Hyperthyroidism

Description

Hyperthyroidism is an endocrine disorder that results in an excess of biologically active thyroid hormones: Thyroxine (T4) and triiodothyronine (T3).
Uncontrolled overt hyperthyroidism can lead to thyroid storm. This is a medical emergency that presents with marked tachycardia, hyperthermia, weakness, and altered levels of consciousness and can result in congestive heart failure (CHF) and shock (1).

Epidemiology

Incidence

~1:1,000 women per year.
~1:10,000 men per year.

Prevalence

General US population:

Subclinical hyperthyroidism: ~1%. Over the age of 55 years, it increases to 2%
Overt hyperthyroidism: ~0.2%

Morbidity

Thyroid hormone increases bone resorption. Patients with hyperthyroidism have low bone density and are at an increased risk of fracture.
Incidence of atrial fibrillation is 2.5 times greater than in patients without hyperthyroidism (2).
Increased incidence of stroke.

Mortality

Increased risk is attributable to an increased incidence of cardiovascular disease.

Etiology/Risk Factors

Female sex (prevalence ratio of 8:1)
Smokers
Elderly
Positive family history
Other autoimmune disorders
Iodide repletion after iodide deprivation

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) that in turn stimulates T3 and T4 release (from the thyroid gland). T3 and T4 feedback to inhibit synthesis and release of TRH and TSH. 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, and release of thyroid hormone. T4 is converted to T3 intracellularly, which binds to thyroid receptor proteins in the cell nucleus, activates DNA transcription, and increases the rate of RNA synthesis, which ultimately affects protein synthesis.
The clinical manifestations of hyperthyroidism are the exaggerated expressions of the physiologic activities of T3 and T4.
Graves' disease is an autoimmune disease whereby autoantibodies to TSH receptors bind to and stimulate thyroid hormone production and secretion.
Hashimoto's thyroiditis is an autoimmune inflammation of the thyroid gland resulting in the release of stored thyroid hormone. After inflammatory "burnout," the patients become hypothyroid.
Toxic multinodular goiter develops when long-standing thyroid goiters become autonomous, resulting in thyroid hormone production and secretion independent of TSH stimulation.
Other less common causes include radiation thyroiditis, excessive replacement therapy, TSH-producing pituitary adenomas, and ectopic sources of thyroid hormone (struma ovarii).

Anesthetic GOALS/GUIDING Principles

Intraoperative risk is directly correlated to the severity of hyperthyroidism, and patients scheduled for elective surgery should be made euthyroid prior to surgery.
In patients requiring nonelective surgery, the avoidance of hyperthyroid crisis is the guiding principle of management.

Diagnosis ⬆ ⬇

Symptoms

Symptoms are due to the supraphysiologic activity of T3 and T4.
Alertness, emotional lability, nervousness, irritability, poor concentration
Muscular weakness, fatigue
Palpitations
Voracious appetite, weight loss
Hyperdefecation
Heat intolerance

History

Focused on the multiple organ systems affected by the supraphysiologic activities of T3 and T4: Neurological, cardiovascular, hematological, GI, metabolic, pulmonary, and musculoskeletal systems.

Signs/Physical Exam

Due to the supraphysiologic activity of T3 and T4.
Hyperkinesia, rapid speech
Proximal muscle (quadriceps) weakness, fine tremors
Moist skin, abundant hair; onycholysis
Lid lag, stare, chemosis, periorbital edema, proptosis
Accentuated first heart sound, tachycardia, atrial fibrillation, widened pulse pressure, dyspnea

Medications

Strategy should involve inhibition of TSH, TRH, peripheral conversion of T4 to the biologically active T3, and the antagonism of beta-adrenergic activity.
Propylthiouracil (PTU) and methimazole are thioamide derivatives that inhibit the synthesis of thyroid hormones. PTU also has the added advantage of inhibiting the peripheral conversion of T4 to T3 (3).
Potassium iodide and glucocorticoids inhibit the release of thyroid hormones. Glucocorticoids also inhibit peripheral conversion of T4 to T3 (3).
Beta-blockers provide adrenergic antagonism by minimizing inotropism, chronotropism, and the potential for arrhythmias (3).
Medical control of hyperthyroidism may require several weeks.

Diagnostic Tests & Interpretation

Labs/Studies

CBC: Anemia
Coagulation panel: Thrombocytopenia and decreased vitamin K-dependent clotting factors.
Chemistry panel: Hypercalcemia and hyperglycemia.
EKG and appropriate cardiac evaluation based on history and physical exam.
CT scan in patients with large goiter may be helpful in assessing airway anatomy.

CONCOMITANT ORGAN DYSFUNCTION

Cardiovascular: Increased risk of myocardial ischemia due to increased resting heart rate, stroke volume, and cardiac output. Increase in beta-receptor sensitivity increases the incidence of atrial fibrillation, premature ventricular contractions, and high-output CHF.
Pulmonary: Weakness of respiratory muscles leading to a reduction in vital capacity and lung compliance.
GI: Impaired drug absorption secondary to rapid GI transit. Hyperdefecation and diarrhea leads to hypokalemia and hypovolemia.
Hematological: Anemia, thrombocytopenia, and decreased vitamin K-dependent factors.
Metabolic: Hypercalcemia from increased bone resorption and impaired glucose tolerance due to up-regulation of beta-adrenergic receptors.
Musculoskeletal: Increased risk of osteopenia and fracture due to bone resorption. Generalized weakness in skeletal muscles from metabolic derangements and the catabolic state associated with severe hyperthyroidism.

Circumstances to delay/Conditions

Thyroid storm is a medical emergency and must be treated prior to surgery.
Signs and symptoms as well as concomitant organ dysfunction must be optimized prior to elective surgery.

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Patients usually have high anxiety. Appropriate use of anxiolytics/sedatives should be balanced against the presence of airway compromise in patients with goiter.

INTRAOPERATIVE CARE

Choice of Anesthesia

Deep general endotracheal anesthesia for thyroidectomy.
Anesthesia technique for nonthyroid surgery should be dictated by the type of surgery and planned position, as well as surgeon/anaesthetist preference.

Monitors

Standard ASA monitors.
Invasive monitoring as dictated by planned surgery and patient comorbidities.
EMG endotracheal tube per surgeon request for thyroid surgery.

Induction/Airway Management

Large goiter can cause tracheal deviation, compression, and tracheomalacia. Preoperative CT of the neck may help to delineate the severity of airway compromise. Awake fiberoptic intubation should be considered if there is a high suspicion of airway compromise. Care should be taken to blunt the adrenergic effect of awake intubation in these patients with sensitized adrenergic tone.
Induction drug should be chosen carefully based on comorbidities. Ketamine should be used with care as this drug may increase adrenergic tone in these sensitized patients.
Succinylcholine or nondepolarizing muscle relaxants with sympathomimetic effects or histamine release should be used with caution.
Patients with exophthalmos require careful application of ointment to the cornea and secure taping of the eyelids.

Maintenance

The avoidance of a thyroid crisis is the guiding principle in managing hyperthyroid patients.
Maintenance of a deep level of surgical anesthesia is prudent.
Medications that increase sympathetic tone should be avoided. Examples include pancuronium, ephedrine, and meperidine.
Anticholinergics for reversal of neuromuscular blockade may also increase sympathetic tone. Careful attention must be paid to prevent an exaggerated sympathetic response. Glycopyrrolate has less chronotropic effect than atropine and therefore may be the preferred choice.

Extubation/Emergence

After a thyroidectomy:
- Coughing/bucking on emergence should be minimized to decrease the likelihood of neck hematoma formation. Preintubation tracheal lidocaine can provide airway analgesia.
- Communication with the surgeon regarding likelihood of recurrent laryngeal nerve injury needs to take place prior to emergence and extubation.

Follow-Up ⬆ ⬇

Bed Acuity

Patients with poorly controlled hyperthyroidism and significant comorbidities should be monitored in the ICU setting.

Complications

Thyroid storm is a rare medical emergency that typically develops postoperatively in patients with hyperthyroidism. Thyroid storm may be difficult to distinguish from malignant hyperthermia, neuroleptic malignant syndrome, or pheochromocytoma. Mortality may be as high as 20–30% (4). Management of thyroid storm involves:
- Oxygen, airway protection, hyperventilation, aggressive fluid replacement.
- Beta-adrenergic blockade, typically with a short-acting titratable beta-blocker like esmolol.
- PTU, methimazole, potassium iodide, corticosteroids.
- Cooling measures involving cool IV fluids, cooling blankets, nasogastric, or bladder lavage.
- Plasmapheresis or peritoneal dialysis can remove excess thyroid hormones (5).
Thyroidectomy
- Airway compromise (most common) from hematoma, airway edema, tracheomalacia, hypocalcemia from hypoparathyroidism, and partial bilateral recurrent laryngeal nerve injury. The RLN innervates all intrinsic laryngeal muscles except the cricothyroid (SLN). Specifically, the RLN innervates a number of adductors, and a single abductor (posterior cricoarytenoid muscles). Injury to the abductor component can result in unopposed adduction (including from the SLN innervated cricothyroid). Complete transection will result in the affected vocal cord lying in the midline (injury to the adductors and abductors).
- Injury to the nearby carotid artery can result in massive bleeding and possible stroke
- Intraoperative carotid sinus irritation may lead to hemodynamic fluctuations and bradyarrhythmias
- Occult pneumothorax can result from lower neck surgical dissection

References ⬆ ⬇

Singer PA , et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of care committee, American Thyroid Association. JAMA. 1995;273:808.
Sherman SI , et al. Clinical and socioeconomic predispositions to complicated thyrotoxicosis: A predictable and preventable syndrome?Am J Med. 1996;101:192.
Cooper DS. Antithyroid drugs. N Engl J Med. 2005;352:905.
Nayak B , et al. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 2006;35:663.
Petry J , et al. Plasmapheresis as effective treatment for thyrotoxic storm after sleeve pneumonectomy. Ann Thorac Surg. 2004;77:1839.

Additional Reading ⬆ ⬇

Franklyn JA. The management of hyperthyroidism. N Engl J Med. 1994;330:1731.
Graham GW , et al. Perioperative management of selected endocrine disorders. Int Anesthesiol Clin. 2000;38:31.

See Also (Topic, Algorithm, Electronic Media Element)

Codes ⬆ ⬇

ICD9

242.90 Thyrotoxicosis without mention of goiter or other cause, and without mention of thyrotoxic crisis or storm
242.91 Thyrotoxicosis without mention of goiter or other cause, with mention of thyrotoxic crisis or storm

ICD10

E05.80 Other thyrotoxicosis without thyrotoxic crisis or storm
E05.90 Thyrotoxicosis, unsp without thyrotoxic crisis or storm
E05.91 Thyrotoxicosis, unspecified with thyrotoxic crisis or storm
E05.81 Other thyrotoxicosis with thyrotoxic crisis or storm

Clinical Pearls ⬆ ⬇

Intraoperative risk is directly correlated to the severity of hyperthyroidism.
Preoperative medical management involves inhibition of thyroid hormone synthesis, release, and peripheral conversion. Commonly used medications include PTU, methimazole, potassium iodide, glucocorticoids, and beta-adrenergic blockade.
Careful airway management and possible awake fiberoptic intubation may be indicated in patients with large goiter.
The avoidance of thyroid crisis by maintaining a deep level of surgical anesthesia while minimizing exposure to sympathomimetic medications is the guiding principle in managing hyperthyroid patients.
Postoperative complications are usually related to airway compromise. Causes include hematoma, airway edema, tracheomalacia, and partial bilateral recurrent laryngeal nerve injury.
Thyroid storm is a medical emergency with high mortality. Decisive emergent management is crucial.

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Basics ⬇