Desarrollo del Proceso de Gestión de Calidad

GERALD DUBOWITZ, MB, CHB

overview

■ Definition: Gastroesophageal reflux disease (GERD) is the reflux of gastric contents into the esophagus

■ GERD suggests incompetence of the lower esophageal sphincter, allowing caustic gastric contents to irritate the lower esophagus.

Hiatal Hernia and Gastroesophageal Reflux Disease 123

■ Definition: Hiatal hernia is the protrusion of the stomach above the diaphragm. Etiology is unclear but may be congenital or acquired.

■ Both hiatal hernia & GERD lead to passive reflux of gastric contents, which may be aspirated during the course of anesthesia.

■ Increased risk in obese pts.

■ Regurgitation is generally a silent process but can have potentially severe consequences:

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Minor pulmonary sequelae (eg, cough)

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Exacerbation of bronchospasm

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Aspiration pneumonitis & ARDS

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Aspiration is most severe w/ high-volume, particulate, acid aspirate

■ Usual Rx: Reduce gastric acidity & therefore the potential damage caused by reflux/aspiration of gastric contents.

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Histamine (H₂) blockers (eg, ranitidine)

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Proton pump inhibitors (eg, omeprazole)

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Antacids (eg, sodium bicitrate)

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Promotility agents to reduce gastric volume (eg, metoclo-pramide)

preop

■ Preop evaluation

➣

Obtain history of reflux:

r Severity of reflux r Frequency

r Assoc w/ eating or all the time r Worse lying down

r Requires sleeping on many pillows

■ Preop mgt

➣

Major goal is to promote low gastric volume, high gastric pH, nonparticulate gastric contents.

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Fast at least 8 hours before surgery to reduce risk of aspiration of particulate matter.

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Continue preop medications for reflux.

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Consider adding promotility agents.

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Important: Administer nonparticulate antacid (eg, Bicitra 30 cc po) within 30 min of induction.

r This is a low-risk medication that is very effective in raising gastric pH.

124 Hiatal Hernia and Gastroesophageal Reflux Disease Hyperaldosteronism

intraop

■ Plan rapid-sequence induction w/ cricoid pressure.

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Minimize time from unconsciousness to tracheal intubation w/

cuffed ETT.

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Apply cricoid pressure properly.

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Succinylcholine has fastest onset of neuromuscular blockade.

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Rocuronium has most rapid onset of nondepolarizing muscle relaxant but has much longer duration than succinylcholine.

Consider this if airway exam suggests difficult intubation.

■ Strategies to minimize risk of aspiration.

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Avoid inhaled induction.

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Consider regional techniques.

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Protect airway w/ cuffed ETT if using general anesthesia.

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Consider NG tube when asleep, though this does not guarantee empty stomach.

■ Extubate when pt is awake, w/ intact airway reflexes. Generally, this occurs when pt is able to clearly follow a command.

postop

■ Monitor mental status closely on emergence. If pt develops altered mental status, consider tracheal intubation for airway protection.

■ Maintain head-up position in PACU, as this may reduce passive reflux.

HYPERALDOSTERONISM

LUDWIG H. LIN, MD

overview

■ Definition: hypersecretion of the mineralocorticoid aldosterone;

may be primary (adrenal cause of excessive production) or sec-ondary (extra-adrenal stimulus for production)

Pathophysiology

■ Primary

➣

Usually caused by an aldosterone-producing adrenal adenoma (Conn’s syndrome)

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Sometimes by adrenal carcinoma or bilateral cortical nodular hyperplasia

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Can be mimicked by inherited disorders involving corticosteroid synthesis, as well as ingestion of licorice

■ Secondary

Hyperaldosteronism 125

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Usually a result of hypoperfusion to the kidneys (eg, renal arte-rial atherosclerosis or fibromuscular hyperplasia), resulting in increased secretion of renin as a compensatory response

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Renin-producing tumors are rarely the cause of secondary aldos-teronism.

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Bartter’s syndrome, characterized by renal juxtaglomerular hyperplasia, is assoc w/ severe hyperaldosteronism because the defect in renal conservation of sodium stimulates renin & aldos-terone production.

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Other diseases producing intravascular volume depletion can lead to increased renin & aldosterone production: cirrhosis, nephrotic syndrome, congestive heart failure.

■ Aldosterone is responsible for sodium & water reabsorption in the distal renal tubule as well as secretion of potassium.

■ Excessive aldosterone results in hypokalemia, hypernatremia, &

hypervolemia, usually presenting as diastolic hypertension.

■ Fatigue & muscle weakness may occur as result of hypokalemia;

polyuria results from impairment of the urinary concentrating ability.

Abnormal Findings

■ Abnormal overnight urinary concentration test

■ Neutral to alkaline urine pH (excessive secretion of ammonium &

bicarbonate ions to compensate for the metabolic alkalosis)

■ Hypokalemia

■ Hypernatremia

preop

Issues/Evaluation

■ Diagnostic criteria for primary hyperaldosteronism

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Diastolic hypertension w/o edema

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Hyposecretion of renin

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Hypersecretion of aldosterone that does not suppress appropri-ately in response to salt loading

■ Diagnostic criteria for secondary hyperaldosteronism

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High renin levels What To Do

■ Usual therapy for primary hyperaldosteronism

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Surgical excision of adenoma.

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Dietary restriction of sodium.

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Use of aldosterone antagonist (spironolactone) also effective.

126 Hyperaldosteronism Hypercalcemia

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Other anti-mineralocorticoids used include triamterene &

amiloride.

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With inherited disorders, replacement w/ dexamethasone, a potent glucocorticoid that suppresses ACTH & endogenous cor-tisol production yet has only weak mineralocorticoid activity, could be the approach.

■ Preop mgt

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Obtain electrolytes & an ECG to look for signs of hypokalemia.

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Elective cases should be delayed if the plasma potassium con-centration is<3 mEq/L.

intraop

■ Issues include pre-existent hypervolemia & electrolyte imbalances, such as hypernatremia & hypokalemia. With secondary hyperaldos-teronism, the cause of the intravascular volume depletion (eg, cir-rhosis, CHF) may predispose the pt to intraop complications.

■ Hypokalemia can lead to myocardial dysfunction, conduction &

rhythm abnormalities. A U wave characteristically appears, along w/ prolonged PR interval. Eventually, a terminal ventricular fibrilla-tion pattern results.

■ Respiratory alkalosis, beta-agonist administration (even as additive to local anesthetics in a regional block), & hyperglycemia can lead to worsening hypokalemia.

■ Nondepolarizing muscle relaxants have an increased effect in pts w/

hypokalemia.

Management

■ Potassium chloride can be given as 0.5–1.0 mEq bolus injections in the event of ECG abnormalities seen w/ hypokalemia. With less urgent replacement, 10–20 mEq of KCl per hour in an IV infusion can be used.

postop

■ Continued telemetry monitoring for pt w/ severe hypokalemia

HYPERCALCEMIA

LUDWIG H. LIN, MD

overview

■ Causes

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Parathyroid related (primary, lithium therapy, familial)

Hypercalcemia 127

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Malignancy-related

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Vitamin D-related (vitamin D intoxication, sarcoidosis, idio-pathic hypercalcemia of infancy)

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Increased bone turnover (hyperthyroidism, immobilization, thi-azides, vitamin A intoxication)

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Renal failure (secondary hyperparathyroidism, aluminum intox-ication, milk-alkali syndrome)

■ Diagnosis: measurement of calcium, albumin, PTH, or ionized calcium

■ Usual Rx: Depends on specific cause, but general measures include hydration w/ saline, w/ or w/o diuresis w/ loop diuretics (furosemide or ethacrynic acid). Other treatments include:

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Bisphosphonates (etidronate, pamidronate)

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^Calcitonin

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Glucocorticoids, in dosages of 40–100 mg QD in four divided doses, increase urinary calcium excretion & decrease intestinal calcium absorption; effective antitumor agent in certain malig-nancies

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^Dialysis

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Gallium nitrate: inhibits bone resorption; nephrotoxin

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Mithramycin: inhibits bone resorption. Can lead to thrombocy-topenia & hepatocellular necrosis

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PO, IV phosphates (can lead to ectopic calcification)

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Parathyroid surgery for primary hyperparathyroidism

preop

Issues/Evaluation

■ For severe symptomatic hypercalcemia, consider postponing elec-tive surgery to determine cause & appropriate therapy.

■ Although most pts have only mild symptoms, hypercalcemia can cause multisystem abnormalities:

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Neuromuscular: generalized weakness, fatigue, mild depression, proximal muscle weakness, confusion

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Renal: renal stones w/ renal colic, polyuria, dehydration, renal insufficiency

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Cardiovascular: shortened QT interval, increased sensitivity to digoxin

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GI: anorexia, constipation, nausea/vomiting

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Other: bone demineralization, arthralgias, bone pain, pruritus

■ Get ECG to assess for prolonged PR or shortened QT intervals &

cardiac arrhythmias.

128 Hypercalcemia Hyperparathyroidism

■ Serum calcium>13 mg/dL leads to calcification in tissue & renal insufficiency.

■ Serum calcium>15 mg/dL is a medical emergency because of the risk of coma & cardiac arrest.

What To Do

■ IV hydration w/ normal saline (2.5–4 L/day).

■ Consider IV furosemide diuresis once hydration is adequate.

➣

Follow other electrolytes closely during this process.

intraop

■ Maintain normocarbia. (Hyperventilation may be deleterious by decreasing plasma potassium, which can counterbalance the effects of calcium, but may be beneficial because it decreases the ionized calcium fraction.)

■ Preop muscle weakness should be considered when dosing muscle relaxants.

Management

■ Avoid thiazide diuretics (they enhance renal tubular resorption of calcium).

■ Avoid prolonged immobilization (calcium release from resorbed bone increases).

postop

■ Treatment options such as calcitonin & mithramycin take hours for onset & hence are not helpful intraop but may be beneficial postop.

HYPERPARATHYROIDISM

BETTY LEE-HOANG, MD

overview

■ Definition: elevated level of parathyroid hormone (PTH)

➣

Primary hyperparathyroidism

r Elevated level of PTH is inappropriate in pt w/ normal or ele-vated serum calcium level.

r Most commonly caused by parathyroid adenoma (75–85%) or parathyroid hyperplasia

➣

Secondary hyperparathyroidism r Related to hypocalcemia

Hyperparathyroidism Hyperthyroidism 129 r Occurs most commonly w/ chronic renal failure & intestinal

malabsorption

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Tertiary hyperparathyroidism

r Refers to pt w/ secondary hyperparathyroidism who sub-sequently develops “autonomous” function of hyperplastic parathyroid glands

■ PTH increases the serum calcium level by stimulating vitamin D pro-duction & absorption of Ca, increasing renal tubular reabsorption of Ca & decreasing reabsorption of phosphate, & promoting movement of Ca from bone.

■ Usual Rx: Depends on the cause of hyperparathyroidism & pt symptoms

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Most symptomatic pts are referred for surgery

■ May occur as part of multiple endocrine neoplasia syndromes (MEN)

preop

■ Presents as hypercalcemia w/ serum calcium>5.5 mEq/L (10.5 mg/

dL)

■ Many pts are asymptomatic, but symptoms can include

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Hypertension

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Pain from renal stones

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^Lethargy

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Muscle weakness, myalgias, arthralgias

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(See also Coexisting Disease: Hypercalcemia)

■ Continue medical mgt, which may include IV hydration, mithramycin, glucocorticoids, calcitonin.

intraop

■ Monitor for dysrhythmias since the QT interval is short, PR interval is prolonged, & QRS complex is wide.

■ Monitor volume status closely to maintain hydration.

postop

■ Pts who have significant muscle weakness may require ventilatory support.

HYPERTHYROIDISM

JEREMY NUSSBAUMER, MD

overview

■ Definition: excessive levels of circulating T3 and/or T4 hormone

130 Hyperthyroidism

■ Causes

➣

Graves’ disease is the most common cause (thyroid-stimulating autoantibodies)

r Other features: exophthalmos, dermopathy

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Excess administration of thyroid replacement hormone

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Toxic nodular goiter

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Thyroiditis

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TSH-secreting tumors (rare)

■ Signs/symptoms

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^Tremor

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Weight loss w/ increased appetite

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Heat intolerance

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Muscle weakness

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Hyperreflexia

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Sinus tachycardia

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CHF (typically high-output)

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Atrial fibrillation

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Possible cardiomyopathy

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Increased cardiac output

■ Usual Rx

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Antithyroid drugs (eg, propylthiouracil, methimazole, carbima-zole)

r Decrease thyroid hormone synthesis

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Iodine compounds (eg, potassium iodide, Lugol’s solution) r Decrease hormone release

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Beta blockers

r Adjunctive therapy to decrease sympathetic activity r May reduce peripheral conversion of T4 to T3

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Surgical removal of tumors

preop

Issues/Evaluation

■ Postpone elective cases until pt is euthyroid.

■ Thyroid storm can be life-threatening.

➣

Check thyroid function tests.

➣

Resting HR should be<85.

■ Consider beta blockade for emergent cases.

What To Do

■ Check T3, T4 levels.

■ Render pt euthyroid before elective surgery.

Hyperthyroidism 131

intraop

■ Avoid meds that stimulate sympathetic nervous system (eg, pan-curonium, ephedrine, epinephrine, ketamine).

■ Consider thiopental for induction (decreases T4 to T3 conver-sion).

■ Carefully protect the eyes of pts w/ exophthalmos.

■ Watch for thyroid storm (see below).

Management

■ Phenylephrine should be used for hypotension.

■ Adequate anesthetic depth should be established to avoid exagger-ated sympathetic response.

postop

■ The most serious complication in the hyperthyroid pt is thyroid storm.

■ Thyroid storm may be precipitated by a variety of conditions.

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Thyroid surgery

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Other surgery

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Acute medical illness (eg, sepsis, stroke, diabetic ketoacidosis)

■ Signs/symptoms of thyroid storm

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^Fever

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Hypotension

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Tachycardia

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Heart failure

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Muscle weakness

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Altered mental status including delirium, coma

■ Thyroid storm can occur intraop or up to 24 h postop. Differential diagnosis includes

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Malignant hyperthermia (characterized by fever, muscle rigidity, increased CK, or severe metabolic acidosis)

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Drug or transfusion reaction

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^Sepsis

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Pheochromocytoma

■ Mgt of thyroid storm should occur in an ICU setting. Therapy includes

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Propylthiouracil (PTU) (250 mg q6h PO, NG, or PR)

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Beta blockade (eg, propranolol 2–4 mg IV q4h)

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Potassium iodide 1 h after PTU (5 drops SSKI PO q6h)

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Glucocorticoid therapy (eg, dexamethasone 2 mg IV q6h)

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IV hydration

132 Hypertrophic Cardiomyopathy

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