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Bowel Disorders. Presnted by Shiva Golian , D.O. Disclosures. None. Objectives. Identify, diagnose and treat irritable bowel syndrome Identify, diagnose and treat fecal incontinence Identify, diagnose and treat pruritis ani. Irritable Bowel Syndrome.

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Bowel Disorders

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Bowel disorders

Bowel Disorders

Presnted by

Shiva Golian, D.O.



  • None



  • Identify, diagnose and treat irritable bowel syndrome

  • Identify, diagnose and treat fecal incontinence

  • Identify, diagnose and treat pruritisani

Irritable bowel syndrome

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

Irritable bowel syndrome1

Irritable Bowel Syndrome

Ibs prevalence and epidemiology

IBSPrevalence 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: 3rdand 4th decades

  • Decreased prevalence in 6th and 7th decades

    • Dx should be made cautiously after age 60

Ibs etiology

IBS Etiology

Ibs pathogenesis


  • Altered Gastrointestinal Motility

    • No predominant pattern: clustered contractions vs prolonged contractions

    • Exaggeration of the normal gut motility

Ibs pathogenesis1


  • 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

Ibs pathogenesis2


  • Intestinal Inflammation

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

Ibs pathogenesis3


  • 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

Ibs pathogenesis4


  • Change in the fecal microflora

    • Is there a role in probiotic use? Need more information

Ibs pathogenesis5


  • 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

Ibs pathogenesis6


  • Food Sensitivity

    • Food allergy: studies have been conflicting

    • Carbohydrate malabsorption: need more investigation

    • Gluten sensitivity:

      • Those without villous atrophy, presence of serum IgGantigliadin antibodies and expression of HLA-DQ2 may have a good response to gluten free diet

      • Make sure to confirm the absence of celiac disease

Ibs pathogenesis7


  • 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

Ibs pathogenesis8


  • 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

Ibs diagnostic criteria

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

Ibs diagnostic criteria1

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

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

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

Diagnosis history1


  • Be careful of alarm symptoms or “red flags”

    • Rectal bleeding

    • Nocturnal/progressive abdominal pain

    • Weight loss

  • Ask about travel history

Diagnosis physical


  • PE generally WNL

  • Abdominal exam

    • Tenderness – generally the LLQ

    • Should not have any rebound or guarding



  • 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%



  • 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



  • 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



  • 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



  • Physical activity: potential benefit

  • Psychosocial therapies

    • May be beneficial in those with IBS symptoms associated with stressors

    • Benefits are controversial



  • Pharmacotherapy

    • Antispasmodic agents

      • Dicyclomine (Bentyl)

      • Hyoscyamine (Levsin, Levbid, NuLev)

      • *Chlordiazepoxide/clidinium (Librax)

      • * Phenobarbital/hyoscyamine/atropine/scopolamine (Donnatal)



  • 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)



  • 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



  • 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



  • Pharmacotherapy

    • Linaclotide (Linzess)

      • Guanylatecyclaseagonist – 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



  • Alternative therapy

    • Peppermint oil

    • Probiotics

    • Acupuncture

    • Enzyme supplementation

    • Hypnotherapy

Fecal incontinence

Fecal Incontinence

Fecal incontinence background

Fecal IncontinenceBackground

  • 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

Fecal incontinence epidemiology

Fecal IncontinenceEpidemiology

  • Varies greatly depending on age, definition, setting: 1-24%

    • This may be an underestimation

  • Occurs in about 47% of nursing home residents

Fecal incontinence risk factors

Fecal IncontinenceRisk 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

Fecal incontinence1

Fecal Incontinence

  • Anatomic considerations

Fecal incontinence2

Fecal Incontinence

Fecal incontinence pathophysiology

Fecal IncontinencePathophysiology

  • Dysfunction of anal sphincters

  • Abnormal rectal compliance

  • Decreased rectal sensation

  • Combination of the above

Fecal incontinence pathophysiology1

Fecal IncontinencePathophysiology

  • 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

Fecal incontinence pathophysiology2

Fecal IncontinencePathophysiology

  • 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

Fecal incontinence pathophysiology3

Fecal IncontinencePathophysiology

  • 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

Fecal incontinence pathophysiology4

Fecal IncontinencePathophysiology

  • Impaired rectal sensation

    • DM

    • MS

    • Dementia

    • Meningomyelocele

    • Spinal cord injury

Fecal incontinence pathophysiology5

Fecal IncontinencePathophysiology

  • Fecal impaction

    • Elderly

    • Constant inhibition of internal anal sphincter

    • Overflow incontinence

Fecal incontinence3

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?

Fecal incontinence4

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

Fecal incontinence diagnostic procedures

Fecal IncontinenceDiagnostic Procedures

  • Anorectalmanometry

    • Measures pressures

    • Decreased resting pressure suggests isolated IAS dysfunction

    • Decreased squeeze pressure suggests isolated EAS dysfunction

Fecal incontinence diagnostic procedures1

Fecal IncontinenceDiagnostic 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

Fecal incontinence diagnostic procedures2

Fecal IncontinenceDiagnostic 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

Fecal incontinence treatment

Fecal IncontinenceTreatment

  • 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

Fecal incontinence treatment1

Fecal IncontinenceTreatment

  • Biofeedback

    • Painless and non-invasive

    • Retrains the pelvic floor and abdominal wall musculature

    • Rates of success: 38-100%

    • Based on the available evidence, the role of biofeedback is unsettled

Fecal incontinence treatment2

Fecal IncontinenceTreatment

  • Surgery

    • Anterior overlap repair: for obstetric damage

    • Gracilisneosphincter: when anal sphincter muscles are irreversible damaged

    • Synthetic sphincter device: for pts with anal leakage

    • Colostomy: when all other txs failed

Fecal incontinence treatment3

Fecal IncontinenceTreatment

  • 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

Fecal incontinence treatment4

Fecal IncontinenceTreatment

  • Dextranomer-hyaluronic acid (Solesta)

    • Four 1 ml injections into deep submucosa

    • Shows promise

Pruritis ani

Pruritis Ani

Pruritis ani1

Pruritis Ani

  • 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

Pruritis ani2

Pruritis Ani

  • Frequency

    • Affects 1-5% of population

  • Sex: M>F

  • Age: 20-40 years (rare in elderly)

Pruritis ani3

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

Pruritis ani4

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)

Pruritis ani5

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

Pruritis ani6

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

Pruritis ani7

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

Pruritis ani8

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

Pruritis ani9

Pruritis Ani

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

Pruritis ani10

Pruritis Ani

Pruritis ani11

Pruritis Ani

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

Pruritis ani12

Pruritis Ani

Pruritis ani13

Pruritis Ani

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

Pruritis ani14

Pruritis Ani

  • Examination

    • Distribution

      • Symmetrical: diet induced

      • Asymmetrical: infection

Pruritis ani15

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

Pruritis ani16

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

Pruritis ani17

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

Pruritis ani18

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

Thank you

Thank You

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