When Fiber is Not Enough: Current Thinking on Constipation Management

   Bowel dysfunction is a common problem and associated with significant morbidity. Chronic constipation affects a significant percentage of the population in Western countries (55% to 30%, depending on the criteria used to define constipation), and laxatives are among the most commonly used drugs.¹ While most individuals respond well to self-treatment, a subset of patients does not respond to standard interventions, underscoring recognition that the pathology of constipation is diverse and multifactorial.^2,3

Understanding Constipation

   Characteristics of normal bowel function. Normal defecation can be characterized as elimination of formed bulky stool with minimal effort - ie, no excessive straining and no sensation of incomplete emptying. Factors contributing to normal defecation include adequate intake of fiber and fluid, normal colonic motility, and coordination between the muscle groups controlling stool elimination (the abdominal and pelvic floor muscles).^4-6 Effective management of the patient with chronic constipation is dependent upon accurate identification of the dysfunctional factor(s) and implementation of appropriate corrective strategies.

   Definition of constipation. The term constipation means different things to different people. Clinicians typically define constipation as abnormal infrequency of bowel movements, while patients frequently use the term to indicate difficult defecation (straining at stool), hard stools, or a sensation of incomplete evacuation.^4,7-9 The most commonly accepted indicators of chronic constipation include the presence of at least two of the following for at least 3 months: 1) straining with defecation at least 25% of the time; 2) lumpy or hard stools at least 25% of the time; 3) sensation of incomplete emptying at least 25% of the time; and 4) less than three bowel movements per week.^4,9 The need to facilitate defecation via perineal support, intravaginal pressure, or manual evacuation of stool is included as a diagnostic criterion in some centers.⁸

   Risk factors for constipation. Although the pathology underlying chronic constipation is not completely understood, the epidemiologic data clearly suggest the following as risk factors: female, aging, low caloric intake, inactivity, number of medications taken, low income level, and low education level. Other factors associated with increased risk are depression, physical abuse, and sexual abuse. Although these factors appear to be associated with chronic constipation, they should not be construed as causative factors; they are based on correlational data only.^1,4,8

Etiology and Pathology of Chronic Constipation

   Chronic constipation is commonly categorized as either primary or secondary. Secondary constipation is caused by an identifiable pathology - ie, factors other than colonic motility and pelvic floor muscle function, while primary (idiopathic) constipation has no apparent cause and is thought to result from intrinsic disorders of colonic motility and/or pelvic floor function.^1,5,7,8

   Secondary constipation. Initial evaluation of the patient presenting with complaints of chronic constipation should include evaluation for specific causative factors. Conditions commonly resulting in constipation include the following:^7-10
   * neurologic disorders such as Parkinson's Disease or spinal cord lesions
   * metabolic disorders including hypothyroidism, hypercalcemia, or diabetes mellitus
   * medications such as opioid analgesics, anticholinergic agents, calcium channel blockers, antiparkinsonian drugs, sympathomimetics (eg, pseudoephedrine), antipsychotics, diuretics, antihistamines, calcium-based antacids and calcium supplements, iron supplements, and nonsteroidal anti-inflammatory agents
   * obstructive lesions such as colorectal tumors, strictures, or large rectoceles
   * lesions causing painful defecation such as anal fissures or hemorrhoids
   * lifestyle factors such as inactivity and low fiber intake.

   Primary constipation. Primary constipation, also known as idiopathic constipation, refers to constipation caused by abnormal colonic motility or pelvic floor dysfunction. The most common types of primary constipation are constipation-predominant irritable bowel syndrome, slow transit constipation, and dyssynergic defecation (loss of coordination between the various muscle groups involved in stool elimination).^1,6,9-13

   Constipation-predominant irritable bowel syndrome. The majority of patients referred to tertiary care centers for chronic constipation fit the profile of constipation-predominant irritable bowel syndrome (IBS).^7,8 Irritable bowel syndrome is a common functional disorder that is more prevalent in women and characterized by abdominal pain, bloating and distention, and alterations in stool frequency and consistency. The causative factors are unknown but theories include disordered motility, visceral hypersensitivity, and extraintestinal factors such as hormonal influences and food sensitivities.^4,7-9 Irritable bowel syndrome is classified as three distinct types: constipation-predominant, diarrhea-predominant, or mixed pattern with alternating episodes of constipation and diarrhea. Patients with constipation-predominant IBS typically report cramping pain triggered by eating, excessive gas production, bloating, and a sensation of incomplete evacuation. Fortunately, this syndrome is fairly responsive to simple therapies such as dietary monitoring and modifications, fiber therapy, stress management, and patient education.^4,8

   Slow transit constipation. Normal colonic motility is characterized by long periods of low-amplitude non-propagating contractions that support water reabsorption and production of formed stool, interspersed by series of high-amplitude propagating contractions that propel the stool distally. These propulsive contractions typically occur once to twice daily, most commonly following a meal with fat; this increased motility following eating is known as the gastrocolonic response.⁵ Slow transit constipation is characterized pathologically by diminished frequency, duration, and amplitude of propagating (propulsive) contractions, which significantly delays stool transit. This, in turn, results in prolonged contact between the stool and the intestinal mucosa, which causes drying and hardening of the stool and increased difficulty with elimination. Patients with slow transit constipation also exhibit impaired gastrocolonic response, compromised relaxation of the internal anal sphincter, and impaired recognition of rectal distention; some patients also have symptoms indicative of impaired gastric emptying and diminished small bowel motility. The cause of these altered motility patterns is unknown; current theories include hormonal influences (either sex hormones or gastrointestinal hormones) or a visceral neuropathy affecting the nerves within the bowel wall. Slow transit constipation is much more common among young women, which explains the interest in a hormonal cause. Patients with slow transit constipation report infrequent bowel movements, hard or lumpy stools, and poor response to fiber therapy and laxatives.^1,4,8,11,12

   Pelvic floor dysfunction. Effective elimination of stool from the rectal vault requires coordination between the abdominal muscles and the pelvic floor muscles. Normal function is characterized by simultaneous contraction of the abdominal muscles (to increase intraabdominal pressure) and pelvic muscle relaxation (to open the outlet and reduce the angle between the anal canal and the rectal vault). Patients with pelvic floor dysfunction (dyssynergic defecation) typically fail to relax the pelvic floor muscles effectively or fail to coordinate pelvic floor relaxation with abdominal muscle contraction. Most of these patients also exhibit impaired sensory awareness of rectal filling.^4,8,9,13 The causative factors are theorized to include unconscious learned behavior resulting from pelvic trauma, painful defecation, or some unknown event. Patients with pelvic floor dysfunction typically present with prolonged straining before stool elimination, feelings of incomplete emptying, hard stools, poor response to fiber and laxative therapy, anorectal pain, and a sensation of perianal fullness or heaviness. When questioned, they may acknowledge using digital maneuvers such as intravaginal pressure and manual disimpaction in attempts to empty the rectum. Biofeedback therapy is the most effective intervention for most of these patients.^4,8,9,13

Patient Assessment

   The first step in effective management of the patient with chronic constipation is to accurately identify the causative factors. Initial assessment should focus on determining whether the constipation is primary or secondary; thus, the initial workup should include measures to identify or rule out specific causative factors (eg, an obstructing rectocele, painful anal fissures, hypothyroidism, or insufficient fiber intake).^7-9,14,15 If no underlying cause is found and the patient is thought to have idiopathic (primary) constipation, the focus should be on identifying the probable pattern. In general, the initial assessment should include a careful history, a focused physical exam, a bowel chart, and baseline laboratory studies (eg, complete blood count; biochemical profile to include electrolytes, BUN, glucose, and Ca++; and TSH levels). Endoscopic and radiographic studies may be indicated for selected patients (eg, those with any evidence of obstructive lesion or reports of rectal bleeding) but are not routine during the initial workup. Advanced diagnostic studies (eg, motility testing, defecography, and anorectal manometry) are typically reserved for patients who fail primary therapy.^7-9,14,15

   History. A carefully elicited history provides important clues to the type of constipation and helps direct the other components of the assessment. Critical information to obtain during the history includes the following:^7-9,14,15
   * Description of the problem to include the patient's definition of the term constipation (Infrequent defecation? Prolonged straining before defecation? Hard stool? Sensation of incomplete evacuation?)
   * Any associated symptoms, such as bloating, nausea, cramping pain, rectal bleeding, recent weight loss, urinary frequency, or urinary incontinence
   * Onset, duration, and any exacerbating or relieving factors; ask specifically about medications, herbal agents, and mechanical strategies (eg, perineal or intravaginal support) used to facilitate elimination and ascertain their effectiveness
   * Description of stool shape, size, and consistency
   * Medical-surgical history
   * Usual dietary and fluid intake patterns (to include usual caloric and fiber intake and the type and volume of fluid intake)
   * Complete list of medications including over-the-counter and herbal agents.

   In reviewing the data gained from the history, the clinician should be aware that acute onset of symptoms, constipation that begins after age 50, or progressive symptoms are suggestive of an organic problem, while constipation extending back to childhood suggests either a congenital or psychological cause. Typical findings for the various types of primary constipation are outlined in Table 1.^7-9

   Bowel record. A carefully maintained bowel record provides objective information regarding stool frequency and consistency that can significantly enhance the data obtained from the history. The patient is asked to record all elimination attempts; data to be recorded include urge to defecate, consistency and volume of stool, straining or other assistive strategies, and use of laxatives, suppositories, or enemas.^7,16
Physical examination. In conducting the clinical examination, the clinician should note general health, nutritional and hydration status, and apparent distress/discomfort. The focused physical exam should include the following:^7-9,16
   * Abdominal inspection, palpation, and percussion, noting distention, masses, tenderness to palpation, and/or dullness to percussion. Generalized distention, tenderness to palpation, and dullness to percussion are indicative of significant retained stool/"loaded colon." (Auscultation of bowel sounds may be performed as well, although bowel sounds primarily reflect small bowel motility)
   * Anorectal examination conducted with patient in the left lateral position and including the following: evidence of fecal soiling; resting tone of the sphincter; ability to voluntarily contract the sphincter and any evidence of sphincter defects; ability to relax the sphincter and expel the examining finger when instructed to do so; volume and consistency of stool in the rectal vault; and observation of the pelvic floor during simulated defecation. (Descent of the perineum > 4 cm in the lateral position is excessive and is associated with chronic straining and ineffective emptying)
   *Vaginal examination if indicated to rule out rectocele and pelvic organ prolapse.

   The assessment data should be integrated and a determination made as to probable diagnosis, the need for additional studies, and initial therapy.

Guidelines for Management

   Effective management of the patient with chronic constipation begins with attention to the specific problems identified during the assessment, as well as general bowel management strategies. Patients who fail to respond to initial therapy require additional assessment and may be candidates for more advanced therapies, such as surgery^7-9,14 (see Table 1).

   Secondary constipation. In managing the patient with constipation secondary to a specific organic problem, the focus is on treatment of the underlying condition in addition to strategies to improve bowel function.^4,8 For example, the patient with an obstructing rectocele requires either a pessary, surgical correction, or instruction in effective use of intravaginal pressure to relieve the obstruction; if her stool is hard, she will also benefit from fiber therapy. Similarly, the patient with evidence of a metabolic or neurologic condition (eg, hypothyroidism or Parkinson's Disease) requires referral for effective management of the primary disease and also may require laxative therapy.

   Primary constipation. The patient with primary constipation should be managed according to the specific type of dysfunction. For example, patients with constipation-predominant IBS usually benefit from fiber therapy (as outlined below), in addition to education regarding IBS and general dietary and lifestyle management guidelines. In contrast, the patient who presents with dyssynergic defecation generally requires referral for biofeedback therapy and pelvic muscle reeducation; these patients benefit from fiber therapy and laxative therapy only if the dyssynergic defecation is complicated by hard stools or infrequent bowel movements. Patients with slow transit constipation are initially managed with fiber therapy and increased activity; most require the addition of one or more laxative agents, and some will require further workup and possibly surgical intervention.^1,7-9,12,13

   Fiber and fluid therapy. Interestingly, few studies have examined the impact of fiber and fluid intake on stool consistency and incidence of constipation, although epidemiologic studies reveal low prevalence of constipation in countries where the typical diet is high in fiber.⁴ Nonetheless, fiber has been demonstrated to increase stool weight and reduce colonic transit time, and adequate fiber and fluid intake are general good health strategies. In addition, fiber therapy has proven beneficial (in uncontrolled studies) both for primary and secondary constipation, including slow transit constipation; it is, therefore, reasonable to begin with these interventions. However, more studies are needed to determine the impact of various types and amounts of fiber on bowel function and stool consistency, and definitive recommendations must await these studies.^{1,4,7-9,17,18} Guidelines for initiation of fiber therapy are outlined below:^4,8,19
   * The goal in fiber therapy is establishment of soft, formed stool. Patients with constipation usually require a total of 20g to 40g of fiber per day, but the dosage for each patient should be titrated based on response.
   * Good sources of fiber include bran cereals, granola, wheat germ, beans, Brussel sprouts, lentils, dried fruits, stewed prunes, and nuts.²⁰ Patients unable or unwilling to maintain a high-fiber diet may elect to routinely take an over-the-counter bulk laxative containing psyllium, polycarbophil, methylcellulose, or carboxymethylcellulose. (Some patients choose a combination approach; they increase their dietary intake of fiber and use bulk laxatives to supplement their dietary fiber.) An alternative to bulk laxatives is a fiber supplement mixture (see Fiber Supplement Recipes). Both recipes call for wheat bran, which has been used effectively in various settings to normalize stool consistency and reduce the need for laxatives and enemas.^21-23
   * Daily dosage of fiber must be titrated based on response. Patients are generally instructed to begin with one bowl of high-fiber cereal, 2 tablespoons of a fiber supplement mixture, or one adult dose of a bulk laxative and to gradually increase the daily dose until the stool is soft and formed. The clinician should explain to the patient that fiber therapy takes about 72 hours to take effect and that adjustments in daily dose should be made no more often than weekly.
   * Adequate intake of fluids is essential when providing fiber therapy; failure to balance fiber with fluid can cause worsening of the constipation or even an intestinal obstruction. The usual goal in fluid intake is 30cc/kg body weight/day; if the patient is on fluid restriction or otherwise unable to ingest adequate fluid, fiber therapy should not be recommended. These patients are usually best managed with use of softener-stimulant combinations such as docusate and casanthranol (Pericolace, Roberts Pharmaceuticals, Eatontown, NJ).²⁴
   * The clinician should caution the patient to expect increased gas and bloating for the first several weeks of fiber therapy (until the bowel has adjusted to the increased fiber intake). Bloating is less common with methylcellulose and carboxymethylcellulose products (eg, Citrucel, SmithKline Beecham, Pittsburgh, Pa.) because they do not undergo bacterial fermentation.

   Increased activity as tolerated. Increased activity has been shown to increase peristalsis. As another good health strategy, the clinician should help the patient identify ways to safely increase daily activity (eg, brisk walking, swimming, wheelchair exercises for wheelchair-bound patients).^1,4,7,19

   Optimal toileting posture. The patient should be taught to respond promptly to the urge to defecate, and toilet height should be adjusted as needed to ensure the optimal position for fecal elimination - ie, feet flat on the floor with hips and knees flexed. A foot stool may be used for patients whose feet do not reach the floor.^4,19

   Laxative therapy. Laxative therapy is an essential component of management for many patients with chronic constipation; unfortunately, appropriate use of laxatives is hampered by myths and misinformation. For example, most patients and health professionals have been taught that routine use of laxatives is always contraindicated due to the risk of cathartic colon, a condition in which laxative abuse causes degeneration of the enteric nerve pathways and renders the colon acontractile (the term laxative abuse suggests inappropriate and unnecessary use). In reality, the concept of cathartic colon is now being challenged; the few studies that have been done on the effects of long-term laxative use showed that a significant portion of patients on long-term therapy had diminished colonic motility, but they failed to differentiate between preexisting motility disorders and motility disorders induced by the laxative therapy.^10,12,17,18 A second misconception is that natural agents (eg, senna-based teas) are inherently safer than laxative medications; in reality, the active agents are frequently the same, and medications are more tightly controlled for dosage and additives. The implication for caregivers is that patient education and reassurance is a critical aspect of effective laxative therapy.

   Current guidelines for use of laxative agents include the following approach to optimizing bowel function while minimizing risk of adverse effects: Begin with bulk agents (fiber therapy), add osmotic agents if needed as second-line therapy, and use stimulant agents only as needed and ideally only on a PRN basis (see Table 2).^8,9,25

      * Osmotic agents. These agents work by pulling fluid into the colon, which distends the bowel and stimulates propagating contractions. The most commonly used osmotic agents are saline laxatives, such as magnesium hydroxide (Milk of Magnesia, Roxane Laboratories, Columbus, Ohio), magnesium citrate (Crystal, Diamond Products, Seffner, Fla.), and sodium phosphate (Fleet Phospho Soda, CB Fleet Company, Lynchburg, Va.). They are a good choice for acute constipation due to their rapid onset of action (30 minutes to 3 hours), and they are generally safe and effective. Saline laxatives are contraindicated for patients in renal failure; as noted, these patients are best managed with softener/stimulant combinations.²⁴ Additional osmotic agents include polyethylene glycol (PEG) solutions (eg, Miralax, Braintree Laboratories, Braintree, Mass.), and sorbitol. They may be used for patients who fail to respond to bulk agents and saline laxatives alone and typically produce a bowel movement within 24 to 48 hours. Polyethylene glycol solutions may be preferred because lactulose and sorbitol are associated with increased gas, cramping, and abdominal distention (due to fermentation by colonic bacteria).^8,12,17

      *Stimulant laxatives. Stimulant laxatives work by altering transport of electrolytes within the intestinal mucosa, causing water retention and stimulating peristalsis. The most commonly used stimulant laxatives are the diphenylmethanes (eg, bisacodyl, or Dulcolax, Novartis Consumer, Summit, NJ) and the anthraquinones (eg, senna or Senokot, Purdue Frederick, Norwalk, Conn.). These agents commonly produce a bowel movement within 6 to 8 hours following oral intake. Chronic use of stimulant agents can cause a reversible pigmentation of the colon (ie, melanosis coli), a benign change. Stimulant agents also contribute to reduced colonic motility (colonic inertia), and some clinicians have expressed concern that anthraquinones might increase the risk for colon cancer. However, no definitive data to support these concerns are currently available. Nonetheless, the most prudent approach is to limit the use of these agents to PRN and short-term use.^8,12,17,26

      *New agents. A number of promotility agents are under investigation. One of the most promising is the serotonin 4 receptor (5-HT4) agonist Tegaserod, which is used for women with constipation-predominant irritable bowel syndrome. Early results indicate positive outcomes in women (ie, reduced number of days per month with cramping and bloating and increased frequency of bowel movements). However, this drug appears to be less effective in men with the same pattern of irritable bowel syndrome.²⁷

   Biofeedback and pelvic muscle reeducation. Patients with dyssynergia of the abdominal and pelvic floor muscle groups are best managed with biofeedback therapy and pelvic muscle reeducation. A number of tools and techniques can be used to help patients learn to effectively coordinate the abdominal and pelvic muscles during defecation, including EMG biofeedback and simulated defecation exercises.^8,13

Indications for Advanced Diagnostics

   Patients who fail to respond to initial therapy should be referred for complex diagnostic studies. Treatment for these patients is dependent on the results of the diagnostic studies and may include colectomy or even colostomy for intractable slow transit constipation.^8,12

Conclusion

   Constipation may occur secondary to another disease process or condition or may have no identifiable cause. It may respond to simple measures or may be refractory to therapy. Effective management requires thorough assessment, correction of reversible factors, and use of general bowel-management strategies such as fiber therapy, increased activity, and judicious use of laxatives.

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