A 60-year-old woman presents with a several-week history of worsening non-bilious emesis and epigastric abdominal pain. She also reports several months of early satiety and decreased appetite and a 15-pound unintentional weight loss over the past 6 months.
Upon examination, the patient is afebrile with normal vital signs. She is a very thin and frail-appearing woman. Her abdomen is soft with focal tympany and tenderness to palpation in the left upper quadrant. There are no palpable abdominal masses. Her laboratory studies are notable for a hypokalemic, hypochloremic metabolic alkalosis.
The incidence of gastric outlet obstruction (GOO) is not precisely known, though it is likely lower in recent years due to the decrease in peptic ulcer disease (PUD). The clinical entities that cause GOO are generally categorized into two well-defined groups—benign and malignant. Before the identification of Helicobacter pylori (H. pylori) and the advent of H2-receptor antagonists, when PUD was more prevalent, benign causes of GOO were more common than malignant causes. Today, this ratio is reversed, with recent reviews reporting that 50% to 80% of all cases are attributable to an underlying malignancy.1, 2, and 3 The leading benign cause of GOO remains PUD, although the incidence is very low, with GOO occurring in only approximately 2% of patients with PUD.4,5 In contrast, the incidence of GOO complicating primary pancreatic, gastric, or duodenal malignancy is reported to be as high as 15% to 25%.6
GOO results from either an intrinsic or an extrinsic obstruction of the pyloric channel or duodenum. The underlying disease process dictates the precise mechanism of the obstruction.
In benign causes, the obstruction is typically the result of inflammation, edema, or scarring in the region of the pyloric channel or duodenal bulb. With PUD, the obstruction typically results from acute inflammation and edema or chronic fibrosis and scarring of the pyloric channel or duodenal bulb. Similarly, gastroduodenal involvement with Crohn’s disease can lead to a Crohn’s-related stricture. With pancreatitis, intense peri-pancreatic inflammation and edema can result in inflammation and fibrosis of the adjacent duodenum. In contrast, obstruction secondary to a large gastric polyp, gastric bezoar, gastric volvulus, or migration of a gastrostomy tube represents a discrete mechanical problem.
In the case of gastric and duodenal malignancies, GOO typically results from intrinsic obstruction by the primary tumor. With pancreatic malignancies, GOO is usually secondary to extrinsic compression by the primary tumor, or by metastatic disease at the gastroduodenal junction.
Emesis and epigastric pain are the cardinal symptoms of GOO, with each occurring in over 90% of patients. Other commonly seen symptoms include early satiety, abdominal distention, and weight loss.7 Initially, patients have intermittent symptoms that then progress until the obstruction is complete. Malnutrition is a ...