GUIDELINES FOR SURGERY 
III. Surgical treatment of goiter with thyroid dysfunction
 
 
 
III-2. HYPOTHYROIDISM
 
Hypothyroidism, defined as a decreased thyroid hormone action at the target tissues, is generally caused by a decreased thyroid hormone production in the thyroid gland.
More than 90% of hypothyroid cases in adults are caused by one of the following conditions: Hashimoto’s thyroiditis, radioactive iodine therapy for hyperthyroidism, or thyroidectomy. Other important causes of primary hypothyroidism include an iodine deficiency and hypothyroidism induced by drugs particularly  amiodarone. Inherited defects in thyroid hormone synthesis and congenital developmental abnormalities of the thyroid gland (thyroid agenesis, ectopic thyroid and thyroid hypoplasia) are rare causes of hypothyroidism in children. Central hypothyroidism is caused by either anterior pituitary gland disease or hypothalamic disorders resulting from diminished TSH secretion or thyrotropin-releasing hormone (TRH) secretion. Another category of hypothyroidism, although very rare, is generalized thyroid hormone resistance, in which hypothyroidism is caused by an abnormal thyroid hormone receptor not by a decreased thyroid hormone production.
Hashimoto’s thyroiditis is the major cause of hypothyroidism in adults. The pathophysiology of hypothyroidism in patients with Hashimoto’s thyroiditis is complex. Thyroid cell damage occurs through immunologic events, as the formation of immune complex and complement is observed in the follicular basement membrane (Kalderon 1977). Thyroid microsomal antibodies, which recognize thyroid peroxidase, are probably the key mediators of complement fixation (Khoury EL 1981). The complement attaches to the thyroid cell, causes an impairment of the thyroid cell function, and leads to the formation of reactive oxygen metabolites (Weetman 1992) which also impair the cell structure and function. The combination of  lymphocytic infiltration and fibrosis decreases  the number of functional units of the thyroid cell (Oertel 1992). Patients with Hashimoto’s thyroiditis are sensitive to an excessive intake of iodine, causing reversible hypothyroidism (Braverman 1971, Tajiri 1986). The presence of TSH-blocking antibody can be responsible for the development of  hypothyroidism in some patients with Hashimoto’s thyroiditis, particularly  non-goitrous cases (Tamaki 1990).

HYPOTHYROIDISM CAUSED BY IODINE-131 THERAPY OR EXTERNAL RADIATION TO THE NECK
Treatment with iodine-131 for Graves-Basedow’s disease is a common cause of hypothyroidism. External irradiation therapy of the neck can cause hypothyroidism in about 25 to 50% of patients with head and neck cancer or lymphoma (Barsano 1992)

HYPOTHYROIDISM AFTER SUBTOTAL OR TOTAL THYROIDECTOMY
Subtotal thyroidectomy for Graves-Basedow’s disease can cause hypothyroidism after surgery.

IODINE DEFICIENCY
Most patients with endemic goiter have a normal thyroid function. However, if the iodine deficiency is severe, they experience hypothyroidism.

DRUG-INDUCED HYPOTHYROIDISM
Amiodarone, lithium, cytokines

THYROID CANCER AND HYPOTHYROIDISM
It is uncommon to see hypothyroidism in patients with thyroid cancers unless the thyroid gland is removed. However, thyroid lymphoma is an exception. Matsuzuka et al. studied 119 cases of primary thyroid lymphoma and found that 40% of the patients were hypothyroid. (Matsuzuka 1993). The high incidence of hypothyroidism in thyroid lymphoma is probably attributable to the coexistence of Hashimoto’s thyroiditis (Matsuzuka 1993)
 
CENTRAL HYPOTHYROIDISM
Hypothyroidism can be caused by abnormalities of the pituitary gland (secondary hypothyroidism) or hypothalamus (tertiary hypothyroidism)

GENERALIZED THYROID HORMONE RESISTANCE
Hypothyroidism resulting from generalized thyroid hormone resistance is  a very rare familial disorder.

SURGERY AND HYPOTHYROIDISM
Surgery for patients with undiagnosed hypothyroidism may cause a catastrophic outcome. It is essential for surgeons to know the precise approach and management of patients with hypothyroidism, who may have to undergo surgery in the hypothyroid state.
 

The first step is to make sure that the patients are actually hypothyroid. After the diagnosis of hypothyroidism is established, it  should be determine whether the patients need urgent surgery.
 

If immediate surgery is not needed, hypothyroidism should be treated with thyroid hormone  to restore the euthyroid state. This eliminates some of the hypothyroid-related surgical complications. At present, the accepted consensus is that emergency surgery can perform  in patients with mild to moderate hypothyroidism. It is important to know the potential complications of surgery for hypothyroid patients (Becker 1985). There are as follows: severe hypotension; cardiac arrest; congestive heart failure; hypothermia; hyponatremia; respiratory insufficiency; coma, confusion, psychosis; ileus; a bleeding tendency; and an adrenal insufficiency.

Three control studies have been reported in which surgery was performed on patients in a hypothyroid state (Weinberg 1983, Ladenson 1984, Drucker 1985). On the basis of these studies, guidelines are established for performing surgery on patients in a hypothyroid state  (Kuma 1997).

Preoperative:

  1. A check should be made on airway obstruction resulting from goiter.
  2. It is ideal to restore the euthyroid state with thyroid hormone therapy if elective surgery is scheduled (particular  care must be taken in patients with coronary artery diease).
  3. Premedication doses should be decreased.
  4. It is necessary to be aware of delayed gastric emptying.
  5. Glucocorticoid coverage should not be forgotten.
Induction of anesthesia:
  1. The dose of induction agents should be decreased.
  2. Some difficulties with intubation should be anticipated if goiter is present.
Maintenance of anesthesia:
  1. Deep anesthesia should be avoided by adjusting anesthetic agents.
  2. Hypotension should be prepared for (inotropic drugs and vasopressors are prepared).
  3. Low pressure temperature most be monitored for.
Extubation:
  1. Alveolar hyperventillation should be borne in mind. Arterial blood gas levels must be cheked for partial pressures of carbone dioxide and oxigen.
  2. Airway obstruction can also be a cause of abnormal blood gas values.
  3. Emergence from anesthesia and extubation requires more time.
Postoperative:
  1. The doses of postoperative sedatives and narcotics are decreased.
  2. Infection may be present without fever.
  3. Checks must be made on the respiratory function and serum electrolytes.
The most difficult case for physicians involves a patient with severe hypothyroidism who needs emergency surgery. The question is whether such patients should be treated with intravenous T4 before  or during surgery. To our  knowledge, no good study is available as regards to the outcome of surgery with and without T4 therapy. However, surgical procedures are the precipitating cause of myxedema coma. Thus, patients with severe hypothyroidism should receive  intravenous T4 before surgery (Kuma 1997).

In addition, diabetic patients with hypothyroidism who undergo surgery should be carefully monitored for the development of hypoglycemia, because episodes of hypoglycemia in response to insulin or oral hypoglycemic agents can be expected more frequently in a hypothyroid state than in a euthyroid state.

A bleeding tendency, particularly in patients with hypothyroidism who are on anticoagulant therapy, should be carefully monitored.

References:

  1. Barsano CP.: Other forms of primary hypothyroidism. In: Braverman LE, Utiger RD (eds): The thyroid, 6th ed. Philadelphia: JB Lippincott, 1992, p 956
  2. Becker C.: Hypothyroidism and atherosclerotic heart disease: Pathogenesis, medical management, and the role of coronary artery bypass surgery Endocr Rev 1985; 6: 432
  3. Braverman LE, Ingbar SH, Vagenakis AG, et al.: Enhanced susceptibility to iodine myxedema in patients with Hashimoto’s disease J Clin Endocrinol Metab 1971; 32: 515
  4. Drucker DJ, Burrow GN.: Cardiovascular surgery in the hypothyroid patient. Arch Intern Med 1985; 145: 1585
  5. Kalderon AE, Bogaars HA.: Immune complex deposits in Graves’ disease and Hashimoto’s thyroiditis. Am J Med 1977; 63: 729
  6. Khoury EL, Hammond L, Botazzo GF, et al.: Presence of organ-specific “microsomal” antigen on the surface of the human thyroid cells in culture: Its involvement in complement-mediated cytotoxicity. Clin Exp Immunol 1981; 45: 316
  7. Kuma K, Fukata S, Sugawara M.: Hypothyroidism  In: Clark OH, Duh QY. (eds) Textbook of Endocrine Surgery. Philadelphia, WB Saunders, 1997, pp 39-46
  8. Ladenson PW, Levin AA, Ridgway EC, et al.: Complications of surgery in hypothyroid patients. Am J Med 1984; 77: 261
  9. Matsuzuka F, Miyauchi A, Katayama S, et al.: Clinical aspects of primary thyroid lymphoma: Diagnosis and treatment based on our experience of 119 cases. Thyroid 1993; 3: 93
  10. Oertel JE, Livolsi VA.: Pathology of thyroid diseases. In: Braverman LE, Utiger RD (eds): The thyroid, 6th ed. Philadelphia:JB Lippincott, 1992, p 603
  11. Tajiri J, Higashi K, Morita M.: Studies of hypothyroidism in patients with high iodine intake. J Clin Endocrinol Metab 1986; 63: 412
  12. Tamaki H, Amino N, Kimura M et al.: Low prevalence of thyrotropin receptor antibody in primary hypothyroidism in Japan. J Clin Endocrinol Metab 1990; 71: 1382
  13. Weetman AP,Tandon N, Morgan BP.: Antithyroid drugs and release of inflammatory mediators by complement-attached thyroid cells. Lancet 1992; 340: 179
  14. Weinberg AD, Brennan MD, Gorman CA, et al.: Outcome of anesthesia and surgery in hypothyroid patients. Arch Intern Med 1983; 143: 893