Surgeons of every specialty face increasingly complex surgical challenges. In addition, modern surgical treatment can be offered to more fragile patients, with successful outcomes. Mastery of the scientific fundamentals of perioperative management is required to achieve satisfactory results. The organ system–based approach presented here allows the surgeon to address the patient’s pre- and postoperative needs with a comprehensive surgical plan. This chapter will serve as a summary guide to best practices integral to conducting surgical procedures in the modern era.

The most common neuropsychiatric complications following abdominal surgery are pain and delirium. Moreover, uncontrolled pain and delirium prevent the patient from contributing to vital aspects of his or her care, such as ambulation and respiratory toilet, and promote an unsafe environment that may lead to the unwanted dislodgment of drains and other supportive devices, with potentially life-threatening consequences. Pain and delirium usually coexist in the postoperative setting, and each can contribute to the development of the other. Despite high reported rates of overall patient satisfaction, pain control is frequently inadequate in the perioperative setting,¹ with high rates of complications such as drowsiness from overtreatment and unacceptable levels of pain from undertreatment. Therefore, it is mandatory that the surgical plan for every patient include close monitoring of postoperative pain and delirium and regular assessment of the efficacy of pain control.

Pain management, like all surgical planning, begins in the preoperative assessment. In the modern era, a large proportion of surgical patients will require special attention with respect to pain control. Patients with preexisting pain syndromes, such as sciatica or interspinal disc disease, or patients with a history of opioid use may have a high tolerance for opioid analgesics. Every patient’s history should include a thorough investigation for chronic pain syndrome, addiction (active or in recovery), and adverse reactions to opioid, nonsteroidal, or epidural analgesia. The pain control strategy may include consultation with a pain control anesthesiology specialist, but it is the responsibility of the operating surgeon to identify complicated patients and construct an effective pain control plan.

Opioid Analgesia

Postoperative pain control using opioid medication has been in use for thousands of years. Hippocrates advocated the use of opium for pain control. The benefits of postoperative pain control are salutary and include improved mobility and respiratory function and earlier return to normal activities. The most effective strategy for pain control using opioid analgesia is patient-controlled analgesia (PCA), wherein the patient is instructed in the use of a preprogrammed intravenous pump that delivers measured doses of opioid (usually morphine or meperidine). In randomized trials, PCA has been shown to provide superior pain control and patient satisfaction compared to interval dosing,² but PCA has not been shown to improve rates of pulmonary and cardiac complications³ or length of hospital stay,⁴ and there is evidence that PCA may contribute to postoperative ileus.⁵ In addition, PCA may be unsuitable for patients with a history of substance abuse, high opioid tolerance, or those with atypical reactions to opioids.

Regional Analgesia

Due to the limitations of PCA, pain control clinicians have turned to regional analgesia as an effective strategy for the management of postoperative pain. Postoperative epidural analgesia involves the insertion of a catheter into the epidural space of the lumbar or thoracic spine, enabling the delivery of local anesthetics or opioids directly to the nerve roots. The insertion procedure is generally safe, with complication rates of motor block and numbness between 0.5% and 7%,⁶ and an epidural abscess rate of 0.5 per thousand.⁷ Potential advantages of epidural analgesia include elimination of systemic opioids, and thus less respiratory depression, and improvement in pulmonary complications and perioperative ileus. There have been several large trials,^8-10 a meta-analysis,⁶ and a systematic review¹¹ comparing PCA with epidural analgesia in the setting of abdominal surgery. These studies indicate that epidural analgesia provides more complete analgesia than PCA throughout the postoperative course. Furthermore, in randomized prospective series of abdominal procedures, epidural analgesia has been associated with decreased rates of pulmonary complications^12,13 and postoperative ileus.^14,15 Epidural analgesia requires a skilled anesthesia clinician to insert and monitor the catheter and adjust the dosage of neuraxial medication. Some clinicians may prefer correction of coagulopathy before inserting or removing the catheter, although the American Society of Anesthesiologists (ASA) has not issued official guidelines on this issue.

Peripheral nerve blocks are also effective in perioperative pain control and do not carry the same potential morbidities as the epidural approach. Using ultrasound guidance, a skilled practitioner can deliver a long-acting local anesthetic into the transversus abdominis plane (TAP) or in the rectus sheath to establish analgesia both intraoperatively and postoperatively. Randomized clinical data have confirmed the efficacy of regional blocks in controlling pain and reducing use of opioid analgesia.^16,17

Analgesia with Nonsteroidal Anti-Inflammatory Drugs

Oral nonsteroidal anti-inflammatory drugs (NSAIDs) have long been used for postoperative analgesia in the outpatient setting and, with the development of parenteral preparations, have come into use in the inpatient population. This class of medication has no respiratory side effects and is not associated with addiction potential, altered mental status, or ileus. In addition, these medications provide effective pain relief in the surgical population. However, use of NSAIDs has not been universally adopted in abdominal surgery due to concerns regarding the platelet dysfunction and erosive gastritis associated with heavy NSAID use. In prospective trials, NSAIDs were found to provide effective pain control without bleeding or gastritis symptoms following laparoscopic cholecystectomy,¹⁸ abdominal hysterectomy,¹⁹ and inguinal hernia repair.^20,21 NSAIDs have also been shown to improve pain control and decrease morphine dosage when used in combination following appendectomy.²²

The sensation of pain is very subjective and personal. Accordingly, the surgeon must individualize the pain control plan to fit the needs of each patient. The pain control modalities discussed above can be used in any combination, and the surgeon should not hesitate to use all resources at his or her command to provide adequate relief of postoperative pain.

Postoperative Delirium

Delirium, defined as acute cognitive dysfunction marked by fluctuating disorientation, sensory disturbance, and decreased attention, is an all too common complication of surgical procedures, with reported rates of 11% to 25%, with the highest rates reported in the elderly population.^23,24 The postoperative phase of abdominal surgery exposes patients, some of whom may be quite vulnerable to delirium, to a large number of factors that may precipitate or exacerbate delirium (Table 2-1). These factors can augment one another: postoperative pain can lead to decreased mobility, causing respiratory compromise, atelectasis, and hypoxemia. Escalating doses of narcotics to treat pain can cause respiratory depression and respiratory acidosis. Hypoxemia and delirium can cause agitation, prompting treatment with benzodiazepines, further worsening respiratory function and delirium. This vicious cycle can result in serious complications or death. Preoperative recognition of high-risk patients and meticulous monitoring of every patient’s mental status are the most effective ways to prevent postoperative delirium; treatment can be remarkably difficult once the cycle has begun.

Patient factors that are associated with high risk of perioperative delirium include age greater than 70 years, preexisting cognitive impairment or prior episode of delirium, history of alcohol or narcotic abuse, and malnutrition.^22,25 Procedural factors associated with high delirium risk include operative time greater than 2 hours, prolonged use of restraints, presence of a urinary catheter, addition of more than 3 new medications, and reoperation.²⁶

Once the patient’s risk for postoperative delirium is identified, perioperative care should be planned carefully to decrease other controllable factors. Epidural analgesia has been associated with less delirium than PCA after abdominal surgery.²⁶ Sedation or “sleepers” should be used judiciously, if at all, with high-risk patients. If the patient requires sedation, neuroleptics such as haloperidol and the atypical neuroleptics such as olanzapine are tolerated much better than benzodiazepines.²⁷ The patient’s mental status, including orientation and attention, should be assessed with every visit and care should be taken to avoid anemia, electrolyte imbalances, dehydration, and other contributing factors.

Once the diagnosis of postoperative delirium is established, it is important to recognize that some of the causes of delirium are potentially life-threatening, and immediate action is necessary. Evaluation begins with a thorough history and physical examination at the bedside by the surgeon. The history should focus on precipitating events such as falls (possible traumatic brain injury), recent procedures, use of opioids and sedatives, changes in existing medications (eg, withholding of thyroid replacement or antidepressants), and consideration of alcohol withdrawal. The vital signs and fluid balance may suggest sepsis, hypovolemia, anemia, or dehydration. The exam should include brief but complete sensory and motor neurologic examinations to differentiate delirium from stroke. Pay attention to common sites of infection such as the surgical wound, the lungs, and intravenous catheters. Urinary retention may be present as a result of medication or infection. Deep venous thrombosis may be clinically evident as limb swelling. Postoperative myocardial infarction (MI) may often present as acute cardiogenic shock.

The history and physical examination should then direct the use of lab tests. Most useful are the electrolytes, blood glucose, and complete blood cell count. Pulse oximetry and arterial blood gases may disclose hypercapnia or hypoxemia. Chest x-ray may disclose atelectasis, pneumonia, acute pulmonary edema, or pneumothorax. Cultures may be indicated in the setting of fever or leukocytosis, but will not help immediately. Electrocardiogram (ECG) and cardiac troponin may be used to diagnose postoperative MI.

Resuscitative measures may be required if life-threatening causes of delirium are suspected. Airway control, supplemental oxygen, and fluid volume expansion should be considered in patients with unstable vital signs. The patient should not be sent out of the monitored environment for further tests, such as head computed tomography (CT), until the vital signs are stable and the agitation is controlled. Treatment of postoperative delirium depends on treatment of the underlying causes. Once the underlying cause has been treated, delirium may persist, especially in elderly or critically ill patients, who regain orientation and sleep cycles slowly. In these patients, it is important to provide orienting communication and mental stimulation during the day and to promote sleep during the night. The simplest ways are the most effective: contact with family members and friends, use of hearing aids, engagement in activities of daily living, and regular mealtimes. Sleep can be promoted by keeping the room dark and quiet throughout the evening and preventing unnecessary interruptions. If nighttime sedation is required, atypical neuroleptics or low-dose serotonin reuptake inhibitors such as trazodone are better tolerated than benzodiazepines. If agitation persists, escalating doses of neuroleptics (or benzodiazepines in the setting of alcohol withdrawal) can be used to control behavior, but underlying organic causes of delirium must be investigated.

Risk Assessment

It has been estimated that 1 million patients have a perioperative MI each year, and the contribution to medical costs is $20 billion annually.²⁸ Thoracic, upper abdominal, neurologic, and major orthopedic procedures are associated with increased cardiac risk. Diabetes, prior MI, unstable angina, and decompensated congestive heart failure (CHF) are most predictive of perioperative cardiac morbidity and mortality, and patients with these conditions undergoing major surgery warrant further evaluation²⁹ (Table 2-2). Patient factors conferring intermediate risk include mild angina and chronic renal insufficiency with baseline creatinine ≥2 mg/dL.³⁰ It is worth noting that women were underrepresented in the studies on which the American College of Cardiology and the American Heart Association (ACC/AHA) guidelines are based.³¹ A retrospective study in gynecologic patients found that hypertension and previous MI were major predictors of postoperative cardiac events, as opposed to the ACC/AHA guidelines, which indicate that they are minor and intermediate criteria, respectively.³² Vascular surgical patients are at highest risk because of the prevalence of underlying coronary disease in this population.^29,33 Other high-risk procedural factors include emergency surgery, long operative time, and high fluid replacement volume. Intraperitoneal procedures, carotid endarterectomy, thoracic surgery, head and neck procedures, and orthopedic procedures carry an intermediate risk and are associated with a 1% to 5% risk of a perioperative cardiac event.³⁰

Perioperative evaluation to identify patients at risk for cardiac complications is essential in minimizing morbidity and mortality. Workup should start with history, physical exam, and ECG to determine the existence of cardiac pathology. Screening with chest radiographs and ECG is required for men over 40 and women over 55. According to the ACC/AHA guidelines, initial preoperative cardiac risk can be assessed using a clinical calculator, the Revised Cardiac Risk Index (RCRI).³⁴ This index includes history of ischemic heart disease, CHF, cerebrovascular disease, diabetes, chronic kidney disease, and planned high-risk procedure. Advanced or invasive testing is reserved for patients with 2 or more of these risk factors. Overall functional ability is the best clinical measure of cardiac fitness. Patients who can exercise without limitations can generally tolerate the stress of major surgery.³⁵ Limited exercise capacity may indicate poor cardiopulmonary reserve and the inability to withstand the stress of surgery. Poor functional status is the inability to perform activities such as driving, cooking, or walking less than 5 km/h.

Intraoperative risk factors include operative site, inappropriate use of vasopressors, and unintended hypotension. Intra-abdominal pressure exceeding 20 mm Hg during laparoscopy can decrease venous return from the lower extremities and thus contribute to decreased cardiac output,³⁶ and Trendelenburg positioning can result in increased pressure on the diaphragm from the abdominal viscera, subsequently reducing vital capacity. Intraoperative hypertension has not been isolated as a risk factor for cardiac morbidity, but it is often associated with wide fluctuations in pressure and has been more closely associated with cardiac morbidity than intraoperative hypotension. Preoperative anxiety can contribute to hypertension even in normotensive patients. Patients with a history of hypertension, even medically controlled hypertension, are more likely to be hypertensive preoperatively. Those with poorly controlled hypertension are at greater risk of developing intraoperative ischemia, arrhythmias, and blood pressure derangements, particularly at induction and intubation. Twenty-five percent of patients will exhibit hypertension during laryngoscopy. Patients with chronic hypertension may not necessarily benefit from lower blood pressure during the preoperative period because they may depend on higher pressures for cerebral perfusion. Those receiving antihypertensive medications should continue them up until the time of surgery. Patients taking β-blockers are at risk of withdrawal and rebound ischemia. Key findings on physical examination include retinal vascular changes and an S₄ gallop consistent with left ventricular hypertrophy. Chest radiography may show an enlarged heart, also suggesting left ventricular hypertrophy.

ECG should be obtained in patients with chest pain, diabetes, prior revascularization, prior hospitalization for cardiac causes, all men age 45 or older, and all women age 55 or older with 2 or more risk factors. High- or intermediate-risk patients should also have a screening ECG. A lower-than-normal ejection fraction demonstrated on echocardiography is associated with the greatest perioperative cardiac risk and should be obtained in all patients with symptoms suggesting heart failure or valvular disease. Tricuspid regurgitation indicates pulmonary hypertension and is often associated with sleep apnea. The chest x-ray is used to screen for cardiomegaly and pulmonary congestion, which may signify ventricular impairment.

Exercise testing demonstrates a propensity for ischemia and arrhythmias under conditions that increase myocardial oxygen consumption. Numerous studies have shown that performance during exercise testing is predictive of perioperative mortality in noncardiac surgery. ST-segment changes during exercise including horizontal depression greater than 2 mm, changes with low workload, and persistent changes after 5 minutes of exercise are seen in severe multivessel disease. Other findings include dysrhythmias at a low heart rate, an inability to raise the heart rate to 70% of predicted, and sustained decrease in systolic pressure during exercise.

Unfortunately, many patients are unable to achieve adequate workload in standard exercise testing because of osteoarthritis, low back pain, and pulmonary disease. In this case, pharmacologic testing is indicated with a dobutamine echocardiogram. Dobutamine is a β-agonist that increases myocardial oxygen demand and reveals impaired oxygen delivery in those with coronary disease. Echocardiography concurrently visualizes wall motion abnormalities due to ischemia. Transesophageal echocardiography may be preferable to transthoracic echocardiography in obese patients because of their body habitus and has been shown to have high negative predictive value in this group.³⁷ Nuclear perfusion imaging with vasodilators such as adenosine or dipyridamole can identify coronary artery disease and demand ischemia. Heterogeneous perfusion after vasodilator administration demonstrates an inadequate response to stress. Wall motion abnormalities indicate ischemia, and an ejection fraction lower than 50% increases the risk of perioperative mortality. Angiography should only be performed if the patient may be a candidate for revascularization.

Coronary Disease

Most perioperative MIs are caused by plaque rupture in lesions that do not produce ischemia during preoperative testing.³⁸ This presents an obvious challenge for detecting patients at risk. Stress testing has a low positive predictive value in patients with no cardiac risk factors and has been associated with an unacceptably high rate of false-positive results.³⁹

Preoperative optimization may include medical management, percutaneous coronary interventions (PCIs), or coronary artery bypass grafting (CABG).⁴⁰ The ACC/AHA guidelines²⁹ recommend revascularization for patients whose preoperative testing reveals severe disease that warrants intervention according to practice guidelines for coronary artery disease, independent of their perioperative status.

Patients warranting emergent CABG will be at greatest risk for that procedure. A recent study from the Veterans Administration hospitals recommends against revascularization in patients with stable cardiac symptoms.⁴¹ Preoperative PCI does not decrease the risk of future MI or mortality in patients with stable coronary disease, and only targets stenotic lesions, rather than those most likely to rupture. One retrospective study found no reduction in morbidity or perioperative MI after percutaneous transluminal coronary angioplasty, and the authors proposed that surgery within 90 days of balloon angioplasty increased the risk of thrombosis.⁴² However, PCI done more than 90 days before surgery did provide benefit when compared to those who had no intervention at all. Another retrospective study found that patients who have surgery within 2 weeks of stenting had a high incidence of perioperative MI, major bleeding, or death.⁴³ Although a retrospective review from the Coronary Artery Surgery Study registry showed a lower mortality rate in patients with coronary artery disease who were post-CABG than those without CABG (0.09% vs 2.4%), this benefit did not include the morbidity associated with CABG itself. Unfortunately, the benefit was overwhelmed by the 2.3% morbidity rate seen with CABG in this cohort.⁴⁴ Survival benefit of CABG over medical management is realized at 2 years or more after surgery,⁴⁵ so preoperative mortality may decrease overall short-term survival. Revascularization and bypass grafting should be restricted to patients who would benefit from the procedure independent of their need for noncardiac surgery. One of the disadvantages of PCI in the preoperative setting is the need for anticoagulation to prevent early stent occlusion. The use of platelet inhibitors to prevent stent occlusion must be included in the overall risk assessment, especially for surgery of the central nervous system.

Catecholamine surges can cause tachycardia, which may alter the tensile strength of coronary plaques and incite plaque rupture.^46,47 Catecholamine surges can also increase blood pressure and contractility, contributing to platelet aggregation and thrombosis after plaque rupture and increasing the possibility of complete occlusion of the arterial lumen.⁴⁸ Perioperative β-blockade mitigates these effects and has been shown to reduce MI and mortality from MI by over 30% in vascular surgical patients with reversible ischemia.⁴⁶ Patients at highest risk still have a cardiac event rate of 10%, even with adequate perioperative β-blockade.²⁹

In 1998, a landmark study⁴⁹ demonstrated a 55% reduction in mortality in noncardiac surgical patients with known coronary disease who were given atenolol perioperatively. This was followed by the DECREASE trial,⁵⁰ which showed a 10-fold reduction in perioperative MI and death compared to placebo. Thereafter, perioperative β-blockade was widely adopted as a quality measure. However, additional later investigations have shown that although perioperative β-blockers benefit patients with known ischemia, low-risk patients may in fact be harmed.⁵¹ Tight rate control has been associated with increased risk of hypotension and bradycardia requiring intervention and stroke without any significant decrease in mortality.^52-55 Furthermore, critical analysis of the literature shows that studies have been inconsistent in the type of medication administered, the duration and timing of administration, and the target for heart rate control.⁵⁶ Consequently, results are difficult to interpret. Thus, prophylactic perioperative β-blockade should be restricted to patients with cardiac ischemia and has a limited role in patients with low or moderate risk of postoperative cardiac events.²⁹

Congestive Heart Failure and Arrhythmia

CHF is associated with coronary disease, valvular disease, ventricular dysfunction, and all types of cardiomyopathy. These are all independent risk factors that should be identified prior to surgery. Even compensated heart failure may be aggravated by fluid shifts associated with anesthesia and abdominal surgery and deserves serious consideration. Perioperative mortality increases with higher New York Heart Association class and preoperative pulmonary congestion. CHF should be treated to lower filling pressures and improve cardiac output before elective surgery. β-Blockers, angiotensin-converting enzyme inhibitors, and diuretics can be employed to this end. The patient should be stable for 1 week before surgery.⁵⁷

Arrhythmias and conduction abnormalities elicited in the history, on exam, or on ECG should prompt investigation into metabolic derangements, drug toxicities, or coronary disease. In the presence of symptoms or hemodynamic changes, the underlying condition should be reversed and then medication given to treat the arrhythmia. Indications for antiarrhythmic medication and cardiac pacemakers are the same as in the nonoperative setting. Nonsustained ventricular tachycardia and premature ventricular contractions have not been associated with increased perioperative risk and do not require further intervention.^58,59

Valvular Disease

Valvular disease should be considered in patients with symptoms of CHF, syncope, and a history of rheumatic heart disease. Aortic stenosis (AS) is a fixed obstruction to the left ventricular outflow tract, limiting cardiac reserve and an appropriate response to stress. History should elicit symptoms of dyspnea, angina, and syncope; examination may reveal a soft S₂, a late-peaking murmur, or a right-sided crescendo–decrescendo murmur radiating to the carotids. AS is usually caused by progressive calcification or congenital bicuspid valve. Critical stenosis exists when the valve area is less than 0.7 cm² or transvalvular gradients are greater than 50 mm Hg and is associated with an inability to increase cardiac output with demand. If uncorrected, AS is associated with a 13% risk of perioperative death. Valve replacement is indicated prior to elective surgery in patients with symptomatic stenosis.²⁹ Myocardial ischemia may occur in the absence of significant coronary artery occlusion in the presence of aortic valve disease. Perioperative management should include optimizing the heart rate to between 60 and 90 beats per minute and avoiding atrial fibrillation if possible. Because of the outflow obstruction, stroke volume may be fixed and bradycardia will lower cardiac output. Similarly, hypotension is also poorly tolerated.

Aortic regurgitation (AR) is associated with backward flow into the left ventricle during diastole and reduced forward stroke volume. Bradycardia facilitates regurgitation by increased diastolic time. Chronic AR causes massive left ventricular dilatation (cor bovinum) and hypertrophy, which is associated with decreased left ventricular function at later stages. AR is most often caused by rheumatic disease or congenital bicuspid valve. Medical treatment includes rate control and afterload reduction. Without valve replacement, survival is approximately 5 years once patients become symptomatic. This is an obvious consideration when planning any other surgical procedures.

Tricuspid regurgitation is usually caused by pulmonary hypertension secondary to severe left-sided failure. Other causes include endocarditis, carcinoid syndrome, and primary pulmonary hypertension. Hypovolemia, hypoxia, and acidosis can increase right ventricular afterload and should be avoided in the perioperative period.

Mitral stenosis is an inflow obstruction that prevents adequate left ventricular filling. The transvalvular pressure gradient depends on atrial kick, heart rate, and diastolic filling time. Tachycardia decreases filling time and contributes to pulmonary congestion. Mitral regurgitation is also associated with pulmonary hypertension with congestion, as the pathologic valve prevents forward flow, causing left atrial dilatation and subsequent atrial arrhythmias. History and physical exam should focus on signs of CHF such as orthopnea, pedal edema, dyspnea, reduced exercise tolerance, and auscultatory findings such as murmurs and an S₃ gallop. Neurologic deficits may signify embolic sequelae of valve disease. Perioperative rate control is essential for maintaining adequate cardiac output. ECG findings will reflect related arrhythmias and medications but will not be specific for valve disease. Laboratory studies should identify secondary hepatic dysfunction or pulmonary compromise. Left ventricular hypertrophy is an adaptive response, which may cause subsequent pulmonary hypertension and diastolic dysfunction.

Prosthetics in the mitral position pose the greatest risk for thromboembolism, and the risk increases with valve area and low flow. Mechanical valves pose a higher risk than tissue valves in patients with a history of valve replacement. Diuretics and afterload-reducing agents will enhance forward flow and minimize cardiopulmonary congestion. Patients with mitral valve prolapse (MVP) should receive antibiotics.

Mitral regurgitation may also impair left ventricular function and lead to pulmonary hypertension. Stroke volume is reduced by backward flow into the atrium during systole. The left ventricle dilates to handle increasing end-systolic volume, eventually causing concentric hypertrophy and decreased contractility. The end result may be decreased ejection fraction and CHF. A decrease in systemic vascular resistance and increase in atrial contribution to the ejection fraction can both improve forward flow and reduce the amount of regurgitation. Echocardiography can clarify the degree of valvular impairment. Medical treatment centers on afterload reduction with vasodilators and diuretics. MVP is present in up to 15% of women and is usually associated with a midsystolic click and late systolic murmur on physical exam. Murmur is indicative of prolapse. Although MVP is associated with connective tissue disorders, it usually occurs in otherwise healthy, asymptomatic patients. Echocardiography is used to confirm the diagnosis and evaluate the degree of prolapse. Chronically, MVP may be associated with mitral regurgitation, emboli, and increased risk of endocarditis. Prolapse may be aggravated by decreased preload, which should be minimized in the perioperative period. Patients with MVP are at risk of ventricular arrhythmias with sympathetic stimulation and endocarditis, which can be addressed with pain control and antibiotic prophylaxis, respectively.

Individuals with underlying structural cardiac defects are at increased risk for developing endocarditis after invasive procedures. Surgical procedures involving mucosal surfaces or infected tissues may cause transient bacteremia that is usually short-lived. Certain procedures are associated with a greater risk of endocarditis and warrant prophylaxis (Table 2-3). Abnormal valves, endocardium, or endothelium can harbor the bloodborne bacteria for a longer period of time, and infection and inflammation can ensue. Although there are no randomized trials regarding endocarditis prophylaxis, the AHA recommends prophylaxis for those⁶⁰ at high and moderate risk for developing the condition. The highest-risk patients have prosthetic heart valves, cyanotic congenital heart disease, or a history of endocarditis (even without structural abnormality).⁶¹ Conditions associated with moderate risk include congenital septal defects, patent ductus arteriosus, coarctation of the aorta, and bicuspid aortic valve. Hypertrophic cardiomyopathy and acquired valvular disease also fall into this category. MVP is a prevalent and often situational condition. Normal valves may prolapse in the event of tachycardia or hypovolemia and may reflect normal growth patterns in young people. Prolapse without leak or regurgitation seen on Doppler studies is not associated with risk greater than that of the general population, and no antibiotic prophylaxis is necessary.^62,63 However, the jet caused by the prolapsed valve increases the risk of bacterial adherence and subsequent endocarditis. Leaky valves detected by physical exam or Doppler warrant consideration for prophylactic antibiotics.⁶⁴ Patients with significant regurgitation are more likely to be older and men, and other studies have shown that older men are more likely to develop endocarditis.^64-66 Some advocate prophylaxis for men older than 45 years with MVP even in the absence of audible regurgitation.⁶⁶ Prolapse secondary to myxomatous valve degeneration also warrants prophylactic antibiotics.^67,68

For patients at risk, the goal should be administration of antibiotics in time to attain adequate serum levels during and after the procedure. For most operations, a single intravenous dose given 1 hour prior to incision will achieve this goal. Antibiotics should generally not be continued for more than 6 to 8 hours after the procedure to minimize the chance of bacterial resistance. In the case of oral, upper respiratory, and esophageal procedures, α-hemolytic Streptococcus is the most common cause of endocarditis, and antibiotics should be targeted accordingly. Oral amoxicillin, parenteral ampicillin, and clindamycin for penicillin-allergic patients are suitable medications. Erythromycin is no longer recommended for penicillin-allergic patients because of gastrointestinal side effects and variable absorption.⁶⁹ Antibiotics given to those having genitourinary and nonesophageal gastrointestinal procedures should target enterococci.⁶⁹ While gram-negative bacteremia can occur, it rarely causes endocarditis. Parenteral ampicillin and gentamicin are recommended for highest-risk patients. Moderate-risk patients may receive amoxicillin or ampicillin. Vancomycin may be substituted in patients allergic to penicillin.

Estimates suggest that 250,000 patients receiving chronic anticoagulation require surgery in the United States each year. Operative bleeding risk must be balanced against thromboembolic risk for the patient off of anticoagulation and requires careful judgment. Factors that influence the risk of thromboembolism include the condition requiring chronic anticoagulation, the duration of the procedure, time expected off of anticoagulation, and the duration of perioperative immobility. Thromboembolic risk increases with the amount of time that the patient’s anticoagulation is subtherapeutic.

Primary indications for chronic anticoagulation include arterial embolism associated with mechanical valves and atrial fibrillation and venous thromboembolism (VTE). Arterial events precipitate stroke, and valvular and atrial clot and systemic emboli are higher risk for morbidity and mortality than venous events. Patients at highest risk for perioperative embolism include those with mechanical prosthetic mitral valves, aortic caged-ball and tilted valves, rheumatic heart disease, or history of stroke or transient ischemic attacks (TIAs) in the past 3 months. The risk of thromboembolism without anticoagulation is higher than 10% per year in these high-risk patients.

Patients at moderate risk of thromboembolism without anticoagulation (4%-10% per year) have atrial fibrillation, a bileaflet valve, or history of stroke or TIA. The CHADS₂ score (CHF, hypertension, age, diabetes, and stroke) further stratifies embolic risk for patients with atrial fibrillation based on comorbidities. One point is assigned for hypertension, diabetes, CHF, and age >75 years; 2 points are assigned for history of stroke or TIA. Patients with a cumulative score of 5 to 6 are highest risk; those with a score of 3 to 4 are moderate risk; and those with a score of 0 to 2 without history of stroke or TIA are low risk.

Chronic anticoagulation is indicated for VTE. Patients with VTE within 3 months of surgery and severe thrombophilia are at highest risk for perioperative events and should receive bridging anticoagulation with therapeutic doses of low-molecular-weight heparin (LMWH) or intravenous unfractionated heparin (UFH). Patients at moderate risk include those with a thromboembolic event 3 to 12 months before surgery and less severe thrombophilias. They can receive therapeutic or subtherapeutic doses of anticoagulation depending on the risk of bleeding associated with the procedure. Patients with a remote event are at lowest risk and do not require bridging anticoagulation. It is generally recommended to stop warfarin 5 days prior to surgery if a normal international normalized ratio (INR) is desired. Vitamin K may be administered in the days leading up to the event if the INR is not correcting quickly enough.

LMWH should be held 24 hours before surgery, and intravenous UFH should be held 4 hours before surgery. Oral anticoagulants may be started 12 to 24 hours postoperatively because they take at least 48 hours to affect coagulation. The timing of resuming intravenous and subcutaneous anticoagulants should be determined on a case-by-case basis.

Low-risk patients receiving clopidogrel or aspirin should have it held 5 to 10 days before surgery. Patients with coronary stents are chronically treated with clopidogrel and aspirin to mitigate the risk of stent thrombosis. Interruptions in therapy are associated with high risk of thrombosis and infarct. Patients with bare metal stents placed within 6 weeks of surgery or drug-eluting stents placed within 12 months of surgery should continue clopidogrel and aspirin in the perioperative period.

The perioperative antithrombotic guidelines⁷⁰ from the American College of Chest Physicians are summarized in Table 2-4.

Pulmonary complications are common after surgery and can prolong hospital stays for 1 to 2 weeks.⁷¹ Complications include atelectasis, pneumonia, exacerbations of chronic pulmonary disorders, and respiratory failure requiring mechanical ventilation. Smoking, underlying chronic obstructive pulmonary disease (COPD), and poor exercise tolerance are the greatest risk factors for postoperative pulmonary complications. Physicians should ask about a history of smoking, decreased exercise capacity, dyspnea, and chronic cough. Examination should note pursed lip breathing, clubbing, and chest wall anatomy that could impair pulmonary function. Pulmonary testing is unnecessary in patients without a clear history of smoking or pulmonary disease. The predictive value of screening spirometry is unclear, and no threshold value has been identified to guide surgical decision-making. Forced expiratory volume in 1 second less than 50% of predicted is indicative of exertional dyspnea and may herald the need for further testing. Preoperative chest x-ray abnormalities are associated with postoperative pulmonary complications,⁷¹ but to this point, there are no recommendations for screening radiographs in patients without pulmonary disease. Any preoperative chest x-ray must be examined for signs of hyperinflation consistent with COPD. While compensated hypercapnia has not been shown to be an independent predictor for postoperative ventilatory insufficiency in patients undergoing lung resection, preoperative arterial blood gas analysis provides useful baseline information for perioperative management of patients with chronic carbon dioxide retention. Transverse and upper abdominal incisions are associated with a higher rate of postoperative pulmonary complications than longitudinal midline incisions and lower abdominal incisions.⁷² Surgery longer than 3 hours is also associated with higher risk.⁷³ General anesthesia is also associated with a higher risk of pulmonary complications than spinal, epidural, or regional anesthesia.⁷⁴

Physiologic changes can be seen in the postoperative period, especially after thoracic and upper abdominal procedures. Vital capacity may decrease by 50% to 60%, and is accompanied by an increased respiratory rate to maintain tidal volumes. Normally, functional residual capacity usually exceeds the closing capacity of the alveoli so they remain open throughout the respiratory cycle. Prolonged effects of anesthetics and narcotics reduce functional reserve capacity postoperatively, causing alveolar collapse. These changes can last for weeks to months. A distended abdomen can impair diaphragmatic excursion; painful incisions around the diaphragm and other respiratory muscles contribute to splinting and inadequate pulmonary toilet. Narcotics can inhibit sighing and coughing reflexes, which normally prevent alveolar collapse during periods of sleep and recumbency. Analgesics must be titrated carefully to permit deep breathing and avoid impairing respiratory effort.

Inspired nonhumidified oxygen and halogenated anesthetics are cytotoxic and interfere with surfactant production and mucociliary clearance. Depressed respiratory reflexes, diaphragm dysfunction, and decreased functional reserve capacity all contribute to alveolar collapse and pooling of secretions. Aspiration risk is also increased. Excess secretions cause further alveolar collapse and create a milieu ripe for bacterial infection and pneumonia. Intubated patients should receive antacid prophylaxis and gastric drainage to minimize the risk of aspiration.

Multiple analyses have found that poor exercise tolerance is the greatest predictor of postoperative pulmonary impairment. The ASA risk classification is a gauge of general status and is highly predictive of both cardiac and pulmonary complications.^75,76 Although advanced age is associated with increased incidence of chronic pulmonary disease and underlying impairment, it is not an independent risk factor for pulmonary complications.

Clearly, all smokers should be urged to stop before surgery. Even in the absence of coexisting pulmonary disease, smoking increases the risk of perioperative complications. Smoking confers a relative risk of 1.4 to 4.3, but a reduced risk of pulmonary complications has been shown in patients who stop smoking at least 8 weeks before cardiac surgery.⁷⁷ Even 48 hours of abstinence can improve mucociliary clearance, decrease carboxyhemoglobin levels to those of nonsmokers, and reduce the cardiovascular effects of nicotine. A nicotine patch may help some patients with postoperative nicotine withdrawal but may not be advisable in patients at risk for poor wound healing.

COPD confers a relative risk of 2.7 to 4.7 in various studies. Symptoms of bronchospasm and obstruction should be addressed before surgery, and elective procedures should be deferred in patients having an acute exacerbation. Preoperative treatment may include bronchodilators, antibiotics, steroids, and physical therapy to increase exercise capacity. Patients with active pulmonary infections should have surgery delayed if possible. Asthmatics should have peak flow equivalent to their personal best or 80% of predicted and should be medically optimized to achieve this goal. Pulse corticosteroids may be used without an increased risk of postoperative infection or other complication.^78,79

Malnourished patients may not be able to meet the demands of the increased work of breathing, increasing their risk for respiratory failure. Obese patients have higher rates of oxygen consumption and carbon dioxide production, which increases their work of breathing. They may also exhibit restrictive physiology due to a large, stiff chest wall. A complete history should inquire about sleeping difficulty and snoring. Obesity increases the amount of soft tissue in the oropharynx, which can cause upper airway obstruction during sleep. Fifty-five percent of morbidly obese patients may have sleep-related breathing disorders such as obstructive sleep apnea and obesity-hypoventilation syndrome.⁸⁰ Symptoms include snoring and daytime sleepiness, and formal sleep studies are employed for definitive diagnosis. Sleep-disordered breathing is associated with hypoxia, hypercapnia, changes in blood pressure, nocturnal angina, and increased cardiac morbidity and mortality including stroke and sudden death.⁸¹ Arterial blood gas with partial arterial oxygen pressure less than 55 mm Hg or partial arterial carbon dioxide pressure greater than 47 mm Hg confirms the diagnosis. An increased incidence of pulmonary hypertension and right-sided heart failure is seen in patients with obesity hypoventilation syndrome, and these patients should have an echocardiogram before surgery. In severe cases, intraoperative monitoring with a pulmonary artery catheter may be prudent.