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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

Bowel Disorders

Presnted by

Shiva Golian, D.O.

objectives
Objectives
  • 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 pathogenesis
IBSPathogenesis
  • Altered Gastrointestinal Motility
    • No predominant pattern: clustered contractions vs prolonged contractions
    • Exaggeration of the normal gut motility
ibs pathogenesis1
IBSPathogenesis
  • 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
IBSPathogenesis
  • Intestinal Inflammation
    • Some studies show an increased number of colonic lymphocytes, mast cells and plasma proinflammatory interleukins in those with IBS
ibs pathogenesis3
IBSPathogenesis
  • 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
IBSPathogenesis
  • Change in the fecal microflora
    • Is there a role in probiotic use? Need more information
ibs pathogenesis5
IBSPathogenesis
  • 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
IBSPathogenesis
  • 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
IBSPathogenesis
  • 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
IBSPathogenesis
  • 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
IBSSubtypes
  • 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
DiagnosisHistory
  • 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
DiagnosisHistory
  • Be careful of alarm symptoms or “red flags”
    • Rectal bleeding
    • Nocturnal/progressive abdominal pain
    • Weight loss
  • Ask about travel history
diagnosis physical
DiagnosisPhysical
  • PE generally WNL
  • Abdominal exam
    • Tenderness – generally the LLQ
    • Should not have any rebound or guarding
diagnosis
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%
diagnosis1
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
treatment
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
treatment1
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
treatment2
Treatment
  • Physical activity: potential benefit
  • Psychosocial therapies
    • May be beneficial in those with IBS symptoms associated with stressors
    • Benefits are controversial
treatment3
Treatment
  • Pharmacotherapy
    • Antispasmodic agents
      • Dicyclomine (Bentyl)
      • Hyoscyamine (Levsin, Levbid, NuLev)
      • *Chlordiazepoxide/clidinium (Librax)
      • * Phenobarbital/hyoscyamine/atropine/scopolamine (Donnatal)
treatment4
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)
treatment5
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
treatment6
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
treatment7
Treatment
  • 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
treatment8
Treatment
  • 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