This week the Renal team presented a really interesting case about myxedema coma. Here is a quick review with important pathophysiology and treatment points to keep in mind.
First thing first, let’s cover some definitions:
- Myxedema coma is a complication of severe hypothyroidism resulting in multi-organ dysfunction
- Myxedema refers to the swelling of skin and soft tissue that occurs with hypothyroidism - most commonly periorbital edema and nonpitting edema of the lower extremities.
Keep in mind that this diagnosis is a misnomer since patients do not require myxedema or a clinical coma for diagnosis. The hallmarks findings are hypothermia and decreased mental status. Other common physical findings are alopecia, delayed reflex relaxation, dry skin, decreased GI motility/ileus, and a myxedematous face (swelling, macroglossia, sparse hair, periorbital edema). Just think of it as extreme symptoms of hypothyroidism. The diagnosis is ultimately clinical with laboratory confirmation of hypothyroidism.
The majority of cases occur in females (80%) that are 60 or older. The vast majority of cases occur in the winter months (>90%).
Patients are often hyponatremic due to decreased free water excretion in the setting of excess ADH and decreased renal perfusion. An ABG often show a respiratory acidosis due to a decreased minute ventilation. Patients’ vitals often show hypotension and bradycardia due to the loss of their compensatory measures, specifically peripheral vasoconstriction and central shunting.
When you are considering this diagnosis, you need to also be thinking about the inciting event for decompensation. Many patients are in homeostatic hypothyroidism, however when an event or condition overcomes their compensatory mechanisms then myxedema coma occurs. Common precipitants are GI bleed, infection (pneumonia, viral, UTI), and medications (general anesthesia, amiodarone, diuretics, phenytoin, rifampin).
All patient with suspected myxedema coma should be treated empirically with IV levothyroxine. In addition to thyroid hormone, all patient should be given empiric IV hydrocortisone until concurrent adrenal insufficiency is ruled out. Failure to give hydrocortisone in the setting of adrenal insufficiency will precipitate adrenal crisis which could be fatal.
Hypovolemia and electrolyte abnormalities should be corrected. Pressors and ionotropes should be avoided if possible since they can provoke arrhythmias when given concurrently with levothyroxine. Avoid warming blankets since they can result in peripheral vasodilation resulting in worsening hypotension and shock. Finally if a precipitation event or condition is identified, treat it.
There is plenty more about there about myxedema coma (controversy of giving T3 vs. T4). Start by reading further info in the review article cited below.
Authored by: GREGORY WIGGER, MD