Complications

Obstruction - Gastric outlet obstruction (GOO) is not a single entity; it is the clinical and pathophysiological consequence of any disease process that produces a mechanical impediment to gastric emptying.

The major benign causes of GOO are PUD, gastric polyps, ingestion of caustics, pyloric stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars. Pancreatic cancer is the most common malignancy causing GOO. Outlet obstruction may occur in 10-20% of patients with pancreatic carcinoma. Other tumors that may obstruct the gastric outlet include ampullary cancer, duodenal cancer, cholangiocarcinomas, and gastric cancer. Metastases to the gastric outlet also may be caused by other primary tumors.

Intrinsic or extrinsic obstruction of the pyloric channel or duodenum is the usual pathophysiology of GOO; as previously noted, the mechanism of obstruction depends upon the underlying etiology.

Nausea and vomiting are the cardinal symptoms of GOO. Vomiting usually is described as nonbilious, and it characteristically contains undigested food particles. In the early stages of obstruction, vomiting may be intermittent and usually occurs within 1 hour of a meal. Early satiety and epigastric fullness are common. Weight loss is late, is most significant in patients with malignant disease. Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer.

Physical examination often demonstrates the presence of chronic dehydration and malnutrition. A dilated stomach may be appreciated as a tympanitic mass in the epigastric area and/or left upper quadrant.

Lab Studies

• Obtain a CBC. Check the hemoglobin and hematocrit - anemia.

• Obtain an electrolyte panel - identifying and correcting electrolyte abnormalities

• Liver function tests may be helpful, when a malignant etiology is suspected.

• A test for H pylori is helpful when the diagnosis of PUD is suspected

Imaging Studies

• Plain abdominal radiographs, contrast upper GI studies (Gastrografin or barium), and CT scans with oral contrast are helpful.

• Plain radiographs, including the obstruction series (ie, supine abdomen, upright abdomen, chest posteroanterior), can demonstrate the presence of gastric dilatation and may be helpful in distinguishing the differential diagnosis.

Diagnostic Procedures

• Upper endoscopy can help visualize the gastric outlet and may provide a tissue diagnosis when the obstruction is intraluminal.

• The sodium chloride load test is a traditional clinical nonimaging study that may be helpful.

  • The traditional sodium chloride load test is performed by infusing 750 cc of sodium chloride solution into the stomach via a nasogastric tube (NGT).

  • A diagnosis of GOO is made if more than 400 cc remain in the stomach after 30 minutes.

Initial management of GOO should be the same regardless of the primary cause. After a diagnosis is made, admit patients for hydration and correction of electrolyte abnormalities. Remembering that the metabolic alkalosis of GOO responds to the administration of chloride is important; therefore, sodium chloride solution should be the initial IV fluid of choice. Potassium deficits are corrected after repletion of volume status and after replacement of chloride.

• Place a NGT to decompress the stomach. Occasionally, a large tube is required because the undigested food blocks tubes with small diameters

When PUD is primary cause of GOO, focus treatment is the reduction of acid production.

Perforation - Involuntary guarding is indicative of peritonitis secondary to gastric perforation.

Penetration – is type of the closed Perforation

Hemorrhage – Upper gastrointestinal bleeding (UGIB) is a common medical condition that results in high patient mortality and medical care costs. Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. Peptic ulcer disease is the most common cause of UGIB.

UGIB is a common medical condition that results in high patient mortality and medical care costs. Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. Peptic ulcer disease is the most common cause of UGIB.

Duodenal ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa. Eradication of H pylori has been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer hemorrhage.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) are the second major etiology of ulcer hemorrhage because of their effect on cyclooxygenase-1, which leads to impaired mucosal defense to acid. The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer hemorrhage, although only when not combined with aspirin therapy. Concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors.

• The patient history findings include weakness, dizziness, syncope associated with hematemesis (coffee ground vomitus), melena (black stools with a rotten odor), and hematochezia (red or maroon stool).

• Patients may have a history of previous dyspepsia (especially nocturnal symptoms), ulcer disease, early satiety, and nonsteroidal anti-inflammatory drug or aspirin use. Many patients with UGIB who are taking NSAIDs present without dyspepsia but with hematemesis or melena as their first symptom. Low-dose aspirin (81 mg) has been associated with UGIB with or without the addition of NSAID therapy.