Hepatic Failure/GI/Endocrine Emergencies

iv.

In patients who are allergic to iodine, lithium carbonate may be used as an alternative. Initial

dose should be 300 mg every 6 hours, with subsequent adjustment to maintain serum lithium

concentration of 0.8–1.2 mEq/L.

Cholestyramine can be given to bind circulating T3 and T4.

ii.

Salicylates should be avoided because use can decrease binding of thyroid hormones to proteins

and therefore increase concentrations of free thyroid hormones.

iii.

In severe cases that do not respond to standard therapy, plasmapheresis and therapeutic plasma

exchange may be considered to decrease T4 and T3 levels.

Reduce heart rate.

Because cardiovascular collapse leads to systemic decompensation, β-blockers should be

initiated as quickly as possible.

ii.

β-Blocker dose should be titrated to achieve heart rate control (typically below 90 beats/minute).

iii.

Traditionally, propranolol is the preferred therapy because it may block T4 to T3 conversion at

high doses. Propranolol is also the agent of choice in women who are pregnant or breastfeeding.

Dosing for this indication is aggressive, starting at 60 mg orally every 4 hours with an optional

initial loading dose of 80 mg.

iv.

Alternative agents include carvedilol, esmolol, and diltiazem. Diltiazem should be reserved for

patients with active bronchospasm or for those who do not tolerate β-blockers.

Myxedema Coma

Clinical presentation

Myxedema coma is defined as decompensated hypothyroidism that leads to multiorgan failure.

Despite its name, the primary manifestation of the disease is decline in mental status rather than

edema or coma.

Diagnosis is made on the basis of clinical presentation, not laboratory evidence of hypothyroidism.

Altered mental status and hypothermia are the most common presenting symptoms. Other

clinical features include hypotension, bradycardia, hypoglycemia, constipation, urinary

retention, puffiness of the hands and face, and pleural, pericardial, or peritoneal effusions.

ii.

Patients may present with shock or arrhythmias, including prolongation of the QT interval that

can lead to torsades de pointes.

iii.

If a patient presents with signs of infection without the systemic inflammatory response

syndrome, myxedema coma should be suspected.

iv.

Patients typically have elevated TSH and low or undetectable T3 and T4, but TSH may be

inappropriately low or normal in cases of central hypothyroidism. The level of change in

thyroid hormones does not correlate well with disease severity.

Myxedema coma is more common in older women and occurs more often during winter months

because of altered temperature regulation.

beyond the scope of this chapter.

Myxedema coma may be the consequence of longstanding hypothyroidism but can also be

precipitated by an acute event such as infection, myocardial infarction, surgery, or cold exposure.

Drugs associated with the development of myxedema coma include sedatives, anesthetics, narcotics,

lithium, immune checkpoint inhibitors, and amiodarone, as well as abrupt discontinuation of

levothyroxine.

Management

Because myxedema coma is an endocrine emergency, treatment should be initiated without waiting

for laboratory data.