What is Salt-Losing Enteropathy?
Salt-losing enteropathy is a pathological condition where the intestine loses more sodium and water into the lumen than it absorbs, resulting in net secretion that leads to dehydration, electrolyte depletion, and secondary hyperaldosteronism if left untreated. 1
Pathophysiology and Mechanisms
Salt-losing enteropathy occurs when the intestinal epithelium becomes abnormally permeable or damaged, allowing sodium-rich fluid to escape into the intestinal lumen at rates exceeding absorptive capacity. 1
Primary Mechanisms
Shortened bowel length: When less than 100 cm of jejunum remains after surgical resection, most patients become "net secretors," losing more fluid from their stoma than they consume orally, with stomal fluid containing approximately 90-100 mmol/L sodium (range 80-140 mmol/L). 1
Epithelial barrier dysfunction: The leaky intestinal epithelium allows both hypotonic fluids (water, tea, coffee) and hypertonic fluids (fruit juices, sodas) to stimulate fluid secretion or increase sodium and fluid influx into the jejunal lumen, paradoxically worsening stomal losses. 1
Inflammatory mucosal damage: Active inflammatory bowel disease, particularly ulcerative colitis, causes impaired colonic capacity to absorb chloride and sodium while retaining the ability to secrete potassium, creating a true salt-losing diarrhea. 2
Secondary Metabolic Consequences
The sodium and water depletion triggers secondary hyperaldosteronism, which compounds the problem by increasing urinary losses of magnesium and potassium. 1 This creates a vicious cycle where magnesium depletion is further worsened by unabsorbed fatty acids binding intraluminal magnesium. 1
Clinical Presentation
Patients with salt-losing enteropathy typically present with:
High-output stomas exceeding 2 liters per 24 hours, placing them at particular risk for significant dehydration and electrolyte disturbances. 1
Dehydration signs including reduced urine output (less than 800 mL/day), concentrated urine with sodium concentration below 20 mmol/L, and clinical volume depletion. 3
Metabolic alkalosis from excessive chloride loss in addition to sodium and water loss, commonly found in active proctocolitis. 2
Refractory hypokalemia and hypocalcemia that will not correct until magnesium deficiency is addressed first. 3
Distinction from Protein-Losing Enteropathy
While both conditions involve intestinal losses, salt-losing enteropathy specifically refers to excessive sodium and water loss, whereas protein-losing enteropathy involves loss of serum proteins (particularly albumin) into the gastrointestinal tract. 4, 5 These are distinct pathophysiological processes that may coexist but require different diagnostic and therapeutic approaches. 6
High-Risk Populations
Patients at greatest risk include:
Short bowel syndrome patients with reduced jejunal length ending in a stoma, particularly those with less than 100 cm of remaining jejunum. 1
Active inflammatory bowel disease patients, especially those with extensive colonic involvement. 2
Post-surgical patients in the immediate postoperative hypersecretory phase following intestinal resection. 3
Critical Diagnostic Indicators
The diagnosis is primarily clinical, based on:
Stomal output volume consistently exceeding 1200 mL/day despite oral intake restriction. 3
Urine sodium concentration below 20 mmol/L with reduced urine volume, indicating inadequate sodium repletion. 3
Elevated renin and aldosterone levels confirming secondary hyperaldosteronism from chronic volume depletion. 3