4. Post Operative Complications

Editors: Doherty, Gerard M.; Way, Lawrence W.

Title: Current Surgical Diagnosis & Treatment, 12th Edition

Copyright 2006 McGraw-Hill

Gerard M. Doherty MD

Postoperative complications may result from the primary disease, the operation, or unrelated factors. Occasionally, one complication results from another previous one (eg, myocardial infarction following massive postoperative bleeding). The clinical signs of disease are often blurred in the postoperative period. Early detection of postoperative complications requires repeated evaluation of the patient by the operating surgeon and other team members.

Prevention of complications starts in the preoperative period with evaluation of the patient's disease and risk factors. Improving the health of the patient before surgery is one goal of the preoperative evaluation. For example, cessation of smoking for 6 weeks before surgery decreases the incidence of postoperative pulmonary complications from 50% to 10%. Correction of gross obesity decreases intra-abdominal pressure and the risk of wound and respiratory complications and improves ventilation postoperatively.

The surgeon should explain the operation and the expected postoperative course to the patient and family. The preoperative hospital stay, if one is necessary, should be as short as possible both to reduce costs and to minimize exposure to antibiotic-resistant microorganisms. Adequate training in respiratory exercises planned for the postoperative period substantially decreases the incidence of postoperative pulmonary complications.

Early mobilization, proper respiratory care, and careful attention to fluid and electrolyte needs are important. On the evening after surgery the patient should be encouraged to sit up, cough, breathe deeply, and walk, if possible. The upright position permits expansion of basilar lung segments, and walking increases the circulation of the lower extremities and lessens the danger of venous thromboembolism. In severely ill patients, continuous monitoring of systemic blood pressure and cardiac performance enables identification and correction of mild derangements before they become severe. Other aspects of prevention of complications are discussed in Chapters 3 and 5.

WOUND COMPLICATIONS

Hematoma

Wound hematoma, a collection of blood and clot in the wound, is one of the most common wound complications and is almost always caused by imperfect hemostasis. Patients receiving aspirin or low-dose heparin have a slightly higher risk of developing this complication. The risk is much higher in patients who have been given systemically effective doses of anticoagulants and those with preexisting coagulopathies. Vigorous coughing or marked arterial hypertension immediately after surgery may contribute to the formation of a wound hematoma.

Hematomas produce elevation and discoloration of the wound edges, discomfort, and swelling. Blood sometimes leaks through skin sutures. Neck hematomas following operations on the thyroid, parathyroid, or carotid artery are particularly dangerous, because they may expand rapidly and compromise the airway. Small hematomas may resorb, but they increase the incidence of wound infection. Treatment in most cases consists of evacuation of the clot under sterile conditions, ligation of bleeding vessels, and reclosure of the wound.

Seroma

A seroma is a fluid collection in the wound other than pus or blood. Seromas often follow operations that involve elevation of skin flaps and transection of numerous lymphatic channels (eg, mastectomy, operations in the groin). Seromas delay healing and increase the risk of wound infection. Those located under skin flaps can usually be evacuated by needle aspiration. Compression dressings should then be applied to seal lymphatic leaks and prevent reaccumulation. Small seromas that recur may be treated by repeated evacuation. Seromas of the groin, which are common after vascular operations, are best left to resorb without aspiration, since the risks of introducing a needle (infection, disruption of vascular structures, etc) are greater than the risk associated with the seroma itself. If seromas persistor if they start leaking through the woundthe wound should be explored in the operating room and the lymphatics ligated.

Wound Dehiscence

Wound dehiscence is partial or total disruption of any or all layers of the operative wound. Rupture of all layers of the abdominal wall and extrusion of abdominal viscera is evisceration. Wound dehiscence occurs in 1-3% of abdominal surgical procedures. Systemic and local factors contribute to the development of this complication.

A. Systemic Risk Factors

Dehiscence is rare in patients under age 30 but affects about 5% of patients over age 60 having laparotomy. It is more common in patients with diabetes mellitus, uremia, immunosuppression, jaundice, sepsis, hypoalbuminemia, and cancer; in obese patients; and in those receiving corticosteroids.

B. Local Risk Factors

The three most important local factors predisposing to wound dehiscence are inadequate closure, increased intra-abdominal pressure, and deficient wound healing. Dehiscence often results from a combination of these factors rather than from a single one. The type of incision (transverse, midline, etc) does not influence the incidence of dehiscence.

Adequacy of closure This is the single most important factor. The fascial layers give strength to a closure, and when fascia disrupts, the wound separates. Accurate approximation of anatomic layers is essential for adequate wound closure. Most wounds that dehisce do so because the sutures tear through the fascia. Prevention of this problem includes performing a neat incision, avoiding devitalization of the fascial edges by careful handling of tissues during the operation, placing and tying sutures correctly, and selecting the proper suture material. Sutures must be placed 2-3 cm from the wound edge and about 1 cm apart. Dehiscence is often the result of using too few stitches and placing them too close to the edge of the fascia. It is unusual for dehiscence to recur following reclosure, implying that adequate closure was technically possible at the initial procedure. In patients with risk factors for dehiscence, the surgeon should do the second closure at the first operation,take extra care to prevent dehiscence. Modern synthetic suture materials (polyglycolic acid, polypropylene, and others) are clearly superior to catgut for fascial closure. In infected wounds, polypropylene sutures are more resistant to degradation than polyglycolic acid sutures and have lower rates of wound disruption. Wound complications are decreased by obliteration of dead space. Ostomies and drains should be brought out through separate incisions to reduce the rate of wound infection and disruption.

Intra-abdominal pressure After most intra-abdominal operations, some degree of ileus exists, which may increase pressure by causing distention of the bowel. High abdominal pressures can also occur in patients with chronic obstructive pulmonary disease who use their abdominal muscles as accessory muscles of respiration. In addition, coughing produces sudden increases in intra-abdominal pressure. Other factors contributing to increased abdominal pressure are postoperative bowel obstruction, obesity, and cirrhosis with ascites formation. Extra precautions are necessary to avoid dehiscence in such patients.

Deficient wound healing. Infection is an associated factor in more than half of wounds that rupture. The presence of drains, seromas, and wound hematomas also delays healing. Normally, a healing ridge (a palpable thickening extending about 0.5 cm on each side of the incision) appears near the end of the first week after operation. The presence of this ridge is clinical evidence that healing is adequate, and it is invariably absent from wounds that rupture.

C. Diagnosis and Management

Although wound dehiscence may occur at any time following wound closure, it is most commonly observed between the fifth and eighth postoperative days, when the strength of the wound is at a minimum. Wound dehiscence may occasionally be the first manifestation of an intra-abdominal abscess. The first sign of dehiscence is discharge of serosanguineous fluid from the wound or, in some cases, sudden evisceration. The patient often describes a popping sensation associated with severe coughing or retching. Thoracic wounds, with the exception of sternal wounds, are much less prone to dehiscence than are abdominal wounds. When a thoracotomy closure ruptures, it is heralded by leakage of pleural fluid or air and paradoxic motion of the chest wall. Sternal dehiscences, which are almost always associated with infection, produce an unstable chest and require early treatment. If infection is not overwhelming and there is minimal osteomyelitis of the adjacent sternum, the patient may be returned to the operating room for reclosure. Continuous mediastinal irrigation through small tubes left at the time of closure appears to reduce the failure rate. In cases of overwhelming infection, the wound is best treated by debridement and closure with a pectoralis major muscle flap, which resists further infection by increasing vascular supply to the area.

Patients with dehiscence of a laparotomy wound and evisceration should be returned to bed and the wound covered with moist towels. With the patient under general anesthesia, any exposed bowel or omentum should be rinsed with lactated Ringer's solution containing antibiotics and then returned to the abdomen. After mechanical cleansing and copious irrigation of the wound, the previous sutures should be removed and the wound reclosed using additional measures to prevent recurrent dehiscence, such as full-thickness retention sutures of No. 22 wire or heavy nylon. Evisceration carries a 10% mortality rate due both to contributing factors (eg, sepsis and cancer) and to resulting local infection.

Wound dehiscence without evisceration is best managed by prompt elective reclosure of the incision. If a partial disruption (ie, the skin is intact) is stable and the patient is a poor operative risk, treatment may be delayed and the resulting incisional hernia accepted. It is important in these patients that skin stitches not be removed before the end of the second postoperative week and that the abdomen be wrapped with a binder or corset to prevent further enlargement of the fascial defect or sudden disruption of the covering skin. When partial dehiscence is discovered during treatment of a wound infection, repair should be delayed if possible until the infection has been controlled, the wound has healed, and 6-7 months have elapsed. In these cases, antibiotics specific for the organisms isolated from the previous wound infection must be given at the time of hernia repair.

Recurrence of evisceration after reclosure of disrupted wounds is rare, though incisional hernias are later found in about 20% of such patientsusually those with wound infection in addition to dehiscence.

Miscellaneous Problems of the Operative Wound

Every new operative wound is painful, but those subject to continuous motion (eg, incisions that cross the costal margin) may be more painful than others. In general, the pain of an operative wound decreases substantially during the first 4-6 postoperative days. Chronic pain localized to one portion of an apparently healed wound may indicate the presence of a stitch abscess, a granuloma, or an occult incisional hernia. Abnormalities on examination of the wound usually allow for easy diagnosis; when this is difficult, ultrasound scanning may help detect a fascial defect or a collection of fluid associated with granulomas or abscesses. Rarely, a neuroma in the wound is responsible for focal pain and tenderness late in the postoperative course. Persistent localized pain is best treated by exploring the area, usually under local anesthesia, and removing a stitch, draining an abscess, or closing a hernia defect. Small sinus tracts usually result from stitch abscesses. The infected stitch can usually be removed with a clamp or crochet hook passed down the tract. If drainage continues, it is occasionally necessary to reopen the skin for better exposure and to remove a series of infected stitches.

Patients with ascites are at risk of fluid leak through the wound. Left untreated, ascitic leaks increase the incidence of wound infection and, through retrograde contamination, may result in peritonitis. Prevention in susceptible patients involves closing at least one layer of the wound with a continuous suture and taking measures to avoid the accumulation of ascites postoperatively. If an ascitic leak develops, the wound should be explored and the fascial defect closed. The rest of the wound, including the skin, should also be closed.

RESPIRATORY COMPLICATIONS

Respiratory complications are the most common single cause of morbidity after major surgical procedures and the second most common cause of postoperative deaths in patients older than 60 years. Patients undergoing chest and upper abdominal operations are particularly prone to pulmonary complications. The incidence is lower after pelvic surgery and even lower after extremity or head and neck procedures. Pulmonary complications are more common after emergency operations. Special hazards are posed by preexisting chronic obstructive pulmonary disease (chronic bronchitis, emphysema, asthma, pulmonary fibrosis). Elderly patients are at much higher risk because they have decreased compliance, increased closing and residual volumes, and increased dead space, all of which predispose to atelectasis.

Atelectasis

Atelectasis, the most common pulmonary complication, affects 25% of patients who have abdominal surgery. It is more common in patients who are elderly or overweight and in those who smoke or have symptoms of respiratory disease. It appears most frequently in the first 48 hours after operation and is responsible for over 90% of febrile episodes during that period. In most cases, the course is self-limited and recovery uneventful.

The pathogenesis of atelectasis involves obstructive and nonobstructive factors. Obstruction may be caused by secretions resulting from chronic obstructive pulmonary disease, intubation, or anesthetic agents. Occasional cases may be due to blood clots or malposition of the endotracheal tube. In most instances, however, the cause is not obstruction but closure of the bronchioles. Small bronchioles (1 mm) are prone to close when lung volume reaches a critical point (closing volume). Portions of the lung that are dependent or compressed are the first to experience bronchiole closure since their regional volume is less than that of nondependent portions. Shallow breathing and failure to periodically hyperinflate the lung result in small alveolar size and decreased volume. The closing volume is higher in older patients and in smokers owing to the loss of elastic recoil of the lung. Other nonobstructive factors contributing to atelectasis include decreased functional residual capacity and loss of pulmonary surfactant.

The air in the atelectatic portion of the lung is absorbed, and since there is minimal change in perfusion, a ventilation/perfusion mismatch results. The immediate effect of atelectasis is decreased oxygenation of blood; its clinical significance depends on the respiratory and cardiac reserve of the patient. A later effect is the propensity of the atelectatic segment to become infected. In general, if a pulmonary segment remains atelectatic for over 72 hours, pneumonia is almost certain to occur.

Atelectasis is usually manifested by fever (pathogenesis unknown), tachypnea, and tachycardia. Physical examination may show elevation of the diaphragm, scattered rales, and decreased breath sounds, but it is often normal. Postoperative atelectasis can be largely prevented by early mobilization, frequent changes in position, encouragement to cough, and use of an incentive spirometer. Preoperative teaching of respiratory exercises and postoperative execution of these exercises prevents atelectasis in patients without preexisting lung disease. Intermittent positive pressure breathing is expensive and less effective than these simpler exercises.

Treatment consists of clearing the airway by chest percussion, coughing, or nasotracheal suction. Bronchodilators and mucolytic agents given by nebulizer may help in patients with severe chronic obstructive pulmonary disease. Atelectasis from obstruction of a major airway may require intrabronchial suction through an endoscope, a procedure that can usually be performed at the bedside with mild sedation.

Pulmonary Aspiration

Aspiration of oropharyngeal and gastric contents is normally prevented by the gastroesophageal and pharyngoesophageal sphincters. Insertion of nasogastric and endotracheal tubes and depression of the central nervous system by drugs interfere with these defenses and predispose to aspiration. Other factors, such as gastroesophageal reflux, food in the stomach, or position of the patient, may play a role. Trauma victims are particularly likely to aspirate regurgitated gastric contents when consciousness is depressed. Patients with intestinal obstruction and pregnant women who have increased intra-abdominal pressure and decreased gastric motility are also at high risk of aspiration. Two-thirds of cases of aspiration follow thoracic or abdominal surgery, and of these, one-half result in pneumonia. The death rate for grossly evident aspiration and subsequent pneumonia is about 50%.

Minor amounts of aspiration are frequent during surgery and are apparently well tolerated. Methylene blue placed in the stomach of patients undergoing abdominal operations can be found in the trachea at completion of the procedure in 15% of cases. Radionuclide techniques have shown aspiration of gastric contents in 45% of normal volunteers during sleep.

The magnitude of pulmonary injury produced by aspiration of fluid, usually from gastric contents, is determined by the volume aspirated, its pH, and the frequency of the event. If the aspirate has a pH of 2.5 or less, it causes immediate chemical pneumonitis, which results in local edema and inflammation, changes that increase the risk of secondary infection. Aspiration of solid matter can produce airway obstruction. Obstruction of distal bronchi, though well tolerated initially, can lead to atelectasis and pulmonary abscess formation. The basal segments are affected most often. Tachypnea, rales, and hypoxia are usually present within hours; less frequently, cyanosis, wheezing, and apnea may appear. In patients with massive aspiration, hypovolemia caused by excessive fluid and colloid loss into the injured lung may lead to hypotension and shock.

Aspiration has been found in 80% of patients with tracheostomies and may account for the predisposition to pulmonary infection in this group. Patients who must remain intubated for long periods should have a low-pressure, high-volume type of cuff on their tube, as this helps to prevent aspiration and limits the risk of pressure necrosis of the trachea.

Aspiration can be prevented by preoperative fasting, proper positioning of the patient, and careful intubation. A single dose of cimetidine before induction of anesthesia may be of value in situations where the risk of aspiration is high. Treatment of aspiration involves reestablishing patency of the airway and preventing further damage to the lung. Endotracheal suction should be performed immediately, as this procedure confirms the diagnosis and stimulates coughing, which helps to clear the airway. Bronchoscopy may be required to remove solid matter. Fluid resuscitation should be undertaken concomitantly. Antibiotics are used initially when the aspirate is heavily contaminated; they are used later to treat pneumonia.

Postoperative Pneumonia

Pneumonia is the most common pulmonary complication among patients who die after surgery. It is directly responsible for deathor is a contributory factorin more than half of these patients. Patients with peritoneal infection and those requiring prolonged ventilatory support are at highest risk for developing postoperative pneumonia. Atelectasis, aspiration, and copious secretions are important predisposing factors.

Host defenses against pneumonitis include the cough reflex, the mucociliary system, and the activity of alveolar macrophages. After surgery, cough is usually weak and may not effectively clear the bronchial tree. The mucociliary transport mechanism is damaged by endotracheal intubation, and the functional ability of the alveolar macrophage is compromised by a number of factors that may be present during and after surgery (oxygen, pulmonary edema, aspiration, corticosteroid therapy, etc). In addition, squamous metaplasia and loss of ciliary coordination further hamper antibacterial defenses. More than half of the pulmonary infections that follow surgery are caused by gram-negative bacilli. They are frequently polymicrobial and usually acquired by aspiration of oropharyngeal secretions. Although colonization of the oropharynx with gram-negative bacteria occurs in only 20% of normal individuals, it is frequent after major surgery as a result of impaired oropharyngeal clearing mechanisms. Aggravating factors are azotemia, prolonged endotracheal intubation, and severe associated infection.

Occasionally, infecting bacteria reach the lung by inhalationeg, from respirators. Pseudomonas aeruginosa and klebsiella can survive in the moist reservoirs of these machines, and these pathogens have been the source of epidemic infections in intensive care units. Rarely, contamination of the lung may result from direct hematogenous spread from distant septic foci.

The clinical manifestations of postoperative pneumonia are fever, tachypnea, increased secretions, and physical changes suggestive of pulmonary consolidation. A chest x-ray usually shows localized parenchymal consolidation. Overall mortality rates for postoperative pneumonia vary from 20% to 40%. Rates are higher when pneumonia develops in patients who had emergency operations; are on respirators; or develop remote organ failure, positive blood cultures, or infection of the second lung.

Maintaining the airway clear of secretions is of paramount concern in the prevention of postoperative pneumonia. Respiratory exercises, deep breathing, and coughing help prevent atelectasis, which is a precursor of pneumonia. Although postoperative pain is thought to contribute to shallow breathing, neither intercostal blocks nor epidural narcotics prevent atelectasis and pneumonia when compared with traditional methods of postoperative pain control. The prophylactic use of antibiotics does not decrease the incidence of gram-negative colonization of the oropharynx or that of pneumonia. Treatment consists of measures to aid the clearing of secretions and administration of antibiotics. Sputum obtained directly from the trachea, usually by endotracheal suctioning, is required for specific identification of the infecting organism.

Postoperative Pleural Effusion & Pneumothorax

Formation of a very small pleural effusion is fairly common immediately after upper abdominal operations and is of no clinical significance. Patients with free peritoneal fluid at the time of surgery and those with postoperative atelectasis are more prone to develop effusions. In the absence of cardiac failure or a pulmonary lesion, appearance of a pleural effusion late in the postoperative course suggests the presence of subdiaphragmatic inflammation (subphrenic abscess, acute pancreatitis, etc). Effusions that do not compromise respiratory function should be left undisturbed. If there is a suspicion of infection, the effusion should be sampled by needle aspiration. When an effusion produces respiratory compromise, it should be drained with a thoracostomy tube.

Postoperative pneumothorax may follow insertion of a subclavian catheter or positive-pressure ventilation, but it sometimes appears after an operation during which the pleura has been injured (eg, nephrectomy or adrenalectomy). Pneumothorax should be treated with a thoracostomy tube.

FAT EMBOLISM

Fat embolism is relatively common but only rarely causes symptoms. Fat particles can be found in the pulmonary vascular bed in 90% of patients who have had fractures of long bones or joint replacements. Fat embolism can also be caused by exogenous sources of fat, such as blood transfusions, intravenous fat emulsion, or bone marrow transplantation. Fat embolism syndrome consists of neurologic dysfunction, respiratory insufficiency, and petechiae of the axillae, chest, and proximal arms. It was originally described in trauma victimsespecially those with long bone fracturesand was thought to be a result of bone marrow embolization. However, the principal clinical manifestations of fat embolism are seen in other conditions. The existence of fat embolism as an entity distinct from posttraumatic pulmonary insufficiency has been questioned.

Fat embolism syndrome characteristically begins 12-72 hours after injury but may be delayed for several days. The diagnosis is clinical. The finding of fat droplets in sputum and urine is common after trauma and is not specific. Decreased hematocrit, thrombocytopenia, and other changes in coagulation parameters are usually seen.

Once symptoms develop, supportive treatment should be provided until respiratory insufficiency and central nervous system manifestations subside. Respiratory insufficiency is treated with positive end-expiratory pressure ventilation and diuretics. The prognosis is related to the severity of the pulmonary insufficiency.

CARDIAC COMPLICATIONS

Cardiac complications following surgery may be life-threatening. Their incidence is reduced by appropriate preoperative preparation.

Dysrhythmias, unstable angina, heart failure, or severe hypertension should be corrected before surgery whenever possible. Valvular diseaseespecially aortic stenosislimits the ability of the heart to respond to increased demand during operation or in the immediate postoperative period. When aortic stenosis is recognized preoperativelyand assuming that the patient is monitored adequately (Swan-Ganz catheterization, central venous pressure, etc)the incidence of major perioperative complications is small. Thus, patients with preexisting heart disease should be evaluated by a cardiologist preoperatively. Determination of cardiac function, including indirect evaluation of the left ventricular ejection fraction, identifies patients at higher risk for cardiac complications. Continuous electrocardiographic monitoring during the first 3-4 postoperative days detects episodes of ischemia or dysrhythmia in about a third of these patients. Oral anticoagulant drugs should be stopped 3-5 days before surgery, and the prothrombin time should be allowed to return to normal. Patients at high risk for thromboembolic disease should receive heparin until approximately 6 hours before the operation, when heparin should be stopped. If needed, heparin can be restarted 3648 hours after surgery along with oral anticoagulation.

General anesthesia depresses the myocardium, and some anesthetic agents predispose to dysrhythmias by sensitizing the myocardium to catecholamines. Monitoring of cardiac activity and blood pressure during the operation detects dysrhythmias and hypotension early. In patients with a high cardiac risk, regional anesthesia may be safer than general anesthesia for procedures below the umbilicus.

The duration and urgency of the operation and uncontrolled bleeding with hypotension have been individually shown to correlate positively with the development of serious postoperative cardiac problems. In patients with pacemakers, the electrocautery current may be sensed by the intracardiac electrode, causing inappropriate pacemaker function.

Noncardiac complications may affect the development of cardiac complications by increasing cardiac demands in patients with a limited reserve. Postoperative sepsis and hypoxemia are foremost. Fluid overload can produce acute left ventricular failure. Patients with coronary artery disease, dysrhythmias, or low cardiac output should be monitored postoperatively in an intensive care unit.

Dysrhythmias

Most dysrhythmias appear during the operation or within the first 3 postoperative days. They are especially likely to occur after thoracic procedures.

A. Intraoperative Dysrhythmias

The overall incidence of intraoperative cardiac dysrhythmias is 20%; most are self-limited. The incidence is higher in patients with preexisting dysrhythmias and in those with known heart disease (35%). About one-third of dysrhythmias occur during induction of anesthesia. These dysrhythmias are usually related to anesthetic agents (eg, halothane, cyclopropane), sympathomimetic drugs, digitalis toxicity, and hypercapnia.

B. Postoperative Dysrhythmias

These dysrhythmias are generally related to reversible factors such as hypokalemia, hypoxemia, alkalosis, digitalis toxicity, and stress during emergence from anesthesia. Occasionally, postoperative dysrhythmias may be the first sign of myocardial infarction. Most postoperative dysrhythmias are asymptomatic, but occasionally the patient complains of chest pain, palpitations, or dyspnea.

Supraventricular dysrhythmias usually have few serious consequences but may decrease cardiac output and coronary blood flow. Patients with atrial flutter or fibrillation with a rapid ventricular response and who are in shock require cardioversion. If they are hemodynamically stable, they should have the heart rate controlled with digitalis, beta-blockers, or calcium channel blockers. Associated hypokalemia should be treated promptly.

Ventricular premature beats are often precipitated by hypercapnia, hypoxemia, pain, or fluid overload. They should be treated with oxygen, sedation, analgesia, and correction of fluid losses or electrolyte abnormalities. Ventricular dysrhythmias have a more profound effect on cardiac function than supraventricular dysrhythmias and may lead to fatal ventricular fibrillation. Immediate treatment is with lidocaine, 1 mg/kg intravenously as a bolus, repeated as necessary to a total dose of 250 mg, followed by a slow intravenous infusion at a rate of 12 mg/min. Higher doses of lidocaine may cause seizures.

Postoperative complete heart block is usually due to serious cardiac disease and calls for the immediate insertion of a pacemaker. First- or second-degree heart block is usually well tolerated.

Postoperative Myocardial Infarction

Approximately 0.4% of all patients undergoing an operation in the USA develop postoperative myocardial infarction. The incidence increases to 5-12% in patients undergoing operations for other manifestations of atherosclerosis (eg, carotid endarterectomy, aortoiliac graft). Other important risk factors include preoperative congestive heart failure, ischemia identified on dipyridamole-thallium scan or treadmill exercise test, and age over 70 years. In selected patients with angina, consideration should be given to coronary revascularization before proceeding with a major elective operation on another organ.

Postoperative myocardial infarction may be precipitated by factors such as hypotension or hypoxemia. Clinical manifestations include chest pain, hypotension, and cardiac dysrhythmias. Over half of postoperative myocardial infarctions, however, are asymptomatic. The absence of symptoms is thought to be due to the residual effects of anesthesia and to analgesics administered postoperatively.

Diagnosis is substantiated by electrocardiographic changes, elevated serum creatine kinase levelsespecially the MB isoenzymeand serum troponin I levels. The mortality rate of postoperative myocardial infarction is as high as 67% in high-risk groups. The prognosis is better if it is the first infarction and worse if there have been previous infarctions. Prevention of this complication includes postponing elective operations for 3 months or preferably 6 months after myocardial infarction, treating congestive heart failure preoperatively, and controlling hypertension perioperatively.

Patients with postoperative myocardial infarction should be monitored in the intensive care unit and provided with adequate oxygenation and precise fluid and electrolyte replacement. Anticoagulation, though not always feasible after major surgery, prevents the development of mural thrombosis and arterial embolism after myocardial infarction. Congestive heart failure should be treated with digitalis, diuretics, and vasodilators as needed.

Postoperative Cardiac Failure

Left ventricular failure and pulmonary edema appear in 4% of patients over age 40 undergoing general surgical procedures with general anesthesia. Fluid overload in patients with limited myocardial reserve is the most common cause. Postoperative myocardial infarction and dysrhythmias producing a high ventricular rate are other causes. Clinical manifestations are progressive dyspnea, hypoxemia with normal CO2 tension, and diffuse congestion on chest x-ray.

Clinically inapparent ventricular failure is frequent, especially when other factors predisposing to pulmonary edema are present (massive trauma, multiple transfusions, sepsis, etc). The diagnosis may be suspected from a decreased Pao2, abnormal chest x-ray, or elevated pulmonary artery wedge pressure. The treatment of left ventricular failure depends on the hemodynamic state of the patient. Those who are in shock require transfer to the intensive care unit, placement of a pulmonary artery line, monitoring of filling pressures, and immediate pre- and afterload reduction. Preload reduction is achieved by diuretics (and nitroglycerin if needed); afterload reduction, by administration of sodium nitroprusside. Patients who are not in shock may, instead, be digitalized. Rapid digitalization (eg, divided intravenous doses of digoxin to a total of 11.5 mg over 24 hours, with careful monitoring of the serum potassium level), fluid restriction, and diuretics may be enough in these cases. Fluids should be restricted, and diuretics may be given. Respiratory insufficiency calls for ventilatory support with endotracheal intubation and a mechanical respirator. Although pulmonary function may improve with the use of positive end-expiratory pressure, hemodynamic derangements and decreased myocardial reserve preclude it in most cases.

PERITONEAL COMPLICATIONS

Hemoperitoneum

Bleeding is the most common cause of shock in the first 24 hours after abdominal surgery. Postoperative hemoperitoneuma rapidly evolving, life-threatening complicationis usually the result of a technical problem with hemostasis, but coagulation disorders may play a role. For example, many of these patients have experienced substantial intraoperative blood loss, and several transfusions have been already given. As a consequence, changes usually observed after transfusion, such as thrombocytopenia, may be present. Other causes of coagulopathy such as mismatched transfusion, administration of heparin, etc, should also be considered. In these cases, bleeding tends to be more generalized, occurring in the wound, venipuncture sites, etc.

Hemoperitoneum usually becomes apparent within 24 hours after the operation. Its manifestations are those of intravascular hypovolemia: tachycardia, decreased blood pressure, decreased urine output, and peripheral vasoconstriction. If bleeding continues, abdominal girth may increase. Changes in the hematocrit are usually not obvious for 46 hours and are of limited diagnostic help in patients who sustain rapid blood loss.

The manifestations may be so subtle that the diagnosis is overlooked. Only a high index of suspicion, frequent examination of patients at risk, and a systematic investigation of patients with postoperative hypotension will result in early recognition of the problem. Preexisting disease and drugs taken before surgery as well as those administered during the operation may cause hypotension. The differential diagnosis of immediate postoperative circulatory collapse also includes pulmonary embolism, cardiac dysrhythmias, pneumothorax, myocardial infarction, and severe allergic reactions. Infusions to expand the intravascular volume should be started as soon as other diseases have been ruled out. If hypotension or other signs of hypovolemia persist, one must reoperate promptly. At operation, bleeding should be stopped, clots evacuated, and the peritoneal cavity rinsed with saline solution.

Complications of Drains

Postoperative drainage of the peritoneal cavity is indicated to prevent fluid accumulation such as bile or pancreatic fluid or to treat established abscesses. Drains may be left to evacuate small amounts of blood, but drain output cannot be used to provide a reliable estimate of the rate of bleeding. The use of drains in operations not expected to have fluid leaks (such as cholecystectomy, splenectomy, and colectomy) increases the rate of postoperative intra-abdominal and wound infection. Latex Penrose drains, which were once popular, should be avoided because of the risk of introducing infection. Large rigid drains may erode into adjacent viscera or vessels and cause fistula formation or bleeding. This risk is lessened with the use of softer Silastic drains, and removing them as early as possible. Drains should not be left in contact with intestinal anastomoses, as they promote anastomotic leakage and fistula formation.

POSTOPERATIVE PAROTITIS

Postoperative parotitisa rare but serious staphylococcal infection of the parotid glandis limited almost entirely to elderly, debilitated, malnourished patients with poor oral hygiene. It appears in the second postoperative week and is associated with prolonged nasogastric intubation. The triggering factors are dehydration and poor oral hygiene, and the pathogenesis consists of a decrease in the secretory activity of the gland with inspissation of parotid secretions that become infected by staphylococci or gram-negative bacteria from the oral cavity. This results in inflammation, accumulation of cells that obstruct large and medium-sized ducts, and, eventually, formation of multiple small abscesses. These lobular abscesses, separated by fibrous bands, may dissect through the capsule and spread to the periglandular tissues to involve the auditory canal, the superficial skin, and the neck. If the disease is not treated at this stage, it may produce acute respiratory failure from tracheal obstruction.

Clinically, parotitis first appears as pain or tenderness at the angle of the jaw. With progression, high fever and leukocytosis develop, and there is swelling and redness in the parotid area. The parotid usually feels firm, and even after abscesses have formed, fluctuance is uncommon.

Prophylaxis includes adequate fluid intake, avoiding the use of anticholinergics, minimizing trauma during intubation, and, most importantly, good oral hygiene (frequent gargles, mouth irrigation, and other mouth cleansing and moistening measures). Stimulation of salivary flow with chewing gum, hard candy, etc, may also be useful. Routine observance of these simple preventive measures has virtually eliminated parotitis, which was once a common postoperative complication.

When signs of acute parotitis appear, fluid obtained from Stensen's duct by gentle compression of the gland should be cultured. Vancomycin should be started while the results of cultures are awaited. Warm moist packs and mouth irrigations may be helpful. In most instances, the disease responds promptly to these measures. If the disease progresses, the parotid must be surgically drained. The procedure consists of elevating a skin flap over the gland and making multiple small incisions parallel to the branches of the facial nerve. The wound is then packed open.

COMPLICATIONS CAUSED BY POSTOPERATIVE ALTERATIONS OF GASTROINTESTINAL MOTILITY

The presence, strength, and direction of normal peristalsis are governed by the enteric nervous system. Anesthesia and surgical manipulation result in a decrease of the normal propulsive activity of the gut, or postoperative ileus. Several factors worsen ileus or prolong its course. These include medicationsespecially opioidselectrolyte abnormalities, inflammatory conditions such as pancreatitis or peritonitis, and pain. The degree of ileus is related to the extent of operative manipulation.

Gastrointestinal peristalsis returns within 24 hours after most operations that do not involve the abdominal cavity. In general, laparoscopic approaches cause less ileus than open procedures. After laparotomy, gastric peristalsis returns in about 48 hours. Colonic activity returns after 48 hours, starting at the cecum and progressing caudally. The motility of the small intestine is affected to a lesser degree, except in patients who have had small bowel resection or who were operated on to relieve bowel obstruction. Normal postoperative ileus leads to slight abdominal distention and absent bowel sounds. Return of peristalsis is often noted by the patient as mild cramps, passage of flatus, and return of appetite. Feedings should be withheld until there is evidence of return of normal gastrointestinal motility. There is no specific therapy for postoperative ileus.

Gastric Dilation

Gastric dilation, a rare life-threatening complication, consists of massive distention of the stomach by gas and fluid. Predisposing factors include asthma, recent surgery, gastric outlet obstruction, and absence of the spleen. Infants and children in whom oxygen masks are used in the immediate postoperative period and adults subjected to forceful assisted respiration during resuscitation are also at risk. Occasionally, gastric dilation develops in patients with anorexia nervosa or during serious illnesses without a specific intercurrent event.

As the air-filled stomach grows larger, it hangs down across the duodenum, producing a mechanical gastric outlet obstruction that contributes further to the problem. The increased intragastric pressure produces venous obstruction of the mucosa, causing mucosal engorgement and bleeding and, if allowed to continue, ischemic necrosis and perforation. The distended stomach pushes the diaphragm upward, which causes collapse of the lower lobe of the left lung, rotation of the heart, and obstruction of the inferior vena cava. The acutely dilated stomach is also prone to undergo volvulus.

The patient appears ill, with abdominal distention and hiccups. Hypochloremia, hypokalemia, and alkalosis may result from fluid and electrolyte losses. When the problem is recognized early, treatment consists of gastric decompression with a nasogastric tube. In the late stage, gastric necrosis may require gastrectomy.

Bowel Obstruction

Failure of postoperative return of bowel function may be the result of paralytic ileus or mechanical obstruction. Mechanical obstruction is most often caused by postoperative adhesions or an internal (mesenteric) hernia. Most of these patients experience a short period of apparently normal intestinal function before manifestations of obstruction supervene. About half of cases of early postoperative small bowel obstruction follow colorectal surgery.

Diagnosis may be difficult because the symptoms are difficult to differentiate from those of paralytic ileus. If plain films of the abdomen show air-fluid levels in loops of small bowel, mechanical obstruction is a more likely diagnosis than ileus. Enteroclysis or an ordinary small bowel series with barium sulfate may aid diagnosis.

Strangulation is uncommon because the adhesive bands are broader and less rigid than is typical of late small bowel obstruction. The death rate is high (about 15%), however, probably because of delay in diagnosis and the postoperative state. Treatment consists of nasogastric suction for several days and, if the obstruction does not resolve spontaneously, laparotomy.

Small bowel intussusception is an uncommon cause of early postoperative obstruction in adults but accounts for 10% of cases in the pediatric age group. Ninety percent of postoperative intussusceptions occur during the first 2 postoperative weeks, and more than half in the first week. Unlike idiopathic ileocolic intussusception, most postoperative intussusceptions are ileoileal or jejunojejunal. They most often follow retroperitoneal and pelvic operations. The cause is unknown. The symptom complex is not typical, and x-ray studies are of limited help. The physician should be aware that intussusception is a possible explanation for vomiting, distention, and abdominal pain after laparotomy in children and that early reoperation will avoid the complications of perforation and peritonitis. Operation is the only treatment, and if the bowel is viable, reduction of the intussusception is all that is needed.

Postoperative Fecal Impaction

Fecal impaction after operative procedures is the result of colonic ileus and impaired perception of rectal fullness. It is principally a disease of the elderly but may occur in younger patients who have predisposing conditions such as megacolon or paraplegia. Postoperative ileus and the use of opioid analgesics and anticholinergic drugs are aggravating factors. Early manifestations are anorexia and obstipation or diarrhea. In advanced cases, marked distention may cause colonic perforation. The diagnosis of postoperative fecal impaction is made by rectal examination. The impaction should be manually removed, enemas given, and digital examination then repeated.

Barium remaining in the colon from an examination done before surgery may harden and produce barium impaction. This usually occurs in the right colon, where most of the water is absorbed, and is a more difficult management problem than fecal impaction. The clinical manifestations are those of bowel obstruction. Treatment includes enemas and purgation with polyethylene glycol-electrolyte solution (eg, CoLyte, GoLYTELY). Diatrizoate sodium (Hypaque), a hyperosmolar solution that stimulates peristalsis and increases intraluminal fluid, may be effective by enema if other solutions fail. Operation is rarely needed.

POSTOPERATIVE PANCREATITIS

Postoperative pancreatitis accounts for 10% of all cases of acute pancreatitis. It occurs in 13% of patients who have operations in the vicinity of the pancreas, and with higher frequency after operations on the biliary tract. For example, pancreatitis occurs in about 1% of patients undergoing cholecystectomy and in 8% of patients undergoing common bile duct exploration. In the latter cases, it does not appear to be related to the performance of intraoperative cholangiograms or choledochoscopy. Postoperative pancreatitis after biliary surgery is worse in patients who have had biliary pancreatitis preoperatively. Pancreatitis occasionally occurs following cardiopulmonary bypass, parathyroid surgery, and renal transplantation. Postoperative pancreatitis is frequently of the necrotizing type. Infected pancreatic necrosis and other complications of pancreatitis develop with a frequency three to four times greater than in biliary and alcoholic pancreatitis. The reason postoperative pancreatitis is so severe is unknown, but the mortality rate is 3040%.

The pathogenesis in most cases appears to be mechanical trauma to the pancreas or its blood supply. Nevertheless, manipulation, biopsy, and partial resection of the pancreas are usually well tolerated, so the reasons that some patients develop pancreatitis are unclear. Prevention of this complication includes careful handling of the pancreas and avoidance of forceful dilation of the choledochal sphincter or obstruction of the pancreatic duct. The 2% incidence of pancreatitis following renal transplantation is probably related to special risk factors such as use of corticosteroids or azathioprine, secondary hyperparathyroidism, or viral infection. Acute changes in serum calcium are thought to be responsible for pancreatitis following parathyroid surgery. Hyperamylasemia develops in about half of patients undergoing heart surgery with extracorporeal bypass, but clinical evidence of pancreatitis is present in only 5% of these patients.

The diagnosis of postoperative pancreatitis may be difficult in patients who have recently had an abdominal operation. Hyperamylasemia may or may not be present. One must be alert to renal and respiratory complications and the consequences of necrotizing or hemorrhagic pancreatitis. Because of the high frequency with which complications develop, frequent monitoring of the pancreas and retroperitoneum with CT scans is useful.

POSTOPERATIVE HEPATIC DYSFUNCTION

Hepatic dysfunction, ranging from mild jaundice to life-threatening hepatic failure, follows 1% of surgical procedures performed under general anesthesia. The incidence is greater following pancreatectomy, biliary bypass operations, and portacaval shunt. Postoperative hyperbilirubinemia may be categorized as prehepatic jaundice, hepatocellular insufficiency, and posthepatic obstruction (Table 4-1).

Table 4-1. Causes of postoperative jaundice.

Prehepatic jaundice (bilirubin overload)Hemolysis (drugs, transfusions, sickle cell crisis)Reabsorption of hematomasHepatocellular insufficiencyViral hepatitisDrug-induced (anesthesia, others)Ischemia (shock, hypoxia, low-output states)SepsisLiver resection (loss of parenchyma)Others (total parenteral nutrition, malnutrition)Posthepatic obstruction (to bile flow)Retained stonesInjury to ductsTumor (unrecognized or untreated)CholecystitisPancreatitisOcclusion of biliary stents

Prehepatic Jaundice

Prehepatic jaundice is caused by bilirubin overload, most often from hemolysis or reabsorption of hematomas. Fasting, malnutrition, hepatotoxic drugs, and anesthesia are among the factors that impair the ability of the liver to excrete increased loads of bilirubin in the postoperative period.

Increased hemolysis may result from transfusion of incompatible blood but more often reflects destruction of fragile transfused red blood cells. Other causes include extracorporeal circulation, congenital hemolytic disease (eg, sickle cell disease), and effects of drugs.

Hepatocellular Insufficiency

Hepatocellular insufficiency, the most common cause of postoperative jaundice, occurs as a consequence of hepatic cell necrosis, inflammation, or massive hepatic resection. Drugs, hypotension, hypoxia, and sepsis are among the injurious factors. Although posttransfusion hepatitis is usually observed much later, this complication may occur as early as the third postoperative week.

Benign postoperative intrahepatic cholestasis is a vague term used to denote jaundice following operations that often involve hypotension and multiple transfusions. Serum bilirubin ranges from 2 to 20 mg/dL and serum alkaline phosphatase is usually high, but the patient is afebrile and postoperative convalescence is otherwise smooth. The diagnosis is one of exclusion. Jaundice clears by the third postoperative week.

Hepatocellular damage occasionally occurs after intestinal bypass procedures for morbid obesity. Cholestatic jaundice may develop in patients receiving total parenteral nutrition.

Posthepatic Obstruction

Posthepatic obstruction can be caused by direct surgical injury to the bile ducts, retained common duct stones, tumor obstruction of the bile duct, or pancreatitis. Acute postoperative cholecystitis is associated with jaundice in one-third of cases, though mechanical obstruction of the common duct is usually not apparent.

One must determine if a patient with postoperative jaundice has a correctable cause that requires treatment. This is particularly true for sepsis (when decreased liver function may sometimes be an early sign), lesions that obstruct the bile duct, and postoperative cholecystitis. Liver function tests are not helpful in determining the cause and do not usually reflect the severity of disease. Liver biopsy, ultrasound and CT scans, and transhepatic or endoscopic retrograde cholangiograms are the tests most likely to sort out the diagnostic possibilities. Renal function must be monitored closely, since renal failure may develop in these patients. Treatment is otherwise expectant.

POSTOPERATIVE CHOLECYSTITIS

Acute postoperative cholecystitis may follow any kind of operation but is more common after gastrointestinal procedures. Acute cholecystitis develops shortly after endoscopic sphincterotomy in 3-5% of patients. Chemical cholecystitis occurs in patients undergoing hepatic arterial chemotherapy with mitomycin and floxuridine with such frequency that cholecystectomy should always be performed before infusion of these agents is begun. Fulminant cholecystitis with gallbladder infarction may follow percutaneous embolization of the hepatic artery for malignant tumors of the liver or for arteriovenous malformation involving this artery.

Postoperative cholecystitis differs in several respects from the common form of acute cholecystitis: It is frequently acalculous (7080%), more common in males (75%), progresses rapidly to gallbladder necrosis, and is not likely to respond to conservative therapy. The cause is clear in cases of chemical or ischemic cholecystitis but not in other forms. Factors thought to play a role include biliary stasis (with formation of sludge), biliary infection, and ischemia.

CLOSTRIDIUM DIFFICILE COLITIS

Postoperative diarrhea due to Clostridium difficile is a common nosocomial infection in surgical patients. The spectrum of illness ranges from asymptomatic colonization torarelysevere toxic colitis. Transmission from hospital personnel probably occurs. The main risk factor is perioperative antibiotic use. The diagnosis is established by identification of a specific cytopathic toxin in the stool or culture of the organism from stool samples or rectal swabs. In severely affected patients, colonoscopy reveals pseudomembranes. Prevention is accomplished by strict handwashing, enteric precautions, and minimizing antibiotic use. Treatment of established infection is with intravenous metronidazole or, for infections with resistant pathogens, oral vancomycin.

URINARY COMPLICATIONS

Postoperative Urinary Retention

Inability to void postoperatively is common, especially after pelvic and perineal operations or operations conducted under spinal anesthesia. Factors responsible for postoperative urinary retention are interference with the neural mechanisms responsible for normal emptying of the bladder and overdistention of the urinary bladder. When its normal capacity of approximately 500 mL is exceeded, bladder contraction is inhibited. Prophylactic bladder catheterization should be performed whenever an operation is likely to last 3 hours or longer or when large volumes of intravenous fluids are anticipated. The catheter can be removed at the end of the operation if the patient is expected to be able to ambulate within a few hours. When bladder catheterization is not performed, the patient should be encouraged to void immediately before coming to the operating room and as soon as possible after the operation. During abdominoperineal resection, operative trauma to the sacral plexus alters bladder function enough so that an indwelling catheter should be left in place for 45 days. Patients with inguinal hernia who strain to void as a manifestation of prostatic hypertrophy should have the prostate treated before the hernia.

The treatment of acute urinary retention is catheterization of the bladder. In the absence of factors that suggest the need for prolonged decompression, such as the presence of 1000 mL of urine or more, the catheter may be removed.

Urinary Tract Infection

Infection of the lower urinary tract is the most frequently acquired nosocomial infection. Preexisting contamination of the urinary tract, urinary retention, and instrumentation are the principal contributing factors. Bacteriuria is present in about 5% of patients who undergo short-term (< 48 hours) bladder catheterization, though clinical signs of urinary tract infection occur in only 1%. Cystitis is manifested by dysuria and mild fever and pyelonephritis by high fever, flank tenderness, and, occasionally, ileus. Diagnosis is made by examination of the urine and confirmed by cultures. Prevention involves treating urinary tract contamination before surgery, prevention or prompt treatment of urinary retention, and careful instrumentation when needed. Treatment includes adequate hydration, proper drainage of the bladder, and specific antibiotics.

CENTRAL NERVOUS SYSTEM COMPLICATIONS

Postoperative Cerebrovascular Accidents

Postoperative cerebrovascular accidents are almost always the result of ischemic neural damage due to poor perfusion. They often occur in elderly patients with severe atherosclerosis who become hypotensive during or after surgery (from sepsis, bleeding, cardiac arrest, etc). Normal regulatory mechanisms of the cerebral vasculature can maintain blood flow over a wide range of blood pressures down to a mean pressure of about 55 mm Hg. Abrupt hypotension, however, is less well tolerated than a more gradual pressure change. Irreversible brain damage occurs after about 4 minutes of total ischemia.

Strokes occur in 1-3% of patients after carotid endarterectomy and other reconstructive operations of the extracranial portion of the carotid system. Embolization from atherosclerotic plaques, ischemia during carotid clamping, and postoperative thrombosis at the site of the arteriotomy or of an intimal flap are usually responsible. Aspirin, which inhibits platelet aggregation, may prevent immediate postoperative thrombosis.

Open heart surgery using extracorporeal circulation or deep cooling is also occasionally followed by stroke. The pathogenesis of stroke is thought to be related to hypoxemia, emboli, or poor perfusion. The presence of a carotid bruit preoperatively increases the risk of postoperative stroke after coronary bypass by a factor of 4. Previous stroke or transient ischemic attacks and postoperative atrial fibrillation also increase the risk. For patients undergoing noncardiac, noncarotid surgery, the risk of stroke is about 0.2%. Predictors of risk in these patients are the presence of cerebrovascular, cardiac, or peripheral vascular disease and arterial hypertension.

Seizures

Epilepsy, metabolic derangements, and medications may lead to seizures in the postoperative period. For unknown reasons, patients with ulcerative colitis and Crohn's disease are peculiarly susceptible to seizures with loss of consciousness after surgery. Seizures should be treated as soon as possible to minimize their harmful effects.

PSYCHIATRIC COMPLICATIONS

Anxiety and fear are normal in patients undergoing surgery. The degree to which these emotions are experienced depends upon diverse cultural and psychologic variables. Underlying depression or a history of chronic pain may serve to exaggerate the patient's response to surgery. The boundary between the normal manifestations of stress and postoperative psychosis is difficult to establish, since the latter is not really a distinct clinical entity.

Postoperative psychosis (so-called) develops in about 0.5% of patients having abdominal operations. It is more common after thoracic surgery, in the elderly, and in those with chronic disease. About half of these patients suffer from mood disturbances (usually severe depression). Twenty percent have delirium. Drugs given in the postoperative period may play a role in the development of psychosis; meperidine, cimetidine, and corticosteroids are most commonly implicated. Patients who develop postoperative psychosis have higher plasma levels of -endorphin and cortisol than those who do not. These patients also lose, temporarily, the normal circadian rhythms of -endorphin and cortisol. Specific psychiatric syndromes may follow specific procedures, such as visual hallucinations and the black patch syndrome after ophthalmic surgery. Preexisting psychiatric disorders not apparent before the operation sometimes contribute to the motivation for surgery (eg, circumcision or cosmetic operations in schizophrenics).

Clinical manifestations are rare on the first postoperative day. During this period, patients appear emotionless and unconcerned about changes in the environment or in themselves. Most overt psychiatric derangements are observed after the third postoperative day. The symptoms are variable but often include confusion, fear, and disorientation as to time and place. Delirium presents as altered consciousness with cognitive impairment. These symptoms may not be readily apparent to the surgeon, as this problem usually occurs in sick patients whose other problems may mask the manifestations of psychosis. Early psychiatric consultation should be obtained when psychosis is suspected so that adequate and prompt assessment of consciousness and cognitive function can be done and treatment instituted. The earlier the psychosis is recognized, the easier it is to correct. Metabolic derangements or early sepsis (especially in burn patients) must be ruled out as the cause. Severe postoperative emotional disturbances may be avoided by appropriate preoperative counseling of the patient by the surgeon. This includes a thorough discussion of the operation and the expected outcome, acquainting the patient with the intensive care unit, etc. Postoperatively, the surgeon must attend to the patient's emotional needs, offering frequent reassurance, explaining the postoperative course, and discussing the prognosis and the outcome of the operation.

Special Psychiatric Problems

A. The ICU Syndrome

The continuous internal vigilance that results from pain and fear and the sleep deprivation from bright lights, monitoring equipment, and continuous noise causes a psychologic disorganization known as ICU psychosis. The patient whose level of consciousness is already decreased by illness and drugs is more susceptible than a normal individual, and the result is decreased ability to think, perceive, and remember. When the cognitive processes are thoroughly disorganized, delirium occurs. The manifestations include distorted visual, auditory, and tactile perception; confusion and restlessness; and inability to differentiate reality from fantasy. Prevention includes isolation from the environment, decreased noise levels, adequate sleep, and removal from the intensive care unit as soon as possible.

B. Postcardiotomy Delirium

Mental changes that occasionally follow open heart surgery include impairment of memory, attention, cognition, and perception and occasionally hysteria, depressive reaction, and anxiety crisis. The symptoms most often appear after the third postoperative day. The type of operation, the presence of organic brain disease, prolonged medical illness, and the length of time on extracorporeal circulation are related to the development of postcardiotomy psychosis. Mild sedation and measures to prevent the ICU syndrome may prevent this complication. In more severe cases, haloperidol (Haldol) in doses of 15 mg given orally, intramuscularly, or intravenously may be required. Haloperidol is preferred over phenothiazines in these patients because it is associated with a lower incidence of cardiovascular side effects.

C. Delirium Tremens

Delirium tremens occurs in alcoholics who stop drinking suddenly. Hyperventilation and metabolic alkalosis contribute to the development of the full-blown syndrome. Hypomagnesemia and hypokalemia secondary to alkalosis or nutritional deficits may precipitate seizures. Readaptation to ethanol-free metabolism requires about 2 weeks, and it is during this period that alcoholics are at greatest risk of developing delirium tremens.

The prodrome includes personality changes, anxiety, and tremor. The complete syndrome is characterized by agitation, hallucinations, restlessness, confusion, overactivity, and, occasionally, seizures and hyperthermia. The syndrome also causes a hyperdynamic cardiorespiratory and metabolic state. For example, cardiac index, oxygen delivery, and oxygen consumption double during delirium tremens and return to normal 2448 hours after resolution. The wild behavior may precipitate dehiscence of a fresh laparotomy incision. Diaphoresis and dehydration are common, and exhaustion may herald death.

Withdrawal symptoms may be prevented by giving small amounts of alcohol, but benzodiazepines are the treatment of choice. Vitamin B1 (thiamine) and magnesium sulfate should also be given.

The aims of treatment are to reduce agitation and anxiety as soon as possible and to prevent the development of other complications (eg, seizures, aspiration pneumonia). General measures should include frequent assessment of vital signs, restoration of nutrition, administration of vitamin B, correction of electrolyte imbalance or other metabolic derangements, and adequate hydration. Physical restraint, though necessary for seriously violent behavior, should be as limited as possible. With proper care, most patients improve within 72 hours.

D. Sexual Dysfunction

Sexual problems commonly occur after certain kinds of operations, such as prostatectomy, heart surgery, and aortic reconstruction. The pathogenesis is unclear. In abdominoperineal resection, severance of the peripheral branches of the sacral plexus may cause impotence. It is important to discuss this possibility with the patient before any operation with a risk of impotence is performed. When sexual dysfunction is psychogenic, reassurance is usually all that is needed. If psychogenic impotence persists beyond 46 weeks, psychiatric consultation is indicated.

COMPLICATIONS OF INTRAVENOUS THERAPY & HEMODYNAMIC MONITORING

Air Embolism

Air embolism may occur during or after insertion of a venous catheter or as a result of accidental introduction of air into the line. Intravenous air lodges in the right atrium, preventing adequate filling of the right heart. This is manifested by hypotension, jugular venous distention, and tachycardia. This complication can be avoided by placing the patient in the Trendelenburg position when a central venous line is inserted. Emergency treatment consists of aspiration of the air with a syringe. If this is unsuccessful, the patient should be positioned right side up and head down, which will help dislodge the air from the right atrium and return circulatory dynamics to normal.

Phlebitis

A needle or a catheter inserted into a vein and left in place will in time cause inflammation at the entry site. When this process involves the vein, it is called phlebitis. Factors determining the degree of inflammation are the nature of the cannula, the solution infused, bacterial infection, and venous thrombosis. Phlebitis is one of the most common causes of fever after the third postoperative day. The symptomatic triad of induration, edema, and tenderness is characteristic. Visible signs may be minimal. Prevention of phlebitis is best accomplished by observance of aseptic techniques during insertion of venous catheters, frequent change of tubing (ie, every 4872 hours), and rotation of insertion sites (ie, every 4 days). Silastic catheters, which are the least reactive, should be used when the line must be left in for a long time. Hypertonic solutions should be infused only into veins with substantial flow, such as the subclavian, jugular, or vena cava. Venous catheters should be removed at the first sign of redness, induration, or edema. Because phlebitis is most frequent with cannulation of veins in the lower extremities, this route should be used only when upper extremity veins are unavailable. Removal of the catheter is adequate treatment.

Suppurative phlebitis may result from the presence of an infected thrombus around the indwelling catheter. Staphylococci are the most common causative organisms. Local signs of inflammation are present, and pus may be expressed from the venipuncture site. High fever and positive blood cultures are common. Treatment consists of excising the affected vein, extending the incision proximally to the first open collateral, and leaving the wound open.

Cardiopulmonary Complications

Perforation of the right atrium with cardiac tamponade has been associated with the use of central venous lines. This complication can be avoided by checking the position of the tip of the line, which should be in the superior vena cava, not the right atrium. Complications associated with the use of the flow-directed balloon-tipped (Swan-Ganz) catheter include cardiac perforation (usually of the right atrium), intracardiac knotting of the catheter, and cardiac dysrhythmias. Pulmonary hemorrhage may result from disruption of a branch of the pulmonary artery during balloon inflation and may be fatal in patients with pulmonary hypertension. Steps in prevention include careful placement, advancement under continuous pressure monitoring, and checking the position of the tip before inflating the balloon.

Ischemic Necrosis of the Finger

Continuous monitoring of arterial blood pressure during the operation and in the intensive care unit requires insertion of a radial or femoral arterial line. The hand receives its blood supply from the radial and ulnar arteries, and because of the anatomy of the palmar arches, patency of one of these vessels is usually enough to provide adequate blood flow through the hand. Occasionally, ischemic necrosis of the finger has followed use of an indwelling catheter in the radial artery. This serious complication can usually be avoided by evaluating the patency of the ulnar artery (Allen's test) before establishing the radial line and by changing arterial line sites every 34 days. After an arterial catheter is withdrawn, a pressure dressing should be applied to avoid formation of an arterial pseudoaneurysm.

POSTOPERATIVE FEVER

Fever occurs in about 40% of patients after major surgery. In most patients the temperature elevation resolves without specific treatment. However, postoperative fever may herald a serious infection, and it is therefore important to evaluate the patient clinically. Features often associated with an infectious origin of the fever include preoperative trauma, ASA class above 2, fever onset after the second postoperative day, an initial temperature elevation above 38.6C, a postoperative white blood cell count greater than 10,000/L, and a postoperative serum urea nitrogen of 15 mg/dL or greater. If three or more of the above are present, the likelihood of associated bacterial infection is nearly 100%.

Fever within 48 hours after surgery is usually caused by atelectasis. Reexpansion of the lung causes body temperature to return to normal. Because laboratory and radiologic investigations are usually unrevealing, an extensive evaluation of early postoperative fever is rarely appropriate if the patient's convalescence is otherwise smooth.

When fever appears after the second postoperative day, atelectasis is a less likely explanation. The differential diagnosis of fever at this time includes catheter-related phlebitis, pneumonia, and urinary tract infection. A directed history and physical examination complemented by focused laboratory and radiologic studies usually determine the cause.

Patients without infection are rarely febrile after the fifth postoperative day. Fever this late suggests wound infection or, less often, anastomotic breakdown and intra-abdominal abscesses. A diagnostic workup directed to the detection of intra-abdominal sepsis is indicated in patients who have high temperatures (> 39 C) and wounds without evidence of infection 5 or more days postoperatively. CT scan of the abdomen and pelvis is the test of choice and should be performed early, before overt organ failure occurs.

Fever is rare after the first week in patients who had a normal convalescence. Allergy to drugs, transfusion-related fever, septic pelvic vein thrombosis, and intra-abdominal abscesses should be considered.

References

Block BM et al: Efficacy of postoperative epidural analgesia: a meta-analysis. JAMA 2003;290:2455.

Eagle KA et al: Guidelines for perioperative cardiovascular evaluation for noncardiac surgery: an abridged version of the report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Mayo Clin Proc 1997;72:524.

McGuire BE et al: Intensive care unit syndrome: a dangerous misnomer. Arch Intern Med 2000;160:906.

Moller AM et al: Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial. Lancet 2002;359:114.

National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2003, issued August 2003. Am J Infect Control 2003;31:481.

Rabinowitz RP, Caplan ES: Management of infections in the trauma patient. Surg Clin North Am 1999;79:1373.

Sitges-Serra A, Girvent M: Catheter-related bloodstream infections. World J Surg 1999;23:589.

van 't Riet M et al: Meta-analysis of techniques for closure of midline abdominal incisions. Br J Surg 2002;89:1350

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