Excess thyroid hormone levels can be caused by Graves’ disease, toxic multinodular goiter, TSH-secreting pituitary tumors, “toxic” or “hot” thyroid adenomas, or overdosage (accidental or intentional) of thyroid replacement hormone. Clinical manifes-tations of excess thyroid hormone concentrations include weight loss, heat intolerance, muscle weak-ness, diarrhea, hyperactive reflexes, and nervous-ness. A fine tremor, exophthalmos, or goiter may be noted, particularly when the cause is Graves’ disease. New onset of atrial fibrillation is a classic presentation of hyperthyroidism, but cardiac signs also include sinus tachycardia and congestive heart failure. The diagnosis of hyperthyroidism is con-firmed by abnormal thyroid function tests, which may include an elevation in serum T4 and serum T3 and a reduced TSH level.
Medical treatment of hyperthyroidism relies on drugs that inhibit thyroid hormone synthe-sis (eg, propylthiouracil, methimazole), prevent hormone release (eg, potassium, sodium iodide), or mask the signs of adrenergic overactivity (eg, propranolol). In addition, although β-adrenergic antagonists do not affect thyroid gland function, they do decrease the peripheral conversion of T4 to T3. Radioactive iodine destroys thyroid cell func-tion and may result in hypothyroidism. Radioactive iodine is not recommended for pregnant patients. Subtotal thyroidectomy is rarely used as an alter-native to medical therapy. Typically, it is reserved for patients with large toxic multinodular goiters or solitary toxic adenomas. Graves’ disease is usually treated with so-called antithyroid drugs or radio-active iodine.
All elective surgical procedures, including subto-tal thyroidectomy, should be postponed until the patient is rendered clinically and chemically euthy-roid with medical treatment. The patient should have normal T3 and T4 concentrations, and should not have resting tachycardia. Antithyroid medica-tions and β-adrenergic antagonists are continued through the morning of surgery. Administration of propylthiouracil and methimazole is particularly important because of their relatively short half-lives. If emergency surgery must proceed despite clinical hyperthyroidism, the hyperdynamic circu-lation can be controlled by titration of an esmolol infusion.
Cardiovascular function and body temperature should be closely monitored in patients with a his-tory of hyperthyroidism. The exophthalmos of Graves’ disease increases the risk of corneal abrasion or ulceration.
Ketamine, indirect-acting adrenergic agonists, and other drugs that stimulate the sympathetic ner-vous system or are unpredictable muscarinic antag-onists are best avoided in patients with current or recently corrected hyperthyroidism because of the possibility of exaggerated elevations in blood pressure and heart rate. Incompletely treated hyperthyroid patients can be chronicallyhypovolemic and prone to an exaggerated hypoten-sive response during induction of anesthesia. Adequate anesthetic depth must be obtained, how-ever, before laryngoscopy or surgical stimulation to avoid tachycardia, hypertension, and ventricular arrhythmias.
Thyrotoxicosis is associated with an increased incidence of myopathies and myasthenia gravis; therefore, neuromuscular blocking agents (NMBs) should be administered cautiously. Hyperthyroidism does not increase anesthetic requirements; that is, there is no increase in minimum alveolar concentration.
The most serious threat to a hyperthyroid patient undergoing surgery is thyroid storm, which is characterized by hyperpyrexia, tachycardia, altered consciousness (eg, agitation, delirium, coma), and hypotension. The onset is usually 6–24 h after sur-gery but can occur intraoperatively, mimicking malignant hyperthermia. Unlike malignant hyper-thermia, however, thyroid storm is not associated with muscle rigidity, elevated creatine kinase, or a marked degree of metabolic (lactic) and respiratory acidosis. Treatment includes hydration and cool-ing, an esmolol infusion or another intravenousblocker (with a target of maintaining heart rate <100/min), propylthiouracil (250–500 mg every 6 horally or by nasogastric tube) followed by sodium iodide (1 g intravenously over 12 h), and correction of any precipitating cause (eg, infection). Cortisol (100–200 mg every 8 h) is recommended to prevent complications from coexisting adrenal gland sup-pression. Thyroid storm is a medical emergency that requires aggressive management and monitoring.
Thyroidectomy is associated with several potential surgical complications. Recurrent laryn-geal nerve palsy will result in hoarseness (unilat-eral) or aphonia and stridor (bilateral). Vocal cord function can be evaluated by laryngoscopy imme-diately following “deep extubation”, however, this is rarely necessary. Failure of one or both cords to move may require reintubation and exploration of the wound. Hematoma formation may cause airway compromise from collapse of the trachea, particu-larly in patients with tracheomalacia. Dissection of the hematoma into the compressible soft tissues of the neck may distort the airway anatomy and may make intubation difficult. Immediate treatment includes opening the neck wound and evacuating the clot, then reassessing the need for reintubation. Anesthesia staff in the postoperative setting must be prepared to open the surgical wound and relieve airway compression if the surgeon is for any reason unavailable.
Hypoparathyroidism from unintentional removal of all four parathyroid glands will cause acute hypo-calcemia within 12–72 h (see the section on Clin-ical Manifestations under Hypoparathyroidism).Pneumothorax is an unusual complication of neck exploration.
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