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Washington University Experience | VASCULAR | Edema - Cerebral | 9A0 Case 8 History - Copy
Case 9 History ---- The patient was a 20 year old right-handed female with hyperthyroidism due to toxic multinodular goiter who presented on June 25th after she complained of feeling hot and then suddenly collapsed. En route via EMS, she apparently had cardiac arrest (duration unrecorded) and was intubated. Upon arrival, she was noted to be tachycardic, tachypneic, and hypotensive with a fever of 105°F. Initial labs were notable for serum K+ and glucose of 8.4 and 19, respectively. Urine drug screen was positive for opiates. Family noted she had a "sinus infection," and was receiving antibiotics and decongestant, but that she had been non-compliant with treatment of her thyroid disease. Free T4 was subsequently found to be 8.09, with an undetectable TSH level. Chest x-ray showed a right upper lobe infiltrate, and her stool was guaiac positive. She was transferred to the ICU with presumed thyroid storm, pneumonia, possible GI bleed, and recent cardiac arrest. Her hyperkalemia and hypoglycemia were corrected. She received IV Decadron, Dopamine, and Ceftriaxone. For her thyroid, PTU, SSKI, and Inderal were given. The following day, she was able to converse with family. Unfortunately, her transaminases had elevated markedly and she had developed acute renal failure. The patient complained of right upper quadrant abdominal pain. By June 28th her AST, ALT and total bilirubin were 2800, 1268, and 5.5, respectively. A viral hepatitis panel was negative. That day, her level of arousal gradually declined and she was re-intubated for transport by helicopter, arriving comatose. No spontaneous movements or eye opening were present, but she would extend her arms and triple-flex her legs to painful stimuli. Pupils were 4 mm bilaterally and minimally reactive. Brainstem reflexes were intact. Reflexes were notable for clonus at both ankles, but Babinski signs were absent. Vital signs included a temperature of 39.2°C and a heart rate of 115. Complete metabolic panel showed hypernatremia (160) and evidence of hepatocellular damage (AST 3033, ALT 1888, TB 4.9), but hyperkalemia and hypoglycemia were corrected. Serum NH3 level was 170. She was coagulopathic, with INR 3.16. Free T4 was up to 16.4. Her initial head CT and LP were normal. A routine EEG showed moderate to severe generalized slowing but no seizure activity. The neurology service felt her coma was multifactorial, due to hepatic failure, anoxic brain injury, hyperthyroidism, and hypernatremia. She received Ampicillin, Ceftriaxone, and Doxycycline for empiric coverage of pneumonia and meningitis. For her thyroid, she received Esmolol, SSKI, and Hydrocortisone IV (PTU was not continued, as it was felt it might have contributed to her liver failure). She was hydrated aggressively and received Vitamin K and Lactulose for coagulopathy and hepatic encephalopathy, respectively. Nonetheless, over the next two days, her condition did not change significantly. On the morning of June 30th, she was still comatose, febrile, tachycardic and hypernatremic, but her transaminase elevations, acute renal failure, and coagulopathy were improving. According to a neurology note that night, her exam changed significantly. She no longer responded to pain at all, pupils were dilated and non-reactive, papilledema was present, and corneal, gag, and oculocephalic reflexes had been lost. For suspected elevated intracranial pressure, she was given Mannitol which failed to help. Head CT showed diffuse cerebral edema with evidence of transtentorial herniation. Neurosurgery felt intervention was unlikely to impact the patient's prognosis. Clinical exams documented absence of brain activity on July 1st. The next day, after a cerebral perfusion scan, brain death was declared. Family withdrew life support and she died. ---- Autopsy showed widespread hypoxic-ischemic injury, involving cerebrum, brainstem and cerebellum, hepatic encephalopathy and diffuse cerebral edema.
