Chapter 4 Postoperative Complications

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 evacuation and injection of tetracycline (1 g in 150 mL saline) as a sclerosant solution. Seromas of the groin, which are common after vascular operations, are best left alone,
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 persist-or if they start leaking through the wound after several days-the 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 called 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. Dehiscences often result from a combination of these factors rather than from a single one. The kind of incision (transverse, longitudinal, etc) does not influence the incidence of dehiscence.
1. 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 undergo dehiscence because the sutures cut 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," ie, 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 stab incisions to reduce the rate of wound infection and disruption.
2. Intra-abdominal pressure-
After any intra-abdominal operation, some degree of ileus is inevitable. High abdominal pressures may 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.
3. 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 surgery. The presence of this ridge is clinical proof 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 flap, which increases 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 infections.
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 patients-usually 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 moderate 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 interferes with these defenses and predisposes 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 produces airway obstruction. Obstruction of distal bronchi, though well tolerated initially, may 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 prevents aspiration and avoids 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. Hydrocortisone, 30 mg/kg/d intravenously, may be useful for the first 3 days. 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 death-or is a contributory factor-in 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 inhalation-eg, 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 tapped. 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 victims-especially those with long bone fractures-and 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 disease-especially aortic stenosis-limits the ability of the heart to respond to increased demand
during operation or in the immediate postoperative period. When aortic stenosis is recognized preoperatively-and 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 of thromboembolic disease should receive heparin until approximately 6 hours before the operation, when heparin should be stopped. If needed, heparin can be restarted 36-48 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 the 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 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 1-2 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 levels-especially the MB isoenzyme-and 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. Dopamine is the best drug for inotropic support. Patients who are not in shock may, instead, be digitalized. Rapid digitalization (eg, divided intravenous doses of digoxin to a total of 1-1.5 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 hemoperitoneum-a rapidly evolving, life-threatening complication-is usually the result of a technical problem with hemostasis, but coagulation disorders may play a role. For example, most of these patients have experienced substantial intraoperative blood loss, and several transfusions have already been 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 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 4-6 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。