Deficient thyroid hormone production can be due to thyroid failure (primary hypothyroidism) or, less commonly, pituitary or hypothalamic disease (secondary hypothyroidism) (Table 170-1). Congenital hypothyroidism is present in 1 of 4000 newborns; the importance of its recognition and prompt treatment for child development has led to the adoption of neonatal screening programs. Transient hypothyroidism may occur in silent or subacute thyroiditis. Subclinical (or mild) hypothyroidism is a state of normal free thyroid hormone levels and mild elevation of thyroid-stimulating hormone (TSH); despite the name, some pts may have minor symptoms. With higher TSH levels and low free T4 levels, symptoms become more readily apparent in clinical (or overt) hypothyroidism. In areas of iodine sufficiency, autoimmune disease and iatrogenic causes are the most common etiologies of hypothyroidism. The peak age of occurrence is around 60 years, and prevalence increases with age.
Symptoms of hypothyroidism include lethargy, dry hair and skin, cold intolerance, hair loss, difficulty concentrating, poor memory, constipation, mild weight gain with poor appetite, dyspnea, hoarse voice, muscle cramping, and menorrhagia. Cardinal features on examination include bradycardia, mild diastolic hypertension, prolongation of the relaxation phase of deep tendon reflexes, and cool peripheral extremities. Goiter may be palpated, or the thyroid may be atrophic and nonpalpable. Carpal tunnel syndrome may be present. Cardiomegaly may be present due to pericardial effusion. The most extreme presentation is a dull, expressionless face, sparse hair, periorbital puffiness, large tongue, and pale, doughy, cool skin. The condition may progress into a hypothermic, stuporous state (myxedema coma) with respiratory depression. Factors that predispose to myxedema coma include cold exposure, trauma, infection, and administration of narcotics. In mild hypothyroidism, the classic findings of overt hypothyroidism may not be present, and the clinical picture may be dominated by fatigue and ill-defined symptoms.
Decreased serum free T4 is common to all varieties of hypothyroidism. An elevated serum TSH is a sensitive marker of primary hypothyroidism but is not found in secondary hypothyroidism. A summary of the investigations used to determine the existence and cause of hypothyroidism is provided in Fig. 170-1. Thyroid peroxidase (TPO) antibodies are increased in >90% of pts with autoimmune-mediated hypothyroidism. Elevated cholesterol, increased creatine phosphokinase, and anemia may be present; bradycardia, low-amplitude QRS complexes, and flattened or inverted T waves may be present on ECG.
Treatment: Hypothyroidism Adult pts <60 years without evidence of heart disease may be started on 50-100 µg of levothyroxine (T4) daily. In the elderly or in pts with known coronary artery disease, the starting dose of levothyroxine is 12.5-25 µg/d. The dose should be adjusted in 12.5- to 25-µg increments every 6-8 weeks on the basis of TSH levels, until a normal TSH level is achieved. The average daily replacement dose is 1.6 µg/kg per day, but dosing should be individualized and guided by TSH measurement. In secondary hypothyroidism, TSH levels cannot be used, and therapy needs to be guided by free T4 measurement. Women on levothyroxine replacement should have a TSH level checked as soon as pregnancy is diagnosed, as the replacement dose typically increases by 30-50% during pregnancy. Failure to recognize and treat maternal hypothyroidism may adversely affect fetal neural development. Therapy for myxedema coma should include levothyroxine (500 µg) as a single IV bolus followed by daily treatment with levothyroxine (50-100 µg/d), along with hydrocortisone (50 mg every 6 h) for impaired adrenal reserve, ventilatory support, space blankets, and treatment of precipitating factors. |
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