33. | Principles of Surgery, Companion Handbook

Chapter 32 Intraabdominal Infections

Principles of Surgery Companion Handbook

CHAPTER

32
INTRAABDOMINAL INFECTIONS

Structure and Function of the Peritoneal Cavity
Physiology of Peritoneal Fluid Exchange
Host Defense Against Intraabdominal Infection
Bacteriology of Peritonitis and Intraabdominal Infection
Evolution of Intraabdominal Infection
Management of Peritonitis
Other Forms of Peritonitis
Management of Localized Abscess
Antimicrobial Therapy for Intraabdominal Infections

Intraabdominal infections are a common occurrence in surgical practice. They may be the initial presenting complaint in a patient with ongoing disease or a complication of surgical therapy. Infections can result in considerable morbidity and mortality as a result of the activation of local and systemic inflammatory responses. A good outcome is highly dependent on prompt and effective decision making. Delay in the treatment of intraabdominal infection allows inflammatory and infectious processes to dominate, resulting in multisystem organ failure or death.

STRUCTURE AND FUNCTION OF THE PERITONEAL CAVITY

The peritoneum lining the abdominal cavity and organs is a single layer of mesothelial cells with a surface area of approximately 1.8 m². There are microvilli that increase the surface area and allow fluid exchange, as well as two distinct populations of cells, cuboidal and flattened. With infection or trauma, the gap between neighboring cells enlarges, allowing free diffusion of molecules and leading to the accumulation of intraabdominal fluid (ascites).

The peritoneal cavity creates several dependent areas where fluid and blood can accumulate. These are the areas where the subsequent development of abscesses is likely. The peritoneum reflects from the posterior aspect of the anterior abdominal musculature to cover the aorta, vena cava, ureters, and kidneys, creating the retroperitoneal space. The reflection continues over the mesentery and becomes the parietal peritoneum, which covers the small bowel, stomach, spleen, liver, gallbladder, ovaries, and uterus.

Normally, the peritoneal cavity is largely a potential space with only a thin film of fluid separating the parietal and visceral layers. This fluid serves as a lubricant that allows the abdominal viscera to slide freely within the peritoneal cavity. The space can be greatly expanded; e.g., during peritoneal dialysis, up to 3 L of fluid can be instilled in the cavity without discomfort. During laparoscopy, up to 5 L of CO₂ can be insufflated, although this requires anesthesia because of the pain of acute abdominal muscle distention.

Potential Spaces for Fluid Accumulation There are several areas created by the compartmentalization of the peritoneal cavity where fluid can accumulate. These include the subphrenic spaces above the liver and spleen, the right and left pericolic gutters between the abdominal wall and the mesentery of the colon, and the pouch of Douglas in the pelvis between the rectum and vagina in females or the rectum and bladder in males. When these become infected, an abscess can occur.

Innervation It is important to understand the innervation of the peritoneal lining to correlate clinical examination with pathophysiology; e.g., a subphrenic collection presents as shoulder pain as a result of irritation of the cervical dermatone extending to the diaphragm. Direct peritoneal irritation as with an inflamed appendix presents as localized pain. Hollow visceral distention as seen in biliary colic, renal colic, or bowel obstruction is referred to the primary dermatome, upper back for gallbladder, groin for kidney, and periumbilical area for bowel.

In localized inflammation of the parietal peritoneum, sensitivity can extend beyond the area of infection. This rebound tenderness is seen on release of the abdominal wall after placing it under tension. Referred pain similarly occurs when compression away from the source of infection refers pain to the site of inflammation.

PHYSIOLOGY OF PERITONEAL FLUID EXCHANGE

The mesothelial lining cells of the peritoneum secrete a serous fluid that circulates within the cavity, with a normal volume of 50–100 mL. Fluid and solutes of less than 30 kD are continuously resorbed by the peritoneal mesothelial lining cells and subdiaphragmatic lymphatics. Infection leads to alterations in molecular permeability, allowing larger particles to be absorbed. Peritoneal fluid movement is based on the balance of two forces; gravity, which pulls fluid to the most dependent areas of the abdomen, and negative pressure, created beneath the diaphragm with each respiratory cycle. Normally, fluid moves from inferiorly to superiorly, with the negative-pressure areas under the diaphragm favored for accumulation of fluid and subsequent abscess.

The normal response to peritoneal injury is rapid filling of the mesothelial defect by adjacent cell movement and healing within 3–5 days. When extensive destruction has occurred leading to basement membrane exposure, adhesions form. These adhesions increase over the first week to 10 days after surgery and become maximal 2–3 weeks after injury.

HOST DEFENSE AGAINST INTRAABDOMINAL INFECTION

There are three major peritoneal defense mechanisms to deal with infection:

Mechanical clearance of bacteria via lymphatics
Phagocytic killing of the bacteria by immune cells
Mechanical sequestration by abscess formation to limit diffusion of bacteria

Diaphragmatic movement produces an influx of fluid into the lymphatics. Because of their small size, bacteria rapidly pass through the diaphragmatic stomata into the thoracic duct and central circulation. This explains why patients with gastrointestinal perforation often present with rigors and fevers. The second defense component is the direct activity of immune cells. Macrophages including peritoneal macrophages are involved in direct microbial killing through phagocytosis via a respiratory burst. This release of proteolytic enzymes is a major component of the inflammatory response and is further mediated by cytokines.

Neutrophils are partially responsible for the parenchymal destruction noted during inflammation. Neutrophils contain granular enzymes that directly digest cell membranes inducing direct toxic effects on bacteria. This defense mechanism has an obligatory requirement for molecular oxygen to create superoxide radicals. Patients with devitalized tissues and shock have inadequate oxygen delivery limiting this defense component.

Endothelial cells lining the blood vessels and lymphatics are injured as bystanders to the inflammatory response. This increases permeability, which allows not only fluid but also additional macrophages and neutrophils to move from the systemic circulation into the abdominal cavity. Mesothelial cells secrete a variety of inflammatory molecules, which attracts neutrophils to the area of infection. Platelet activation and adherence result in the release of platelet-activating factors. Monocyte mediation releases immunoglobulins.

Mechanisms of Cell Recruitment to the Site of Injury: Cytokines and Other Chemoattractants Systemic inflammatory cells must be drawn to the area of infection. The release of chemoattractants recruits neutrophils to the area and induces them to adhere to the endothelium and then pass into the area of inflammation. Leukocytes also must exit the systemic circulation to migrate into the area of infection. The cell initially moves from the circulating state in the center of the bloodstream, rolling along the wall of the capillary. At some point, the leukocyte adheres firmly and is activated by the aforementioned chemotactic agents. Migration is mediated by adherence to integrins and subsequent movement to the extravascular space.

BACTERIOLOGY OF PERITONITIS AND INTRAABDOMINAL INFECTION

Most bacteria in the colon are anaerobic and contribute little to intraabdominal infection. The most common bacteria isolated in clinical infections, Escherichia coli, Enterobacter, Klebsiella, and Pseudomonas, make up less than 0.1 percent of normal colonic flora. Even the most common anaerobic pathogen, Bacteroides fragilis, accounts for only 1 percent. The presence of a large number of nonpathogenic bacteria provides a measure of protection to the host by suppressing the growth of potentially pathogenic bacteria. This balance often is altered with chronic broad-spectrum antibiotic treatment, leaving the remaining bacteria increasingly virulent (Table 32-1). The concentration of bacteria also varies along the length of the gastrointestinal tract. The stomach, because of its high acid content, contains fewer than 10³ bacteria/mm³, which rises with acid-reduction therapy. The proximal small bowel contains 10⁴ – 10⁵ bacteria/mm³, rising to 10⁹/mm³ in the terminal ileum and 10¹²/mm³ in the colon, with more anaerobic bacteria predominant distally.

TABLE 32-1 BACTERIA COMMONLY ENCOUNTERED IN INTRAABDOMINAL INFECTIONS

After perforation, multiple species of bacteria adhere to the peritoneum and colonize the mesothelium. B. fragilis emerges as the predominant organism and becomes a major factor in the development of intraabdominal abscess. The synergy between anaerobic and aerobic bacteria increases the virulence of the infection. In animal studies, pure cultures of E. coli caused peritonitis with moderate mortality but no intraabdominal abscess. The coinjection of B. fragilis led to both abscess formation and a significant mortality. The inoculum of bacteria needed to establish a significant infection is less if there are adjunctive substances such as blood present. In experimental E. coli models, hemoglobin alone decreased the lethal dose of bacteria by five orders of magnitude. Other substances, including bile salts and pancreatic secretions, as well as foreign materials such as talc, fragments of cotton sponges, sutures, or barium, also increased morbidity and mortality associated with peritoneal contamination.

EVOLUTION OF INTRAABDOMINAL INFECTION

A single inoculum of intraperitoneal bacteria does not invariably lead to infection. The combination of bacteria and devitalized tissues in the presence of other facultative media increases the risk of developing peritonitis. The sooner that the contamination is contained and the debris evacuated, the better is the chance of resolution. Although early diagnosis is key, the classic combination of fever, leukocytosis, and abdominal pain is not present in all patients. The initial physiologic response is to dilute the noxious influence by the third spacing of fluid. Patients will then show signs of volume depletion but may not have localized peritonitis. A pneumonic process such as lower lobe pneumonia can mimic an intraabdominal process via referred somatic pathways. It is important to examine and image the chest before proceeding with any type of intervention of the abdomen.

Plain radiographs of the abdomen will reveal free air in the presence of visceral perforation. Abdominal abscesses can be seen without free air. Air-fluid levels above the liver or spleen suggest subphrenic abscess.

The preoperative preparation of patients with peritonitis involves the restoration of intravascular volume. Therapeutic doses of broad-spectrum antibiotics should be started. Patients developing ongoing acidosis or respiratory compromise should be intubated promptly and their respiratory status supported. Metabolic acidosis should not be attributed to infection only but also may reflect inadequate resuscitation. Determination of blood pressure plus monitoring of urinary output is an important measure of the adequacy of resuscitation.

The administration of pharmacologic doses of corticosteroids to septic patients should not be done. Some studies have shown that large doses of steroids may delay immediate mortality in sepsis, but overall outcome is not altered. One situation where steroids are useful is that of acute adrenal insufficiency, where the hypotensive and febrile state may mimic that of peritonitis. Patients at risk for bilateral adrenal hemorrhages include those on large doses of anticoagulation and postinjury patients.

MANAGEMENT OF PERITONITIS

When the patient has been resuscitated, celiotomy should commence promptly. A long midline incision allows wide exploration of the abdomen. Specific areas of perforation should be controlled quickly either with clamps or with sutures pending definitive therapy. It is important to explore the dependent areas of the abdomen carefully because multiple abscesses can occur in the subphrenic, subhepatic, and pelvic areas. The small bowel often will form interloop abscesses that should be gently exposed and evacuated. The definitive management of peritonitis depends on its cause. The perforation associated with stomach and duodenum is more chemical as opposed to bacterial peritonitis. Simple patching can treat duodenal perforations. Gastric perforations require resection, especially if there is concern regarding malignancy. Unless the gastric perforation is clearly associated with a high-acid ulcer, vagotomy is unnecessary. Small bowel perforations usually result from bowel obstruction with ischemia or embolic events. After resection, the question of reanastomosis depends on the location of the bowel and the underlying state and extent of the peritonitis. It is safer to exteriorize proximal and distal ends of the bowel in cases of severe peritonitis, especially when the perforation is more distal. Proximal perforations that are exteriorized can lead to difficulties with a high ostomy output state requiring long-term total parenteral nutrition, although subsequent reanastomosis is possible. Colonic perforation is a result of diverticulitis, acute colitis, carcinoma, or distal obstruction. Resection of the perforated colon with the obstruction is appropriate, and exteriorization of the bowel should be undertaken.

Postoperative peritonitis usually results from an anastomotic leak. Rather than developing the fulminate form of sepsis often seen in acute perforation, this is a more indolent type of syndrome beginning 5–8 days postoperatively. It often is associated with a rising white blood cell count and spiking temperatures. Computed tomography (CT) will demonstrate a fluid collection that can be drained percutaneously under ultrasound or radiologic guidance.

OTHER FORMS OF PERITONITIS

Not all peritonitis is a result of contamination from the gastrointestinal tract. Patients with cirrhosis and those with autoimmune diseases can develop primary bacterial peritonitis as a monomicrobial infection. Treatment is antibiotics and expectant management. Patients with peritoneal dialysis catheters often manifest infections, usually related to the presence of a chronic foreign body that is accessed on a regular basis. Treatment normally is nonoperative using parenteral and intradialytic antibiotics. Nonresponse mandates catheter removal. Other forms of peritonitis not associated with bacteria include postoperative bile leak, retained foreign bodies, or chemical peritonitis from a perforated and sealed duodenal ulcer.

MANAGEMENT OF LOCALIZED ABSCESS

Intraabdominal abscess often is diagnosed by CT scan. Rectal and vaginal examinations confirming a mass in the lumen allows diagnosis and subsequent drainage.

There are some patients who cannot be drained percutaneously or transrectally. Subphrenic abscesses are amenable to drainage under ultrasound or radiologic guidance, although there is concern about passing the catheter through the previously sterile pleural space. In this situation, a small subcostal or posterolateral incision often allows open drainage. Abscesses in the retroperitoneum usually can be drained percutaneously. If surgical intervention is undertaken, the incision should remain in the retroperitoneal space.

ANTIMICROBIAL THERAPY FOR INTRAABDOMINAL INFECTIONS

In addition to drainage, a cornerstone of therapy for peritonitis is adequate tissue levels of antibiotics. Broad-spectrum empirical therapy is started before identification of the offending organism and is based on expected organisms. Most intraabdominal infections are caused by E. coli, B. fragilis, Pseudomonas, or Streptococcus. Perforations of the upper gastrointestinal tract such as the stomach often yield only isolates of yeast because of the high-acid state of the stomach.

Aminoglycosides have been the mainstay of therapy for serious gram-negative infections for many years. Although they do have nephro- and ototoxicity, careful monitoring can minimize these effects. Aminoglycosides are synergistic with penicillins, yielding improved response. Aminoglycosides work through suppression of bacterial DNA and RNA synthesis at the nucleus. Penicillin-type antibiotics open the bacterial cellular wall, allowing for greater entrance of the aminoglycocides. Beta-lactam antibiotics such as the cephalosporins have more gram-positive than gram-negative activity. They should be combined with metronidazole or clindamycin for anaerobic coverage.

The fluoroquinolones are a relative newcomer whose effect results from targeting DNA gyrase, a repair enzyme. The quinolones have a fairly wide spectrum of activity against gram-negative bacilli including Pseudomonas. They can be used in either an oral or an intravenous form and have minimal nephrotoxicity (Table 32-2).

TABLE 32-2 APPROPRIATE ANTIBIOTIC CHOICES IN PERITONITIS*

Pharmacology of Antibiotics It is important that suitable tissue levels of antibiotics are maintained depending on their activity. The aminoglycocides are most effective when a certain peak is reached between dosages, whereas the other beta-lactam antibiotics are most effective when the minimum inhibitory concentrations (MICs) are maintained at a relatively high level over the entire 24-h period. Frequent, small doses may accomplish this. Some antibiotics such as cefoperazone, piperacillin, and mezlocillin are excreted in the bile, achieving high levels within the biliary tree and lumen of the bowel. Route, timing, and dosages will maximize response.

For a more detailed discussion, see Solomkin JS, Wittman DW, West MA, and Barie PS: Intraabdominal Infections, chap. 32 in Principles of Surgery, 7th ed.