Fatigue, somnolenee, eold intoleranee, syneope, exertional Bradyeardia, hair changes (sparse, eoarse, dry, brittle), puffy face, loss of lateral aspeets of the dyspnea, weight gain, arthralgias, nausea, anorexia, eyebrows, penorbital edema, maeroglossia, voiee deepening and hoarsening, skin ehanges (sealy, indigestion, eonstipation, menstrual abnormalities thiek, doughy, eoarse, dry, earotenemia), bnttle nails, nonpitting edema, galaetorrhea, effusions
Data from Mitehell JM: Thyroid disease in the emergeney department: Thyroid fune~tion tests and hypothyroidism and myxedema eoma Emerg Med Clin North Am 1989;7:885-902; Mazzafern EL: Adult hypothyroidism: 1. Manifestations and elinical presentation. Postgrad Med 1986;79:64 72; Myers L, Hays J: Myxedema eoma. Cnt Care Clinie 1991;7:43 56; and iQaminsld HJ, Ruff RL: Neurologie eomDheations of endoenne diseases. Neurol Clin 7:489 508.
hypothyroidism,^1 its reported incidence among adult hypothyroid patients varies. y Minor evidence of polyneuropathy, such as distal lower extremity sensory dysfunction and absent ankle jerks, is observed in approximately 10 percent of patients, y and rarely, a moderately severe sensorimotor polyneuropathy has been described. Carpal tunnel syndrome (i.e., median mononeuropathy at the wrist) occurs in 15 to 30 percent of hypothyroid patients, is usually bilateral, and is the most common mononeuropathy encountered.
Myopathy can be a feature of hypothyroidism and manifests with proximal muscle weakness. Regardless of the cause of the hypothyroidism, weakness is observed in about one third of these patients.y Increased muscle size and firmness, which is most obvious in the limb musculature, as well as slowed muscle contraction are important features to identify. Exertional pain, stiffness, and cramps may be noted, and myoedema may be observed. Myoedema, a mounding of the muscle in response to direct percussion, is painless and electrically silent, and occurs in one third of hypothyroid patients. y Difficulty relaxing the hand grip and exacerbation by cold weather may suggest myotonia. However, unlike myotonia, hypothyroid myopathy involves a slowness of muscle relaxation and contraction, and resolves with correction of the hypothyroid state. y Although sleep apnea is usually of the obstructive type, other possibilities include a central abnormality, chest muscle weakness, and blunted responses to hypoxia and hypercapnia. y Reports have associated hypothyroidism with SIADH,y idiopathic intracranial hypertension, y and myasthenia gravis.
Differential Diagnosis. Ihe differential diagnosis of hypothyroidism includes nonthyroidal illness (i.e., decreased I 3 or I4 , or both, without clinical hypothyroidism), euthyroid hypothyroxinemia (decreased I4 caused by decreased thyroid-binding globulin), and drugs that inhibit 14 binding (salicylates, phenytoin, and phenobarbital). Once hypothyroidism has been diagnosed, the most important clinical distinction is between primary and secondary hypothyroidism. Ihe clinical and laboratory similarities between myxedema coma and other life-threatening causes of the comatose state may make its diagnosis extremely difficult. Regarding hypothyroid myopathy, the muscular appearance, stiffness, and exacerbation by cold may suggest a mild form of myotonia congenita, which can present in adulthood. Although the stiffness noted in patients with pyramidal and extrapyramidal diseases may appear similar to that of hypothyroid myopathy, the characteristic history, appearance, and laboratory studies usually permit the diagnosis of hypothyroidism.
Evaluation. The combination of a low T4 level and an elevated thyroid-stimulating hormone (TSH) level is virtually diagnostic of primary hypothyroidism, because TSH elevation does not occur in central hypothyroidism. Further delineation between primary and secondary hypothyroidism is dependent on history, examination, and other laboratory studies. In addition to TFTs, other laboratory abnormalities have been described, including anemia (normocytic-normochromic, microcytic-hypochromic, or macrocytic) and hyponatremia (factitious due to hyperlipidemia or secondary to impaired free water excretion), as well as elevated serum creatine kinase, myoglobin,1™1 and prolactin. Because of the possibility of concomitant adrenal insufficiency, a serum cortisol level should also be obtained. The EEG may show slowing of the posterior dominant rhythm and a generalized voltage decrease, as well as triphasic waves that disappear with replacement therapy. y CSF analysis may reveal an elevated protein content which may exceed 100 mg/dl.
Management. The treatment of hypothyroidism, regardless of cause, consists of thyroid hormone replacement. Even in the setting of hypothyroid-induced seizures, achievement of the euthyroid state facilitates control. y Precipitants of myxedema coma (e.g., infection, cold exposure, certain drugs [phenothiazines, narcotics, and sedative-hypnotics, phenytoin, rifampin], and other stressors [surgery, trauma]) require correction. y
Prognosis and Future Perspectives. With early recognition and treatment, as well as improved intensive supportive care, the mortality rate of myxedema coma has decreased from roughly 50 to 70 percent to around 15 to 20 percent. y Without early recognition and prompt institution of replacement therapy, the prognosis is grave.y
Pathogenesis and Pathophysiology. Thyroid hormones affect mitochondrial oxidative capacity, protein synthesis and degradation, tissue sensitivity to catecholamines, muscle fiber differentiation, and capillary growth. y Excess thyroid hormone produces accelerated muscle protein catabolism and enhanced lysosomal protease activity, and interferes with the anabolic effects of insulin on muscle. y Despite this understanding, the exact pathophysiology of thyrotoxic myopathy remains unknown. CNS observations include elevated rates of cerebral circulation, faster posterior dominant rhythms, alterations in the sensitivity of some brain enzymes and neurotransmitter systems, and altered metabolic responses.y At present, the specific pathophysiological processes causing these manifestations remain unknown. It has been proposed that alterations in central and peripheral beta-adrenergic tone may be responsible for hyperthyroid-related tremor and chorea, and that brisk tendon reflexes may reflect faster muscle contraction and relaxation times.
Epidemiology and Risk Factors. Hyperthyroidism is more common in women than in men (10:1 ratio) and often shows a strong familial predisposition. During pregnancy, hyperthyroidism occurs more commonly than hypothyroidism, with an incidence ranging from 0.05 to 0.2 percent, most commonly related to Graves' disease, acute (i.e., subacute) thyroiditis, toxic nodular goiter, and toxic adenoma. y , y The incidence of low-birth-weight infants is significantly increased, and neonatal mortality is slightly increased. y
Clinical Features and Associated Disorders. The general clinical features of thyrotoxicosis are numerous (... Table. ,3.8.-8 ). Neuropsychiatry signs include impaired attention, concentration, and memory, as well as emotional lability, nervousness, hypervigilance, lethargy, depression (i.e., apathetic hyperthyroidism), mania, psychosis, insomnia, and agitated delirium.y Apathetic hyperthyroidism most frequently occurs in the elderly, lacks the usual hyperadrenergic features, and may easily be confused with depression or dementia.
ERAL FEATURES OF THYROTOXICOSIS
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