The questionable discharge

Story:

Mrs. EG was a 71-year-old woman who presented to her community hospital emergency department with complaints of 2-3 weeks of muscle weakness making it difficult to go up and down the stairs. She also complained of nonspecific abdominal discomfort with nausea, and a recent rash for which she had received corticosteroids (prednisone 10 mg daily for 1 week). Her medical history included chronic obstructive pulmonary disease with active tobacco abuse, hypertension, and hyperlipidemia. Her simvastatin had been recently discontinued by her primary care physician as a result of mildly elevated liver enzymes discovered about 4 weeks prior to her current presentation. Her medications upon presentation included a fluticasone/salmeterol inhaler, amlodipine, and hydrochlorothiazide. In the ED, the laboratory studies revealed multiple abnormalities including hyponatremia (sodium, 128 mmol/L), a low serum bicarbonate (23 mmol/L) level, thrombocytopenia (platelets, 136,000/mcL), and elevated creatine kinase (2,035 U/L) and liver enzymes (AST 245 U/L and ALT 268 U/L).

Mrs. EG was admitted for further management to Dr. Hospitalist-1 (H1).

©Marcin Kempski/iStockphoto.com

Dr. H1 ordered imaging studies and a battery of laboratory tests. The diuretic was discontinued and intravenous hydration provided. He consulted neurology, rheumatology, and gastroenterology to aid in his evaluation. Mrs. EG was ruled out for myocardial infarction/myocarditis, and she had a CT of the abdomen/pelvis with contrast that was normal. Mrs. EG was not febrile and her blood cultures were negative. Routine primary care cancer screening was normal. Coagulation tests, thyroid-stimulating hormone level, erythrocyte sedimentation rate, C-reactive protein level, serum osmolarity, and urinalysis testing were normal. Serum aldolase was elevated 3x normal. Mrs. EG ’s muscle weakness combined with her creatine kinase, liver transaminase, and serum aldolase elevations were consistent with an inflammatory myositis. Dermatomyositis, SLE, and viral myositis with rhabdomyolysis were also a consideration but thought to be less likely. Additional neuromuscular testing was recommended by both neurology and rheumatology (electromyogram and a muscle biopsy), and both consultants felt that these tests could be safely performed in a facilitated fashion in the outpatient setting. Empiric steroid therapy for myositis was not recommended out of concern that it would limit the interpretation of the muscle biopsy. Mrs. EG qualified for skilled nursing facility care based on her physical therapy assessment; however, she declined this recommendation in favor of going home with her family.

Dr. H1 ultimately discharged Mrs. EG home on hospital day 3 without a final diagnosis, although her work-up and evaluation were still proceeding as an outpatient with a presumed autoimmune myositis. She did have abnormalities (sodium, 127 mmol/L; HCO₃, 18 mmol/L; platelets, 106,000/mcL) on her morning labs. Mrs. EG left the hospital with her daughters at approximately 4 p.m.

Ten hours later, Mrs. EG returned to the hospital with profound weakness, but also worsening nausea, more diffuse and severe abdominal pain, and new complaints of shortness of breath, diarrhea, dizziness, cold sweats, and associated hypotension. Dr. Hospitalist-2 readmitted Mrs. EG, and at the time of the initial assessment and despite intravenous fluid support, Mrs. EG was hypotensive (92/59 mm Hg) with acute kidney injury (serum creatinine, 1.9 mg/dL with a baseline value of 1.0 mg/dL). Empiric antibiotics were ordered along with additional imaging studies. There was no evidence of bleeding. Unfortunately, later that morning, Mrs. EG had a respiratory arrest (HCO₃, 15 mmol/L; arterial pH, 7.1). Over the next 24 hours, Mrs. EG went on to suffer multiorgan dysfunction and refractory shock, and ultimately died 5 days after her initial presentation to the hospital. Diffuse ischemic colitis was found on autopsy.

Complaint:

Three months after Mrs. EG died, the daughters filed a lawsuit on behalf of the estate for wrongful death. They alleged that Mrs. EG was discharged prematurely, as evidenced by her abnormal laboratory values on the day of discharge, the absence of a definitive discharge diagnosis, and readmission and death just 10 hours and 2 days, respectively, following her hospital release. They asserted that Mrs. EG more likely than not had an underlying endocrinopathy (such as adrenal insufficiency) and if she was to be discharged, empiric steroids should have been given to prevent her from going into adrenal crisis and shock. Had Dr. H1 kept Mrs. EG in the hospital, her condition would have been monitored, and she would have had empiric therapy with steroids and intravenous fluids before she developed hypotension and shock and the ischemic colitis that resulted in systemic acidemia and death. Furthermore, Dr. H1 discharged Mrs. EG without consideration for endocrinopathy, and this was a breach in the standard of care. Had Dr. H1 considered adrenal insufficiency, he would not have discharged Mrs. EG until the diagnosis was confirmed and the patient appropriately treated.

Scientific principles:

The decision regarding the need for acute hospital care is a combination of the acuity of the patient’s illness and the intensity of the treatment that is to be provided. Similarly, the discharge decision is related to satisfying the reason for admission. A safe discharge home typically requires patients to have the ability to perform basic activities of daily living independently or the presence of qualified family/personnel to provide assistance with such activities. There should also be assurance that the patient is able to obtain food and medications independently or with assistance from family or friends.

A final diagnosis or completely normal labs are not required for hospital discharge unless there are foreseeable consequences that such uncertainty or the degree and type of laboratory abnormality would lead to patient harm.

Complaint rebuttal and discussion:

Mrs. EG presented with a complex clinical picture at the outset for which a unifying diagnosis was uncertain. She was admitted for further evaluation and treatment, both of which she received. She was seen by several consultants and had numerous radiographic and laboratory tests. Dr. H1 testified that he considered secondary adrenal insufficiency as a cause for some of Mrs. EG’s complaints and her laboratory abnormalities (despite the historical lack of steroid exposure to the degree that one would expect to see secondary adrenal impairment); however, secondary adrenal insufficiency would not explain Mrs. EG’s thrombocytopenia or elevated serum aldolase. In addition, hypotension is associated with primary adrenal insufficiency. Mrs. EG did not demonstrate hypotension at any point in her first hospital stay. On the morning of discharge, Mrs. EG had a normal blood pressure (124/72 mm Hg) and heart rate (81 beats/min) without intravenous fluid support. Mrs. EG was afebrile with little evidence for systemic infection; her WBC was normal. She did not have diarrhea, cold sweats, or progressive abdominal complaints prior to her discharge. Her weakness was reasonably attributed to her documented myositis. In addition, Dr. H1 ordered a physical therapy assessment to evaluate Mrs. EG’s functional activities of daily living and to determine the need for inpatient rehabilitation prior to her discharge. The physical therapy assessment was limited as Mrs. EG declined to ambulate.

Despite Mrs. EG’s concerns about being discharged and her complaints of ongoing weakness, Mrs. EG herself was not interested in inpatient rehabilitation (that is, transfer to a skilled nursing facility) that would have provided a greater level of monitoring as opposed to going home. Further, the nursing staff documented that Mrs. EG was comfortable and resting in bed approximately 1 hour before she left the hospital.

The autopsy concluded that Mrs. EG died of severe systemic acidemia resulting from ischemic colitis secondary to profound hypotension. However, her ischemic colitis may have been the sole cause of the hypotension (via translocation of gram-negative bacteria and resulting sepsis) or may have resulted from it (hypoperfusion of the bowel, ischemia, and systemic acidemia). It is unlikely that her hypotension was due to adrenal crisis, as no mechanism for primary adrenal insufficiency was found at autopsy. In fact, the pathologist noted that the adrenal glands were normal (thus, autoimmune adrenalitis was ruled out).

Mrs. EG was discharged with laboratory abnormalities, but the differential diagnosis for these abnormalities did not include an immediately life-threatening entity. Dr. H1 had no basis for which to foresee Mrs. EG ’s return to the ED less than 10 hours later.

Conclusion:

Patients are discharged with laboratory abnormalities all the time. Patients have chronic conditions, and most patients will go home with laboratory abnormalities that may be unrelated to the reason for hospital admission. Hospitalists typically deal with the primary reason for admission, and once that is satisfied, the patient is transitioned to a lower level of care. However, all hospitalists need to recognize that abnormal vital signs, physical findings, or laboratory tests should be explained in the discharge summary.

Better documentation of the reason for discharge and the explanation and consideration of abnormal findings will protect the hospitalist from unnecessary litigation. Following a thorough expert review on behalf of the defense and a subsequent report outlining the questionable causation, this case was dropped without prejudice.

Dr. Michota is director of academic affairs in the hospital medicine department at the Cleveland Clinic and medical editor of Hospitalist News. He reported having no relevant financial conflicts.

Story:

Mrs. EG was a 71-year-old woman who presented to her community hospital emergency department with complaints of 2-3 weeks of muscle weakness making it difficult to go up and down the stairs. She also complained of nonspecific abdominal discomfort with nausea, and a recent rash for which she had received corticosteroids (prednisone 10 mg daily for 1 week). Her medical history included chronic obstructive pulmonary disease with active tobacco abuse, hypertension, and hyperlipidemia. Her simvastatin had been recently discontinued by her primary care physician as a result of mildly elevated liver enzymes discovered about 4 weeks prior to her current presentation. Her medications upon presentation included a fluticasone/salmeterol inhaler, amlodipine, and hydrochlorothiazide. In the ED, the laboratory studies revealed multiple abnormalities including hyponatremia (sodium, 128 mmol/L), a low serum bicarbonate (23 mmol/L) level, thrombocytopenia (platelets, 136,000/mcL), and elevated creatine kinase (2,035 U/L) and liver enzymes (AST 245 U/L and ALT 268 U/L).

Mrs. EG was admitted for further management to Dr. Hospitalist-1 (H1).

©Marcin Kempski/iStockphoto.com

Dr. H1 ordered imaging studies and a battery of laboratory tests. The diuretic was discontinued and intravenous hydration provided. He consulted neurology, rheumatology, and gastroenterology to aid in his evaluation. Mrs. EG was ruled out for myocardial infarction/myocarditis, and she had a CT of the abdomen/pelvis with contrast that was normal. Mrs. EG was not febrile and her blood cultures were negative. Routine primary care cancer screening was normal. Coagulation tests, thyroid-stimulating hormone level, erythrocyte sedimentation rate, C-reactive protein level, serum osmolarity, and urinalysis testing were normal. Serum aldolase was elevated 3x normal. Mrs. EG ’s muscle weakness combined with her creatine kinase, liver transaminase, and serum aldolase elevations were consistent with an inflammatory myositis. Dermatomyositis, SLE, and viral myositis with rhabdomyolysis were also a consideration but thought to be less likely. Additional neuromuscular testing was recommended by both neurology and rheumatology (electromyogram and a muscle biopsy), and both consultants felt that these tests could be safely performed in a facilitated fashion in the outpatient setting. Empiric steroid therapy for myositis was not recommended out of concern that it would limit the interpretation of the muscle biopsy. Mrs. EG qualified for skilled nursing facility care based on her physical therapy assessment; however, she declined this recommendation in favor of going home with her family.

Dr. H1 ultimately discharged Mrs. EG home on hospital day 3 without a final diagnosis, although her work-up and evaluation were still proceeding as an outpatient with a presumed autoimmune myositis. She did have abnormalities (sodium, 127 mmol/L; HCO₃, 18 mmol/L; platelets, 106,000/mcL) on her morning labs. Mrs. EG left the hospital with her daughters at approximately 4 p.m.

Ten hours later, Mrs. EG returned to the hospital with profound weakness, but also worsening nausea, more diffuse and severe abdominal pain, and new complaints of shortness of breath, diarrhea, dizziness, cold sweats, and associated hypotension. Dr. Hospitalist-2 readmitted Mrs. EG, and at the time of the initial assessment and despite intravenous fluid support, Mrs. EG was hypotensive (92/59 mm Hg) with acute kidney injury (serum creatinine, 1.9 mg/dL with a baseline value of 1.0 mg/dL). Empiric antibiotics were ordered along with additional imaging studies. There was no evidence of bleeding. Unfortunately, later that morning, Mrs. EG had a respiratory arrest (HCO₃, 15 mmol/L; arterial pH, 7.1). Over the next 24 hours, Mrs. EG went on to suffer multiorgan dysfunction and refractory shock, and ultimately died 5 days after her initial presentation to the hospital. Diffuse ischemic colitis was found on autopsy.

Complaint:

Three months after Mrs. EG died, the daughters filed a lawsuit on behalf of the estate for wrongful death. They alleged that Mrs. EG was discharged prematurely, as evidenced by her abnormal laboratory values on the day of discharge, the absence of a definitive discharge diagnosis, and readmission and death just 10 hours and 2 days, respectively, following her hospital release. They asserted that Mrs. EG more likely than not had an underlying endocrinopathy (such as adrenal insufficiency) and if she was to be discharged, empiric steroids should have been given to prevent her from going into adrenal crisis and shock. Had Dr. H1 kept Mrs. EG in the hospital, her condition would have been monitored, and she would have had empiric therapy with steroids and intravenous fluids before she developed hypotension and shock and the ischemic colitis that resulted in systemic acidemia and death. Furthermore, Dr. H1 discharged Mrs. EG without consideration for endocrinopathy, and this was a breach in the standard of care. Had Dr. H1 considered adrenal insufficiency, he would not have discharged Mrs. EG until the diagnosis was confirmed and the patient appropriately treated.

Scientific principles:

The decision regarding the need for acute hospital care is a combination of the acuity of the patient’s illness and the intensity of the treatment that is to be provided. Similarly, the discharge decision is related to satisfying the reason for admission. A safe discharge home typically requires patients to have the ability to perform basic activities of daily living independently or the presence of qualified family/personnel to provide assistance with such activities. There should also be assurance that the patient is able to obtain food and medications independently or with assistance from family or friends.

A final diagnosis or completely normal labs are not required for hospital discharge unless there are foreseeable consequences that such uncertainty or the degree and type of laboratory abnormality would lead to patient harm.

Complaint rebuttal and discussion:

Mrs. EG presented with a complex clinical picture at the outset for which a unifying diagnosis was uncertain. She was admitted for further evaluation and treatment, both of which she received. She was seen by several consultants and had numerous radiographic and laboratory tests. Dr. H1 testified that he considered secondary adrenal insufficiency as a cause for some of Mrs. EG’s complaints and her laboratory abnormalities (despite the historical lack of steroid exposure to the degree that one would expect to see secondary adrenal impairment); however, secondary adrenal insufficiency would not explain Mrs. EG’s thrombocytopenia or elevated serum aldolase. In addition, hypotension is associated with primary adrenal insufficiency. Mrs. EG did not demonstrate hypotension at any point in her first hospital stay. On the morning of discharge, Mrs. EG had a normal blood pressure (124/72 mm Hg) and heart rate (81 beats/min) without intravenous fluid support. Mrs. EG was afebrile with little evidence for systemic infection; her WBC was normal. She did not have diarrhea, cold sweats, or progressive abdominal complaints prior to her discharge. Her weakness was reasonably attributed to her documented myositis. In addition, Dr. H1 ordered a physical therapy assessment to evaluate Mrs. EG’s functional activities of daily living and to determine the need for inpatient rehabilitation prior to her discharge. The physical therapy assessment was limited as Mrs. EG declined to ambulate.

Despite Mrs. EG’s concerns about being discharged and her complaints of ongoing weakness, Mrs. EG herself was not interested in inpatient rehabilitation (that is, transfer to a skilled nursing facility) that would have provided a greater level of monitoring as opposed to going home. Further, the nursing staff documented that Mrs. EG was comfortable and resting in bed approximately 1 hour before she left the hospital.

The autopsy concluded that Mrs. EG died of severe systemic acidemia resulting from ischemic colitis secondary to profound hypotension. However, her ischemic colitis may have been the sole cause of the hypotension (via translocation of gram-negative bacteria and resulting sepsis) or may have resulted from it (hypoperfusion of the bowel, ischemia, and systemic acidemia). It is unlikely that her hypotension was due to adrenal crisis, as no mechanism for primary adrenal insufficiency was found at autopsy. In fact, the pathologist noted that the adrenal glands were normal (thus, autoimmune adrenalitis was ruled out).

Mrs. EG was discharged with laboratory abnormalities, but the differential diagnosis for these abnormalities did not include an immediately life-threatening entity. Dr. H1 had no basis for which to foresee Mrs. EG ’s return to the ED less than 10 hours later.

Conclusion:

Patients are discharged with laboratory abnormalities all the time. Patients have chronic conditions, and most patients will go home with laboratory abnormalities that may be unrelated to the reason for hospital admission. Hospitalists typically deal with the primary reason for admission, and once that is satisfied, the patient is transitioned to a lower level of care. However, all hospitalists need to recognize that abnormal vital signs, physical findings, or laboratory tests should be explained in the discharge summary.

Better documentation of the reason for discharge and the explanation and consideration of abnormal findings will protect the hospitalist from unnecessary litigation. Following a thorough expert review on behalf of the defense and a subsequent report outlining the questionable causation, this case was dropped without prejudice.

Dr. Michota is director of academic affairs in the hospital medicine department at the Cleveland Clinic and medical editor of Hospitalist News. He reported having no relevant financial conflicts.

Story:

Mrs. EG was a 71-year-old woman who presented to her community hospital emergency department with complaints of 2-3 weeks of muscle weakness making it difficult to go up and down the stairs. She also complained of nonspecific abdominal discomfort with nausea, and a recent rash for which she had received corticosteroids (prednisone 10 mg daily for 1 week). Her medical history included chronic obstructive pulmonary disease with active tobacco abuse, hypertension, and hyperlipidemia. Her simvastatin had been recently discontinued by her primary care physician as a result of mildly elevated liver enzymes discovered about 4 weeks prior to her current presentation. Her medications upon presentation included a fluticasone/salmeterol inhaler, amlodipine, and hydrochlorothiazide. In the ED, the laboratory studies revealed multiple abnormalities including hyponatremia (sodium, 128 mmol/L), a low serum bicarbonate (23 mmol/L) level, thrombocytopenia (platelets, 136,000/mcL), and elevated creatine kinase (2,035 U/L) and liver enzymes (AST 245 U/L and ALT 268 U/L).

Mrs. EG was admitted for further management to Dr. Hospitalist-1 (H1).

©Marcin Kempski/iStockphoto.com

Dr. H1 ordered imaging studies and a battery of laboratory tests. The diuretic was discontinued and intravenous hydration provided. He consulted neurology, rheumatology, and gastroenterology to aid in his evaluation. Mrs. EG was ruled out for myocardial infarction/myocarditis, and she had a CT of the abdomen/pelvis with contrast that was normal. Mrs. EG was not febrile and her blood cultures were negative. Routine primary care cancer screening was normal. Coagulation tests, thyroid-stimulating hormone level, erythrocyte sedimentation rate, C-reactive protein level, serum osmolarity, and urinalysis testing were normal. Serum aldolase was elevated 3x normal. Mrs. EG ’s muscle weakness combined with her creatine kinase, liver transaminase, and serum aldolase elevations were consistent with an inflammatory myositis. Dermatomyositis, SLE, and viral myositis with rhabdomyolysis were also a consideration but thought to be less likely. Additional neuromuscular testing was recommended by both neurology and rheumatology (electromyogram and a muscle biopsy), and both consultants felt that these tests could be safely performed in a facilitated fashion in the outpatient setting. Empiric steroid therapy for myositis was not recommended out of concern that it would limit the interpretation of the muscle biopsy. Mrs. EG qualified for skilled nursing facility care based on her physical therapy assessment; however, she declined this recommendation in favor of going home with her family.

Dr. H1 ultimately discharged Mrs. EG home on hospital day 3 without a final diagnosis, although her work-up and evaluation were still proceeding as an outpatient with a presumed autoimmune myositis. She did have abnormalities (sodium, 127 mmol/L; HCO₃, 18 mmol/L; platelets, 106,000/mcL) on her morning labs. Mrs. EG left the hospital with her daughters at approximately 4 p.m.

Ten hours later, Mrs. EG returned to the hospital with profound weakness, but also worsening nausea, more diffuse and severe abdominal pain, and new complaints of shortness of breath, diarrhea, dizziness, cold sweats, and associated hypotension. Dr. Hospitalist-2 readmitted Mrs. EG, and at the time of the initial assessment and despite intravenous fluid support, Mrs. EG was hypotensive (92/59 mm Hg) with acute kidney injury (serum creatinine, 1.9 mg/dL with a baseline value of 1.0 mg/dL). Empiric antibiotics were ordered along with additional imaging studies. There was no evidence of bleeding. Unfortunately, later that morning, Mrs. EG had a respiratory arrest (HCO₃, 15 mmol/L; arterial pH, 7.1). Over the next 24 hours, Mrs. EG went on to suffer multiorgan dysfunction and refractory shock, and ultimately died 5 days after her initial presentation to the hospital. Diffuse ischemic colitis was found on autopsy.

Complaint:

Three months after Mrs. EG died, the daughters filed a lawsuit on behalf of the estate for wrongful death. They alleged that Mrs. EG was discharged prematurely, as evidenced by her abnormal laboratory values on the day of discharge, the absence of a definitive discharge diagnosis, and readmission and death just 10 hours and 2 days, respectively, following her hospital release. They asserted that Mrs. EG more likely than not had an underlying endocrinopathy (such as adrenal insufficiency) and if she was to be discharged, empiric steroids should have been given to prevent her from going into adrenal crisis and shock. Had Dr. H1 kept Mrs. EG in the hospital, her condition would have been monitored, and she would have had empiric therapy with steroids and intravenous fluids before she developed hypotension and shock and the ischemic colitis that resulted in systemic acidemia and death. Furthermore, Dr. H1 discharged Mrs. EG without consideration for endocrinopathy, and this was a breach in the standard of care. Had Dr. H1 considered adrenal insufficiency, he would not have discharged Mrs. EG until the diagnosis was confirmed and the patient appropriately treated.

Scientific principles:

The decision regarding the need for acute hospital care is a combination of the acuity of the patient’s illness and the intensity of the treatment that is to be provided. Similarly, the discharge decision is related to satisfying the reason for admission. A safe discharge home typically requires patients to have the ability to perform basic activities of daily living independently or the presence of qualified family/personnel to provide assistance with such activities. There should also be assurance that the patient is able to obtain food and medications independently or with assistance from family or friends.

A final diagnosis or completely normal labs are not required for hospital discharge unless there are foreseeable consequences that such uncertainty or the degree and type of laboratory abnormality would lead to patient harm.

Complaint rebuttal and discussion:

Mrs. EG presented with a complex clinical picture at the outset for which a unifying diagnosis was uncertain. She was admitted for further evaluation and treatment, both of which she received. She was seen by several consultants and had numerous radiographic and laboratory tests. Dr. H1 testified that he considered secondary adrenal insufficiency as a cause for some of Mrs. EG’s complaints and her laboratory abnormalities (despite the historical lack of steroid exposure to the degree that one would expect to see secondary adrenal impairment); however, secondary adrenal insufficiency would not explain Mrs. EG’s thrombocytopenia or elevated serum aldolase. In addition, hypotension is associated with primary adrenal insufficiency. Mrs. EG did not demonstrate hypotension at any point in her first hospital stay. On the morning of discharge, Mrs. EG had a normal blood pressure (124/72 mm Hg) and heart rate (81 beats/min) without intravenous fluid support. Mrs. EG was afebrile with little evidence for systemic infection; her WBC was normal. She did not have diarrhea, cold sweats, or progressive abdominal complaints prior to her discharge. Her weakness was reasonably attributed to her documented myositis. In addition, Dr. H1 ordered a physical therapy assessment to evaluate Mrs. EG’s functional activities of daily living and to determine the need for inpatient rehabilitation prior to her discharge. The physical therapy assessment was limited as Mrs. EG declined to ambulate.

Despite Mrs. EG’s concerns about being discharged and her complaints of ongoing weakness, Mrs. EG herself was not interested in inpatient rehabilitation (that is, transfer to a skilled nursing facility) that would have provided a greater level of monitoring as opposed to going home. Further, the nursing staff documented that Mrs. EG was comfortable and resting in bed approximately 1 hour before she left the hospital.

The autopsy concluded that Mrs. EG died of severe systemic acidemia resulting from ischemic colitis secondary to profound hypotension. However, her ischemic colitis may have been the sole cause of the hypotension (via translocation of gram-negative bacteria and resulting sepsis) or may have resulted from it (hypoperfusion of the bowel, ischemia, and systemic acidemia). It is unlikely that her hypotension was due to adrenal crisis, as no mechanism for primary adrenal insufficiency was found at autopsy. In fact, the pathologist noted that the adrenal glands were normal (thus, autoimmune adrenalitis was ruled out).

Mrs. EG was discharged with laboratory abnormalities, but the differential diagnosis for these abnormalities did not include an immediately life-threatening entity. Dr. H1 had no basis for which to foresee Mrs. EG ’s return to the ED less than 10 hours later.

Conclusion:

Patients are discharged with laboratory abnormalities all the time. Patients have chronic conditions, and most patients will go home with laboratory abnormalities that may be unrelated to the reason for hospital admission. Hospitalists typically deal with the primary reason for admission, and once that is satisfied, the patient is transitioned to a lower level of care. However, all hospitalists need to recognize that abnormal vital signs, physical findings, or laboratory tests should be explained in the discharge summary.

Better documentation of the reason for discharge and the explanation and consideration of abnormal findings will protect the hospitalist from unnecessary litigation. Following a thorough expert review on behalf of the defense and a subsequent report outlining the questionable causation, this case was dropped without prejudice.

Dr. Michota is director of academic affairs in the hospital medicine department at the Cleveland Clinic and medical editor of Hospitalist News. He reported having no relevant financial conflicts.