Peritoneum and Related Diseases

Embryology

The peritoneum development begins in the fifth week of gestation at the gastrulation stage, during which a trilaminar layer of endoderm, mesoderm, and ectoderm develops. The future parietal peritoneum will originate from the lateral parietal plate of the mesoderm and the ectoderm, as with the visceral peritoneum from the visceral plate of the mesoderm and the endoderm. Between this, two layers of the mesothelial membrane will form and its visceral portion will cover most of the surface of intraperitoneal organs and anterior aspect of retroperitoneal organs. The peritoneal cavity contains approximately 100 mL of sterile fluid, which lines the visceral organs and aids in defense. The intraperitoneal organs are suspended by peritoneal ligaments. Meyers et al. describe 11 peritoneal ligaments and mesenteries; these allow continuity of anatomic planes and direct the circulation of fluid within the peritoneal cavity. This leads to the spread of infection or malignancy between intraperitoneal and extraperitoneal compartments.

Anatomy and Physiology

The omentum is a protective vascular peritoneal fold, walling off inflammatory processes, infection, or malignancy. The greater omentum (gastrocolic omentum, or ligament) is the largest peritoneal fold; it drapes over from the greater curvature of the stomach overlying the abdominal viscera. The upper end of the left border is continuous with the gastrosplenic ligament, and the upper end of the right border extends to the first portion of the duodenum. The greater omentum is usually a thin, delicate layer of fibroelastic tissue; it usually also contains some adipose tissue and may accumulate a large amount of fat in an obese patient.

The lesser sac peritoneum on the posteroinferior surface of the stomach and the greater sac peritoneum on the anterosuperior surface meet at the greater curvature of the stomach and course inferiorly to the free border of the greater omentum, where they turn superiorly to the transverse colon.

The lesser omentum (gastrohepatic omentum, or ligament), hepatogastric ligaments, and hepatoduodenal ligaments extend from the posteroinferior surface of the liver to the lesser curvature of the stomach and the beginning of the duodenum. The lesser omentum is extremely thin, on the left portion, and sometimes fenestrated, while the right is thicker and ends in a free, rounded margin that contains the common bile duct to the right, the hepatic artery to the left, and the portal vein posterior to these; it then forms the anterior border of the epiploic foramen. In addition to these structures, the lesser omentum contains the right and left gastric arteries close to the lesser curvature of the stomach and the accompanying veins, lymphatics, and autonomic nerve plexuses. The peritoneum forming the anterior layer of this omentum and continuing onto the anterosuperior surface of the stomach is the greater sac peritoneum, and that forming the posterior layer and continuing onto the posteroinferior surface of the stomach is the lesser sac peritoneum. The lesser omentum reaches the liver at the porta, and to the left of the porta it extends to the bottom of the fossa for the ligamentum venosum.

The blood supply and innervation of the peritoneum is distinct from the visceral and parietal. The parietal peritoneum receives its blood supply from intercostal, lumbar, and iliac vessels while the visceral blood supply is from the splanchnic vasculature. The visceral peritoneum is supplied by nonsomatic nerves and parietal supplied by somatic nerves. Visceral pain will be vague and generalized, stimulated by irritation of splanchnic nerves. Parietal pain is sharp and localized due to direct stimulation of phrenic, thoracoabdominal, subcostal, or lumbar sacral nerves. This distinction is critical for clinical assessment.

Diagnosis

The diagnosis of peritonitis depends on history, examination, and laboratory and radiologic findings. Early features depend on the severity and extent of the peritonitis. Clinically, pain may be localized or generalized. Extensive peritonitis that involves subdiaphragmatic abscess or collection may be accompanied by shoulder pain. Vomiting often occurs early in the disease course, as well malaise and fevers. As disease process progresses, abdomen may become more distended.

The differential diagnosis for acute peritonitis includes appendicitis, perforated peptic ulcers, pelvic inflammatory disease or ruptured ovarian cyst, diverticulitis, ischemic bowel and perforation, gangrenous cholecystitis, or necrotizing pancreatitis.

Abdominal radiography reveals free subdiaphragmatic gas from hollow viscus perforation. Abdominal ultrasound and computed tomography (CT) should be reserved for cases requiring further confirmation to obtain an accurate diagnosis. Ultrasound is an effective tool to evaluate the acute abdomen and to rapidly assess multiple organs. Doppler imaging reveals any vascular abnormalities, including embolic or thrombotic site, aortic and visceral arterial aneurysm, or arteriovenous fistula.

CT is a safe, noninvasive, and efficient method that provides sensitive detection of free air, abscesses, calcifications, and collections of intraperitoneal fluid, as well as detailed information of the bowel wall, mesentery, and retroperitoneum—in particular, kidneys, pancreas, duodenum, and the aorta. Use of intravenous and oral contrast materials is recommended to delineate obstruction, collections, and vasculature. Special attention must be given to patients with impaired renal function and/or contrast allergy. In addition, CT magnetic resonance imaging (MRI) requires more time and is generally less useful than CT.