DI D V I E V R E T R I T C I U C LA L R DI D S I EA E SE Dr Förhécz Zsolt

Transcription

1 DIVERTICULARDISEASE Dr Förhécz Zsolt

2 Diverticula: the formation of small bulging pouches out from the colon wall. The diverticula usually range in diameter from 5-10 mm, but it can exceed 2 cm. The medical condition that refers to the presence of diverticula is known as diverticulosis

3

4

5 Diet low in fiber results in low stool volume, which prolongs transit time. This low stool volume also causes an increase in intraluminal pressure based on LaPlace slaw (P [pressure] = kt[wall tension]/r[radius]), which states that there is an inverse relationship between intraluminal pressure and lumen diameter. This increased intraluminal pressure can in turn cause herniation of the colonic mucosa in areas of weakness such as the penetration point of vasa recta that supplies the submucosa and mucosa. This might explain the reason why diverticula are usually present in parallel rows.

6 RISK FACTORS ENVIRONMENTAL AND LIFESTYLE FACTORS ARE IMPORTANT RISK FACTORS FOR DIVERTICULAR DISEASE. Fiber The role of fiber in the development of diverticulosis is unclear. the risk of diverticular disease was significantly increased with diets that were low in fiber and were high in total fat or red meat Nut, corn, and popcorn consumption arenotassociated with an increase in risk of diverticulosis, diverticulitis or diverticular bleeding. Physical activity It is unclear if lack of vigorous exercise is a risk factor for diverticular disease. However, vigorous physical activity appears to reduce the risk of diverticulitis and diverticular bleeding. Obesity Obesity has been associated with an increase in risk of both diverticulitis and diverticular bleeding. Other Current smokers appear to be at increased risk for perforated diverticulitis and a diverticular abscess as compared with nonsmokers Caffeine and alcohol are not associated with an increased risk for symptomatic diverticular diseas Several medications are associated with an increased risk of diverticulitis and diverticular bleeding including nonsteroidal antiinflammatorydrugs, steroids, and opiates. In contrast, statins may be associated with a decreased risk of diverticular perforation

7

8 As a diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa.over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media. These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen. DIVERTICULAR BLEEDING

9 The management of colonic diverticular bleeding includes resuscitation and, if the bleeding does not stop spontaneously, treatment of the bleeding site. If active bleeding or a visible vessel (similar to stigmata of ulcer hemorrhage) can be localized to a particular diverticulum during colonoscopy, endoscopic therapy can be attempted. Angiography is an alternative to colonoscopy for treatment in cases where the bleeding site cannot be identified with colonoscopy or if a bleeding site is identified but attempts to stop the bleeding endoscopically are unsuccessful. If the bleeding cannot be controlled with endoscopic or angiographic therapy, or if there is persistent instability despite aggressive resuscitation, surgery is typically required.

10 The underlying cause of diverticulitis is micro-or macroscopic perforation of a diverticulum. It was previously believed that obstruction of diverticula (eg, by fecaliths) increased diverticular pressure and caused perforation. However, such obstruction is now thought to be rare. The primary process is thought to be erosion of the diverticular wall by increased intraluminal pressure or inspissated food particles.inflammation and focal necrosis ensue, resulting in perforation DIVERTICULITIS

11 CLINICAL MANIFESTATIONS The clinical presentation of acute diverticulitis depends on the severity of the underlying inflammatory process and the presence of associated complications. The mean age at admission for acute diverticulitis is 63 years. While the incidence of acute diverticulitis is lower in younger individuals, approximately 16 percent of admissions for acute diverticulitis are in patients under 45 years of age

12 CLINICAL MANIFESTATIONS Abdominal pain is the most common complaint in patients with acute diverticulitis. The pain is usually in the left lower quadrant due to involvement of the sigmoid colon. However, patients may have right lower quadrant or suprapubic pain due to the presence of a redundant inflamed sigmoid colon or, much less commonly, right-sided (cecal) diverticulitis which has a higher incidence in Asian populations The pain is usually constant and is often present for several days prior to presentation.approximately 50 percent of patients have had one or more prior episodes of similar pain.

13 Nausea and vomiting (20 to 62 percent)due to a bowel obstruction or an ileus due to peritoneal irritation low grade fever Hemodynamic instability with hypotension and shock are rare and are associated with perforation and peritonitis. A tender mass is palpable in approximately( 20%) due to pericolonic inflammation or a peridiverticular abscess. localized peritoneal signs with localized guarding, rigidity, and rebound tenderness Rectal examination may reveal a mass or tenderness to palpation in the presence of a distal sigmoid abscess. Stool may be positive for occult blood change in bowel habits, with constipation reported in approximately 50% and diarrhea in 25 to 35 % Approximately 10 to 15 percent of patients with acute diverticulitis have urinary urgency, frequency, or dysuria due to irritation of the bladder from an inflamed sigmoid colon

14

15 A diverticular abscess may be noted on abdominal CT scan at initial presentation or may develop subsequently. A diverticular abscess should therefore be suspected in patients with uncomplicated diverticulitis who have no improvement in abdominal pain or a persistent fever despite three days of antibiotic treatment. DIVERTICULAR ABSCESSES OCCUR IN APPROXIMATELY 17 PERCENT OF PATIENTS HOSPITALIZED WITH ACUTE DIVERTICULITIS

16 because of relative luminal narrowing due to pericolonicinflammation or compression from a diverticular abscess. However, high-grade colonic obstruction is rare in the acute setting and is usually associated with the subsequent development of a stricture due to chronic diverticular inflammation also cause a small bowel obstruction if a loop of small intestine becomes incorporated in a pericolonic inflammatory mass OBSTRUCTION DURING AN ATTACK OF ACUTE DIVERTICULITIS, PARTIAL COLONIC OBSTRUCTION CAN OCCUR

17 colovesical fistula may have pneumaturia, fecaluria, or dysuria. colovaginal fistula may report vaginal passage of feces or flatus. FISTULA INFLAMMATION FROM ACUTE DIVERTICULITIS MAY RESULT IN THE FORMATION OF A FISTULA BETWEEN THE COLON AND ADJACENT VISCERA. FISTULAS MOST COMMONLY INVOLVE THE BLADDER

18 In patients with a free perforation, the abdomen is distended and diffusely tender to light palpation. There is diffuse guarding, rigidity, and rebound tenderness, and bowel sounds are absent. ALTHOUGH ONLY 1 TO 2 PERCENT OF PATIENTS WITH ACUTE DIVERTICULITIS HAVE A PERFORATION WITH PURULENT OR FECAL PERITONITIS, MORTALITY RATES APPROACH 20 PERCENT

19 mild leukocytosis. However, the white count may be normal in up to 45 percent of patients Serum amylase and lipase may be normal or mildly elevated, especially in patients with a free perforation and peritonitis. Urinalysis may reveal sterile pyuria due to adjacent inflammation. The presence of colonic flora on urine culture suggests the presence of a colovesical fistula LABORATORY FINDINGS

20 Computed tomography scan Computed tomography (CT) findings suggestive of acute diverticulitis include the presence of localized bowel wall thickening (>4 mm), an increase in soft tissue density within the pericolonicfat secondary to inflammation or fat stranding, and the presence of colonic diverticula IMAGING

21 Ultrasound features suggestive of acute diverticulitis include: A hypoechoic peridiverticular inflammatory reaction Mural and peridiverticular abscess formation with or without gas bubbles Bowel wall thickening(segmental mural thickening greaterthan4 mm) atthepointof maximaltenderness Presence of diverticula in the surrounding segments ABDOMINAL ULTRASOUND

22 Magnetic resonance imaging Abdominal magnetic resonance imaging (MRI) findings suggestive of acute diverticulitis include colonic wall thickening, presence of diverticula, and pericolonic exudates and edema Abdominal and chest radiographs Nonspecific abnormalities can be seen on abdominal radiographs in 30 to 50 percent of patients with acute diverticulitis. These findings include air-fluid levels with small or large intestinal dilation due to an ileus or obstruction and soft tissue densities due to the presence of an abscess.an upright chest radiograph may demonstrate the presence of pneumoperitoneumwith air under the diaphragm in 3 to 12 percent of patients with acute diverticulitis

23 Colorectalcancer Acuteappendicitis Inflammatory bowel disease Infectiouscolitis Ischemiccolitis DIFFERENTIAL DIAGNOSIS

24 Colonoscopy has no role in establishing the diagnosisof acute diverticulitis, as the inflammation is peridiverticular. Endoscopic evaluation of the colon should be avoided in the acute setting due to the risk of perforation or exacerbation of the existing inflammation. After the complete resolution of symptoms associated with acute diverticulitis (typically in six to eight weeks), a colonoscopy is performed, except for those who have had a colonoscopy within the previous yea EXCLUSION OF AN UNDERLYING MALIGNANCY

25 In patients with acute diverticulitis, mortality rates vary depending on the presence of complications and patient comorbidities. In patients with acute uncomplicated diverticulitis, conservative treatment is successful in 70 to 100 percent of patients and mortality is negligible In patients with complicated diverticulitis undergoing an operation,the mortality rate is approximately 0.6 to 5 percent Although mortality rates are up to 20 percent in patients with perforated diverticulitis with purulent or fecal peritonitis, these complications are rare in the absence of diffuse peritoniti MORTALITY

26 Patients with acute diverticulitis should receive inpatient treatment if CT showscomplicateddiverticulitisdefinedbythepresenceof perforation, abscess, obstruction, or fistulization. CT shows uncomplicated diverticulitis but the patient has one or more of the following characteristics: Sepsis Immunosuppression(eg, poorlycontrolleddiabetes mellitus, chronichigh-dosecorticosteroiduse, useof other immunosuppressive agents, advanced HIV infection, B or T cell leukocyte deficiency) High fever(>102.5 F/39 C) Significant leukocytosis Severe abdominal pain or diffuse peritonitis Advanced age Significant comorbidities Intolerance of oral intake Noncompliance/unreliability for return visits/lack of support system Failed outpatient treatment CRITERIA FOR INPATIENT TREATMENT

27 Antibiotics used to treat diverticulitis must cover the usualgastrointestinalfloraof Gram-negativerodsand anaerobes, particularly E. coli and B. fragilis We use one of the following outpatient antibiotic regimensin adultpatientswithnormalrenaland hepatic function: Ciprofloxacin(500 mg PO every12 hours) plusmetronidazole(500 mg PO every8 hours) Trimethoprim-sulfamethoxazole(1 double-strengthtablet [sulfamethoxazole800 mg;trimethoprim160 mg] every12 hours) plus metronidazole(500 mg PO every 8 hours) Amoxicillin-clavulanate(1 tablet [875 mgamoxicillin; 125 mg clavulanic acid] every 8 hours) or Augmentin XR (2 tablets[each tablet containing1 g amoxicillin; 62.5 mg clavulanicacid] every12 hours) Moxifloxacin(400 mg PO daily; usein patientsintolerantof both metronidazole and beta lactam agents) INITIAL OUTPATIENT CARE

28 The outpatient treatment of acute colonic diverticulitis typically consists of oral antibiotics for 7 to 10 days. Patients are reassessed clinically two to three days after the initiation of antibiotic therapy and weekly thereafter until the complete resolution of all symptoms. Repeat imaging studies arenotindicated unless the patient fails to improve clinically. Patients who fail outpatient treatment are admitted for inpatient treatment. OUTPATIENT TREATMENT

29 There is no evidence for dietary restrictions in acute uncomplicated diverticulitis. Some guidelines allow regular diet in patients who can tolerate it while others endorse a "modified" diet One approach is to limit patients to a clear liquid diet until they can be reassessed in two to three days, after which their diet can be liberalized to soft or regular if they demonstrate clinical improvement. OUTPATIENT DIET

30 Acute diverticulitis that presents with frank perforation is lifethreatening and mandates emergency surgery Microperforationshould be treated with intravenous antibiotics in a fashion that is similar to patients with uncomplicated diverticulitis. CT-guided drainage is typically performed for abscesses that are amenable to percutaneous drainage Abscesses not amenable to percutaneous drainage-patients who fail to improve after two to three days of antibiotic therapy will require surgery. Obstruction-surgicalresection of the involved bowel segment is mandatory to rule out cancer. Diverticular fistulas rarely close spontaneously, and a resection of the affected bowel segment is generally required. INPATIENTTREATMENTOF COMPLICATIONS

31 typically begins with administration of intravenous antibiotics, fluids, and pain medications. Patients are discharged with oral antibiotics to complete a course of 10 to 14 days Failure of inpatient medical treatment Surgery is indicated at any point during admission INPATIENTTREATMENTOF DIVERTICULITIS

32 After successful out-or inpatient treatment of acute diverticulitis, patients are reassessed in six to eight weeks. Those who have persistent symptoms may have chronic smoldering diverticulitis and are referred for surgical evaluation. Those who are symptom-free should undergo colonoscopy to rule out colon cancer. Patients who have had complicated diverticulitis or who are immunosuppressed should be referred for elective surgery, while others may be observed with dietary and behavioral modifications to reduce the risk of recurrence. Additionally, patients who reside in or frequently travel to remote areas that lack medical resources may benefit from elective surgery to reduce the risk of recurrences.

33 After nonoperative management of acute diverticulitis, patients have a 16 to 42 percent risk of developing recurrent diverticulitis. However, prior uncomplicated attacks do not predict a higher incidence nor a higher severity of recurrence. Thus, the number of prior attacks is no longer used as a sole criterion for surgery. Overall, approximately 20 percent of patients with acute diverticulitis will require surgical intervention at some time during the course of their disease because of symptoms, nearly all of whom have had either a complicated episode or several uncomplicated episodes of diverticulitis

34 COLONIC ISCHEMIA is the most frequent form of intestinal ischemia, most often affecting older adults. It is due to a reduction in blood flow to a level that is insufficient for the delivery of oxygen and nutrients needed for cellular metabolism. It can be related to acute arterial occlusion (embolic, thrombotic), venous thrombosis, or hypoperfusionof the mesenteric vasculature causing nonocclusive ischemia. The incidence is estimated at 16 cases per 100,000 person-years, which has increased over time The majority of patients have transient, nongangrenousischemia, which resolves without sequelae. Some patients develop colonic necrosis and gangrene, which can be lifethreatening. Long-term complications include persistent segmental colitis and the development of a stricture

35

36 of colonic ischemia vary depending upon the clinical setting and the extent and duration of the ischemia. Patients with acute colonic ischemia usually present with rapid onset of mild abdominal pain and tenderness over the affected bowel, most often the left colon. Mild-to-moderate amounts of rectal bleeding or bloody diarrhea usually develop within 24 hours of the onset of abdominal pain. Approximately 20 percent of patients develop chronic ischemic colitis. THE CLINICAL MANIFESTATIONS

37 Three progressive clinical stages have been described: Hyperactive phase Soon after occlusion or hypoperfusion, severe pain dominates with frequent passage of bloody, loose stools. Blood loss is usually mild without the need for transfusion. Paralytic phase The pain usually diminishes, becomes more continuous, and diffuses. The abdomen becomes more tender and distended without bowel sounds. Shock phase Massive fluid, protein, and electrolytes start to leak through a damaged, gangrenous mucosa. Severe dehydration with shock and metabolic acidosis may develop, requiring rapid surgical intervention. Fortunately, this most severe form affects only 10 to 20 percent of patients.

38 Laboratory studies are routinely obtained during the initial evaluation of the patient with abdominal pain or gastrointestinal bleeding, including complete blood count, metabolic panel, and coagulation studies. Although these are not diagnostic for colonic ischemia, they may aid the assessment of disease severity There are no specific laboratory markers for ischemia, although an increased serum lactate, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), or amylase may indicate advanced tissue damage. Decreased hemoglobin levels may reflect intestinal blood loss LABORATORY STUDIES

39 Plain abdominal radiography A plain abdominal radiograph is frequently nonspecific signs such as signs such as thumbprinting (indicating submucosal edema) and hemorrhage could be identified in only 30 percent of patients with mesenteric infarction

40 Chronicischemiccolitis A protractedtimecourseand less severe symptoms distinguish these patients from those with acute colonic ischemia. Patients with episodes of chronic recurrent colonic ischemia can present with recurrent abdominal pain, bloody diarrhea, weightlossfromprotein-losingenteropathy, recurrent bacteremia, persistent sepsis, or symptomatic colonic strictures.

41

42 DIAGNOSIS A diagnosis of colonic ischemia is usually suspected based upon the history, physical examination, and clinical setting. It is confirmed with imaging when possible, typically with computed tomography (CT) of the abdomen. Suspicion for colonic ischemiashould be increased in patients (particularly in older adults) with any of the risk factors and with lower abdominal pain with bloody diarrhea or hematochezia; however, these symptoms are nonspecific, the presence of four or more risk factors (ie, older than 60, hemodialysis, hypertension, hypoalbuminemia, diabetes mellitus, constipation-inducing medications) was 100 percent predictive of colonic ischemia.

43 For patients who present with fulminant gangrenous colonic ischemia with peritonitisand/orcolon perforation, a definitive diagnosis will necessarily be made in the operating room. In certain acute settings and for those with chronic symptoms, lower endoscopy (sigmoidoscopy or colonoscopy) or arteriography may be used in an effort to identify colonic ischemia and differentiate it from other causes of abdominal pain and bloody stools

44 TREATMENT Supportive care Supportive care with bowel rest and observation is appropriate provided there is no evidence of colon perforation, necrosis, or gangrene. Intravenous fluids/infusioshould be given to ensure adequate colonic perfusion. A nasogastric tube should be inserted if an ileus is present. Any precipitating conditions should be treated, and medications known to promote intestinal ischemia (eg, vasopressors, digitalis) should be promptly discontinued if feasible. Cardiac function and oxygenation should be optimized.

45 Antibiotics There is no strong evidence supporting the routine use of antibiotics for the treatment of all patients with colonic ischemia. However, we agree with major society guidelines that suggest empiric broad-spectrum antibiotics for most patients with colonic ischemia, except possibly those with mild disease and no evidence for bleeding from ulceration

46 Antithrombotic therapy Antithrombotic therapy is not indicated for most patients with colonic ischemia, as the majority have nonocclusive ischemia. However, anticoagulant therapy is indicated for patients who develop ischemia due to mesenteric venous thrombosis or from cardiac thromboembolism

47 Surgery is required in up to 20 percent of cases Patients with colon infarction and necrosis require urgent surgical intervention, which can be life-saving Clinical suspicion of ischemia (eg, ongoing pain that is out of proportion to clinical examination, hemodynamic instability) is a common indication for surgical exploration. Other indications for abdominal exploration include endoscopic evidence of full-thickness irreversible necrosis of the colonic muscularisor lesser degrees of ischemia in patients who do not respond appropriately to nonsurgical supportive care Abdominal exploration

48 Prior to abdominal exploration (open or laparoscopic), bowel preparation should not be used, as it can precipitate perforation or toxic dilation of the colon. Once the abdomen is exposed (open or laparoscopic), the bowel should be systematically inspected from the ligament of Treitz to the peritoneal reflection overlying the rectum Second-look procedure In most cases following exploration or colonic resection, repeat exploration (ie, "second-look" operation [open or laparoscopic]) should be performed within 12 to 24 hours to assess the viability of the remaining bowel and integrity of any anastomose

49 Among patients with embolic or thrombotic arterial occlusion, pharmacomechanical thrombolysis with or without vascular angioplasty and stenting may be indicated. unlike mesenteric ischemia, embolectomy, bypass graft, or endarterectomy is not performed in cases of primary colonic ischemia, which is not generally related to large artery obstruction VASCULAR INTERVENTION

50 IRRITABLE BOWEL SYNDROME (IBS) Irritable bowel syndrome (IBS) is a functional disorder of the gastrointestinal tract characterized by chronic abdominal pain and altered bowel habits. The estimated prevalence of IBS globally is approximately 11 percent with a higher prevalence in younger individuals and in women. IBS is associated with other conditions including fibromyalgia, chronic fatigue syndrome(also known as systemic exertionintolerancedisease), gastroesophagealreflux disease, functional dyspepsia, non-cardiac chest pain, and psychiatric disorders including major depression, anxiety, and somatization

51 PATHOPHYSIOLOGY OF IRRITABLE BOWEL SYNDROME Although motor abnormalities of the gastrointestinal tract (increased frequency and irregularity of luminal contractions, abnormal transit time) are detectable in some patients with IBS, no predominant pattern of motor activity has emerged as a marker for IBS. Selective hypersensitization of visceral afferent nerves in the gut has been observed in patients with IBS and is one explanation for IBS symptoms. Immunohistologicinvestigation has revealed mucosal immune system activation characterized by alterations in particular immune cells and markers in some patients with IBS.

52 The development of IBS following infectious gastroenteritis has been suspected clinically based upon a history of an acute diarrheal illness preceding the onset of irritable bowel symptoms in some patients. The cause of bowel symptoms following acute infection is uncertain although several theories (malabsorption, increased enteroendocrinecells/lymphocytes,and antibiotic use) have been proposed. The complex ecology of the fecal microflora has led to speculation whether changes in its composition could be associated with IBS. An association between IBS and small intestinal bacterial overgrowth has been conflicting. The role of food in the pathophysiology of IBS is not clear. Investigations have centered on the development of food specific antibodies, carbohydrate malabsorption, and gluten sensitivity. A genetic susceptibility to IBS is suggested by several twin studies, although familial patterns may also reflect underlying social factors. Associations between specific genes and IBS are under investigation. Psychosocial factors may influence the expression of IBS symptoms.

53 CLINICAL MANIFESTATIONS Abdominal pain in IBS is usually described as a cramping sensation with variable intensity and periodic exacerbations. The pain is frequently related to defecation. While in some patients abdominal pain is relieved with defecation, a substantial portion of patients report worsening of pain with defecation. Symptoms of IBS include diarrhea, constipation, alternating diarrhea and constipation, or normal bowel habits alternating with either diarrhea and/or constipation. Diarrhea is usually characterized as frequent loose stools of small to moderate volume. Bowel movements generally occur during waking hours, most often in the morning or after meals. Patients may have constipation with interludes of diarrhea or normal bowel function.

54 DIAGNOSTIC CRITERIA IN THE ABSENCE OF A BIOLOGIC DISEASE MARKER, SEVERAL SYMPTOM-BASED CRITERIA HAVE BEEN PROPOSED TO STANDARDIZE THE DIAGNOSIS OF IBS. Rome IV criteria for IBS IBS is defined as recurrent abdominal pain, on average, at least one day per week in the last three months, associated with two or more of the following criteria: Related to defecation Associated with a change in stool frequency Associated with a change in stool form (appearance)

55 IBS subtypes Subtypes of IBS are recognized based on the patient's reported predominant bowel habit on days with abnormal bowel movements. The Bristol stool form scale (BSFS) should be used to record stool consistency. IBS subtypes are defined for clinical practice as follows: IBS with predominant constipation: Patient reports that abnormal bowel movements are usually constipation (type 1 and 2 in the BSFS) IBS with predominant diarrhea: Patient reports that abnormal bowel movements are usually diarrhea (type 6 and 7 in the BSFS) IBS with mixed bowel habits: Patient reports that abnormal bowel movements are usually both constipation and diarrhea (more than one-fourth of all the abnormal bowel movements were constipation and more than one-fourth were diarrhea) IBS unclassified: Patients who meet diagnostic criteria for IBS but cannot be accurately categorized into one of the other three subtypes.

56 INITIAL EVALUATION in all patients with suspected IBS includes a history and physical examination, and limited testing to evaluate for the presence of alarm features concerning for organic disease(medical history!) In all patients with suspected IBS, we perform a complete blood count and age appropriate colorectal cancer screening. In patients with diarrhea, we perform the following: -C-reactive protein or fecal calprotectin -Serologic testing for celiac disease

57 ALARM FEATURES CONCERNING FOR UNDERLING ORGANIC DISEASE INCLUDE: Age of onset after age 50 years Rectal bleeding or melena Nocturnal diarrhea Progressive abdominal pain Unexplained weight loss Laboratory abnormalities (iron deficiency anemia, elevated C-reactive protein or fecal calprotectin) Family history of inflammatory bowel disease or colorectal cancer In patients who meet diagnostic criteria for IBS and have no alarm features, we do not routinely perform any additional testing beyond the initial evaluation In patients with alarm features, we perform additional evaluation to exclude other causes of similar symptoms. The diagnostic evaluation is based on the clinical presentation and usually includesendoscopic evaluation in all patients and imaging in selected cases

58 Most patients with IBS have chronic symptoms that vary in severity over time. Patients may also experience a change in IBS subtype over time with the most frequent change being from predominant constipation or diarrhea to mixed bowel habits

59 Establishment of a clinician-patient relationship and continuity of care are critical to the management of all patients with irritable bowel syndrome (IBS). In patients with mild and intermittent symptoms that do not impair quality of life, we initially recommend lifestyle and dietary modification alone rather than specific pharmacologic agents INITIAL THERAPY

60 A careful dietary history may reveal patterns of symptoms related to specific foods. Patients with IBS may benefit from exclusion of gas-producing foods; a diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs); and in select cases, lactose and gluten avoidance. Food allergy testing The role of food allergy in IBS is unclear Physical activity Physical activity should be advised DIETARY MODIFICATION

61 ADJUNCTIVE PHARMACOLOGIC THERAPY WE TREAT PATIENTS WITH MODERATE TO SEVERE SYMPTOMS OF IRRITABLE BOWEL SYNDROME (IBS) THAT IMPAIR QUALITY OF LIFE WITH PHARMACOLOGIC AGENTS Constipation In patients with IBS with constipation(ibs-c) who have failed a trial of soluble fiber(eg, psyllium/ispaghula), we suggest polyethylene glycol(peg)/osmotic laxatives. We treat patients with persistent constipation despite treatment with PEG with lubiprostone or linaclotide. Diarrhea we use antidiarrheals(eg,loperamide) as initial treatment and use bile acid sequestrants as second-line therapy Abdominal pain and bloating In patients with abdominal pain due to IBS, we use antispasmodicson an as-needed basis. In patients with IBS with constipation, we initiate antispasmodics only if the abdominal pain persists despite treatment of constipation. In patients with persistent abdominal pain despite antispasmodics, we recommend a trial of antidepressants. In patients with moderate to severe IBS without constipation, particularly those with bloating, who have failed to respond to other therapies, we suggest a two-week trial of rifaximin Probiotics Probiotics are not routinely recommended in patients with IBS

62