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Flashcards in 26 Colon Physiology and Pathophysiology Deck (30):
1

Colon Anatomy and Physiology--Introduction (p.4-5+10-12)

  • functions of the colon
  • The colon is divided by convention into 6 anatomic regions
    • the cecum, the ascending, and transverse colon
      • derived from/
      • supplied by/
    • the descending and sigmoid colon and upper rectum 
      • derived from/
      • served by/
    • The lower rectum 
      • comes from/
      • supplied by/
  • the colon has both circular and longitudinal smooth muscles,
    • the longitudinal muscle is arranged/
    • The taenia are thought to be important in/

  • Although not essential to life, the colon
    • important role in gut homeostasis.
    • absorbs 1 to 1.8 L of electrolyte-rich fluid entering it daily from the small intestine,
    • salvages unabsorbed nutrients via bacteria that colonize it,
    • permits defecation to occur less frequently and at appropriate times.
  • The colon is divided by convention into 6 anatomic regions
    • the cecum, the ascending, and transverse colon
      • derived from the embryonic midgut
      • supplied by the superior mesenteric artery and vein,
    • the descending and sigmoid colon and upper rectum
      • derived from the hindgut 
      • served by the inferior mesenteric artery and vein.
    • The lower rectum
      • comes from the cloaca
      • supplied by hemorrhoidal vessels.
  • the colon has both circular and longitudinal smooth muscles,
    • the longitudinal muscle is arranged in 3 bunches called taenia which end (coalesce into 1 layer) at the rectum
    • The taenia are thought to be important in retarding propulsion and enhancing residence time in the ascending colon (ideal for reabsorption and solidification of fecal material).

2

Colonic Function and Motor Activity

  • The functions of the large intestine are:
  • There are three main types of physiological motor activity of the colon, and each corresponds to a function:

  • The functions of the large intestine are:
    • mixing and dehydration of fecal material,
    • storage until evacuation is socially convenient,
    • salvaging electrolytes and water not absorbed in the small intestine,
    • fermentation of monosaccharides to yield free fatty acids that are taken up by colonic epithelial cells.
  • There are three main types of physiological motor activity of the colon, and each corresponds to a function:
    • Segmentation: mixing, dehydration
    • Compliance: storage
    • High amplitude peristaltic contractions: mass movements

3

Colonic motility is influenced by several factors:
Neural elements (p.13-16)

  • The large intestine receives extrinsic innervation (from extra-intestinal ganglia, the spinal cord and CNS) via/
    • These nerves
      • part of the/
      • not influenced by/
    • Most motor activities of the colon are directed by/
    • extrinsic innervation/
  • efferent parasympathetic and sympathetic fibers
    • most terminate in/
    • some sympathetic axons terminate/
  • Parasympathetic innervation 
    • arises from two sources: 
    • Stimulation of efferent vagal cholinergic neurons activates/
    • Inhibitory neural input is mediated by/
    • Pelvic nerve stimulation evokes/

  • The large intestine receives extrinsic innervation (from extra-intestinal ganglia, the spinal cord and CNS) via the parasympathetic (stimulatory) and the sympathetic (inhibitory) nervous systems
    • These nerves
      • part of the autonomic nervous system
      • not influenced by volitional activity.
    • Most motor activities of the colon are directed by intrinsic nerves,
    • extrinsic innervation serves mostly a modulatory role.
  • efferent parasympathetic and sympathetic fibers
    • most terminate in the myenteric plexus
    • some sympathetic axons terminate directly on sphincteric smooth muscle.
  • Parasympathetic innervation
    • arises from two sources:
      • the vagus nerve (myelinated) supplies the right and proximal transverse colon,
      • the pelvic nerve which is derived from sacral segments 2-4 (S2-4) supplies the colon as far as the mid-transverse colon.
    • Stimulation of efferent vagal cholinergic neurons activates nicotinic receptors within enteric ganglia.
    • Inhibitory neural input is mediated by vasoactive intestinal peptide (VIP) and nitric oxide (NO).
    • Pelvic nerve stimulation evokes generalized colonic contractile activity and accelerates colonic transit with induction of defecation.

4

Colonic motility is influenced by several factors:
Neural elements (p.13-16)

  • Sympathetic innervation 
    • arises from
    • Nerve fibers/
  • normal motility is usually maintained 
    • even if the colon/
    • This is due to/
    • non-adrenergic, non-cholinergic (NANC) neurotransmitters

  • Sympathetic innervation
    • arises from the lateral part of the low cervical to third lumbar segments of the spinal cord.
    • Nerve fibers enter the paravertebral sympathetic ganglia, emerge as splanchnic nerves which pass to the preaortic ganglia and give rise to the postganglionic adrenergic fibers which supply the colonic musculature.
  • normal motility is usually maintained
    • even if the colon is deprived of its extrinsic (parasympathetic and sympathetic) innervation.
    • This is due to the intrinsic (enteric) nervous system whose ganglia are located in the myenteric and submucosal plexuses
    • In addition to sympathetic and parasympathetic pathways that modulate the enteric nervous system, non-adrenergic, non-cholinergic (NANC) neurotransmitters also play an important role in modulating colon and anorectal motility.

5

Colonic motility is influenced by several factors:
Myogenic elements (motor patterns and myoelectric complexes) (p.17+22-23)

  • Colonic contractions are dictated by/
    • These signals are called/
    • When necessary, coordination between the two layers may occur via/
  • Giant Migrating Contractions:
    • mediate/
    • generated by/
    • induced by/
    • reduced by/

  • Colonic contractions are dictated by pacemaking electrical signals in smooth muscle.
    • These signals are called electrical slow waves or electrical control activity (ECA) and differ in the circular and longitudinal layers.
    • When necessary, coordination between the two layers may occur via the interstitial cells of Cajal (ICC).
  • Giant Migrating Contractions:
    • mediate the mass movement of feces occurs once or twice daily
    • generated by migrating long spike bursts (MLSB), which are thought to be generated from myenteric potential oscillations.
    • Rectal distension and intra-colonic glycerol (i.e. glycerin suppositories for constipation) induce GMCs, which are also more frequent in the setting of diarrhea.
    • reduced by atropine, and hence the use of anti-cholinergic agents in irritable bowel syndrome.

6

Colonic motility is influenced by several factors:
Myogenic elements (motor patterns and myoelectric complexes) (p.20-21+23)

  • Short Duration Contractions:
    • ?
    • Short spike bursts (SSB)
    • These contractions last and originate
  • Long Duration Contractions:
    • assist in /
    • can be/
      • To facilitate mixing/
      • To facilitate emptying/
    • Long spike bursts (LSB)
    • Because they are highly variable in frequency, amplitude, and wave shape, the long spike bursts/

  • Short Duration Contractions:
    • stationary colonic motor patterns that facilitate water extraction.
    • Short spike bursts (SSB) are the myoelectric phenomena underlying the generation of short duration contractions.
      • These bursts occur in phase with colonic slow wave activity.
    • These contractions last less than 15 sec and are thought to originate from the circular muscles.
      • Their frequency in humans is 2-13 cycles per min
  • Long Duration Contractions:
    • assist in the mixing and local propulsion of feces.
    • can be stationary or they may propagate in an oral or aboral direction.
      • To facilitate mixing, these contractions migrate orally (towards the mouth) in the ascending colon.
      • To facilitate emptying, they migrate aborally (away from the mouth) in the distal colon.
    • Long spike bursts (LSB)
      • the myoelectric phenomena underlying the generation of long duration contractions.
      • action potentials generated by contractile electrical complexes (CEC's) or intermittent bursts of membrane potential oscillation likely in the longitudinal muscle layer.
      • aka "high frequency slow waves".
    • Because they are highly variable in frequency, amplitude, and wave shape, the long spike bursts tend to be irregular.
      • They generally persist for 40-60 sec.

7

Colonic motility is influenced by several factors:
Neurohormonal element (p.25-30)

  • CCK, motilin, serotonin and gastrin/
    • what stimulate colonic contractions
    • what inhibit smooth muscle contractions
    • NO /
  • gastrocolonic response
    • Following a meal, colonic motor activity/
      • This accounts for/
      • because/
    • Colonic motor activity usually starts within and lasts for/
    • fat
    • This response is mediated in part by

  • CCK, motilin, serotonin and gastrin excite intestinal contractions.
    • Neuropeptides such as substance P, neurotensin, and gamma-amino butyric acid (GABA) also stimulate colonic contractions
    • secretin, glucagon, VIP, neuropeptide Y and nitric oxide (NO) inhibit smooth muscle contractions.
    • NO is a major NANC (non-adrenergic, non-cholinergic) neurotransmitter in the colon and anorectum.
  • gastrocolonic response
    • Following a meal, colonic motor activity increases, often associated with propulsive contractions or mass movements
      • This accounts for the frequent need to defecate after a meal, especially in the morning.
      • Defecation is often stimulated after a meal because increased colonic motor activity propels stool into the rectum; this is particularly true of the HAPCs
    • Colonic motor activity usually starts within 10 minutes and lasts for 45-60 minutes, depending upon the size and caloric content of the meal.
    • The most important dietary stimulant is fat, which must be in contact with gastroduodenal mucosa (proteins and carbohydrates have little effect on motility).
    • This response is mediated in part by CCK, although gastrin, neurotensin and substance P may also play a role.
      • The muscarinic cholinergic nervous system and enkephalins also mediate this response, which may be partially inhibited by secretin, thoracic cord resection, atropine and naloxone.

8

Colonic motility is influenced by several factors:
Neurohormonal element (p.25-30)

  • Motor activity in the colon exhibits strikingly diurnal variability
  • colonic tone
    • measured by/
    • A decrease in volume indicates/
    • an increase in volume indicates/
    • Normally, eating/
  • Colonic sensation
    • primarily mediated by/
    • sensitive only to/
    • sensory localization/
    • Visceral sensitivity appears to be enhanced (hyperalgesia) in many patients with/

  • Motor activity in the colon exhibits strikingly diurnal variability
    • Activity is minimal during sleep but increases dramatically upon awakening
    • This likely contributes for the prevalent pattern of early morning defecation.
  • In addition to phasic motor activity, colonic tone also is an important factor in colonic motor function.
    • This can be measured by inflating a compliant balloon in various regions of the colon and measuring the volume of air displaced or augmented when keeping pressure at a set level.
    • A decrease in volume indicates increased colonic tone,
    • an increase in volume indicates muscle relaxation.
    • Normally, eating increases colonic tone, reduces storage capacity and produces pressure gradients to move intraluminal contents into areas of lower pressure.
  • Colonic sensation
    • primarily mediated by visceral afferents
    • sensitive only to increased wall tension, either generated by intraluminal pressure or muscular wall contractions.
    • sensory localization is poor throughout the colon.
    • Visceral sensitivity appears to be enhanced (hyperalgesia) in many patients with irritable bowel syndrome and inflammatory conditions.

9

Anorectal Anatomy and Physiology (p.32+34-35)

  • The anorectum functions to/
  • The rectum 
    • acts as/
    • contains/
    • defecation and continence are regulated by/
  • The important components which maintain rectal continence 

  • The anorectum functions to store and eliminate fecal waste in a socially acceptable manner.
  • The rectum
    • acts as a storage reservoir
    • contains a sensory mechanism to allow awareness of rectal filling and impending defecation,
    • defecation and continence are regulated by the internal (IAS), the external anal sphincter (EAS), and the puborectalis muscle (PRM)
  • The important components which maintain rectal continence
    • rectal sensation,
    • rectal storage capacity,
    • resting tone of the IAS,
    • contractile responses of the PRM and EAS at appropriate moments and
    • motivation to be continent.

10

Internal and External Anal Sphincters (IAS and EAS) (p.32+34-35)

  • IAS
  • EAS
  • Both the IAS and the EAS are important for/
  • Anteroposterior angulation of the anorectum 
    • maintained by/
    • Contraction of the puborectalis narrows/
    • relaxation/
    • Assessment of puborectalis function can be made by/
    • The PRM also receives efferent innervation from the/

  • Approximately 80-85% of the resting pressure of the anal canal is derived from the tone of the IAS, which arises from the circular smooth muscle of the rectum at the dentate line
  • Anal canal pressure can be augmented by voluntary contraction of the EAS, a striated muscle which is innervated by the second, third and fourth sacral nerves.
    • The EAS can also be stimulated to contract in response to rectal distension, postural changes, cough and perianal pinprick.
  • Both the IAS and the EAS are important for continence.
  • Anteroposterior angulation of the anorectum
    • maintained by the striated puborectalis muscle which forms a sling with its insertions attached anteriorly to the symphysis pubis 
    • Contraction of the puborectalis narrows the anorectal angle
    • relaxation widens the anorectal angle to decrease resistance to the passage of stools
    • Assessment of puborectalis function can be made by digital examination or by imaging of the anorectum (proctogram).
    • The PRM also receives efferent innervation from the lower sacral nerves

11

Rectal and Anal Sensation & Rectal Reservoir Capacity (p.32+34-35)

  • Rectal and Anal Sensation
    • The rectum is supplied with/
    • the mechanoreceptors which mediate this perception lie in the/
    • the anal epithelium is richly supplied with/
  • Rectal Reservoir Capacity
    • The rectum acts as/
    • It does so through/
    • This can be measured by/

  • Rectal and Anal Sensation
    • The rectum is supplied with afferent nerves which allow the perception of rectal distension of as little as 5 ml of air.
    • the mechanoreceptors which mediate this perception lie in the perirectal tissues.
    • the anal epithelium is richly supplied with sensory nerve endings which allow the distinction between gas, liquid and solid.
  • Rectal Reservoir Capacity
    • The rectum acts as a reservoir for fecal material until defecation becomes socially convenient.
    • It does so through adaptive compliance, in which rectal pressures increase by relatively small amounts in response to increases in rectal contents.
    • This can be measured by determining pressure-volume relationships in response to stepwise filling of a rectal balloon

12

Anorectal Continence Mechanisms (p.32+34-35+36)

  • Reservoir Elements
  • Sensorimotor Elements
  • defecation
    • partly controlled by/
    • During defecation/
    • Colonic segmentive activity/
    • Simultaneously, the pelvic floor muscles/
    • After defecation is completed/

  • Reservoir Elements
    • Rectal compliance/accommodation
    • Colonic compliance/accommodation
  • Sensorimotor Elements
    • Anorectal angle
    • Rectal sensation
    • Anal sensory nerves
    • Internal anal sphincter
    • External anal sphincter
  • defecation
    • partly controlled by the central nervous system.
    • During defecation, contraction of abdominal muscles and closure of the glottis increases intra-abdominal pressure.
    • Colonic segmentive activity is temporarily inhibited and feces are propelled towards the rectum.
    • Simultaneously, the pelvic floor muscles relax, which leads to descent of the rectum, and relaxation of the anal sphincters allows expulsion of feces.
    • After defecation is completed, the pelvic floor ascends and anorectal angulation and anal sphincter tone are restored.

13

Pathology

  • primary associated symptoms
  • Diarrhea of colonic origin is typically/
  • abdominal pain of colonic origin (irritable bowel syndrome) involves/
  • The pathogenesis of constipation may involve/
  • fecal incontinence largely is a consequence of/
  • Constipation 
    • may reflect
    • Slow transit may occur /
    • Patients with no obvious cause for constipation are presumed to have/

  • Because storage and elimination are the principal functions of the colon and anorectum, abnormal bowel frequency, abdominal pain, and/or fecal incontinence are the primary associated symptoms.
  • Diarrhea of colonic origin is typically infectious or inflammatory in origin
  • abdominal pain of colonic origin (irritable bowel syndrome) involves peripheral and/or central sensitization of afferents
  • The pathogenesis of constipation may involve colonic dysfunction, anorectal dysfunction or both,
  • fecal incontinence largely is a consequence of anorectal dysfunction.
  • Constipation
    • may reflect delayed transit through the colon and or anorectum.
    • Slow transit may occur
      • because of a primary disorder of motility,
      • in association with many diseases (some of which involve neurologic dysfunction),
      • as a side effect of certain medications.
    • Patients with no obvious cause for constipation are presumed to have an underlying disorder of colonic or anorectal motor function

14

Classification of Functional Constipation (p.51+54)

  • Classification
  • colonic inertia,
    • ?
    • occurs because/
    • may occur in a colon/
    • gender
    • In affected patients, approaches to treat constipation include/
  • outlet delay constipation,
    • ?
    • implies a disorder of/

  • Classification
    • Normal Transit
    • Colonic Inertia
    • Outlet Delay
  • colonic inertia,
    • transit through the colon proximal to the rectum is delayed
    • occurs because of decreased propulsive motor activity
    • may occur in a colon of normal caliber or in one that is dilated (megacolon).
    • overwhelmingly a female disorder that can present in one’s teens or as late as one’s 40s.
      • Women present with infrequent defecation and/or excessive straining with defecation and respond poorly or not at all to fiber supplements, laxatives and other bowel aids.
      • because decreased enteric neurons are less responsive to agents that would normally stimulate colonic motility.
    • In affected patients, approaches to treat constipation include osmotic laxatives such as polyethylene glycol (PEG) with stimulant laxatives (anthraquinones or diphenylmethanes), prostaglandins (i.e. misoprostrol), and prokinetic agents.
      • In highly selected patients, subtotal colectomy with ileorectal anastomosis may be required.
  • outlet delay constipation,
    • markers move normally through the colon but are not emptied from the rectum and sigmoid colon in a timely fashion.
    • implies a disorder of anorectal function (when voluntary withholding behavior has been excluded)
      • specifically indicates a disorder of defecation.

15

Anorectal mechanisms which may produce disorders of defecation can be divided into 4 major categories

  • Weak Propulsion
  • Misdirection of Propulsion
  • Failure of IAS (interal anal sphincter) Relaxation
  • Failure of Striated Muscle Relaxation

  • Weak Propulsion
    • Megarectum
    • Pain Syndromes
    • Neuromuscular diseases
  • Misdirection of Propulsion
    • Rectocele (occasional)
  • Failure of IAS (interal anal sphincter) Relaxation
    • Hirschsprung’s disease
  • Failure of Striated Muscle Relaxation
    • Dyssynergic defecation

16

Hirschsprung’s Disease (HD) (p.61-62)

  • ?
  • always involves/
  • may be/
  • genetic defects
  • gender
  • The result
  • Treatment

  • generalized embryonic defect in the normal migration of neural crest cells in the gut leading to an absence of intramural ganglion cells of the submucosal and myenteric plexuses in the distal bowel.
  • always involves the IAS as the most distal circular smooth muscle plus various lengths of rectum and colon.
  • may be sporadic or familial
    • if familial, may be autosomal dominant or recessive.
  • At least 6 genetic defects have been recognized, the most frequent being a deletion or mutation of the RET proto-oncogene that codes for a tyrosine kinase receptor expressed in cells of neural crest lineage.
  • Males are far more often affected than females.
  • The result is poor relaxation of the denervated bowel with functional obstruction associated with megacolon of the normally innervated colon proximally.
  • Treatment
    • Patients with HD require surgery to relieve functional obstruction.
    • This is done either by excising the aganglionic segment (i.e. Swenson procedure) or bypassing the diseased segment (i.e. Duhamel procedure)

17

Hirschsprung’s Disease (HD) Diagnosis (p.61-62)

  • Barium X-ray: 
    • Obtaining a barium enema is important for 2 reasons: 
    • A barium enema is diagnostic/
  • Anorectal Manometry: 
  • Rectal Biopsy: 
    • Biopsies must be/
    • ganglion cells
    • Tissue can be stained with
    • The diagnostic accuracy
  • Normally, rectal distension leads to /

  • Barium X-ray:
    • Obtaining a barium enema is important for 2 reasons:
      • to demonstrate whether there is a functional or mechanical obstruction;
      • to demonstrate a transition zone between ganglionic and aganglionic bowel.
    • A barium enema is diagnostic in only 80% of patients and requires confirmatory studies.
  • Anorectal Manometry:
    • In HD, the IAS is always affected and this can be evaluated with manometry
  • Rectal Biopsy:
    • Biopsies must be deep enough to include the submucosa and should be obtained >3 cm proximal to the anal verge.
    • A normal number of submucosal ganglion cells excludes HD whereas absence of ganglion cells is consistent with HD.
    • Tissue can be stained with acetylcholinesterase (ACE) to delineate excessive ACE-positive nerves in the muscularis mucosa and lamina propria and the absence of ganglion cells.
    • The diagnostic accuracy of this stain is nearly 100% 
  • Normally, rectal distension leads to reflex inhibition of the IAS which is absent in HD.
    • The finding of IAS relaxation excludes HD but failure to demonstrate relaxation is not diagnostic.

18

Dyssynergic Defecation (p.64)

  • ?
  • characterized by/
  • In the lab, the diagnosis is suggested by/
  • Manometrically, dyssynergia is characterized by
  • treatment

  • abnormal defecation pattern in some children and adults with defecation difficulty,
  • characterized by contraction or failure to relax the PRM (puborectalis muscle) and EAS (external anal sphincter) during attempted defecation.
  • In the lab, the diagnosis is suggested by inability to expel a water filled balloon from the rectum or to empty contrast from the rectum.
  • Manometrically, dyssynergia is characterized by inappropriate increase in anal canal pressures or EAS EMG activity when bearing down as if to defecate 
  • an unconscious learned behavior that can be modified by muscle retraining or biofeedback techniques.
    • Such treatment is considered beneficial in adults but not in children.

19

Acute Megacolon: A Disorder of Neuromuscular Elements (p.67)

  • ?
  • occurs primarily in/
  • develops/
  • The pathophysiology

  • Colon pseudoobstruction without a mechanical or functional obstruction (i.e. HD) is known as idiopathic or functional megacolon.
    • Megacolon may be acute or chronic;
    • if acute, it is known as Ogilvie’s syndrome
  • occurs primarily in hospitalized patients who have undergone orthopedic, gynecologic or abdominal surgeries, systemic infections and cardiac or neurologic illness.
  • develops over 1-7 days with a mean of 4-5 days after often uneventful surgery.
  • The pathophysiology is an imbalance of parasympathetic and sympathetic regulation of colonic motor activity.
    • As parasympathetic input increases and sympathetic input decreases motility, a relative predominance of sympathetic input appears to induce this disorder.
    • This results in colonic atony and pseudoobstruction.

20

Acute Megacolon: A Disorder of Neuromuscular Elements

  • Treatment of acute megacolon begins with/
  • Treatment of acute megacolon
  • More Aggressive Interventions
  • Colonoscopic Decompression
  • Surgical Decompression or even resection

  • Treatment of acute megacolon begins with conservative measures pharmacologic agents, colonic decompression with a colonoscope or surgery to decompress the colon.
  • Treatment of acute megacolon
    • Nothing by mouth
    • Correct fluid and electrolyte imbalances
    • Nasogastric suction
    • Rectal tube decompression
    • Stop offending medications
    • Frequent position changes; ambulate if possible
  • More Aggressive Interventions
    • Neostigmine is a reversible acetylcholinesterase (ACE) inhibitor which increases parasympathetic input to correct the imbalance in autonomic regulation of colonic motor function.
    • intravenous neostigmine often rapidly decompresses the colon in most patients with approximately a 10% recurrence.
  • Colonoscopic Decompression is often successful if previous measures fail or if neostigmine is contraindicated.
    • The recurrence rate after decompression is about 40-50%.
  • Surgical Decompression or even resection is usually reserved for patients who show evidence of ischemia or perforation.
    • Surgery is associated with increased morbidity and mortality and is reserved for the most refractory patients with life threatening complications.

21

Fecal Incontinence: A Disorder Involving Multiple Mechanisms

  • defined as/
  • It is a much underreported problem which often has/
  • Patients exhibit
  • diagnosis

  • defined as recurrent uncontrolled passage of fecal material which occurs in an individual who is older than the established age of achieving bowel control.
  • It is a much underreported problem which often has devastating psychosocial and economic consequences.
  • Patients exhibit one or more abnormalities of continence mechanisms which may require specific treatment interventions.
  • Some may be diagnosed on clinical grounds whereas others require specific diagnostic testing. 

22

Fecal Incontinence:
Overflow Incontinence

  • Pathophysiology:
  • Diagnosis:
  • Populations:
  • Treatment of Overflow Incontinence
    • Medical
    • Surgical

  • Pathophysiology:
    • Fecal impaction
    • Megarectum
    • Blunting of rectal sensation
  • Diagnosis:
    • Digital Exam
    • Abdominal X-Ray
  • Populations:
    • Children (encopresis)
    • Institutionalized elderly
    • Dementia/Psychosis
  • Treatment of Overflow Incontinence
    • Medical
      • Disimpaction
      • Bowel cleansing
      • Habit training
    • Surgical
      • None

23

Fecal Incontinence:
Reservoir Incontinence (p.78)

  • Pathophysiology:
  • Diagnosis:
  • Populations:
  • Treatment of Reservoir Incontinence
    • Medical
    • Surgical

  • Pathophysiology:
    • Decreased Rectal compliance
    • Rectal resection/tumor
  • Diagnosis:
    • History
    • Sigmoidoscopy
  • Populations:
    • Inflammatory bowel diseases
    • Radiation (pelvic)
    • Rectal surgery
  • Treatment of Reservoir Incontinence
    • Medical
      • Reduce dietary fiber
      • Treat inflammation
      • Loperamide, diphenoxylate
    • Surgical
      • Colostomy

24

Fecal Incontinence:
Internal Sphincter Incontinence

  • Pathophysiology:
  • Diagnosis:
  • Populations:
  • Treatment

  • Pathophysiology:
    • Weakness of IAS
      • Trauma
      • Degeneration
      • Autonomic
  • Diagnosis:
    • History (see page only)
    • Decreased anal tone
  • Populations:
    • Middle aged to older adults
    • Scleroderma
    • Sphincterotomy (fissures)
  • Treatment of IAS Weakness (Passive Incontinence)
    • Loperamide
    • Cotton Plug

25

Rectosphincteric Incontinence

  • occurs predominantly in/
    • There may be a history of/
  • Manometry may demonstrate/
  • Anorectal radiographs suggest/
  • In patients with severe weakness/
  • what may contribute to weakening of continence mechanisms.
  • Anorectal manometry often demonstrates/

  • a multifactorial condition that occurs predominantly in middle-aged and elderly women who may have no history of anorectal disease or trauma.
    • There may be a history of constipation or excessive straining with defecation, multiple and difficult childbirths.
  • Manometry may demonstrate diminished anal sphincter pressures at rest and/or during voluntary contraction.
  • Anorectal radiographs suggest weakness of the PRM and pelvic floor muscles which are thought to develop because of repetitive damage to the pudendal nerves associated with abnormal descent of the pelvic floor.
  • In patients with severe weakness, rectal prolapse of varying degrees may occur.
  • In some women with incontinence, occult defects of either anal sphincter due to remote injury during childbirth may contribute to weakening of continence mechanisms.
  • Anorectal manometry often demonstrates patterns of dysfunction of continence mechanisms which suggest pathophysiology

26

Patterns of Rectosphincteric Fecal Incontinence

  • For each
    • IAS Weakness
    • EAS Trauma
    • Neurogenic
      • Peripheral
      • Central
  • Resting Pressure
  • Squeeze Pressure
  • PRM
  • Rectal Sensation
  • Rectal Compliance

  • Resting Pressure
    • IAS Weakness: decreased
    • EAS Trauma: normal
    • Neurogenic
      • Peripheral: normal
      • Central: normal
  • Squeeze Pressure
    • IAS Weakness: normal
    • EAS Trauma: decreased
    • Neurogenic
      • Peripheral: decreased
      • Central: decreased
  • PRM
    • IAS Weakness: normal
    • EAS Trauma: normal
    • Neurogenic
      • Peripheral: decreased
      • Central: decreased
  • Rectal Sensation
    • IAS Weakness: normal
    • EAS Trauma: normal
    • Neurogenic
      • Peripheral: normal
      • Central: decreased
  • Rectal Compliance
    • IAS Weakness: normal
    • EAS Trauma: normal
    • Neurogenic
      • Peripheral: normal
      • Central: normal

27

Certain systemic diseases are associated with fecal incontinence, either through neurologic dysfunction or involvement of GI smooth or striated muscles. Some examples of these diseases are as follows:

  • Diabetes Mellitus (A peripheral neurologic disease)
  • Multiple Sclerosis (A central neurologic disease)
  • Spinal Cord Injury
  • Systemic Sclerosis (A disorder of gastrointestinal smooth muscle)

28

Diabetes Mellitus (A peripheral neurologic disease)

  • Fecal incontinence occurs in/
  • prevalence
  • Most diabetics with fecal incontinence have/
  • \in the vast majority of incontinent diabetic patients
  • In contrast, continent diabetic patients exhibit/

  • Fecal incontinence occurs in up to 4-5% of insulin dependent diabetic patients, most of whom have diarrhea associated with peripheral and autonomic neuropathy.
  • The prevalence of fecal incontinence in diabetic patients has been underestimated since patients often do not volunteer this symptom because of embarrassment at their loss of bowel function.
  • Most diabetics with fecal incontinence have daily stool volumes within the normal range or in amounts which are only moderately increased.
  • Rather, multiple abnormalities of anorectal function occur in the vast majority of incontinent diabetic patients.
  • In contrast, continent diabetic patients exhibit normal anorectal neuromuscular function.

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Spinal Cord Injury

  • sacral cord lesions,
    • ?
    • Fecal incontinence can be prevented by/
  • suprasacral cord lesions
    • associated with/
    • incontinence is often prevented by/

  • sacral cord lesions,
    • no rectal sensation, rectal hypotonia, modest or no changes in resting anal sphincter tone and loss of voluntary contraction of the EAS.
      • Reflex defecation and warning of impending defecation are also absent.
    • Fecal incontinence can be prevented by evacuation of the rectum on a regular basis and includes the use of stimulant laxatives to promote evacuation.
  • suprasacral cord lesions
    • associated with preservation of reflex defecation, normal resting anal pressures and not uncommonly, autonomic signs of impending defecation.
    • Despite the absence of rectal sensation and voluntary muscle control in these patients, incontinence is often prevented by planned defecation by rectal stimulation.

30

Multiple Sclerosis & Systemic Sclerosis

  • Multiple Sclerosis (A central neurologic disease)
    • what occur frequently in MS patients with fecal incontinence.
    • what may have an additive effect in some women with MS
  • Systemic Sclerosis (A disorder of gastrointestinal smooth muscle)
    • Gastrointestinal involvement by systemic sclerosis is characterized by/
    • frequently abnormal
    • The most consistent findings
    • Patients with fecal incontinence had/
    • the EAS and PRM/

  • Multiple Sclerosis (A central neurologic disease)
    • Alterations of rectal sensation and EAS occur frequently in MS patients with fecal incontinence.
    • Pudendal nerve injury or occult anal sphincter injury occurring during childbirth may have an additive effect in some women with MS.
  • Systemic Sclerosis (A disorder of gastrointestinal smooth muscle)
    • Gastrointestinal involvement by systemic sclerosis is characterized by atrophy and replacement of circular smooth muscle with collagen.
    • Anorectal motility is as frequently abnormal as esophageal motility in this disease.
    • The most consistent findings are decreased resting anal canal pressures and a blunted or absent rectoanal inhibitory reflex.
    • Patients with fecal incontinence had lower resting anal canal pressures than did those who were continent.
    • In contrast to the IAS, the EAS and PRM are generally normal in systemic sclerosis.