What are the electrolyte abnormalities associated with gastric outlet obstruction?

From the Guidelines

Gastric outlet obstruction commonly causes several electrolyte abnormalities, primarily metabolic alkalosis with hypochloremia and hypokalemia, which can be managed with fluid replacement, potassium supplementation, and addressing the underlying obstruction. This occurs because the obstruction leads to persistent vomiting, which results in significant loss of gastric acid containing hydrochloric acid and potassium, as noted in the management of malignant alimentary tract obstruction 1. The loss of hydrogen and chloride ions creates a metabolic alkalosis, while potassium depletion further exacerbates this alkalosis by promoting hydrogen ion movement into cells. Patients may also develop hyponatremia due to dehydration and inappropriate ADH secretion.

Key Considerations

• Treatment involves correcting fluid deficits with isotonic saline (0.9% NaCl) at rates based on the severity of dehydration, typically starting with a 1-2 liter bolus followed by maintenance fluids.
• Potassium chloride supplementation (typically 20-40 mEq/L of IV fluids) should be administered once urine output is established, with more aggressive replacement for severe hypokalemia (K+ <3.0 mEq/L), considering the definition of hypokalemia as K<3.5 mEq/L 1.
• Proton pump inhibitors like pantoprazole (40mg IV daily) help reduce gastric acid production.
• Addressing the underlying obstruction through nasogastric decompression and definitive treatment (endoscopic intervention or surgery) is essential for long-term correction of these abnormalities, with surgical gastrojejunostomy considered for patients with a life expectancy greater than 2 months, good functional status, and who are surgically fit 1.
• Regular monitoring of electrolytes every 4-6 hours initially is crucial to guide replacement therapy and prevent overcorrection.

From the Research

Gastric Outlet Obstruction and Electrolyte Abnormalities

• Gastric outlet obstruction (GOO) is a medical condition characterized by mechanical obstruction, which can lead to various electrolyte abnormalities 2.
• The commonest cause of GOO is pyloric stenosis secondary to peptic ulcer disease or gastric carcinoma, resulting in unique metabolic sequelae 3.
• Patients with GOO often experience hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria and hypocalcaemia 3.

Management and Treatment

• Treatment of GOO depends on the underlying cause, which can include proton pump inhibitors, H. pylori eradication, endoscopic treatments, or surgery 2.
• Endoscopic management of GOO includes balloon dilation, enteral stenting, and endoscopic ultrasound-guided gastroenterostomy (EUS-GE) to relieve mechanical blockage and reestablish per oral intake 4.
• Minimally invasive endoscopic options can provide similar clinical outcomes with fewer adverse events, faster resumption of oral feeding, and shorter hospitalizations compared to surgery 4.

Electrolyte Abnormalities in GOO

• The metabolic abnormalities associated with GOO, such as hypochloraemic, hypokalaemic metabolic alkalosis, are crucial to recognize and manage 3.
• The treatment of these electrolyte abnormalities is essential to prevent further complications and improve patient outcomes 3.
• The management of GOO should include monitoring and correction of electrolyte abnormalities, in addition to relieving the mechanical obstruction 3, 5.