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Bowel Disorders Presnted by Shiva Golian, D.O.. Disclosures None.

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Presentation on theme: "Bowel Disorders Presnted by Shiva Golian, D.O.. Disclosures None."— Presentation transcript:

1 Bowel Disorders Presnted by Shiva Golian, D.O.

2 Disclosures None

3 Objectives Identify, diagnose and treat irritable bowel syndrome Identify, diagnose and treat fecal incontinence Identify, diagnose and treat pruritis ani

4 Irritable Bowel Syndrome Syndrome: group of signs or symptoms that characterize a specific disorder Type of functional GI disorder: chronic disorders of the GI tract in which an organic or structural lesion responsible for symptom development cannot be identified

5 Irritable Bowel Syndrome

6 IBS Prevalence and Epidemiology Prevalence in North America: 10-15% 2:1 female prevalence Only 15% of those affected seek medical attention Comprises 25-50% of all referrals to the gastroenterologist After the common cold, second highest cause of work absenteeism Peak prevalence: 3 rd and 4 th decades Decreased prevalence in 6 th and 7 th decades Dx should be made cautiously after age 60

7 IBS Etiology

8 IBS Pathogenesis Altered Gastrointestinal Motility No predominant pattern: clustered contractions vs prolonged contractions Exaggeration of the normal gut motility

9 IBS Pathogenesis Visceral Hypersensitivity Distention Balloon distention sensed at lower volumes Rectal distention increased cerebral cortical activity Bloating Increased abdominal girth Impaired transit of intestinal gas loads

10 IBS Pathogenesis Intestinal Inflammation Some studies show an increased number of colonic lymphocytes, mast cells and plasma proinflammatory interleukins in those with IBS

11 IBS Pathogenesis Postinfectious Associated with bacterial, protozoal, helminthic and viral infections Thabane et al (meta-analysis of 18 studies) Incidence of postinfectious IBS is 10% Odds of developing IBS increase sixfold after acute GI infection Risk factors: young age, prolonged fever, anxiety, depression Causes of postinfectious bowel symptoms Malabsorption: idiopathic bile acid malabsorption Increase in enteroendocrine cells/lymphocytes: increased serotonin levels causes increased GI motility and visceral hypersensitivity Antibiotic use

12 IBS Pathogenesis Change in the fecal microflora Is there a role in probiotic use? Need more information

13 IBS Pathogenesis Small intestinal Bacterial Overgrowth (SIBO) Pimental et al 78% of 202 pts that met Rome I criteria for IBS had abnormal lactulose breath test suggestive of bacterial overgrowth Very exciting news: this means that IBS can be cured with antibiotics Unfortunately, more recent studies have failed to find any association between IBS and SIBO

14 IBS Pathogenesis Food Sensitivity Food allergy: studies have been conflicting Carbohydrate malabsorption: need more investigation Gluten sensitivity: Those without villous atrophy, presence of serum IgG antigliadin antibodies and expression of HLA-DQ2 may have a good response to gluten free diet Make sure to confirm the absence of celiac disease

15 IBS Pathogenesis Genetics Many studies with twins showing concordance rates ranging from 2-22% One study found that having a parent with IBS was a greater independent predictor of IBS than having an affected twin Thus it could be due to social learning Genotyping studies Perhaps an association with IBS and polymorphisms of serotonin transporter gene

16 IBS Pathogenesis Psychosocial Dysfunction More lifetime and daily stressful events than control groups Those with IBS have increased anxiety, depression, phobias and somatization Positive association between IBS and abuse Fukudo et al Administration of corticotropin releasing factor (CRF – mediator of stress response) increases abdominal pain and colonic motility in IBS pts

17 IBS Diagnostic Criteria Manning Criteria Pain relieved with defecation More frequent stools at the onset of pain Looser stools at the onset of pain Visible abdominal distention Passage of mucus Sensation of incomplete evacuation

18 IBS Diagnostic Criteria Rome III criteria Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with 2 or more of the following: Improvement with defecation Onset associated with a change in frequency of stool Onset associated with a change in form (appearance) of stool Symptom onset at least 6 months prior to diagnosis **Developed for clinical investigation; no emphasis on postprandial urgency, abdominal pain, diarrhea

19 IBS Subtypes IBS with constipation (IBS-C): hard or lumpy stools >/= 25% or loose/watery stools <25% of BMs IBS with diarrhea (IBS-D): loose or watery stools >/=25% or hard/lumpy stools <5% of BMs Mixed IBS (IBS-M): hard/lumpy stools >/=25% or loose/watery stools >/=25% of BMs (most common group) Unsubtyped IBS: insufficient abnormality of stool consistency to meet the above subtypes

20 Diagnosis History 2 most common complaints Abdominal pain Required for diagnosis of IBS Should be temporally related to defecation in some way Location of pain varies from person to person, but is consistent over time in the individual Altered bowel habits But also remember bloating Remember – these pts have an altered tolerance to normal amounts of distention

21 Diagnosis History Be careful of alarm symptoms or “red flags” Rectal bleeding Nocturnal/progressive abdominal pain Weight loss Ask about travel history

22 Diagnosis Physical PE generally WNL Abdominal exam Tenderness – generally the LLQ Should not have any rebound or guarding

23 Diagnosis Good history and physical exam Routine labwork (normal in IBS pts) CBC Chemistries ESR Stool samples for those with diarrhea TSH for those with constipation History with chronic symptoms, normal PE, normal labwork: accuracy of diagnosis is 95-97%

24 Diagnosis Colonoscopy Caucasians 50 or older African Americans 45 or older Strong family history of colorectal cancer or inflammatory bowel disease Those with anemia Those with stool WBCs Those with alarm symptoms Those with abnormal labwork Diagnosis of exclusion

25 Treatment No cure Treatment focused on symptom relief Must have a good therapeutic relationship Kaptchuck et al Pts with positive relationship with their healthcare provider have significantly more improvement Patient education Chronicity of syndrome Normal life span

26 Treatment Dietary Efficacy of dietary modification not well established Lactose Exclusion of gas-producing foods Food allergy testing: not well studied Gluten sensitivity Carbohydrate malabsorption: not enough large studies Fiber: efficacy not proven

27 Treatment Physical activity: potential benefit Psychosocial therapies May be beneficial in those with IBS symptoms associated with stressors Benefits are controversial

28 Treatment Pharmacotherapy Antispasmodic agents Dicyclomine (Bentyl) Hyoscyamine (Levsin, Levbid, NuLev) *Chlordiazepoxide/clidinium (Librax) * Phenobarbital/hyoscyamine/atropine/scopolamine (Donnatal)

29 Treatment Pharmacotherapy Antidepressants May be beneficial in those with neuropathic pain TCAs have anticholinergic properties which help to slow intestinal transit time (helps with IBS-D) Improvement in pain with TCAs occurs at lower doses than doses used for treatment of depression TCAs to try: Amitriptyline (Elavil), imipramine (Tofranil), nortriptyline (Pamelor), desipramine (Norpramin) Be careful with those with IBS-C Other meds: paroxetine (Paxil), fluoxetine (Prozac), sertraline (Zoloft)

30 Treatment Pharmacotherapy Antidiarrheal agents Loperamide (Imodium) – effective for tx of diarrhea, but not for tx of global IBS symptoms or abdominal pain Alosetron (Lotronex) 5-HT3 receptor antagonist Used in females with IBS-D Complications: ischemic colitis, severe constipation FDA has brought this back under tight control

31 Treatment Pharmacotherapy Tegaserod (Zelnorm) 5-HT4 receptor agonist Used in IBS-C Removed from market d/t cardiovascular side-effects Lubiprostone (Amitiza) Locally acting chloride channel activator Best to use with for those with IBS with severe constipation where other approaches have failed Used in IBS-C

32 Treatment Pharmacotherapy Linaclotide (Linzess) Guanylate cyclase agonist – stimulates intestinal fluid secretion and transit Used for IBS-C Antibiotics Rifaximin – a nonabsorbable antibiotic Improvement in bloating, abd pain, or altered bowel habits Used in IBS without constipation Benefits may be due to suppression of gas producing bacteria in colon

33 Treatment Alternative therapy Peppermint oil Probiotics Acupuncture Enzyme supplementation Hypnotherapy

34 Fecal Incontinence

35 Fecal Incontinence Background In 1988 Cost of adult diapers thought to exceed $400 million annually Second leading cause of nursing home placement Definition Continuous/recurrent uncontrolled passage of feces (>10ml) for at least 1 month in someone > 3-4 yrs old

36 Fecal Incontinence Epidemiology Varies greatly depending on age, definition, setting: 1-24% This may be an underestimation Occurs in about 47% of nursing home residents

37 Fecal Incontinence Risk Factors Increasing age Occurs in 15% of those >/= 70 Poor general health Physical limitations COPD IBS Urinary incontinence Chronic diarrhea In women: depression and white race

38 Fecal Incontinence Anatomic considerations

39 Fecal Incontinence

40 Fecal Incontinence Pathophysiology Dysfunction of anal sphincters Abnormal rectal compliance Decreased rectal sensation Combination of the above

41 Fecal Incontinence Pathophysiology Dysfunction of anal sphincters Vaginal delivery Anal sphincter tears Trauma to pudendal nerve: may cause incontinence years after delivery Risks: Forceps High birth weight infant Long second stage of labor Occipitoposterior presentation of fetus

42 Fecal Incontinence Pathophysiology Dysfunction of anal sphincters Surgical trauma Anal fistula Hemorrhoidectomy After injection of botulinum toxin Diabetes mellitus Reduced internal anal sphincter resting pressure Can be due to autonomic neuropathy

43 Fecal Incontinence Pathophysiology Decreased rectal compliance Ability of rectum to store fecal debris is reduced Leads to increased frequency and urgency Leads to incontinence even if sphincter function is normal Common conditions Ulcerative colitis Radiation proctitis

44 Fecal Incontinence Pathophysiology Impaired rectal sensation DM MS Dementia Meningomyelocele Spinal cord injury

45 Fecal Incontinence Pathophysiology Fecal impaction Elderly Constant inhibition of internal anal sphincter Overflow incontinence

46 Fecal Incontinence History Differentiate true incontinence from frequency and urgency History of: Prior vaginal delivery Anorectal surgery Pelvic irradiation Diabetes Neurologic disease Do symptoms occur with a background of diarrhea?

47 Fecal Incontinence Physical exam Appropriate inspection of the perianal area Fistula, prolapsing hemorrhoids, rectal prolapse Anocutaneous reflex (anal wink sign) Absence suggests nerve damage Digital Rectal Exam Mass, fecal impaction Pt should be instructed to bear down and then squeeze against the finger

48 Fecal Incontinence Diagnostic Procedures Anorectal manometry Measures pressures Decreased resting pressure suggests isolated IAS dysfunction Decreased squeeze pressure suggests isolated EAS dysfunction

49 Fecal Incontinence Diagnostic Procedures Endorectal ultrasound/MRI Good for identifying structural abnormalities of the anal sphincters, rectal wall, puborectalis muscle Ultrasound much more economical Findings correlate well with manometric findings

50 Fecal Incontinence Diagnostic Procedures Defecography Barium paste is instilled into rectum Pt is then seated on a radiolucent commode and films are taken at rest and during straining and defecation

51 Fecal Incontinence Treatment Medical therapy Aimed at reducing frequency of stool and improving consistency of stools Bulking agents Antidiarrheal drugs: Loperamide and Lomotil Loperamide also increases internal anal sphincter tone Anticholinergics: hyoscyamine TCAs: may help with idiopathic fecal incontinence Those with mental dysfunction/physical debility: regular defecation program Stool impaction: disimpaction and bowel regimen to prevent further impaction

52 Fecal Incontinence Treatment Biofeedback Painless and non-invasive Retrains the pelvic floor and abdominal wall musculature Rates of success: % Based on the available evidence, the role of biofeedback is unsettled

53 Fecal Incontinence Treatment Surgery Anterior overlap repair: for obstetric damage Gracilis neosphincter: when anal sphincter muscles are irreversible damaged Synthetic sphincter device: for pts with anal leakage Colostomy: when all other txs failed

54 Fecal Incontinence Treatment Sacral nerve stimulation Effective in those with neurological disorders Electrode is inserted into the S3 sacral foramen The electrode then provides low grade stimulation via an implanted stimulator Improvement in both resting and squeeze pressures Drawback: follow up studies show high rate of revision (41%) Infection, electrode displacement, electrode breakage, increased impedance, pain, battery depletion, partial or total loss of efficacy

55 Fecal Incontinence Treatment Dextranomer-hyaluronic acid (Solesta) Four 1 ml injections into deep submucosa Shows promise

56 Pruritis Ani

57 Anal itching Most common anorectal symptom presenting to dermatologist Rich nerve supply to perianal area is thought to be the primary reason for sensitivity to potential irritants

58 Pruritis Ani Frequency Affects 1-5% of population Sex: M>F Age: years (rare in elderly)

59 Pruritis Ani Secondary causes Anorectal conditions: Rectal prolapse, hemorrhoids, fistula in ano, fissure, skin tag, mucosal extropion, villous adenoma, hidradenitis suppurativa Infections: HSV, condyloma acuminata, gonorrhea, syphilis, TB, erythrasma, fungal infection Surgical procedures: those involving weakening of anus causing seepage

60 Pruritis Ani Secondary causes: Skin disorders: contact dermatitis, psoriasis, eczema, lichen planus, lichen sclerosis et atrophicus, lichen simplex leukiplakia Neoplastic disorders: Paget’s disease, Bowen’s Disease Ingested drugs: mineral oil, colchicine, quinidine, anabolic hormones, antibiotics (secondary diarrhea)

61 Pruritis Ani Secondary cause: Systemic disorders: obstructive jaundice, uremia, diabetes Primary (idiopathic) cause Once all secondary causes are ruled out Mostly diet induced: Coffee is most common agent Tea, cola, chocolate, beer, milk, tomatoes, citrus fruits, vitamin C, nuts, cheese, milk products, alcohol, smoking

62 Pruritis Ani Primary causes Compulsive anal cleaners Farouk manometry results: Internal sphincter pressure decrease was greater in pruritis patients compared with control patients Prolonged duration of internal sphincter relaxation after rectal distention Symptoms of seepage

63 Pruritis Ani Examination Skin changes may be staged Stage 0: skin normal Stage 1: skin red and inflamed Stage 2: white, lichenified skin Stage 3: coarse ridging of skin with ulceration superimposed on lichenification

64 Pruritis Ani Stage I (mild): No lesion seen at inspection of anal verge but the patient finds palpation and/or anoscopy painful, and other anal lesions have been excluded

65 Pruritis Ani Stage 2 (moderate): Red dry skin only, at times weeping skin with superficial round splits and longitudinal superficial fissures

66 Pruritis Ani

67 Stage 3(severe): Reddened, weeping skin, with superficial ulcers and excoriations disrupted by pale, whitish areas with no more hairs

68 Pruritis Ani

69 Stage 4 (chronic): whitened, thickened, dry, leathery, scaly skin with no hairs and no superficial ulcers or excoriations

70 Pruritis Ani Examination Distribution Symmetrical: diet induced Asymmetrical: infection

71 Pruritis Ani Treatment Specific treatment for any secondary causes with antifungal/antibiotic/antiparasitic Add bulking agent (e.g. metamucil) absorbs liquid from stool and helps diminish seepage associated with minor int sphincter weakness Stop the offending drug Stop using any soaps, topical antipruritics, etc to perianal skin

72 Pruritis Ani Treatment Stop scratching the skin After BM bathe or wash area using water without soap Pat skin dry with cotton towel – do not rigorously rub No scented toilet paper Loose underclothes

73 Pruritis Ani Treatment Use elimination diet to identify etiologic agent (may take 2-3 wks for itching to stop after agent is stopped) May use bulb tip syringe to flush out any fecal residue after BMs Apply small cotton ball on anal canal to absorb any further seepage

74 Pruritis Ani Treatment Steroidal anti-inflammatory cream with second layer of barrier cream (calamine, calmoseptine, zinc oxide) Do not exceed 3 wks of steroid use to prevent atrophy If all treatments fail, skin bx and consider referral to dermatologist

75 Thank You


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