MEDSCAPE Clinical Case a Home-Bound 65-Year-Old Woman With Chronic Constipation]

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CME/CE Information

CME/CE Released: 08/14/2009; Valid for credit through 08/14/2010

This activity has expired.

The accredited provider can no longer issue certificates for this activity. Medscape cannot attest to the timeliness of

expired CME activities.

Target Audience

This activity is intended for family medicine/primary care practitioners, internal medicine practitioners,

gastroenterologists, geriatrics practitioners, nurses, and pharmacists involved in the care of patients with chronic

constipation.

Goal

The goal of this activity is to increase clinicians’ recognition of the higher prevalence of chronic constipation in elderly

patients as well as raise clinician awareness to the factors for the increased prevalence of CC in this population; allow

clinicians to examine lifestyle measures often used by elderly patients to manage their constipation and evaluate their

effectiveness; describe special considerations for targeting therapy in the elderly population; and review the evidence

and provide a practical guide to the screening, diagnosis, and treatment of CC in the elderly population.

Learning Objectives

Upon completion of this activity, participants will be able to:

1. Recognize the higher prevalence of chronic constipation in elderly patients and the potential reasons for the

increased prevalence in this population

2. Examine lifestyle measures often used by elderly patients to manage their constipation and evaluate their

effectiveness

3. Describe special considerations for targeting therapy in the elderly population

4. Review the evidence and provide a practical guide to the screening, diagnosis, and treatment of chronic

constipation in this population

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23/4/2011 A Home-Bound 65-Year-Old Woman Wi…

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Author

Brennan M.R. Spiegel, MD, MSHS

Assistant Professor in Residence, Digestive Diseases, UCLA David Geffen School of Medicine,

Los Angeles, California; Attending Physician, Department of Gastroenterology, Los Angeles,

California

Disclosure: Brennan M.R. Spiegel, MD, MSHS, has disclosed the following relevant financial

relationships:

Received grants for clinical research and educational activities from: Amgen Inc.; Takeda

Pharmaceuticals North America, Inc.; Bristol-Myers Squibb Company

Served as an advisor or consultant to: Prometheus Laboratories Inc.; AstraZeneca

Pharmaceuticals LP

Editor

Elizabeth Samander, PhD

Scientific Director, MedscapeCME

Disclosure: Elizabeth Samander, PhD, has disclosed no relevant financial relationships.

Nurse Plannner

Laurie E. Scudder, MS, NP

Accreditation Coordinator, Continuing Professional Education Department, MedscapeCME; Clinical Assistant

Professor, School of Nursing and Allied Health, George Washington University, Washington, DC; Nurse Practitioner,

School-Based Health Centers, Baltimore City Public Schools, Baltimore, Maryland

Disclosure: Laurie E. Scudder, MS, NP, has disclosed no relevant financial relationships.



From MedscapeCME Gastroenterology

The following test-and-teach case is an educational activity modeled on the interactive grand rounds approach.

The questions within the activity are designed to test your current knowledge. After each question, you will be

able to see whether you answered correctly and will then read evidence-based information that supports the most

appropriate answer choice. Please note that these questions are designed to challenge you; you will not be

penalized for answering the questions incorrectly. At the end of the case, there will be a short post-test

assessment based on material covered in the activity.

Patient History

Sue F., a 65-year-old woman, is referred to you by her primary care provider for

evaluation of chronic constipation. The patient reports straining with defecation;

hard, lumpy stools; and a sense of incomplete evacuation with bowel movements.

She often spends a prolonged period on the toilet to defecate, usually without

success. She defecates 1 to 2 times per week on average. She reports

intermittent lower abdominal "bloating" and "tightness" but no visual distention and

no abdominal pain. Defecation somewhat relieves the bloating and tightness, but

there are usually residual symptoms despite stool passage. She recalls having

constipation for most of her life, but has only recently developed progressive

worsening of her symptoms over the past 2 years. It is now severe enough that it

affects her quality of life. She says the symptoms are "devitalizing" and "draining,"

and she reports that it has negatively affected her social life to the point where she

stays at home and avoids social engagements due to embarrassment and worry about her bowel symptoms. She

worked as a bank teller for over 40 years and just recently retired. She has never smoked tobacco and rarely drinks

alcohol. Her husband of 35 years recently died of metastatic colon cancer. She now lives alone in her home and is

intermittently visited by her older daughter, who lives locally. She often cooks for herself and "tries to eat well," but

admits that since her husband died it has become harder to prepare nutritious meals. There is no family history of

gastrointestinal cancer.

Sue F. presents with a major complaint of constipation. She has difficulty with each bowel movement

and is using over-the-counter laxatives. She has had these symptoms for 2 years. She does not report

any changes in her weight or appetite or any blood in her stool. However, the severity of symptoms

has been gradually increasing. Her medical history is unremarkable except for high blood pressure

and high cholesterol. On physical examination she has a body mass index (BMI) of 31 kg/m2, and vital

signs are stable. General physical examination, including abdominal examination, is unremarkable.

Digital rectal examination reveals 1 small external hemorrhoid. On the first clinic visit, you provided her

with a diary to track the frequency and quality of her bowel movements. You notice that she had 4

bowel movements during the past week, producing minimally hard stool, while she was not taking any

laxatives.

MedscapeCME Staff involved in the planning and review of this activity have disclosed no relevant financial

relationships.

A Home-Bound 65-Year-Old Woman With Chronic ConstipationBrennan M.R. Spiegel, MD, MSHS

CME/CE Released: 08/14/2009; Valid for credit through 08/14/2010



What would be your next step in managing this patient?

Explain that she does not have constipation and that her bowel habits could be considered

normal on the basis of the frequency of her bowel habits

Explain that most likely she has irritable bowel syndrome and that she may benefit from stress

management and fiber

Send her for further evaluation for her symptoms

Ask her to continue the over-the-counter laxatives

Save and Proceed

Defining Chronic Constipation

"Constipation" means different things to different people. This insight, although potentially obvious, is important to

help guide diagnostic and therapeutic decision-making. Because patients cite a variety of symptoms to describe

constipation, and because these different symptoms may require widely disparate therapies, it is vital for treating

clinicians to fully understand and explore each patient's individual illness experience and to tailor therapy accordingly.

What is constipation? Historically constipation has been defined as infrequent defecation, and traditionally cite a

frequency of fewer than 3 bowel movements per week as evidence of clinically important constipation. However,

patients do not uniformly report infrequent defecation as their defining symptom.[1] Moreover, constipation can be

correctly diagnosed in the absence of infrequent defecation. Certainly a patient with hard, round stools; straining; and

a sense of incomplete evacuation may have constipation even if she passes multiple bowel movements daily.

Constipation often includes abnormalities of both frequency and form -- namely, infrequent bowel movements or

alterations in the consistency of the bowel movements. Therefore, stool frequency alone is only part of the story.

Because most patients understandably lack a working knowledge of normative stool consistency, it is instructive to

use the Bristol Stool Scale (Figure 1) when asking patients to classify their bowel movements.[2-4] The scale provides

7 prototypical stool forms ranging from hard, rounds "nuts" (type 1) to watery without formed elements (type 7).

Patients with constipation typically point to type 1 and type 2 bowel movements as their predominant stool form.

They may also experience straining with defecation, a nagging sense of incomplete evacuation, prolonged bouts of

defecation often resulting in unsuccessful evacuation, or even resorting to manual maneuvers to aid stool passage.



Figure 1. The Bristol Stool Scale.

The Rome III criteria (Table 1) provide a working definition of chronic constipation (CC).[3] The criteria highlight the

difference between stool frequency and stool form and emphasize that infrequent bowel movements alone do not

necessarily define constipation. It is important to emphasize the difference between acute constipation and CC. The

Rome III criteria define CC as the presence of cardinal symptoms for at least 12 weeks in the previous 12 months.

Acute constipation has a shorter time course and a different differential diagnosis than CC. Finally, it is useful to note

the difference between CC and irritable bowel syndrome (IBS) with constipation (IBS-C). Whereas the hallmark

symptom of IBS-C is abdominal pain in association with constipation, patients with CC do not report pain as a

predominant feature of their illness experience.[3,5] Practically, however, many patients do not comply with this tidy

dichotomy. It is common to encounter patients who have mild or moderate abdominal discomfort in CC but who do

not report discomfort as a predominant symptom. Similarly, patients with IBS-C may have abdominal pain on some

occasions but not consistently. These variations in patient assessment of abdominal discomfort make it difficult to

clearly distinguish IBS-C from CC. If in doubt, ask the patient whether pain or discomfort is a predominant feature or

whether the "main problem" is limited to the constipation itself. Patients who acknowledge that abdominal pain is a

major factor are more likely to have IBS-C than CC. Those principally concerned with improving stool frequency or

form independent of abdominal pain probably have CC.[5]

Table I. Rome III Diagnostic Criteria* for Constipation

Chronic constipation must include 2 or more of the following in > 25% of defecations:

Straining

Lumpy or hard stools

Sensation of incomplete evacuation



Sensation of anorectal obstruction/blockage

Manual maneuvers

< 3 defecations a week

Loose stools are rarely present without the use of laxatives

Insufficient criteria for irritable bowel syndrome (IBS)

*Criteria fulfilled for at least 3 months with symptom onset at least 6 months before diagnosis.

From Longstreth et al. Gastroenterology. 2006;140:1480.

Patient History (cont'd)

She does not report alarm features. Specifically, there is no unintended weight loss; no nausea or vomiting; no fevers,

chills, or sweats; and no blood in her bowel movements. Her stool caliber has not changed over time; it is usually

round, "like pebbles, like it's been for years." She has not had to use manual disimpaction to assist stool passage,

but says she's "almost getting to that point." Her only abdominal surgery was an appendectomy when she was 30

years old. She has a history of 2 normal spontaneous vaginal deliveries without complications. Her medical history

includes osteoarthritis for which she takes intermittent ibuprofen as needed, hypertension for which she receives

lisinopril, and hypercholesterolemia for which she takes simvastatin. She has been receiving all of these medications

for over 5 years without a change in dose.

Her primary care provider ordered a complete blood count, liver chemistries, and serum electrolytes, all of which were

normal. Fecal occult blood testing was negative on 3 occasions over the past year. She had a colonoscopy 5 years

ago that revealed sigmoid diverticula and melanosis coli. No polyps were documented.

Sue F. had a colonoscopy 5 years ago and asks whether she needs to have this test done again. You

recommended that she get a colonoscopy.

What would be your next step in managing this patient?

Explain that she does not have constipation and that her bowel habits could be considered

normal on the basis of the frequency of her bowel habits

Explain that most likely she has irritable bowel syndrome and that she may benefit from stress

management and fiber

Send her for further evaluation for her symptoms

Ask her to continue the over-the-counter laxatives

Save and Proceed

Pathophysiology and Differential Diagnosis of CC

To understand the pathophysiology of CC, it is useful to first review key aspects of normal intestinal physiology.

Typically around 1500 mL of dietary fluid is delivered to the small intestine daily, where it joins with nearly 7 L of

additional secretions intrinsically produced from the parotids, stomach, liver, and pancreas. Thus, between 8 and 9 L

of fluid enters the jejunum. All but 1500 mL of this volume is subsequently reabsorbed before exiting the ileum. The

colon receives the remaining 1500 mL of fluid, where it is stored and admixed with feces. The colon ultimately



absorbs nearly 90% of the remaining fluid load, leaving only 100-150 mL to be excreted with the feces. The main

learning point here is that the intestines have a remarkable ability to absorb fluid; it is not easy to overwhelm the

system with oral hydration. This is clinically relevant because patients often attempt to "treat" constipation by

drinking large volumes of water and, in fact, many well-intentioned clinicians advise their constipated patients to stay

well hydrated. But this advice does not necessarily comport with physiology. Excess fluid is excreted by the kidneys,

not the bowels. Although staying well hydrated is good general advice, it does not follow that increasing oral hydration

will alter stool consistency or frequency. The intestines will readily reabsorb the excess fluid before it could provide a

substantive effect on feces stored in the colon.

Whereas CC is generally unrelated to the amount of oral hydration, it may be precipitated by alterations in intestinal

transit. Normally the colon is a well-coordinated organ that intermittently propels feces through synchronized

contractions of the smooth muscle apparatus investing its walls. This occurs through a variety of signals, including

serotonin (namely 5HT-4), which coordinates proximal contraction, distal relaxation, and secretion.[6] In addition,

chloride channels (namely chloride channel-2, or ClC-2) serve as a key regulator of intestinal secretory function by

promoting water and sodium transport into the lumen.[7,8] The timing of these effects is partly coordinated by the

interstitial cells of Cajal (ICCs) found in the myenteric plexus. The ICCs are thought to play a vital role in organizing

colonic motility.[9] If ICCs are diminished, as occurs in "colonic inertia" -- a severe and recalcitrant form of

constipation -- colonic motility slows, propagation is inefficient, and feces become firm and desiccated.[9,10] Loss of

ICCs over time is one possible explanation for why CC is more prevalent with increasing age,[9] as discussed further

below.

In addition to slow-transit constipation, some patients develop constipation from rectal outlet obstruction or delay.

This may occur through anatomic or functional barriers to proper evacuation. The classic example of a functional

obstruction is Hirschsprung's disease, which arises from failure of the neural crest cells to migrate to the end of the

bowel during normal embryogenesis. This results in an aganglionic segment of bowel that is dysfunctional. The

disease is characterized by a lack of reflex inhibition of the internal anal sphincter due to lack of enteric inhibitory

neurons. The segment may be long, in which case the disease is typically detected shortly after birth in neonates

who are unable to pass meconium. But short segments of Hirschsprung's disease may evade detection for years and

only present with longstanding constipation in adults.[11] Nonetheless, this is a very uncommon cause of CC in

adults, and is especially uncommon in elderly patients with CC.

Sue F. reports no abdominal pain, blood in her stool, or change in appetite. Her blood pressure is

130/85 mm Hg and pulse rate is 75 beats/min. General physical examination is unremarkable and her

abdomen is mildly distended with normal bowel sound. There is no organomegaly or palpable mass.

Digital rectal examination reveals perianal dried brown stool. Anal sensation is intact and the tone of

the rectum is normal. She has thick pasty brown stool in the vault. On review of her medications you

notice that she is taking an antidiarrheal medicine, 1 tablet twice a day, to help with her incontinence.

Which of these tests is the first that you would obtain to provide you with more useful information

about this patient?

Balloon expulsion test

Anorectal manometry for evaluation of rectal tone and compliance

Abdominal radiography

Defecography for evaluation of pelvic floor function

Save and Proceed



In contrast to Hirschsprung's disease, pelvic dyssynergia is a highly prevalent cause of functional outlet delay in

adults, including the elderly.[12] To understand pelvic dyssynergia, it is important to first understand normal anorectal

function. During a normal bowel movement, pressure in the rectum increases while pressure in the anal canal

decreases. The anal sphincters are striated muscles under voluntary control. To easily evacuate a stool, the anal

sphincter should relax to reduce the physical barrier to expulsion. But some people are literally "anal retentive." They

keep their external anal sphincter paradoxically "tight" at the very moment when they should be relaxing. The tip-off

on anorectal manometry is a paradoxical increase in the anal pressure that correlates with the increase in rectal

pressure (Figure 2).[12] The increase in rectal pressure is a normal consequence of the Valsalva maneuver and is the

initiating event for defecation. This is accompanied by a relaxation of the puborectalis sling, which allows a

straightening of the anorectal angle. The final part of a normal reflex is the relaxation of the anal sphincter, which is

normally detected with a decrease -- not increase -- in the anal pressure. In the case depicted in Figure 2, the

pressure in the anal canal is rising, not falling. As a crude analogy, the pressure profile in Figure 2 is akin to

squeezing toothpaste out of the tube while keeping the cap on. The cap needs to come off first so that the toothpaste

can be squeezed out. Stool is no different. Pelvic dyssynergia can be detected by a standard balloon expulsion test,

in which a patient has a rectal balloon instilled with 50-60 mL of water and then has 2 minutes to expel the balloon

while on a commode (easier said than done, even for nondyssynergic patients).[12] If the balloon cannot be expelled

within 2 minutes, potential dyssynergic defecation is suggested.[12]

Figure 2. Anorectal manometry in pelvic dyssynergia.

Another approach to diagnosis is to use a radiopaque marker study (SitzmarkTM study),[13] described further below. If

the markers collect in the rectum without being expelled, it provides further evidence for possible anorectal outlet

obstruction. The definitive treatment for pelvic dyssynergia is biofeedback therapy, in which patients learn to literally

relax their external anal sphincter during defecation -- a process that typically requires several sessions with active

coaching and real-time feedback regarding sphincter tone.[14] Traditional laxative therapy is not very effective in this

condition because the problem is not one of motility but of outlet delay.



Other causes of anatomic outlet obstruction include rectoceles and rectal prolapse. It is rare for rectal cancer to

present with CC, although presence of alarm features, as detailed further below, should always raise awareness for

underlying malignancy.[5]

Finally, a long list of underlying disorders may present with CC. These include endocrinopathies, such as

hypothyroidism and advanced diabetes; degenerative neurologic conditions, including Parkinson's disease and spinal

lesions; metabolic abnormalities, such as hypercalcemia and hypokalemia; and a variety of systemic disorders,

including amyloidosis, systemic sclerosis, and myopathies.[5] Figure 3 provides a comprehensive list of potential

underlying secondary causes of CC.

Figure 3. Secondary causes of chronic constipation.

Adapted from: Candelli M, et al. Hepatogastroenterology. 2001;48:1050.


She has used bisacodyl tablets for the past 15 years to help normalize her bowel movements. As the symptoms

became worse 2 years ago she began to use psyllium powder on the advice of her primary care provider, but she

reported that it caused bloating and did not improve her constipation. She now seeks additional treatment options and

wonders why nothing has worked to date.

Burden of Illness and Epidemiology

CC is an extraordinarily common healthcare problem. In fact, the population prevalence of CC is nearly twice that of

diabetes or asthma, both highly prevalent diseases in their own right.[15] Although there is some variability in the

estimated prevalence of CC among studies, up to 27% of individuals report symptoms consistent with CC.[5] Recent

data indicate that over 3 million physician visits annually are the principal reason for consultation, making CC the

second most common outpatient gastrointestinal tract diagnosis behind acid reflux disease.[16] Although CC is

especially common among the elderly, it is prevalent among all age groups. In fact, the rate of consultation for CC is

higher in children younger than 15 years of age than in adults older than 65 years of age.[16] Nonetheless, physician

visits for CC among adults rise in lockstep with increasing age.[16]

There are a variety of potential reasons why older patients have a higher prevalence of CC. In particular, many

medications are known to precipitate or at least contribute to constipation (Table 2). Because older patients tend to



use more medications than younger patients, medication use alone probably explains much of the increased

prevalence in the elderly population. Bed-bound patients, especially nursing home residents, are especially prone to

developing CC, a possible consequence of being sedentary and immobile (although it remains unclear whether

immobility itself can cause constipation).[17] These patients are also commonly prescribed narcotics for chronic pain.

Narcotic-related CC can be severe and difficult to treat.[18] Pelvic floor laxity can also promote constipation through

dyssynergic defecation.[12] Older or sedentary patients (especially women) may develop weakness and laxity of the

pelvic floor musculature, which diminishes the bolstering effect of perirectal structures and, ultimately, promotes

constipation through discoordinated fecal expulsion.[12] In addition, some forms of constipation may represent a sort

of "dementia" of the gut. Just as the function of the central nervous system can decrease over time, as occurs with

Alzheimer's disease and other progressive forms of dementia, the function of the enteric nervous system can also

decrease as patients age.[9] The ICCs, in particular, play a vital role as the "gut pacemaker" for intestinal transit and,

with time, may fall in numbers.[9,10] Patients with "colonic inertia," a severe form of CC marked by diminished or

absent colonic transit, have a dramatically lower density of ICCs on intestinal biopsy compared with healthy

controls.[10] Although the analogy between colonic inertia and Alzheimer's dementia is imperfect, both conditions

have in common an age-related abatement in neural function with resulting functional impairment.

Table 2. Common Medication Classes Associated With Chronic Constipation

Medication Class Example

Anticholinergic medications NA

Antihistamines Diphenhydramine

Antispasmodics Hyoscyamine, dicyclomine

Antidepressants Amitriptyline

Calcium-channel blockers Verapamil

Iron supplements NA

Aluminum-containing products Aluminum hydroxide, sucralfate

Opiates Morphine, meperidine, codeine

5-HT3 Antagonists Alosetron

NA = not applicable

Without relief of symptoms, patients with chronic constipation are most likely to report:

Impairment of daily activities

Inability to afford treatment

Absenteeism from work or school

Decrease in productivity

Save and Proceed

The burden of illness of CC is more than an epidemiologic phenomenon --it can also severely affect the health-related

quality of life (HRQOL) of patients themselves.[19] Data indicate that patients with CC score lower on all 8 scales of

the Short Form-36 HRQOL questionnaire compared with "normal" cohorts without CC. Decrements in HRQOL are



especially large in the "vitality" subscale of the SF-36, which is consistent with the common clinical report of feeling

"tired," "worn down," "devitalized," or "drained," as with the current case. Data indicate that HRQOL decrements in

patients with CC are directly related to the frequency of physician visits.[19] In addition, the HRQOL burden of CC

leads to diminished work productivity and higher rates of work absenteeism compared with controls. One study found

that patients report an average of 2.4 days per month of productivity from CC and that there are over 13 millions days

of restricted work activity annually from CC.[20,21] In short, it is important to ask patients about how CC affects their

HRQOL; failure to recognize and address the HRQOL effect of CC could undermine the provider-patient relationship,

lead to dissatisfaction with care, and even affect work productivity.


On physical examination she is noted to be obese, with a BMI of 31 kg/m2. Her vital signs are normal. She has a

blunt affect and appears dispirited. There is no conjunctival pallor. Visual inspection of her abdomen reveals

protuberance consistent with her body habitus and an old scar from a right-lower-quadrant appendectomy. Bowel

sounds are present and unremarkable. Deep palpation in her left lower quadrant elicits mild discomfort. Digital rectal

examination reveals 1 small external hemorrhoid. She has normal sphincter tone, no evidence of a rectocele or rectal

prolapse, and a normal expulsion effort with a normal amount of perineal descent. There is solid stool in her rectal

vault that is guaiac negative. The remainder of her general examination is unremarkable.

Clinical Clues From the Patient History and Physical Examination in CC

The patient history and physical examination provide important clinical clues in CC. Through a careful and directed

history and examination, the astute clinician can often predict underlying disorders even in the absence of diagnostic

testing. In particular, the history and examination should focus on whether the patient has an underlying medical

condition leading to CC ("secondary" CC) or primary CC. If the latter, the clinician should estimate whether the

underlying cause of primary CC is slow-transit constipation, normal-transit constipation, outlet obstruction, or a

combination thereof as discussed further below.

First and foremost, it is vital to screen for "alarm features" when evaluating any patient with CC, regardless of age.

However, this is especially important in the elderly because the prevalence of underlying gastrointestinal malignancy

is higher in this age group. Table 3 lists alarm symptoms and signs that should be elicited in any patient presenting

with CC.[5] Although the predictive validity of these features for malignancy is somewhat unreliable, their presence

should never be ignored. Patients with alarm features should be evaluated for possible gastrointestinal malignancy,

especially if there is rectal bleeding, unintended weight loss, occult blood-positive stools, recent decrease in stool

caliber (not just frequency or consistency), or unexplained iron deficiency anemia. Any of these symptoms or signs

should mandate a structural examination of the colon, preferably colonoscopy.

Table 3. Alarm Features in Chronic Constipation

Family history of colon cancer/organic gastrointestinal disease

Overt rectal bleeding

Iron deficiency anemia

Positivity on fecal occult blood test

Significant unintended weight loss (>10 pounds of weight in 2-3 months)

Severe, persistent constipation

Recent narrowing of stool caliber

Lack of response to traditional treatments



New-onset constipation in an elderly patient

From Brandt et al. Am J Gastroenterol. 2005;100(suppl 1):S5.

Assuming the patient does not have alarm features, the next step is to estimate whether the patient has a functional

outlet obstruction. This is especially important in elderly women, who are at highest risk for outlet obstruction from

rectoceles or prolapse.[12] Patients reporting excessive straining, incomplete evacuation, prolonged defecation with

minimal success, or need for manual maneuvers may have a functional outlet obstruction, such as dyssynergic

defecation. In these patients it is helpful to perform a careful digital rectal examination to estimate rectal tone, screen

for paradoxical contraction of the external anal sphincter during forced expulsion, and measure the degree of perineal

descent.[12,22] Normally the perineum remains within 2 to 3 cm of the ischial tuberosities both at rest and with

straining. Excessive perineal descent may indicate a rectocele.[19] In contrast, lack of any perineal descent might

indicate pelvic dyssynergia with "tenting" of the perineum from forced contraction of the external anal sphincter.[22]

Although estimating the degree of perineal descent can be an unreliable exercise, this variable is nonetheless worth

evaluating because extremes in either direction might help direct additional diagnostic testing, such as balloon

expulsion or anorectal manometry. The larger point is that clinicians must remember outlet obstruction early on

because traditional therapies for CC, such as laxatives, may not be effective at all if the underlying problem is pelvic

dyssynergy. Failure to detect outlet obstruction early in the diagnostic course can lead to delays in providing effective

treatment, dissatisfaction with care, and unnecessary extension of HRQOL decrements.

Patients without evidence of secondary CC or primary outlet obstruction may have slow-transit or so-called normal-

transit CC.[5] Both forms of CC may also coexist with outlet delay but by definition cannot coexist with each other.

True slow-transit constipation, described previously, is actually quite rare. In one series of 277 Patients with CC

undergoing colon transit studies, only 11% were found to have slow-transit constipation.[23] Instead, normal-transit

constipation is the most common subgroup within primary CC, making up over 70% of cases.[5,23] These patients

may have underlying visceral hypersensitivity and misperceive normal peristalsis as pathologic. Many of these

patients have concurrent abdominal pain and either meet criteria for IBS-Cor fluctuate between CC and IBS-C.

Elevated psychosocial distress, although not necessarily etiologic, is commonly observed in patients with normal

transit constipation.[5]

In reviewing the current case, several historical and physical clues help narrow the diagnostic decision making. First,

the patient does not report alarm features, has no recent change in stool caliber, and had no polyps or masses found

on colonoscopy 5 years ago. All of this makes underlying colon cancer unlikely. Second, her medical history,

medication history, and general physical examination do not point to obvious secondary causes of CC. Although

further diagnostic testing is warranted, as outlined below, the data from the history and examination suggest that

primary CC is more likely than secondary CC. Third, although she reports straining and incomplete evacuation, she

has not resorted (yet) to manual maneuvers, has normal perineal descent on rectal examination, has a normal

expulsion effort without paradoxical external anal sphincter, and does not have an obstetrical history that would raise

suspicion for pelvic floor disruptions. These findings suggest that outlet delay may not be a predominant mechanism

for her constipation. Fourth, although she reports some bloating and "tightness," she has no abdominal pain and her

abdominal symptoms do not fully resolve with defecation. This suggests that CC is more likely than underlying IBS-C

because the latter is marked by predominant abdominal pain that typically improves with defecation. Fifth, she reports

recent HRQOL decrements related to the death of her husband, and is devitalized and possibly depressed. This

raises the possibility of normal-transit constipation with an underlying functional gastrointestinal disorder. However, it

is important to emphasize that the relationship between psychological distress and CC is not necessarily causal, and

true slow-transit constipation is still possible. The longstanding nature of her symptoms is also relevant because the

symptoms predate the recent death of her husband by many years. The finding of melanosis coli on a previous

colonoscopy indicates longstanding use of stimulant laxatives, again suggesting that her symptoms have been

troubling her for a long time. Anecdotally, this sort of longstanding CC, particularly in the absence of typical IBS-C

characteristics or outlet delay, suggests underlying and progressive slow-transit constipation.

Cost-Effective Diagnostic Testing in CC



As outlined above, it is important to recognize that many underlying organic conditions can lead to CC. This is

especially relevant in the elderly population, which harbors more diseases, on average, than younger patients.

Clinicians should bear this in mind when performing diagnostic testing but should also recognize that most testing

strategies have low yield in the absence of alarm signs or symptoms.

In 2005, the American College of Gastroenterology (ACG) conducted a systematic review of the literature to identify

data supporting diagnostic testing strategies in CC.[5] The ACG concluded that almost all the standard laboratory

tests, including a complete blood count, serum electrolytes, and thyroid function testing, provide minimal data in

patients with CC. However, the ACG points out that high-quality data regarding diagnostic test yield in CC are

generally lacking and that patients should be approached in an individualized manner depending on the pretest

likelihood for underlying organic disease. The ACG further emphasizes that there are inadequate data to recommend

the routine use of flexible sigmoidoscopy, colonoscopy, or barium enema but that patients older than age 50 years

should undergo routine colorectal cancer screening independent of their CC diagnosis.[5] Data from a study by Pepin

and Ladabaum[24] revealed that colonoscopy identified adenomas and cancer in 19% and 2% of patients with CC,

respectively -- values that were statistically similar to the yield in control patients undergoing routine colorectal cancer

screening (20% and 1% for adenomas and cancer, respectively). In short, colonoscopy in young patients without

alarm features is an exercise in diminishing returns and is probably not cost-effective. However, presence of alarm

features should generally prompt colonoscopy, regardless of age. In addition, patients eligible for colorectal cancer

screening should be screened, regardless of CC. Finally, routine laboratory tests have low yield in CC and should be

ordered on the basis of pretest likelihood of underlying disease determined from a careful and detailed history and

physical examination, as reviewed above.

Once secondary constipation has been ruled out on the basis of the history and physical examination and judicious

diagnostic testing, the next step is to evaluate whether the patient has normal-transit, slow-transit, or outlet delay as

the basis of their symptoms. This can be estimated in advance of testing from a careful history and examination, as

described above. Moreover, many providers opt to treat patients empirically before conducting additional tests. I

typically begin with empirical treatment unless I suspect underlying outlet delay. If outlet delay is being considered,

then it is useful to perform an objective test before starting therapy because the treatment for pelvic dyssynergia in

particular is very different from that for other forms of constipation (ie, biofeedback therapy vs medical therapy).

Balloon expulsion is a simple test that can be easily completed in the office setting.[25,26] An inexpensive rig can be

created with a nasogastric tube, latex glove, suture, and 60-mL syringe. The first step is to cut the index finger off the

glove and fit it over the end of the nasogastric tube while ensuring the outlet ports are covered by the latex. A suture

(or even a string) is then tied tightly at the bottom of the latex to form a seal; the result is an oblong "balloon" at the

end of the tube (Figure 4).



Figure 4. Balloon expulsion test rig. Copyright 2009 Brennan M.R. Spiegel, MD, MSHS.

After leak testing is performed, the tube is inserted into the rectum digitally, and 50-60 mL of fluid is instilled through

the tube with the syringe. The patient is then asked to sit on a commode or toilet and spontaneously evacuate the

balloon. If the balloon cannot be expelled after 2 minutes of effort, then the test result is considered to be positive.[26]

Of note, this relatively simple office examination has an 88% sensitivity and 89% specificity when compared with the

gold standard of specialized anorectal manometry.[25] Its negative predictive value is 97%.[25] Thus, if a patient can

spontaneously evacuate the balloon within 2 minutes, then outlet obstruction is highly unlikely. In contrast, the

positive predictive value of the balloon expulsion test is only 64%, indicating that additional confirmatory testing with

anorectal manometry or defecography may be required if the balloon expulsion result is positive but the diagnosis

remains in question.[25] I tend to use defecography -- especially in the elderly -- because it can screen for anatomic

barriers such as a rectocele or prolapse.[26]Although these diagnoses can often be found on digital rectal

examination, they are often elusive. Thus, defecography may help confirm the suspicion. This is an important step

because surgery, not medical therapy alone or biofeedback therapy, may be the treatment of choice if there is a

clinically important rectocele or prolapse.

Patients with a normal balloon expulsion test result usually have normal-transit constipation but may have slow-transit

constipation. I typically do not discriminate but treat empirically, as described further below. Patients with an

incomplete response may require further diagnostic testing. If slow-transit constipation is suspected, a radio-opaque

marker study may be warranted. There are a variety of techniques for interpreting the marker study results, but the

most common is to administer a capsule with 24 markers and obtain an abdominal radiograph 5 days later.[26] If more

than 20% of the markers remain distributed throughout the colon at day 5, then slow-transit constipation is likely.[26]

If the markers remain but are co-located in the rectum, then outlet obstruction may still be present despite the normal

balloon expulsion test result. If fewer than 20% of the capsules remain, the diagnosis is normal-transit

constipation.[26]



On the basis of your experience, which of the following options is most effective in managing

constipation in elderly patients?

Bulking agents

Stool softeners

Enemas

Stimulants/irritants

Osmotic agents

Lubricants

Chloride channel activator

Serotonergic agents

Save and Proceed

Treatment Options in CC

There are a variety of approaches for treating CC, including lifestyle modifications, bulking agents, osmotic laxatives,

stool softeners, stimulant laxatives, and chloride channel activators, among others.

Lifestyle Modifications

Lifestyle modifications are often recommended to help treat CC symptoms.[5,17] This typically includes increasing

intake of dietary fiber, staying well hydrated, and exercising. However, minimal data support the effectiveness of these

interventions. As discussed above, oral hydration does not substantially alter stool frequency or form because the

small bowel and colon are highly efficient at absorbing excess water. Dietary fiber may help, but it can be difficult to

consume enough fiber (20 to 30 g per day) from dietary sources alone to alter intestinal transit. Elderly patients, in

particular, may be less motivated to change longstanding and habituated diets to achieve sufficient levels of fiber

intake. Finally, exercise is important for all sorts of reasons, but probably not for initiating or aiding colonic motility.

Moreover, in frail or debilitated elderly patients it may be hard to initiate an exercise routine. In short, it is reasonable

to counsel patients about healthy living practices, but this alone is unlikely to improve CC; concurrent therapies

should be used.

Bulking Agents

Bulking agents include organic and inorganic polymers that work by retaining water in the stool. In theory, this helps

to emulsify stools and speed transit time, ultimately improving CC symptoms. Common bulking agents include

psyllium, calcium polycarbophil, methylcellulose, and bran. Of these, psyllium has the highest-quality data supporting

its efficacy in CC.[5] Five randomized controlled trials have compared psyllium with placebo.[27-31] Most of these

studies indicate that psyllium, at doses of 7 to 24 g daily, improves stool frequency and consistency compared with

placebo. However, the quality of these studies is generally poor, and the data are not entirely consistent.

Furthermore, psyllium undergoes bacterial fermentation in the colon and can generate gas and bloating. In patients

with preexisting bloating, such as the current case, psyllium should be discouraged. In patients without bloating

psyllium may be well tolerated. There is often an initial discomfort and bloating upon initiation of therapy, but over time

this may decrease, particularly with the advice to "start low and go slow" with dosing. Patients with substantial

bloating might benefit from calcium polycarbophil or methylcellulose, both inorganic bulking agents that are not

fermentable.[5] However, only one uncontrolled, low-quality study to date has evaluated this calcium polycarbophil.[32]

Similarly, there is only one low-quality study supporting methylcellulose; this study showed equivalency between



methylcellulose and psyllium.[33] The ACG concluded that it is "not possible to make any recommendation" about

use of calcium polycarbophil or methylcellulose.[5]

Osmotic Laxatives

Osmotic laxatives entrain fluid in the intestinal lumen and act to break up and liquefy stool. A wide variety of osmotic

laxatives are available, including fermentable carbohydrates (such as sorbitol and lactulose), milk of magnesia, and

polyethylene glycol (PEG). Of these, both lactulose and PEG have received grade A evidence from the ACG,

indicating that both have been proven effective in randomized controlled trials.[5] The ACG systematic review identified

3 randomized, placebo-controlled trials of lactulose in CC.[34,35] All the trials revealed that lactulose significantly

improves stool consistency and increases the mean number of daily bowel movements compared with placebo.

However, initial dosing of lactulose may produce transient flatulence and intestinal cramping, along with nausea and,

rarely, vomiting. PEG has a lower incidence of adverse effects than lactulose but is more expensive. Data from 5

randomized trials reveal that PEG is superior to placebo.[36-39] Compared with lactulose, PEG yields looser stools,

less frequent straining, and better overall effectiveness.[40,41] PEG is well tolerated and flavorless, which is appealing

to many patients. High doses may produce diarrhea, excessive stool frequency, nausea, bloating, cramping, and

flatulence. However, discontinuation of PEG because of adverse events is rare.

Stool Softeners

Stool softeners available in the United States include docusate sodium and docusate calcium. These medications are

widely used in both the ambulatory and inpatient setting. Yet despite their popularity, there are surprisingly few data

supporting their efficacy, much less their specific mode of action.[5] Stool softeners are though to work as surface-

acting agents that "soften" stool by acting as a detergent. It actually remains unclear whether docusate actually

works this way or whether its mode of action is altogether different -- possibly even acting as a stimulant in the colon.

Mechanism aside, the data supporting stool softeners are sparse and weak.[5] The effectiveness of docusate from the

existing data is inconsistent. In its guidance document, the ACG concluded that it is not possible to make a

recommendation about the efficacy of stool softeners as a treatment for CC symptoms.[5] Nonetheless, stool

softeners are relatively inexpensive and well tolerated. In patients with severe symptoms, or in patients in whom other

forms of therapy have failed, it is unlikely that stool softeners alone will be adequate.

Stimulant Laxatives

The most commonly available stimulant laxatives are senna and bisacodyl. These agents are thought to treat CC by

triggering high-amplitude propagating contractions (HAPCs) that promote motility and also by inhibiting water

absorption.[5] As with stool softeners, there are surprisingly few data supporting the effectiveness of stimulant

laxatives. The existing studies are of variable quality and reveal inconsistent results. The ACG was unable to make

any recommendation about the efficacy of stimulant laxatives.[5] Practically speaking, however, many patients report

clinically relevant benefits from these agents and symptom recurrence upon discontinuation. Long-term use of

stimulant laxatives is common, and there are historical concerns that they may cause a "cathartic colon" marked by

diminished motility from a "burned out" myenteric plexus.[42] However, there are few data in humans showing that this

occurs.[42] Stimulant laxatives may cause abdominal discomfort, electrolyte imbalances, and even hepatotoxicity, so

they are not entirely benign. Still, stimulant laxatives represent an important rung in the therapeutic ladder.

Chloride Channel Activators

Lubiprostone is a first-in-class locally acting chloride channel activator that has shown benefits in CC.[43-48] The

agent is a gastrointestinal-targeted bicyclic functional fatty acid that increases intestinal fluid secretion by selectively

activating ClC-2 chloride channels. Data in animals suggest that this agent may also restore mucosal barrier function,

although the significance of this finding remains unclear.[8,49] Clinically, lubiprostone reveals important benefits vs

placebo in patients with longstanding CC. In randomized controlled trials, lubiprostone produced significantly more

spontaneous bowel movements per week compared with placebo, along with improvements in abdominal bloating,



discomfort, straining with defecation, and stool frequency.[45,46] Side effects include nausea, which occurred in nearly

30% of patients -- a rate that was nearly 6 times higher than that in patients receiving placebo in the clinical trials.

Nausea with lubiprostone appears dose dependent and often improves with continued use. Diarrhea occurs in 13% of

patients, but discontinuation from diarrhea is rare. The US Food and Drug Administration-approved dose is 24 µg

twice daily with meals. As with most medications for CC, lubiprostone has not been specifically tested in the elderly

population. Most clinicians currently reserve lubiprostone for patients with severe symptoms who have not responded

to less expensive therapies. However, lubiprostone fills an important void in patients with HRQOL decrements in

whom multiple therapies have failed. In addition, because lubiprostone shows benefits for bloating, it makes sense to

consider the agent in the subset of patients with CC with comorbid bloating or tightness, as with the current patient.

Novel Therapies

Several novel therapeutic approaches for CC are currently available or will soon become available. Currently available

approaches include botulinum therapy for outlet dysfunction, sacral nerve stimulation (SNS), and acupuncture. Of

these, SNS requires special attention because it has shown benefit for the most difficult-to-treat forms of recalcitrant

constipation.[50-53] SNS involves implantation of a stimulator device into the sacral nerve plexus. It is a common

treatment for urinary and fecal incontinence. Of note, urologists have found that in patients receiving SNS for urinary

incontinence, underlying CC symptoms often improve. Although the mechanism of action remains unclear, SNS is

thought to work through modulating afferent pathways and rectal sensation in patients with CC. In a prospective,

multicenter, uncontrolled European trial of SNS in 66 patients with recalcitrant CC, Kamm and colleagues found that

66% of patients responded to an initial SNS trial.[53] The SNS improved stool frequency, time per bowel movement,

straining, bloating, and even abdominal pain when measured before vs after the SNS trial. Although a sham-controlled

trial is lacking, the SNS data are intriguing. Because total colectomy is sometimes required in the most severe cases

of CC (particularly those with colonic inertia), SNS provides an appealing alternative that is less invasive.

Nonetheless, future research is needed before SNS will become more widely accepted and practices.

In addition to nonpharmacologic approaches such as SNS, a variety of new pharmacologic approaches are being

developing. These include subcutaneous neostigmine (which can promote utility through anticholinesterase inhibition),

prucalopride (a high-affinity 5-HT4 agonist), and subcutaneous methylnaltrexone for patients with opioid-related CC,

an increasingly common and difficult-to-treat form of CC that is especially prevalent among nursing home patients.


A balloon expulsion test was performed in the office. The patient was able to easily expel the 60-mL balloon in under

2 minutes, making outlet delay unlikely. The lack of alarm symptoms and signs, coupled with the history of a

previously normal colonoscopy and normal complete blood count, argued against an underlying organic disease.

Repeated colonoscopy reconfirmed melanosis coli but found no polyps or masses. Because normal-transit CC is

more prevalent than slow-transit CC, and because the patient also exhibited recent psychosocial distress, normal-

transit CC was presumed. The patient was treated empirically without further testing. Because she had already

received bisacodyl and psyllium with limited success, she was prescribed a course of lactulose. She tolerated the

medicine poorly and reported the medication's unappealing taste and its effect in worsening her bloating. She was

then prescribed a course of 17 g of PEG powder mixed in water daily. She initially responded well and had more

frequent bowel movements and less straining. However, she still reported "bloating and tightness." Moreover, after

several weeks the PEG became less effective and her straining returned. She began receiving lubiprostone, 24 µg

twice daily, which resulted in substantially improved stool frequency and form, along with a reduction in her bloating

symptoms. She developed transient nausea during the first week of therapy that subsided in time, and she did not

stop the therapy. She continued the medication for several months but slowly found that it lost its effect. She was

then referred for a radio-opaque marker study that confirmed slow-transit constipation (18 of the 24 markers remained

scattered throughout her colon after 5 days).

Conclusion



Given the progressive nature of the symptoms, the age-related worsening, and the slow transit documented with the

marker study, colonic inertia was ultimately diagnosed in the patient. Her HRQOL is poor and she is depressed. More

definitive treatment is necessary. She is being evaluated for SNS vs colectomy because traditional medical therapies

have been ineffective. Sacral nerve stimulation, although still considered experimental, might provide some relief

through as yet poorly understood mechanisms. The definitive treatment is colectomy; however, this is clearly a

draconian step and it is worth considering less invasive alternative, such as SNS, before colectomy.

This activity is supported by an independent educational grant from Sucampo Pharmaceuticals Inc. and Takeda

Pharmaceuticals North America Inc.

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Disclaimer

The material presented here does not necessarily ref lect the view s of MedscapeCME or companies that support educational programming

on www .medscapecme.com. These materials may discuss therapeutic products that have not been approved by the US Food and Drug

Administration and off-label uses of approved products. A qualif ied healthcare professional should be consulted before using any

therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies

described in this educational activity.

MedscapeCME Gastroenterology © 2009 MedscapeCME.

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Abstract 198.



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