HYPERTHYROIDISM
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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