Sandbox spinalcord

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.
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.
Even in severe hypothyroidism a balance of metabolic homeostasis is achieved through adaptive neurovascular mechanisms. However in conditions such as respiratory or urinary tract infections, cardiac, acute myocardial infarction or stroke interfere with this adaptive mechanisms by decreasing the blood volume and ventilation triggering myxedema coma.

Treatment

Myxemeda 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).