Opioid Induced Constipation


The normal amount of stools that are passed on a weekly basis is 3 (1). The clinical definition of constipation involves having (a) less than 3 stools per week for women and 5 stools per week for men despite a diet high in dietary fiber, or a period of more than 3 days without a bowel movement (b) or straining at stool greater than 25% of the time, or 2 or fewer stools per week and © or straining when defecation and having less than 1 stool daily with minimal effort occurs (1)


However, opioid induced constipation does not only include symptoms such as hard dry stools, straining, incomplete evacuation; it also includes a combination of gastrointestinal effects such as abdominal cramping, bloating and gastroesophageal reflux (1). Tolerance to the constipating aspects of opioids is rare. (1) The constipating effects of the opioids are not dose dependent (1). Having less than 3 bowel movements per week is considered to be constipation (1).


Opiates affect all the segments of the bowel; however the colon is the most receptive to its effects (1). The proposed mechanism in which opiates cause constipation is due to the prolongation of the intestinal transit time, which is due to causing spastic nonpropulsive contractions (2). An additional proposed mechanism may be due to an increase in the electrolyte absorption (1,2). All of the opiate derivatives are linked to causing constipation, but the severity of the constipation varies among the different agents (1,2).

OIC is more pronounced with codeine than the other agents (1,2). Furthermore, transdermal opioids have less constipating effects than the oral or parenteral opioids (1,2).

In order to understand the basis behind opioid induced constipation, it is important to note that the GI tract is innervated by the enteric nervous system, which is composed of the myenteric plexus (located between circular and longitudinal smooth muscle layers of the bowel), and the submucosal plexus (2). The enteric neurons also synthesize opioid peptides, which co-cordinate the contractile process under the normal conditions and help in suppressing the intestinal motility as needed (2). Specifically, it is the mu-opioid receptors that are responsible for the agonistic effects of the opioids (2). When the opioid agonists bind to the receptors, excitatory and inhibitory neurotransmitter release is prohibited, and this interrupts the co-ordinate rhythmic contraction that is required for intestinal motility and reduces the mucosal secretions (2). The lower GI transit time results in excessive water and electrolyte reabsorption from feces and the decreased biliary and pancreatic secretion will further dehydrate the stool (2).


Concurrent use of other constipating drugs such as tricyclic antidepressants, antihistmaines, phenothiazines, antacids containing calcium carbonate or aluminum hydroxide, calcium channel blockers, non potassium sparing diuretics, other opiates also increase the likelihood of constipation (1). Dehydration, advancing age, immobility, metabolic abnormalities (such as hypercalcemia), and chemotherapy also contribute to constipation. (1)


Complications that are associated with uncontrolled constipation include fecal impaction and overflow diarrhea (feces become so hard that they cannot be expelled and fecal fluid will flow around the block), pseudo-obstruction (decreased ability of the intestines to push food through) of the bowel causing abdominal pain (increase amplitude of nonpropulsive segmental contractions), nausea, vomiting; and interference with drug administration and absorption (2,3). The risk of GERD will also increase due to decreased gastric motility and emptying (3).


Patients that experience severe pain with bowel movements, or blood in the stools should seek medical attention (1). There is no normal bowel movement as this varies greatly from person to person (1). However, treatment for constipation should improve the number of bowel movements from baseline (1).


  1. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. p. 623-628
  2. Panchal SJ, Muller-Schwefe P, Wurzelmann JI. Opioid-induced bowel dysfunction: prevalence, pathophysiology and burden. International Journal of Clinical Practice. 2007;61(7):1181-1187.
  3. Clemens KE, Klaschik E. Management of constipation in palliative care patients. Curr Opin Support Palliat Care 2008;2:22.


This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers

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