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 laxativesSecond-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