Perioperative Management

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Chapter 182 Perioperative Management

Basheal M. Agrawal, Seth M. Zeidman, Laurence Rhines, Nathan H. Lebwohl, Gregory R. Trost

The spectrum of spine surgery ranges from straightforward cervical procedures in healthy, young adults to emergent fixation of unstable thoracolumbar spine fractures in clinically unstable patients with multiple traumatic injuries. Preoperative evaluation and postoperative care share equal importance with the surgical procedure. The continuum of care begins at the initial meeting of the surgeon and patient and continues long after surgery. The clinician should be cognizant of coexisting medical problems and their implications, commonly used anesthetic and surgical techniques, potential postoperative complications, and prophylactic measures that can minimize postoperative morbidity. This chapter provides an overview of these issues.

The purpose of preoperative evaluation is to identify problems affecting surgical risk and, in so doing, reduce perioperative morbidity and mortality. Preoperative evaluation often uncovers other health problems that need attention, regardless of whether they directly affect the proposed operation. A complete health history should be obtained, including the present illness, past illnesses, and associated diseases. One should inquire about bleeding tendencies, current medications, and allergies. Coexisting medical problems are common in spine surgery patients and can be associated with an increased incidence of postoperative complications and a lengthy hospital stay.

General Conditions Affecting Surgical Risk

Age

Patients at either extreme of the life span are at risk for complications or death from operation because of their narrower margin of safety. Small errors that are well tolerated by young, healthy adults are quickly compounded in children or geriatric patients, sometimes with catastrophic results.

Infants and young children have a relatively low tolerance for infection, trauma, blood loss, and nutritional and fluid disturbances.1 The management of these disorders in infants and children differs from their treatment in adults. Particular aspects of surgical care deserving special attention include fluid and electrolyte management, nutrition, and temperature maintenance.1,2

Advanced age is an independent risk factor for postoperative morbidity, and the prevalence of coexisting medical problems increases with age.3 As a result, elderly patients who undergo spine procedures have higher rates of postoperative complications, including excessive bleeding, postoperative confusion, and urinary tract infections.4 They tend to recuperate more slowly than do their younger counterparts. A recent study has shown that age is a positive risk factor for postoperative complications in multilevel thoracolumbar spine fusion surgery. Furthermore, it is correlative with higher rates of reoperation.5

It is safe to consider every patient older than 65 years of age to be at high risk for generalized atherosclerosis and for potential limitation of myocardial and renal reserve. Elderly patients often develop cardiac failure if they are fluid overloaded. Close monitoring of vital signs, intake, output, body weight, and serum electrolytes is mandatory. Elderly patients generally require smaller doses of narcotics, sedatives, and anesthetics than do younger patients. Barbiturates, sedatives, and steroids may cause confusion, and narcotics can produce respiratory depression.6

Osteoporosis and falls are common in the geriatric population and result in an increased incidence of spine fractures with advancing age. Elderly patients with spine fractures after a fall pose special problems. In addition to assessing the overall medical condition, the clinician should evaluate the cause of the fall because it may uncover an important coexisting medical condition and, in turn, help to prevent future injury. Nonoperative measures may be more appropriate in the elderly patient with a spine fracture if he or she is unable to tolerate the rigors of a prescribed treatment. Furthermore, bracing of the elderly patient is different from that of younger patients. For example, use of a halo vest in the geriatric population is fraught with morbidity.

Although most falls are results of accidents or environmental factors, they can also be caused by important cardiovascular or neurologic disorders, including arrhythmia, orthostatic hypotension, and cerebral ischemia. Special consideration should also be given to alcohol and drug use as possible causes. The incidence of falls in the elderly has been correlated with use of benzodiazepines, antidepressants, and diuretics.

Finally, advanced age is an important independent risk factor for postoperative deep venous thrombosis and pulmonary embolism, which are major causes of morbidity and mortality after surgical procedures.

Obesity

Obesity increases the technical difficulty of surgery and anesthesia. Obese surgical patients have a greater incidence of serious concomitant disease and higher rates of postoperative wound breakdown, thromboembolic complications, and pulmonary disease. Early patient mobilization, aggressive pulmonary toilet, and appropriate prophylaxis against deep venous thrombosis are all necessary adjuncts to good perioperative care. Occasionally, it may be advisable to delay elective surgery until the patient loses weight by appropriate dietary measures. There are increasing data to suggest that minimally invasive techniques, including tubular surgery, diminish the risks incurred by obesity.7

Coagulation Abnormalities

Spine procedures may result in substantial blood loss. Excessive bleeding at the surgical site increases the chances of wound infection and impaired wound healing. Although the prevalence of underlying coagulopathies is no higher in patients undergoing spine surgery, many regularly take nonsteroidal anti-inflammatory drugs (NSAIDs). Because NSAIDs are reversible inhibitors of platelet aggregation, their use can increase postoperative bleeding. NSAIDs should be discontinued at least 1 week before a major spine procedure. NSAIDs have also been shown to inhibit the healing of spine fusions. In patients undergoing spine fusion, NSAIDs should be avoided in the postoperative period as well.8,9

Malnutrition

Increasing evidence suggests that many surgical patients are moderately to severely malnourished.10 The increased metabolic demands of patients undergoing or recovering from spine surgery are often unmet because of insufficient caloric intake. With inadequate caloric intake, the hypercatabolic state induced by trauma or surgery results in significant visceral and skeletal protein depletion. Malnourished patients have increased rates of mortality and morbidity from sepsis, wound complications, impaired healing, and protracted rehabilitation. Although no single test demonstrates malnutrition conclusively, a variety of laboratory studies and physical measurements can help reveal nutritional inadequacies.11 These include preoperative weight loss of more than 10 pounds, a serum albumin level of less than 3.5 g/dL, and a total lymphocyte count less than 1500 to 2000 cells/μL.12

If malnutrition is identified, a vigorous regimen of nutritional supplementation should begin, preferably before surgery, and the patient should be monitored throughout the perioperative period.11 Total or peripheral parenteral nutrition should be considered in patients who either cannot tolerate or cannot meet their caloric needs with enteral nutrition alone.13–16

Smoking

The harmful effects of smoking tobacco on the rate of postoperative pulmonary, cardiac, and thromboembolic complications are well known. In a recent study of 875 patients undergoing orthopaedic reconstructive surgery, the incidence of cardiopulmonary complications in smokers was double that of nonsmokers. In that study, smoking was identified as the single most important risk factor for the development of complications after elective hip or knee arthroplasty. Similarly increased rates of pulmonary complications were identified in a multicenter review of 400 patients undergoing abdominal surgery.17–20

A review of wound infections after dorsal spine operations involving instrumentation implicated smoking as a significant risk factor for development of an infection.21

Wound complications in soft tissue procedures have also been reported to occur much more frequently in smokers. In a study of 425 patients undergoing reconstruction after breast cancer surgery, the risk of skin flap necrosis was nine times as high in heavy smokers as in nonsmokers. Similarly, in a review of patients undergoing face lift, the risk of skin slough was 12.5 times as high in smokers compared with nonsmokers.22,23 In spine surgery, current smoking increases the rate of postoperative wound infection and subsequently increases hospital stay and 30-day mortality rates.24

Stopping smoking before surgery has been shown to decrease the rate of postoperative complications, but only if a significant amount of time elapses between smoking cessation and surgery. A 2-week smoke-free period in a study of 60 patients before colorectal surgery did not decrease the rate of postoperative complications. In contrast, 4 weeks of smoking cessation significantly reduced the rate of wound infections in a randomized, controlled trial of minor dermatologic procedures. In another randomized trial of 120 patients scheduled to undergo hip or knee replacement, enrollment in a smoking cessation program at least 6 weeks before surgery resulted in a substantial decrease in complication rates. The rate of wound complications decreased from 31% to 5%, and of cardiovascular complications from 10% to 0%.25–27

In addition to the aforementioned general postoperative problems, tobacco smoking has been associated with unique complications after spine surgery. Smoking was identified as a significant risk factor in the development of postoperative airway obstruction after cervical corpectomy. In a review of 133 patients undergoing cervical corpectomy, 6 of 7 patients who developed airway obstruction were smokers. Two of these patients died as a result of this complication. Other risk factors were myelopathy and multilevel surgery. In patients with these risk factors, the authors recommend delayed extubation and careful assessment of the airway for swelling before extubation.28

Smoking has been shown to inhibit the healing of spine fusions in many clinical reviews. This effect has been well documented in patients undergoing spine fusion surgery and in animal models. In a randomly selected retrospective study of 50 smokers and 50 nonsmokers undergoing uninstrumented lumbar dorsolateral fusion, the pseudarthrosis rate was 40% for smokers and 8% for nonsmokers. A corresponding diminution in resting oxygen saturation was identified. The authors theorized that this relative hypoxia was responsible for the failure of the arthrodesis to heal.29

Animal studies, however, have shown that the inhibition of fusion can be attributed directly to the pharmacologic effects of systemically administered nicotine, without hypoxia.30 Inhibition of bone graft vascularization has been shown in animal models. Cytokine expression is decreased, suggesting that the inhibitory effects of nicotine involve more than just local vasoconstriction.31,32

Although the effect of hypoxia has not been studied independently, these observations suggest that the negative effects of smoking on arthrodesis cannot be avoided by switching from inhaled tobacco to oral or transdermal nicotine.

Smoking has been demonstrated to be a risk factor for nonunion after thoracic and cervical fusion surgery as well. In a review of 90 patients undergoing ventral instrumented spine fusion for adolescent scoliosis, 4 of 5 patients who developed a nonunion were smokers.33

A retrospective review of 131 patients who had multilevel cervical discectomies and fusions with autogenous interbody graft without instrumentation found a pseudarthrosis rate of 50% in smokers compared with 24% in nonsmokers.34

In animal models, bone morphogenetic protein was effective in reversing the inhibitory effects of nicotine on spine fusion.35

In some clinical series, the use of instrumentation and electrical stimulation has been reported to help overcome the inhibitory effects of smoking on spine fusion.36,37

Two studies have assessed whether the negative effects on fusion can be reversed by smoking cessation, with conflicting results. Glassman et al.9 reported that whereas smokers had a nonunion rate of 26.5% after lumbar fusion surgery, those who stopped smoking for more than 6 months after surgery had a successful arthrodesis rate of 82.9%. This was not significantly different than the union rate of 85.8% in nonsmokers. However, Deguchi et al.8 found no improvement in arthrodesis rate in their patients who stopped smoking.

Infection

Urinary tract infections are frequent in patients undergoing spine surgery. When associated with bacteremia, these infections are of particular concern because of the possibility of bacterial seeding of hardware. Thus, it is important to identify and treat established urinary tract infections before spinal instrumentation is applied.38

Compromised Host

The capacity of a compromised host to respond to infection or trauma is significantly impaired by disease or medication. Increased susceptibility to infection and delayed wound healing are the major postoperative problems in these patients and may arise from drugs such as corticosteroids, immunosuppressive agents, or cytotoxic agents and from prolonged antibiotic therapy. Infections in these patients can be caused by either common or opportunistic organisms. Malnutrition, renal failure, diabetes mellitus, and other immunocompromising diseases, including acquired immunodeficiency syndrome, significantly increase susceptibility to infection.

Multiple Trauma

Many spine surgery patients are the victims of severe accidents and have sustained multiple concomitant traumatic injuries. In such cases, urgent repair of spine injuries almost always takes precedence over assessment and treatment of chronic medical problems because acute spine stabilization dramatically reduces mortality, incidence of acute respiratory distress syndrome, length of hospital stay, and need for mechanical ventilation. Nonetheless, it is important to realize that the severity of neurologic injury, number of comorbidities, and use of high-dose steroids increase the risk of complication after thoracolumbar spine fracutrues.39

Patients with multiple trauma are often in their best state of health on admission. Efforts to delay spine stabilization may not be in their best interest.

After surgery, it is important to search for factors contributing to the accident, including alcohol and drug abuse, and unrecognized or untreated conditions such as liver disease, withdrawal syndromes, myocardial infarction (MI), arrhythmias, seizures, and hypoglycemia. All these conditions have postoperative implications and may require specific diagnostic and therapeutic interventions.

Rheumatologic Conditions

Patients with rheumatoid arthritis undergo a variety of spine procedures, particularly cervical fusion. These patients experience high complication rates for all surgical procedures. Wound breakdown, infection, loosening of instrumentation, and pseudarthrosis occur more frequently in patients with rheumatoid arthritis and can be attributed to poor tissue integrity, compromised vascular status, and the use of immunosuppressive drugs.40,41

Patients with rheumatoid arthritis should be examined for cervical spine involvement. Dynamic flexion and extension radiographs should be obtained to exclude occult instability before the administration of general endotracheal anesthesia. A variety of other problems, including anemia, pulmonary fibrosis, and pleural effusions, may be present. Chronic steroid use often results in adrenal suppression, requiring administration of perioperative stress-dose steroids. Similarly, patients with systemic lupus erythematosus and other rheumatologic conditions require thorough preoperative evaluation and may prove difficult to manage.42

Particular attention should be paid to patients with ankylosing spondylitis. These patients warrant very different management than the typical spine surgery patient with degenerative disease, especially with regard to positioning, traction, and orthoses.

Nonsurgical Diseases Affecting Surgical Risk

Cardiac Disease

Preoperative Evaluation

The most common symptoms of heart disease are dyspnea, fatigue, chest pain, and palpitation. It is important to inquire about exercise tolerance, paroxysmal nocturnal dyspnea, orthopnea, peripheral edema, irregular heartbeat, and chest pain. One should document significant past illnesses such as congenital heart disease, rheumatic fever, MI, atherosclerotic cerebrovascular and peripheral vascular disease, diabetes mellitus, hypertension, and autoimmune disease. Also, use of cardiac pacemakers, previous cardiac surgery, and past or present use of diuretics, digitalis, coronary vasodilators, antihypertensive drugs, and antiarrhythmic drugs should be noted. A history of angina pectoris, MI, Adams-Stokes attacks, stroke, cerebral ischemic attacks, intermittent claudication, or previous treatment for heart disease or hypertension should alert the surgeon to the possibility of a cardiac abnormality requiring further evaluation.

Conditions contraindicating elective surgery because of increased risk are acute MI, recent or crescendo angina pectoris, aortic stenosis, and atrioventricular block.

Physical Examination

The heart rate and rhythm must be recorded and any cyanosis, clubbing, petechiae, neck vein distention, and peripheral edema noted. The lungs should be auscultated for rales or wheezes. Auscultation permits evaluation of the first and second heart sounds, as well as of gallops and murmurs.

Radiologic Examination

Most preoperative patients require an anteroposterior chest radiograph to exclude cardiac enlargement, pulmonary vessel distention, and pulmonary infiltrates. Lateral views permit diagnosis of individual chamber enlargement.

Electrocardiography

An electrocardiogram (ECG) can help detect arrhythmias, conduction defects, chamber enlargement, and myocardial ischemia. Routine preoperative ECGs are obtained on all adult patients undergoing spine surgery. The ECG is useful diagnostically and also as a baseline measurement to evaluate subsequent changes in the myocardium and conduction system. In general, a stable abnormality on the ECG, in the absence of cardiac failure or angina pectoris, is indicative of only slightly increased perioperative risk.

Laboratory Tests

Serum concentrations of hemoglobin, sodium, potassium, and calcium may be relevant in the assessment of cardiac function. Arterial blood gas and pH studies indicate the adequacy of oxygenation.

Hemodynamic Studies

Pulse rate and cuff blood pressure are useful indicators of cardiac function. Monitoring arterial pressure with an intra-arterial line provides a more accurate value and permits waveform analysis. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) indicate cardiac preload. PCWP reflects left ventricular filling pressure and left ventricular performance, whereas CVP reflects right ventricular function.

Elevations of CVP above 10 mm Hg suggest right ventricular failure. In most patients, left heart function correlates with right heart function. CVP exceeding PCWP by greater than 5 mm Hg indicates pulmonary artery hypertension; PCWP exceeding CVP by more than 5 mm Hg indicates isolated left ventricular failure. However, presence of a normal CVP does not exclude left ventricular failure. A PCWP below 10 mm Hg may be associated with shock and a PCWP above 25 mm Hg, with pulmonary edema.

For patients with cardiac or pulmonary disease, monitoring of PCWP with a Swan-Ganz catheter provides the best indication of left ventricular preload. Cardiac output can be measured by thermodilution using a Swan-Ganz catheter. Serial measurements can guide fluid therapy, even in the presence of left ventricular failure.

Echocardiography is a noninvasive method of studying cardiac anatomy and function. Cardiac catheterization with coronary angiography remains the most definitive cardiac diagnostic study, showing the vascular supply to different areas of the myocardium. This type of study is not without inherent risks.

Preoperative Preparation

The cardiac status of a spine surgery patient with cardiac dysfunction should be optimized before surgery. Special attention should be paid to correction of electrolyte imbalance, fluid excess, and anemia. It is important to avoid hypotension, hypoxia, fluid overload, and undue pain or excitement.

Cardiac Contraindications

Relative cardiac contraindications to operation are recent MI, uncontrolled congestive heart failure (CHF), unstable angina pectoris, intractable cardiac arrhythmias and conduction defects, and uncontrolled hypertension. Preoperative evaluation is directed toward detecting and treating these conditions.

The mortality rate after a major operation is 25% if the surgery is within 3 weeks of MI, 10% if within 3 months, and 5% if within 6 months. A patient with a healed MI has an added mortality risk of about 3%. Only emergent and urgent operations are indicated within 3 months; only semiurgent procedures are indicated from 3 to 6 months. Elective operations should be postponed until 6 to 12 months after MI.

Treatable causes of CHF include myocardial ischemia and its sequelae, valvular disease, bacterial endocarditis, sepsis, arrhythmias, hyperthyroidism, and hypertension. Careful perioperative management of these conditions will certainly decrease morbidity. Anginal chest pain may reflect severe coronary artery disease. Symptoms and signs denoting severe angina include associated sweating and nausea, poor response to coronary vasodilators (nitroglycerin), no relief with rest, frequent attacks, prolonged pain, and ECG evidence of ischemia.

High-risk coronary artery lesions include left main coronary artery occlusion, high left anterior descending artery lesions, and lesions in multiple vessels. Elective procedures should be postponed in patients with such lesions. Nonelective procedures may necessitate preliminary or coincident coronary artery bypass surgery. Patients who need urgent or emergent procedures require intensive perioperative management.

In hypertensive patients the blood pressure should be normalized before surgery. There is a linear correlation between preoperative blood pressure and postoperative myocardial ischemia.34

Postoperative Management

Patients with significant cardiac disease require close postoperative monitoring. Monitoring typically includes treatment in an intensive care setting for the first 24 hours after surgery.

Most postoperative MIs occur on the second or third postoperative day, and hence serial ECGs for 3 days are indicated in patients with known coronary artery disease. Chest pain is often difficult to evaluate in the postoperative period, and an MI may become apparent only because of hypotension or arrhythmia. Serial cardiac isoenzyme studies are especially useful for identifying postoperative infarcts, and should be obtained as well. Postoperative treatment for MI entails vigorous support and monitoring. Arrhythmias and cardiac failure should be treated as they arise.

Typically, cardiac failure shows symptoms of hypotension or oliguria and is most often a result of hypovolemia in the postoperative patient. If hypotension or oliguria persists after IV fluids are administered, the patient must undergo complete evaluation. When cardiac failure results from hypertensive crisis, blood pressure can be reduced with nitroprusside.

Cardiac failure unresponsive to other measures may respond to afterload reduction. Judicious use of drugs with a positive inotropic effect (e.g., dopamine, dobutamine, isoproterenol, and digitalis) may also prove to be beneficial. Heart performance is most efficient at a rate of 100 to 120 beats/min.

Pericardial restriction resulting from constrictive pericarditis or pericardial effusion is suggested by a decreased cardiac output with a high CVP. Typically, jugular veins are distended, and a paradoxical pulse may be present. Echocardiography may assist in making the diagnosis. Treatment consists of pericardiocentesis or pericardiotomy.

In the presence of bradycardia, one should look for anesthetic excess, hypoxia, atrioventricular block, or vagal stimulation by visceral traction, carotid sinus compression, or traction on extraocular muscles.

In the presence of falling blood pressure, one should look for anesthetic excess, myocardial ischemia, or inadequate preload caused by blood or fluid losses, obstruction of venous return, or vasodilation. Absence of blood pressure, carotid pulse, or respiration is an ominous sign. Treatment should include identification of the underlying cause and immediate correction of the abnormality (e.g., for ventricular fibrillation, electrical defibrillation should be used; for asystole, cardiac massage, vagolytic or sympathomimetic drugs, or cardiac pacing should be used). Cardiopulmonary resuscitation should be initiated immediately and continued until the underlying problem has been corrected. Four minutes without blood flow to the brain results in a fatal ischemic injury. Preexisting inadequacy of cerebral blood flow and oxygenation shortens the time available for correction. Closed chest cardiopulmonary resuscitation is the initial method of resuscitation. Open chest cardiac massage should be undertaken only as a last resort.

Treatment of the major arrhythmias is a complex problem requiring close collaboration of the internist and surgeon. If the surgeon is required to provide emergency treatment until the internist arrives, a general knowledge of cardiac arrhythmias and their treatment is important. Diagnosis of the arrhythmia is made from the ECG.

Atrial fibrillation decreases cardiac efficiency and may cause congestive failure. Treatment involves slowing the rate by adequate digitalization. Calcium channel blockers can be used in patients with no history of heart failure or cardiomyopathy. Conversion to normal sinus rhythm by quinidine or direct current (DC) countershock may be required if shock or pulmonary edema is noted.

Atrial flutter often causes congestive failure. Digitalization will slow the rate, either by increasing the degree of block or converting the flutter to sinus rhythm or atrial fibrillation. DC countershock is the treatment of choice, especially if the rhythm is poorly tolerated.

Paroxysmal supraventricular tachycardia often occurs in patients with otherwise normal hearts. In the absence of heart disease, serious effects are rare. Digitalis toxicity must be excluded as a cause. Vagal stimulation (carotid sinus massage, Valsalva maneuver) should be tried initially. If mechanical measures fail, pharmacotherapy is indicated. There is, however, no unanimity on the most effective medical therapy. Digitalis, vasopressors, procainamide, and propranolol can all be tried. Continuous ECG and blood pressure monitoring are essential. DC cardioversion may be indicated if the patient’s condition deteriorates.

Ventricular tachycardia and ventricular fibrillation are usually associated with myocardial damage, especially MI. Lidocaine is the drug of choice for emergency treatment because of its short duration of action. If the arrhythmia recurs, an IV infusion may be given or the IV injection repeated. If lidocaine has no effect, DC cardioversion is preferable to additional pharmacotherapy.

Ventricular fibrillation produces cardiac arrest and requires defibrillation and cardiopulmonary resuscitation. DC cardioversion is often effective in converting patients back to sinus rhythm. If the initial attempt at cardioversion is unsuccessful, repetition with sequentially higher energy levels is indicated.

Pulmonary Disease

Preoperative Evaluation

The most common symptoms of pulmonary disease are dyspnea at rest or after minor exertion, cough, sputum production, wheezing, chest pain, and hemoptysis. It is important to document any history of tuberculosis, recent upper respiratory infection, chronic pulmonary disease, or asthma. One must determine the degree of tobacco and alcohol use as well as previous occupational exposures to coal dust, asbestos, and silica dusts. Establishment of a medication history, particularly regarding the use of corticosteroids, is especially important.

Physical Examination

The examiner must look for physical signs of pulmonary disease such as cyanosis or nail clubbing. It is important to observe the respiratory rate and respiratory effort as well as to percuss the chest for dullness or hyperresonance and to determine inspiratory diaphragm excursion. Auscultation of the chest allows the examiner to hear rales, rhonchi, wheezes, and decreased breath sounds.

Radiologic Examination

The chest radiograph may demonstrate pulmonary infiltrates, granulomas, atelectasis, hyperlucency, pneumothorax, abnormalities of pulmonary vasculature, or a mass. A negative radiograph does not exclude pulmonary disease. If any question exists, a CT scan of the chest may be obtained.

Laboratory Examination

Yellow, green, or brown sputum suggests active infection. Sputum culture is indicated to identify specific organisms and to determine antibiotic sensitivities. Arterial blood gas measurements help evaluate pulmonary gas exchange. The arterial partial pressure of oxygen (Pao2) is an indicator of oxygen uptake by the blood in its passage through the lungs. Pao2 is affected by the fraction of inspired oxygen, right-to-left shunting, and diffusion capacity across the alveolocapillary membrane. Normally, Pao2 is 70 mm Hg or greater. A Pao2 of 60 mm Hg indicates mild respiratory failure; a Pao2 of 50 mm Hg or less indicates severe pulmonary disease. The oxygen saturation (Sao2) reflects the percentage of hemoglobin actually bound by oxygen. Normally, Sao2 is 93% or more; an Sao2 of 90% indicates mild respiratory failure; an Sao2 of 84% or less indicates severe pulmonary disease. The arterial partial pressure of carbon dioxide (Paco2) reflects the adequacy of ventilation. Normally, Paco2 is 38 to 43 mm Hg. A Paco2 of 44 to 54 mm Hg indicates mild impairment of ventilation; a Paco2 of 55 mm Hg or greater indicates severely impaired ventilation. Arterial blood pH is affected by both metabolic and respiratory factors. Normally, the arterial blood pH is 7.38 to 7.42.

Spirometry

The vital capacity (VC) is the maximum volume expired after a maximum inspiration. VC is decreased in restrictive disease but is usually normal in obstructive disease. A VC that is 50% or less of predicted indicates severe disease. The forced expiratory volume is the maximum volume expired after a maximum inspiration. Forced expiratory volume equals VC in restrictive disease but is less than VC in obstructive disease.

Preoperative Preparation

Patients without pulmonary symptoms can be expected to tolerate surgery from a respiratory standpoint. If a patient can climb two flights of stairs without shortness of breath, further evaluation of respiratory status is generally unnecessary. Factors that can predispose a patient to postoperative pulmonary complications are long-term cigarette smoking, chronic obstructive pulmonary disease, upper abdominal and thoracic procedures, acute respiratory infections, and restrictive disorders such as obesity, pulmonary fibrosis, and neuromuscular and skeletal disease. Patients with one or more of these factors require careful preoperative preparation, and most should undergo complete pulmonary evaluation. Elective procedures should be postponed until maximum pulmonary function has been achieved. All patients should stop smoking at least 2 weeks before any elective operation. Overweight patients should try to achieve ideal body weight. All patients should receive preoperative instruction in coughing, deep breathing, and use of the incentive spirometer.

Respiratory infections should be treated before elective operations. Viral infections resolve with symptomatic treatment; bacterial infections can be treated with the appropriate antibiotics. Whenever possible, preoperative preparation and treatment should be performed on an outpatient basis to avoid superinfection with hospital-acquired antibiotic-resistant organisms. Adequate hydration, humidified air, and expectorants can help liquefy sputum. Postural drainage and chest percussion can help clear these secretions. Bronchodilators are often helpful for patients with chronic obstructive pulmonary disease. In addition, patients with bronchospasm or asthma may benefit from the administration of bronchodilators either by aerosol or by intermittent positive-pressure ventilation. Corticosteroids may be necessary for patients with severe asthma or pulmonary fibrosis.

If aspiration is observed, endotracheal intubation, airway suctioning, and saline lavage should be performed immediately. Bronchorrhea will neutralize the acidic gastric juices within 10 minutes so lavage after this interval is of no benefit. Moreover, steroid treatment has no objective benefit. Antibiotics should be reserved to treat specific organisms and should not be used prophylactically.

No patient should be denied operation for emergent and urgent conditions because of pulmonary disease. Whenever possible, the risks should be recognized and pulmonary function optimized.

Postoperative Management

The postoperative effects of major procedures under general anesthesia include decreases in total lung capacity, vital capacity, functional residual volume, and compliance. Aggressive postoperative care minimizes these effects. Administering low doses of analgesics at frequent intervals promotes improved respiration by controlling pain without compromising respiratory drive. Frequent change of position and early ambulation are also beneficial. Changing the volume of ventilation prevents atelectasis. Incentive spirometry promotes deep inspiration that can also help prevent atelectasis.

Oxygen administration should be used when necessary but with judiciousness; 100% oxygen promotes atelectasis and may result in oxygen toxicity. Administering oxygen to patients with chronic hypercapnia may depress respiratory drive. The elderly and patients with acutely impaired respiratory function may require ventilatory support over the first postoperative night. Arterial blood gases and fluid therapy should be closely monitored; administration of both insufficient and excessive fluid impairs respiratory function. Patients with bronchospasm may benefit from bronchodilator therapy.

Pulmonary Complications

Ventilatory impairment is typical after ventral thoracic and lumbar approaches to the spine. In most instances, the impairment does not prevent spontaneous breathing. However, if the operative procedures are extensive, if there has been massive trauma, if the patient is elderly, or if the patient has preexisting chronic disease or malnutrition, ventilatory impairment may be so great that a period of assisted ventilation is necessary.

The first postoperative hours are critical because this is when acute ventilatory failure most commonly occurs. The effects of muscle relaxants may not have worn off completely, and muscle weakness can cause reduced vital capacity. If a respiratory complication develops, decreased lung compliance may also contribute to inadequate ventilatory function.

Pneumothorax is an uncommon complication in elective surgical procedures, but it should be considered in any patient who develops acute respiratory distress or intraoperative deterioration. The principal cause of pneumothorax in hospitalized patients is iatrogenic lung puncture during percutaneous central venous catheter placement. It can also occur in a patient who coughs and thereby ruptures a pulmonary bleb or bulla. Diagnosis is made on the basis of decreased or absent breath sounds on the affected side, with hyperresonance to percussion. When a tension pneumothorax develops there may also be a lateral shift of the trachea away from the affected side. Any patient who develops respiratory distress after insertion of a central venous catheter should be presumed to have a pneumothorax, and a chest tube should be inserted immediately and not delayed for the radiograph. If pneumothorax is suspected but the patient is comfortable, one should first obtain the chest radiograph and insert a chest tube if indicated.

Atelectasis is the most common complication in the first 2 to 3 postoperative days. It results from collapse of the most dependent portions of the lung. Clinical signs include fever, tachypnea, and tachycardia that typically develop within the first 2 postoperative days. Chest radiographs usually show linear densities in dependent segments of the lungs or frank areas of collapse. There is often radiographic evidence of volume loss in the affected lung. Treatment entails deep breathing and coughing to expand underventilated lung segments. The patient should be mobilized if there are no contraindications. Mechanical devices, including the incentive spirometer and devices to maintain positive airway pressure, help achieve adequate ventilation.

If the preceding methods fail to reverse atelectasis, bronchoscopy may be indicated for suctioning secretions out of the atelectatic segment. This is rarely necessary and should be used only when the atelectasis is severe and involves an entire lobe, if the patient is developing respiratory distress, or if blood gas levels are deteriorating.

Acute pulmonary edema is common in elderly patients with compromised cardiac function or in patients with significant cardiac disease. Typically, it develops on the second or third postoperative day as third-space fluid is mobilized. Alternatively, it can occur with excessive administration of fluid during surgery or immediately after surgery if cardiac or renal function is compromised. Healthy patients with normal cardiac and renal function usually tolerate fluid overload with prompt diuresis and no pulmonary symptoms.

The diagnosis of acute pulmonary edema is made by the presence of tachypnea, tachycardia, shortness of breath, and orthopnea. These symptoms are often coupled with elevated CVP, distended neck veins, and wet rales bilaterally in the basilar lung segments. These rales may extend two thirds of the way up the lungs. In addition, the sputum is often frothy and pink. Chest radiographs show symmetrical perihilar fluffy infiltrates, cardiac enlargement, prominent pulmonary vascular shadows, and lymphatic congestion in the costophrenic angles (Kerley B lines).

Pneumonia in the postoperative patient usually results from inadequately treated atelectasis, airway contamination, or preexistent pulmonary disease, most commonly a consequence of cigarette smoking. Pneumonia rarely develops earlier than 4 to 5 days after operation unless an unusual event, such as aspiration, occurs. The source is almost always bacterial, and if the patient has been given prophylactic or therapeutic antibiotics from the time of surgery, one may assume that the organism causing the pneumonia is resistant to the antibiotics.

The diagnosis is made by the presence of fever, leukocytosis, increased sputum production, decreased breath sounds or rales on physical examination, and a localized or diffuse infiltrate on radiographs. Gram staining of the sputum usually reveals heavy colonization by a single organism, and a large number of polymorphonuclear leukocytes are present. If pneumonia is diagnosed, antibiotic therapy should be started immediately, on the basis of the Gram stain. Confirmatory cultures must be obtained, and the antibiotic sensitivities checked. Antibiotic therapy can then be guided by these sensitivities. Therapy should include supportive care as well as measures directed at the underlying cause of the pneumonia. Blood gases should be monitored and endotracheal intubation and ventilation carried out if the patient’s status deteriorates.

Acute Respiratory Distress Syndrome

In rare instances after extensive surgery or massive trauma, patients develop tachypnea, hypoxemia, diffuse pulmonary infiltrates, and decreased compliance of the lungs. Physical examination does not reveal rales, bronchospasm, or evidence of alveolar edema. In these situations, the diagnosis of acute respiratory distress syndrome (ARDS) is made. In many cases, ARDS appears to be related to pulmonary microembolism, and the findings are similar to those described for fat embolism. Evidence of intravascular coagulation is common with this syndrome, but the role of intravascular coagulation as a specific cause has not been proved. ARDS normally does not develop until 3 days after surgery, and it is often associated with sepsis.

When the disease is mild, supportive care with oxygen administration may be sufficient. In most cases, the symptoms are severe and hypoxemia mandates intubation and mechanical ventilation. In severe cases, positive end-expiratory pressure must be used to improve oxygenation.

A pulmonary artery catheter to monitor PCWP is mandatory for careful titration of fluid therapy. Because of the high mortality associated with the development of renal failure in patients with ARDS, attempts must be made to preserve renal function by adequate hydration. At the same time, one must avoid overhydration, which can increase pulmonary interstitial edema. PCWP should be kept as low as possible, while adequate peripheral perfusion and a urine output of 0.5 mL/kg/hr are maintained. PCWP should not exceed 15 mm Hg. Steroids and diuretics have not been shown to be of benefit.

Fat embolism syndrome may occur after extensive trauma. Although the true etiology of this syndrome is poorly defined, it was initially postulated to result from embolization of marrow fat to the pulmonary capillaries, producing symptoms by mechanical obstruction and inflammation. Arguing against this mechanism are the pathologic findings of fat in pulmonary, renal, and cerebral capillaries in traumatized patients without fractures or evidence of bony injury. The symptoms are nearly indistinguishable from those of ARDS: tachypnea, hypoxemia, pulmonary infiltrates, and decreased lung compliance. The only clinical difference is a higher incidence of cerebral symptoms, including disorientation, confusion, and progressive obtundation without localizing signs.

Pulmonary Embolism

Dyspnea, pleuritic chest pain, and hemoptysis are the classic symptoms of pulmonary embolism. Physical examination may reveal decreased breath sounds, pleural rub, or pleural effusion. Moreover, chest radiographs may demonstrate a wedge-shaped density and the ECG may show evidence of right ventricular strain. Ventilation-perfusion scan of the lungs often reveals areas of decreased perfusion. Pulmonary angiography, the gold standard for diagnosis, occasionally shows obstruction of large pulmonary arteries.

Pulmonary embolism accompanied by circulatory and respiratory instability mandates treatment with high-dose IV heparin. Placement of a Greenfield filter or ligation of the inferior vena cava may be required if anticoagulants are contraindicated, if bleeding complications develop in a patient receiving anticoagulants, or if pulmonary embolism recurs in a fully anticoagulated patient.

Renal Disease

Preoperative Evaluation

Urinary frequency and volume, dysuria, nocturia, poor stream, incontinence, and hematuria must be checked. It is important to note any history of renal disease, calculi, diabetes mellitus, or hypertension and to establish whether there has been any use of diuretics or nephrotoxins.

A history of the use of acetaminophen, a potential nephrotoxin, is particularly revealing in patients who undergo spine surgery. Often, patients with low back pain consume substantial quantities of acetaminophen without recognizing its potential harm. Symptoms and signs of renal disease frequently reflect the degree of renal failure; however, it is not uncommon for patients with marked impairment of renal function to be asymptomatic.

Urinary tract obstruction should be suspected in any anuric patient. Upper tract obstruction must be bilateral for azotemia to occur. A renal hippurate scan, infusion IV pyelography, renal ultrasonography, and retrograde ureteral catheterization are important diagnostic tests. Renal scans are very useful for detecting acute obstruction. Sonography, infusion IV pyelography, and retrograde catheterization are indicated in patients with chronic obstruction. Obstruction of the lower tract is recognized by the inability to insert a Foley catheter.

Physical Examination

The patient must be carefully checked for edema or dehydration. Metabolic acidosis may result in hyperventilation, and pericardial effusions can sometimes produce a friction rub.

Laboratory Examination

Blood urea nitrogen (BUN), serum creatinine measurements, and routine urinalysis are adequate screening tests for renal disease. A freshly voided urine sample yields much information about renal status.

Hematuria may be secondary to glomerular disease or to a lesion in the collecting system. In addition, the finding of different types of casts in the urine may be a sign of advancing renal disease. Red cell casts are suggestive of acute glomerular dysfunction, whereas white cell casts are indicative of acute pyelonephritis. It must be kept in mind that in patients with reduced muscle mass, serum creatinine levels can remain within the normal range even though creatinine clearance is no more than 20% of normal values. BUN-to-creatinine ratios greater than 10:1 may reflect prerenal azotemia, gastrointestinal bleeding, or enhanced catabolic states or may be secondary to catabolic drug effects.

Random urine samples usually have a specific gravity of 1.012 to 1.015. A higher specific gravity reflects dehydration or the presence of solutes, such as radiograph contrast medium, glucose, or mannitol. Dilute urine (specific gravity <1.007) reflects overhydration, diuretic therapy, water intoxication, or diabetes insipidus. A fixed specific gravity of 1.010 to 1.014 (isosthenuria) signifies a lack of renal tubular concentrating ability and occurs in renal parenchymal disease, congenital tubular defects, and acute tubular necrosis (ATN).

The normal pH range of the urine is 4.3 to 5.0. This range can be affected by diet and other factors. Aciduria may result from metabolic or respiratory acidosis, potassium depletion, starvation, or fever. Alkaline urine results from metabolic or respiratory alkalosis, certain urinary infections, and carbonic anhydrase-B–inhibiting diuretics.

Transient proteinuria may result from fever, cold exposure, strenuous exercise, and acute stress. Persistent proteinuria may signify true renal disease. Proteinuria is the earliest sign of aminoglycoside toxicity. Glucosuria usually signifies diabetes mellitus but may result from benign renal glucosuria, renal tubular disorders, pregnancy, or glucose infusion. The presence of reducing agents in the urine may also yield significant information about the patient’s status. Ketonuria occurs with diabetic ketoacidosis, excessive vomiting, starvation, or cachexia and after strenuous exercise and cold exposure. One must keep in mind that ascorbic acid, cephalosporins, salicylates, paraldehyde, and chloral hydrate can alter reactions that measure urinary reducing agents. The dipstick test for occult blood is a useful screening test. It is positive with more than 10 red blood cells per high-power field in a spun urine sediment. However, myoglobinuria and hemoglobinuria can also give a positive reaction.

BUN concentration varies with dietary nitrogen consumption, hepatic urea production, and endogenous protein catabolism. It is increased by dehydration, gastrointestinal hemorrhage, hemolysis, corticosteroid therapy, and the tissue breakdown associated with trauma, shock, or sepsis.

Finally, the serum creatinine concentration is an important value because it reflects glomerular filtration. Creatinine production is correlated to muscle mass and, in a given individual, remains nearly constant in the absence of muscle destruction. Creatinine clearance (CLcr) is a more exact indicator of glomerular filtration and is defined by the equation

image

where U[cr] = urine creatinine concentration in mg/dL, P[cr] = serum creatinine concentration in mg/dL, and V = urine volume in mL/min. Normal creatinine clearance is 125 ± 25 mL/min/1.73 m2. A minimum clearance of 10 mL/min/1.73 m2 is needed to maintain life without dialysis. Serum creatinine level may remain normal until the clearance is reduced by more than half.

Preoperative Preparation

In the preoperative period, it is important to assess renal function carefully and correct any electrolyte abnormalities. Anephric patients, if managed carefully, tolerate operations well. Preoperative preparation should maximize renal function and is important for preventing postoperative failure. Urinary tract infection should be treated preoperatively with appropriate antibiotics as determined by urine culture and sensitivity tests.

Obstructive lesions of the urinary tract should be removed or corrected, if possible, before other major operations are planned. Dehydration, hypovolemia, and electrolyte imbalance should be corrected, and adequate urine volume should be ensured before surgery. Metabolic acidosis, even though compensated, should be corrected with sodium bicarbonate.

Anemia is a frequent finding in patients with renal disease and should be evaluated preoperatively. A hemoglobin level of 9 g/dL and a hematocrit of 25% are satisfactory for patients with chronic renal insufficiency. Patients on hemodialysis adapt to hematocrits in the range of 20% and do not need transfusions unless there is significant blood loss. Blood transfusion should be used cautiously to avoid cardiac decompensation.

Coagulation defects in patients with chronic renal disease should be identified and corrected. Patients with severe renal failure often have platelet dysfunction that can cause bleeding. Elective procedures should be delayed until platelet dysfunction is corrected with hemodialysis on the day before surgery. Follow-up hemodialysis, with its attendant anticoagulation and fluid shifts, can be delayed until the second or third postoperative day.

It is important to maintain all antihypertensive medications, including beta-blockers and catecholamine-depleting drugs, until the night before surgery. Discontinuation of clonidine may result in paroxysmal hypertension, and abrupt withdrawal of certain beta-blockers can produce cardiac dysrhythmia. Patients who take diuretics may require correction of volume contraction and hypokalemia. When possible, one should avoid nephrotoxic drugs and be on the alert for medications that accumulate because of decreased renal excretion. Use of nephrotoxic IV contrast media should be limited.

Postoperative Management

The diseased kidney is unable to concentrate urine and must excrete a urine volume greater than normal to rid the body of metabolic end products. At the same time, the kidney may be unable to excrete water and electrolytes. There is a slim margin between further renal insufficiency from dehydration and CHF secondary to excess salt and water retention. Effective management requires monitoring of body weight, intake and output, serum electrolytes, pH, CVP, and PCWP. Keeping track of urine electrolyte concentrations and of all measurable fluid losses helps guide appropriate fluid therapy. By themselves, however, urine output and specific gravity do not reliably reflect the state of hydration.

Nephrotoxic drugs must be administered carefully and in reduced doses to patients with impaired renal function. These agents include aminoglycoside antibiotics, cephaloridine, colistin, polymyxin B, and amphotericin B. Spot checks for urine protein are useful for detecting early aminoglycoside toxicity. Drugs requiring major dose modification in the renally impaired patient include allopurinol, digoxin, methotrexate, phenobarbital, procainamide, quinidine, and tolbutamide.

Postoperative urine output less than 25 mL/hr requires immediate evaluation. Oliguria suggests prerenal or renal parenchymal failure. Anuria suggests vascular obstruction, cortical necrosis, or urinary tract obstruction.

Acute Renal Failure

The hallmark of acute renal failure is rapidly progressive azotemia, generally accompanied by oliguria (urine output <400 mL/24 hr). Prerenal azotemia results from renal hypoperfusion caused by volume depletion (dehydration or blood loss) or decreased cardiac output from pump failure (CHF). An expeditious diagnosis of prerenal azotemia is essential because the condition is easily reversible and persistent renal hypoperfusion results in ATN.

The physician must assess the patient’s volume status frequently (i.e., fullness of neck veins, skin turgor, orthostatic changes in blood pressure and heart rate, and peripheral perfusion). Examination of the heart and lungs may reveal signs of CHF.

Bladder catheterization can be helpful for obtaining urine specimens and monitoring urine output carefully. Measurements of serum BUN, creatinine, electrolytes, and osmolality, as well as of urine electrolytes and osmolality, can also be of diagnostic value.

Following the aforementioned suggestions should help distinguish whether prerenal azotemia is secondary to hypovolemia or CHF. In patients with tenuous cardiac function, measurement of CVP or even PCWP may be necessary before therapy is instituted.

Hypovolemic patients should be given normal saline solution at a rate of 100 to 500 mL/hr depending on the severity of volume depletion. Diuretics should not be administered before hypovolemia is corrected.

If there is no improvement in urine output after blood volume has been replenished, a bolus of furosemide or mannitol may be administered. Mannitol should be infused carefully because if oliguria persists, failure to excrete mannitol will produce volume expansion and pulmonary edema. If there is no response to these diuretics, ATN or obstructive uropathy is probably present.

The clinical setting and the laboratory tests, especially the results of urinalysis, are generally sufficient to establish the diagnosis of ATN. ATN may be a consequence of ischemia, nephrotoxins, or unknown mechanisms. The course of ATN is divided into three phases: pre-ATN, oliguric, and diuretic phases. As the kidneys recover, the urine output gradually increases. Occasionally, this postoliguric diuresis is massive. The severity of renal damage varies. In mild cases, there may be high urinary output rather than oliguria (nonoliguric ATN). Anuria (urine output <50 mL/24 hr) is rare in ATN. Bilateral cortical necrosis, acute glomerulonephritis, urinary obstruction, and thrombosis of the major renal vessels are more likely to produce anuria.

The abnormalities described in chronic renal failure also occur in acute renal failure, frequently with greater severity because of the acuteness of renal dysfunction. Fluid and electrolyte abnormalities are invariably present, and profound acidosis and severe hyperkalemia are common. In ATN, infection and gastrointestinal bleeding are the major associated complications. Infection is the principal cause of death.

Treatment of ATN is supportive and is directed at preventing or treating complications until renal function returns to normal. There is no evidence that the course of established ATN is modified by the administration of furosemide or mannitol. Diuretics should not be given.

Measurable fluid losses and insensible losses should be replaced. Fluid intake, fluid output, and body weight should be meticulously assessed. In addition, sodium losses from urine or other measurable sources should be replaced. Hyponatremia developing in the course of ATN is usually indicative of fluid excess rather than of sodium deficit and is best treated by fluid restriction. In addition, hyperkalemia frequently occurs in these patients. A variety of factors contribute to hyperkalemia, including acidosis and potassium release from tissues secondary to excessive catabolism, trauma, or hemolysis. The serum potassium concentration and the ECG must be monitored.

Severe hyperkalemia (serum potassium level >7 mEq/L) requires more urgent therapy, including administration of sodium bicarbonate or hypertonic glucose solution and an insulin drip. Life-threatening cardiac arrhythmias due to hyperkalemia should be treated by IV calcium gluconate, or calcium chloride dialysis may be required to remove excess potassium. It is advisable to restrict magnesium and check for hypocalcemia. Acidosis in ATN may be treated cautiously with sodium bicarbonate, but this may result in hypernatremia and heart failure. Acidosis associated with volume overload is best treated by dialysis.

Adequate nutrition is fundamental in the treatment of ATN. Dosages of drugs, including antibiotics, digoxin, and magnesium-containing antacids, must be modified. If a nephrotoxin may have caused the ATN, it should be discontinued.

As suggested previously, the indications for dialysis include uncontrollable hyperkalemia or acidosis, overhydration, and the development of uremic symptoms. Peritoneal dialysis and hemodialysis are equally effective. Early and aggressive dialysis seems to result in improved survival in patients with ATN.

ATN has an overall mortality rate of 50%. Mortality is approximately 80% in patients with burns, trauma, or surgical procedures and only 30% with medical ATN. This is presumably because there are more complications of the underlying condition in the surgical group.

Urinary Retention

Inability to urinate after surgery is a frequent problem and may be seen after any operation. Causes include reflex spasm of the voluntary sphincter because of pain or anxiety, medications (usually anticholinergics and narcotics), preexisting partial bladder outlet obstruction (e.g., enlarged prostate), and intraoperative overdistention.

Preoperative voiding patterns should be evaluated if a bladder outlet obstruction is suspected. Obstruction can be corrected before operation, or catheter drainage may be instituted immediately after surgery. Excessive use of narcotics and parasympatholytic drugs should be avoided. Patients scheduled for lengthy operations should be catheterized preoperatively and the bladder drained throughout the procedure.

If a patient is unable to pass urine for several hours after surgery, and there is no urge to urinate, one must explore the possibility of oliguria as a consequence of diminished volume status. Occasionally, a heavily sedated patient does not recognize the sensation of fullness and does not urinate for that reason.

A palpable bladder in the midline above the symphysis pubis is highly suggestive of acute urinary retention. Any patient who does not urinate for 6 hours after operation should be evaluated carefully. In this way, overdistention of the bladder, which may induce bladder atony and even myogenic damage to the bladder wall, can be avoided.

Urinary retention can be relieved in a variety of ways. Narcotics or sedatives may help relieve local pain. Moreover, if the condition permits, the patient can be positioned in the standing or sitting position instead of the supine position for urination. Cholinergic drugs such as bethanechol chloride may be administered.

When all other measures fail, if the bladder is markedly distended and severe bladder contractions occur without voiding, single-pass, straight catheterization should be performed so that patients can void on their own. A preoperative history of any voiding difficulty is very important to help decide on the duration of catheter drainage. If there was minimal preoperative obstruction, the patient should be able to resume normal voiding spontaneously. Under no circumstances should the bladder be allowed to overdistend. If the patient cannot void spontaneously after two catheterizations and there is evidence of overstretching or mild mechanical obstruction, a Foley catheter should be left in place for 2 to 3 days before testing for spontaneous voiding again. It is of note that men after middle age often have mechanical obstruction secondary to prostatic enlargement. Women are more susceptible to detrusor atony after overstretching, especially if the period of overstretching is prolonged.

Gastrointestinal Complications

Gastric Distention and Dilation

The stomach frequently becomes distended with gas during anesthesia induction, and further quantities of air are swallowed in the postoperative period. Gastric juices and duodenal secretions that reflux into the stomach contribute to this distention. Marked gastric distention can result in nausea and vomiting. Moreover, the distended stomach may impair diaphragmatic excursion and cause tachypnea. Nasogastric intubation for 12 to 24 hours is usually sufficient treatment; however, intubation for longer periods is occasionally necessary.

Vomiting immediately after an operation may be the result of a direct anesthetic effect or the result of gastric distention. Regardless of the cause, the best management is nasogastric intubation and suction to maintain an empty stomach for 12 to 24 hours. Medications that suppress nausea are less effective and can have untoward side effects, including vasodilation. Vomiting later in the postoperative period may be the result of drugs, ileus, mechanical obstruction of the gut, or other problems and should be investigated. Gastric stress ulcers and acid reflux must be considered in patients with multiple traumas, ICU patients, and patients who were in the prone position for an extended period of time. Appropriate prophylaxis against gastrointestinal bleeding should be considered in these patients. Agents include a low-dose proton pump inhibitor or a histamine type 2 receptor antagonist.

Gastric dilation occurs when the stomach becomes massively distended. Hemorrhage from the gastric mucosa can develop. This uncommon surgical complication is an occult cause of shock in the first few hours after operation. If the fluid is vomited, aspiration may occur. The distended, tympanitic stomach may be visible in the epigastrium or on a radiograph. Typically, nasogastric intubation yields dark, bloody fluid. Fluid and electrolyte losses must be replaced. Acute gastric dilation can be fatal if it is unrecognized, and prompt treatment usually results in dramatic improvement.

Paralytic ileus is the cessation of effective gastrointestinal motility after trauma, severe illness, or surgery. Ileus is primarily a gastric phenomenon because the remainder of the gut can usually handle fluids earlier than the stomach. Vomiting and abdominal distention are the main manifestations. Decreased bowel sounds are an unreliable finding. Abdominal radiographs show gas in the stomach, small bowel, and colon. Mechanical bowel obstruction must be excluded in such patients. Any patient with ileus should be given bowel rest (given nothing by mouth) and should have a nasogastric tube inserted and left in place until the ileus resolves.

Another potential gastrointestinal complication is constipation. Several factors contribute to postoperative constipation. First, taking nothing by mouth eliminates gastrocolic reflexes and reduces fecal bulk. Second, dehydration encourages fluid absorption from the colonic contents, desiccating the stool. Third, ileus has a component of impaired colonic motility. Finally, incisional pain makes patients unwilling to increase intra-abdominal pressure, eliminating an important force contributing to defecation. Physical inactivity removes stimuli to movement of feces through the colon. Furthermore, opiates and antacids containing calcium or aluminum exacerbate constipation. Often, attempts to defecate on a bedpan are unsuccessful because the patient is semirecumbent. The normal sitting or squatting position raises abdominal pressure and helps evacuate the rectum.

Hiccups are another potential complication. Typically, they are self-limited; however, they can be sufficiently persistent and exhausting to endanger life in a severely debilitated patient. They are produced by any process that stimulates the afferent or efferent phrenic nerve pathways. Therefore, the causes are quite varied and include central nervous system, cardiopulmonary, and gastrointestinal conditions, as well as renal failure, infectious diseases, and steroid therapy.

Treatment should be directed at the cause when possible, but therapy is frequently only symptomatic. Breath holding, drinking a large glass of water, or gastric lavage with a warm 1% solution of sodium bicarbonate may be effective. Rebreathing into a paper bag or administration of 10% to 15% carbon dioxide by face mask induces hyperventilation and may interrupt the reflex. Tranquilizing drugs such as chlorpromazine hydrochloride or other phenothiazine preparations are worth trying in patients with prolonged hiccups. Barbiturate sedation may be effective.

Disorders of Hemostasis

Patients with preexisting hemostatic disorders undergo operations more frequently than in the past. Because specific replacement therapies are available, it is essential to identify the exact defect before surgery whenever possible. Occasionally, the first sign of a hemostatic defect is excessive bleeding at operation. This distressing situation will seldom arise from a preexisting disorder if a bleeding history and screening laboratory tests are obtained before surgery.

Screening Procedures

Blood is potentially the most dangerous substance prescribed by most physicians. Complications are common and may be fatal. Transmission of syphilis, malaria, bacteria, and viruses is infrequent with current blood banking practices. Hepatitis, however, remains a problem. Blood products carry a hepatitis risk proportional to the number of donors contributing to the blood pool. Recently, available assays for hepatitis have greatly reduced the potential of distributing blood from hepatitis carriers, but most cases of hepatitis that occur after transfusion in the United States are not a result of hepatitis B or other known viruses. The statistical risk of hepatitis is unknown because the majority of cases are subclinical. Blood is an allograft, and the recipient may become immunized against human leukocyte antigens, platelet antigens, and red cell antigens. Reactions to leukocyte antigens are the probable cause of many febrile responses to transfusions. Reactions to transfusions of proteins, especially immunoglobulin A, are frequently severe and may be hemolytic in nature.

Administration of blood to the wrong recipient is the most common error and is usually the result of a clerical error such as incorrect specimen labeling. Such an error can cause serious immunologic complication. Massive hemolysis may occur, leading to renal failure and death. Symptoms of early hemolysis are chills, fever, back pains, circulatory collapse, and hemorrhage. Delayed hemolysis occurs from several days to 1 month after transfusion and is manifested by anemia or mild jaundice.

Transfusion Reactions

In the case of a transfusion reaction, the transfusion should be immediately halted and the remaining blood returned to the bank for investigation of the appropriateness of the cross-match, the Rh compatibility, and the Coombs test. The patient should be adequately hydrated. Samples of plasma and urine should be tested for hemoglobin. The presence of hemoglobin in these fluids implies hemolysis. Cultures should be obtained of the recipient’s blood and the donor’s blood. If a severe reaction has occurred, renal function should be evaluated and protected by administration of mannitol and bicarbonate. Febrile reactions, without hemolysis, should be treated with antihistamines and acetaminophen. Isoimmunized patients who require subsequent transfusions should receive washed red cells.

Surgical patients usually receive blood transfusions for the restoration of red cell mass or blood volume. Anemic patients who are asymptomatic are able to tolerate operations of almost any magnitude if operative blood loss is minimal. If a surgical procedure commonly associated with substantial blood loss is planned, anemia should be corrected 1 to 2 days before operation so that the storage-related defects of transfused blood can be normalized. Moreover, preoperative transfusion permits preoperative detection of transfusion reactions. Red cell concentrates are preferred for correction of preoperative anemia in stable patients.

The need for transfusion to correct mild postoperative anemia is assessed by measurement of the reticulocyte count. If the count is elevated and the patient does not have postural hypotension or dyspnea, transfusion is not indicated. If the reticulocyte count is low, the response to oral or parenteral iron should be determined before giving blood. Chronically ill patients frequently have a regenerative anemia and may require serial blood transfusions.

Banked blood lacks functioning platelets. Platelets lose their aggregability in cold storage, and preservatives do not maintain platelet viability beyond 72 hours. In addition, most banks with component programs routinely remove the platelets from donated blood. Absent or nonfunctioning platelets contribute to posttransfusion bleeding, and the magnitude of the problem is proportional to the number of units of blood administered. Platelet concentrates (or platelet packs) should be given to patients receiving 10 or more units of blood within 1 hour.

Whole blood is preferable for patients with exsanguinating hemorrhage because red cell concentrates cannot be rapidly administered.

Prophylaxis

Autologous Blood Donation

Autologous blood transfusion avoids most of the complications associated with transfusion of homologous blood, including transmission of disease, hemolytic transfusion reactions, and other immune phenomena. Despite existing medical problems, most patients are able to donate at least two units of autologous blood before surgery. This could potentially enable over 90% of patients to avoid homologous transfusion during major spine procedures. Autologous blood can normally be stored for up to 40 days (longer storage requires an expensive and complex freezing process). One unit of autologous blood can be processed from a given patient every 3 days up to 3 days before surgery, provided the hematocrit remains at least 34%. Iron supplementation is recommended. Treatment with erythropoietin can increase the patient’s hematocrit and allow more blood to be stored in advance of surgery. It can also be used without predonation to minimize the need for transfusion at the time of surgery.43

There are two forms of autotransfusion. In one type, a patient donates blood in advance of elective operation, and this blood is stored for transfusion back into the donor, should it be required. This practice permits stimulation of erythropoiesis and results in restoration of red cell mass to near-normal levels by the time of operation. A further advantage is the availability of the safest possible blood, should the patient require it.

The other type of autotransfusion is useful in emergencies. Blood lost by the patient is collected into an apparatus designed for this purpose (e.g., the cell-saver), anticoagulated, and immediately returned to the circulation. This type of autotransfusion is most useful in cases of massive bleeding. It may be life saving when compatible blood is unavailable. Reinfusion of large amounts of blood, however, can cause coagulopathies.

Antibiotic Prophylaxis

Prophylactic antibiotics are administered routinely to patients undergoing spine surgery, particularly those undergoing spinal instrumentation, because of the severe consequences of infected prostheses. Short courses of antibiotics are safe and effective. Longer courses have been associated with Clostridium difficile colitis. Prophylaxis for endocarditis is not necessary for clean spine procedures, because the risk of bacteremia is low.

Prophylaxis for Thromboembolism

The most important prophylaxis issue in patients undergoing spine surgery is the prevention of deep venous thrombosis and pulmonary embolism. The incidence of deep venous thrombosis in spine surgery is not known. Estimates as high as 60% have been made. Prophylaxis for thromboembolism should therefore be considered in all patients undergoing major spine procedures, especially if patients are not immediately ambulatory. Thigh-length sequential compression devices, thromboembolic stockings, and low-dose heparin serve as prophylaxis for deep venous thrombosis in elective spine surgery. Initial studies suggest that low-molecular-weight heparin and heparinoids may be effective and safe in these patients. The benefits of prophylactic anticoagulation must be balanced against the risk. Cain et al.44 reported a high rate of complications due to therapeutic heparinization after pulmonary embolus in spine surgery patients. In a poll of Scoliosis Research Society members representing more than 13,000 thoracic and lumbar fusions, they identified 9 patients who were treated with heparin anticoagulation. Complications attributable to anticoagulation were reported in two thirds of these patients.

Anticoagulation

Anticoagulation is defined as suppression of the coagulation mechanism. The term is used loosely in clinical practice, however, and it may refer to the suppression of clotting or the inhibition of platelet aggregation.

The only absolute anticoagulant is heparin, a physiologic substance present in mast cells that suppresses thrombin formation. Oral anticoagulant agents are less effective. They block coagulation indirectly by depressing certain factors in the clotting cascade. Antiplatelet agents interfere with platelet aggregation and thus inhibit coagulation.

Venous clots are composed of fibrin. As a result, anticoagulants are effective for preventing and treating venous thrombosis. Arterial clots are composed mainly of platelets. Therefore, antiplatelet medications are useful for preventing arterial thrombosis.

Heparin can be administered either subcutaneously or intravenously. Subcutaneous heparin is used only when small amounts of heparin are required, most often for prophylaxis against clotting. Larger doses of heparin required to treat thrombotic states should be administered intravenously.

In general, for clotting prophylaxis, sufficient heparin is administered to decrease the coagulation tendency without altering coagulation parameters. This avoids the complications inherent in systemic anticoagulation. Clotting measures such as the Lee-White clotting time, the activated partial thromboplastin time, or the prothrombin time are all used for this purpose. These tests help to quantify the effect of a given dose of anticoagulant.

A dose of heparin is metabolized in 4 to 8 hours. In the presence of bleeding complications, it may be necessary to reverse the heparin immediately by infusing protamine sulfate. Not more than 1 mg of protamine should be given for every 100 units of heparin. Administration of too much protamine can produce hypotension or bleeding complications. Protamine, therefore, should be administered slowly and carefully.

Anaphylactic reactions to heparin are very rare. Hemorrhage is the primary complication. Patients at risk should have their hematocrit checked frequently (at least twice daily). Typically, bleeding occurs into wounds or into the retroperitoneum and is not serious if the problem is promptly recognized and appropriately treated. Cerebral hemorrhage is a rare but serious complication.

Depression of platelet function occurs in some patients after 3 to 4 days of heparin therapy. The risk of hemorrhage is greatest in these patients. This complication can often be anticipated, however, because it is usually preceded by a decrease in the platelet count to below 100,000/mm3.

Heparin should be given in adequate doses. The rate of heparin infusion should be adjusted to maintain a partial thromboplastin time that is 1.5 to 2 times the control value. Enoxaparin, a low-molecular-weight heparin, is an alternative that does not require continuous infusion or such careful monitoring and regulation of laboratory values. The usual dose for prophylaxis is 40 mg given subcutaneously once daily. The dose for treatment of deep venous thrombosis is 1 mg/kg body weight given subcutaneously every 12 hours. Special caution is necessary when treating the elderly, those with renal impairment, or patients weighing less than 45 kg.

Warfarin is less effective than heparin but is practical for prophylaxis, especially in outpatients, because it is administered orally. The dosage required in individual patients varies considerably. The preferred regimen for initiation of oral anticoagulation is 10 mg of warfarin orally each day until anticoagulation is obtained. The dose is then adjusted to maintain a prothrombin time that is 1.5 to 2 times the normal value. The average maintenance dose is 5 mg/day.

The prothrombin time returns to normal within 3 to 4 days after warfarin is discontinued. Rapid reversal is obtained by administering 5 to 10 mg of IV vitamin K. Immediate reversal can be obtained by the administration of fresh-frozen plasma IV.

The most common complication of oral anticoagulation is hemorrhage, frequently into the retroperitoneum or into the urinary or gastrointestinal tract. The urine and stool should be monitored for the presence of blood. Abdominal pain suggests retroperitoneal hemorrhage.

Antiplatelet agents are used to treat arterial thrombotic conditions. These agents carry less risk of hemorrhage than do anticoagulants, but they are not as effective. Aspirin, dipyridamole, and related drugs depress platelet aggregation for the life span of the platelet. Reversal of drug effect therefore depends on generation of new platelets. The half-life of platelets is approximately 4 days; therefore, these agents are effective for 1 to 2 days.

Plasma volume expanders can also depress platelet aggregation. Low-molecular-weight dextran reduces viscosity, increases microcirculatory flow, and decreases the tendency toward platelet aggregation. This agent is often used postoperatively.

Postoperative Complications

Nonspecific Complications

Fever

Pulmonary atelectasis is the most common cause of fever during the first 2 days after major spine procedures. Typically, the pulse and respiratory rates are elevated along with the temperature (the “triple response”). Pneumonia seldom develops before the third postoperative day unless pulmonary disease was present at the time of operation or unless the patient aspirates.

Wound infection caused by beta-hemolytic streptococci or clostridia can develop within hours of operation. Other bacterial wound infections require several days before they progress sufficiently to cause fever.

In general, cystitis alone does not cause fever, but infection of the upper urinary tract does. Infection in the operative site (deep to the incision) can also cause fever. Examples include epidural abscess, empyema, meningitis, and graft infection. IV catheters can become infected quickly unless rigid aseptic precautions are used during and after insertion.

Reactions to drugs, notably antibiotics, may cause fever. The extent to which fever is investigated by laboratory tests and radiographs depends on the interval between operation and the appearance of fever, the severity of fever, and the physician’s certainty about the cause on the basis of the history and physical examination. The patient must be questioned about symptoms (e.g., dysuria, unusual pain) that may be clues to the source of fever. Physical examination, including auscultation of the chest, inspection of the wound, and examination of IV sites, is essential.

Leukocyte count and urinalysis are ordered in nearly every case. Cultures of urine, sputum, blood, and drainage fluid may be indicated. Chest radiographs are not necessary for patients with a clinical diagnosis of atelectasis in the first day or two after operation. Persistent fever of suspected pulmonary origin, however, requires a chest radiograph. Radiographs of other areas (e.g., the abdomen) are obtained as indicated. The search for deep infections may require special tests such as gallium scan, liver scan, ultrasonography, CT, or MRI scans.

Postoperative fever is treated best by correction of the underlying cause. Because high fever (temperature >38.5°C) is itself debilitating, antipyretic drugs (e.g., acetaminophen or aspirin) can be given by mouth or rectal suppository while the cause is being investigated. Application of ice packs or 70% alcohol to the skin surface or placement of the patient on a refrigerated blanket are other methods of lowering body temperature.

If the cause of fever remains undefined, IV catheters and central lines should be removed and new ones placed. Potentially fever-causing drugs should be changed or discontinued.

Confusion and Delirium

Elderly patients and those who are acutely and severely ill may experience postoperative psychosis. Causative factors include pain, sleep deprivation, isolation, and unfamiliar surroundings. The patients may become disoriented, hallucinatory, agitated, combative, and fearful of personnel who are caring for them, particularly at night. The derangements are transient, and patients usually regain their former mental status as the recovery from the operation progresses. It is essential to determine whether a patient with these symptoms is hypoxemic. Hypoxemia is a common cause of postoperative restlessness and mental status alteration, and the administration of analgesics or sedatives to a hypoxic patient may be lethal.

Simple helpful measures include keeping a light on in the room and providing a companion. Efforts should be made to reorient confused patients as often as possible. Mechanical restraints should be avoided unless the patient is at risk of self-injury or injury to others. Tranquilizers should be used cautiously, especially in elderly patients.

Delayed Wound Healing and Dehiscence

Many systemic factors contribute to wound healing failure by altering collagen metabolism or impairing oxygen delivery to the wound. Local and technical problems may cause impaired blood supply or inadequate resistance to mechanical forces. Infection, corticosteroid or cytotoxic drug use, malnutrition, hypovolemia, hypoxemia, increased blood viscosity, tissue irradiation, and errors in technique may all contribute to impaired wound healing.

Wounds may dehisce because tissue is devitalized by dissection or strangulated by placement of too many sutures or by tying sutures too tightly. The latter is a common technical cause of dehiscence, which is confirmed when intact sutures are found to have cut through the tissue on one side of the wound. Inadequate suture strength or number or premature suture removal may also lead to similar complications. Absorbable sutures may not maintain their tensile strength long enough for secure healing, especially in debilitated patients.

Dehiscence of the skin is apparent on inspection. Fascial dehiscence is manifested by spontaneous serosanguineous fluid drainage from the wound. One must assume that fascia has dehisced when this type of drainage appears, especially when it persists. Fluid from a seroma or hematoma is not serosanguineous, and it usually does not continue to drain.

Obvious major dehiscence of the fascia should be treated by resuture under anesthesia in the operating room. Minor disruptions of fascia may be managed without resuture; however, the extent of fascial disruption is often underestimated until the skin is opened and the wound is explored. It is best to do this under aseptic conditions in the operating room.

Bleeding from the incision is apparent within minutes to hours after the operation is completed. Bleeding vessels may be in the skin, in the cutaneous fat, or at the fascial level.

Decubitus Ulcers

Decubitus ulcers are caused by sustained pressure on the skin, usually over bony prominences such as the sacrum, ischium, trochanter, and heel. Poor nutrition is the most important factor leading to decubitus formation. The ulcers occur in bedridden patients who are weak, aged, malnourished, or paralyzed and who are receiving inadequate nursing care. Soiling of the bed because of bowel or urinary incontinence frequently leads to skin irritation, which in turn increases the risk of ulcer development. Unrelieved pressure of only a few hours may be sufficient to produce a decubitus ulcer in a susceptible individual. Usually, decubitus ulcers begin as small areas of erythema and tenderness that soon break down to form indolent ulcers, unless they are protected from further pressure. In neglected cases, large defects in skin and soft tissues may result from the combined effects of pressure, infection, and poor healing capability. Osteomyelitis of underlying bone may occur.

The most important elements in prevention of decubitus ulcers are vigilant nursing care, mobilization, and nutrition. Bedridden patients should be inspected frequently for areas of skin damage that may progress to ulcer formation. Soiling of the bed by incontinent patients should be prevented as much as possible. An alternating pressure or foam rubber mattress may be used to decrease pressure on the skin. Washable sponge pads under pressure points are also protective.

It is essential to change patient position frequently and protect involved skin areas by pillows and pads. The clothing and skin must be kept clean and dry. Correction of malnutrition and anemia and control of infection are often critical to healing.

Decubitus ulcers should be kept clean and well debrided. They may be exposed to air or covered with dry sterile dressings. Topical applications have little value. Invasive local infection should be treated with drainage, saline compresses, and systemic antibiotics, as indicated.

Surgical treatment of large, resistant lesions consists of complete debridement, including removal of any bony prominences or sequestra, and closure of the wound with a local myocutaneous flap. This provides an adequate pad over the bone and avoids suture lines over the critical area of pressure. The donor area may be closed frequently by direct approximation, but a split-thickness skin graft may be required.

Postoperative Complications Specific to Spine Surgery

Infection

Spine Surgical Wound Infection

Spangfort45 reviewed more than 10,000 laminectomy cases and reported an operative infection rate of approximately 2.9%. More recent series indicate that preoperative antibiotic prophylaxis may lower the incidence of infection.46,47

In 1980, Ramirez and Thisted48 reported an incidence of infection of 0.3% in an analysis of 28,395 patients who underwent lumbar laminectomy for radiculopathy in the United States.

The clinical and radiographic characteristics of interspace infection were described first by Milward,49 in 1936, after the inadvertent introduction of microorganisms into a disc space during lumbar puncture. Gieseking50 reported the first postoperative interspace infection in 1951. Typically, patients with aseptic necrosis or interspace infection are asymptomatic immediately after surgery but begin to experience excruciating spasms in the lower back, with or without radiation into the legs, within 2 weeks. Typically, the white blood cell count and temperature are normal but the erythrocyte sedimentation rate is elevated, often to more than 100 mm/hr. Lumbosacral radiographs may reveal erosion of the cartilaginous plates as the disease progresses. Needle aspirations of the interspace may reveal the offending organisms but are often negative.51 Patients with a clear-cut syndrome should be placed on IV antibiotics.

Wound infection should be suspected when persistent temperature elevation occurs several days after surgery. The wound should be examined for erythema, swelling, tenderness, and drainage. Management should include a Gram stain and culture, with antibiotic treatment if the clinical suspicion is strong. In the presence of probable infection or persistent infection despite antibiotic treatment, the patient should be returned to the operating room and the wound reopened, thoroughly debrided, and irrigated. Hardware should not be removed. If there is substantial tissue necrosis, the wound can be managed open, with frequent dressing changes. If the tissues look healthy and well vascularized, the wound can be closed over drains.

Discitis

The incidence of postoperative intervertebral disc space infection (discitis) is 0.75%. Disc space infection rates vary from 0.1% to 3.8%.45,52–55 The higher incidence of disc space infection with microsurgery has been attributed to the presence of the microscope over the open wound.56 Postoperative discitis produces persistent, intense back pain with unremarkable associated physical findings 2 weeks to 3 months after discectomy.

Elevated erythrocyte sedimentation rates are typical. Bone scan, CT, and MRI are quite sensitive for detecting discitis and can identify changes associated with discitis earlier than can plain radiographs. CT is effective in the early diagnosis of discitis, with hypodensity of the affected disc space being detected as early as 10 days after surgery. The responsible bacteria are identified in less than 50% of cases, with Staphylococcus species the most common organisms cultured.51 Early diagnosis and immediate treatment are important for preventing chronic infection. Immobilization is often effective for pain relief, and 4 to 6 weeks of IV antibiotic therapy is recommended. Uncomplicated discitis should not require surgery, and most patients undergo spontaneous interbody fusion. Occasionally, lumbar epidural abscesses may develop that produce paresis. Under these circumstances, immediate decompressive laminectomy is indicated.

Postoperative Osteomyelitis

Infection may be introduced directly into the intervertebral disc space during surgery and can spread to the adjacent vertebral bodies, producing osteomyelitis. Surgery for protruding or herniated discs is the most frequent factor in the direct introduction of infection into the intervertebral disc space. This complication occurs in less than 1% of patients who undergo disc surgery. Organisms may be inadvertently inoculated at the time of surgery, and residual hematoma, necrotic tissue, and foreign bodies provide an environment conducive to bacterial proliferation. Weeks, months, or even years may elapse before the diagnosis of a disc space infection is established. Symptoms may not be apparent immediately after operation. Often there is initial pain relief followed by recurrence several days to weeks later. Fever may be transient, intermittent, or absent, and there is often no evidence of infection when symptoms develop. The degree of pain may appear to be out of proportion to the objective findings and may be attributed erroneously to malingering or even psychoneurosis.

The typical radiologic changes of vertebral osteomyelitis may not be apparent for months. Radionuclide bone scans are quite sensitive and often demonstrate evidence of infection before plain films of the spine show any changes. However, they are not specific; surgical edema and disc changes may yield false-positive results.57 Furthermore, early in the course of disc space infection, the bone scan may be negative in a significant proportion of patients.58 CT scans may show destructive changes of the vertebral bodies before these are evident on plain films. End-plate irregularities on CT scan, however, are not specific for discitis, and normal curettage changes in vertebral end plates may mimic erosions of discitis.59 MRI may show changes of discitis long before any changes are apparent radiologically.60 It is, however, important to note that MRI and CT studies may be negative early in the course of postoperative or posttraumatic discitis,58 and a high index of suspicion is necessary. Any patient with increasing back pain more than 2 weeks after surgery and an erythrocyte sedimentation rate greater than 50 mm/hr should be considered to have discitis until proven otherwise.60 Percutaneous disc biopsy can be helpful in the diagnosis of postoperative discitis,61 but this often produces false-negative results.

In a study comparing MRI, plain radiographs, and radionuclide studies in the evaluation of vertebral osteomyelitis, MRI was judged to be as accurate and sensitive as combined bone and gallium scanning and more sensitive than plain radiography.60 The MRI appearance of pyogenic infection is characteristic, making MRI a rapid, noninvasive method for the detection of vertebral osteomyelitis and its complications, including epidural abscess. On T1-weighted images, infected disc material shows decreased signal intensity from the intervertebral disc space and contiguous vertebral bodies relative to the normal vertebral signal. On T2-weighted images, these tissues show increased signal. MRI provides more anatomic detail than radionuclide scanning and allows differentiation of neoplasm and degenerative disease from osteomyelitis. The disc space is nearly always spared in neoplastic disease, whereas degenerative disease with nucleus desiccation produces decreased disc signal on T2-weighted images. Gallium scans may show positive results earlier than MRI in the course of infection, and this technique is more sensitive to changes arising from treatment and decreasing inflammation.

In many patients, postoperative discitis and vertebral osteomyelitis resolve spontaneously, and a diagnosis is never made.62 In some patients with postoperative vertebral osteomyelitis, intermittent antibiotic therapy obscures the diagnosis and permits the illness to go undetected for years.63,64 Kern63 reported a patient in whom vertebral osteomyelitis and meningitis became manifest 2.5 years after lumbar spine surgery. The ability of infections to remain dormant and recur after long periods is illustrated by a patient in whom postoperative staphylococcal lumbar vertebral osteomyelitis developed and cleared after 3 years of treatment. Thirty-four years later, after 30 years without symptoms, the patient developed a staphylococcal psoas abscess.64

Epidural Abscess

Spinal epidural abscess (SEA) is an uncommon entity, but its clinical importance overshadows its rarity. Although SEA is rare, it should be considered in any patient with increasing neurologic symptoms and signs in the early postoperative period. It may be difficult to differentiate from an expanding hematoma in the absence of systemic evidence of infection.

The importance of early diagnosis of SEA was emphasized by Heusner as early as 1948. Several studies have emphasized the frequently rapid deterioration and substantial permanent morbidity associated with this infection. Despite the recognition of SEA as a potential neurosurgical emergency and the increased sophistication of diagnostic studies, the morbidity and mortality associated with SEA remain significant. Advances in imaging have made the diagnosis of SEA less elusive and the options for therapeutic intervention more rational.65

SEAs are categorized as acute lesions (gross pus in the epidural space), usually with accompanying sepsis, or chronic lesions (granulation tissue in the epidural space) that may persist for months. The clinical presentation of an acute SEA is often stereotypical, but it can be difficult to appreciate in its earliest stages. The classic triad is intense localized back pain, progressive neurologic deficit, and fever. The initial complaint is almost uniformly axial pain. Paresthesias are also very common. Fever or other symptoms of infection are present about 50% of the time. Without treatment, the progression and time course of symptoms beyond this point are astoundingly uniform. Within 3 days, patients generally note radicular symptomatology, followed within 36 hours by weakness. Rapid deterioration to paralysis occurs typically over the next 24 hours. This pattern of symptoms is so uniform that some authors suggest that this establishes the diagnosis until proven otherwise.65

Laboratory findings are often unhelpful. Fever and leukocytosis are useful markers when present but are absent in more than 50% of the cases. Leukocytosis is common in the acute group (average white blood cell count of <16,000/mm3). The erythrocyte sedimentation rate is almost universally elevated but is a nonspecific indicator.

Plain radiographs are typically unremarkable in the absence of concomitant osteomyelitic involvement of adjacent vertebral bodies. The vertebral end plates directly adjacent to the disc space may show erosion. This often develops as late as 4 to 6 weeks after the onset of infection. The degree of local bone destruction from associated osteomyelitis is best appreciated by CT, and this information is often essential to formulation of the optimal management strategy.

CT myelography is an excellent technique that is often diagnostic. Lateral C1-2 puncture is our preferred method. This identifies the upper limit of any epidural mass but may not define the lower edge, and a second puncture below the block is required occasionally. Myelography has the added benefit of providing a cerebrospinal fluid sample for a cell count with differential, protein and glucose levels, Gram stain, and culture. The cerebrospinal fluid profile is generally consistent with parameningeal inflammation, although up to 15% of patients have concurrent meningitis. Myelography, however, carries the risk of converting an epidural process into a subdural empyema by subarachnoid contamination from puncture of the thecal sac during traversal of an unsuspected focus of epidural infection. Because of this potential morbidity, MRI is used as a first-line diagnostic imaging modality.

MRI is indispensable for diagnosing SEA and is extremely valuable in guiding the patient’s management. MRI is considered the diagnostic test of choice, and it is diagnostic in nearly every case. MRI rapidly and accurately identifies inflammatory foci, defines the degree of spinal cord compression, and shows the predominant location of the abscess; in addition, it will often dictate the surgical approach. MRI provides more information than does CT about the extent of abscess involvement and degree of cord compromise.

The traditional therapy for SEA has been immediate surgical spinal cord decompression. Early studies of SEA recommended this policy and warned of patients who had deteriorated before delayed surgical decompression could be performed. The fundamental principles of surgical management are drainage of pus, debridement of granulation tissue, copious irrigation, and postoperative drainage.

Summary

The perioperative management of the spine surgery patient is both straightforward and potentially complex. It is critical to evaluate patients carefully, both before surgery, to avoid intraoperative catastrophes, and after surgery, to eliminate development of preventable associated morbidities. Perfect surgical procedures are often negated by suboptimal perioperative care. Spine surgery should never be considered potentially less morbid than other areas of neurosurgery.

Key References

Brooks-Brunn J.A. Predictors of postoperative pulmonary complications following abdominal surgery. Chest. 1997;111:564-571.

Brown M.D., Seltzer D.G. Perioperative care in lumbar spine surgery. Orthop Clin North Am. 1991;22:353-358.

Forrest J.B., Rehder K., Cahalan M.K., et al. Multicenter study of general anesthesia: III. Predictors of severe perioperative adverse outcomes. Anesthesiology. 1992;76:3-15.

Glassman S.D., Rose S.M., Dimar J.R., et al. The effect of postoperative nonsteroidal anti-inflammatory drug administration on spinal fusion. Spine (Phila Pa 1976). 1998;23:834-838.

Hilibrand A.S., Fye M.A., Emery S.E., et al. Impact of smoking on the outcome of anterior cervical arthrodesis with interbody or strut-grafting. J Bone Joint Surg [Am]. 2001;83:668-673.

Howell S.J., Hemming A.E., Allman K.G., et al. Predictors of postoperative myocardial ischaemia: the role of intercurrent arterial hypertension and other cardiovascular risk factors. Anaesthesia. 1997;52:107-111.

Lapp M.A., Bridwell K.H., Lenke L.G., et al. Prospective randomization of parenteral hyperalimentation for long fusions with spinal deformity, its effect on complications and recovery from postoperative malnutrition. Spine (Phila Pa 1976). 2001;26:809-817.

Moller A.M., Villebro N., Pedersen T., et al. Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial. Lancet. 2002;359:114-117.

Rubinstein E., Findler G., Amit P., et al. Perioperative prophylactic cephazolin in spinal surgery: a double-blind placebo-controlled trial. J Bone Joint Surg [Br]. 1994;76:99-102.

References

The complete reference list is available online at expertconsult.com.

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