Myxedema coma pathophysiology

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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]

Pathophysiology

Risk factors Common risk factors that can trigger myxedema coma in patients with hypothyroidism include:

Hypothermia CVA CHF Infections ( pneumonia, influenza, UTI, sepsis) Drugs ( Anesthestics, narcotics, amidirone, Lithium carbonate) 6486153 GI bleeding Metabolic disturbances(Hypoglycemia, hyponatremia, acidosis, hypercalcemia, hypoxemia, hypercapneia) History History of antecedent thyroid disease History of radioiodine therapy or thyroidectomy Discontinuation of medications. 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 harmone can lead to cretinism and myxedema. In 1891, Murray was the first physician to discover cure for myxedema by using hypodermic injections of sheep thyroid extract. Pathophysiology Myxedema coma occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism. Myxedema coma is usually precipitated by a systemic illness. Causes Myxedema coma can result from any of the causes of hypothyroidism, most commonly chronic autoimmune thyroiditis. Myxedema coma can also occur in patients who had thyroidectomy or underwent radioactive iodine therapy for hyperthyroidism. Rare causes may include secondary hypothyroidism and medications such as lithium and amiodarone. Pathogenesis 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. [5] Reduced metabolism results in hypothermia. Reduced metabolism and decreased oxygen also results in decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents; this can precipitate myxedema coma. The following table summarizes the various effects of reduced thyroid hormone on different organ systems

Organ System Effect due to Decreased Thyroid Hormone Manifestation Cardiovascular Cardiac contractility is impaired Leading to reduced stroke volume

Low cardiac output

Bradycardia

Sometimes hypotension

Reduced stroke volume in severe cases may also be due to pericardial effusions

caused by the accumulation of fluid rich in mucopolysaccharides within the pericardial sac

Hypotension Narrowed pulse pressure

Fluid accumulation in tissue

Pericardial effusions.

Neurologic Altered brain function due to Reduced oxygen delivery and consumption

Decreased glucose utilization

Reduced cerebral blood flow.

Altered consciousness Pulmonary Central depression of ventilatory drive Decreased responsiveness to hypoxia and hypercapnia

Hypoventilation Renal Reduced glomerular filtration rate because of

Low cardiac output

Peripheral vasoconstriction

Rhabdomyolysis

Electrolyte abnormalities

Low volume stimulates

Antidiuretic hormone impairs water excretion leading to hyponatremia

Gastrointestinal mucopolysaccharide infiltration and edema malabsorption

gastric atony

impaired peristalsis,

paralytic ileus

megacolon.

GI bleeding Ascites

Constipation

Hematologic Coagulopathy due to decrease in production of factors V, VII, VIII, IX, and X

Hemorrhage and vitamin B12 deficiency

Bleeding Anemia

Treatment Myxedema coma is a medical emergency and requires a prompt treatment. All patients must be shifted to ICU.

Supportive Therapy Prevention of further heat loss by covering the patient with blankets but avoid external rewarming because it may produce vascular collapse. Consider warmed IV fluids. Cardiac monitoring of the patient. Acute Mecial Therapy Preffered regimen (1):- Levothyroxine 5 to 8 mcg/kg (200 to 500 mcg) IV infused over 15 min, then 50 to 100 mcg IV q24h until transition to an oral formulation is possible. Glucocorticoids should also be empirically administered until coexistent adrenal insufficiency can be ruled out. Hydrocortisone hemisuccinate 100 mg IV bolus is initially given, followed by 100 mg IV q8h until initial plasma cortisol level is confirmed normal. • IV hydration with D 5 NS is used to correct hypotension and hypoglycemia (if present); avoid overhydration and possible water intoxication because clearance of free water is impaired in these patients. • Rule out and treat precipitating factors (e.g., antibiotics in suspected sepsis).

ECG Electrocardiographic findings may 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