A perforated bowel (e.g., caused by a perforated duodenal ulcer) often leads to the release of gas into the peritoneal cavity. This peritoneal gas can be easily visualized on an erect chest radiograph—gas can be demonstrated in extremely small amounts beneath the diaphragm. A patient with severe abdominal pain and subdiaphragmatic gas needs a laparotomy (Fig. 4.58).
In the clinic
The greater omentum
When a laparotomy is performed and the peritoneal cavity is opened, the first structure usually encountered is the greater omentum. This fatty double-layered vascular membrane hangs like an apron from the greater curvature of the stomach, drapes over the transverse colon, and lies freely suspended within the abdominal cavity. It is often referred to as the “policeman of the abdomen” because of its apparent ability to migrate to any inflamed area and wrap itself around the organ to wall off inflammation.
When a part of bowel becomes inflamed, it ceases peristalsis. This aperistaltic area is referred to as a local paralytic ileus. The remaining noninflamed part of the bowel continues to move and “massages” the greater omentum to the region where there is no peristalsis. The localized inflammatory reaction spreads to the greater omentum, which then adheres to the diseased area of bowel.
The greater omentum is also an important site for metastatic tumor spread. Direct omental spread by a transcoelomic route is common for carcinoma of the ovary. As the metastases develop within the greater omentum, it becomes significantly thickened.
In computed tomography imaging and during laparotomy, the thickened omentum is referred to as an “omental cake.”
In the clinic
Epithelial transition between the abdominal esophagus and stomach
The gastroesophageal junction is demarcated by a transition from one epithelial type (nonkeratinized stratified squamous epithelium) to another epithelial type (columnar epithelium). In some people, the histological junction does not lie at the anatomical gastroesophageal junction but occurs more proximally in the lower third of the esophagus. This may predispose these people to esophageal ulceration and is also associated with an increased risk of adenocarcinoma. In certain conditions, like gastroesophageal reflux, the stratified squamous epithelium in the esophagus can undergo metaplasia and the epithelium in the lower esophagus is replaced by columnar epithelium, a condition called Barrett’s esophagus. The presence of Barrett’s esophagus predisposes these people to the development of esophageal malignancy (adenocarcinoma).
In the clinic
Duodenal ulcers usually occur in the superior part of the duodenum and are much less common than they were 50 years ago. At first, there was no treatment and patients died from hemorrhage or peritonitis. As surgical techniques developed, patients with duodenal ulcers were subjected to extensive upper gastrointestinal surgery to prevent ulcer recurrence and for some patients the treatment was dangerous. As knowledge and understanding of the mechanisms for acid secretion in the stomach increased, drugs were developed to block acid stimulation and secretion indirectly (histamine H2-receptor antagonists) and these have significantly reduced the morbidity and mortality rates of this disease. Pharmacological therapy can now directly inhibit the cells of the stomach that produce acid with, for example, proton pump inhibitors. Patients are also screened for the bacteria Helicobacter pylori, which when eradicated (by antibiotic treatment) significantly reduces duodenal ulcer formation.
Anatomically, duodenal ulcers tend to occur either anteriorly or posteriorly.