Hypothyroidism

Description

Hypothyroidism is a clinical state resulting from decreased circulating levels of the thyroid hormones thyroxine (T4) and triiodothyronine (T3) or from peripheral hormone resistance.

Epidemiology

Incidence

~4:1,000 women per year.
~0.6:1,000 men per year.

Prevalence

1.9% of the female US population.
0.1% of the male US population.
6.9%–7.3% of patients age 55 or over.
Women are 10 times more likely to be hypothyroid compared to men (1).

Morbidity

Patients with hypothyroidism are at increased risk for atherosclerotic heart disease due to increased incidence of hypercholesterolemia.
Increased incidence of dementia and depression

Mortality

Severe hypothyroidism may lead to coma and death if untreated.
Increased incidence of suicide

Etiology/Risk Factors

Female sex
Elderly
Positive family history
History of autoimmune disorders
History of treatment with radioactive iodine or antithyroid medications such as propylthiouracil (PTU) or methimazole
History of radiation to the neck
History of thyroid surgery

Physiology/Pathophysiology

Thyroid hormone functions in several capacities, including normal heart, liver, kidney, and skeletal muscle metabolism, as well as cell differentiation and growth.
T4 and T3 are produced by follicular cells in the thyroid gland in a classic negative feedback system. Thyroid-releasing hormone (TRH; from the hypothalamus) stimulates the release of thyroid-stimulating hormone (TSH; from the anterior pituitary), which in turn stimulates T3 and T4 release (from the thyroid gland). T3 and T4 inhibit synthesis and release of TRH and TSH, via a feedback loop. Additionally, high levels of iodide ion can inhibit T4 synthesis and release.
Hormone synthesis involves iodide uptake into the gland, iodination of thyroglobulin, coupling of iodotyrosines to form T4 and T3. T4 and T3 are released from the thyroid gland into the bloodstream (20:1 ratio).
When T4 enters target cells, it is converted to T3 (more potent). Both T4 and T3 bind to thyroid receptor proteins within the cell nucleus and activate DNA transcription and increase the rate of RNA synthesis, which ultimately affects protein synthesis.
Hypothyroidism manifests as the lack of physiologic activities of T3 and T4. Primary hypothyroidism (95% of cases) is defined by the inability of the thyroid gland to produce thyroid hormones, while secondary hypothyroidism is defined as a functional thyroid gland that is deprived of TSH (2).

Anesthetic GOALS/GUIDING Principles

Determine the severity and tailor an anesthetic plan to the concomitant organ dysfunction.
Mild or well controlled hypothyroidism likely poses no increased surgical risk.

Diagnosis ⬆ ⬇

Symptoms

General: Lethargy, decreased vigor, cold intolerance, diminished food intake, and weight gain.
Neurologic: Slow thinking.
Integument: Dry skin, thickened hair, hair loss, broken nails.
Gastrointestinal (GI): Constipation.
Gynecologic: Menorrhagia, diminished libido.

History

Focus on the multiple systems affected by the lack of physiologic activity of T3 and T4.
Symptoms are insidious in onset and easily overlooked despite multisystem involvement.
In patients with a history of Hashimoto's thyroiditis, a careful review of associated autoimmune diseases such as lupus erythematosus, rheumatoid arthritis, primary adrenal insufficiency, and Sjögren's syndrome is necessary.

Signs/Physical Exam

Neurologic: Slow speech, mental slowing, depression.
HEENT: Round puffy face, periorbital edema, hoarseness.
Integument: Cold/thick/dry/scaling skin, dry/coarse/brittle hair, dry and longitudinally ridged nails.
Cardiovascular: Bradycardia, decreased stroke volume, narrow pulse pressure, cardiac enlargement, pericardial effusion.
GI: Ascites.
Extremities: Ankle edema.
In severe hypothyroidism or myxedema, there can be impaired mentation, coma, enlarged tongue, decreased upper airway tissue tone, hypoventilation, CHF, hypothermia, and hyponatremia secondary to SIADH.

Medications

Replacement therapy is typically with synthetic T4 (levothyroxine) which may take up to 2 weeks before symptomatic improvement is seen.
Synthetic T3, which is the biologically active form of thyroid hormone, can be used to attain a more acute response.

Diagnostic Tests & Interpretation

Labs/Studies

Increased TSH for primary hypothyroidism; decreased TSH for secondary hypothyroidism.
Decreased thyroid hormones T3 and T4.
Decreased radioiodine uptake by the thyroid gland.
Macrocytic anemia.
Elevated serum cholesterol and CK level.
Hypoglycemia, hyponatremia.
Low voltage EKG.

CONCOMITANT ORGAN DYSFUNCTION

Degree of organ dysfunction is concomitant with the severity of hypothyroidism.
Cardiac involvement includes pericardial effusion, QT prolongation, T-wave inversion, and CHF; also, decreased cardiac output (stroke volume and heart rate), pulse pressure, and blood volume hinders the heart's ability to respond to circulatory stress.
Pulmonary involvement includes decreased respiratory drive in response to hypoxemia and hypercarbia, decreased maximal breathing capacity, and decreased diffusion capacity for carbon monoxide.
CNS involvement includes increased sensitivity to sedative medications and decreased level of consciousness progressing to coma.

Circumstances to delay/Conditions

Patients with signs and symptoms of severe hypothyroidism or myxedema should have elective surgery postponed until after adequate replacement therapy.
Patients with severe hypothyroidism or myxedema requiring emergent surgery require immediate hormone replacement with T3, stress dose steroids, and intensive monitoring of their response to therapy.
In patients with coronary artery disease, care must be taken during thyroid replacement therapy. Several studies have shown that replacement therapy may exacerbate angina and even induce myocardial infarction.
Most experts believe mild hypothyroidism poses no increased surgical risk (3).

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Carefully titrate sedatives and analgesics because hypothyroid patients may be more sensitive to these medications.
Aspiration prophylaxis should be considered because severe hypothyroidism or myxedema may have a significant delay in gastric emptying.

INTRAOPERATIVE CARE

Choice of Anesthesia

General endotracheal anesthesia is indicated for thyroidectomy.
Anesthesia technique for nonthyroid surgery should be dictated by the type of surgery, planned position, as well as surgeon/anaesthetist preference.
Patients with severe hypothyroidism or myxedema should be intubated and have their ventilation controlled due to decreased respiratory response to hypoxemia and hypercarbia.

Monitors

Standard ASA monitors.
Invasive monitoring as dictated by the type of surgery, patient comorbidities, and severity of hypothyroidism.
Patients with severe hypothyroidism or myxedema are particularly susceptible to CHF. Pulmonary artery catheter, peripheral arterial catheter, and transesophageal echocardiography may be helpful to guide ionotropic support and fluid management.
EMG endotracheal tube per surgeon request for thyroid surgery.

Induction/Airway Management

Large goiter can cause tracheal deviation, compression, and tracheomalacia. In addition, the frequently associated findings of obesity, large tongue, and decreased upper airway tone among hypothyroid patients can make airway management difficult. Awake fiberoptic intubation should be considered, if there is a high suspicion for airway compromise.
Ketamine may be the induction agent of choice in patients with severe hypothyroidism or myxedema due to its inotropism and ability to maintain sympathetic tone.
Rapid or modified rapid sequence induction may be warranted in patients with significant delay in gastric emptying.

Maintenance

Mixed technique of a volatile agent, nitrous oxide, and short-acting opioid may be the technique of choice. The presence of nitrous oxide and opioid will allow for a lower concentration of the volatile agent, resulting in less cardiac depression and vasodilation.
Controlled ventilation is necessary in patients with severe hypothyroidism or myxedema due to impaired ventilatory response to hypercarbia and hypoxemia.
Minimum alveolar concentration is unchanged in patients with hypothyroidism (4).
Warming blanket and warm IV fluids should be used to minimize risk of hypothermia.

Extubation/Emergence

for thyroidectomies, coughing/bucking on emergence should be minimized to decrease the likelihood of neck hematoma formation. Preintubation tracheal lidocaine can provide airway analgesia.
Because of increased sensitivity to sedatives and analgesics, the use of non-narcotic analgesics may help prevent delayed emergence.
Complications:
- Delayed emergence due to increased sensitivity to sedatives and analgesics.
- Hypothermia.
- Postoperative dependence on mechanical ventilation.
- Thyroidectomy: Airway compromise such as hematoma, airway edema, tracheomalacia, and bilateral recurrent laryngeal nerve injury. Massive bleeding and stroke may occur when injury to the nearby carotid artery occurs. Carotid sinus irritation may lead to hemodynamic fluctuations and bradyarrhythmias. Respiratory compromise from an occult pneumothorax may result from lower neck surgical dissection.

Follow-Up ⬆ ⬇

Bed Acuity

Patients with severe hypothyroidism or myxedema should be monitored in the ICU postoperatively.

Complications

for thyroid surgery, postoperative respiratory distress may be the result of a neck hematoma or hypocalcemia causing laryngospasm and decreased upper airway tone. The latter may be difficult to differentiate in the myxedematous patient that has decreased upper airway tone.

References ⬆ ⬇

Singer PA , et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of care committee, American thyroid association. JAMA. 1995;273:808.
Vanderpump MP , et al. The epidemiology of thyroid disorders in the community: A twenty-year follow-up of the Whickham Survey. Clin Endocrinol. 1995;43:55.
Farling PA. Thyroid disease. Br J Anaesth. 2000;85:15.
Weinberg AD , et al. Outcome of anesthesia and surgery in hypothyroid patients. Arch Intern Med. 1983;143:893.

Additional Reading ⬆ ⬇

Graham GW , et al. Perioperative management of selected endocrine disorders. Int Anesthesiol Clin. 2000;38:31.
Kohl BA , Schwartz S. How to manage perioperative endocrine insufficiency. Anesthesiol Clin. 2010;28:139.

See Also (Topic, Algorithm, Electronic Media Element)

Codes ⬆ ⬇

ICD9

244.9 Unspecified acquired hypothyroidism

ICD10

E03.9 Hypothyroidism, unspecified

Clinical Pearls ⬆ ⬇

The overriding goal of management is determining the severity of the hypothyroidism and designing an anesthetic plan tailored to the concomitant organ dysfunction.
In patients with history of Hashimoto's thyroiditis, a careful review of associated autoimmune diseases is necessary.
Most experts believe mild hypothyroidism poses no increased surgical risk and patients may be able to proceed for surgery.
Patients with severe hypothyroidism or myxedema must be medically optimized prior to surgery. Replacement therapy with T4 or more acutely with T3 should be undertaken with monitoring of symptomatic improvement.
Careful airway management and possible awake fiberoptic intubation may be indicated in patients with large goiter, large tongue, and/or decreased airway tone.
Severely hypothyroid and myxedematous patients should have appropriate invasive monitoring, induction with ketamine, and airway intubation with controlled ventilation. Careful titration of short-acting opioid analgesics or the use of nonopioid analgesics may help in minimizing the risk of delayed emergence.

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Basics ⬇