Gastric Outlet Obstruction Clinical Presentation

Updated: Jun 08, 2017
  • Author: Andres E Castellanos, MD; Chief Editor: John Geibel, MD, DSc, MSc, AGAF  more...
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Presentation

History

Nausea and vomiting are the cardinal symptoms of gastric outlet obstruction (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.

Patients with GOO resulting from a duodenal ulcer or incomplete obstruction typically present with symptoms of gastric retention, including early satiety, bloating or epigastric fullness, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss. They are frequently malnourished and dehydrated and have a metabolic insufficiency. 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, peptic ulcer disease [PUD] or pancreatic cancer).

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Physical Examination

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 blood urea nitrogen (BUN) and creatinine are late features of dehydration.

Prolonged vomiting causes loss of hydrochloric 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.

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