Pyloric Obstruction and the Effects of Vomiting

Clinical Picture

When the outlet of the stomach becomes narrowed to the point of interference with gastric emptying, the gastric musculature responds at first with increased peristalsis in an effort to build up sufficient pressure to overcome the resistance at its pyloric end. At this stage, the patient may experience a sensation, or burning, in the epigastrium or left hypochondrium. With persisting obstruction and further stagnation of ingested food and gastric secretion, the stomach begins to dilate; the musculature becomes atonic, and peristaltic activity is minimal. At this stage, the patient reports fullness, vomiting of undigested food consumed many hours earlier, and foul-smelling eructation. If the obstruction is unrelieved, vomiting becomes more frequent and more copious. With so little gastric content now passing into the intestine because of the profound gastric atony, the patient is powerless to keep up with the fluid and electrolytes lost in the vomitus. Dehydration, hypochloremia, hypokalemia, and alkalosis supervene, which in turn affect renal function, with development of oliguria, azotemia, and retention of other electrolytes. Clinically, the patient is weak, anorexic, and drowsy. Unless measures are instituted to correct the metabolic disorder and to relieve the obstruction, the condition progresses to irreversible tissue damage and death.

Pyloric obstruction is not the only cause of vomiting (see Chapter 27 ), but the diagnosis may be suspected because of the history just described, the pattern of the emesis, and the appearance of the vomitus. In duodenal ulcer, which is the most common cause of pyloric obstruction, the patient usually gives a history of ulcer symptoms. The vomiting is at first intermittent, perhaps 2 or 3 days apart, and the vomitus often contains recognizable particles of food eaten the previous day.

As with excessive vomiting from any cause, the patient has appreciable losses of fluids and hydrogen (H ⁺ ), chloride (Cl ⁻ ), and potassium (K ⁺ ) ions. Because the gastric juice is poor in sodium (Na ⁺ ), usually no sodium deficiency occurs, and although Na ⁺ remains in the blood, bicarbonate (HCO ₃ ⁻ ) substitutes for Cl ⁻ . Loss of K ⁺ occurs because parietal cells secrete significant amounts of this ion.

Vomiting does not usually occur in uncomplicated ulcer disease, except when the ulcer is located in the pyloric canal. However, many patients with ulcers empty the stomach through vomiting to obtain pain relief.