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Diagnosis and management of chronic constipation

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Diagnosis and management of chronic constipation

Diagnosis is a challenge because patients and clinicians often define constipation differently. The history, physical examination, and appropriate diagnostic procedures are key.

Jennifer Drost, MMSc, PA-C; Lucinda A. harris, MS, MD

Jennifer Drost works in the Division of Internal Medicine and Lucinda Harris is Senior Associate Consultant, Division of Gastroenterology and Hepatology, both at the Mayo Clinic Arizona, Scottsdale. Dr. Harris reports grant support from Novartis.

Constipation is a common GI motility disorder that affects 2% to 27% of North Americans, with most estimates at 12% to 19%.1 Constipation afflicts more than twice as many women as men.1 Although most people experience occasional bouts of constipation, for many it is a chronic condition.

The activities and relationships of those with chronic constipation (CC) are generally affected. Health-related quality of life is more negatively impacted in people with CC and other GI motility disorders than in the general healthy population—and even than in people with other chronic conditions, such as asthma.2 Relatively few people with symptoms of CC seek medical treatment, and those who do are often not effectively treated.3,4 CC imposes a substantial economic burden through direct (physician and hospital visits and medications) and indirect (absence from or reduced productivity at work) costs.5-7

Defining chronic constipation

One challenging issue facing the patient and the clinician is determining what constipation actually is. There is no formal clinical definition, and clinicians, patients, and diagnostic criteria define constipation differently8-10 (see Table 1). Another challenge is deciding when to consider the condition chronic, which is often arbitrarily defined by most criteria—including the Rome II criteria—as lasting at least 3 months.9 Rome II states that the symptoms should be present for at least 1 year.

New definition Because the Rome II criteria can be restrictive in clinical practice, the American College of Gastroenterology (ACG) recently recommended an expanded definition of constipation: “Unsatisfactory defecation characterized by infrequent stools, difficult stool passage, or both. Difficult stool passage includes straining, a sense of difficulty passing stool, incomplete evacuation, hard/lumpy stools, prolonged time to stool, or need for manual maneuvers to pass stool.”11 The ACG Chronic Constipation Task Force also clarified what is meant by chronic, stating that “Chronic constipation is defined as the presence of these symptoms for at least 3 months.”11 Additionally, the Task Force recognized that this disorder can have a significant impact on quality of life. Realizing the restrictive nature of the Rome II criteria for constipation, the Rome III Criteria were recently released. The differences between Rome II and Rome III are outlined in Table 1.12

Types of constipation Defining CC is essential for accurate diagnosis and satisfactory treatment. Understanding its causes is crucial for proper diagnosis. Constipation can be classified into two broad categories: primary and secondary (see the tables on the Web13-17). Secondary causes of constipation should be considered before proceeding with diagnostic testing or therapy.

Evaluation and diagnosis

A thorough evaluation is needed to assess the patient’s condition, rule out systemic disease, and determine the best course of treatment. "Diagnostic workup for constipation" offers a helpful algorithm.17,18

Diagnostic tools Given the sensitive nature of the subject, a useful tool for evaluating stool consistency is the Bristol Stool Form Scale, which helps the patient describe bowel movements in an objective and minimally embarrassing manner.19 Another helpful tool is a daily diary for recording bowel movement frequency (date and time), daily symptoms of constipation (straining, bloating, feelings of incomplete evacuation), and frequency and dosage of any medications taken for symptom relief.

These tools are useful for comparing the patient’s definition of constipation with the clinician’s and determining whether any misconceptions exist regarding what constitutes “normal” bowel habits. Unfortunately, there is no standard definition of a “normal” number of bowel movements, but the literature suggests a range from three per day to three per week.20,21

Physical examination It is important to determine if alarm features suggestive of possible underlying disease are present. A thorough neurologic examination can help determine the presence or absence of systemic illness. Palpation of the abdomen will reveal masses, distention, tenderness, abnormal bowel sounds, presence of stool throughout the colon, and surgical scars.

The rectal examination is an important part of the process, and explaining what is involved will elicit better cooperation from the patient. The left lateral recumbent position is optimal for the visual part of the examination. Closely inspect the perianal area by gently spreading the buttocks to look for fissures, hemorrhoids, masses, skin tags, or evidence of previous surgery. Fissures most often occur anteriorly and posteriorly; their presence elsewhere may indicate Crohn’s disease. Digital rectal examination is important to identify internal hemorrhoids, anal strictures, rectal masses, or impaction.13

Diagnosis A positive diagnosis of chronic constipation can be made based on the symptoms, medical history, and rectal examination. Diagnostic testing should be reserved for patients who exhibit alarm features, have symptoms refractory to empiric therapy, or are thought to have a particular disorder.22,23 Primary care clinicians may perform the diagnostic laboratory tests themselves or refer the patient to a specialist for more specific testing.

Management options

Clarify the patient’s expectations of treatment. Setting realistic goals leads to satisfaction with care and promotes a better therapeutic outcome. Does the patient expect symptoms to be completely alleviated? Is she or he willing to deal with minor adverse effects of treatment? Is the goal simply to be able to lead a normal life without being tied to a bathroom? Review treatment options with the patient, including potential symptom relief and possible adverse effects.

Diet and lifestyle modifications, which include increases in dietary fiber intake, water consumption, and exercise, often constitute the first approach to treatment. Although these measures are good health practices that may help dehydrated or sedentary patients, few data support their overall effectiveness. Additionally, increased fiber intake may actually worsen symptoms, causing abdominal discomfort and bloating in patients with moderate to severe constipation.24

Laxatives When diet and lifestyle measures are ineffective, laxatives are generally the next treatment choice. See Table 2 for a summary of the classes of laxatives—bulk forming, emollient, osmotic, and stimulant—and their various mechanisms, onsets of action, adverse effects, and therapeutic roles.17,25-29 Despite the widespread use of laxatives, reliable, evidence-based data evaluating their benefit for patients with CC are lacking.


Only two recently published reviews of clinical trials data support laxative use for CC.30,31 Based on parameters set forth by Ramkumar and Rao, polyethylene glycol (PEG) was the only substance shown to improve bowel movement frequency, stool consistency, and colonic transit time.30 PEG earned a grade A rating since the data supporting its use are based on randomized, placebo-controlled trials.30 It is important to note, however, that although this analysis included all formulations of PEG, only PEG 3350 is approved by the FDA for use in patients with occasional constipation.

In another review, the ACG Chronic Constipation Task Force concluded that the data were insufficient in most cases to make recommendations about the efficacy of psyllium, calcium polycarbophil, methylcellulose, bran, stool softeners, milk of magnesia, and stimulant laxatives in patients with CC.31 Lactulose and PEG each received a grade A recommendation. However, this review also included all formulations of PEG and a trial in patients with opioid-induced constipation. The two trials involving PEG 3350 were not randomized controlled trials and were of short duration (2 weeks); one was of crossover design with a small number of patients (n = 23).31 These two systematic reviews highlight the paucity of good clinical data to support the use of many commonly used laxatives in treating patients with CC.

Serotonergic agents Research in the past two decades has provided increasingly insightful information about GI motility, particularly the role of the enteric nervous system (ENS) and how it communicates with the CNS—often referred to as the brain-gut axis. The ENS acts semiautonomously from the CNS to regulate gut function. Alterations in neurotransmitters have been identified among many potential underlying abnormalities associated with constipation.32 Although several neurotransmitters are involved in regulating GI tract function, serotonin (5-hydroxytryptamine [5-HT]) appears to be a common link—important for GI motility, intestinal secretion, and pain perception.33 Many people are aware of serotonin’s role in the CNS, but most do not realize that 95% of the body’s total serotonin content originates from enterochromaffin cells within the GI tract, where it functions as part of the ENS.32,34

Dysfunction of the serotonin signaling pathways may result in increased GI tract sensitivity, increased or decreased GI motility, and altered intestinal secretions. These changes in GI physiology may manifest as symptoms associated with GI motility disorders.33,35 Recent evidence suggests an association between CC and alterations in serotonin synthesis and signaling.32 In addition, a link between alterations in serotonin signaling and IBS has recently been shown.32,33,35

Of the serotonin receptor subtypes identified to date, types 1P (5-HT1P), 3 (5-HT3), and 4 (5-HT4) are important in regulating GI tract function.33,34 Modulation of 5-HT3 and 5-HT4 receptor subtypes can affect peristaltic reflexes and thus intestinal motility; 5-HT4 receptor agonists enhance the peristaltic reflex,33 increase stool fluid content,36 and reduce visceral sensation.32 Clinically, blocking or activating specific 5-HT receptors affects symptoms, including altered bowel habits, abdominal pain/discomfort, bloating, straining, feelings of incomplete evacuation, and the urge to defecate.

Selective 5-HT4 receptor agonists Tegaserod has been approved by the FDA for the treatment of women who have irritable bowel syndrome with constipation and of men and women younger than 65 years with chronic idiopathic constipation. Two large clinical studies demonstrated that treatment with tegaserod (2 mg twice daily or 6 mg twice daily) for 12 weeks produced statistically significant improvement over placebo in low bowel frequency and other constipation symptoms.37-39 Tegaserod was safe and well tolerated, with no significant differences in adverse events among treatment groups. Tegaserod received a grade A recommendation from the ACG Task Force for the treatment of patients with CC.11

Chloride channel activators Lubiprostone increases the frequency of bowel movements and relieves other symptoms of constipation.40-43 Fluid secretion in the gut depends on chloride secretion, which is mediated by chloride channels located in epithelial cells that line the intestine. Activators of chloride channels increase fluid secretion and soften stool. The FDA recently approved lubiprostone for CC and associated symptoms in those aged 18 years or older.

Conclusion

Because of the stigma surrounding open discussion of bowel disorders, consider using dialogue, open-ended questions, and questionnaires that can be completed in private to initiate discussion. Educating patients that CC is not always related to lifestyle and dietary habits also can make them feel more comfortable and less alone. In addition, advising patients that viable treatment options are available will help decrease anxiety. If pharmacotherapy is indicated, counseling regarding proper dosage guidelines, potential adverse effects, and realistic therapy goals will help manage expectations. If reasonable treatment trials are not effective, referral to a gastroenterologist may be warranted.

The authors would like to acknowledge the editorial assistance of Cathy Winter, PhD, and Maribeth Bogush, PhD, in the preparation of this manuscript.

REFERENCES

1. Higgins PD, Johanson JF. Epidemiology of constipation in North America: a systematic review. Am J Gastroenterol. 2004;99(4):750-759.

2. Chang L. Review article: epidemiology and quality of life in functional gastrointestinal disorders. Aliment Pharmacol Ther. 2004;20(suppl 7):31-39.

3. Schiller LR, Dennis E, Toth G. An Internet-based survey of the prevalence and symptom spectrum of chronic constipation [abstract]. Am J Gastroenterol. 2004;99(10 suppl):S234. Abstract 723.

4. Palsson OS, Whitehead WE, Levy RL, et al. Constipation less effectively treated than other functional bowel problems in a health maintenance organization (HMO) [abstract]. Am J Gastroenterol. 2004;99(10 suppl):S287. Abstract 878.

5. Martin BC, Barghout V. National estimates of office and emergency room constipation-related visits in the United States [abstract]. Am J Gastroenterol. 2004;99(10 suppl):S244. Abstract 754.

6. Singh G, Kahler K, Bharathi V, et al. Adults with chronic constipation have significant health care resource utilization and costs of care [abstract]. Am J Gastroenterol. 2004;99(10 suppl):S227. Abstract 701.

7. Bracco A, Kahler K. Burden of chronic constipation must include estimates of work productivity and activity impairment in addition to traditional healthcare utilization [abstract]. Am J Gastroenterol. 2004;99(10 suppl):S233. Abstract 719.

8. Herz MJ, Kahan E, Zalevski S, et al. Constipation: a different entity for patients and doctors. Fam Pract. 1996;13(2):156-159.

9. Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut. 1999;45(suppl 2):1143-1147.

10. Pare P, Ferrazzi S, Thompson WG, et al. An epidemiological survey of constipation in Canada: definitions, rates, demographics, and predictors of health care seeking. Am J Gastroenterol. 2001;96(11):3130-3137.

11. American College of Gastroenterology Chronic Constipation Task Force. Evidence-based approach to the management of chronic constipation in North America. Am J Gastroenterol. 2005;100(suppl 1):S1-S21.

12. Longstreth GF, Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology. 2006;130(5):1480-1491.

13. Lembo A, Camilleri M. Chronic constipation. N Engl J Med. 2003;349(14):1360-1368.

14. Rao SS. Constipation: evaluation and treatment. Gastroenterol Clin North Am. 2003;32(2):659-683.

15. Wald A. Constipation. Med Clin North Am. 2000;84(5):1231-1246.

16. Locke GR 3rd, Pemberton JH, Phillips SF. AGA technical review on constipation. American Gastroenterological Association. Gastroenterology. 2000;119(6):1766-1778.

17. Faigel DO. A clinical approach to constipation. Clin Cornerstone. 2002;4(4):11-21.

18. Borum ML. Constipation: evaluation and management. Prim Care. 2001;28(3):577-590.

19. Lewis SJ, Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol. 1997;32(9):920-924.

20. Tucker DM, Sandstead HH, Logan GM Jr, et al. Dietary fiber and personality factors as determinants of stool output. Gastroenterology. 1981;81(5):879-883.

21. Connell AM, Hilton C, Irvine G, et al. Variation of bowel habit in two population samples. Br Med J. 1965;5470:1095-1099.

22. Arce DA, Ermocilla CA, Costa H. Evaluation of constipation. Am Fam Physician. 2002;65(11):2283-2290.

23. Schiller LR. Review article: the therapy of constipation. Aliment Pharmacol Ther. 2001;15(6):749-763.

24. Müller-Lissner SA, Kamm MA, Scarpignato C, Wald A. Myths and misconceptions about chronic constipation. Am J Gastroenterol. 2005;100(1):232-242.

25. Pampati V, Fogel R. Treatment options for primary constipation. Curr Treat Options Gastroenterol. 2004;7(3):225-233.

26. DiPalma JA. Current treatment options for chronic constipation. Rev Gastroenterol Disord. 2004(suppl 2):S34-S42.

27. Christer R, Robinson L, Bird C. Constipation: causes and cures. Nurs Times. 2003; 99(25):26-27.

28. MiraLax [package insert]. Braintree, Mass: Braintree Laboratories; 1998.

29. Wanitschke R, Goerg KJ, Loew D. Differential therapy of constipation—a review. Int J Clin Pharmacol Ther. 2003;41(1):14-21.

30. Ramkumar D, Rao SS. Efficacy and safety of traditional medical therapies for chronic constipation: systematic review. Am J Gastroenterol. 2005;100(4):936-971.

31. Brandt LJ, Prather CM, Quigley EM, et al. Systematic review on the management of chronic constipation in North America. Am J Gastroenterol. 2005;100(suppl 1):S5-S21.

32. Crowell MD, Shetzline MA, Moses PL, et al. Enterochromaffin cells and 5-HT signaling in the pathophysiology of disorders of gastrointestinal function. Curr Opin Investig Drugs. 2004;5(1):55-60.

33. Crowell MD. The role of serotonin in the pathophysiology of irritable bowel syndrome. Am J Manag Care. 2001;7(8 suppl):S252-S260.

34. Gershon MD. Serotonin and its implication for the management of irritable bowel syndrome. Rev Gastroenterol Disord. 2003;3(suppl 2):S25-S34.

35. Coates MD, Mahoney CR, Linden DR, et al. Molecular defects in mucosal serotonin content and decreased serotonin reuptake transporter in ulcerative colitis and irritable bowel syndrome. Gastroenterology. 2004;126(7):1657-1664.

36. Stoner MC, Arcuni JC, Lee J, Kellum JM. A selective 5-HT4 receptor agonist induces CAMP-mediated Cl¯ efflux from rat colonocytes [abstract]. Gastroenterology. 1999; 116(4 suppl 2):A648. Abstract G2827.

37. Johanson JF. Review article: tegaserod for chronic constipation. Aliment Pharmacol Ther. 2004;20(suppl 7):20-24.

38. Kamm MA, Muller-Lissner S, Talley NJ, et al. Tegaserod for the treatment of chronic constipation: a randomized, double-blind, placebo-controlled multinational study. Am J Gastroenterol. 2005;100(2):362-372.

39. Johanson JF, Wald A, Tougas G, et al. Effect of tegaserod in chronic constipation: a randomized, double-blind, controlled trial. Clin Gastroenterol Hepatol. 2004;2(9):796-805.

40. Schiller LR. New and emerging treatment options for chronic constipation. Rev Gastroenterol Disord. 2004;4(suppl 2):S43-S51.

41. Cuppoletti J, Malinowska DH, Tewari KP, et al. SPI-0211 activates T84 cell chloride transport and recombinant human ClC-2 chloride currents. Am J Physiol Cell Physiol. 2004;287:C1173-C1183.

42. Johanson JF, Gargano MA, Holland PC, et al. Phase III efficacy and safety of RU-0211, a novel chloride channel activator, for the treatment of constipation [abstract]. Gastroenterology. 2003;124:A104.

43. Johanson JF, Gargano MA, Patchen ML, Ueno R. Efficacy and safety of a novel compound, RU-0211, for the treatment of constipation [abstract]. Gastroenterology. 2002;122:A-315.





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