

  • “Find one hospital you are comfortable with, [where] your family physician is on staff, and use it exclusively if possible,” says David M. Grace, MD, a hospitalist with The Schumacher Group in Lafayette, La. “By utilizing one hospital, all of your previous records and test results are immediately available when needed. Often this translates into a much shorter hospitalization as there are no delays in obtaining old records, and it minimizes the chance of duplicate tests/procedures being performed.”
  • “Know who your doctors are [and] what their role is, and understand their input into your healthcare,” says Dr. Farnan, who is extensively involved in medical residents’ training. And “be cognizant of the physician work hours,” she advises. “We often have families who demand to speak with ‘their’ doctor at all hours of the early morning and night.” She tells friends and relatives, “I think more patients need to understand the nature [and] structure of the system [and] what kind of information a covering physician can provide. If the family of the patient has questions [and] wants to speak with the primary MD, it may be best to attempt in the daytime when the primary service is more likely to be present.”
  • “Know the full names, and preferably [the] phone numbers, of all your outpatient physicians,” says Dr. Grace. “One area will often have multiple doctors with the same last name, and, frequently, records need to be requested from them. Up-to-date contact information on your physicians helps us request the right records from the right physicians with minimal delay.”
 

 

What to Bring to the Hospital

Some hospital Web sites advise patients on what to bring with them for their hospital stay, suggesting everything from your own robe, slippers, pajamas, or nightgown to an advance directive. Definitely, the latter is an important point.

“Whether it’s an elective or emergent admission,” says Dr. Grace, “there are a few things [you] can do to ensure [your] hospitalization is as safe, efficient, and productive as possible,” he tells friends and relatives. Among them, he says, is to “have a Living Will or advance directives completed, ensure the hospital has a copy, and discuss your wishes with your family prior to admission. Clear and concise plans, coupled with good family awareness, will help ensure your wishes and values are honored appropriately.”

And, as several of his hospitalist colleagues suggest, “Bring all of the medications you are currently using, including any over-the-counter medicines and herbs or homeopathic treatments. It’s imperative that physicians know what medications you are taking [because] many cannot be stopped abruptly, and [they may] have interactions with medications you may receive in the hospital.”

In addition, “know what medications you’re truly allergic to [e.g., hives, swelling, breathing problems],” Dr. Grace advises, “and which medications you have had side effects from [e.g., stomach upset, sleepiness, and so on]. Many patients confuse the two. Occasionally the best or only option involves using medications with potential unwanted side effects. Rarely do we use medications to which the patient has a true allergy.”

Communication: The Key to the Hospital Kingdom

Dr. Sachdeva recommends being ready to communicate even before going to the hospital. “In the case of an emergency admission,” he says, “they should have all their information readily available because at the time for a needed hospitalization, they may be sick and confused.” Have it “on their person” or in “an easily identifiable place,” he says, and, like his colleagues, he reiterates that this information should include a list of medications, problems, doctors, and phone numbers, along with a list of patient advocates and their phone numbers.

“Most of the time, patients are able to notify a family member, but if that doesn’t happen, then the ER can notify the appropriate person to be present to supervise and oversee the care from a patient perspective,” he says.

Communication was mentioned by all the hospitalists we interviewed. “Be prepared to ask questions and take an active role in your healthcare,” says Dr. Grace. “Ask your nurse what each medication you receive is and what it’s for. Ensure you know what medications to continue taking when you return home and which ones to stop. If you don’t understand your diagnosis, prognosis, or treatment plan, make sure you ask.”

One hospitalist’s advice pertained to the patient’s and family’s behavior and is based on an experience in her own family: “Be really nice to everybody,” Alison Holmes, MD, a hospitalist with Concord Hospital, Concord, N.H., advises friends and family. “This is hard to do when you’re sick and scared, but it’s incredibly important.”

Dr. Holmes speaks of her own parents’ experience: “My mother was admitted to the hospital for pneumonia about a year ago. She had very long wait in the emergency room. My father got very upset and called me and said, ‘Oh, they were so angry at me, I was yelling at everybody.’

“That won’t get you anywhere!” I told him. “That will get you worse care.” I asked, “Where is she now?” and he said, ‘Oh, she’s still in the emergency room,’ and I said, “You’re at home? You left her there?” Dr. Holmes then advised her father to return to the hospital right away.

 

 

Finally, all the hospitalists we interviewed emphasized that they would tell their family members to designate a point person for communication. And you can’t assume that that would be their doctor son or daughter, even if they happened to be in the same locale.

“When possible, don’t stay in the hospital alone,” says Dr. Holmes. “Try to always have a family member present so that there is someone available for questions. It’s not always clear where [the physician] can reach someone or how far away [that person is]. It can take a little coordination and multiple people to do it,” she says.

Also, Dr. Farnan points out, “It is often difficult [because of time limitations] for [physicians] to repeat the same information to multiple family members.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital. If they don’t have family close by, they should have “a close friend or neighbor who is willing to take on that job, someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?”

Dr. Sachdeva advises relatives that they might be distressed or unable to focus, so having a healthy advocate with them may be extremely important, “the difference between life and death,” although, no doubt, he’d leave that last comment out of his advice to family. “Because a lot of the time, it is not that we don’t try to do a good job, but it’s just [that] the advocate might bring something to our attention that we might not have otherwise noticed.” TH

Andrea Sattinger has been writing for The Hospitalist since 2005.

Issue
The Hospitalist - 2007(02)
Publications
Sections

In YOU: The Smart Patient: An Insider's Handbook for Getting the Best Treatment, authors Michael F. Roizen, MD, and Mehmet C. Oz, MD, well-credentialed celebrity physicians, tell the reader that being a smart patient may make the difference between good and poor care and may even save your life. Everyone can be a “medical detective,” they suggest, seeking and supplying the facts that providers and administrators need in order to avoid errors or mix-ups.

The Joint Commission Resources, a collaborator on this publication, announces on its Web site that this book “empowers patients” (www.jcrinc.com/generic.asp?durki=11727&site=11&return=405.). Dr. Oz, in a Web post to customers who might purchase the book, puts it this way: “[T]he Joint Commission, our nation’s healthcare safety advocate, approached us to help with a big problem. Medical errors cost us 98,000 lives per year, and the Joint Commission could not squash this crazily large number without pulling in the biggest ally of all, the Smart Patient.” It’s a “scary statistic,” but true, he writes, “You have a two in five chance of being affected by a major medical complication in your life.” (For more information on the book, visit www.amazon.com/YOU-Insiders-Handbook-Getting-Treatment/dp/0743293010.)

The Hospitalist asked some hospitalists what they would recommend to a friend or relative headed for a hospital stay. Do they have any tips that only an insider would know? As might be expected, some of their advice echoes that already available in print, in broadcasts, and on the Web. And some things that were mentioned in these publications were also on our hospitalists’ list, including bringing along statistics, dates, and other healthcare specifics that might be crucial to providers. In fact, Drs. Roizen and Oz recommend assembling a thorough health history and bringing two copies of it to hospital admission—one especially for “the admitting nurse who welcomes you to your bed.”

Assume Nothing

In their book chapter on hospital stays, Drs. Oz and Roizen emphasize that patients and their visitors should keep an eye out to make certain hospital staff wash their hands and give the patient the right treatments, tests, and medications. “It’s astounding the amount of diligence you and your family will have to exercise during a hospital stay,” a reader-reviewer writes on the book’s Web page on the Amazon.com site. Some of the warnings posted in a book excerpt at the Joint Commission on Accreditation of Healthcare Organizations (JCAHO)’s site include “Don’t touch that remote!” and “wear rubber gloves” if you do want to watch TV. Readers are told that “a study found that the TV remote control is one of the most germ-infested things in a hospital room.”

Patients are also cautioned to “insist on being scanned,” to “insist on a clean stethoscope,” and to keep “an industrial-sized jug of alcohol hand-sanitizing gel” by the bed. In fact, the authors write: “Stethoscopes are filthy from being used on several patients an hour. Most doc[tor]s now wash their stethoscopes with alcohol between patients, but we’d always ask.” Our hospitalists agreed.

Ian Jenkins, MD, a hospitalist with the University of California at San Diego, would tell his friends and family to remind providers to wash their hands. “Don’t let anyone touch you unless you’ve seen them wash or gel their hands correctly—and their stethoscopes, too.”

Drs. Oz and Roizen say, “You might even post a sign that reads ‘Thank You for Washing Your Hands’ as a gentle reminder.”

Trust your intuition, one hospitalist tells people facing hospitalization. “If you sense that something is awry, it probably is,” says Jeanne Farnan, MD, a hospitalist scholar at The University of Chicago Hospitals. “Discuss concerns with physicians/nurses. Write down your questions in case they come to you spontaneously.”

 

 

On the other hand, she tells friends and relatives, “Patients, when asked questions, will often respond, ‘it’s in my chart.’ We often don't have access to a primary MD’s notes/chart, and not all documentation is pristine. When we are asking questions regarding your medical history, it is only to provide you with the best care—not to be a nuisance.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital … someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?

Be Selective about Your Providers and Hospital

One recommendation from JCAHO’s patient education Web pages is a section entitled “Finding Dr. Right.” “Choose wisely and you could rest easy for many years to come,” it says.

Sandeep Sachdeva, MD, lead hospitalist at Swedish Medical Center’s Stroke Program and clinical instructor at the University of Washington at Seattle, says this may apply even to a patient’s relationship with a hospitalist.

“Sometimes patients come in and tell us their stories [about how providers treat them]. It’s just amazing; I think patients who have family members providing close supervision seem to get better care than somebody [who] is not asking questions,” he says. “And some care providers find questions intimidating, but the patient should not get discouraged by that. … If they feel that the care provider is not listening to them or not being attentive to them, they can always have a recourse: They can talk to the supervisor of that provider or somebody else [to get] a different provider. Patients sometimes have the fear that if they speak up against somebody that their care might be jeopardized.”

Dr. Sachdeva advises friends and relatives that they talk to the nursing supervisor or ask for the physician supervisor or an administrative person or social worker so that they get the attention they need.

Dr. Jenkins agrees. “Informed consent” is one of his tips for friends and family: “If your doctor won't talk to you about the risks and benefits of your treatments, and alternatives to them, you need a new doctor.”

Our hospitalists suggest being discriminating, savvy, and proactive:

  • “Find one hospital you are comfortable with, [where] your family physician is on staff, and use it exclusively if possible,” says David M. Grace, MD, a hospitalist with The Schumacher Group in Lafayette, La. “By utilizing one hospital, all of your previous records and test results are immediately available when needed. Often this translates into a much shorter hospitalization as there are no delays in obtaining old records, and it minimizes the chance of duplicate tests/procedures being performed.”
  • “Know who your doctors are [and] what their role is, and understand their input into your healthcare,” says Dr. Farnan, who is extensively involved in medical residents’ training. And “be cognizant of the physician work hours,” she advises. “We often have families who demand to speak with ‘their’ doctor at all hours of the early morning and night.” She tells friends and relatives, “I think more patients need to understand the nature [and] structure of the system [and] what kind of information a covering physician can provide. If the family of the patient has questions [and] wants to speak with the primary MD, it may be best to attempt in the daytime when the primary service is more likely to be present.”
  • “Know the full names, and preferably [the] phone numbers, of all your outpatient physicians,” says Dr. Grace. “One area will often have multiple doctors with the same last name, and, frequently, records need to be requested from them. Up-to-date contact information on your physicians helps us request the right records from the right physicians with minimal delay.”
 

 

What to Bring to the Hospital

Some hospital Web sites advise patients on what to bring with them for their hospital stay, suggesting everything from your own robe, slippers, pajamas, or nightgown to an advance directive. Definitely, the latter is an important point.

“Whether it’s an elective or emergent admission,” says Dr. Grace, “there are a few things [you] can do to ensure [your] hospitalization is as safe, efficient, and productive as possible,” he tells friends and relatives. Among them, he says, is to “have a Living Will or advance directives completed, ensure the hospital has a copy, and discuss your wishes with your family prior to admission. Clear and concise plans, coupled with good family awareness, will help ensure your wishes and values are honored appropriately.”

And, as several of his hospitalist colleagues suggest, “Bring all of the medications you are currently using, including any over-the-counter medicines and herbs or homeopathic treatments. It’s imperative that physicians know what medications you are taking [because] many cannot be stopped abruptly, and [they may] have interactions with medications you may receive in the hospital.”

In addition, “know what medications you’re truly allergic to [e.g., hives, swelling, breathing problems],” Dr. Grace advises, “and which medications you have had side effects from [e.g., stomach upset, sleepiness, and so on]. Many patients confuse the two. Occasionally the best or only option involves using medications with potential unwanted side effects. Rarely do we use medications to which the patient has a true allergy.”

Communication: The Key to the Hospital Kingdom

Dr. Sachdeva recommends being ready to communicate even before going to the hospital. “In the case of an emergency admission,” he says, “they should have all their information readily available because at the time for a needed hospitalization, they may be sick and confused.” Have it “on their person” or in “an easily identifiable place,” he says, and, like his colleagues, he reiterates that this information should include a list of medications, problems, doctors, and phone numbers, along with a list of patient advocates and their phone numbers.

“Most of the time, patients are able to notify a family member, but if that doesn’t happen, then the ER can notify the appropriate person to be present to supervise and oversee the care from a patient perspective,” he says.

Communication was mentioned by all the hospitalists we interviewed. “Be prepared to ask questions and take an active role in your healthcare,” says Dr. Grace. “Ask your nurse what each medication you receive is and what it’s for. Ensure you know what medications to continue taking when you return home and which ones to stop. If you don’t understand your diagnosis, prognosis, or treatment plan, make sure you ask.”

One hospitalist’s advice pertained to the patient’s and family’s behavior and is based on an experience in her own family: “Be really nice to everybody,” Alison Holmes, MD, a hospitalist with Concord Hospital, Concord, N.H., advises friends and family. “This is hard to do when you’re sick and scared, but it’s incredibly important.”

Dr. Holmes speaks of her own parents’ experience: “My mother was admitted to the hospital for pneumonia about a year ago. She had very long wait in the emergency room. My father got very upset and called me and said, ‘Oh, they were so angry at me, I was yelling at everybody.’

“That won’t get you anywhere!” I told him. “That will get you worse care.” I asked, “Where is she now?” and he said, ‘Oh, she’s still in the emergency room,’ and I said, “You’re at home? You left her there?” Dr. Holmes then advised her father to return to the hospital right away.

 

 

Finally, all the hospitalists we interviewed emphasized that they would tell their family members to designate a point person for communication. And you can’t assume that that would be their doctor son or daughter, even if they happened to be in the same locale.

“When possible, don’t stay in the hospital alone,” says Dr. Holmes. “Try to always have a family member present so that there is someone available for questions. It’s not always clear where [the physician] can reach someone or how far away [that person is]. It can take a little coordination and multiple people to do it,” she says.

Also, Dr. Farnan points out, “It is often difficult [because of time limitations] for [physicians] to repeat the same information to multiple family members.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital. If they don’t have family close by, they should have “a close friend or neighbor who is willing to take on that job, someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?”

Dr. Sachdeva advises relatives that they might be distressed or unable to focus, so having a healthy advocate with them may be extremely important, “the difference between life and death,” although, no doubt, he’d leave that last comment out of his advice to family. “Because a lot of the time, it is not that we don’t try to do a good job, but it’s just [that] the advocate might bring something to our attention that we might not have otherwise noticed.” TH

Andrea Sattinger has been writing for The Hospitalist since 2005.

In YOU: The Smart Patient: An Insider's Handbook for Getting the Best Treatment, authors Michael F. Roizen, MD, and Mehmet C. Oz, MD, well-credentialed celebrity physicians, tell the reader that being a smart patient may make the difference between good and poor care and may even save your life. Everyone can be a “medical detective,” they suggest, seeking and supplying the facts that providers and administrators need in order to avoid errors or mix-ups.

The Joint Commission Resources, a collaborator on this publication, announces on its Web site that this book “empowers patients” (www.jcrinc.com/generic.asp?durki=11727&site=11&return=405.). Dr. Oz, in a Web post to customers who might purchase the book, puts it this way: “[T]he Joint Commission, our nation’s healthcare safety advocate, approached us to help with a big problem. Medical errors cost us 98,000 lives per year, and the Joint Commission could not squash this crazily large number without pulling in the biggest ally of all, the Smart Patient.” It’s a “scary statistic,” but true, he writes, “You have a two in five chance of being affected by a major medical complication in your life.” (For more information on the book, visit www.amazon.com/YOU-Insiders-Handbook-Getting-Treatment/dp/0743293010.)

The Hospitalist asked some hospitalists what they would recommend to a friend or relative headed for a hospital stay. Do they have any tips that only an insider would know? As might be expected, some of their advice echoes that already available in print, in broadcasts, and on the Web. And some things that were mentioned in these publications were also on our hospitalists’ list, including bringing along statistics, dates, and other healthcare specifics that might be crucial to providers. In fact, Drs. Roizen and Oz recommend assembling a thorough health history and bringing two copies of it to hospital admission—one especially for “the admitting nurse who welcomes you to your bed.”

Assume Nothing

In their book chapter on hospital stays, Drs. Oz and Roizen emphasize that patients and their visitors should keep an eye out to make certain hospital staff wash their hands and give the patient the right treatments, tests, and medications. “It’s astounding the amount of diligence you and your family will have to exercise during a hospital stay,” a reader-reviewer writes on the book’s Web page on the Amazon.com site. Some of the warnings posted in a book excerpt at the Joint Commission on Accreditation of Healthcare Organizations (JCAHO)’s site include “Don’t touch that remote!” and “wear rubber gloves” if you do want to watch TV. Readers are told that “a study found that the TV remote control is one of the most germ-infested things in a hospital room.”

Patients are also cautioned to “insist on being scanned,” to “insist on a clean stethoscope,” and to keep “an industrial-sized jug of alcohol hand-sanitizing gel” by the bed. In fact, the authors write: “Stethoscopes are filthy from being used on several patients an hour. Most doc[tor]s now wash their stethoscopes with alcohol between patients, but we’d always ask.” Our hospitalists agreed.

Ian Jenkins, MD, a hospitalist with the University of California at San Diego, would tell his friends and family to remind providers to wash their hands. “Don’t let anyone touch you unless you’ve seen them wash or gel their hands correctly—and their stethoscopes, too.”

Drs. Oz and Roizen say, “You might even post a sign that reads ‘Thank You for Washing Your Hands’ as a gentle reminder.”

Trust your intuition, one hospitalist tells people facing hospitalization. “If you sense that something is awry, it probably is,” says Jeanne Farnan, MD, a hospitalist scholar at The University of Chicago Hospitals. “Discuss concerns with physicians/nurses. Write down your questions in case they come to you spontaneously.”

 

 

On the other hand, she tells friends and relatives, “Patients, when asked questions, will often respond, ‘it’s in my chart.’ We often don't have access to a primary MD’s notes/chart, and not all documentation is pristine. When we are asking questions regarding your medical history, it is only to provide you with the best care—not to be a nuisance.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital … someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?

Be Selective about Your Providers and Hospital

One recommendation from JCAHO’s patient education Web pages is a section entitled “Finding Dr. Right.” “Choose wisely and you could rest easy for many years to come,” it says.

Sandeep Sachdeva, MD, lead hospitalist at Swedish Medical Center’s Stroke Program and clinical instructor at the University of Washington at Seattle, says this may apply even to a patient’s relationship with a hospitalist.

“Sometimes patients come in and tell us their stories [about how providers treat them]. It’s just amazing; I think patients who have family members providing close supervision seem to get better care than somebody [who] is not asking questions,” he says. “And some care providers find questions intimidating, but the patient should not get discouraged by that. … If they feel that the care provider is not listening to them or not being attentive to them, they can always have a recourse: They can talk to the supervisor of that provider or somebody else [to get] a different provider. Patients sometimes have the fear that if they speak up against somebody that their care might be jeopardized.”

Dr. Sachdeva advises friends and relatives that they talk to the nursing supervisor or ask for the physician supervisor or an administrative person or social worker so that they get the attention they need.

Dr. Jenkins agrees. “Informed consent” is one of his tips for friends and family: “If your doctor won't talk to you about the risks and benefits of your treatments, and alternatives to them, you need a new doctor.”

Our hospitalists suggest being discriminating, savvy, and proactive:

  • “Find one hospital you are comfortable with, [where] your family physician is on staff, and use it exclusively if possible,” says David M. Grace, MD, a hospitalist with The Schumacher Group in Lafayette, La. “By utilizing one hospital, all of your previous records and test results are immediately available when needed. Often this translates into a much shorter hospitalization as there are no delays in obtaining old records, and it minimizes the chance of duplicate tests/procedures being performed.”
  • “Know who your doctors are [and] what their role is, and understand their input into your healthcare,” says Dr. Farnan, who is extensively involved in medical residents’ training. And “be cognizant of the physician work hours,” she advises. “We often have families who demand to speak with ‘their’ doctor at all hours of the early morning and night.” She tells friends and relatives, “I think more patients need to understand the nature [and] structure of the system [and] what kind of information a covering physician can provide. If the family of the patient has questions [and] wants to speak with the primary MD, it may be best to attempt in the daytime when the primary service is more likely to be present.”
  • “Know the full names, and preferably [the] phone numbers, of all your outpatient physicians,” says Dr. Grace. “One area will often have multiple doctors with the same last name, and, frequently, records need to be requested from them. Up-to-date contact information on your physicians helps us request the right records from the right physicians with minimal delay.”
 

 

What to Bring to the Hospital

Some hospital Web sites advise patients on what to bring with them for their hospital stay, suggesting everything from your own robe, slippers, pajamas, or nightgown to an advance directive. Definitely, the latter is an important point.

“Whether it’s an elective or emergent admission,” says Dr. Grace, “there are a few things [you] can do to ensure [your] hospitalization is as safe, efficient, and productive as possible,” he tells friends and relatives. Among them, he says, is to “have a Living Will or advance directives completed, ensure the hospital has a copy, and discuss your wishes with your family prior to admission. Clear and concise plans, coupled with good family awareness, will help ensure your wishes and values are honored appropriately.”

And, as several of his hospitalist colleagues suggest, “Bring all of the medications you are currently using, including any over-the-counter medicines and herbs or homeopathic treatments. It’s imperative that physicians know what medications you are taking [because] many cannot be stopped abruptly, and [they may] have interactions with medications you may receive in the hospital.”

In addition, “know what medications you’re truly allergic to [e.g., hives, swelling, breathing problems],” Dr. Grace advises, “and which medications you have had side effects from [e.g., stomach upset, sleepiness, and so on]. Many patients confuse the two. Occasionally the best or only option involves using medications with potential unwanted side effects. Rarely do we use medications to which the patient has a true allergy.”

Communication: The Key to the Hospital Kingdom

Dr. Sachdeva recommends being ready to communicate even before going to the hospital. “In the case of an emergency admission,” he says, “they should have all their information readily available because at the time for a needed hospitalization, they may be sick and confused.” Have it “on their person” or in “an easily identifiable place,” he says, and, like his colleagues, he reiterates that this information should include a list of medications, problems, doctors, and phone numbers, along with a list of patient advocates and their phone numbers.

“Most of the time, patients are able to notify a family member, but if that doesn’t happen, then the ER can notify the appropriate person to be present to supervise and oversee the care from a patient perspective,” he says.

Communication was mentioned by all the hospitalists we interviewed. “Be prepared to ask questions and take an active role in your healthcare,” says Dr. Grace. “Ask your nurse what each medication you receive is and what it’s for. Ensure you know what medications to continue taking when you return home and which ones to stop. If you don’t understand your diagnosis, prognosis, or treatment plan, make sure you ask.”

One hospitalist’s advice pertained to the patient’s and family’s behavior and is based on an experience in her own family: “Be really nice to everybody,” Alison Holmes, MD, a hospitalist with Concord Hospital, Concord, N.H., advises friends and family. “This is hard to do when you’re sick and scared, but it’s incredibly important.”

Dr. Holmes speaks of her own parents’ experience: “My mother was admitted to the hospital for pneumonia about a year ago. She had very long wait in the emergency room. My father got very upset and called me and said, ‘Oh, they were so angry at me, I was yelling at everybody.’

“That won’t get you anywhere!” I told him. “That will get you worse care.” I asked, “Where is she now?” and he said, ‘Oh, she’s still in the emergency room,’ and I said, “You’re at home? You left her there?” Dr. Holmes then advised her father to return to the hospital right away.

 

 

Finally, all the hospitalists we interviewed emphasized that they would tell their family members to designate a point person for communication. And you can’t assume that that would be their doctor son or daughter, even if they happened to be in the same locale.

“When possible, don’t stay in the hospital alone,” says Dr. Holmes. “Try to always have a family member present so that there is someone available for questions. It’s not always clear where [the physician] can reach someone or how far away [that person is]. It can take a little coordination and multiple people to do it,” she says.

Also, Dr. Farnan points out, “It is often difficult [because of time limitations] for [physicians] to repeat the same information to multiple family members.”

All patients, but especially the elderly, says Dr. Sachdeva, should have a patient advocate with them at the hospital. If they don’t have family close by, they should have “a close friend or neighbor who is willing to take on that job, someone who can be there in the room and ask these questions: What medicine are you giving me? What’s the next step? What are the options?”

Dr. Sachdeva advises relatives that they might be distressed or unable to focus, so having a healthy advocate with them may be extremely important, “the difference between life and death,” although, no doubt, he’d leave that last comment out of his advice to family. “Because a lot of the time, it is not that we don’t try to do a good job, but it’s just [that] the advocate might bring something to our attention that we might not have otherwise noticed.” TH

Andrea Sattinger has been writing for The Hospitalist since 2005.

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