INTRODUCTION: Myxedema coma is considered an endocrine emergency presenting with symptoms of slowed multi-organ dysfunction, including abnormal mental status and hypothermia. The diagnosis is typically clinical and must be differentiated from other causes of altered mental status.  To the best of our knowledge, subclinical hypothyroidism is a rare cause of myxedema coma with very few reported cases in the medical literature.

DESCRIPTION: We present a 62-year-old female with a longstanding history of bipolar disorder and epilepsy presenting with myxedema coma and subclinical hypothyroidism. Our patient had been transferred to the emergency department with reported hypotension and altered mental status. On admission, the patient was found to have evidence of delirium, bradyphasia, and delayed response to noxious stimuli. On examination, she was hypothermic (temperature of 31.1C), blood pressure was 113/58 mmHg, respiratory rate 16 breaths per minute, and Glasgow Coma Scale (GCS) was 11/15. She initially met clinical criteria for Myxedema and was started on levothyroxine, liothyronine, and hydrocortisone. She also met 2/4 SIRS criteria. Intravenous fluids and antibiotics were initiated while undergoing further diagnostic testing. Soon after Hospital admission the patient’s condition quickly deteriorated with the presence of hypotension (75/48 mmHg), hypoxia (SpO2 82%), heart rate of 80 beats per minute, and findings consistent with hypercapnic respiratory failure, her GCS worsened to 5/15. She was intubated and admitted to the Intensive care unit. Laboratory evaluation revealed elevated thyroid-stimulating hormone (TSH) (13.4mU/L) with a normal free thyroxine (T4) (0.85 ng/dL) consistent with subclinical hypothyroidism. The patient cortisol level was unremarkable,hyperammonemia (43), mildly elevated lipase (505), and hypoglycemia (48) were found. Blood cultures, bronchial fluid culture, and CSF analysis were unrevealing. No infectious source was identified; thus, antibiotics were discontinued, and based on her labs, the concern for adrenal insufficiency was excluded. Subsequently, the patient’s condition gradually improved, she was transitioned to oral levothyroxine and by the time of discharge on week three, she had returned to her baseline. 

DISCUSSION: Our patient had myxedema coma with laboratory findings consistent with Subclinical hypothyroidism. Although biochemical hypothyroidism is usually expected, this case highlights the importance of identifying Myxedema Coma when evaluating a patient presenting with altered mental status and hypotension. In adition, recognizing the absence of laboratory features of hypothyroidism (E.g., presence of subclinical hypothyroidism) doesn’t exclude the diagnosis. Treatment shouldn’t be delayed considering mortality remains very high.

Subclinical hypothyroidism is characterized by a serum thyroid-stimulating hormone (TSH) level above the upper limit of the reference range and normal free thyroxine (T4) level; before making this diagnosis, transient elevation of serum TSH should be ruled out by repeating the measurement of TSH in 2 to 3 months. Also, subclinical hypothyroidism is an early form of primary hypothyroidism affecting up to 10% of the population. Since guidelines differ regarding when to treat subclinical hypothyroidism, is important to follow up on TSH levels given that thyroid hormone replacement therapy can result in clinical benefits and may have a significant effect on cardiovascular events or mortality as we can see in our patient. We strongly believe that treatment in the outpatient setting could have prevented her hospitalization and further deterioration.