Surgical Peritonitis and Other Diseases of the Peritoneum, Mesentery, Omentum, and Diaphragm

Gross Anatomy

The peritoneum is the largest serous membrane of the human body, with an estimated surface area of 1.8 m ² , which is almost the same area as the skin (or total body surface area). The embryologic development of the peritoneum occurs in the gastrulation phase, where the 3 layers of the embryo—the ectoderm, mesoderm, and endoderm—further differentiate into the visceral plate mesoderm and the parietal plate mesoderm. The parietal peritoneum secretes serous fluid, whereas the visceral peritoneum invests organs and the mesentery that suspends the gut tube from the abdominal wall, thus providing a pathway for vessels, nerves, and lymphatics. The peritoneal sac, as it is often referred to, is sealed in men and open to the exterior via the ostia of the fallopian tubes in women.

The parietal peritoneum in a completely developed fetus covers the internal surfaces of the abdominal wall including the diaphragms and the pelvis, whereas the visceral peritoneum invests all intraperitoneal organs (such as small intestine, gall bladder, stomach) and the anterior surface of retroperitoneal organs (pancreas, kidneys, ascending and descending colon). Remarkably, the understanding of the anatomy of the peritoneum, omentum, and mesentery is evolving. Meyers identified numerous ligaments and 2 mesenteries including the coronary, gastrohepatic, hepatic, duodenal, falciform, gastrocolic, duodenocolic, gastrosplenic, splenorenal, and phrenicocolic ligaments and the transverse mesocolon and the small bowel mesentery. Although important in understanding and predicting spread of disease and inflammation that manifests in clinically relevant situations, this is an oversimplification of the anatomy. For instance, patients with perforated peptic ulcer disease may present with RLQ pain due to dependent drainage along the right paracolic gutter. Prior to imaging techniques, patients would be placed in semi-recumbent positions (Fowler position) in order to encourage dependent accumulation of infected fluid with the goal that the eventually encapsulated pelvic abscess could be drained transrectally.

Current understanding of the mesentery and the parietal peritoneum suggest that the mesentery distal to the duodenojejunal flexure is a contiguous and extra-retroperitoneal organ. The right and left mesocolic regions and the mesosigmoid are flattened against the abdominal wall, held in place by Toldt fascia. It has been suggested that the intestine and mesentery are contiguous from diaphragm to pelvic floor and that the mesogastrium and mesoduodenum are indeed contiguous with the mesentery. This description of the mesentery is broken into 6 flexures: duodenojejunal, ileocecal, hepatic, splenic, between descending and sigmoid, and sigmoid and rectum. The peritoneal reflections, although contiguous, are variably named as Jackson membrane, anterior reflection, pouch of Douglas, and the lateral peritoneal reflection ( Fig. 39.1 ). This understanding is translating into “total mesocolic or mesorectal” excisions for oncologic purposes.

The greater omentum is an intraperitoneal organ derived from the greater curvature of the stomach and spleen, draping across the transverse colon, which separates the abdomen into the greater and lesser sacs. The lesser omentum attaches the lesser curvature of the stomach to the liver and is also referred to as the gastrohepatic omentum. The right edge of the lesser omentum is also known as the hepatoduodenal ligament, and the opening posterior to this (the epiploic foramen of Winslow) is the only connection between the lesser and greater sacs.

Microscopic Anatomy

The word peritoneum is derived from the Greek peri- , meaning “around” and tonos, meaning “a stretching around.” The visceral and parietal peritoneum have a similar structure and consist of 3 layers: the mesothelium, the basal lamina, and the submesothelial stroma. The mesothelium is formed by a monolayer of cuboidal mesothelial cells approximately 25 μm in diameter. Mesothelial cells possess both epithelial and mesenchymal characteristics and peritoneal pathology can lead to epithelial-mesenchymal transitions. The peritoneum contains stomata, which are direct portals to the lymphatic system. These are abundantly present on the diaphragm. At the apical surface of the peritoneum are numerous microvilli and occasional cilia in which lamellar bodies are embedded. These release surfactant that allows a friction-free state. On top of the microvilli and lamellar bodies, a glycocalyx is present consisting of proteoglycans and glycosaminoglycans. These are responsible for intercellular contact, inflammatory regulation, tissue remodeling, and possibly transport. Mesothelial cells are joined by well-defined intercellular junctional complexes, including tight junctions, adherens junctions, gap junctions, and desmosomes that establish and maintain the semipermeable barrier for fluid, solutes, and particles.

Blood Supply and Innervation

The visceral peritoneum is supplied by the splanchnic blood vessels, and the parietal peritoneum by intercostal, subcostal, lumbar, and iliac vessels. The venous blood from the visceral peritoneum returns via the portal vein, whereas the parietal peritoneum drains via the inferior vena cava. The visceral peritoneum is supplied by nonsomatic nerves, whereas the parietal peritoneum is supplied by somatic nerves. Therefore, visceral pain is poorly localized, diffuse, and vague (see Chapter 11 ). Visceral pain is caused by stretching, distention, torsion, and twisting. The visceral peritoneum does not produce pain when it is cut or burned. When visceral pain fibers of midgut structures are stimulated, a vague periumbilical discomfort results because the visceral pain fibers enter the spinal cord at the same level as the T10 dermatome somatic fibers (see Chapters 11 and 12 ). This sensation is, therefore, experienced as discomfort in a dermatomal distribution. Likewise, visceral stimulation from foregut structures produces epigastric (T8 distribution) discomfort, and visceral stimulation in the hindgut produces suprapubic (T12) discomfort. Parietal (somatic) pain fibers are activated by such stimuli as cutting, burning, and inflammation. This type of pain is sharply localized. A good example of this process is acute appendicitis. Early in the disease process the patient experiences periumbilical discomfort secondary to distention of the appendiceal lumen, and this progresses to localized RLQ pain and tenderness as the inflammation becomes transmural and involves the parietal peritoneum.

Physiology

The mesothelial cell maintains homeostasis of the peritoneal cavity and synthesizes the matrix proteins on the basal surface that maintain the architecture of the peritoneal membrane ( Fig. 39.2 ). The peritoneum can regenerate after injury or surgery. The peritoneum can also cause fibrosis by exerting epithelial-mesenchymal transitions. In addition, these cells also can promote degradation of fibrin by converting plasminogen to plasmin, thereby activating tissue plasminogen activator. In animal models of abdominal wall hernias repaired with composite mesh grafts, a functional neoperitoneum covers the graft in 7 to 14 days.

Under conditions of inflammation, the mesothelial cell initiates and regulates the inflammatory response by synthesis of cytokines, chemokines, and growth factors. The peritoneal mesothelial cell is capable of phagocytosis and can serve as an antigen-presenting cell.

Finally, in health and in inflammatory conditions, the mesothelial cell facilitates transport of fluids, solutes, and particulate matter across the peritoneal membrane. Fluid and solute movement are governed by convection and diffusion. Particles are absorbed from the peritoneal cavity by 2 different anatomic routes. Particles smaller than 2 kd may be absorbed through peritoneal venous pores and are directed to the portal circulation. Particles larger than 3 kd are absorbed through peritoneal lymphatics, entering the lymphatic thoracic duct and from there the systemic circulation. This last route of absorption plays an important role in controlling abdominal infections because it has a huge capacity for absorption. The anatomic structure of these large channels between the peritoneal cavity and the diaphragmatic vessels and the negative pressure of the thorax during inspiration make this mechanism extremely effective in the removal of bacteria and cells. The large surface area and semi-permeability of the peritoneal membrane can be exploited therapeutically in peritoneal dialysis ( Fig. 39.3 ).

Causes and Pathogenesis

The diagnosis of secondary peritonitis is based on history, physical examination, imaging studies, and operative exploration. History and physical examination are very important in secondary peritonitis, and a good history and physical examination can often reduce or eliminate the need for further studies. Secondary peritonitis has numerous causes. Some of the more common causes of secondary peritonitis include perforated peptic ulcer disease, appendicitis, diverticulitis, acute cholecystitis, pancreatitis, and postsurgical complications. Other sources of inflammation such as autoimmune serositis (e.g., SLE), endometriosis, and malignancies cause peritoneal inflammation but rarely cause clinical peritonitis.

Other nonbacterial causes of peritonitis include leakage of blood into the peritoneal cavity due to rupture of a tubal pregnancy, ovarian cyst, or aneurysmal vessel. Blood is highly irritating to the peritoneum and may cause abdominal pain (hemorrhagic peritonitis) similar to that found in septic peritonitis. Bile leakage into the peritoneal cavity also can cause signs and symptoms of peritonitis, especially when there is also bacterial contamination of the bilious contents. However, sterile bile in the abdomen can be surprisingly asymptomatic. Large bilomas may have minimal symptoms.

Bacteria can reach the peritoneal cavity by a variety of pathologic processes: transmural inflammation with luminal obstruction (see Chapter 123 ), perforation of the GI tract, bacterial translocation (see Chapter 58 ), and intestinal ischemia (see Chapter 118 ). The initial inoculum of bacteria is determined by the normal flora in the involved portion of the GI tract (see Chapter 3 ).

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 11 ). 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 ICU patients. Analgesics typically will not relieve the findings of peritonitis on physical examination, but may relieve some discomfort. Diabetic patients may have deficits in both 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 SBP unless the parietal peritoneum becomes involved with the inflammatory process (see Chapter 93 ).

On examination, the patient with surgical peritonitis usually prefers to remain 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 in sepsis. Fever is a fundamental 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. The absence of hepatic dullness to percussion 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 board-like 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 include rebound tenderness, involuntary guarding, and extreme tenderness on palpation. Peritonitis can be diffuse, such as that associated with perforated ulcer, or localized, such as in sigmoid colonic diverticulitis confined to the LLQ. 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 120 ) can be helpful in detecting retroperitoneal or pelvic inflammation and abscesses.

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

Laboratory Tests and Imaging

The most common and widely available laboratory test that is abnormal in otherwise immunocompetent patients with peritonitis is an increased WBC count with left shift. The presence of circulating juvenile forms (i.e., bands) reflects an increasing demand for new white cells from the bone marrow. A low WBC count during a bacterial infection, associated at times with gram-negative septicemia, may indicate the presence of an exhausted bone marrow and carries a poorer prognosis. In addition, metabolic acidosis, hemoconcentration, and prerenal azotemia may be present.

Free air may be evident on upright chest radiograph or on upright or decubitus abdominal films, but the finding of pneumoperitoneum by radiography has limited sensitivity in gut perforation. The absence of free air should not delay surgical intervention in an otherwise appropriate clinical setting. US can be helpful in demonstrating abscesses, bile duct dilation, and large fluid collections but is usually not the best first-line choice for diagnostic imaging. CT of the abdomen and pelvis, generally with both oral (and occasionally rectal) and IV 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 3-dimensional sets of images. 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. 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 valuable in confirming the diagnosis of surgical peritonitis. CT is less invasive, but if not available, or if a patient is too hemodynamically unstable to undergo scanning, peritoneal lavage is an effective alternative that can be rapidly performed. Peritoneal lavage involves insertion under sterile conditions of a catheter into the peritoneal cavity and infusing 1 L of normal saline. If the effluent contains more than 500 WBCs/mm ³ , effluent amylase or bilirubin levels greater than the corresponding serum value, or bacteria are visible on Gram stain, there is approximately a 90% likelihood of surgical peritonitis. Surgery is usually indicated in this setting. Finally, diagnostic laparoscopy is highly accurate in the diagnosis of surgical peritonitis, and many of the underlying diseases can be dealt with laparoscopically, avoiding the need for laparotomy.

Treatment

Two principles in the management of secondary peritonitis cannot be overemphasized. First, not all patients with peritonitis require surgery. For example, a patient with localized LLQ peritonitis secondary to sigmoid colonic diverticulitis can be managed with bowel rest and IV 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 29 ). The second principle is that 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 physical examination findings (see Chapter 11 ). Likewise, a complete mechanical SBO generally requires emergency operation before the development of peritoneal signs that indicate progression to perforation or vascular compromise (see Chapter 123 ).

For most cases of secondary peritonitis, fluid resuscitation and antibiotic therapy followed by urgent laparotomy or laparoscopy are the mainstays of treatment. The patient should be aggressively fluid resuscitated to treat intravascular volume depletion secondary to movement of fluid out of the vascular space. Fluid resuscitation (bolus of 30 mL/kg) is guided by frequent monitoring of physiologic parameters in an intensive care setting, including blood pressure (by arterial line if shock is present), heart rate, central venous pressure, mixed venous oxygen saturation, 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. Vasopressor therapy should be initiated only after adequate volume resuscitation has failed to correct hypotension and hypoperfusion. Measurement of serum lactate levels to guide resuscitative efforts has been included in the new update for surviving sepsis guidelines. Glucocorticoids that were previously empirically administered are restricted to patients who fail to respond to fluid and vasopressor therapy. Surgical intervention for source control should be pursued as soon as the patient is hemodynamically stable for operation.