Peritoneal Lesion – Biopsy

Anatomy

The peritoneum consists of a single sheet of simple squamous epithelium of mesodermal origin, termed mesothelium, lying on a thin connective tissue stroma. The surface area is 1.0 to 1.7 m ² , approximately that of the total body surface area. In males, the peritoneal cavity is sealed, whereas in females it is open to the exterior through the ostia of the fallopian tubes. The peritoneal membrane is divided into parietal and visceral components. The parietal peritoneum covers the anterior, lateral, and posterior abdominal wall surfaces and the inferior surface of the diaphragm and the pelvis. The visceral peritoneum covers most of the surface of the intraperitoneal organs (i.e., stomach, jejunum, ileum, transverse colon, liver, spleen) and the anterior aspect of the retroperitoneal organs (i.e., duodenum, left and right colon, pancreas, kidneys, adrenal glands).

The peritoneal cavity is subdivided into interconnected compartments or spaces by 11 ligaments and mesenteries. The peritoneal ligaments or mesenteries include the coronary, gastrohepatic, hepatoduodenal, falciform, gastrocolic, duodenocolic, gastrosplenic, splenorenal, and phrenicocolic ligaments and the transverse mesocolon and small bowel mesentery ( Figure 4-1-1 ). These structures partition the abdomen into nine potential spaces – right and left subphrenic, subhepatic, supramesenteric and inframesenteric, right and left paracolic gutters, pelvis, and lesser space. These ligaments, mesenteries, and peritoneal spaces direct the circulation of fluid in the peritoneal cavity and thus may be useful in predicting the route of spread of infectious and malignant diseases. For example, perforation of the duodenum from peptic ulcer disease may result in the movement of fluid (and the development of abscesses) in the subhepatic space, right paracolic gutter, and pelvis. The blood supply to the visceral peritoneum is derived from the splanchnic blood vessels, whereas the parietal peritoneum is supplied by branches of the intercostals, subcostal, lumbar, and iliac vessels.

Physiology

The peritoneum is a bidirectional, semipermeable membrane that controls the amount of fluid in the peritoneal cavity, promotes the sequestration and removal of bacteria from the peritoneal cavity, and facilitates the migration of inflammatory cells from the microvasculature into the peritoneal cavity. Normally, the peritoneal cavity contains less than 100 mL of sterile serous fluid. Microvilli on the apical surface of the peritoneal mesothelium markedly increase the surface area and promote the rapid absorption of fluid from the peritoneal cavity into the lymphatics and portal and systemic circulations. The amount of fluid in the peritoneal cavity may increase to many liters in some diseases, such as cirrhosis, nephrotic syndrome, and peritoneal carcinomatosis.

The circulation of fluid in the peritoneal cavity is driven in part by the movement of the diaphragm. Intercellular pores in the peritoneum covering the inferior surface of the diaphragm (termed stomata ) communicate with lymphatic pools in the diaphragm. Lymph flows from these diaphragmatic lymphatic channels through subpleural lymphatics to the regional lymph nodes and, ultimately, the thoracic duct. Relaxation of the diaphragm during exhalation opens the stomata and the negative intrathoracic pressure draws fluid and particles, including bacteria, into the stomata. Contraction of the diaphragm during inhalation propels the lymph through the mediastinal lymphatic channels into the thoracic duct. It is postulated that this so-called diaphragmatic pump drives the movement of peritoneal fluid in a cephalad direction toward the diaphragm and into the thoracic lymphatic vessels. This circulatory pattern of peritoneal fluid toward the diaphragm and into the central lymphatic channels is consistent with the rapid appearance of sepsis in patients with generalized intra-abdominal infections, as well as the perihepatitis of Fitz-Hugh Curtis syndrome in patients with acute salpingitis.

The peritoneum and peritoneal cavity respond to infection in five ways:

• 1.

  Bacteria are rapidly removed from the peritoneal cavity through the diaphragmatic stomata and lymphatics.

• 2.

  Peritoneal macrophages release proinflammatory mediators that promote the migration of leukocytes into the peritoneal cavity from the surrounding microvasculature.

• 3.

  Degranulation of peritoneal mast cells releases histamine and other vasoactive products, causing local vasodilation and the extravasation of protein-rich fluid containing complement and immunoglobulins into the peritoneal space.

• 4.

  Protein in the peritoneal fluid opsonizes bacteria, which, along with activation of the complement cascade, promotes neutrophil- and macrophage-mediated bacterial phagocytosis and destruction.

• 5.

  Bacteria become sequestered within fibrin matrices, thereby promoting abscess formation and limiting the generalized spread of the infection.

Peritoneal Disorders