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Abstract

Introduction: Hypothermia remains a challenging clinical problem in US. Causes of hypothermia include cold exposure, medical condition such as hypothyroidism, adrenal insufficiency, sepsis, toxin, and medications. Hypothermia is also complicated by other comorbidities such as arrhythmia, lactic acidosis, coagulopathy, infection, and rhabdomyolysis which are life threatening. This can explain high mortality rate of this condition (40%). We present a case of hypothermia as a presentation of hypothyroidism. 74-year-old Hispanic female was brought to the ER as Jane Doe after she was found unresponsive on the street. At ER, she was alert but confused. Medical history was not available at that time. On examination, there were multiple abrasions on extremities. Vital signs were as follows: rectal temerature 28.1 c, blood pressure 122/67 mmHg, heart rate 78/min, respiration 14/min, and oxygen saturation 100% on room air. Her examination was notable for dry mucous membranes, very cold and moist skin, irregular heart rhythm, pupils 3 mm sluggishly reacted to light, and her GCS score was 10. EKG demonstrated atrial fibrillation rate of 93/min with prominent Osborne waves. Active rewarming process was initiated immediately by warm IVF, Bair hugger, bladder irrigation with warm saline, and warmed humidified air. Thirty minutes later, she was more responsive but her blood pressure dropped to 88/52 mmHg and temperature was 30 c. EKG was same as previous. She receives 3 L of NS as bolus and was started on vasopressor. Empiric antibiotics were given. She was then monitored closely in MICU. Laboratory revealed the following results: pH 7.28, pCO2 59, pO2 136, bicarbonate 29, sodium 139, potassium 2.7, creatinine 1.02, lactic 4.5, troponin I 0.05, CPK 869, urine myoglobin < 1, d-dimer 5.41, WBC 14.5, TSH 14.378 mcunit(high), free T4 0.9 ng/dL(normal), cortisol 40, urine drug screen - negative, ammonia 31. CT brain and CT chest was negative for any intracranial lesion and pulmonary embolism. Cardiology was consulted for elevated troponin and possible myocardial infarction. Echocardiography revealed no wall motion abnormality. Elevated troponin was likely reflect rhabdomyolysis. Endocrinology thought that myxedema coma was less likely and recommended to start patient on levothyroxine 50 mcg daily without loading dose for treatment of hypothyroidism. Later on that day, Her son was successfully contacted by hospital and gave information that patient has hypertension, dyslipidemia and worsened memory loss in the past 2 months. After 6 hours of rewarming process, the core temperature normalized (37.1 c). Her EKG converted to normal sinus rhythm. During the hospital course, her CPK trending up to 5,324 then trending down with aggressive IV fluid while her kidney function was maintain normal. Neurological investigations were done reveal normal MRI brain, normal EEG, normal level of vitamin B12. Neurologist confirmed diagnosis of dementia likely secondary to hypothyroidism. She was transferred to general floor at 48 hours. Her consciousness improved back to baseline at 72 hours and was discharged on the sixth day in good condition on levothyroxine 50 mcg oral daily. There are various causes of hypothermia. In this case, it was possible to assume that this patient who was hospitalized with hypothermia and altered mental status suffers from hypothyroidism. The acute decompensation of hypothyroidism is typically precipitated by environment cold exposure, infection, medication or withdrawal. In patients suspected to have this condition, the passive rewarming is preferred compared to active rewarming which carries risk of vasodilation and hypotension which happened in our patient. Our patient also had sign of hypothyroidism (dementia) preceding this incidence. This should raise importance of checking TSH as a routine work up in dementia for early diagnosis and treatment to prevent patient from myxedema coma which has high mortality rate.