Bowel disorders
1 / 75

Bowel Disorders - PowerPoint PPT Presentation

  • Uploaded on

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.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about ' Bowel Disorders' - reia

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Bowel disorders

Bowel Disorders

Presnted by

Shiva Golian, D.O.


  • 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

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 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 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 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 ani11
Pruritis Ani

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

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