Handbook of Clinical Anesthesia

Chapter 49

Endocrine Function

An understanding of the pathophysiology of endocrine function is important in the management of anesthesia for patients with disorders of the hormone-producing glands (Schwartz JJ, Akhtar S, Rosenbaum SH: Endocrine function. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1279–1304).

1. Thyroid Gland
2. Thyroid Metabolism and Function.Thyroxine (T₄) and triiodothyronine (T₃) are the major regulators of cellular metabolic activity. The thyroid gland is solely responsible for the daily secretion of T₄ (80–100 µg/day; elimination half-time, 6–7 days). About 80% of T₃ is produced by extrathyroidal deiodination of T₄ (elimination half-time, 24–30 hours). Thyroid hormone synthesis occurs in four stages (Fig. 49-1). Most of the excess effects of thyroid hormones (hyperadrenergic state) are mediated by T₃ (Table 49-1).
3. Tests of Thyroid Function(Table 49-2)
4. Hyperthyroidism
5. Treatment and Anesthetic Considerations(Table 49-3)
6. A combination of propranolol (effective in attenuating the manifestations of excessive sympathetic nervous system activity, as evidenced by a heart rate <90 bpm) and potassium iodide (inhibits hormone release) is effective in rendering patients “euthyroid” before anesthesia and surgery. Esmolol may be administered as a continuous intravenous (IV) infusion to maintain the heart rate below 90 bpm.

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1. The goal of intraoperative management is achievement of a depth of anesthesia (often with isoflurane or desflurane) that prevents an exaggerated sympathetic nervous system response to surgical stimulation. Drugs that activate the sympathetic nervous system (e.g., ketamine) or increase the heart rate (e.g., pancuronium) are not likely to be recommended.
2. If a regional anesthetic is selected, epinephrine should not be added to the local anesthetic solution.

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3. Anesthesia for thyroid surgery(subtotal thyroidectomy) is an alternative to prolonged medical therapy. Complications associated with surgery occur more frequently when preoperative preparation is inadequate (Tables 49-4 and 49-5).
4. It is useful to evaluate vocal cord function in the early postoperative period by asking patients to say the letter “e.”
5. Unexpected difficult intubation is increased in the presence of goiter. (Inhalation induction or awake fiberoptic intubation should be considered if there is evidence of significant airway obstruction or tracheal deviation or narrowing.)

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1. Postoperative airway obstruction caused by hematoma or tracheomalacia may require urgent reintubation of the trachea.
2. Operating on an acutely hyperthyroid patient may provoke thyroid storm.
3. Hypothyroidism
4. Hypothyroidism is a relatively common disease (0.5%–0.8% of the adult population) that results from inadequate circulating levels of T₄, T₃, or both (Table 49-6).
5. Treatment and Anesthetic Considerations
6. No evidence supports postponement of elective surgery (including coronary artery bypass graft surgery) in the presence of mild to moderate hypothyroidism.
7. No evidence supports the choice of a specific anesthetic technique or selection of drugs for hypothyroid patients, although opioids and volatile anesthetics are often considered to have increased depressant effects in these patients. There appears to be little, if any, decrease in anesthetic requirements as reflected by the minimum alveolar concentration.
8. Meticulous attention must be paid to maintaining body temperature.
9. Myxedema coma is a medical emergency that requires aggressive therapy (Table 49-7).

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1. Parathyroid Glands
2. Calcium Physiology.Parathyroid hormone secretion is regulated by the serum ionized calcium concentration (negative feedback mechanism) to maintain calcium levels in a normal range (8.8–10.4 mg/dL).
3. Hyperparathyroidism
4. Hypercalcemia is responsible for a broad spectrum of signs and symptoms (e.g., nephrolithiasis, confusion).
5. Treatment and Anesthetic Considerations.Preoperative IV administration of normal saline and furosemide may lower serum calcium concentrations. There is no evidence that a specific anesthetic drug or technique is preferred. A cautious approach to the use of muscle relaxants is suggested by the unpredictable effect of hypercalcemia at the neuromuscular junction. Careful positioning of osteopenic patients during surgery is necessary to minimize the likelihood of pathologic bone fractures.
6. Hypoparathyroidism.Clinical features are manifestations of hypocalcemia, and treatment is with calcium gluconate (10–20 mL of 10% solution IV) (Table 49-8).

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III. Adrenal Cortex

1. The biologic effects of adrenal cortex dysfunction reflect cortisol or aldosterone excess or deficiency (Table 49-9).
2. Glucocorticoid Excess (Cushing's Syndrome)(Table 49-10)
3. The diagnosis of hyperadrenocorticism is established by failure of the exogenous administration of dex-amethasone to suppress endogenous cortisol secretion.
4. Anesthetic Management(Table 49-11). Etomidate has been used for temporizing medical treatment of severe Cushing's disease because of its inhibition of steroid synthesis.

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1. Mineralocorticoid excessshould be considered in nonedematous hypertensive patients who have persistent hypokalemia and are not receiving potassium-wasting diuretics.
2. Adrenal Insufficiency (Addison's Disease)
3. Clinically, primary adrenal insufficiency is usually not apparent until at least 90% of the adrenal cortex has been destroyed.
4. Clinical presentationalmost always includes hypotension. (A high degree of suspicion should be maintained for patients who demonstrate cardiovascular instability without a defined cause.)
5. Treatment and Anesthetic Considerations.Immediate therapy consists of electrolyte resuscitation (glucose in normal saline) and steroid replacement (100 mg IV every 6 hours for 24 hours). Inotropic support is indicated if hemodynamic instability persists despite adequate fluid resuscitation.
6. Steroid Replacement During the Perioperative Period
7. Patients with adrenal insufficiency and those with hypothalamic–pituitary adrenal (HPA) axis suppression from chronic steroid use require additional corticosteroids to mimic the increased output of the normal adrenal gland during stress.
8. Normal adrenal gland can secrete up to 200 mg/day of cortisol and may secrete between 200 and 500 mg/day during stress.
9. The HPA axis is considered to be intact if plasma cortisol levels are greater than 22 µg/dL during acute stress.
10. Regional anesthesia postpones the elevation in plasma cortisol levels evoked by surgery, and deep

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general anesthesia suppresses the elevation of stress hormones.

1. Despite symptoms of clinically significant adrenal insufficiency during the perioperative period, these findings have rarely been documented in direct association with glucocorticoid deficiency.
2. Identifying patients who require steroid supplementation is not practical. (Provocative testing with adrenocorticotrophic hormone [ACTH] stimulation is too costly compared with the risk of brief steroid supplementation.)
3. HPA axis suppression may occur after five daily doses of prednisone of 20 mg or more. Suppression may also occur with topical, regional, and inhaled steroids. (Alternate-day therapy decreases the risk of suppression.)
4. Recovery of HPA axis function occurs gradually and can take up to 9 to 12 months.
5. There is no proven optimal regimen for perioperative steroid replacement (low-dose vs high-dose replacement) (Table 49-12). Patients who are using steroids at the time of surgery should receive their usual dose on the morning of surgery and are supplemented at a level that is at least equivalent to the usual daily replacement. Cortisol coverage is rapidly tapered to the patient's normal maintenance dosage during the postoperative period.
6. Although no conclusive evidence supports an increased incidence of infection or abnormal wound healing when supraphysiologic doses of supplemental steroids are used acutely, the goal of therapy is to use the minimal drug dosage necessary to adequately protect the patient.
7. Exogenous Glucocorticoid Therapy(see Table 49-9)

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1. Adrenal Medulla

The adrenal medulla is analogous to a postganglionic neuron, although the catecholamines it secretes function as hormones, not as neurotransmitters.

1. Pheochromocytoma.These tumors produce, store, and secrete catecholamines that may result in life-threatening cardiovascular effects (Table 49-13).
2. Diagnosisof pheochromocytoma is based on measurement of catecholamines in the plasma and catecholamine metabolites (vanillylmandelic acid) in the urine. Excess production of catecholamines is diagnostic for pheochromocytoma. Computed tomography or magnetic resonance imaging may be used to localize these tumors.
3. Anesthetic Considerations
4. Preoperative preparationconsists of α blockade (phentolamine, prazosin) initiated before surgery, if possible, and restoration of intravascular fluid volume. β blockade is indicated only if cardiac dysrhythmias or tachycardia persists after institution of α blockade. The goals of medical therapy are to control heart rate, suppress cardiac dysrhythmias, and prevent paroxysmal increases in blood pressure.
5. Perioperative Anesthetic Management(Table 49-14)
6. Postoperatively, plasma catecholamine levels return to normal over several days, and about 75% of patients become normotensive within 10 days.
7. Diabetes Mellitus

Diabetes mellitus is the most common endocrine disease present in surgical patients (25% to 50% of diabetics require surgery). It is a disease with a broad range of severity, and its manifestations can be altered (unmasked for the first time) in response to stress as produced by surgery.

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1. Classification(Table 49-15)
2. Treatment(Table 49-16)
3. Anesthetic Management
4. Preoperative(Table 49-17). It is axiomatic that the patient should be in the best state of metabolic control that is possible preoperatively.
5. Intraoperative.The details of the anesthetic plan depend ultimately on the presence of end-organ

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disease. Invasive monitoring may be indicated for the patient with heart disease. Fluid management and drug selection may be influenced by renal function, and aspiration considerations may be affected by the presence of gastroparesis.

1. Blood glucose levels should be measured preoperatively and postoperatively. The need for additional measurements is determined by the duration and magnitude of surgery and the stability of the patient's diabetes.
2. Dehydration may be present on the patient's arrival in the operating room based on osmotic diuresis.

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1. It is important to note the amount of glucose administered IV to avoid an overdose. (The standard glucose dose for adults is 5–10 g/hr or 100–200 mL of 5% glucose/hr.)
2. Another area of patient monitoring that is extremely important in patients with diabetes is positioning on the operating table. These patients' peripheral nerves may already be partly ischemic and are therefore uniquely susceptible to pressure or stretch injuries.
3. Glycemic Goals(Table 49-18). Although the association between perioperative hyperglycemia and poor outcomes is strong, the value of controlling glucose levels tightly intraoperatively has not been proven conclusively. It may be prudent to maintain glucose levels at 180 mg/dL or below, especially in the perioperative period.
4. Management of Perioperative Hyperglycemia.Many factors influence glucose levels in the perioperative period and the regimen selected to control hyperglycemia (Table 49-19). The goal of any regimen is to minimize metabolic derangements and avoid hypoglycemia (Table 49-20).
5. Emergencies
6. Hyperosmolar Nonketotic Coma(Table 49-21)
7. Diabetic Ketoacidosis.Manifestations of diabetic ketoacidosis reflect insufficient insulin to block the

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metabolism of fatty acids, resulting in the accumulation of acetoacetate and β-hydroxybutyrate (Table 49-22). Because leukocytosis, abdominal pain, ileus, and mildly elevated amylase levels are common in the presence of diabetic ketoacidosis, an occasional

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patient is misdiagnosed as having an intra-abdominal surgical problem. Treatment of diabetic ketoacidosis includes insulin administration and fluid and electrolyte evaluation and management (Table 49-23).

3. Hypoglycemiaproduces signs of sympathetic nervous systemic stimulation (tachycardia, hypertension, diaphoresis), which may be masked or misdiagnosed in an anesthetized patient as an inadequate level of anesthesia relative to surgical stimulation.
4. Diabetic surgical patients are more likely to de-velop hypoglycemia if insulin or sulfonylureas are given without supplemental glucose.
5. Renal insufficiency prolongs the action of insulin and oral hypoglycemic drugs.
6. Pituitary Gland

The pituitary gland is divided into the anterior pituitary (thyroid-stimulating hormone, ACTH, gonadotropins, growth hormone) and posterior pituitary (vasopressin, oxytocin). Both are under the control of the hypothalamus.

1. Anterior Pituitary.Acromegaly poses several problems for anesthesiologists (Table 49-24).
2. Diabetes insipidusreflects a relative or absolute deficiency of antidiuretic hormone (ADH), resulting in

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hypovolemia (inability to concentrate urine) and hypernatremia. ADH is also used in vasodilatory shock as an adjuvant to other pressors.

1. Inappropriate secretion of antidiuretic hormonemanifests as dilutional hyponatremia and decreased serum osmolarity. These changes typically occur in the presence of head injury or an intracranial tumor. Initial treatment is restriction of daily fluid intake to 800 mL.

VII. Endocrine Responses to Surgical Stress

Anesthesia, surgery, and trauma elicit a generalized endocrine metabolic response (increased plasma levels of cortisol, ADH, renin, catecholamines, endorphins) and metabolic changes (hyperglycemia, negative nitrogen balance). Regional anesthesia may block part of the metabolic stress response during surgery (blockade of neural communications from the surgical area).

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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