During the perinatal period, there is an absolute requirement for thyroid hormone for the development and maturation of the nervous and musculoskeletal systems. In the perinatal nervous system, thyroid hormone plays a critical role in normal growth of the cerebral and cerebellar cortices, the proliferation of axons, the branching of dendrites, synaptogenesis, myelination, cell migration, and so on.
Thyroid hormone also plays a major role in the maturation of bone. A deficiency of thyroid hormone in early life leads to both delay in and abnormal development of epiphyseal centers of ossification (epiphyseal dysgenesis). Hypothyroidism-induced impairment of linear growth can lead to dwarfism in which the limbs are disproportionately short in relation to the trunk with the apparent bone age retarded in relation to chronological age.
The hallmarks of infantile hypothyroidism (e.g., retardation of mental development and growth) become manifest only in later infancy and are largely irreversible. Consequently, early recognition and initiation of replacement therapy are crucial. In the absence of thyroid hormone therapy, the symptoms of infantile hy-pothyroidism include feeding problems, failure to thrive, constipation, a hoarse cry, and somnolence. In succeeding months, especially in severe cases, protuberance of the abdomen, dry skin, poor growth of hair and nails, delayed eruption of the deciduous teeth, and delay in reaching the normal milestones of development (e.g., holding up the head, sitting, walking, and talking) become evident.
In adults, the signs and symptoms of hypothyroidism include somnolence, slow mentation, dryness and loss of hair, increased fluid in body cavities (e.g., the pericardial sac), low metabolic rate, tendency to gain weight, hy-perlipidemia, subnormal temperature, cold intolerance, bradycardia, reduced systolic and increased diastolic pulse pressure, hoarseness, muscle weakness, slow return of muscle to the neutral position after a tendon jerk, constipation, menstrual abnormalities, infertility, and sometimes myxedema (hard edema of subcutaneous tissue with increased content of proteoglycans in the fluid). A goiter (i.e., enlargement of the thyroid gland) may be present.
Juvenile or adult patients with primary hypothyroidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and reducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing dietary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism.
Patients with secondary or tertiary hypothyroidism are also usually treated with thyroxine, but the serum TSH concentration is not a reliable guide to therapy. The efficacy of thyroid hormone replacement in these patients must be assessed clinically and by measurement of the serum T4 concentration.
The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support and treated with intravenous T4 (or sometimes T3). Until coexisting adrenal insufficiency is ruled out, hydrocortisone should also be administered.
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