2) Hyperthyroidism

    a) Etiology

  i) Hyperthyroidism is a state of thyroid gland hyperfunction (goiter) with excessive secretion of thyroid hormones. Thyroid hyperfunction causes suppression of TSH levels.

    b) Causes

  i) Graves disease

1) Multinodular diffuse autoimmune disease affecting females between 20 and 40 years due to circulating stimulating IgG antibodies to the TSH thyroid receptor.

  ii) Thyroid single adenoma or multi-nodular goiter

1) Autonomic functioning thyroid tissue that is not down regulated by increased thyroid hormone levels.

  iii) Endemic goiter due to iodine deficiency

  iv) Subacute (de Quervain) thyroiditis

1) Inflammation of the thyroid with flu-like symptoms and thyroid pain that develops usually after an upper respiratory infection and is treated with anti-inflammatory medications.

  v) Ectopic thyroid tissue/neoplasm

  vi) Exogenous, usually iatrogenic, administration of thyroid hormone or iodine/iodine rich medications (e.g., amiodarone) in patients with chronically low iodine intake or nodular goiters (1,2).

    c) Prevalence

  i) More common in females.

  ii) 60% to 80% of patients have Graves disease (3–5).

    d) Signs and Symptoms (Table 82-1)

Table 82-1
Hyperthyroidism Signs

  i) Hypermetabolism and sympathetic overstimulation

    e) Associated findings

  i) Graves disease is associated with myasthenia gravis and exophthalmos opthalmopathy (2,3,5,6).

    f) Treatment (2,5,7) Can be pharmacologic with β-adrenergic antagonists, antithyroid agents, glucocorticoids or with radioactive iodine or with surgical intervention.

  i) Pharmacologic. This is recommended for children and pregnant/breast-feeding women.

1) β-adrenergic antagonists (propanolol, metoprolol, esmolol). Control of adrenergic manifestations. Propanolol additionally reduces peripheral conversion of T4 to T3.

2) Antithyroid agents. Decrease thyroid hormone production, and circulation.

    a) Thionamides (propylthiouracil [PTU] or methimazole). Block the production of T3, T4. PTU additionally prevents peripheral conversion of T4 to T3.

    b) Non-radioactive iodines (Lugol iodine, potassium iodine, sodium iodine). Reduce thyroid gland vascularity and block release of T3, T4. They are iodine substrates and should be given 2 to 3 hours after administration of thionamides to avoid a thyrotoxic crisis in a hyperthyroid patient.

    c) Glucocorticoids (dexamethasone, hydrocortisone). Inhibit peripheral conversion of T4 to T3 and correct subsequent adrenal suppression.

  ii) Radioactive iodine Reduces thyroid hormone production through thyroid gland destruction. It is not used for pregnant/ breastfeeding women or patients with Graves ophthalmopathy (may deteriorate ophthalmopathy). A thionamide should be administered prior to radioactive iodine to avoid thyrotoxic crisis.

  iii) Surgical thyroidectomy. In patients refractory to medication treatment, retrosternal or large goiter, thyroid cancer or lymphoma, and obstructive symptoms.

    g) Preoperative anesthesia evaluation

  i) All patients undergoing elective procedures should be euthyroid (normal thyroid function tests). This is usually clinically represented by a heart rate <85 bpm and no hand tremor before the procedure.

  ii) Usually takes 1 to 8 weeks of treatment to become euthyroid (5,6).

  iii) Patients undergoing emergency surgery

1) β-adrenergic antagonist (usually propanolol), thionamide and a stress dose of glucocorticoid should be given.

2) Inorganic iodine should be given 2 to 3 hours after the thionamide (5).

  iv) Labs

1) Thyroid function tests (TSH and free T4 and T3), CBC, comprehensive metabolic panel and urinalysis.

2) An ECG to evaluate for ischemia, left ventricular hypertrophy, tachycardia, atrial fibrillation.

1) Chest xray (CXR) to evaluate for tracheal compression/deviation and for retrosternal thyroid extension should be ordered in large goiters.

   (a) A CT or MRI should be done to further evaluate the airway if there is >50% narrowing of the trachea, a retrosternal thyroid mass, or any signs/symptoms of airway compression.

4) An ENT consult or fiberoptic evaluation may be needed to document for vocal cord dysfunction or paralysis due to laryngeal nerve damage and pharyngeal displacement in patients with neoplasms or previous neck surgeries.

   (a) Fiberoptic evaluation should be considered in patients with a difficult airway or airway obstruction (2,6).

  v) Preoperative medications (1,5,6)

1) Goals are to reduce thyroid hyperfunction, sympathetic stimulation, anxiety, and pain.

2) All anti-thyroid and β-adrenergic antagonists medications should be continued through the morning of surgery.

   (a) Consider an esmolol IV infusion perioperatively to control tachycardia to <90 bpm.

   (b) Benzodiazepines can be useful as anxiolytics.

1) Regional anesthesia with a superficial and deep cervical block may be used for intraoperative sympathetic blockade and for postoperative analgesia.

4) Consider omitting epinephrine to avoid stimulation of an up-regulated sympathetic system.

5) If a patient has signs of tracheal compression, an awake fiberoptic bronchoscopy (FOB) or an inhalational induction may be indicated.

    h) Intraoperative treatment (1,4,6,8)

  i) Maintain adequate anesthesia and pain control.

  ii) Complications to be prepared for include:

(1) Difficult ventilation/intubation

(2) Cardiac arrhythmias

(3) Sympathetic hyperactivity

(4) Hyperthermia requiring active cooling and excessive airway pressures during surgical manipulations

  iii) Patient’s head and neck should be positioned in a slight head-up tilt position.

(1) Careful eye padding in exophthalmos patients

  iv) Medications

1) Avoid adrenergic stimulation or parasympathetic blockade to avoid exacerbated responses from an up regulated sympathetic system. Medications that cause hypertension or tachycardia are best avoided and when needed smaller doses should be used to avoid exacerbated elevations of blood pressure and heart rate.

   (a) Avoid ketamine, halothane, pancuronium, anticholinergics, indirect acting vasopressors (e.g., ephedrine), and epinephrine.

   (b) For hypotension, a decreased dose of a direct acting vasopressor (e.g., phenylephrine) can be used.

   (c) Esmolol and lidocaine can be used for tachycardia or supraventricular arrhythmias.

   (d) If β-adrenergic antagonist intolerance consider diltiazem for heart rate reduction.

2) Patients are often hypovolemic and vasodilated.

   (a) Give all IV medications slowly and titrate to effect.

1) Minimal alveolar concentration (MAC) of volatile anesthetics is increased in hyperthermic patients (5% MAC increase for every degree above 37°C).

4) Muscle relaxants: Initial and maintenance doses of muscle relaxants should be reduced since subclinical myopathy may be present and reversal with an anticholinergic medication may be unwanted.

5) Avoid salicylates, NSAIDs or furosemide which can increase levels of thyroid hormones by increasing f T3 and f T4.

   (a) Consider ethacrinic acid for diuretic.

  v) Postoperative treatment

1) Supplemental O₂

2) Monitor patient’s vital signs including temperature

1) Provide adequate pain control

    j) Thyroid storm (TS) A life threatening condition that develops rapidly in patients with poorly treated hyperthyroidism.

  i) TS is due to marked hypersensitivity to increased catecholamine secretion.

  ii) Due to acute emotional or physical stress from conditions such as:

1) Emergent surgery

2) Surgical manipulations of an overactive thyroid gland

1) Cardiovascular stress

4) Trauma

5) Infection

6) Diabetic ketoacidosis

7) Pregnancy-induced hypertension

  iii) Symptoms that may present

1) Anxiety

2) Agitation

1) Delirium

4) Hyperthermia

5) Hypertension

6) Tachycardia

7) Arrhythmias

8) Nausea/vomiting

9) Diffuse abdominal pain/obstruction

10) Myocardial ischemia

11) Congestive heart failure (CHF)

  iv) TS most commonly presents 6 to 18 hours postoperatively.

  v) Mortality rates can be up to 10% to 75%.

1) Immediate diagnosis of TS is critical (2,5,6,8).

  vi) Treatment and resuscitation

1) Treatment should focus on ventilation and cardiovascular support.

   (a) Supplemental O₂ to maximize oxygen delivery.

   (b) Maintaining a HR < 100 bpm.

   (c) Decreasing temperature.

   (d) Treating the precipitating factor.

2) Since drug metabolism is slowed, consider reducing drug dosages.

1) The following should be given promptly:

   (a) β-adrenergic antagonist (esmolol infusion or propranolol 10 to 40 mg po q4–6h)

   (b) Corticosteroids (hydrocortisone 100 to 200 mg IV q6h) to reduce peripheral T4 to T3 conversion and because relative adrenal deficiency may be present.

   (c) Antithyroid medications (PTU 200 to 400 mg po/NGT q8h)

   (d) Give iodine (Lugol iodine or potassium iodine) 3 to 4 hours after PTU

4) Invasive monitoring including arterial, central venous and potentially a pulmonary artery catheter and continuous temperature monitoring should be established.

5) Consider ice packs or hypothermic blankets for cooling. Give acetaminophen for temperature control (8,9).

6) Correct fluid deficits and metabolic abnormalities. Dehydrate with IV saline and glucose.

7) Avoid salicylates or furosemide which can increase levels of thyroid hormone.

8) Thyroid levels return to normal after 24 to 48 hours and recovery occurs after 1 week.

9) If conventional therapy is not successful, consider direct removal of circulating thyroid hormones with cholestyramine,

1) Hypothyroidism

    a) Etiology

  i) Hypothyroidism is a state of thyroid gland hypofunction with decreased production of thyroid hormones.

    b) Primary hypothyroidism

  i) TSH is increased above the upper limit of normal.

  ii) The most common causes are iatrogenic.

(1) Surgical resection

(2) Iodine or amiodarone treatment

   (a) High iodine content causes a reduction in thyroid hormone synthesis and release.

(3) Lithium use

   (a) Lithium blocks thyroid hormone synthesis and release.

(4) Hashimoto disease

   (a) Autoimmune disease with lymphocytic infiltration of the thyroid gland

(5) Other causes are thyroiditis (e.g., de Quervain thyroiditis that initially can cause hyperthyroidism)

    c) Secondary hypothyroidism (pituitary)

  i) Thyroid hormone and TSH levels are decreased due to decreased TRH

  ii) Due to any pituitary abnormality

(1) Postpartum pituitary necrosis (Sheehan syndrome)

(2) Expansive pituitary mass

(3) Surgical resection

(4) Intracranial radiation

    d) Secondary hypothyroidism (hypothalamic)

  i) Thyroid hormone and TSH levels are decreased due to decreased TRH.

  ii) Due to neoplasms and surgical resection (7,10)

    e) Prevalence

  i) Hypothyroidism is seen in 1% to 2% of patients.

  ii) More common in females and older patients (10).

    f) Signs and symptoms

  i) Often insidious in onset

  ii) Decreased metabolism

  iii) Lethargy

  iv) Depressed cardiac and respiratory function

(1) Bradycardia

(2) ↓CO

(3) ↓ventilatory response to hypoxia and hypercapnia

  v) Cold intolerance (4,5,11)

    g) Associated findings in untreated hypothyroidism

  i) Obesity

  ii) Obstructive sleep apnea

  iii) Hyperlipidemia

  iv) Hypothermia

  v) Delayed gastric emptying

  vi) Cardiomegaly

  vii) CHF

  viii) Pericardial/pleural effusions

  ix) Peripheral edema

  x) Anemia

  xi) Adrenal insufficiency

  xii) Hyponatremia

  xiii) Hashimoto disease

(1) Associated with other autoimmune diseases including primary adrenal insufficiency and diabetes mellitus (2,4,5,7,10).

    h) Treatment

  i) Pharmacologic

1) Thyroid replacement

   (a) Levothyroxine is most commonly used at doses of 1.6 μg/kg/day.

   (b) 6 to 8 weeks after initiation of treatment, T4 and TSH levels should be checked and doses modified accordingly. (7,10).

2) Drug interactions are common.

   (a) Levothyroxine can increase warfarin levels.

   (b) Iron sulfate, sucralfate and aluminum hydroxide interfere with levothyroxine absorption.

   (c) Phenytoin, rifampin, and carbamazepine decrease levothyroxine levels (7).

  i) Preoperative anesthesia evaluation

  i) For patients with mild-moderate hypothyroidism elective surgery is probably safe.

  ii) For patients with severe hypothyroidism or pregnant, a euthyroid state (HR > 60) should be established prior to elective surgery (5,6,8).

  iii) Hypothyroid patients with coronary artery disease (CAD) are at increased risk of myocardial ischemia during establishment of a euthyroid state due to a sudden increase in metabolic O₂ demands.

(1) Should be assessed for β-adrenergic antagonist therapy or emergency coronary revascularization (2,4,6,9).

  iv) For patients undergoing emergency surgery with severe hypothyroidism, aggressiveness of therapy should be based on the patient’s clinical status (4).

  v) Labs. The same labs should be obtained as for patients with hyperthyroidism.

  vi) Preoperative medications

(1) Treatment goals are to protect from respiratory depression, hypovolemia, hypoglycemia, hyponatremia and hypothermia (5,6,9).

(2) Levothyroxine has a t_1/2 of 5 to 7 days but ideally should be continued perioperatively.

(3) Thyroid hormone medications are associated with wrong dose safety issues with conversions from μg to mg and adjusting IV to PO dosing.

   (a) Oral dosing has 50% bioavailability versus IV dosing with 100% bioavailability (2).

(4) Patients may have heightened sensitivity to respiratory depression from sedatives.

(5) Since patients may have delayed gastric emptying and occult adrenal insufficiency, consider histamine H₂ antagonists, metoclopramide, rapid sequence induction, non-particulate antacid and corticosteroids (1,10).

    j) Intraoperative treatment (1,4,5,6)

  i) Anticipate the potential for difficult intubation (generalized edema, tracheal compression/deviation) in patients with goiter and complications:

(1) Exaggerated effects of cardiodepressant drugs

(2) Prolonged muscle relaxation with neuromuscular blockade

(3) Hypocarbia

(4) Hyponatremia

(5) Hypoglycemia

(6) CHF

  ii) For patients with refractory hypotension, consider adrenal insufficiency.

  iii) For patients with severe hypothyroidism, consider invasive monitoring.

  iv) Preventing hypothermia

(1) Increase ambient OR temperature.

(2) Warm IV fluids

(3) Use forced air warming devices

    k) Postoperative treatment

  i) Anesthesia recovery may be delayed.

  ii) Ensure patients have adequate muscle strength and are normothermic prior to extubation.

  iii) Non-opioid analgesics like ketorolac and peripheral and or central neuraxial blockade are preferable for postoperative pain management (1,5,7,9).

4) Myxedema coma (MXC) (2,5,8–10)

    a) A life threatening condition of severe hypothyroidism.

    b) Sepsis, omission of thyroid replacement therapy, trauma, or surgery can precipitate MXC in hypothyroid patients.

    c) Mortality can be as high as 15% to 60%.

    d) Strong mortality predictors include:

     (i) Low mean arterial pressure (MAP)

     (ii) Need for mechanical ventilation

     (iii) Sepsis

    e) The diagnosis can be made by very low blood levels of free T4, T3 with or without TSH elevation.

    f) Signs and Symptoms

     (i) Impaired mental status

     (ii) Seizures

     (iii) Loss of deep tendon reflexes

     (iv) Hypoventilation

     (v) Hypothermia

     (vi) Hyponatremia

(1) Due to inappropriate antidiuretic hormone (ADH) secretion.

     (vii) Hypoglycemia

(1) Due to concomitant adrenal insufficiency.

     (viii) Ileus

     (ix) Effusions

     (x) ECG abnormalities

(1) Sinus bradycardia

(2) Low-voltage

(3) Non-specific ST and T wave changes

     (xi) CHF

(1) Dilated cardiomyopathy

(2) Pericardial effusion

    g) Treatment and Resuscitation

     (i) Patients should be in an ICU setting.

(1) Mechanical ventilation

(2) Cardiovascular support

(3) IV thyroid hormone

(4) Steroids

(5) Saline

(6) Glucose for gradual correction of hyponatremia and hypoglycemia.

     (ii) A loading dose of levothyroxine 200 to 500 μg is given until the patient regains consciousness.

(1) Followed by a maintenance dose of 50 to 200 μg daily.

     (iii) Continuous ECG monitoring should be done.

     (iv) Steroid replacement with hydrocortisone 100 mg every 8 hours should be given to prevent adrenal insufficiency.

     (v) Patients become euthyroid after 3 to 5 days.

     (vi) External warming for correction of hypothermia should be done gradually to avoid cardiovascular collapse due to sudden peripheral vasodilatation of a hypovolemic patient.

5) Complications after thyroid surgery (5,8)

    a) Superior laryngeal nerve damage

  i) Hoarseness.

  ii) Loss of sensation above the vocals cords which can place the patient at risk for aspiration.

b ) Recurrent laryngeal nerve damage

  i) Unilateral can present with hoarseness.

  ii) Bilateral can present with airway obstruction and aphonia.

  iii) To assess vocal cord function postoperatively, ask the patient to say “e.”

    c) Tracheal compression

  i) Can be secondary to hematoma or tracheomalacia.

  ii) May require surgical intervention and/or reintubation.

    d) Hypoparathyroidism

  i) Due to inadvertent removal of the parathyroid glands.

  ii) Typically presents with hypocalcemia 24 to 96 hours postoperatively.

  iii) Patients may present with laryngospasm.

  iv) Treatment is with calcium carbonate/gluconate.

(1) Magnesium levels should also be followed.

References

1. McQuillan PM, Allman KG, Wilson IH. Endocrine and metabolic disease, endocrine surgery. In: Oxford American Handbook of Anesthesiology. Oxford 1st ed. New York, NY: Oxford; 2008:155–192, 575–586.

2. Breivik H. Perianaesthetic management of patients with endocrine disease. Acta Anaesthesiol Scand 1996;40:1004–1015.

3. Little JW. Thyroid disorders. Part I: Hyperthyroidism. Oral Surg Oral Med Oral Path Oral Radiol Endod 2006;101(3):276–284.

4. Connery LE, Coursin DB. Assessment and therapy of selective endocrine disorders. Anesth Clin N Am 2004;22:93–123.

5. Wall, RT. Endocrine disease. In: Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-Existing Disease. 5th ed. Philadelphia, PA: Churchill Livingstone; 2008:378–393.

6. Roizen MF, Fleisher LA. Anesthetic implications of concurrent diseases. In: Miller RD, ed. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2009:1067–1089.

7. Arora N, Dhar P, Fahey TJ, et al. Seminars: local and regional anesthesia for thyroid surgery. J Surg Oncol 2006;94:708–713.

8. Schwartz JJ, Shamsuddin A, Rosenbaum SH. Endocrine function. In: Barash, PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1279–1286.

9. Vedig AE. Thyroid emergencies. In: Bersten AD, Soni N, Oh TE, eds. Oh’s Intensive Care Manual. 5th ed. Edinburgh, UK: Butterworth Heinemann; 2003:559–566.

10. Little JW. Thyroid disorders. Part II: Hypothyroidism and thyroiditis. Oral Surg Oral Med Oral Path Oral Radiol Endod 2006;102(2): 148–153.

11. Farling PA. Thyroid disease. Br J Anaesth 2000;85(1):15–28.

Adrenal Disorders

Jessica Spellman, MD

1) Overview

    a) The adrenal glands are small (4 to 5 g) triangular shaped endocrine glands that sit on top of the kidneys

  i) Synthesize and store essential hormones

  ii) Release hormones in conjunction with stress

  iii) Divisions of the adrenal glands

(1) Adrenal cortex produces and stores three hormones

   (a) Mineralocorticoids (aldosterone) responsible for regulation of extracellular volume via urinary sodium and potassium exchange in the Renin–Angiotensin–Aldosterone system

   (b) Glucocorticoids (cortisol) responsible for gluconeogenesis, elevation of blood glucose, promotion of glycogen storage, protein, lipid and carbohydrate metabolism, anti-inflammatory actions, and blood pressure maintenance

   (c) Androgens

(2) Adrenal medulla produces catecholamines that function as hormones throughout the body

   (a) Epinephrine and norepinephrine

   (b) Embryologically derived from neuroectodermal cells

    b) Disorders of the adrenal gland can be described in four main categories

  i) Disorders which cause increased output

(1) Increased catecholamine production

   (a) Pheochromocytoma

   (b) Paragangliomas

(2) Increased aldosterone production

   (a) Primary (Conn syndrome)

   (b) Secondary from increased renin production

(3) Increased cortisol

   (a) Cushing syndrome

   (b) Exogenous administration

  ii) Disorders which cause decreased output

(1) Decreased cortisol

   (a) Addison disease

   (b) Secondary to decreased ACTH production

   (c) Tertiary (iatrogenic)

2) Disorders of increased output

    a) Pheochromocytoma

  i) Rare but significant disease

1) Incidence is <0.2% of patients with hypertension

2) Sometimes associated with familial syndromes such as multiple endocrine neoplasia (MEN), von Hippel–Lindau, Neurofibromatosis-1, and familial paragangliomas (1)

1) High perioperative mortality

    a) Without preoperative treatment mortality can be as high as 45%

    b) With appropriate preoperative treatment mortality is <3%

4) Surgical excision of the tumor is curative in >90% of patients (1)

  ii) Pathophysiology

1) Pheochromocytomas are tumors that arise from chromaffin cells of the adrenal medulla

2) Secrete epinephrine and norepinephrine which leads to clinical manifestations

1) Paragangliomas are pheochromocytomas that grow outside of the adrenal glands

  iii) Signs and symptoms result from catecholamine release

1) Hypertension, headache, palpitations, tremor, sweating, anxiety, hyperglycemia, and catecholamine induced cardiomyopathy (2)

2) Signs and symptoms may be sustained or paroxysmal as a result of episodic increased secretion of catecholamines

1) Paroxysmal catecholamine release may be precipitated by:

    a) Stimulation, including: laryngoscopy, displacement of abdominal contents, pneumoperitoneum, tumor manipulation

    b) Tyramine containing foods

    c) Certain drugs such as TCAs and metoclopromide

    d) Micturition, in the case of urinary bladder tumors (1)

  iv) Diagnosis

1) Excess catecholamines or metabolites (metanephrine, normetanephrine, or VMA) found in urine or plasma testing

    a) Plasma-free metanephrines or urinary-fractionated metanephrines are the most sensitive tests for diagnosis and exclusion of pheochromocytoma (1)

    b) False positive elevated catecholamine levels may occur with physiologic stimuli

    c) True positive elevated catecholamines can be distinguished by the magnitude of elevation often two to three times the upper reference limit (1,4)

2) Imaging allows localization of the tumor (1)

    a) CT imaging with and without contrast

     (i) Contrast may have an effect on plasma catecholamines

     (ii) Patients should be protected from catecholamine release by alpha and beta blockade (see below) prior to contrast administration

    b) MRI is preferred for extra-adrenal tumors or tumors found in pregnant patients, children, or patients allergic to CT contrast

    c) MIBG scanning allows for functional and anatomic coupling which may be required for metastatic or multifocal tumors

  v) Perioperative management

1) Preoperative goals are to prevent the effects of tumor released catecholamines

    a) α-Blockade

     (i) Prevents the hypertensive effects of catecholamines (4).

     (ii) α-Blockade is continued for 10 to 14 days before surgery along with intravascular volume expansion to avoid excessive orthostatic hypotension.

     (iii) α-Blockers

(1) Long acting α-blockers (irreversible, noncompetitive)

   (a) Phenoxybenzamine 10 mg BID, increasing every 2 to 3 days by 10 to 20 mg to maximum dose of 1 mg/kg

(2) Short acting α–blockers (competitive)

   (a) Doxazosin increasing from 1 to 16 mg/day

   (b) Prazosin 2 to 5 mg two to three times a day

   (c) Terazosin 2 to 5 mg/day

    b) β-Blockade

     (i) Patients with dysrhythmias or persistent tachycardia require β-blockade

     (ii) β-blockade should only be added after several days of α-blockade to avoid the possibility of unopposed α-constriction resulting in severe hypertension, ischemia, and heart failure as well as other hypertension related end-organ dysfunction (1)

     (iii) β-Blockers

(1) Propranolol 20 to 80 mg one to three times a day

(2) Atenolol 12.5 to 25 mg two to three times a day

(3) Metoprolol 25 to 50 mg three to four times a day (4)

    c) Other agents

     (i) Labetalol is a nonselective α and β blocker with predominant effects at β-receptors

     (ii) Calcium channel blockers do not completely prevent hemodynamic instability

     (iii) α-methyl-paratyrosine or metirosine can be used to block catecholamine synthesis

    d) Preoperative treatment endpoints

     (i) Blood pressure control of <160/90 for more than 24 hours

     (ii) Presence of orthostatic hypotension (not <80/45 standing)

     (iii) Less than one premature ventricular contraction every 5 minutes

     (iv) Absence of ST segment changes and T wave inversions on ECG for 1 week (1)

     (v) Hematocrit decrease of 5% to suggest the adequacy of intravascular volume expansion and satisfactory α-blockade (3)

     (vi) Intraoperative considerations

1) Arterial blood pressure monitoring should be initiated prior to induction and intubation.

2) Large bore IV access and/or central venous access should be established for administration of fluids and vasoactive infusions.

1) Adequate monitoring for ischemia from catecholamine induced acute, severe hypertension should be used.

    a) ECG

    b) Transesophageal echocardiography (TEE) in patients with cardiomyopathy or uninterpretable ECG

4) Adequate depth of anesthesia should be achieved prior to laryngoscopy to minimize catecholamine responses

5) Acute increases in blood pressure can be treated with short acting agents such as: sodium nitroprusside, phentolamine, nicardipine, or magnesium infusions.

6) Tachycardia can be treated with esmolol

7) Short acting agents are preferred as hypotension may ensue following ligation of the venous drainage of the tumor

8) If hypotension occurs, IV fluids and phenylephrine or norepinephrine infusions are the initial treatment.

  vii) Postoperative considerations

1) Hypotension may result from an abrupt fall in circulating catecholamine levels combined with the residual effects of preoperative α blockade.

2) Hypoglycemia may ensue from a rebound hyperinsulinemia effect due to insulin release after tumor excision (1)

1) Following surgery patients should remain in a close watch unit for 24 hours for monitoring of blood pressure and glucose.

    b) Adrenal pathology with increased aldosterone production (2)

  i) Two types

1) Primary increased adrenal cortex production (Conn syndrome)

2) Secondary to increased renin production

  ii) Pathophysiology

1) Increased aldosterone causes increased urinary sodium and potassium exchange that leads to sodium and water retention, potassium loss

  iii) Signs/symptoms of increased aldosterone

1) Hypertension, extracellular volume expansion, weakness

  iv) Perioperative management

1) Normalization of intravascular fluid volume and electrolytes

2) Preoperative sodium restriction

1) Aldosterone antagonists (spironolactone)

4) Potassium repletion

    c) Adrenal pathology with increased cortisol production (Cushing syndrome) (2)

  i) Cortisol production is regulated by the hypothalamic-pituitary-adrenal (HPA) axis

1) Hypothalamic corticotrophin-releasing factor (CRF) stimulates anterior pituitary adrenocorticotropic hormone (ACTH) release, which stimulates the adrenal cortex to release cortisol.

2) Normal daily production of cortisol is 20 mg, with up to 300 mg produced in times of stress.

  ii) Excess cortisol production caused by adrenocortical overproduction (pituitary microadenoma or neuroendocrine tumors producing excess ACTH, adrenal neoplasm), or exogenous administration of cortisol

  iii) Signs/symptoms

1) Truncal obesity, hypertension, hyperglycemia, increased intravascular fluid volume, hypokalemia, osteoporosis, and muscle weakness

  iv) Perioperative management

1) Management of hypertension

2) Management of blood glucose

1) Normalization of intravascular fluid volume and electrolytes

4) When adrenalectomy is performed on these patients, glucocorticoid replacement must be initiated (see below)

1) Adrenal Disorders with decreased output

    a) Adrenal pathology with decreased cortisol production

  i) Adrenal Insufficiency (AI) (5)

(1) Three types

    a) Primary adrenal insufficiency

  i) Loss of adrenal tissue

  ii) Results from autoimmune destruction (Addison’s), infection (tuberculosis, advanced HIV, sepsis), malignancy, or hemorrhage

  iii) Patients are deficient in both mineralocorticoids and glucocorticoids

    b) Secondary adrenal insufficiency

  i) Decreased pituitary ACTH production

  ii) Patients usually have intact mineralocorticoid function via the renin–angiotensin system

    c) Tertiary or iatrogenic HPA axis suppression

  i) Most common form of AI

  ii) Results from chronic exogenous corticosteroid therapy

  iii) Patients usually have intact mineralocorticoid function via the rennin–angiotensin system

(2) AI may be seen in critically ill patients

(3) Signs/Symptoms

    a) AI is characterized by fatigue, weakness, anorexia, weight loss, hypotension, and hyperkalemia

    b) Acute AI may result in refractory distributive shock

(4) Treatment of AI

    a) Mineralocorticoid and glucocorticoid administration

  i) Patients suspected of acute AI should receive immediate steroid replacement with hydrocortisone (100 mg IV every 6 hours continued for 24 hours), doses may be reduced following stabilization

  ii) electrolyte correction

(5) Perioperative management (5)

    a) All patients with AI who undergo a procedure should receive their normal daily corticosteroid dose orally or intravenously.

    b) Patients with primary or secondary AI are often unable to increase endogenous cortisol production during stress and should receive supplemental corticosteroid therapy.

    c) Patients on hydrocortisone doses >50 mg/day do not require additional mineralocorticoid supplementation (see Table 83-1 for steroid equivalencies among different glucocorticoid preparations)

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