Chapter 22: Peritoneal Cavity

The peritoneum is the thin serous membrane that lines the peritoneal cavity. It is the largest serous surface layer in the human body and its surface area is similar to the skin. The structure is made up of a single, flat, layer of mesothelial cells, rich in microvilli. Beneath the mesothelium are a basement membrane and a loose collagen network containing vascularized connective tissue with scattered fibroblasts and macrophages. Normally there is between 5 and 20 mL of free peritoneal fluid, this can vary in women, peaking after ovulation. Normal peritoneal fluid has a specific gravity less than 1.016, protein concentration less than 3g/dL, pH between 7.5 and 8, and a white blood cell count less than 3000/μL. The peritoneum is divided anatomically into parietal and visceral components. The parietal peritoneum underlies the anterior, later, and posterior abdominal walls as well as the undersurface of the diaphragm and pelvic basin. The visceral peritoneum is reflected over the viscera within the abdominal cavity.

Once thought to be a passive barrier, the peritoneum is now understood to have numerous functions. The mesothelial cells secrete phosphatidylcholine, which provides a near frictionless environment within the peritoneum and allows intraperitoneal organs to glide over one another during peristalsis and movement. With its large surface area and semi permeable nature, it participates in fluid exchange with the extracellular fluid space at rates of over 500 mL/h. The circulation of peritoneal fluid is directed toward lymphatics on the undersurface of the diaphragm where particulate matter, up to 20 μm in size, is cleared via stomas in the diaphragmatic mesothelium and emptied into the right thoracic duct.

The peritoneum has a vigorous response to injury and inflammation. Normally sterile, the peritoneum participates in recognizing and eliminating bacteria. Mesothelial cells secrete opsonins that promote bacterial destruction, express CD40 and are aid in antigen presentation, and express intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) which aid in attachment and activation of lymphocytes, granulocytes, and monocytes in response to infectious pathogens. The mesothelial cells secrete tPA under normal conditions which participates in intraperitoneal adhesiolysis. The peritoneum has significant wound healing functions as well, secreting multiple inflammatory mediators including vascular endothelial growth factor (VEGF), PAI, and nitrogen monoxide, TGF beta, and TNF alpha in response to trauma. In response to injury, the peritoneum produces a large proinflammatory response with fibrin deposition and activation of coagulation pathways as well. Imbalance between fibrin deposition and fibrinolysis following peritoneal traumatization can lead to the organization of fibrin deposits between adjacent structures and development of intraperitoneal adhesions which will be discussed further in later sections. Unlike with cutaneous wound healing, following injury to the mesothelium there is uniform recreation of the mesothelial monolayer within 5-10 days.

PRIMARY PERITONITIS

Primary (spontaneous) peritonitis occurring in the absence of gastrointestinal perforation is caused mainly by hematogenous spread but occasionally by transluminal or direct bacterial invasion of the peritoneal cavity. Impairment of the hepatic reticuloendothelial system and compromised peripheral destruction of bacteria by neutrophils promotes bacteremia, which readily infects ascitic fluid that has reduced bacterium-killing capacity. Primary peritonitis is most closely associated with cirrhosis and advanced liver disease with a low ascitic fluid protein concentration. It is also seen in patients with the nephrotic syndrome or systemic lupus erythematosus, or after splenectomy during childhood. Recurrence is common in cirrhosis and often proves fatal.

Clinical Findings

The clinical presentation simulates secondary bacterial peritonitis, with abrupt onset of fever, abdominal pain, distention, and rebound tenderness. However, one-fourth of patients have minimal or no peritoneal symptoms. Most have clinical and biochemical manifestations of advanced cirrhosis or nephrosis. Leukocytosis, hypoalbuminemia, and a prolonged prothrombin time are characteristic findings. The diagnosis hinges upon examination of the ascitic fluid, which reveals a white blood cell count greater than 500/μL and more than 25% polymorphonuclear leukocytes. A blood-ascitic fluid albumin gradient greater than 1.1 g/dL, a raised serum lactic acid level, or a reduced ascitic fluid pH (< 7.31) supports the diagnosis. Bacteria are seen on Gram-stained smears in only 25% of cases. Culture of ascitic fluid inoculated immediately into blood culture media at the bedside usually reveals a single enteric organism, most commonly Escherichia coli, Klebsiella, or streptococci, but Listeria monocytogenes has been reported in immunocompromised hosts.

Treatment

Antibiotic prophylaxis is of no proven value. Systemic antibiotics with third-generation cephalosporins (eg, cefotaxime) or a β-lactam-clavulanic acid combination along with supportive treatment are begun once the diagnosis has been established.

TUBERCULOUS PERITONITIS

Pathophysiology

Tuberculosis peritonitis is encountered in 0.5% of new cases of tuberculosis. It presents as a primary infection without active pulmonary, intestinal, renal, or uterine tube involvement. Its cause is reactivation of a dormant peritoneal focus derived from hematogenous dissemination from a distant nidus or breakdown of mesenteric lymph nodes. Some cases occur as a systemic manifestation of extra-abdominal infection. Multiple small, hard, raised, whitish tubercles studding the peritoneum, omentum, and mesentery are the distinctive finding. A cecal tuberculoma, matted lymph nodes, or omental involvement may form a palpable mass.

The disease affects young persons, particularly women, and is more prevalent in countries where tuberculosis is still endemic. AIDS patients are especially susceptible to development of extrapulmonary tuberculosis such as this.

Clinical Findings

Chronic symptoms (lasting more than a week) include abdominal pain and distention, fever, night sweats, weight loss, and altered bowel habits. Ascites is present in about half of cases, especially if the disease is of long standing, and may be the primary manifestation. A mass may be felt in a third of cases. The differential diagnosis includes Crohn disease, carcinoma, hepatic cirrhosis, and intestinal lymphoma. One-fourth of patients have acute symptoms suggestive of acute bowel obstruction or peritonitis that mimics appendicitis, cholecystitis, or a perforated ulcer.

Detection of an extra-abdominal site of tuberculosis, evident in half of cases, is the single most useful diagnostic clue. Pleural effusion is present in up to 50% of patients. Paracentesis, laparoscopy, or peritoneal biopsy is applicable only in patients with ascites. The peritoneal fluid is characterized by a protein concentration above 3 g/dL with less than 1.1 g/dL serum-ascitic fluid albumin difference and lymphocyte predominance among white blood cells. Definitive diagnosis is possible in 80% of cases by culture (often taking several weeks) and direct smear. A purified protein derivative (PPD) skin test is useful only when positive (about 80% of cases). Hematologic and biochemical studies are seldom helpful, and leukocytosis is uncommon. The sedimentation rate is elevated in many cases. The presence of high-density ascites or soft tissue masses on ultrasonography or computed tomography (CT) scan supports the diagnosis. Young patients from endemic areas who present with classic symptoms or who have suggestive imaging findings should undergo diagnostic laparoscopy, which may obviate laparotomy.

Treatment

In chronic cases, nonoperative therapy is preferable if the diagnosis can be established. Most patients presenting with acute symptoms are diagnosed only by laparotomy. In the absence of intestinal obstruction or perforation, only a biopsy of a peritoneal or omental nodule should be taken. Obstruction due to constriction by a tuberculous lesion usually develops in the distal ileum and cecum, although multiple skip areas along the small bowel may exist. Localized short segments of diseased bowel are best treated by resection with primary anastomosis. Multiple strictured areas may be managed either by side-to-side bypass or a stricturoplasty of partially narrowed segments.

Combination antituberculosis chemotherapy should be started once the diagnosis is confirmed or considered likely. A favorable response is the rule, but isoniazid and rifampin must be continued for 18 months postoperatively.

GRANULOMATOUS PERITONITIS

Pathophysiology

Talc (magnesium silicate), cornstarch glove lubricants, gauze fluffs, and cellulose fibers from disposable surgical fabrics may elicit a vigorous granulomatous (a delayed hypersensitivity) response in some patients 2-6 weeks after laparotomy. The condition is uncommon now that surgeons wipe clean their gloves before handling abdominal viscera. Less rarely, granulomatous peritonitis may develop as a hypersensitivity reaction to other foreign material (eg, intestinal ascariasis or food particles from a perforated ulcer).

Clinical Findings

Besides abdominal pain, which is often out of proportion to the low-grade fever, there may be nausea and vomiting, ileus, and other systemic complaints. Abdominal tenderness is usually diffuse but mild. Free abdominal fluid, if detectable, should be tapped and inspected for the diagnostic Maltese cross pattern of starch particles.

Treatment

Reoperation achieves little and should be avoided if the diagnosis can be made. Most patients undergo reexploration because they present an erroneous impression of postoperative bowel obstruction or peritoneal sepsis. The diffuse hard, white granulomatous masses studding the peritoneum and omentum are easily mistaken for cancer or tuberculosis unless a biopsy specimen is taken to demonstrate foreign body granulomas.

If granulomatous peritonitis is suspected, the response to treatment with corticosteroids or other anti-inflammatory agents is often so dramatic as to be diagnostic in itself. After clinical improvement, intravenous methylprednisolone can be replaced by oral prednisone for 2-3 weeks. The disease is self-limited and does not predispose to late intestinal obstruction.

ACUTE BACTERIAL SECONDARY PERITONITIS

Pathophysiology

Peritonitis is an inflammatory or suppurative response of the peritoneal lining to direct irritation. Peritonitis can occur after perforating, inflammatory, infectious, or ischemic injuries of the gastrointestinal or genitourinary system. Common examples are listed in Table 22–1. Secondary peritonitis results from bacterial contamination originating from within viscera or from external sources (eg, penetrating injury). It most often follows disruption of a hollow viscus. Extravasated bile and urine, although only mildly irritating when sterile, are markedly toxic if infected and provoke a vigorous peritoneal reaction. Gastric juice from a perforated duodenal ulcer remains mostly sterile for several hours, during which time it produces a chemical peritonitis with large fluid losses; but if left untreated, it evolves within 6-12 hours into bacterial peritonitis. Intraperitoneal fluid dilutes opsonic proteins and impairs phagocytosis. Furthermore, when hemoglobin is present in the peritoneal cavity, E coli growing within the cavity can elaborate leukotoxins that reduce bactericidal activity. Limited, localized infection can be eradicated by host defenses, but continued contamination invariably leads to generalized peritonitis and eventually to septicemia with multiple organ failure.

Factors that influence the severity of peritonitis include the type of bacterial or fungal contamination, the nature and duration of the injury, and the host’s nutritional and immune status. The grade of peritonitis varies with the cause. Clean (eg, proximal gut perforations) or well-localized (eg, ruptured appendix) contaminations progress to fulminant peritonitis relatively slowly (eg, 12-24 hours). In contrast, bacteria associated with distal gut or infected biliary tract perforations quickly overwhelm host peritoneal defenses. This degree of toxicity is also characteristic of postoperative peritonitis due to anastomotic leakage or contamination. Conditions that ordinarily cause mild peritonitis may produce life-threatening sepsis in an immunocompromised host.

Causative Organisms

Systemic sepsis due to peritonitis occurs in varying degrees depending on the virulence of the pathogens, the bacterial load, and the duration of bacterial proliferation and synergistic interaction. Except for spontaneous bacterial peritonitis, peritonitis is almost invariably polymicrobial; cultures usually contain more than one aerobic and more than two anaerobic species. The microbial picture reflects the bacterial flora of the involved organ. As long as gastric acid secretion and gastric emptying are normal, perforations of the proximal bowel (stomach or duodenum) are generally sterile or associated with relatively small numbers of gram-positive organisms. Perforations or ischemic injuries of the distal small bowel (eg, strangulated hernia) lead to infection with aerobic bacteria in about 30% of cases and anaerobic organisms in about 10% of cases. Fecal spillage, with a bacterial load of 10¹² or more organisms per gram, is extremely toxic.

Aerobic bacteria account for the majority of bacterial contamination and include both Gram-negative and Gram-positive species. The most frequent Gram-negative organisms encountered include E coli, Klebsiella, Enterobacter, Proteus mirabilis, and infrequently Pseudomonas aeruginosa. Among the more common Gram-positive organisms seen are Enterococcus, Streptococcus, and less commonly Staphylococcus aureus, and Coagulase-negative Staphylococcus. Bacteroides, clostridia, and other anaerobes make up the common anaerobic pathogens encountered. Fungi are rarely encountered though may be present in immunocompromised patients, when present, Candida are the predominant species.

Intraoperative cultures were obtained frequently in the past if purulence was encountered in the surgical field. Given the polymicrobial nature of peritonitis following intestinal tract perforations these cultures may provide little information that impact postoperative management.

Clinical Findings

By estimating the severity of peritonitis from clinical and laboratory findings, the need for specific organ-supportive care and surgery can be determined.

See Chapter 21 for details of radiologic and other investigations.

Symptoms & Signs

The clinical manifestations of peritonitis reflect the severity and duration of infection and the age and general health of the patient. Physical findings can be divided into: (1) abdominal signs arising from the initial injury and (2) manifestations of systemic infection. Acute peritonitis frequently presents as an acute abdomen. Local findings include abdominal pain, tenderness, guarding or rigidity, distention, free peritoneal air, and diminished bowel sounds—signs that reflect parietal peritoneal irritation and resulting ileus. Systemic findings include fever, chills or rigors, tachycardia, sweating, tachypnea, restlessness, dehydration, oliguria, disorientation, and, ultimately, refractory shock. Shock is due to the combined effects of hypovolemia and septicemia with multiple organ dysfunction. Recurrent unexplained shock is highly predictive of serious intraperitoneal sepsis.

The findings in abdominal sepsis are modified by the patient’s age and general health. Physical signs of peritonitis are subtle or difficult to interpret in both very young and very old patients as well as in those who are chronically debilitated, immunosuppressed, or receiving corticosteroids and in postoperative patients. Paracentesis or diagnostic peritoneal lavage may be occasionally useful in equivocal cases and in senile or confused patients. A white blood cell count of greater than 200 cells/μL is indicative of peritonitis, with virtually no false-positive and minimal false-negative errors. Delayed recognition is a major cause of the high mortality rate of peritonitis.

Familial Mediterranean fever (periodic peritonitis, familial paroxysmal polyserositis) is a rare genetic condition that affects individuals of Mediterranean genetic background. Its exact cause is unknown. Patients present with recurrent bouts of abdominal pain and tenderness along with pleuritic or joint pain. Fever and leukocytosis are common. Colchicine prevents but does not treat acute attacks. Provocative testing by infusion of metaraminol (10 mg) induces abdominal pain within 2 days.

Laparoscopy has superseded laparotomy in suspect individuals. Free fluid and inflamed peritoneal surfaces are found, but smears and cultures are negative. The appendix should be removed to simplify diagnosis in subsequent episodes. Secondary amyloidosis with renal failure is a late complication that is preventable by a long-term colchicine therapy.

Treatment

A. Preoperative Care

The presentation of patients with pertitoneal inflammation following bacterial contamination can range from mild to life threatening. It is necessary to approach each patient with the same goals of diagnosis and prompt treatment in mind. Initial management consists of assessing the patient’s resuscitative needs and determining underlying pathology. Once resuscitation is begun, antibiotics administration and other supportive care measures should be pursued followed by imaging and treatment considerations.

Antibiotic administration should be initiated once the diagnosis is made. Antibiotics should be directed against the most likely source and cover the aerobic and anaerobic organisms commonly encountered in gut perforation. Intravenous antibiotics are first line to ensure therapeutic serum levels in the early course of treatment given like ileus and unreliable oral absorption.

While antibiotics are a mainstay in the preoperative treatment of secondary peritonitis, their role in the postoperative period is less clear. Extended postoperative antibiotic courses may offer little benefit when compared with discontinuing antibiotics in the first 24 hours postoperatively in the prevention of intraperitoneal abscess or surgical site infection but can place patients at higher risk for antibiotic related complications and add to resistance in the community.

If the decision is made to continue antibiotics in the postoperative course historically they have been continued until the patient has been afebrile with a normal white blood cell count and a white blood cell count differential with less than 3% band forms. Provided the patient is tolerating a diet there is no added benefit to using intravenous antibiotics over comparable oral agents.

In diffuse peritoneal contamination, irrigation with copious amounts of warm isotonic crystalloid solution removes gross particulate matter as well as blood and fibrin clots. The addition of antiseptics or antibiotics to the irrigating solution is generally useless or even harmful because of induced adhesions (eg, tetracycline, povidone-iodine). All fluid in the peritoneal cavity should be aspirated because it may hamper local defense mechanisms by diluting opsonins and removing surfaces upon which phagocytes destroy bacteria.

In cases of localized peritoneal contamination irrigation of the peritoneum is not advisable. Recent publications discourage the use of peritoneal irrigation in the surgical bed, favoring the use of suction alone, when encountering collections of purulence and spillage intraoperatively as it is associated with reduced rates of postoperative intraperitoneal abscess and surgical site infections.

Complications

Postoperative complications are frequent and may be divided into local and systemic problems. Deep wound infections, residual abscesses and intraperitoneal sepsis, anastomotic breakdown, and fistula formation usually become manifest toward the end of the first postoperative week. Persistent high or swinging fever, inability to wean off cardiac inotropes, generalized edema with unexplained continued high fluid requirements, increased abdominal distention, prolonged mental apathy and weakness, or general failure to improve despite intensive treatment may be the sole indicators of residual intra-abdominal infection. This should prompt a thorough examination of the patient for infected catheters and an abdominal CT scan. Percutaneous catheter drainage of localized abscesses or open reexploration is undertaken as needed (see next section).

Prognosis

The overall mortality rate of generalized peritonitis is about 40% (Table 22–1). Factors contributing to a high mortality rate include the type of primary disease and its duration, associated multiple organ failure before treatment, and the age and general health of the patient. Mortality rates are consistently below 10% in patients with perforated ulcers or appendicitis, in young patients, in those having less extensive bacterial contamination, and in those diagnosed and operated upon early. Patients with distal small bowel or colonic perforations or postoperative sepsis tend to be older, to have concurrent medical illnesses and greater bacterial contamination, and to have a greater propensity to renal and respiratory failure; their mortality rates are about 50%. Markedly poor physiologic indices (eg, APACHE II or Mannheim Peritonitis Index), reduced cardiac status, and low preoperative albumin levels identify high-risk patients who require intensive treatment to reduce a daunting mortality rate.

INTRAPERITONEAL ABSCESSES

Pathophysiology

An intra-abdominal abscess is a collection of infected fluid within the abdominal cavity. Gastrointestinal perforations, postoperative complications, and penetrating injuries are the most common etiologies. An abscess forms by one of two modes. It may develop: (1) adjacent to a diseased viscus (eg, with perforated appendix, Crohn enterocolitis, or diverticulitis) or (2) as a result of external contamination (eg, postoperative subphrenic abscesses). In one-third of cases, the abscess occurs as a sequela of generalized peritonitis. Interloop and pelvic abscesses form if extravasated fluid gravitating into a dependent or localized area becomes secondarily infected (Figure 22–1).

Bacteria-laden fibrin and blood clots and neutrophils contribute to the formation of an abscess. The pathogenic organisms are similar to those responsible for peritonitis, but anaerobic organisms occupy an important role. Experimentally, mixed aerobic (E coli) and anaerobic (Bacteroides fragilis) infections, especially in conjunction with adjuvants (eg, feces or barium), reduce intraperitoneal O₂ and pH, thereby fostering anaerobic proliferation and abscess formation.

Sites of Abscesses

The areas in which abscesses commonly occur are defined by the configuration of the peritoneal cavity with its dependent lateral and pelvic basins (Figure 22–1), together with the natural divisions created by the transverse mesocolon and the small bowel mesentery. The supracolic compartment, located above the transverse mesocolon, broadly defines the subphrenic spaces (Figure 22–2A). Within this area, the subdiaphragmatic (suprahepatic) and subhepatic areas of the subphrenic space may be distinguished. The subdiaphragmatic space on each side occupies the concavity between the hemidiaphragms and the domes of the hepatic lobes. The inferior limits of its posterior recess are the attachments of the coronary and triangular ligaments on the dorsal—not superior—aspect of the diaphragm. Anteriorly, the lower limits are defined on the right by the transverse colon and on the left by the anterior stomach surface, omentum, transverse colon, spleen, and phrenicocolic ligament. Although each subdiaphragmatic space is continuous over the convex liver surface, inflammatory adhesions may delimit an abscess in an anterior or posterior position (Figure 22–2B). The falciform ligament separates the right and left subdiaphragmatic divisions.

The right subhepatic division (Figure 22–2B) of the subphrenic space is located between the undersurfaces of the liver and gallbladder superiorly and the right kidney and mesocolon inferiorly. The anterior bulge of the kidney partitions this space into an anterior (gallbladder fossa) and posterior (Morison pouch) section.

The left subhepatic space also has an anterior and posterior part (Figure 22–2C). The smaller anterior subhepatic space lies between the undersurface of the left lobe and the anterior surface of the stomach. Left subdiaphragmatic collections often extend into this anterior subhepatic area. The posterior subhepatic space is the lesser sac, which is situated behind the lesser omentum and stomach and lies anterior to the pancreas, duodenum, transverse mesocolon, and left kidney. It extends posteriorly to the attachment of the left triangular ligament superiorly on to the hemidiaphragm. The lesser sac communicates with both the right subhepatic and right paracolic spaces through the narrow foramen of winslow.

The infracolic compartment, below the transverse mesocolon, includes the pericolic and pelvic areas (Figure 22–3). The diagonally aligned root of the small bowel mesentery divides the mid-abdominal area between the fixed right and left colons into right and left infracolic spaces. Each lateral paracolic gutter and lower quadrant area communicates freely with the pelvic cavity. However, while right paracolic collections may track upward into the subhepatic and subdiaphragmatic spaces, the phrenicocolic ligament hinders fluid migration along the left paracolic gutter into the left subdiaphragmatic area.

The most common abscess sites are in the lower quadrants, followed by the pelvic, subhepatic, and subdiaphragmatic spaces (Table 22–2).

Clinical Findings

A. Symptoms and Signs

An intraperitoneal abscess should be suspected in any patient with a predisposing condition. Fever, tachycardia, and pain may be mild or absent, especially in patients receiving antibiotics. A deep-seated or posteriorly situated abscess may exist in seemingly well individuals whose only symptom is persistent fever. Not infrequently, prolonged ileus or a sluggish recovery in a patient who has had recent abdominal surgery or peritoneal sepsis, rising leukocytosis, or nonspecific radiologic abnormality provides the initial clue. A mass is seldom felt except late in patients with lower quadrant or pelvic lesions. Irritation of contiguous structures may produce lower chest pain, dyspnea, referred shoulder pain or hiccup, or basilar atelectasis or effusion in subphrenic abscesses; or diarrhea or urinary frequency in pelvic abscesses. The diagnosis is more difficult in postoperative, chronically ill, confused, or diabetic patients and in those receiving immunosuppressive drugs, a group particularly susceptible to septic complications.

Sequential multiple organ failure—principally respiratory, renal, or hepatic failure—or stress-induced gastrointestinal bleeding with disseminated intravascular coagulopathy is highly suggestive of intra-abdominal infection.

B. Laboratory Findings

A raised leukocyte count, abnormal liver or renal function test results, hyperglycemia, and abnormal arterial blood gases are nonspecific signs of infection. Serial postoperative measurement of serum lysozyme (derived from phagocytic cells) is a promising but not widely available test that appears to be highly specific for intra-abdominal pus. Persistently positive blood cultures point strongly to an intra-abdominal focus. A cervical smear demonstrating gonococcal infection is of specific value in diagnosing tubo-ovarian abscess.

C. Imaging Studies

Plain x-rays may suggest an abscess in up to one half of cases. In subphrenic abscesses, the chest x-ray may show pleural effusion, a raised hemidiaphragm, basilar infiltrates, or atelectasis. Abnormalities on plain abdominal films include an ileus pattern, soft tissue mass, air-fluid levels, free or mottled gas pockets, effacement of properitoneal or psoas outlines, and displacement of viscera. Many of these findings are vague or nonspecific, but they may suggest the need for a CT scan. Barium contrast studies interfere with and have been largely superseded by other imaging techniques. A water-soluble upper gastrointestinal series may reveal an unsuspected perforated viscus or outline perigastric and lesser sac abscesses.

Real-time ultrasonography is sensitive (about 80% of cases) in diagnosing intra-abdominal abscesses. The findings consist of a sonolucent area with well-defined walls containing fluid or debris of variable density. Bowel gas, intervening viscera, skin incisions, and stomas interfere with ultrasound examinations, limiting their efficacy in postoperative patients. Nevertheless, the procedure is readily available, portable, and inexpensive, and the findings are specific when correlated with the clinical picture. Ultrasonography is most useful when an abscess is clinically suspected, especially for lesions in the right upper quadrant and the paracolic and pelvic areas.

CT scan of the abdomen, the best diagnostic study, is highly sensitive (over 95% of cases) and specific. Neither gas shadows nor exposed wounds interfere with CT scanning in postoperative patients, and the procedure is reliable even in areas poorly seen on ultrasonography. Abscesses appear as cystic collections with density measurements of between 0 and 15 attenuation units. Resolution is increased by contrast media (eg, sodium diatrizoate) injected intravenously or instilled into hollow viscera adjacent to the abscess. One drawback of CT scan is that diagnosis may be difficult in areas with multiple thick-walled bowel loops or if a pleural effusion overlies a subphrenic abscess, so occasionally a very large abscess is missed. CT-guided or ultrasonography-guided needle aspiration can distinguish between sterile and infected collections in uncertain cases.

The scanning time, patient inaccessibility during scan acquisition, and upper respiratory motion have limited the usefulness of MRI in the investigation of upper abdominal abscesses. CT scan is generally preferable.

Treatment

Treatment consists of prompt and complete drainage of the abscess, control of the primary cause, and adjunctive use of effective antibiotics. Depending upon the abscess site and the condition of the patient, drainage may be achieved by operative or nonoperative methods. Percutaneous drainage is the preferred method for single, well-localized, superficial bacterial abscesses that do not have fistulous communications or contain solid debris. Following CT scan or ultrasonographic delineation, a needle is guided into the abscess cavity, infected material is aspirated for culture, and a suitably large drainage catheter is inserted.

Postoperative irrigation is vital to remove debris and ensure catheter patency. This technique is not appropriate for multiple or deep (especially pancreatic) abscesses or for patients with ongoing contamination, fungal infections, or thick purulent or necrotic material. Percutaneous drainage can be performed in about 75% of cases. The success rate exceeds 80% in simple abscesses but is often less than 50% in more complex ones. It is heavily influenced by the availability of appropriate equipment and the experience of the radiologist performing the drainage. Complications include septicemia, fistula formation, bleeding, and peritoneal contamination.

Open drainage is reserved for abscesses for which percutaneous drainage is inappropriate or unsuccessful. These include many cases where there is a persistent focus of infection (eg, diverticulitis or anastomotic dehiscence) that needs to be controlled. In cases without evidence of continued soiling, the direct extraperitoneal route has the advantage of establishing dependent drainage without contaminating the rest of the peritoneal cavity. Only light general anesthesia or even local anesthesia is necessary, and surgical trauma is minimized. Right anterior subphrenic abscesses can be drained by a subcostal incision (Figure 22–4). Posterior subdiaphragmatic and subhepatic lesions can be decompressed posteriorly through the bed of the resected twelfth rib (Figure 22–4) or by a lateral extraperitoneal method. Most lower quadrant and flank abscesses can be drained through a lateral extraperitoneal approach. Pelvic abscesses can often be detected on pelvic or rectal examination as a fluctuant mass distorting the contour of the vagina or rectum. If needle aspiration directly through the vaginal or rectal wall returns pus, the abscess is best drained by making an incision in that area. In all cases, digital or direct exploration must ensure that all loculations are broken down. Penrose and sump drains are used to allow continued drainage postoperatively until the infection has resolved. Serial sonograms or imaging studies help document obliteration of the abscess cavity.

Transperitoneal exploration is indicated if the abscess cannot be localized preoperatively, if there are several or deep-lying lesions, if an enterocutaneous fistula or bowel obstruction exists, or if previous drainage attempts have been unsuccessful. This is especially likely in postoperative patients with multiple abscesses and persistent peritoneal soiling. The need to achieve complete drainage fully justifies the greater stress of laparotomy and the small possibility that infection might be spread to other uninvolved areas. Laparoscopy alone is often inadequate, especially in critically toxic patients without a localized focus.

Satisfactory drainage is usually evidenced by improving clinical findings within 3 days after starting treatment. Failure to improve indicates inadequate drainage, another source of (or ongoing) sepsis, or organ dysfunction. Additional localizing studies and repeated percutaneous or operative drainage should be undertaken urgently (ie, within 24-48 hours, depending on the seriousness of the case). Failure to acknowledge adequate progress delays essential studies and incurs higher mortality.

Prognosis

The mortality rate of serious intra-abdominal abscesses is about 30%. Deaths are related to the severity of the underlying cause, delay in diagnosis, multiple organ failure, and incomplete drainage. Right lower quadrant and pelvic abscesses are usually caused by perforated ulcers and appendicitis in younger individuals. They are readily diagnosed and treated, and the mortality rate is less than 5%. Diagnosis is often delayed in older patients; this increases the likelihood of multiple organ failure. Decompensation of two major organ systems is associated with a mortality rate of over 50%. Subphrenic, deep, and multiple abscesses frequently require operative drainage and are associated with a mortality rate of over 40%. An untreated residual abscess is nearly always fatal. Postoperative abscesses, in addition to their deleterious effects on patient’s health, add a significant cost to hospitalizations due to extended length of stay, diagnosis, and treatment.

RETROPERITONEAL & RETROFASCIAL ABSCESSES

Pathophysiology

The large retroperitoneal space, extending from the diaphragm to the pelvis, is divided into anterior and posterior compartments (Figure 22–1). The anterior portion includes structures between the posterior peritoneum and the perinephric fascia (pancreas, parts of the duodenum, and the ascending and descending colon). The posterior portion contains the adrenals, kidneys, and perinephric spaces. The compartment posterior to the transversalis fascia is involved in retrofascial abscesses.

Abscesses occur less commonly in the retroperitoneum than in the peritoneal cavity. Retroperitoneal abscesses arise chiefly from injuries or infections in adjacent structures: gastrointestinal tract abscesses due to appendicitis, pancreatitis, penetrating posterior ulcers, regional enteritis, diverticulitis, or trauma; genitourinary tract abscesses due to pyelonephritis; and spinal column abscesses due to osteomyelitis or disk space infections.

Psoas abscesses may be primary or secondary. Primary psoas abscesses, which occur without associated disease of other organs, are caused by hematogenous spread of S aureus from an occult source and are predominantly seen in children and young adults. They are more common in underdeveloped countries. Secondary psoas abscesses result from spread of infection from adjacent organs, principally from the intestine, and are therefore most often polymicrobial. The most common cause is Crohn disease.

The pyogenic bacteria (E coli, Bacteroides, Proteus, Klebsiella) have replaced Mycobacterium tuberculosis as the major causative organism. Surprisingly, only a single causative organism is involved in over one-half of cases. A positive blood culture—especially with Bacteroides—is an ominous finding.

Clinical Findings

Although they may be symptomless, retroperitoneal abscesses tend to develop in patients with obvious acute illnesses. Fever and abdominal or flank pain are prominent features, sometimes accompanied by anorexia, weight loss, and nausea and vomiting. The clinical findings in patients with psoas abscess consist of hip pain, flexion of the hip with pain on extension, and a positive iliopsoas sign. Abdominal, thigh, and back pain may also occur. The diagnosis is apt to be overlooked when pain in the hip aggravated by walking is the major complaint. The differential diagnosis includes retroperitoneal tumors and hematomas. Radionuclide scanning, bowel contrast studies, and urograms are the common preliminary investigations, but CT scanning most accurately delineates these lesions. Gas bubbles are diagnostic of an abscess. Awareness of the overall clinical picture is essential for CT scanning to differentiate retroperitoneal abscesses from neoplasms or hematomas. Abscesses are confined to specific compartments, whereas malignant lesions, by contrast, frequently violate peritoneal and fascial barriers and can invade bone.

Treatment

Principles of antibiotics and drainage are the mainstay of treating these abscesses as well. Drainage by catheter has a lower success rate for retroperitoneal than intraperitoneal abscesses for the following reasons: (1) retroperitoneal abscesses often dissect along planes, giving a stellate instead of globular shape; (2) they often contain necrotic debris that will not pass through catheters; and (3) they often invade adjacent muscle (eg, psoas abscess). Operation is indicated if there is no clinical improvement following percutaneous drainage. An extraperitoneal approach via the flank is preferred for upper retroperitoneal and perinephric abscesses—and one via the perineum presacrally between the anus and the coccyx for pelvic lesions. Transperitoneal exploration may be unavoidable for deep anterior retroperitoneal abscesses. Resection of necrotic or diseased organs, debridement of the affected compartment, and thorough drainage should be accomplished.

The surgical mortality rate is about 25%. Failure of the fever to subside within 3 days indicates inadequate drainage and persistent sepsis that will prove fatal if not corrected promptly.

Adhesions

Peritoneal adhesions are a frequent and complex problem following intra-abdominal and pelvic surgery. They are a source of major morbidity and significant health care spending, estimated at over a billion dollars annually. Postoperative peritoneal adhesions form in over 90% of open abdominal surgery. Pelvic adhesions account for 12% of infertility cases in women. They can cause pain and are a source of bowel obstructions. They impair operative exposure in future operations, increase operative times as well as intraoperative complications. Peritoneal trauma and ischemia leads to an imbalance between fibrin deposition and the normal fibrinolytic capacity within the peritoneal cavity, favoring the former. Following injury and ischemia, the peritoneum secretes a serosanguinous exudate rich in fibrin, protoglycans, glycosaminoglycans, and hyaluranoic acid. The injured mesothelial cells express tissue factor causing activation of the coagulation cascade which augments fibrin deposition within the secreted exudate. Various chemokines and cytokines attract inflammatory cells to the peritoneum. Hypoxia leads to expression of a fibroblast phenotype that has less fibrinolytic capacity than in the unperturbed state. These fibroblasts infiltrate areas of fibrin deposition and form collagen to create more organized adhesive bands. Transforming growth factor beta1 (TGF-beta1) is upregulated in peritoneal inflammation and has a significant role in adhesion formation through reduction in fibrinolysis. Plasminogen activator inhibitor (PAI) is secreted by the mesothelium following peritoneal injury and ischemia; it acts to promote fibrin deposition by binding 1:1 with both tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA). The binding of PAI to uPA and tPA inhibits the conversion of plasminogen to plasmin which is critical for fibrinolysis. Tumor necrosis factor alpha (TNF-alpha) upregulation leads to decreased tPA production and simultaneous increased PAI-1 production by mesothelial cells. VEGF is an angiogenic factor responsible for the neovascularization of peritoneal adhesions, transforming simple adhesions into dense and vascularized fibrous bands that are unable to undergo fibrinolysis. Substance P, a proinflammatory peptide, is upregulated within the peritoneum following peritoneal insult; its interaction with neurokinin-1 receptor leads to a down regulation of metalloproteinases which are integral in fibrinolysis within the peritoneum as well as changes in tPA and PAI-1 expression.

Prevention & Treatment

Current available strategies to minimize adhesions include careful operative technique and barrier methods. Precise surgical technique and gentle tissue handling is critical to minimize peritoneal and serosal damage to limit the inflammatory response responsible for adhesion formation. Minimizing hemorrhage and obtaining complete hemostasis is necessary as activation of the coagulation cascade causes increased fibrin deposition within the peritoneal cavity which further potentiates adhesion formation. It is also important to avoid contaminating the peritoneum with foreign materials such as particles from powdered gloves, fibers from gowns, gauze pads, surgical drapes, and towels which can all promote foreign body reaction and inflammation. Sutures should be minimally reactive as well to limit foreign body reactions. Laparoscopy has been associated with decreased intraperitoneal adhesions through multiple proposed mechanisms including the haemostatic effect of intraperitoneal tamponade during carbon dioxide insufflations of the abdomen and decreased tissue manipulation leading to decreased denudation of the mesothelium.

To date the only commercially available tools used to prevent postoperative adhesions are barrier methods. Barriers exist in solid, liquid, and sprayable forms. They inhibit postoperative adhesion formation by physically separating areas of inflamed and injured peritoneum during the most active early stages of adhesiogensis. Barriers such as hyaluronic acid carboxymethycellulose, Seprafilm Genzyme, are dissolvable and typically remain present within the peritoneal cavity for up to 2 weeks. A large disadvantage of solid barrier methods is that they are only effective at the site the barrier is placed, also they are often difficult to handle and use during laparoscopy. These barriers are associated with the risk of anastomotic leak if wrapped around fresh bowel anastomoses, as well as small increased fistula and peritonitis rates. Liquid barriers have the added benefit of conferring hydro-flotation in between loops of bowel to help prevent adhesions, though this effect is often shortlived depending on the rate of absorption of the liquid by the peritoneum.

There is significant research using pharmacologic agents, by both systemic and by intraperitoneal injection, in adhesion prevention. HMG-CoA reductase inhibitors have been studied for their role in augmenting the profibrinolytic environment of the peritoneum. Angiotensin receptor blocking agents have been shown to downregulate TGF-beta expression and decrease intraperitoneal adhesion formation. Neurokinin-1 receptor antagonists have been shown to decrease adhesion formation in animal models by blocking the actions of Substance P, increasing concentrations of matrix metalloproteinases, and altering tPA and PAI-1 levels within the peritoneum.

TUMORS OF THE PERITONEUM AND RETROPERITONEUM

Tumors affecting the peritoneum are of both primary peritoneal origin and more commonly secondary implants from intraperitoneal malignancies. Primary peritoneal malignancies include mesothelial tumors, epithelial tumors, and smooth muscle tumors. Secondary peritoneal tumors can arise from metastatic lesions, infectious origins, and other nonmalignant origins such as endometriosis.

Peritoneal Mesothelioma

Peritoneal mesothelioma is one of few primary peritoneal neoplasms. It arises from the mesothelium which lines the peritoneal cavity. Mesothelioma of the peritoneum can be diffuse or localized, localized having a more favorable prognosis. Four subtypes, epithelioid, sarcomatoid, mixed or biphasic, and well-differentiated papillary exist. Well-differentiated papillary is usually found in women of reproductive age, has a high cure rate following resection alone distinguishing it from the others. Epithelioid subtypes have a more favorable prognosis when compared with sarcomatoid, which is rarer and more aggressive. Mixed, or biphasic, subtypes are those with both epithelioid and sarcomatoid components. Its incidence is approximately 300-500 new cases being diagnosed in the United States each year. As with pleural mesothelioma, there is an association with an asbestos exposure history. The peritoneal cavity is the second most common site for malignant mesothelioma accounting for approximately 10%-15% of all new malignant mesothelioma cases. Mean age of presentation is in the fifth decade of life. Men are affected more often than women though the divide is less striking when compared with pleural-based mesothelioma.

Clinical Findings

Presenting symptoms are vague, nonspecific, and frequently cause a delay in diagnosis as patients and practitioners pursue workup and treatment of more benign gastrointestinal tract diseases. Patients most often present with abdominal pain and later increased abdominal girth. Additional presenting signs and symptoms include new hernia, abdominal mass, anorexia, nausea, constipation, and diarrhea. Intestinal obstruction is a late finding in the course of peritoneal mesothelioma.

Diagnosis can be difficult not only given the vague presenting symptoms but also because it can mimic other peritoneal malignancies. Laboratory tests are often unrevealing. CA125 and soluble mesothelin related protein are both commonly elevated, though they have a low specificity. Other tumor markers are not useful in the diagnosis. CT with intravenous contrast typically will demonstrate sheet like thickening of the peritoneum with peritoneal nodules in diffuse cases and distinct masses with peritoneal studding in localized subtypes. In patients who cannot receive iodinated contrast for CT imaging, MRI can be used. Presence of ascites on CT can be variable, ranging from minimal to massive amounts. Laparoscopy with tissue biopsy or CT guided tissue biopsy with immunohistochemical staining for calretinin, cytokeratin 5/6, mesothelin, and Wilms tumor 1 antigen remain the gold standard for diagnosis. If peritoneal mesothelioma is suspected, laparoscopic tracts should be excised at the time of operation given its propensity to seed port sites. Cytology is of little use in making the diagnosis.

Treatment

Peritoneal mesothelioma is highly malignant neoplasm; mean time from diagnosis to death is less than 1 year without treatment. Current advances in the past decade with debulking surgery and intraperitoneal chemotherapy has extended survival in many patients though these treatments are not yet standardized. At laparotomy the goal is cytoreduction with excision of all tumor deposits greater than 2.5 mm. A midline laparotomy is used for adequate exposure of the abdomen and pelvic contents. Right and left upper peritoneal quadrants, splenectomy, antrectomy, greater omentectomy, lesser omentum stripping, cholecystectomy, sigmoid colectomy, and pelvic peritoneal resection are performed as required to eliminate all tumor deposits larger than 2.5 mm. Completeness of cytoreduction is the most important factor influencing survival.

Hyperthermic (40.5-43°C) intraperitoneal chemotherapy (HIPEC) is being used as adjuvant therapy and has been associated with median survival times of 54 months. Not yet standardized, common regimens include intraperitoneal mitomycin c, doxorubicin, and cisplatin. No prospective comparisons between cytoreduction with and without HIPEC are available. Factors that are contraindications to undergo cytoreduction and HIPEC include inability to perform adequate cytoreduction, advanced age, poor function status, extra-abdominal metastases, hepatic parenchymal metastases, and bulky retroperitoneal disease.

DESMOPLASTIC SMALL ROUND CELL TUMOR

Desmoplastic small round cell tumors are rare primary peritoneal tumors which are highly aggressive and confer a poor prognosis when diagnosed. This predominantly affects young men, greater than 90% of cases, in the third and fourth decade of life. As with other peritoneal malignancies the presenting signs and symptoms are nonspecific leading to delays in diagnosis. CT is the main imaging modality; typical findings include peritoneal thickening, nodules, heterogeneous intraperitoneal masses often with calcifications and central, low attenuation foci representing necrotic cores within the masses. Mesenteric lymphadenopathy is often present. Given the rarity of the disease, few consensus guidelines exist for its treatment to date and survival even with resection remains less than 20% at 5 years.

PSEUDOMYXOMA PERITONEI

This unusual disease is caused by a low-grade mucinous cystadenocarcinoma of the appendix or ovary that secretes large amounts of mucus-containing epithelial cells. It should be distinguished from benign appendiceal mucocele, which may also have local mucinous deposits but carries a favorable outlook. Patients seldom complain until advanced stages of disease, at which time they have abdominal distention and pain and, in many instances, intermittent or chronic partial small bowel obstruction. Weight loss and other features of cancer are uncommon. The shed neoplastic cells spread freely to two main areas: the upper abdominal sites of peritoneal fluid resorption (undersurface of diaphragm and omentum) and the dependent peritoneal areas (pelvis and lateral abdominal gutters). Distant metastases and visceral involvement are rare. CT scans show a distinctive peritoneal scalloping of the liver margin, calcified plaques, ascites, and low-density masses. Ultrasound features include anechoic areas in the peritoneum, starburst and scalloped appearance of the liver and mobile echogenic foci in the pelvis.

Treatment

At laparotomy, the surgeon should remove as much of the primary lesion and gelatinous material as possible. The omentum also should be resected. This often necessitates right hemicolectomy. If there is no apparent primary tumor, the appendix, and, in women, both ovaries should be removed. Some surgeons advocate radical peritonectomy (including splenectomy, cholecystectomy, appendectomy, sigmoid colectomy, and hysterectomy) to eliminate potential areas of microscopic spread. Whether the higher morbidity incurred is justified remains debated.

Current therapy favors very early intraperitoneal fluorouracil-based adjuvant chemotherapy. Systemic chemo­-therapy is generally useless. Adjuvant intracavitary radiotherapy has also been advocated, especially for patients with residual disease. Reexploration should be undertaken either as a planned second-look laparotomy or to debulk residual tumor responsible for recurrent obstruction or debilitating mucous ascites. Recent studies quote 10 and 15 year respective survival rates of 63% and 59% when combining cytoreductive surgery with HIPEC.

RETROPERITONEAL FIBROSIS

This uncommon entity, is characterized by extensive fibrotic encasement of retroperitoneal tissues. Over two-thirds of cases are idiopathic and the rest secondary to drugs (eg, methysergide, beta-adrenergic blocking agents), retroperitoneal hemorrhage, perianeurysmal inflammation, irradiation, urinary extravasation, or cancer. The fibrosis represents an allergic reaction to insoluble lipid (ceroid) that has leaked from atheromatous plaques, especially those within the aorta. The urinary tract may be involved with a diagnostic triad of hydronephrosis and hydroureter (usually bilateral), medial deviation of the ureters, and extrinsic ureteric compression near the L4-5 level. Desmoplastic involvement of the small and large bowel may give rise to obstructive symptoms. Most patients are men older than 50 who present with renal failure or obstructive uropathy. Pain in the low back or flank is common. Pyuria is present in most patients. The diagnosis is suggested by a CT scan that shows the fibrotic process and any coexisting aneurysmal changes in the aorta. MRI may distinguish fibrosis from lymphoma or metastatic carcinoma. Withdrawal of suspect drugs is usually followed by gradual improvement.

Severe urinary obstruction should be decompressed by ureteric stents or nephrostomy. Prednisone (30-60 mg daily) and immunosuppression have been tried but with inconclusive benefits. These agents should be started early postoperatively before marked fibrosis develops. Tamoxifen has produced regression of desmoid tumors. If surgery becomes necessary, a thick rubbery or fibrotic plaque containing chronic inflammatory cells is found at exploration. Multiple biopsy specimens should be taken to exclude cancer. Ureterolysis should be attempted, and there may be some advantage to wrapping omentum around the freed ureters to reduce the risk of subsequent entrapment. Laparoscopic ureterolysis may occasionally be feasible. The outlook is good as long as there is no underlying cancer.

THE OMENTUM

The omentum is an organ consisting of highly vascularized tissue containing mostly adipose and some lymphoid tissue, described as milky patches, within folds of peritoneum. It is pliable, mobile, and concentrates itself in areas of inflammation within the peritoneal cavity. Anatomically it consists of both greater and lesser components. The greater omentum drapes from the greater curvature of the stomach anteriorly, descends to cover the small intestines, and turns back on itself inserting onto the transverse colon posteriorly, comprising four layers of peritoneum when fused. During embryology, it derives from the dorsal mesogastrium beginning in the fourth week of gestation. Its blood supply is from the right and left gastroepiploic arteries which arise from the gastroduodenal and splenic arteries respectively and its venous drainage exits to the portal system. The lesser omentum is a much thinner structure and extends from the porta hepatis to the inferior curvature of the stomach. During embryology the lesser omentum derives from the septum transversum. Containing mostly fat and lymphocytes, it has active roles in immune function, inflammation, and infection control within the peritoneal cavity. Its role in maintaining the intraperitoneal cavity is a long known function of the omentum, describe as “the abdominal policeman” by Rutherford Morrison in the early 20^th century as he noted it frequently to be in areas of infection and perforation within the peritoneal cavity. Its role in the immune and inflammatory function has grown considerably since that time. If foreign bodies are present in the peritoneal cavity the omentum enlarges in size and mass with expansion of stromal cells rich in tissue and vascular growth factors as well as pleuripotent stem cells. These functions allow it to participate in both tissue regeneration and revascularization in areas of intraperitoneal injury, infection, and inflammation.

Torsion & Infarction

Primary (spontaneous) torsion of the omentum may develop if a free portion is fixed by an adhesion or trapped within a hernia. Rotation around the pedicle occludes the blood supply and leads to ischemic necrosis.

Clinically, torsion presents as acute abdominal pain with nausea and vomiting. Tenderness is confined to the involved area, usually on the right side but away from McBurney’s point. A mobile, tender mass is noted in one-third of cases. These features may suggest acute appendicitis or cholecystitis but are not typical of those diseases. The clinical findings usually mandate surgical exploration, which reveals serosanguineous fluid, a normal appendix, and the hemorrhagic necrotic segment of omentum. Resection of the affected portion is curative.

Tumors & Cysts

The omentum is frequently involved secondarily by intra-abdominal malignant tumors, especially gastrointestinal and ovarian adenocarcinomas. Primary cysts or vascular anomalies, usually incidentally discovered at laparotomy, are readily resected.