DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema co...
DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation. The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy.
• Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
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MYXEDEMA COMA By PINKY RATHEE M.Sc. NURSING
Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold. Myxedema Coma
Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation . The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy. Myxedema Coma
Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area. Myxedema Coma
It is deficiency of thyroid hormone resulting in- slowed body metabolism, decreased heat production, decreased oxygen consumption by tissues. HYPOTHYROIDISM
Chronic autoimmune thyroiditis , Thyroidectomy Underwent radioactive iodine therapy for hyperthyroidism, Secondary hypothyroidism. ETIOLOGY AND RISK FACTORS of Myxedema Coma
Poor compliance and lack of knowledge about managing levothyroxine therapy in acute illness. Undiagnosed hypothyroidism ETIOLOGY AND RISK FACTORS of Myxedema Coma
Medications – sedatives, narcotics, amiodarone , rifampin , beta blockers. Decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents; this can precipitate myxedema coma. PRECIPITATING FACTORS
CVS – cardiac contractility is impaired leading to reduced stroke volume, low cardiac output, bradycardia and hypotension. CNS –Brain function is affected by reduction in oxygen delivery and subsequent consumption, decreased glucose utilization and reduced cerebral blood flow. PATHOPHYSIOOGY of Myxedema Coma
Pulmonary – hypoventilation due to central depression of ventilatory drive with decreased responsiveness to hypoxia and hypercapnia Renal - Hyponatremia is common in patients with myxedema coma and is caused by increased serum antidiuretic hormone and impaired water excretion and reduced GFR due to low cardiac output. PATHOPHYSIOOGY of Myxedema Coma
GI - malabsorption , impaired peristalsis, paralytic ileus . Ascites may occur due to increased capillary permeability, heart failure, or other mechanisms. Gastrointestinal bleeding secondary to an associated coagulopathy may occur. PATHOPHYSIOOGY of Myxedema Coma
History -Most patients with myxedema coma have a history of hypothyroidism. Some patients may have developed hypothyroidism after thyroidectomy or iodine therapy for hyperthyroidism. Symptoms of hypothyroidism, including fatigue, weight gain, cold intolerance, constipation, and dry skin, may be elicited. Patients have depressed mental state with lethargy, delirium, or coma. Cold extremities, non pitting edema of the upper and lower extremities. Confusion, stupor, slow speech, delayed reflexes, seizures, coma Symptoms of the precipitating illness can be seen such as infection (commonly pneumonia), stroke, myocardial infarction, trauma, or heart failure. CLINICAL MANIFESTATION
Hypoventilation leading to respiratory acidosis. Hypothermia Hypotension Hypoglycaemia Hyponatremia Hypercapnia hypoxia Drastic decrease in metabolic rate.
TFTs – TSH (0.4-4mU/L) is elevated, fT3 and fT4 is low. A low or normal TSH level with low levels of free T4(0.7-1.9ng/dl) and free T3 (80-180ng/dl) may indicate that the disorder is due to pituitary or hypothalamic dysfunction Other tests – Serum osmolality ( hyponatremia ), serum creatinine (because of decreased renal perfusion), CBC (infection), serum cortisol . LABORATORY INVESTIGATIONS
CXR (signs of Pulmonary Edema , cardiomegaly , CHF, pericardia effusion), ECG (sinus bradycardia , low-amplitude QRS complexes, a prolonged QT interval, flattened or inverted T waves, or arrhythmias). Imaging studies –
Levothyroxine sodium- lifelong therapy. Myxedema Coma- Maintain a patent airway Oxygen administration I/V fluids. Vital signs to be monitored. Correct hypothermia Vasopressor for tissue perfusion Levothyroxine sodium with I/V glucose, corticosteroids MANAGEMENT
Airway maintenance is crucial, mechanical ventilation is commonly required during the first 36-48 hours, but some patients require prolonged respiratory support for as long as 2-3 weeks. Thyroid hormone replacement – controversial, some favor levothyroxine (T4) while others favor combination of T4 and liothyronine (T3).An intravenous loading dose of 300-600 micrograms of levothyroxine (T4) is followed by a daily intravenous dose of 50-100 micrograms. ICU setting with continuous cardiac monitoring
Because the rate of conversion of T4 to the active hormone T3 can be reduced in these patients, the addition of T3 along with T4 has been recommended. T3 has a quicker onset of action than T4, as increases in body temperature and oxygen consumption has been reported to be faster with T3 therapy compared to T4.T3 therapy is given as bolus of 5-20 micrograms intravenously and to be continued at a dosage of 2.5-10 micrograms every 8 hours. Measurement of thyroid hormones every 1-2 days is suggested. Failure of TSH to decrease or of thyroid hormone levels to increase suggests the need to increase doses of T4 and/or add T3. The treatment is changed to the oral form once the patient is able to take medications by mouth.
Patients with primary hypothyroidism may have concomitant primary adrenal insufficiency while patients with secondary hypothyroidism may have associated hypopituitarism and secondary adrenal insufficiency. The other rationale for the treatment with corticosteroids is the potential risk of precipitating acute adrenal insufficiency caused by the accelerated metabolism of cortisol that follows T4 therapy. Hydrocortisone at a dose of 50-100 mg every 8 hours is administered. An alternative is dexamethasone at a dose of 2-4 mg every 12 hours. Glucocorticoid therapy –
Treat hypothermia with passive rewarming using ordinary blankets and a warm room. Treat associated infection. Correct severe hyponatremia with saline and free water restriction. Correct hypoglycemia with IV dextrose. Hypotension is usually corrected with thyroid hormone therapy. If blood pressure continues to be low, cautious use of intravenous fluids with normal saline is advised. Refractory hypotension can be cautiously treated with vasopressors such as dopamine. Supportive measures –
Activity intolerance related to fatigue. Space activities to promote rest and exercise. Assist with self-care activities when patient is fatigued. Risk for imbalanced body temperature related to decreased metabolism. Provide extra layer of blanket/clothing. Monitor vital signs. Protect from exposure to cold and drafts. NURSING MANAGEMENT
Constipation related to depressed GI function. Encourage increased fluid intake. Provide food rich in roughage, fibre. Avoid abuse of laxatives. Encourage increased mobility. Deficient knowledge about the therapeutic regimen. Explain rational for lifelong thyroid hormone replacement therapy. Explain side-effects, action, overdose, symptoms of medication. Follow-up visits.
Ineffective breathing patterns related to depressed ventilation. Monitor respiratory rate, pattern, depth . Encourage deep breathing exercises, coughing exercises. Maintain patent airway. Disturbed thought process related to hypothyroidism Orient patient to time, place and person. Provide stimulation through conversation and activities.
Myxedema & myxedema coma related to the disease process. Monitor for complications. Monitor compliance and response to therapy.