Hyperthyroidism

Anesthesia for Hyperthyroidism

•  Preop

• General: Euthyroid status preferred (risk of thyroid storm), check TFTs, continue antithyroid meds & β-blockers to the day of surgery

• Airway: Check for compression, tracheal deviation, & substernal thyroid mass consider awake fiberoptic intubation if airway looks challenging

• Benzodiazepines for preop sedation

•  Intraop

• General: Avoid/use sympathetic nervous system stimulants cautiously

(epinephrine, ketamine, ephedrine, phenylephrine) → severe HTN/tachycardia

• Ensure patient eye protection (pt often have exophthalmos)

• Thiopental possesses antithyroid activity in high doses

• Watch for signs of thyroid storm (hyperthermia, tachycardia, ↑ BP)

• Autoimmune thyrotoxicosis may be associated with myopathies

•  Postop

• Complications: Hormonal disturbances & airway management issues

• Thyroid storm: Life-threatening condition, can develop 6–24 hrs after surgery; caused by massive release of T₃ & T₄

Signs: Tachycardia, fever, confusion, vomiting, dehydration, CHF, agitation

(unlike MH, not associated with ↑ CPK, muscle rigidity or acidosis)

• Parathyroid gland damage/removal → hypocalcemia in 24–72 hrs postop

• Recurrent laryngeal n. damage → causes hoarseness if unilateral, stridor if bilateral diagnosis by fiberoptic laryngoscopy

• Neck hematoma → partial/complete upper airway obstruction

Treatment = prompt opening of neck wound & drainage

Hypothyroidism

Anesthesia for Hypothyroidism

•  Preop

• Thyroid supplements should be continued through surgery

• Delay elective surgeries in case of untreated hypothyroidism (risk of cardiovascular instability & myxedema coma)

• Subclinical hypothyroidism not associated with ↑ surgical risk

• In emergency cases: Consider pretreatment with IV thyroxine & steroids

• Pts usually obese, may have large tongue, short neck, delayed gastric emptying

•  Intraop

• Hypothyroid pts sensitive to narcotics & sedatives

• Induction: Maintain stable hemodynamics (consider ketamine or etomidate)

• Hypotension due to abnl baroreceptor fx, ↓ cardiac output, hypovolemia

• Hypothermia develops very fast & difficult to treat

• Metabolic disturbances common: ↓ Na & ↓ blood sugar

• Hypoventilation common (blunted response to hypoxia)

• Myxedema coma (severe form of decompensated hypothyroidism) can occur (see table below)

•  Postop

• Hypothermia, slow drug metabolism, & resp depression may delay extubation

• Extubation should be done in awake & normothermic pt

• Regional anesthesia & ketorolac = preferable for pain control (use opioids with caution)

PARATHYROID GLANDS

Hyperparathyroidism

Anesthesia for Hyperparathyroidism

•  ECG: Short PR & QT intervals, cardiac conduction disorders (↑ Ca levels)

•  Maintain hydration & good urine output

•  Consider using lower doses of nondepolarizing muscle relaxants in weak/somnolent pts

Hypoparathyroidism

Anesthesia for Hypoparathyroidism

•  Preop—serum & ionized Ca should be normalized, especially for pts with cardiac symptoms

•  Intraop—preexisting hypocalcemia may augment neuromuscular block

• Blood products containing citrate (as well as 5% albumin) will ↓ serum Ca level

•  Postop—hypocalcemia may cause prolonged recovery from neuromuscular blockade

Pheochromocytoma

•  May be associated with autosomal dominant multiple endocrine neoplastic synd (MEN types 2a & b)

•  Secretes epinephrine, norepinephrine, & occasionally dopamine

• Secretion may be intermittent or continuous

•  Change in tumor blood flow, direct pressure, & meds can trigger catecholamine release

Anesthesia for Pheochromocytoma

•  Preop: Goal = control BP & restore of intravascular volume

• Start α-blockade 10–14 d prior to surgery & prior to β-blockade

• If one accidentally starts β-blockade prior to α-blockade → severe HTN from unopposed α-stimulus

• Phenoxybenzamine = α-antagonist of choice (another option is prazosin)

• Starting dose = 10 mg qd or bid, then inc dose by 10–20 mg in divided doses every 2–3 d as needed to control BP (goal final dose = 20–100 mg qd)

• Propranolol 10 mg qid (should be initiated 3–4 d prior to the surgery)

• Ca-channel blockers—nicardipine 30 mg bid to supplement α- and β-blockade if BP is poorly controlled

• Hydrate all patients with pheochromocytoma—carefully in pts with signs of CHF

• Nitroprusside infusion (also phentolamine IV) for treatment of acute HTN crisis

• Metyrosine—catecholamine synthesis inhibitor, sometimes used preop

•  Intraop

• GA vs. regional—no influence on patient outcome

• Avoid desflurane, sympathetic stimulants (ketamine, ephedrine), & hypoventilation (cause nonneurogenic release of catecholamines), atracurium & morphine (histamine release)

• Prepare nitroprusside & phenylephrine infusions in advance

• A-line before induction, ± central line (assessment of intravascular volume), ± PA line

• Gentle induction—intubation may cause massive release of catecholamines

• Tumor manipulation—may cause massive catecholamine release → HTN crisis

• Suprarenal vein ligation → acute drop in blood catecholamine level → cause hypotension (treat with fluid administration and direct sympathomimetics)

• Catecholamine-resistant vasoplegia: Can also use vasopressin to reverse

• Refractory tachycardia: Treat with esmolol (25–300 mcg/kg/min)

•  Postop

• Maintain normal BP; in about 50% pts BP will remain elevated

• Bilateral adrenalectomy → steroid support may be necessary

DIABETES

Anesthesia for Diabetes

•  Preoperative

• Check type, duration, and severity of diabetes—the more severe, poorly controlled and longstanding is the disease, the higher is the risk of long-term complications

• Check current therapy for type and dose (diet, oral hypoglycemic drug or insulin)

• Morning blood sugar and HbA1c assay help to assess status of diabetic control. Creatinine level and electrolytes may reflect degree of nephropathy

• Check for the presence of coronary artery disease, HTN, cerebrovascular disease and peripheral vascular disease, check EKG for presence of rhythm disturbances and prior MIs

• Consider Na bicitrate and metoclopramide in pts with GERD and gastroparesis

• Severe peripheral neuropathy may preclude use of regional anesthesia

• Long-acting insulins should be stopped and substituted by protamine and lente insulins

• Long-acting sulfonylurea drugs such as chlorpropamide should be stopped and substituted by short-acting agents. Metformin stopped if concern for intraop metabolic acidosis. Type-2-diabetic patients with marked hyperglycemia on oral treatment should be switched to insulin before operation

•  Emergency surgery

• Stabilize metabolic control/volume status as much as possible (delay surgery if possible)

• Maximize glucose, electrolyte, acid–base status—insulin & glucose infusions

• Saline infusion if volume is depleted (depending on renal function & cardiac status)

• K⁺ infusion if renal function is normal & serum K⁺ normal or low

• Bicarbonate infusion only in pts with severe acidosis

•  Intraoperative management

• Monitoring blood sugar = mandatory for all insulin dependent pts & poorly controlled pts

• Pts on NPH (neutral protamine Hagedorn) or PZI (protamine zinc insulin)

• ↑ risk for anaphylactic protamine reactions (2° to prior sensitization)

• Insulin requirements in diabetics vary during surgery; must individualize

•  Postop

• Treat N/V in pts with gastroparesis with metoclopramide as pts have increased risk of infection, MI, hyper/hypoglycemia, CV, and renal dysfunction

•  Diabetic emergencies

• Diabetic ketoacidosis: Usually triggered by trauma or infection in Type I DM

• Nausea, vomiting, dehydration, polyuria, polydipsia, somnolence → coma

• Hyperglycemia, wide anion gap metabolic acidosis, ketones in blood & urine, ↓ K⁺

• Management: Place A-line, consider intubation for severe CNS depression

• Start insulin infusion (10 U IV, then 5–10 U/hr)

• Normal saline at 5–10 ml/kg/hr (fluid deficit of 3–8 L not uncommon) add 5% glucose when blood sugar <250 mg/dL

• Replenish K (0.3–0.5 meq/kg/hr)

• Bicarbonate not usually required

• Hyperosmolar, hyperglycemic, nonketotic coma (usually type II DM)

• Severe dehydration & associated with acute hyperglycemia (>600 mg/dL)

• Treatment: Correct hypovolemia & hyperglycemia

Fluid resuscitation with 0.45% saline

Give 10 U regular insulin IV stat → insulin drip (see protocol above)

• Hypoglycemia—result of stress, missed meal, exercise, alcohol consumption

• Hypoglycemia is much more dangerous in unconscious pt than hyperglycemia (safer to err on the side of hyperglycemia)

• Symptoms: Diaphoresis, tachy, impaired cognition, confusion, loc & seizures

• Treatment: 50% IV glucose, initial dose 25 mL

ADRENAL INSUFFICIENCY

Anesthesia for Adrenal Insufficiency

•  Preop—administer stress dose of corticosteroid (usually 100 mg hydrocortisone IV)

•  Intraop

• Risk of poor fluid loading tolerance, hypoglycemia, ↑ K⁺, dysrhythmias

• Unexplained hypotension (that is unresponsive to fluids & vasopressors)

→ Treat with glucocorticoid

• Avoid etomidate (suppresses adrenal function)

•  Postop

• Provide adequate corticosteroid supplementation

Excess of Corticosteroids (Cushing’s Syndrome)

•  Causes

• 1°—Adrenal adenoma/hyperplasia

• 2°—ACTH-secreting pituitary microadenoma (Cushing’s dz), ACTH-secreting tumors, exogenous steroid usage

•  Clinical features: Moon facies, buffalo hump, central obesity, hirsutism, skin atrophy, osteoporosis, easy bruising, diabetes, proximal myopathy, aseptic hip necrosis, mental status changes, pancreatitis, polyuria/polydipsia

Anesthesia for Cushing’s Syndrome

•  Preop: Risk of hypokalemia & glucose intolerance (check both)

• Cushingoid pts may have HTN, CHF, fragile skin, osteoporosis

• Use stress dose steroids in case of iatrogenic Cushing’s syndrome

•  Intraop

• Obese (potentially difficult airway/IV access), often HTN

• Special attention to positioning (skin breaks down easily)

• High-dose opioids may cause resp depression & difficulty with extubation

•  Postop course

• Poor ventilatory performance (↓ FRC), poor mobilization, pressure sores, ↑ infections

Hyperaldosteronism (Conn’s Syndrome)

•  Causes

• 1°—(Conn’s syndrome) excess secretion of aldosterone by an adrenal adenoma (60%), bilateral adrenal hyperplasia (30%), carcinoma (rare)

• 2°—high plasma levels of renin & aldosterone (due to CHF/liver cirrhosis)

•  Clinical features

• Malignant HTN (centrally mediated or aldosterone-induced)

• ↓ K⁺ often severe & may be exacerbated by diuretics → weakness & tetany

• HTN pts often hypovolemic (hypovolemia & ↓ K⁺ indicate severe total K⁺ deficit)

• Metabolic alkalosis from H⁺ loss

Anesthesia for Conn’s Syndrome

•  Preop: Correct ↑ BP, metabolic alkalosis, hypokalemia

• Spironolactone (up to 400 mg qd) may control HTN & moderate hypovolemia/ ↓ K⁺

•  Intraop: If CHF, uncontrolled HTN, hypovolemia present → place A-line

• Surgical manipulation of adrenal may release catecholamines → CV instability

• Give corticosteroid & mineralocorticoids in cases of bilateral adrenalectomy

•  Postop: Goal = maintain normal BP, electrolyte balance

• Continue corticosteroid & mineralocorticoids in cases of bilateral adrenalectomy

POSTERIOR PITUITARY GLAND

•  Posterior pituitary releases oxytocin & antidiuretic hormone (ADH, vasopressin)

•  ADH stimulates kidneys to conserve water

• Low ADH → diabetes insipidus

• High ADH → syndrome of inappropriate antidiuretic hormone (SIADH) secretion

Diabetes Insipidus (DI)

•  Causes: Central DI—insufficient ADH by pituitary (damage from head injuries, genetic disorders, infections, vascular dz, tumors)

• Nephrogenic DI—lack of kidney response to ADH (from drugs, chronic kidney dz)

•  Clinical features: Thirst, polyuria (up to 20 L/d), low BP, & dehydration

•  Diagnosis: Urine specific gravity of ≤1.005, urine osmolality <200 mOsm/kg, random plasma osmolality > 287 mOsm/kg

•  Treatment: SQ/nasal/PO vasopressin analogues (desmopressin), chlorpropamide, carbamazepine, thiazide diuretics

•  Anesthetic management

• Preop—restore intravascular volume, nasal desmopressin 10 mcg bid–tid

• Intraop

• Total lack of ADH: 100 mU vasopressin before surgery followed by infusion (100–200 mU/hr titrated to urine output)

• Partial ADH deficiency: No vasopressin (unless plasma osmolality >290)

• Postop—continue desmopressin & monitor electrolyte balance

Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion

•  Clinical features: ↓ Na superimposed upon symptoms of underlying pathology

• ↓ Na due to a dilutional effect, not Na depletion (may be no clinical symptoms)

• Symptoms: May include nausea, weakness, anorexia; Na <110 mmol/L → coma

•  Diagnosis: Must distinguish SIADH from other causes (such as dilutional hyponatremia) (causes of dilutional ↓ Na: Excess infusion of dextrose/saline drips/use of diuretics)

• Diagnosis confirmed by serum Na <130 mmol/L, plasma osmolality <270 mOsm/L, urinary Na >20 mEq/L & elevated urine osmolality

•  Treatment: Address underlying problem

• Release of ADH (from hypophysis or tumor) cannot be suppressed by medical therapy

• Symptomatic relief: Water intake restriction to 500–1000 mL per 24 hrs

(plasma & urine osmolality should be measured regularly)

• Fluid restriction may not be appropriate in SAH—may promote vasospasm

• Demeclocycline: When fluid restriction is difficult

•  Anesthetic management

• Correct hyponatremia, monitor volume status by CVP or PA catheter

• Monitor electrolytes (urine osmolarity, plasma osmolarity, serum Na) (including immediately after surgery)

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