A 62-year-old white female collapsed at home after a period of shortness of breath and "foaming at the mouth." Her brother, who has Down's syndrome, witnessed these events. A basic life support team began cardiopulmonary resuscitation approximately 15 minutes later, noting absent pulse and respirations. An advanced cardiac life support team arrived 30 minutes after her collapse. Evaluation at that time confirmed absent respirations and pulse with asystole on electrocardiogram. Atropine was administered followed by epinephrine. The patient's pulse was restored about 35 minutes after her collapse. She was intubated and transferred to the emergency department.
There, she had pulmonary edema, inferior Q waves, primary atrioventricular block and a right bundle branch block with right ventricular strain. Abnormal lab values included white blood cell count, 15.7; hematocrit, 25.8; prothrombin time, 22.3; INR, 2.0; PTT, 84.0; CO2, 10; BUN, 41; creatinine, 1.7; and glucose, 594.
She had a history of hypothyroidism, chronic renal insufficiency, hypertension, coronary artery disease, non-insulin dependent diabetes mellitus, and psoriatic arthritis. Her daily medications included aspirin, levothryoxine, lisinopril, glipizide, simvastatin, omeprazole, lasix, amlodipine, prednisone, paroxetine, digoxin, and metoprolol.
A neurological consultation four hours after admission revealed an intubated woman who did not respond to noxious stimuli. The pupillary, corneal, oculocephalic, gag and cough reflexes were absent. Caloric testing was not performed at this time. Her temperature was 33.1°C.
Her profound hypothermia and history of hypothyroidism led us to initiate investigating thyroid functions. Treatment included re-warming and control of hyperglycemia.
Seven hours after admission, a head CT demonstrated loss of the gray/white junction, diffuse low density, loss of sulci, and obliterated cisterns suggesting diffuse, severe hypoxic injury.
An apnea test conducted 10 hours after admission did not induce breathing during the 10-minute evaluation. Concurrently, she had absent pupillary, corneal, gag, cough, oculocephalic and caloric responses. There was no response to deep pain stimulation. At this time she met the three clinical neurological requirements to diagnose death by neurological criteria, however, we learned that her TSH was strikingly elevated at 67.38 uIU/mL (normal 0.4 – 6.00), indicating profound hypothyroidism. Free T4 was low at 0.4 ng/dl (normal 0.8 – 1.8). T3 uptake was normal (34%). Her last prior TSH level was 2.18 uIU/mL 10 weeks earlier.
From an ethical perspective, we felt justified in offering the opinion that even if death by neurological criteria was inappropriate because of hypothyroidism, treatment could be withdrawn based on her dismal prognosis and the support of a surrogate decision-maker. Unfortunately, the only known relative was mentally retarded and incapable of participating in the decision to terminate care for futility.
Given the profound hypothyroidism confounding a diagnosis of brain death, a technetium radionuclide perfusion study was obtained and revealed absent intracranial blood flow compatible with brain death. Almost simultaneously, remote relatives were contacted who agreed support should be terminated. This was done and the patient expired.