Epidemiology


Etiology


Pathophysiology


Clinical features


Diagnostics


Treatment


Approach

  • First-line: nonpharmacological measures (e.g., high-fiber diet, increased fluid intake, and exercise) and/or trial of bulk-forming laxatives
  • Second-line: step-wise pharmacotherapy with laxatives from other classes
    • Begin with an osmotic laxative.
    • If symptoms persist, add a short course of a stimulant laxative.

Laxatives

  • Bulk-forming laxatives (fiber)
    • Mechanism
      • Bulk-forming laxatives are indigestible, not systemically absorbed.
      • Soluble fibers increase water absorption in the intestinal lumen → stretching of the bowel wall → stimulation of peristalsis
  • Osmotic laxatives
    • Agents: Polyethylene glycol (PEG) and lactulose
  • Stimulant laxatives (secretory laxatives)
    • Agents: Bisacodyl and sodium picosulfate
    • Mechanism
      • Stimulation of epithelial cell secretion of electrolytes into the colonic lumen → ↑ Secretion of fluid into the colon (with bisacodyl, this secretory activity is nitric oxide-mediated)
      • Myenteric neuronal depolarization → colon contractions (peristalsis)
  • Surfactant (eg, docusate)
    • Decreases stool surface tension, enabling water to enter stool
  • Chloride channel agonist (eg, lubiprostone)
    • Causes chloride efflux into intestinal lumen, which is followed by sodium and watered
  • Peripherally acting µ-opioid receptor antagonists (eg, methylnaltrexone)
    • Counteracts inhibitory effect of opioids on peristalsis