A Case of Atypical Thyroid Storm Presentation With Subsequent DIC, Hypoglycemia, Kidney Failure and Shock Liver

Background: Thyroid storm is a rare and life-threatening emergency requiring prompt intervention that is diagnosed based on a combination of clinical, physical and biochemical findings. Presented here is a case of thyroid storm which proved a diagnostic challenge due to its atypical presentation and whose management was further complicated by uncommon sequelae including DIC, hypoglycemia, kidney failure and shock liver. Clinical Case: A 37-year-old female with Graves’ disease presented to the Emergency Department with a chief complaint of facial swelling with concern for recent food allergy. Initial labs revealed elevated fT4 of 5.17 ng/dL (n 0.6-1.12 ng/dL) and suppressed TSH <0.01 uIU/mL (n 0.45-4.12 uIU/mL), but otherwise normal range BMP and CBC. While awaiting admission in the ED, she had normal cognition, stable vitals and scored 25 per Burch-Wartofsky scale. Given significant thyrotoxicosis and history of non-compliance with Graves’ treatment, patient was nevertheless empirically started on treatment for suspected thyroid storm in addition to treatment for possible allergic reaction. In the ED patient suddenly went into cardiac arrest with ROSC achieved after 2 rounds of CPR. Following ROSC, labs showed BG of 24 mg/dL (n<115 mg/dL), WBC to 24 thousand/mcL (n 4.0-10.5 thousand/mcL), lactate >10 mmol/L (n< 2mmol/L), D-dimer >20,000 ng/mL (n<500 ng/mL), AST 1869 U/L (n<52 U/L). Patient underwent a prolonged hospital course requiring treatment for hypoglycemia, shock liver, acute kidney injury, heart failure, atrial fibrillation, DIC and embolic CVA. Her initial shock liver improved and transitioned into a cholestatic picture, prompting a change in her thionamides from PTU to Methimazole, then back to PTU later on. Her multi-organ failure improved gradually over 3 weeks with mechanical ventilation, CRRT, blood transfusion, stress dose steroids and comprehensive critical care treatment. Patient was eventually discharged with close endocrine, ENT, cardiology, and neurology follow up. Conclusion: In diagnosing and treating this rare but life-threatening endocrine emergency, a strong clinical suspicion should not be detracted by an atypical presentation and prompt action is needed. It is vital to remember that this is first and foremost a clinical diagnosis that can be further supported with laboratory and physical findings. Furthermore, this case is an example of the extent of multi-organ failure that can result from thyroid storm.

Clarithromycin-Associated Acute Liver Failure Leading to Fatal, Massive Upper Gastrointestinal Hemorrhage from Profound Coagulopathy: Case Report and Systematic Literature Review

While erythromycin has caused numerous cases of acute liver failure (ALF), clarithromycin, a similar macrolide antibiotic, has caused only six reported cases of ALF. A new case of clarithromycin-associated ALF is reported with hepatic histopathology and exclusion of other etiologies by extensive workup, and the syndrome of clarithromycin-associated ALF is better characterized by systematic review. A 60-year-old nonalcoholic man, with normal baseline liver function tests, was admitted with diffuse abdominal pain and AST = 499 U/L and ALT = 539 U/L, six days after completing a 7-day course of clarithromycin 500 mg twice daily for suspected upper respiratory infection. AST and ALT each rose to about 1,000 U/L on day-2 of admission, and rose to ≥6,000 U/L on day-3, with development of severe hepatic encephalopathy and severe coagulopathy. Planned liver biopsy was cancelled due to coagulopathies. Extensive evaluation for infectious, immunologic, and metabolic causes of liver disease was negative. Abdominal computerized tomography and abdominal ultrasound with Doppler were unremarkable. The patient developed massive, acute upper gastrointestinal bleeding associated with coagulopathies. Esophagogastroduodenoscopy was planned after massive blood product transfusions, but the patient rapidly expired from hemorrhagic shock. Autopsy revealed a golden-brown heavy liver with massive hepatic necrosis and sinusoidal congestion. Rise of AST/ALT to about 1,000 U/L each was temporally incompatible with shock liver because this rise preceded the hemorrhagic shock, but the subsequent AST/ALT rise to ≥6,000 U/L each may have had a component of shock liver. The six previously reported cases were limited by failure to exclude hepatitis E (4), lack of liver biopsy (2), and uninterpretable liver biopsy (1) and by confounding potential etiologies including disulfiram, israpidine, or recent acetaminophen use (3), clarithromycin overdose (1), active alcohol use (1), and severe heart failure (1). Review of 6 previously reported and current case of clarithromycin-associated ALF revealed that patients had AST and ALT values in the thousands. Five patients died and 2 survived.