Inflammatory, Functional, and Other Intestinal Disorders

4.1 Irritable Bowel Syndrome

Am J Gastro 2009;104 Suppl 1:S1; GE 2002;123:2105; Nejm 2003;349:2136

Epidem: In a large U.S. householder survey, the prevalence of irritable bowel syndrome (IBS) sx was 9.4% (Dig Dis Sci 1993;38:1569). In a large U.S. county survey, the prevalence of IBS sx was 17% (GE 1991;101:927). In contrast, only 2.9% of the population reports a medical dx of IBS, because most people with sx of IBS do notbecome pts with IBS (GE 1990;99:409). Women are more than twice as likely to have IBS sx and even more likely to seek care for IBS sx (GE 1991;100:998). Sx reporting decreases with age, suggesting the benign course of these sx (Scand J Gastroenterol 1994;29:102). There are no differences between the physical or psychological sx of men and women, but there are few studies of sx in men (Am J Gastro 2000;95:11). The economic cost is huge. Pts with IBS lose twice as many work days due to illness, require greater numbers of physician visits for GI and non-GI sx (Dig Dis Sci 1993;38:1569), and undergo many more appendectomies, cholecystectomies, hysterectomies, and back surgeries (GE 2004;126:1665).

Pathophys:

Definition of IBS: A working definition of IBS is needed to conduct sound clinical studies. This has proved to be difficult. The most widely used criteria to define IBS are referred to as the Rome criteria, which were published in 1992 and then substantially revised (Gut 1999;45[suppl 2]:II43). Given the limited number of GI sx possible with any gut disorder, it is impossible to develop a definition, based on clinical sx, that will distinguish IBS from other bowel diseases (Am J Med 1999;107:5S). As a practical matter, IBS is considered when a pt presents with abdominal pain and disordered defecation for more than 3 months in the absence of structural disease.
Abnormal motility and IBS: Resting motility is similar in IBS and non-IBS pts, but IBS pts have increased motility in response to stimuli such as food or psychological stress. The severity of pain does notcorrelate with abnormal motility (Gastroenterologist 1994;2:315).
Abnormal visceral perception and IBS: (Gut 2002;51[suppl 1]:i67) There is a body of evidence suggesting that enhanced visceral sensitivity is a factor in IBS pathophysiology. IBS pts
perceive pain from balloon distension of the rectum or ileum at pressures and volumes much lower than controls do. The mechanisms of enhanced sensitivity are unclear. It is thought that multiple inciting factors (genetic factors, chronic inflammation, psychological stresses, peripheral nerve irritation) alter afferent pain pathways to the brain and leave them permanently revved up long after the inciting stimulus goes away. In a sense, the IBS pt develops a pain memory that causes stimuli, which an ordinary subject would notperceive, to be experienced as pain. These stimuli are further modulated by the CNS in ways that might further enhance the perception of pain. Serotonin is an important signaling molecule within the GI tract and enteric nervous system (GE 2007;132:397), and effective serotonergic drugs have been developed for rx of IBS.
Psychosocial factors and IBS: Up to 60% of IBS pts have psychosocial difficulties, including major psychiatric disorders, personality disorders, stressful life events, a hx of physical or sexual abuse, and chronic pain behaviors. These psychosocial factors distinguish IBS pts from pts with IBS sx who do notseek medical attention. Psychosocial factors play a major role in explaining why the IBS pt experiences sx as being more severe than the individual who has the same IBS sx and copes without medical evaluation. These psychosocial problems translate into worse outcomes (measured by more disability days, more physician visits, and more medicines). A hx of sexual or physical abuse is one of the strongest predictors of poor outcome. Those with the most severe IBS have the greatest psychosocial stressors (Am J Med 1999;107:41S).
Food intolerance: A subgroup of pts have sx of IBS in response to specific foods. These intolerances have been verified with blinded administration of the offending foods through an NG tube. The mechanism does notappear to be allergic, but it does provide a rational basis for the use of food and sx diaries in pts with moderate sx. Some clinicians have pts pursue strict exclusion diets to find the offending food (Lancet 1982;2:1115).
Bacterial overgrowth: Bacterial overgrowth may be an important factor in subgroups of pts with diarrhea or bloating as evidenced by the response to antibiotic therapy (see Rx).

Sx: Since IBS cannot be defined by any test or structural abnormality, it is recognized by its sx. Three sx patterns are recognized. The patterns require different diagnostic workups and respond differently to rx (Am J Med 1999;107:20S). Common to all 3 subtypes are that: (1) the pts have pain or closely related noxious sx; (2) the sx are chronic, typically lasting years; (3) the sx typically begin insidiously in young adulthood; and (4) there are no findings to suggest structural diseases (ie, no weight loss, bleeding, fever, etc). Sudden-onset sx, especially in older pts, are usually notIBS. Sx that awaken pts from sleep are less common but do notrule out IBS. The recognized sx patterns are:

Diarrhea-predominant IBS: The pts have pain associated with loose, watery BMs and great urgency. Pts often describe the stools as explosive, and typically several will be passed in a short period requiring several trips to the toilet. The BMs often cluster in the morning. Pts are usually well once the flurry of activity passes. Sometimes bouts are directly related to stressful events (taking tests, job-related stress, Monday morning).
Constipation-predominant IBS: These pts have crampy lower abdominal pain associated with infrequent BMs. The stool is hard and looks like it is composed of individual pellets packed together. There is a sense of incomplete evacuation and straining at stool. Pain is relieved by passage of a BM. Interestingly, such constipation-predominant pts are more likely to have dyspepsia, musculoskeletal pain, poor sleep, and sexual dysfunction (Am J Med 1999;107:20S).
Mixed-diarrhea/constipation IBS: This group presents with complaints of constipation alternating with diarrhea. These pts have crampy pain and go days without BMs. Eventually they pass hard, dry BMs. After the initial hard, dry stool has passed, a number of looser BMs may follow and the pt may complain of diarrhea. The pt then may be without sx for a day or 2 and the pattern often repeats.
Pain/discomfort-predominant IBS: This group presents with complaints of generalized discomfort/pain, usually associated with bloating, a perception of abdominal distension, and a sensation of gas. Their sx may or may notbe related to meals, and the relief with BMs is variable. They tend to experience sx over a greater part of the day. The distension is often thought by physicians to be imaginary, but increases in abdominal girth are seen in IBS pts compared to controls without a clearly defined mechanism (Gut 1991;32:662).

Si: PE is useful only for detecting structural diseases by palpation of masses, detection of blood, and identification of abdominal wall pain. No positive finding on physical exam makes IBS more likely or predicts clinical outcome or response to rx (Am J Med 1999;107:33S).

Crs: Combining results of observational studies, it is evident that more than 50% of pts have improvement in their sx over the course of years. Complaints vary in severity over time but tend notto change in their quality. Psychological distress and a long duration of complaints correlate with poorer outcome (Scand J Gastroenterol 1998;33:561).

Diff Dx: One approach to diff dx in IBS is to list all disorders known to humankind that cause diarrhea, constipation, or abdominal pain. This can lead to a lengthy list and the compulsion to rule out each dx on the list with a specific test. In practice, such a complete diff dx and subsequent workup is unnecessary. It is more fruitful to consider a short diff dx for the specific set of pt complaints, taking into account the age of the pt and the duration and severity of sx.

For pts with diarrhea as a predominant sx routine, celiac disease testing (p 119) should be considered. The prevalence of celiac disease in pts meeting diagnostic criteria for IBS is substantially increased (Arch IM 2009;169:651). Other conditions to consider include lactose intolerance (p 102), drug-induced diarrhea, bacterial overgrowth (p 169) sorbitol ingestion (p 11), surreptitious laxative use, and IBD. Infections are uncommon if the sx are long standing, except in areas endemic for parasitic infections. The malabsorptive diseases, such as pancreatic insufficiency, rarely present with the crampy lower abdominal pain typical of diarrhea-predominant IBS. Uncommonly, collagenous colitis and selective bile salt malabsorption are considerations. Only in refractory cases does a more extensive diff dx for chronic diarrhea need to be considered (p 17).

For pts with constipation-predominant sx, age and duration of sx guide testing. In those with a short-duration sx and in those >40 yr of age, colonic obstruction due to malignancy is a consideration. The reader should review the discussion of constipation (p 11).

The diff dx for pts with pain/discomfort-predominant IBS is more complex. Consider lactose intolerance (p 102), sorbitol ingestion (p 11), partial mechanical obstruction (p 123), Crohn’s disease (p 105), pseudo-obstruction (p 126), malabsorption (p 19), gastroparesis (p 77), and bacterial overgrowth (p 169).

Lab: A CBC and CMP are commonly performed to find clues to more serious illness. Stool testing for FOBT is reasonable. TSH should be done for specific reasons such as diarrhea or constipation. Stool studies for infectious causes are of very low yield if the sx are long
standing and notrecently changed. Stool testing can be considered in areas endemic for parasitic infection or in pts with recent exacerbation of diarrheal sx. In refractory diarrhea, a 72-hr stool collection for weight and fat can help identify those with a structural cause of diarrhea by demonstrating stool weight >300 gm/day or malabsorption of fat (p 19).

X-ray: CT enterography or SBFT is indicated if Crohn’s disease is suspected or if there are other clues to mechanical obstruction. CT colonography or ACBE in combination with sigmoidoscopy can be used in the small number of pts in whom obstructing neoplasm must be ruled out. However, colonoscopy would be the test of choice in pts over the age of 50 yr, who might have the secondary benefit of the most effective screening for polyps.

Endoscopy: Endoscopy is notindicated in the vast majority of pts with IBS. The threshold to perform colonoscopy to evaluate possible IBS sx should be lower in older pts, in pts with sudden-onset sx, and in pts with refractory diarrhea. The yield will be higher in these pts, and they gain the additional benefit of clearing the colon of polyps as a means of preventing future CRC. Sigmoidoscopy should notbe part of the routine workup of IBS but should be done for specific clues that pathology is within reach of the sigmoidoscope.

Rx:

Initial approach:

Evaluation of the pt’s complaints can be therapeutic: Pts with long-standing complaints seek care for a variety of reasons. Many are concerned that they may have a dangerous underlying illness, while others simply seek relief of sx. It is important to know the pt’s reason for seeking care. A detailed hx, obtained with empathy, is crucial to demonstrate to the pt that the physician takes the complaints seriously and is competent to evaluate them. A cursory hx and blind reassurance on that basis can be destructive even if the physician is entirely correct with the dx. Explain to the pt the diff dx being considered and the planned evaluation to rule out structural illness. Reassure the pt that if he/she fails to respond to the initial therapeutic approach and if the initial testing is unrevealing, further testing and rx will be carefully considered. However, it is important to notcreate unrealistic expectations about the goals of rx or the extent of diagnostic testing needed.
Dietary fiber: Establish the importance of diet in the pt’s sx with a detailed dietary hx. Estimate the pt’s daily fiber intake in grams by determining the pt’s intake of whole-grain bread, cereal, beans, fruits, and vegetables (Am Fam Phys 1995;51:419). A fiber intake of 25 gms will generally improve pts with constipation and helps some with diarrheapredominant IBS. Its use in diarrhea-predominant pts is controversial, given limited evidence of efficacy (Am J Med 1999;107:27S). Some pts will experience bloating as fiber is increased due to fermentation/degradation, so the amount of fiber should be increased gradually. Fluid intake should be increased as dietary fiber is increased. As an alternative, fiber supplements containing psyllium seed, methylcellulose, or polycarbophil can be used (p 13), but diet should be tried first in those who are willing.
Trial of lactose exclusion: Establish the daily intake of lactose-containing products. In pts with diarrhea or bloating, a therapeutic trial of exclusion of lactose (for 7-14 days) is worthwhile. Some authors do breath testing for lactose intolerance instead. This spares some pts an unneeded trial but does notanswer the question as to whether lactose intolerance is responsible for sx (p 102).
Exclusion of excessive sorbitol: In pts with diarrhea or bloating, determine the intake of sorbitol. Sorbitol is notabsorbed and is then fermented by bacteria, causing distress or diarrhea. It can be found in sugarless gum, breath mints, some hard candy, apples, pears, peaches, prunes, and foods sweetened for diabetics.
Legumes: Determine the intake of beans, cabbage, broccoli, and cauliflower. For pts with bloating and gas, consider a trial of exclusion or of an alpha-galactosidase preparation such as Beano (J Fam Pract 1994;39:441).
Fatty foods: In IBS there can be abnormal motility in response to a variety of triggers, and for some pts this includes fatty foods.

In pts without a good response to the initial approach, consider:

Rethinking of the dx: If pts do notimprove with initial management, the physician should rethink the dx and workup. For example, failure of constipation to respond to a high-fiber diet might prompt excluding obstruction. Failure of diarrhea to improve after excluding milk and sorbitol may cause reconsideration of other causes of chronic diarrhea (p 17), especially celiac disease or IBD.
Antidiarrheal agents: Loperamide is effective in treating chronic diarrhea due to IBS. It reduces diarrhea and diminishes urgency but may notimprove pain. The dosage should be gradually increased from 2 mg to a max of 16 mg daily in 4 divided doses. Pts should be cautioned about the risk of impaction with excessive loperamide. A second-line agent is cholestyramine, which may relieve the diarrhea due to the malabsorption of bile salts that occurs frequently in pts with functional diarrhea and treats those with the uncommon disease of idiopathic bile salt malabsorption (Am J Med 1999;107:27S). A dosage of 4 gm tid can be used as a trial. Some pts prefer 1-gm colestipol hydrochloride tablets when low doses are required.
Smooth muscle relaxants: In the U.S., dicyclomine (10-20 mg po qid prn) and hyoscyamine (0.125-0.25 mg po qid prn or as a timed-release preparation [eg, Levsinex] 0.375 mg po q 12 hrs) are widely used for relief of pain in IBS. There are limited data to support their use due to methodological limitations in the available trials. A meta-analysis of smooth muscle relaxants in IBS showed that they achieved some benefit in control of pain and resulted in global improvement (Aliment Pharmacol Ther 1994;8:499). Peppermint oil appears to be effective, but data are limited (BMJ 2008;337:a2313).
Antibiotics: Treatment with the nonabsorbable antibiotic rifaximin improves sx of IBS, especially diarrhea and bloating (Am J Gastro 2009;104 Suppl 1:S1; Ann IM 2006;145:557). Presumably, some of the pts who respond have bacterial overgrowth. A course of 400 mg po tid for 10-14 days may give relief for 3 months, but recurrence is common. There are no data on long-term use.
Probiotics: Probiotics appear to be effective in IBS, but the degree of benefit and the most effective agents and strains are unknown (Gut 2008 Dec 17 Epub ahead of print; PMID 19091823). Bifidobacterium infantis was effective in a large study of women with a mix of subtypes of IBS (Am J Gastro 2006;101:1581). It is commercially available in the U.S. OTC as Align.
Antidepressants: Tricyclic antidepressants are appropriate for pts whose sx are persistent over months, especially if there is associated depression or anxiety. They probably work centrally as analgesics. Doses needed for IBS are often lower than doses needed for depression (10-25 mg of amitriptyline, 50 mg of desipramine). Trials of 2-3 months seem
appropriate, and a second agent should be tried if the first fails, as success will be seen about 50% of the time on a second trial (Aliment Pharmacol Ther 1994;8:409). Selective serotonin reuptake inhibitors (SSRIs) also appear to be effective, but data are limited (Gut 2009;58:367).
Alosetron: Alosetron is a 5-HT3 receptor antagonist that improves pain and BM frequency in pts with diarrhea-predominant IBS (Lancet 2000;355:1035). It was temporarily withdrawn from the U.S. market because of a possible association with cases of ischemic colitis. It has been re-released under a special prescribing program for use in women with severe sx of diarrhea-predominant IBS.
Lubiprostone: Lubiprostone is a chloride channel activator that is effective in idiopathic constipation. Low-dose therapy (8 mcg po bid) improves sx in pts with constipationpredominant IBS with a low incidence of side effects (Aliment Pharmacol Ther 2009;29:329).
Tegaserod: Agonists of the 5-HT4 receptors appear beneficial in constipationpredominant IBS. Tegaserod (2-6 mg po bid) improves sx of pain and constipation (Aliment Pharmacol Ther 2001;15:1655). Unfortunately, it was withdrawn from the market in 2007 for a 0.11% rate of adverse cardiovascular events.
Chinese herbs: Chinese herbal remedies reduce sx but are notreadily available or standardized (Jama 1998;280:1585; Jama 1998;280:1569).

If pts are refractory to anything on the preceding list:

Reconsider the diagnosis: At this point if the pt has refractory sx, especially if they are long standing and constant, the dx is likely secure. Additional testing is unlikely to be needed. However, pts with IBS are notprevented from coming down with serious unrelated illnesses, and the physician should guard against failing to listen to the pt’s sx.
Review the abuse history: Hopefully, long before this point in rx, the physician will be able to establish whether there is a hx of verbal, physical, or sexual abuse. However, because this hx is so depressingly common in pts with refractory sx (Ann Intern Med 1995;123:782), the physician must reexplore this area.
Refer for psychological rx: (Arch IM 2003;163:265) A variety of modalities are available, which may be of benefit to pts whose sx are more severe and substantially affect their quality of life (Ann IM 1995;123:688). These include stress management, psychotherapy, behavioral rx, hypnotherapy, and biofeedback/relaxation training. Choice of rx is usually made by the mental health professional on the basis of pt’s needs and resources.

4.2 Physical and Sexual Abuse and GI

Ann IM 1995;123:782

Pts with chronic, functional GI complaints have a distressingly high (44%) incidence of prior physical or sexual abuse (Int J Colorectal Dis 1995;10:200; Ann IM 1990;113:828). Most of these pts never report these tragic life experiences to their physicians. A large number of factors that suggest a hx of abuse have been identified (Ann IM 1995;123:782). The link between abuse hx and GI sx may be that chronic or traumatic stimulation increases sensitivity of visceral afferent receptors (Am J Med 1994;97:105). As a simple rule of thumb, always consider physical or sexual abuse in pts with functional complaints that do notrespond readily to routine measures and in pts who have seen multiple providers for the same complaint.
Eliciting a hx of abuse can be easily done in the routine office setting. Sometimes the pt may make a veiled reference to prior difficulties in life that open a door of inquiry. At other times a supportively phrased question is most helpful. For example, say, “Many pts I have seen with difficult or long-lasting belly pain have told me that they have been sexually or physically abused in their lifetimes—has that ever happened to you?” Most pts are surprised at the question, and most have never been previously asked about abuse by a physician. Most pts will respond well to a supportive inquiry. In an academic center, only 3% of pts required urgent counseling after the inquiry (Ann IM 1995;123:782). It is then useful to go on to explain the possible connection between chronic GI complaints and the abuse hx and to reassure pts that many others have had similar difficult experiences. For pts who answer affirmatively to an abuse hx, it is often sensible to limit testing and to try to work with dietary and other therapies while the process of counseling is initiated. The pt is followed along with mental health clinicians until the picture improves. Occasionally, the inquiry throws a schedule into disarray, but there is greater satisfaction in steering such a pt to expert help than in being on time for the next endoscopy.

4.3 Food Allergy

Am J Gastro 2003;98:740; Lancet 2002;360:701; BMJ 1998;316:1299

Cause: The most common causes of true food allergy are cow’s milk, hen’s eggs, cod (and other fish), shrimp (and other shellfish), peanuts (and other nuts), soybeans, wheat, and food additives. Those allergic to pollen may have reactions with a variety of foods.

Epidem: The confirmed prevalence of food allergy in adults is only 1.4-2.4% compared with a 20% pt-perceived prevalence (Lancet 1994;343:1127). Rates of true allergy are higher in children.

Pathophys: Adverse reactions to food can be (1) IgE-mediated allergy (involving basophils and mast cells [GE 1992;103:1075]); (2) delayed non-IgE-mediated immunologic reactions (eg, eczema from milk); (3) nonallergic food intolerance (eg, scromboid fish poisoning due to high histamine levels, reaction to monosodium glutamate in Chinese food); and (4) food aversion. The last category is the most common, and sx are nonspecific and cannot be confirmed by blinded food challenge. Food additives (benzoates, sulfites, tartrazine, food colorings, and salicylates) may cause a nonimmunologic, harmless, contact urticaria.

Sx: Pts develop specific and reproducible sx or si involving the mouth, gut, skin, and respiratory systems. At least 2 of these systems should be involved. Sx include oral itching and swelling, nausea, vomiting, abdominal pain, diarrhea, asthma, cough, rhinitis, atopic dermatitis, or anaphylaxis. In a subgroup, sx develop only after exercise.

Si: Angioedema, urticaria.

Crs: About one-third of children and adults lose clinical reactivity to food allergens, though lab testing can remain positive for years.

Cmplc: Anaphylaxis.

Diff Dx: Food aversion is the major differential point and is much more common than allergy. Reactions to additives and other intolerances can be difficult to separate from allergy.
When sx suggest allergy, the dx is confirmed by lab testing followed by eliminating and then rechallenging (under medical supervision) with the offending food.

Lab: Antigen-specific IgE to water-soluble extracts of food antigens can be evaluated in serum. Many clinically insignificant cross-reactivities create false positives. Skin prick testing with food extracts is the alternative.

Rx: Rx is food avoidance. Epinephrine should be available to the pt at home, along with a userfriendly delivery device (eg, EpiPen). Anti-IgE and immunomodulatory therapies are being developed. Methods are being developed to produce hypoallergenic foods (GE 2005;128:1089).

4.4 Colonic Diverticulosis and Diverticulitis

Lancet 2004;363:631; Am J Gastro 1999;94:3110

Epidem: Rare in children. In Western countries, the prevalence of diverticula is <10% in those under age 40 yr, 20-30% in those over age 50 yr, and >50% in those over age 80 yr. Rare in rural Africa and Asia. Based on prevalence of data and hospitalization data, only 0.5% of pts are hospitalized for diverticular disease.

Pathophys: (Gastroenterologist 1994;2:299) Left-sided diverticula are pseudodiverticula that contain only mucosa and submucosa rather than all layers of bowel. They form between the longitudinal muscle layers of the colon that are present in 3 bands called the tenia coli. Diverticula form between the mesenteric and the 2 antimesenteric tenia, where the nutrient arteries pierce the circular muscle layers. These arteries create weak points where herniation can occur. The association of each diverticulum with a nutrient artery predisposes to diverticular hemorrhage.

In Western countries, 90% of pts have left-sided disease, and in Asia, right-sided disease dominates. The number of diverticula can range from a few to hundreds and are usually 5-10 mm in diameter. Resected specimens with diverticular disease show a shortening of the tenia, thickening of the colon wall, and deposition of elastin in teniae, though nottrue muscular hypertrophy. The thickening of the circular muscle folds is due to shortening of the tenia (Gastroenterologist 1994;2:299). The colon in pts with diverticular disease appears to be less elastic and pliable. New diverticula may be formed when dysmotility causes high-pressure segments to develop within the sigmoid.

Because of the epidemiology, it was hypothesized that diverticulosis was a fiber deficiency disease. Fiber increases the bulk of stool, increases luminal diameter, and decreases intraluminal pressure. A high-fiber diet reduced the risk of symptomatic diverticular disease (RR = 0.63) in the prospective U.S. Health Professionals Study (J Nutr 1998;128:714). Nut and popcorn consumption was associated with a lower risk of diverticulitis in this cohort (Jama 2008;300:907). A study of 1800 rats also demonstrated a protective effect of a high-fiber diet (Am J Clin Nutr 1985;42:788).

Diverticulitis is the result of a small perforation of a diverticulum. This is thought to occur when undigested food debris blocks the neck of the diverticulum. This results in bacterial fermentation and mucus secretion in a closed space, which increases pressure in the diverticulum. The vascular supply becomes compromised and perforation occurs. Most of these perforations are walled off by the mesocolon or appendices epiploicae (Nejm 1998;338:1521). The walled abscess (stage I) may lead to other intra-abdominal or pelvic
abscesses (stage II), or to peritonitis from rupture of the abscess (stage III). Bowel contents do notspill into the abdomen in stage III because the diverticulum is swollen shut at its neck. In stage IV disease there is a large hole in the colon that allows free spillage of stool into the abdomen with its attendant morbidity and mortality.

Diverticular bleeding is arterial. Thus, it tends to be fairly large volume and abrupt in onset. Bleeding occurs from the rupture of the artery in the diverticulum as it courses over the dome of the diverticulum. Inflammation is notpart of the picture histologically (GE 1976;71:577). It is notclear what predisposes an artery to thinning. NSAID use is associated with diverticular hemorrhage (Dig Dis Sci 1997;42:990).

Sx: Most pts with diverticular disease have no sx. A subgroup will present with abdominal pain without evidence of diverticulitis. It is notclear if the pain is related to the diverticulosis. The pain is typically crampy, LLQ, associated with bloating, and has features similar to IBS, though in many cases the hx is of recent-onset pain (Am J Clin Nutr 1985;42:788). Diverticulitis typically presents as sudden onset of LLQ pain and fever, usually associated with a change in bowels. There may be minor bleeding or pain elsewhere in the belly. Pneumaturia suggests colovesical fistula, and feculent vaginal discharge may indicate colovaginal fistula. Dysuria and frequency may occur from inflammation of the bladder. Diverticular bleeding presents as a sudden, large-volume bleed, usually reddish bloody stool with clot, as would be expected from rupture of an artery. Intermittent, chronic, small-volume hematochezia should notbe attributed to diverticular bleeding. Melena from bleeding right-sided diverticula is rare.

Si: Tenderness to palpation is almost universal in diverticulitis and is usually in the LLQ. Percussion tenderness and localized or diffuse peritoneal signs are variably present and reflect the severity of the episode. Fever is usually present. A palpable mass may be evident in more severe cases. FOBT may be positive, but gross bleeding is rare in diverticulitis.

Crs:

Diverticulitis: The risk of recurrence after a first attack of diverticulitis managed medically is about 25%, but the rate reported in the literature does vary widely (Am J Gastro 1999;94:3110). Older case series suggested that if a second attack occurs, it is much less likely to respond to medical rx, more likely to have complications such as abscess, and more likely to require surgery in 2 stages (BMJ 1969;4:639). More recent data suggest that 80% of pts with diverticulitis are never hospitalized again with the illness and only 5-7% undergo colectomy (J Am Coll Surg 2004;199:904). Diverticulitis recurs in 10% of pts treated surgically and requires reoperation in 3%, especially if the anastomosis is to distal sigmoid rather than rectum.
Diverticular hemorrhage: Bleeding stops spontaneously in 80% of pts. It recurs in 22-38% of pts, and the chance of a third bleed after a second bleed may be as high as 50% (Am J Gastro 1999;94:3110). Pts who require less than 4 units of blood per 24 hr usually stop spontaneously (Ann Surg 1994;220:653).

Cmplc: Pylephlebitis (inflammation or infection of the portal vein and/or its tributaries); fistulae to bladder, vagina, or skin; intra-abdominal abscess.

Diff Dx: Many causes of acute abdominal pain need to be considered (p 1). The most important differential considerations for diverticulitis are (1) ischemic colitis (in which there is usually prominent bloody stool and crampy pain is prominent); (2) CRC (where the hx of sx is usually longer); (3) Crohn’s or ulcerative colitis (where extraintestinal manifestations and
chronic diarrhea may be a clue); (4) appendicitis (especially if diverticulitis is right sided); (5) pain from an ovarian source (cyst, abscess, or torsion); (6) ectopic pregnancy; (7) bacterial colitis, including C. diff (where diarrhea is prominent); and (8) perforated ulcer disease. The diff dx for diverticular hemorrhage includes brisk UGI bleeding, bleeding from angioectasias, cancer, or ischemia (p 21).

Lab: In diverticulitis severe enough for hospitalization, the wbc is usually elevated, but may be normal (Surgery 1994;115:546).

X-ray: An abdominal series to look for free air under the diaphragm is indicated in pts in whom perforation is suspected. However, since diverticulitis is really an extraluminal disease, the best imaging test is CT scan. CT with oral and, if needed, rectal contrast can reveal thickening of the colon, infiltration of the pericolonic fat (so-called “greying” of the fat), abscess, or air or contrast outside the bowel wall. If abscess is seen, CT can be used for percutaneous drainage. In addition, CT may show an alternative dx. False-negative rates for CT vary widely and are reported in 2-21% of pts (Nejm 1998;338:1521). Contrast enemas are often nondiagnostic (since the disease is outside the bowel), but force the dx to be reconsidered if there are no diverticula seen. US has its advocates but is very operator dependent, and studies on its use have been small (Am J Gastro 1999;94:3110).

Endoscopy: Endoscopy should be avoided in acute diverticulitis for fear of creating free perforation from the air or the instrument. Limited sigmoidoscopy is appropriate acutely if there is strong diagnostic concern for IBD or infectious colitis and stool studies are negative. After the pt recovers from a clinically diagnosed bout of diverticulitis, the entire colon should be evaluated (generally with colonoscopy). This is typically done several weeks after recovery from the acute bout. Diverticular inflammation can be an incidental finding in asymptomatic pts that does notrequire treatment (Am J Gastro 2003;98:802).

Rx: (Am J Gastro 1999;94:3110; Dis Colon Rectum 1995;38:125)

Diet and exercise: A high-fiber diet is reasonable for pts with asymptomatic diverticular disease with the hope of reducing the risk of diverticulitis. Nuts and popcorn do notneed to be restricted. Vigorous physical activity is associated with a lower risk diverticulitis and might be considered.
Medical rx of diverticulitis: Mild to moderate episodes in otherwise healthy pts can be treated on an outpatient basis with oral antibiotics. Severity is judged by fever, wbc count, physical exam, and reported sx severity. Pts must be well enough to be hydrated orally and be in a safe setting in case they become more ill. A 10-day course of oral antibiotics with aerobic and anaerobic coverage is prescribed. There are many acceptable choices, including amoxicillinclavulanate (500 mg po tid × 10 days); trimethoprim-sulfamethoxazole (1 DS tab po bid) plus metronidazole (500 mg po tid); or ciprofloxacin (500 mg po bid) plus metronidazole. Because the majority of pts who recover from their first attack of diverticulitis never have a recurrence, surgery should notbe offered after a single uncomplicated bout.
Surgical rx of recurrent uncomplicated diverticulitis: For years it has been argued that each attack of diverticulitis makes it more likely that another attack will occur and less likely that the next attack will respond to medical rx. This theory has led to consideration of surgery after a second bout of diverticulitis. However, these recommendations are based on data from small case series. Decision analysis based on more recent larger studies suggests that delaying surgery until after a fourth episode lowers cost, death rate, and
the need for colostomy. There are no hard-and-fast rules, and the decision should be individualized. The medical fitness of the pt for an operation, the severity of the attack, the response to medical rx, and the desires of the pt all factor into the decision. If pts are treated while notacutely ill, they can undergo resection of the diseased segment and anastomosis in a single operation (primary anastomosis). A 1-stage operation may notbe possible in complicated disease.
Complicated diverticulitis: Abscess, fistula, free perforation, and obstruction define complicated diverticulitis. All pts with complicated diverticulitis should be offered surgery unless the medical risk is prohibitive. Small pericolic abscesses may resolve with antibiotics (Surgery 1994;115:546). Larger abscesses can be drained with CT-guided drainage or surgery. If CT drainage is successful, the pt can usually have a 1-stage operation with primary anastomosis. If CT drainage is notpossible or is unsuccessful, laparotomy with resection is done. If contamination is substantial, a Hartmann procedure is done. In this operation, the diseased segment is resected, an ostomy is created for the portion of bowel still in the fecal stream, and the free end of the defunctionalized bowel is closed. In the fit pt who makes a good recovery, a reanastomosis can be performed (a 2-stage operation). Pts with obstruction often respond to medical rx initially and can undergo resection with primary anastomosis electively. Pts with free perforation should have resection with colostomy. This group has high morbidity and mortality (6-35%).
Diverticulitis in the young: Some authors have suggested that diverticulitis in young pts is a more virulent disease that requires surgery more than 70% of the time (Am J Surg 1994;167:562). However, other series suggest that the rate of perforation and the need for urgent surgery are notincreased in a first episode of diverticulitis in the younger pt (J Am Coll Surg 1994;179:156). There does notappear to be compelling evidence to change the therapeutic approach in young pts.
Diverticular hemorrhage: The approach to suspected lower GI bleeding is outlined on p 23. In suspected diverticular bleeding, an anorectal cause should be excluded by anoscopy. Upper endoscopy may be needed to exclude an upper source. If the pt is bleeding actively, a tagged rbc scan or CT angiogram is obtained to try to localize the bleeding site. If the site is localized and bleeding does notstop, angiographic rx or a surgical resection is performed. Some centers offer urgent angiography with selective embolization as therapy. Angiography can be diagnostic and therapeutic but is associated with a high incidence of complications, requires more vigorous bleeding than a rbc scan requires for visualization (≥0.5 mL/min), and surgery is still frequently required (GE 2000;118:978). If bleeding stops or slows enough for a colonoscopy prep, the pt should undergo colonoscopy to look for a treatable cause of the bleeding. Some authors advocate urgent colonoscopy following vigorous bowel prep with polyethylene glycol lavage. The purpose is to stratify the pt’s risk of rebleeding (by identifying those with active bleeding, visible vessels, and adherent clots) and to treat high-risk lesions endoscopically. Endoscopic rx includes injection of the base of the actively bleeding diverticulum with 1-2 mL of 1:20,000 epinephrine in 4 quadrants and bipolar electrocoagulation for visible vessels. Endoscopic clips can be used (Gastro Endosc 2004;59:433). A nonrandomized trial suggests benefit (Nejm 2000;342:78), and a small RCT showed no effect on outcomes (Am J Gastro 2005;100:2395). A large, randomized, multicenter trial is needed to assess the safety and efficacy of this approach. Retrospective data suggest a high risk of recurrence for those treated endoscopically (Am J Gastro 2001;96:2367).

4.5 Lactose Intolerance

Aliment Pharmacol Ther 2008;27:93; Am Fam Phys 2002;65:1845; Postgrad Med 1998;104:109

Cause: Low levels of lactase, a small intestinal enzyme.

Epidem: The prevalence of adult lactase deficiency is low in northern Europeans (2-7%) and U.S. Caucasians (6-22%) and is higher in Hispanics (50-80%), African Americans (60-80%), Native Americans (80-100%), and Asians (98-100%). The prevalence rises with age (Dig Dis Sci 1994;39:1519).

Pathophys: Lactase is normally present in the brush border of small intestinal epithelial cells. At birth, levels of the enzyme are high but decline rapidly after weaning in most populations. In some groups, especially northern Europeans, single nucleotide polymorphisms in the lactase gene cause levels of lactase to remain abnormally high into adulthood. Thus the normal condition is to become lactase deficient after weaning, but mutations have allowed some populations to remain lactose tolerant into adulthood. In some cases, lactase deficiency is acquired due to infection (eg, Giardia), drugs, or other diseases of the bowel. When dietary lactose is notappropriately broken down into glucose and galactose, it passes unabsorbed into the colon. In the colon, bacteria ferment lactose, producing gas and other metabolites that cause net fluid secretion into the colon. Not all pts who maldigest lactose become symptomatic; some live blissfully with their deficiency. Most of the sx are associated with the gas production. Sx from less than 12 gm lactose (1 cup of milk) are minimal to nonexistent, and sx increase in a dose-related fashion thereafter (Aliment Pharmacol Ther 1995;9:589).

Sx: Abdominal pain, bloating, flatulence, and diarrhea after the consumption of lactose.

Si: Distension is usually notdetectable clinically.

Crs: Surprisingly, sx can improve with continued lactose exposure in pts who are lactase deficient. This occurs notby improved lactose digestion but by colonic adaptation (Am J Clin Nutr 1993;58:879).

Diff Dx: Since the sx of lactose intolerance are similar to those of IBS, the 2 conditions are easily confused. Lactose intolerance is as common in IBS as in the general population.

Lab: Several tests are available for the dx of lactase deficiency. The most widely used is the breath hydrogen test that measures the amount of hydrogen produced after the ingestion of lactose. Breath hydrogen is produced by intestinal bacteria that ferment the malabsorbed lactose. If breath hydrogen rises more than 20 ppm, lactase deficiency is diagnosed. False-negative results can occur in up to 20% of pts with recent antibiotics or if the pt’s flora uses the available hydrogen to produce methane. Small bowel bx is the gold standard but is largely a research tool. Other serum tests have been described (Scand J Gastroenterol [suppl] 1994;202:26). There is controversy regarding which pts to test for lactase deficiency. Since notall pts with lactose maldigestion have sx and some pts have sx without proven maldigestion, it seems reasonable to do a trial of exclusion of lactose without a diagnostic test. However, this approach risks making a dx of a lifelong condition with a trial of questionable validity (Aliment Pharmacol Ther 1995;9:589). If this
approach is taken, a rechallenge with lactose should be considered after the pt has been asymptomatic for some time.

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