Myxedema coma

Myxedema coma, refers to the extreme manifestation of hypothyroidism.

It is potentially lethal.



Patients with hypothyroidism may decompensate into myxedema coma, when their homeostatic mechanisms fail: 


when the body’s compensatory responses to hypothyroidism are overwhelmed by a precipitating factor, such as infection.



Patients with hypothyroidism typically have a history of fatigue, weight gain, constipation and cold intolerance. 



Patients myxedema coma should be admitted to an intensive care unit for pulmonary and cardiovascular support, and treatment with intravenous levothyroxine (T4) as opposed to intravenous liothyronine (T3). 



Hydrocortisone treatment is administered until coexisting adrenal insufficiency is ruled out.



Myxedema coma is an extreme complication of hypothyroidism with  multiple organ abnormalities and progressive mental deterioration. 



Myxedema coma is a misnomer because most patients exhibit neither the nonpitting edema known as myxedema nor coma.



The main manifestation of myxedema coma is a deterioration of the patient’s mental status.



Mortality ranges from 30 to 60 percent.



Hypothyroidism is four times more common in women than in men.



80 percent of cases of myxedema coma occur in females.



It occurs almost exclusively in persons 60 years and older.



More than 90 percent of myxedema coma cases occur during the winter months: sense temperature and lower heat production secondary to hypothyroidism.



Patients with myxedema coma usually have longstanding hypothyroidism. even although iid not not have been previously diagnosed. 



Patients often demonstrate symptoms of hypothyroidism: fatigue; constipation; weight gain; cold intolerance; a deep voice; coarse hair; and dry, pale, cool skin. 



The elderly with hypothyroidism often have atypical presentations, such as decreased mobility, and some patients with compensated hypothyroidism are asymptomatic.



Hypothyroidism decompensation into myxedema coma occurs when the hypothyroid patient’s homeostatic mechanisms are disrupted. 



Common precipitating factors of myxedema coma include, infections, particularly pneumonia and urosepsis, certain medications, and failure to reinstate thyroid replacement therapy during hospitalization.



Factors Known to Precipitate Myxedema








Carbon dioxide retention



Gastrointestinal hemorrhage


















Urinary tract infection/urosepsis


















Beta blockers

































Physical findings in myxedema coma may include:



Myxedematous face, which is characterized by generalized puffiness, macroglossia, ptosis, periorbital edema, and coarse, sparse hair. 



Nonpitting edema of the lower extremities is sometimes present. 



The thyroid examination are usually normal, but a goiter may be present in some patients. 



Neurological examination may reveal decreased reflex tendon relaxation and will invariably reveal altered mentation.



Altered mentation









Dry, cool, doughy skin



Gastrointestinal-Decreased motility






Paralytic ileus



Fecal impaction



Myxedema megacolon









Myxedematous face



Generalized swelling









Periorbital edema



Coarse, sparse hair



Nonpitting edema



All patients with myxedema coma manifest deterioration of their mental status: apathy, neglect or a decrease in intellectual function, confusion, psychosis and, rarely, coma. 



Hypothermia is  common clinical feature of myxedema coma: temperature is usually less than 35.5°C (95.9°F).



Hypoglycemia and cold exposure may exacerbate the hypothermia. 



With compensated hypothyroidism patients often exhibit diastolic hypertension, but decreased oxygen consumption and lowered body temperature result in peripheral vasoconstriction and central shunting.



With decompensation neurovascular mechanisms fail, and the patient may then display hypotension characteristically associated with myxedema coma. 



Bradycardia, low cardiac output and overall blood volume deficit frequently exacerbate the hypotension.



Myxedema coma hypoventilation results from the decreased ventilatory response to hypoxia and hypercapnia.



Myxedema coma respiratory dysfunction may lead to sleep apnea, and respiratory difficulties exacerbated by myxedematous infiltration of the tongue and pharynx.



Hypothyroidism causes weakness of the diaphragm.



Myxedema coma diagnostic findings  include abnormal thyroid hormone levels, electrolyte levels, and creatine kinase (CPK) levels.



Typically, patients with myxedema coma have primary hypothyroidism manifested by low serum levels of thyroxine (T4) and triiodothyronine (T3) and a high thyroid stimulating hormone (TSH) level. 



Myxedema coma should be considered in all patients with altered mental status or symptoms of psychiatric illness. 



Secondary hypothyroidism is a result of pituitary dysfunction.



Tertiary hypothyroidism is caused by a hypothalamic abnormality. 



With hypopituitarism TSH levels is not increased, therefore a low T4 level and low-normal or decreased TSH level mandate a search for pituitary abnormalities. 



Hyponatremia seen in myxedema coma is a result of decreased free water clearance due to elevated levels of antidiuretic hormone and/or diminished blood flow to the brain and kidneys.



Myxedema coma hyponatremia is associated with a low serum osmolality, and a high serum creatinine.



Hypoglycemia may be a result of the down-regulation of metabolism.



Increased CPK and other transaminases are thought to result from altered membrane permeability, and may lead to misdiagnosis of myocardial infarction.



The fractionation of the CPK reveals such changes are from skeletal muscle.



Myxedema coma ECG changes include bradycardia, decreased voltages, non-specific ST and T changes, varying types of block and a prolonged QT interval. 



Arterial blood gas analysis often reveals respiratory acidosis, hypoxia and hypercapnia. 



Leukopenia and a normocytic anemia are also frequently present. 



Macrocytic anemia and pernicious anemia caused by associated immune dysfunction are sometimes present.



Cardiomegaly and pleural effusions may be noted on chest x-ray.



Lumbar puncture typically reveals elevated protein levels, with  a high opening pressure. 






Admission to ICU, correction of 


hypovolemia and electrolyte abnormalities



Mechanical ventilation may be necessary. 



Intravenous thyroid hormone replacement.



The  necessity of intravenous thyroid hormone replacement is  clear: initial levothyroxine dose of 100 to 500 μg administered intravenously should be followed by 75 to 100 μg administered intravenously daily until the patient is able to take oral replacement. 



The lower initial doses are administered to patients who are frail or have other comorbidities, such as cardiovascular disease. 



Elderly patients typically require 100 to 170 μg of oral levothyroxine daily.



Because an infection is often the cause of the patient’s decompensation; evaluation for the presence of infection is taken, and administration of antibiotics is considered.



Hydrocortisone should be administered intravenously at a dosage of 100 mg every eight hours, until adrenal insufficiency is ruled out, to prevent adrenal crisis.



The mortality rate ranges from 30-60% percent.



Poor prognosis associated with advanced age, bradycardia and persistent hypothermia, adrenal insufficiency, decreased level of consciousness,and delayed treatment.



Myxedema coma is the most severe form of hypothyroidism, with the hallmark symptom being altered mental status.



Unusual presentations of hypothyroidism include dementia, delirium, psychosis, aggression, and hallucinations.



Triggers of myxedema coma:  medications, gastrointestinal tract bleeding, and sepsis, cerebrovascular accidents and cold exposure.



Cardiac manifestations of myxedema coma include pericardial effusion, bradycardia, prolonged QT interval, congestive heart failure, and diastolic hypertension. 



Laboratory findings in MC:  normocytic anemia, hyponatremia, hyperlipidemia, and an elevated creatinine kinase level. 



Hyponatremia likely due to increased levels of antidiuretic hormone.



Creatinine kinase is often elevated, likely secondary to increased muscle membrane permeability.








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