Myxedema coma overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Myxedema coma constitutes the highest expression of untreated hypothyroidism and results from depletion severe and prolonged thyroid hormones. The term coma is considered to be misleading because the majority of patients with this syndrome are not initially in a comatose condition. Myxedematous coma is believed to triggered by a variety factors that cause a systemic compromise with fatal outcome if not mediating an early diagnosis and intensive treatment. The typical picture of myxedematous coma is lethargy that progresses to stupor and finally coma. In addition to coma, the clinical characteristics of hypothyroidism such as dry skin, alopecia, hoarse voice, periorbital edema and generalized macroglossia and hyporeflexia are also present.
Historical Perspective
In 874, Gull was the first physician to describe hypothyroidism under the name myxedema due to its characteristics of swollen skin and its mucin content. In 1883, Semon was the first to establish a relationship between patients undergoing thyroidectomy and later developing symptoms of myxedema. In 1888, Clinical Society of London presented a paper describing that extreme loss of thyroid hormone can lead to cretinism and myxedema.
Classification
There is no established classification system for myxedema coma.
Pathophysiology
Myxedema coma occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism. Myxedema coma is usually precipitated by a systemic illness. Thyroid hormone plays an important role in cell metabolism. Long-standing hypothyroidism is associated with reduced metabolic rate and decreased oxygen consumption, which affects all body systems. Reduced metabolism and decreased oxygen results in hypothermia and decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents and can precipitate myxedema coma.
Causes
Common causes of myxedema coma include sepsis, exposure to cold weather, central nervous system depressants (sedatives, narcotics, antidepressants), trauma, surgery, stroke, congestive heart failure, burns, intravascular volume contraction (GI blood loss, diuretic use), myocardial infarction, and metabolic derangements.
Differentiating Myxedema coma from Other Diseases
Myxedema must be differentiated from other causes of lower limb edema-like chronic venous insufficiency, acute deep venous thrombosis, lipedema, lymphatic filariasis, cellulitis and causes of generalized edema.
Epidemiology and Demographics
Myxedema coma is the extreme expression of severe hypothyroidism and fortunately is rare, with an incidence rate of 0.022 per 100,000 per year. Myxedema coma is more commonly seen in older age group.
Risk Factors
Common risk factors in the development of myxedema coma include hypothermia, cerebrovascular accidents, congestive heart failure, infections, drugs,gastrointestinal bleeding, trauma, and electrolyte disturbances.
Screening
There is insufficient evidence to recommend routine screening for myxedema coma.
Natural History, Complications, and Prognosis
If left untreated, myxedema coma can be fatal leading to death. Common complications of myxedema coma include treatment-induced congestive heart failure in patients with coronary artery disease, increased susceptibility to infection and organic psychosis with paranoia. The mortality rate in myxedema coma is 20% to 25% despite aggressive therapy.
Diagnosis
Diagnostic Criteria
The diagnosis of myxedema coma is made when the three key diagnostic features of myxedema coma are present, which include altered mental status, hypothermia or absence of fever and a precipitating event such as cold exposure, infection, drugs.
History and Symptoms
The function of all organ systems and various metabolic pathways are compromised in hypothyroidism. The cardinal symptoms of myxedema coma are the sensory impairment and hypothermia. The accumulation in the interstitial tissue of mucopolysaccharides and water leads to myxedema that compromises large part of the tissues. Myxedema coma patients may be disoriented, therefore, the patient interview may be difficult. In such cases, history from the care givers or the family members may need to be obtained.
Physical Examination
The physical examination findings of myxedema coma will reveal the characteristic signs of hypothyroidism, and not being able to obtain patient's history, it is often very useful to search for of other signs that guide the diagnosis of myxedema coma such as a cervical scar (history of thyroid surgery), vitiligo, hyperpigmentation, ophthalmopathy.
Laboratory Findings
Myxedematous coma should be considered in any patient who is comatose or who has some degree of deterioration of the sensorium with hypothermia or absence of fever in the presence of infection, hyponatremia and / or hypercapnia. Performing a thyroid routine test is considered best initial step in management of patients with myxedema coma.
Electrocardiogram
Electrocardiographic findings of myxedema coma include bradycardia, varying degrees of block, low voltage, nonspecific ST-segment changes, flattened or inverted T waves, prolonged Q-T interval, and ventricular or atrial arrhythmias.
X-ray
There are no x-ray findings associated with myxedema coma. However, an x-ray may be helpful in the diagnosis of complications of myxedema coma, which include cardiomegaly, pericardial effusion, congestive heart failure, or pleural effusion
Ultrasound
There are no echocardiography/ultrasound findings associated with myxedema coma.
CT scan
There are no CT scan findings associated with myxedema coma but a CT scan of brain is done to rule out CNS etiology.
MRI
There are no MRI findings associated with myxedema coma.
Other Imaging Findings
There are no other imaging findings associated with myxedema coma.
Other Diagnostic Studies
There are no other diagnostic studies associated with myxedema coma.
Treatment
Medical Therapy
All the patients with myxedema coma should be shifted to ICU and treatment should be started as quickly as possible. Given the clinical suspicion of myxedema coma, initiate replacement therapy without waiting for results of endocrine laboratory. The empirical use of glucocorticoids should be part of the initial therapeutic protocol, in view of the observations which indicate that severe hypothyroidism induces a lower adrenal response to stress. This is independent of whether or not there is simultaneous adrenal insufficiency. Since thyroid hormone speeds up metabolism of cortisol and its plasma levels may be decreased in the presence of adrenal insufficiency, the glucocorticoids should always be given prior to thyroid replacement because otherwise they could precipitate an adrenal crisis. Hydrocortisone will be given in doses of stress, 50- 100 mg intravenously (IV) every 6-8 h for 7 to 10 days or until hemodynamically stabilizes the patient. Suspend if laboratory commitment is discarded of the adrenal axis. Identify and properly treat the precipitating factor.
Surgery
Surgical intervention is not recommended for the management of myxedema coma.
Primary Prevention
Effective measures for the primary prevention of myxedema coma include regular follow-up care, undergoing regular blood testing in order to adapt hormone replacement therapy and compliant with medications once the diagnosis of hypothyroidism is made.
Secondary Prevention
There are no secondary preventive measures available for myxedema coma.