ANATOMY AND PHYSIOLOGY

SURGICAL PERITONITIS

Secondary (surgical) peritonitis is a result of an inflammatory process in the peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure. Surgical intervention is typically required to treat these processes, although antibiotics often are useful while the process resolves (e.g., uncomplicated diverticulitis). If untreated, secondary peritonitis will, in most cases, lead to septic shock and death.

ICAM, intercellular adhesion molecule; VCAM, vascular cell adhesion molecule.

Peritoneal Clearance of Bacteria

Once bacteria enter the peritoneal cavity, clearance of the offending microorganisms begins immediately. Within 6 minutes of intraperitoneal inoculation of bacteria in dogs, bacteria can be cultured in thoracic lymph, indicating passage of organisms through the diaphragm. Twelve minutes later, bacteremia may be evident. This clearance mechanism is probably important in survival because blockade of the thoracic duct in an animal model of peritonitis decreases bacteremia episodes⁴ but increases mortality and induces liver necrosis. This appears to be directly related to the amount of endotoxin to which the liver is exposed.⁹ Decades before it was known that the diaphragm was the predominant site of clearance of bacteria, Fowler, in 1900, proposed his head-up, pelvis-down position for prevention of absorption of toxins from infected peritoneal cavities. In the preantibiotic era, documentation of the delayed clearance of bacteria from experiments in infected dogs in the head-down position confirms the wisdom of this positioning for patients with peritonitis.

Killing Mechanisms

In addition to mechanisms of bacterial clearance through the diaphragm, intraperitoneal defense mechanisms include cellular and humoral responses (see Chapter 2). Macrophages and neutrophils are attracted to the peritoneal cavity, and in this setting, microvilli of the mesothelial cells play a significant role in leukocyte migration into the peritoneal cavity by providing the needed substrates for their adhesion, namely intercellular adhesion molecule-1 (ICAM-1, or CD 54), and vascular cell adhesion molecule-1 (VCAM-1, or CD 106).¹⁰

The degree of cellular recruitment may be a key factor in a patient’s survival because a prolonged peritoneal inflammatory response has been observed to be adversely correlated with survival in an animal model of peritonitis.¹¹ Humoral antibacterial agents, such as complement factors, fibronectin, and globulins, are released into the peritoneal cavity. These opsonins coat bacteria and render them recognizable as foreign; then they are entrapped and killed by phagocytes.¹²

Sequestration Mechanisms

Sequestration mechanisms include fibrin trapping of bacteria, fibrinous adhesions, and omental loculation of foci of infection (see Table 37-1).¹³ It has been known since 1950 that bacteria are more readily destroyed on a surface than in a liquid medium. The microscopic and macroscopic networks of surfaces provided by fibrin and the omentum assist phagocytes in locating, trapping, ingesting, and killing bacteria. The volume of peritoneal fluid in which infection develops has a remarkable effect on mortality; 20% of rats inoculated with E. coli diluted in 1 mL of saline die, whereas 75% of rats inoculated with the same number of viable bacteria but diluted in 30 mL of saline die.¹⁴ This phenomenon explains in part the risk of development of spontaneous bacterial peritonitis in relation to the ascitic fluid total protein concentration.¹⁵ The more voluminous the ascitic fluid, the lower the concentration of proteins and opsonins, the less efficient the trapping of bacteria, and the higher the risk of an uncontrolled infection (see Chapter 91). Patients undergoing chronic ambulatory peritoneal dialysis may be vulnerable to peritonitis because of dilution of opsonins by dialysis fluids.

Bacterial contamination in the peritoneal cavity and the subsequent response of immune cells such as neutrophils and macrophages lead to an inflammatory response including the release of cytokines. The systemic inflammatory response syndrome (SIRS) is marked by fever, a hyperdynamic cardiovascular response, muscle protein breakdown,¹⁶ and respiratory failure. If the underlying cause is treated by surgical intervention, antibiotics, or the body’s own defense mechanisms, these processes can be thwarted or reversed. However, if the process goes unchecked, multisystem organ failure and death will result. In addition, even if the underlying cause is treated, the inflammatory response can lead to multisystem organ failure and death if the treatment is delayed or the inflammatory response is particularly vigorous.

Patients with severe peritonitis may have a higher mortality from a shift from type 1 to type 2 T-helper cells leading to greater immunosuppression.¹⁷ When treating peritonitis or operating within the abdomen, the clinician’s goal is to minimize or eliminate inflammation. For instance, laparoscopic operations may induce less of a systemic inflammatory response than their open counterparts.^18,19 In addition, laparoscopy differs from laparotomy in regard to peritoneal macrophage response,²⁰ less cortisol release,²¹ and less reduction in natural killer (NK) cell subsets.²² Laparoscopic operations may well confer an immunologic advantage over conventional open operations.²³ The additional benefits of smaller incisions, less tissue trauma, decreased postoperative pain, and shorter recovery are driving a trend to laparoscopic operations over open operations even in acute settings.

HISTORY AND PHYSICAL EXAMINATION

Clinical history and careful physical examination are the key factors in making a timely diagnosis of surgical peritonitis. In general, the sooner the diagnosis is made, the better the prognosis. Abdominal pain is the hallmark of peritonitis. The exact details of the onset of pain can be helpful in drawing attention to the affected organ (see Chapter 10). The pain’s character, location, area of radiation, change over time, and provocative and palliative factors are key pieces of information in assisting with the diagnosis. Peritoneal inflammation is typically associated with ileus, and therefore nausea and vomiting are common symptoms.

The ability of the clinician to elicit an accurate history of abdominal pain and peritoneal signs is limited in patients with neurologic and immunologic compromise. The pain of peritonitis can be reduced or even absent in older adult patients. Infants and children may be incapable of furnishing any history or cooperating with the physical examination. Notoriously difficult patients to assess for secondary peritonitis include emergency room patients under the influence of alcohol or illicit drugs, trauma patients with central nervous system or spinal cord injuries, and sedated and ventilated intensive care unit (ICU) patients. Analgesics typically will not relieve the pain of peritonitis on examination but may relieve some discomfort as related to the history of present illness. In fact, it has been shown that early provision of analgesia to patients with undifferentiated abdominal pain does not affect diagnostic accuracy.²⁴ Diabetic patients have deficits in neurologic and immune function. Patients receiving immunosuppressive and anti-inflammatory drugs, such as glucocorticoids and chemotherapeutic drugs, may have blunted perception of pain and minimal signs of peritoneal irritation. Patients with cirrhosis and ascites may show no pain during episodes of spontaneous bacterial peritonitis unless the parietal peritoneum becomes involved with the inflammatory process (see Chapter 91).

On examination, the patient with surgical peritonitis is usually immobile because any movement acutely worsens the pain. Fever of 100° F or higher is typical, as is tachycardia, which may be in part secondary to pain. Hypotension is usually a late finding accompanying sepsis. Fever is a basic endogenous mechanism to help fight infection. In fact, the increase in body temperature that is usually found during bacterial infections, including peritonitis, seems to be essential for optimal host defense against bacteria.²⁵ The absence of percussible hepatic dullness suggests the presence of free air in the peritoneal cavity. Exquisite tenderness to percussion should lead to very gentle palpation. Overly vigorous palpation of a very tender abdomen may cause patients such pain that they are subsequently unable to cooperate for the remainder of the examination.

Palpation should begin farthest from the area that the patient identifies as the source of the most pain. Palpation of a truly boardlike abdomen is so impressive to the examiner that it cannot be forgotten. Lesser degrees of rigidity must be compared with this extreme end of the spectrum. Voluntary guarding in the presence of mild tenderness may be misinterpreted as rigidity by the inexperienced examiner if the patient is anxious and palpation too vigorous. It is usually not necessary to check for rebound tenderness to palpation if rebound tenderness is noted during auscultation or percussion. Often, the presence of rebound tenderness can be inferred if the patient’s pain is exacerbated when the bed or stretcher is jarred.

Peritoneal signs signify inflammation of the parietal peritoneum secondary to an intra-abdominal process. Peritoneal signs consist of rebound tenderness, involuntary guarding and extreme tenderness on palpation. Peritonitis can be diffuse, such as that associated with perforated ulcer, or localized, such as that of diverticulitis confined to the left lower quadrant. Significant septic processes may be confined to the pelvis by overlying bowel and omentum with a resulting absence of peritoneal signs in the anterior abdominal wall. Therefore, careful rectal and pelvic exams are essential in order to detect pelvic peritonitis. The presence of iliopsoas and obturator signs (described in Chapter 116) can be helpful in detecting retroperitoneal or pelvic inflammation and abscesses.

Repeated physical examinations by the same examiner will provide evidence of progressive peritoneal irritation. The evolution of the physical exam over time provides additional information for diagnosis and evaluation of response to initial conservative therapy. This, together with laboratory tests and imaging procedures described below, will indicate the need for surgical intervention.

LABORATORY TESTS AND IMAGING

The most common laboratory sign of peritonitis in an immunocompetent patient is an increased white blood cell count with left shift. The presence of circulating juvenile forms (e.g., bands) is a reflection of an increasing demand of white cells from the bone marrow. A low white blood cell count in the course of a bacterial infection associated at times with gram-negative septicemia may indicate the presence of an exhausted bone marrow, with a poorer prognosis. In addition, metabolic acidosis, hemoconcentration, and prerenal azotemia may be present.

Free air may be detected on upright chest radiograph or on upright or decubitus abdominal films, but this finding may be only 60% sensitive in detecting gut perforation.²⁶ The absence of free air should not delay surgical intervention in an otherwise appropriate clinical setting. Ultrasonography can be helpful in demonstrating abscesses, bile duct dilatation, and large fluid collections. CT scan of the abdomen and pelvis, generally with both oral (occasionally rectal) and intravenous contrast, is increasingly preferred as the most sensitive and specific imaging modality for acute abdominal pain. Multidetector CT scanners are capable of imaging the entire abdomen and pelvis in a single breath-hold. The axial images are of extremely high resolution and can be reconstructed in coronal, sagittal, and three dimensional sets of images.²⁷ CT is much more sensitive than plain films for the detection of free air, and with multidetector CT it is possible to visualize the actual site of perforation.²⁸ Although CT images are increasingly accurate and the images compelling, they should not delay surgical consultation, resuscitation, and operation in a patient with suspected peritonitis.

DIAGNOSIS

The diagnosis of surgical peritonitis is suspected on the basis of history, physical examination, and laboratory and imaging tests and is confirmed at laparotomy or laparoscopy when purulent fibrinous peritonitis is found. In those patients whose history and physical examinations are unreliable, CT and peritoneal lavage are extremely valuable in confirming the diagnosis of surgical peritonitis. CT is less invasive but peritoneal lavage can be performed quickly in hemodynamically unstable patients. Peritoneal lavage is performed by inserting a catheter under sterile conditions into the peritoneal cavity and infusing 1 L of normal saline. If the effluent contains more than 500 white blood cells (WBCs) per cubic millimeter, an amylase or bilirubin level greater than the corresponding serum value, or bacteria on Gram stain, there is approximately a 90% likelihood of surgical peritonitis.²⁹ Laparotomy is usually indicated in this setting. Finally, diagnostic laparoscopy is extremely accurate in making the diagnosis of surgical peritonitis and many of the underlying diseases can be dealt with laparoscopically, avoiding the need for laparotomy.³⁰

TREATMENT

The following two principles in the management of surgical peritonitis cannot be overemphasized. First, not all patients with peritonitis require surgery. For example, a patient with localized left lower quadrant peritonitis secondary to diverticulitis can be managed with bowel rest and intravenous antibiotics alone. Another patient with the same clinical presentation and findings of a diverticular abscess on CT scan can be successfully treated with antibiotics and percutaneous drainage (see Chapter 26). Second, the absence of peritonitis does not exclude the possibility of surgical emergency. The classic example of this clinical situation is early acute mesenteric ischemia with abdominal pain out of proportion to findings on physical examination findings. Likewise, a complete mechanical small bowel obstruction without peritoneal signs, an indication of perforation or vascular compromise, still requires operation.

For most cases of secondary peritonitis fluid resuscitation and antibiotic therapy followed by urgent laparotomy or laparoscopy are the mainstays of treatment. Fluid resuscitation is guided by frequent monitoring of physiologic parameters in an ICU, including blood pressure (by arterial line if shock is present), heart rate, central venous pressure or pulmonary capillary wedge pressure, and urine output. Hematocrit, WBC, electrolytes, glucose, creatinine, and blood gases should also be monitored. Hypovolemia, hypotension, metabolic acidosis, hypoxia, and hemoconcentration from loss of plasma into the peritoneal cavity are expected. Glucocorticoids have been shown not to provide benefit in the setting of septic shock.³¹

The patient should be aggressively fluid resuscitated to treat intravascular fluid depletion secondary to movement of fluid out of the vascular space. Pressors are generally to be avoided, if possible, and surgical intervention should be pursued when indicated as soon as the patient is hemodynamically stable for operation.