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. [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.

Cardiovascular Cardiac contractility is impaired, leading to reduced stroke volume, low cardiac output, bradycardia and sometimes hypotension. [6] 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. Congestive heart failure is rarely seen in the absence of preexisting cardiac disease. 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. [7] The reduction of the effect of beta-adrenergic receptors leads to prevalence of the effect of alpha-adrenergic receptors, increased catecholamines, and increased systemic vascular resistance, causing some patients to have diastolic hypertension and a narrowed pulse pressure. Plasma volume is decreased, and capillary permeability is increased, leading to fluid accumulation in tissue and spaces and pericardial effusions. [8] Neurologic

Despite the term myxedema coma, many patients do not present in coma, but manifest variable degrees of altered consciousness. [1] Brain function is affected by reduction in oxygen delivery and subsequent consumption, decreased glucose utilization and reduced cerebral blood flow. Hyponatremia can also contribute to altered mental function. Pulmonary The main pulmonary effect of myxedema coma is hypoventilation, which results from central depression of ventilatory drive with decreased responsiveness to hypoxia and hypercapnia. [9, 10] Other contributing factors to hypoventilation include respiratory muscle weakness, mechanical obstruction by a large tongue, and obesity-hypoventilation syndrome. Fluid accumulation may cause pleural effusions and decreased diffusing capacity. Renal Kidney function may be compromised with reduced glomerular filtration rate because of low cardiac output and peripheral vasoconstriction or because of rhabdomyolysis. [11, 12] Hyponatremia is common in patients with myxedema coma and is caused by increased serum antidiuretic hormone and impaired water excretion. [13, 14] Gastrointestinal The gastrointestinal tract in myxedema coma can be marked by mucopolysaccharide infiltration and edema. In addition, neuropathic changes can cause malabsorption, gastric atony, impaired peristalsis, paralytic ileus, and megacolon. [15] Ascites may occur due to increased capillary permeability, heart failure, or other mechanisms. [16] Gastrointestinal bleeding secondary to an associated coagulopathy may occur. [17] Hematologic Myxedema coma is associated with a higher risk of bleeding caused by coagulopathy related to an acquired von Willebrand syndrome (type 1) and decreases in factors V, VII, VIII, IX, and X. [18, 19] Patients may also have microcytic anemia secondary to hemorrhage, or macrocytic anemia caused by vitamin B12 deficiency, or normocytic normochromic anemia, which may be secondary to decreased oxygen requirement and reduced erythropoietin

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).