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).
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.
