Introduction
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.
Clinical entities that can result in GOO generally are categorized into 2 well-defined groups of causes—benign and malignant. This classification facilitates discussion of management and treatment. In the past, when peptic ulcer disease (PUD) was more prevalent, benign causes were the most common; however, one review shows that only 37% of patients with GOO have benign disease and the remaining patients have obstruction secondary to malignancy.1
Problem
GOO can be a diagnostic and treatment dilemma. As part of the initial workup, exclude the possibility of functional nonmechanical causes of obstruction, such as diabetic gastroparesis.
Once a mechanical obstruction is confirmed, differentiate between benign and malignant processes because definitive treatment is based on recognition of the specific underlying cause.
Carry out diagnosis and treatment expeditiously because delay may result in further compromise of the patient's nutritional status.
Frequency
The incidence of GOO has been reported to be less than 5% in patients with PUD, which is the leading benign cause of the problem.
The incidence of GOO in patients with peripancreatic malignancy, the most common malignant etiology, has been reported as 15-20%.
Etiology
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.
PUD manifests in approximately 5% of all patients with GOO. Ulcers within the pyloric channel and first portion of the duodenum usually are responsible for outlet obstruction. Obstruction can occur in an acute setting secondary to acute inflammation and edema or, more commonly, in a chronic setting secondary to scarring and fibrosis. Helicobacter pylori has been implicated as a frequent associated finding in patients with GOO, but its exact incidence has not been defined precisely.
Within the pediatric population, pyloric stenosis constitutes the most important cause of GOO. Pyloric stenosis occurs in 1 per 750 births. It is more common in boys than in girls and also is more common in first-born children. Pyloric stenosis is the result of gradual hypertrophy of the circular smooth muscle of the pylorus.
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.
Pathophysiology
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.
Patients present with intermittent symptoms that progress until obstruction is complete. Vomiting is the cardinal symptom. Initially, patients may demonstrate better tolerance to liquids than solid food.
In a later stage, patients may develop significant weight loss due to poor caloric intake. Malnutrition is a late sign, but it may be very profound in patients with concomitant malignancy.
In the acute or chronic phase of obstruction, continuous vomiting may lead to dehydration and electrolyte abnormalities.
When obstruction persists, patients may develop significant and progressive gastric dilatation. The stomach eventually loses its contractility. Undigested food accumulates and may represent a constant risk for aspiration pneumonia.
Presentation
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 frequent when the condition approaches chronicity and 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.
Dehydration and electrolyte abnormalities can be demonstrated by routine laboratory examinations. Increases in BUN and creatinine are late features of dehydration. Prolonged vomiting causes loss of hydrochloric (HCl) acid and produces an increase of bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is a hypokalemic hypochloremic metabolic alkalosis. Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum positive potassium is increased factitiously. With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia.
Indications
Once the diagnosis is suspected, request a surgical consultation.
Patients with GOO due to benign ulcer disease may be treated medically if results of imaging studies or endoscopy determine that acute inflammation and edema are the principle causes of the outlet obstruction (as opposed to scarring and fibrosis, which may be fixed). If medical therapy conducted for a reasonable period fails to alleviate the obstruction, then surgical intervention becomes appropriate. The choice of surgical procedure depends upon the patient's particular circumstances; however, vagotomy and antrectomy should be considered the criterion standard against which the efficacy of other procedures should be measured.
Weigh the extent of surgical intervention for the relief of GOO against the type and extent of malignancy and the patient's anticipated long-term prognosis. As a guiding principle, undertake major tumor resections in the absence of metastatic disease in a patient who can withstand such a procedure from a nutritional standpoint. In patients with largely metastatic disease, determine the degree of surgical intervention for palliation in light of the patient's realistic prognosis and personal wishes.
Relevant Anatomy
The stomach is located mainly in the left upper quadrant beneath the diaphragm and is attached superiorly to the esophagus and distally to the duodenum. The stomach is divided into 4 portions, the cardia, the body, the antrum, and the pylorus. Inflammation, scarring, or infiltration of the antrum and pylorus are associated with the development of GOO.
The duodenum begins immediately beyond the pylorus and mostly is a retroperitoneal structure, wrapping around the head of the pancreas. The duodenum classically is divided into 4 portions. It is intimately related to the gallbladder, liver, and pancreas; therefore, a malignant process of any adjacent structure may cause outlet obstruction due to extrinsic compression.
Contraindications
Contraindications for surgery relate to the underlying medical condition.
Most patients benefit from an initial period of gastric decompression, hydration, and correction of electrolyte imbalances. In patients who are severely malnourished, postponing surgical intervention until the nutritional status has been optimized may be wise. In selective cases, some patients may benefit from total parenteral nutrition (TPN) or distal tube feeding (eg, placed via a percutaneous jejunostomy).
One of the relative contraindications for surgery is the presence of advanced malignancy; in these cases, life expectancy may be limited to a few months.
Overall, every patient with GOO deserves evaluation by a surgeon. Even if the patient has unresectable disease, other palliative surgical measures may improve the quality of life.
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Further Reading
Keywords
GOO, gastric obstruction, proximal bowel obstruction, peptic ulcer disease, PUD, peripancreatic malignancy
