Thyroid disease is the second most common endocrinopathy encountered in the perioperative period (after diabetes mellitus). The thyroid is a butterfly-shaped gland that lies anterior of the trachea, just below the larynx. It produces three major hormones: thyroxine (T4), tri-iodothyronine (T3), and calcitonin. T4 and T3 regulate the growth and rate of function of many other systems in the body, whereas calcitonin is involved with calcium homeostasis. Production and exposure of tissue to excessive thyroid hormone results in hyperthyroidism.
The vast majority of cases of hyperthyroidism are caused by intrinsic thyroid disease such as Graves’ disease (most common), thyroid adenoma (second most common cause), or toxic multinodular goiter (Table 105-1). Other etiologies include thyroiditis and iatrogenic causes (iodine therapy, thyroid hormone replacement, or amiodorone). A clinical picture of hyperthyroidism characterized by suppressed TSH and high or high normal T3 or T4 (or both) confirms the diagnosis.
TABLE 105-1Causes of Thyrotoxicosis |Favorite Table|Download (.pdf) TABLE 105-1 Causes of Thyrotoxicosis
|Thyroid Hormone Overproduction ||Uncontrolled Release of Preformed Thyroid Hormone |
|Graves’ disease ||Subacute thyroiditis |
|Toxic multinodular goiter ||Painless thyroiditis |
|Toxic adenoma ||Postpartum thyroiditis |
|Metastatic thyroid carcinoma ||Amiodorone-induced thyroiditis |
|Thyroid stimulating hormone mediated ||Excessive thyroid hormone replacement |
|Iodide excess (Jod–Basedow) || |
|Human chorionic gonadotropin mediated || |
The term thyrotoxicosis is the clinical condition resulting from the action of excess thyroid hormone on tissues. Thyrotoxicosis is a hypermetabolic state and its clinical presentation depends on the severity, duration of the disease, and the patient’s age. Common nonspecific constitutive signs of thyrotoxicosis include nervousness, fatigue, weakness, sweating, heat intolerance, poor concentration, increase appetite, and weight loss.
Hyperthyroidism leads to a variety of physiologic effects:
Cardiovascular—Tachycardia; atrial fibrillation; complete heart block; ventricular dysrhythmias; increased contractility, stroke volume, oxygen consumption, and cardiac output; high output congestive heart failure (in severe cases)
Pulmonary—Tachypnea; hypercarbia; increased oxygen consumption; decreased vital capacity and compliance; pulmonary edema
Neurologic—Anxiety; agitation; tremors; sweating; insomnia; muscle weakness; poor concentration; confusion, delirium, seizure, stupor, obtundation, coma (in severe cases)
Gastrointestinal—Diarrhea; weight loss
Hematological—Anemia; neutropenia; thrombocytopenia
Untreated hyperthyroidism can lead to hypertension, heart failure, atrial fibrillation, bone mass loss or thyroid storm. There are readily available and effective treatments for all common types of hyperthyroidism (Table 105-2). With thyrotoxicosis, the catecholamine receptor number is increased leading to symptoms such as tremor and palpitations. These symptoms can be treated with beta-adrenergic receptor blockers (such as propranolol) which play an important role in blocking catecholamine response. In addition, beta-adrenergic receptor blockers can also block the conversion of T4 to T3 (the active form).
TABLE 105-2Medical Treatment of Thyrotoxicosis