The myxedematous coma is the severe manifestation of hypothyroidism, a condition that occurs when the body lacks enough thyroid hormone. Patients with hypothyroidism often suffer from physiological alterations as a result of the body trying to compensate for the lack of thyroid hormone.
The thyroid is a small gland located in the front of the neck that releases hormones that the body needs to regulate energy and balance the growth and degree of functionality of different body systems.
If these homeostatic mechanisms are affected by causes such as infections, the patient can decompensate leading to myxedema coma.
Patients with myxedema coma present with considerable organ abnormalities and progressive mental decline. A common mistake is to believe that a patient must be in a coma to be diagnosed with this pathology.
However, myxedematous coma is a misnomer because most patients are neither comatose nor present with the edema known as myxedema..
Hypothyroidism is four times more common in women than in men. 80% of cases of myxedematous coma occur in women and occur almost exclusively in people over 60 years of age. Low temperatures are also often a major factor in the development of the condition.
Given the importance of thyroid hormones in cellular metabolism, myxedematous coma is normally associated with a reduced metabolic rate and lower oxygen consumption, affecting all body systems..
Before a patient develops myxedema coma, the features of hypothyroidism are usually present and may have gone unnoticed for a prolonged period..
Despite the term myxedematous coma, many patients do not present in a coma but do manifest varying degrees of altered consciousness. Brain function is affected by reduced oxygen supply and subsequent consumption, decreased glucose utilization, and reduced cerebral blood flow.
The altered mental state can range from mild confusion, apathy, and lethargy to clouding and coma. Although all patients with myxedematous coma have some degree of altered mental status, only a few present with true coma
Hypoventilation also occurs in myxedema as a result of a depressed hypoxic ventilatory drive (a poor response to low oxygen levels) and a hypercapnic ventilatory response (accumulation of carbon dioxide)..
As a result, the concentrations of these gases in the body are altered, and gas exchange in the lungs does not occur properly..
Renal function can be compromised with a reduced glomerular filtration rate due to decreased renal blood flow and increased vascular resistance in the afferent and efferent arterioles..
The gastrointestinal tract in myxedematous coma may be marked by mucopolysaccharide infiltration and edema. The most common gastrointestinal presentation is constipation, which occurs as a result of decreased intestinal motility.
Myxedema coma is associated with an increased risk of bleeding caused by coagulopathy related to an acquired von Willebrand syndrome and a decrease in factors V, VII, VIII, IX, and X.
Patients may present with classic myxedematous facies, characterized by generalized swelling, ptosis, macroglossia, scant, rough hair, and periorbital edema. The skin is dry, pale, and thickened with unresectable edema.
Cardiovascular manifestations include bradycardia and low cardiac output due to decreased cardiac contractility; however, overt congestive heart failure is rare.
Reduced stroke volume in severe cases may also be due to pericardial effusions caused by accumulation of fluid rich in mucopolysaccharides within the pericardial sac.
Hypothermia is usually present, with a body temperature that can drop as low as 24 ° C.
Clearly the term "myxedematous coma" is nothing more than an extreme representation of some symptoms of hypothyroidism: "coma" as a result of reduced neurological and metabolic function, and "myxedema" as a result of fluid accumulation of form prolonged in declining areas of the body.
The latter requires a little more explanation, since the determining factor for myxedema is, initially, the accumulation of proteins in these sloping areas, normally mobilized by lymph into the circulation (a phenomenon favored by a high metabolic rate).
These stagnant proteins are osmotically active, that is, they attract water with considerable power, and they cannot cross membranes. For these reasons, patients with hypothyroidism tend to develop this characteristic edema..
Most patients with myxedema coma have a history of hypothyroidism. Some patients may have developed hypothyroidism after thyroidectomy or iodine therapy for hyperthyroidism.
Almost entirely, the problem is caused by the inability of the thyroid gland to produce thyroid hormone. Very rarely it is caused by the failure of the pituitary gland or hypothalamus to properly signal the thyroid gland to perform its normal functions..
Myxedema coma is a physiological decompensation of untreated hypothyroidism that is usually caused by a trigger such as the following:
-Exposure to cold temperatures
-Congestive heart failure
-Medications such as the following:
-Metabolic disturbances such as hypoglycemia, hyponatremia, acidosis, and hypercapnia
It can also develop when someone stops taking their thyroid medicine..
Many patients who develop myxedema coma are initially hospitalized for an unrelated condition. During hospitalization, the patient slowly develops a change in mental state. The diagnosis may not be suspected initially, especially when narcotics or sedatives are used.
Myxedema coma is an acute medical emergency and must be treated in the intensive care unit. Continuous monitoring of the patient's cardiovascular and pulmonary status is required, and respiratory support is often required.
The method to replace thyroid hormone involves taking a synthetic version of the T4 hormone known as levothyroxine. Once T4 hormone levels are restored, symptoms become more manageable, although this can take several weeks. You may need to continue taking this medicine for the rest of your life..
The ideal mode of therapy and doses of thyroid hormone therapy in myxedema coma remain controversial due to the rarity of the condition and the lack of clinical trials.