|Mr. Halvorsen is an 82-year-old man who has resided in an assisted-living facility for 3 years. He originally relocated there due to progressive difficulty with ambulation in his two-story home secondary to osteoarthritis and degenerative joint disease. Mr. Halvorsen has a long history of chronic constipation symptoms, which he has managed with bulking agents and stimulant laxatives as needed. Six months ago his physician initiated PEG 3350 at a daily dose of 17 gm per day and while this has helped a bit, Mr. Halvorsen still complains about significant straining and is concerned that he only has one bowel movement per week. He describes his BMs as extremely hard and "like rocks." He is taking the following medications:
- Ibuprofen 800 mg BID-TID
- Omeprazole 20 mg qD
- Furosemide 20 mg po qD
- Enalapril 10 mg po qD
- Acetaminophen 500 mg po BID-TID prn joint pain
- Zolpidem 10 mg po qhs prn insomnia
- Psyllium 1 TBSP po BID
- PEG 3350 17 gm PO qD
Physical examination, including a rectal examination, is unremarkable. Colonoscopy at age 79 showed diffuse diverticulosis but was otherwise normal. Colonic marker study demonstrates retention of 18 markers in the cecum and ascending colon at day 5.
The evaluation of a patient who presents with chronic constipation starts with a thorough history and physical exam. Questions to consider include reasons for current appointment, duration of symptoms, the effect of symptoms on daily activity, previous use of laxatives (including herbal medications and fiber), the need for digitation to enhance defecation, and the frequency of feeling the urge to defecate.(1)
Patients should be evaluated for alarm symptoms and signs including unexplained weight loss, blood in stool, new onset constipation in a person over 50 years, severe or persistent constipation unresponsive to treatment, and family history of colorectal cancer.(2) If any of these are present, further investigation may be warranted.
Idiopathic constipation can be classified into three broad categories based on underlying pathophysiology: normal transit constipation, slow transit constipation, and dyssynergic defecation. More than one mechanism may contribute to idiopathic constipation in any one patient.(3,4) Histopathological studies in patients with slow transit constipation have shown alterations of myenteric plexus neurons, abnormalities of inhibitory transmitters,(5) and reduction in the number of interstitial cells of Cajal.(6) Slow transit constipation can be diagnosed through a colonic marker study. In one version of this test, a gelatin capsule containing 24 markers is swallowed and an abdominal x-ray is obtained 5 days later.(7) Normal values are defined as the passage of (at least) 80% of the markers. In another version, one capsule with 24 markers is swallowed on each of 3 consecutive days and an abdominal x-ray is obtained on day 4.(8) If more than 34 markers are identified, a second abdominal x-ray is obtained on day 7. Markers are counted in the right, left, and rectosigmoid colons as defined by bony landmarks to obtain total and segmental colon transit times. A colonic transit time of <70 hours is defined as normal transit based upon the 95th percentile value.
Identification and modification of causes of secondary constipation is always indicated as a primary intervention in patients with chronic constipation symptoms. In Mr. Halvorsen's case, he is on several medications that have been associated with chronic constipation (NSAIDs, thiazide diuretics) but his physician is reluctant to change these medications. He is currently being treated for his constipation with medications from several therapeutic classes, including fiber supplements and osmotic agents, with minimal success. Since slow transit constipation has been confirmed as the probable cause of his symptoms, it would be reasonable to discontinue his current laxative medications in favor of a stimulant laxative such as senna or cascara. Depending on his response, the addition of a laxative of a different class, such as PEG 3350 or lubiprostone, may be required. There is not currently any evidence to suggest that long term laxative therapy is addictive or harmful to the colon.
Case contributed by:
Brooks D. Cash, MD, FACP, FACG, CDR, MC, USN
CDR, Medical Corps, US Navy
National Naval Medical Center
Division of Gastroenterology
(1) Locke GR, Pemberton JH, Phillips SF. AGA technical review on constipation. Gastroenterology. 2000;119:1766-1778.
(2) Brandt LJ, Prather CM, Quigley EM, Schiller LR, Schoenfeld P, Talley NJ. Systematic review on the management of chronic constipation in North America. Am J Gastroenterology 2005;100(Suppl 1):S5-S21.
(3) Rao SSC. Constipation: evaluation and treatment. Gastroenterol Clin N Am. 2003;32:659.
(4) Lembo A, Camilleri M. Chronic constipation. N Engl J Med. 2003;349:1360-1368.
(5) Tzavella K, Riepl RL, Klauser AG, Voderholzer WA, Schindlbeck NE, Muller-Lissner SA. Decreased substance P levels in rectal biopsies from patients with slow transit constipation. Eur J Gastroenterol Hepatol. 1996;8:1207-1211.
(6) He CL, Burgart L, Wang L, et al. Decreased interstitial cell of Cajal volume in patients with slow-transit constipation. Gastroenterology. 2000;118:14-21.
(7) Hinton JM, Lennard-Jones JE, Young AC. A new method for studying gut transit times using radiopaque markers. Gut. 1969; 10:842-847
(8) Metcalf AM, Phillips SF, Zinsmeister AR, et al. Simplified assessment of segmental colonic transit. Gastroenterology. 1987;92:40-47.