What is myxedema coma?
Myxedema coma is a loss of brain function as a result of severe, longstanding low level of thyroid hormone in the blood (hypothyroidism). Myxedema coma is considered a life-threatening complication of hypothyroidism and represents the far more serious side of the spectrum of thyroid disease.
Who is affected by myxedema coma?
Myxedema coma is not common, but tends to be seen more frequently in elderly patients and in women. There is an increased incidence in the winter months, which is likely secondary to the extremes in temperature. Myxedema coma can actually result in death. Fortunately, the condition is rare.
What are the symptoms of hypothyroidism?
Before a patient develops myxedema coma, features of hypothyroidism are usually present and may have gone unsuspected for a long period of time.
These symptoms include:
- mental impairment,
- cold intolerance,
- dry skin,
- weight gain,
- change in menstrual cycles,
- constipation, and
Hypothyroidism definition and facts
- Hypothyroidism refers to any state in which a person's thyroid hormone production is below normal.
- There are many disorders that result in hypothyroidism, for example, autoimmune disorders, thyroid removal, prescription medications, pituitary disease, and iodine deficiency.
- The thyroid gland is regulated by another gland that is located in the brain, the pituitary.
- Hypothyroidism is a very common condition.
- The symptoms of hypothyroidism are depend on the deficiency of thyroid hormone, but can include
- increased cholesterol levels,
- hair loss
- memory loss,
- dry, rough skin, and
- A blood test is used to confirm hypothyroidism.
- With the exception of certain conditions, the treatment of hypothyroidism requires life-long medication.
What causes myxedema coma?
Most patients with myxedema coma have a history of hypothyroidism, thyroid surgery, or radioactive iodine treatment for thyroid disease. Very rarely, the problem is not caused by the inability of the thyroid gland to make thyroid hormone; but rather is caused by the failure of the pituitary gland or the hypothalamus to correctly signal the thyroid gland to perform its normal functions. In this situation, the thyroid gland is normal, but it is not receiving the signals from the pituitary gland or hypothalamus to make the thyroid hormone it is capable of producing.
Picture of the Thyroid Gland
Picture of the Pituitary Gland
What are triggers of myxedema coma?
Certain factors may suddenly trigger myxedema coma in a person with poorly controlled hypothyroidism. These include:
- drugs (particularly sedatives, narcotics, anesthesia, lithium (Eskalith, Lithobid), and amiodarone (Cordarone),
- heart failure,
- gastrointestinal bleeding,
- hypothermia (abnormally low body temperature), and
- failing to take thyroid medications as prescribed.
What are the symptoms of myxedema coma?
When a patient presents with myxedema coma the following may be present:
- the body temperature is usually abnormally low (hypothermia), the core temperature may be as low as 80 F (26.6 C);
- severe mental changes including hallucinations, disorientation, seizures, and ultimately, deep coma;
- significant swelling (edema) all over the body with swollen eyes and thickening of the tongue,
- sparse, dry hair, and loss of the outer thirds of the eyebrows;
- difficulty breathing;
- collections of fluid around the lungs and heart (pleural effusion and pericardial effusions);
- the heart may slow down and its ability to pump blood forward can be impaired;
- the gastrointestinal tract does not function well and sometimes it becomes paralyzed, thereby necessitating surgery; and
- blood test abnormalities are a result of the increased fluid in the body. For example, sodium levels drop because of dilution, which is caused by the body retaining extra water.
How is myxedema coma diagnosed?
Initial laboratory evaluation usually includes a test for thyroid function (TSH, T3 and T4 levels). Other blood tests, as well as heart and lung function testing, may also be needed.
What is the treatment for myxedema coma?
Treatment may include assisting the patient to breathe and warming them to raise the body temperature to normal. Often, antibiotics are started until it is certain that an infection is not present.
The method of replacing thyroid hormone in patients with myxedema coma is controversial. Many different approaches are used. In general, initial replacement is done by intravenous infusion, since the intestinal system may not be absorbing properly.
While common hypothyroidism without myxedema is usually treated with T4 replacement (the hormone produced in greatest quantity by the thyroid gland), in the case of myxedema coma, management is different. The thyroid gland also produces a small amount of another hormone, T3. This is the more metabolically active of the two hormones. In patients who are well, T4 is converted into T3 in the bloodstream. However, patients with myxedema coma are often so sick that this conversion is impaired. As a result, many doctors choose to treat these patients with T3 initially and start T4 therapy as well. Since T4 therapy can take a month or so to work, there is usually an overlap of these two hormones. Care is taken to avoid heart rhythm abnormalities (arrhythmias) and stress on the heart, which can be caused by replacing thyroid hormone too quickly, particularly in elderly patients.
While mild thyroid disorders can be managed by primary care physicians, myxedema coma is generally managed by a thyroid specialist (endocrinologist) because treatment can be complicated and critical.
How can myxedema coma be prevented?
The ideal way to manage this condition is to prevent it from occurring in the first place. An individual with hypothyroidism should visit their doctor regularly for follow-up and blood testing to be certain that their replacement dose is appropriate.
If an individual has symptoms that concerns them, but has not beendiagnosed with hypothyroidism, they should visit their health care practitioner to discuss their concerns and explore the option of testing for thyroid imbalance.
Medically reviewed by John A. Seibel, MD; Board Certified Internal Medicine with a subspecialty in Endocrinology & Metabolism
"Clinical manifestations of hypothyroidism"