Late Electrolyte Disturbance in Gastric Outlet Obstruction
The most likely late electrolyte disturbance in Gastric Outlet Obstruction (GOO) is hypokalemic metabolic alkalosis (option B). 1
Pathophysiology of Electrolyte Disturbances in GOO
Gastric outlet obstruction leads to a characteristic pattern of electrolyte abnormalities through the following mechanisms:
- Initial phase: Persistent vomiting of gastric contents
- Loss of components: Significant loss of hydrogen ions, chloride, and potassium
- Compensatory response: Kidneys retain bicarbonate and excrete hydrogen ions
- Result: Hypochloremic, hypokalemic metabolic alkalosis
This metabolic alkalosis is often accompanied by:
- Elevated serum bicarbonate
- Elevated blood pH
- Paradoxical aciduria (due to potassium depletion affecting renal function)
- Hypochloremia (due to loss of chloride-rich gastric secretions)
Clinical Presentation and Diagnosis
Patients with GOO typically present with:
- Epigastric pain
- Postprandial vomiting
- Early satiety
- Signs of dehydration
- Laboratory findings showing metabolic alkalosis with hypokalemia and hypochloremia 2
Management Considerations
When treating patients with GOO and associated metabolic alkalosis:
Fluid resuscitation and electrolyte correction:
- Chloride replacement is crucial (normal saline)
- Aggressive potassium repletion
- Correction of volume depletion
Addressing the underlying cause:
Common Pitfalls to Avoid
- Underestimating potassium depletion: Total body potassium deficit is often greater than reflected in serum levels
- Inadequate chloride replacement: Chloride is essential for correcting the alkalosis
- Overlooking volume status: Patients are often severely dehydrated
- Failing to monitor electrolytes during rehydration: Rapid shifts can occur during initial treatment
Why Not the Other Options?
- Aciduria (option A): While paradoxical aciduria can occur in GOO, it's a manifestation of the underlying alkalosis, not the primary electrolyte disturbance
- Metabolic alkalosis without hypokalemia (option C): Incomplete description, as hypokalemia is a characteristic feature of the alkalosis in GOO
The metabolic alkalosis in GOO is specifically characterized by hypokalemia due to gastric losses and renal compensation mechanisms, making hypokalemic metabolic alkalosis (option B) the most accurate answer.