12/7/2019 1

CHROHN’s DESEASE
EPIDEMIOLOGI

•Crohn’s disease (CD) is a chronic relapsing inflammatory

condition
usually with flare-ups alternating with periods of remission, and
an
increasing disease severity and incidence of complications as
time goes on.

•It can affect any part of the gastrointestinal tract from the
mouth to the anus. For typical sites & proportion of patients
affected see below:
Epidemiology

Extensive Small Terminal Ileum

Bowel – 5% only – 20%

Ileocaecal – 45% Colon only – 25%

Other: anorectal,
gastroduodenual, oral only
– 5%
Epidemiology

World wide distribution Incidence: 7/100 000

but more common in pop/yr
the West.

The incidence is lower in

Females are non-white races.
affected more Epidemiology
than males
1.2:1 Jews are more affected
than non-Jews

Bimodal age distribution:

20-40 yrs/60-80 yrs The incidence is rising

Prevalence: 100/100 000 pop/yr

Pathology
Some of the complications of CD are outlined below:

Fistula formation – abnormal channels of communication

can form in CD between loops of bowel, bladder and skin.
If the CD is in the colon, fistulae can form between the
colon and vagina or between the colon and perineum. The
diagram on the right shows the beginning of a fistula
formation with a fissure extending though mucosa towards
the muscular wall. Below is a cartoon representation of a
fistula starting from an area of ulceration
Obstruction - typically
occurs from strictures
or adhesions which
narrow the lumen,
blocking the passage
of the intestinal
contents. This can be
seen in the barium
follow-through to the
right.
Aetiology & Pathogenesis
The aetiology of Crohn’s disease is unknown. There are many proposed
pathogenic mechanisms, some of which are represented in this diagram.

Genetic Environmental
susceptibility factors

Host
Immune
Response

Crohn’s Disease

As there is no one cause, it is likely that Crohn’s disease is an outcome of

interactions between genetic predisposition, environmental factors and the
subsequent reaction of the host immune system.
Genetic Factors
There are 3 mutations on the CARD15 gene on
Genetic Chromosome 16 that are associated with some forms of
susceptibility CD. The risk of developing CD in increased forty-fold if
homozygous for all three mutations.

The mutations appear to alter monocyte recognition of the constituent flora of the
gut. It is possible that functional defects in CARD15 prevent innate immunity from
balancing resistance to the microbes in the gut in CD patients, leading to
uncontrolled inflammation and mucosal damage.

However the CARD15 mutations only account for 20-30% of cases of CD and CD is
not found in oriental populations who have the mutations. Therefore this gene is
not necessary for CD.

It is likely that there are other susceptibility genes that influence how the immune
system interacts with the gut flora which may be discovered in the future. Putative
loci have been mapped to chromosome 12 (IBD2), 6 (IBD3) and 14 (IBD4).
Environmental Factors
A wide range of environmental factors have been
Environmental
factors found to play a role:

 Smoking – Patients with CD are more likely to have been smokers and smoking
may worsen CD and increase the risk of relapse/surgical intervention.

 Diet – Active CD may improve when a normal diet is changed to a liquid

formula diet.

 Bacterial infection – There is some evidence implicating E. coli, M.

paratuberculosis, the measles virus and L. monocytogenes in the pathogenesis of
CD. This data is controversial and requires further research to clarify.

 Drugs – the oral contraceptive pill has been linked epidemiologically with CD.
Relapse may be precipitated by NSAIDs.
 Immune response
Host Both the potential genetics underlying CD and the
Immune
Response
environmental and host factors surrounding the patient
may be considered as initiating factors for CD, but the
exact aetiology is unknown.

What is known is that mucosal immunity is dysregulated in CD leading to a

prolonged inflammatory response in the gut.

In CD, a dominant CD4 Th1 reaction is induced. The mechanisms for this are
displayed diagrammatically on the next page.
The immune system and CD
Luminal antigen’s (from
CD mucosal bacteria/food)
macrophages Gut epithelium – limits but doesn’t
produce large exclude antigens from entering the
amounts of lamina propria. In CD there is an
cytokines increased permeability.
IL-12 & IL-18 M
Th1
CD4
which induce Interferon- - recruits
the Th1
leukocytes to the site
recruitment CD4
resulting in increased
of Th1 cells Th1
inflammation.
CD4
Th1 also have abnormal apoptosis TNF- -causes
sustained by these cytokines. increased inflammation.

Adhesins ( ) are important in assisting the migration of

leukocytes through endothelial cells to the area
Clinical Features
The clinical presentation can be very variable
depending upon the site and predominant
pathology of that site.

Major symptoms include:

• Diarrhoea (can be bloody with colonic involvement,

or steatorrhoea in small bowel disease)
• Abdominal pain
• Weight loss
• Constitutional symptoms such as malaise, anorexia,
nausea, vomiting and a low grade fever.
Clinical Features
Ileocecal (45%) & terminal ileum (20%)

Patients present with pain and/or tender mass

in right iliac fossa with or without diarrhoea
and weight loss.

The nature of the pain can distinguish between

the underlying pathology: constant pain with
fever suggests inflammation and abscess;
fibrosis/stricture formation has more
generalised, intermittent colicky pain with
signs of bowel obstruction.

CD here can sometimes present as an

emergency with acute right iliac fossa pain
which mimics appendicitis.
 Clinical Features
Crohn’s colitis (25%)

Symptoms such as diarrhoea

(mucous/blood), sense of urgency
and occasionally abdominal
pain/malaise.

Similar to ulcerative colitis but less

blood in the diarrhoea.

Extra-intestinal features are more

common in CD of the colon than
CD of the small bowel.
Clinical Features
Gastroduodenal & oral
(5%)

Very rare.

The former presents with

upper abdominal pain or
dyspepsia with anorexia,
nausea and weight loss.

The latter presents with

mouth ulcers or induration.
 Clinical Features

Extensive small bowel

(5%)

Presents with typical pain,

diarrhoea and weight loss
in addition to features of
malabsorption (e.g.
steatorrhoea) and
anaemia.

Due to the malabsorption,

undernutrition is
frequently a problem
Clinical Features
Perianal CD – complication

Characterised by perianal pain

and/or discharge. It’s due to
fistula, fissure or abscess
formation and can be confirmed
by examination. It is not as
painful as it looks but sedation is
often needed for sigmoidoscopy.

Direct questions about

pneumaturia (air bubbles in the
urine) and faeculent vaginial
discharge may be needed to elicit
this when taking a history.
Intestinal Complications
Anal and perianal complications
•Fissure in ano or fistula in ano
•Haemorrhoids
•Skin tags
•Perianal or ischiorectal abscess
•Anorectal fistulae

Undernutrition
•Caused by reduced food intake, malabsorption,
increased protein loss from inflamed bowel and
the increased metabolic demands of being sick.
Short bowel syndrome
•Develops when extensive bowel resection
leads to excessive malabsorption of fluids,
electrolytes and nutrients.

Cancer
•With Crohn’s colitis, there is a increased risk of
colorectal carcinoma
•There is an small increased risk of rarer small
intestinal and anal cancers occurring in cites of
prolonged inflammation.
Extra-intestinal complications
There are many systemic associations and complications of CD, most affecting the
liver and biliary tree, joints, skin and eyes:

Sclerosing Cholangitis – occurs in a small

proportion of patients. The pathogenesis is
unknown and the condition is characterised by
an inflammatory obliterative fibrosis of the
biliary tree (the white in the diagram->). It
progresses slowly and a liver transplant is the
only cure.

Ankylosing spondylitis – affects about 5% of patients

with Crohn’s colitis. The patient presents with back
pain and stiffness and the diagnosis can come years
before the CD.
Extra-intestinal complications
Erythema nodosum – occurs in ~8% of Crohn’s
colitis patients when disease is active. Hot, red
tender nodules appear on the arms and legs and
subside after a few days.

Pyoderma gangrenosum – occurs in ~2% of CD

patients, starting as a small pustule, then
developing into a painful, enlarging ulcer, most
commonly on the leg.

In addition to these conditions, other complications and associations include

episcleritis and uveitis (occuring in 5% of patients with active disease), osteoporosis
(as a consequence of chronic inflammation, malabsortion and treatment with
corticosteroids) and arthropathy.
Diagnosis
Radiology and imaging

Barium follow-through
Colonoscopy, terminal ileoscopy – findings consistent
& biopsy: These allow direct with Crohn’s include
visualisation and allows for a an asymmetrical
biopsy of the mucosa to be alteration in mucosal
taken. This is central to pattern with deep
macroscopic and microscopic ulceration and areas of
diagnosis. narrowing or
stricturing.

Ultrasound & CT
scanning: Can help
define thickness of the
bowel and mesentery
and can be useful to
evaluate disease
progress & chart
fistula formation.
Diagnosis
Blood tests

Haematology: results suggesting anaemia,  platelet count &  ESR suggests an

inflammatory bowel condition.

Biochemistry:  C-reactive protein and  serum albumin suggests active CD. Liver
biochemistry may be abnormal.

Stool cultures

Faecal calprotectin: provides accurate marker of inflammatory activity. Calprotectin is

a neutrophil-derived cytosolic protein that is resistant to bacterial degradation and if
present in the stools provides an accurate index of intestinal inflammatory activity. It
is not routinely available but has the potential to be a simple, cheap, non-invasive
marker.

Stool cultures should be done to rule out infection as a differential diagnosis.

Differential Diagnosis
There are many differential diagnosis for Crohn’s disease, complicated further
by the differing presentations of CD depending upon the site and pathology.
Some major differential diagnoses are outline below:

•Yersinia infections and appendicitis cause an acute ileitis

•If diarrhoea is bloody (as it sometimes is with colonic CD), other causes could
be ulcerative colitis, infective colitis, colorectal cancer, ischaemia or iatrogenic
causes (NSAIDs or antibiotics)

•Causes of abdominal pain, diarrhoea and weight loss include ulcerative colitis,
infective colitis and other forms of colitis, cancer (of pancreas, colorectal, small
bowel lymphomas or endocrine tumours), ischaemia coeliac disease and
irritable bowel disease.
Medical management
•Dietary advice and nutritional support including vitamin supplementation to
counter-act any deficiencies that develop.

•Diarrhoea can be controlled by anti-diarrhoeals such as loperamide, codeine

phosphate or co-phenotrope. If the diarrhoea is due to bile acid malabsorption,
then this can be treated with colestyramine.

•Likely to be beneficial in inducing remission:

•Corticosteroids (oral)
•Aminosalicylates
•(azathioprine/mercaptopurine – trade off between benefits and harms)
•Methotrexate
•Infliximab

•Likely to maintain remission:

•Smoking cessation
•(Unknown if the following are effective: enteral nutrition, fish oil, probiotics)

•The BNF information about the drugs on this page can be seen HERE
Surgical management
•Surgery is indicated for perforation or haemorrhage (emergency) or for small-bowel
obstruction, Crohn's colitis, abscess (intra-abdo and perianal), fistulas and
inflammation unresponsive to medical therapy.

•Approximately 80% of patients with CD will require surgery at some point.

•The principle of surgery is to conserve as much bowel as possible as 60% of

patients need further surgery.

•Surgery is not curative.

In small bowel CD – resection is likely to be beneficial whereby discrete sections are

removed and an end-to-end anastomosis created. The benefits of strictureplasty to
widen a narrowed lumen are unknown at this time.

In colonic CD – segmental and subtotal colectomy is likely

to be beneficial. In a segmental colectomy the part of the
colon affected is removed and an end-to-end anastomosis
created in remaining colon and in a subtotal colectomy the
ileum is sewn/stapled to the sigmoid colon as seen in diagram.
Prognosis
Mortality
The cumulative mortality is approximately twice that of the general population.
Death is primarily due to sepsis, pulmonary embolism and complications of the
surgery or immunosuppressive agents used as treatments.

Morbidity
The pattern of CD is a lifelong duration with periods of active disease alternating
with periods of remission. The disease causes significant disability with only 75% of
patients being fully capable of work in the first year of disease and 15% of patients
unable to work after 5-10years of the disease.

People with CD are also more at risk of developing certain cancers and other
complications as mentioned under the clinical features section of this module.
Epidemiology
 Increases with age

 Age 40 <5%

 Age 60 30%

 Age 85 65%
Epidemiology
 Gender prevalence depends on age

 M>>F Age less than 40

 M>F Age 40-50

 F>M Ages 50-70

 F>>M Ages > 70

Anatomic location of diverticuli varies with
the geographic location
 “Westernized” nations (North America, Europe,
Australia) have predominantly left sided diverticulosis

 95% diverticuli are in sigmoid colon

 35% can also have proximal diverticuli

 4% have only right sided diverticuli

What exactly is a diverticulum?
 Colonic diverticulosis is actually not a true
diverticulum but rather a pseudo-diverticulum
 True diverticulum contains all layers of the GI wall
(mucosa to serosa)
 Colonic pseudo-diverticulum more like a local hernia
 Mucosa-submucosa herniates through the muscle
layer (muscularis propria) and then is only covered by
serosa
Pathophysiology
 Diverticuli develop in ‘weak’ regions of the colon.
Specifically, local hernias develop where the vasa recta
penetrate the bowel wall
 Mucosa

Submucosa

Muscularis Vasa recta

Serosa
Pathophysiology
 Segmentation = motility process in which the segmental
muscular contractions separate the lumen into chambers

 Segmentation  increased intraluminal pressure 

mucosal herniation  Diverticulosis

 May explain why high fiber prevents diverticuli by creating a larger

diameter colon and less vigorous segmentation
Lifestyle factors associated with
diverticular disease
 Low fiber  diverticular disease

 Not absolutely proven in all studies but strongly

suggested

 Western diet is low in fiber with high prevalence of

diverticulosis

 In contrast, African diet is high in fiber with a low

prevalence of diverticulosis
Lifestyle factors associated with
diverticular disease
 Obesity associated with diverticulosis – particularly in
men under the age of 40

 Lack of physical activity

Uncomplicated diverticulosis
 Usually an incidental finding at time of colonoscopy
Diverticulitis
 Diverticulitis = inflammation of diverticuli

 Most common complication of diverticulosis

 Occurs in 10-25% of patients with diverticulosis

Pathophysiology of Diverticulitis
 Micro or macroscopic perforation of the diverticulum
 subclinical inflammation to generalized peritonitis
 Previously thought to be due to fecaliths causing
increased diverticular pressure; this is really rare
Pathophysiology of Diverticulitis
 Erosion of diverticular wall from increased
intraluminal pressure  inflammation  focal
necrosis  perforation

 Usually inflammation is mild and microperforation is

walled off by pericolonic fat and mesentery
Diagnosis of Diverticulitis
 Classic history: increasing, constant, LLQ abdominal
pain over several days prior to presentation with fever
 Crescendo quality – each day is worse
 Constant – not colicky
 Fever occurs in 57-100% of cases

 In one study, less than 17% of pts with diverticulitis had

symptoms for less than 24 hours
Diagnosis of Diverticulitis
 Previous of episodes of similar pain

 Associated symptoms
 Nausea/vomiting 20-62%
 Constipation 50%
 Diarrhea 25-35%
 Urinary symptoms (dysuria, urgency, frequency)
10-15%
Diagnosis of Diverticulitis
Right sided diverticulitis tends to cause RLQ abdominal
pain; can be difficult to distinguish from appendicitis
Diagnosis of Diverticulitis
 Physical examination
 Low grade fever
 LLQ abdominal tenderness
 Usually moderate with no peritoneal signs
 Painful pseudo-mass in 20% of cases
 Rebound tenderness suggests free perforation and peritonitis

 Labs : Mild leukocytosis

 45% of patients will have a normal WBC
Diagnosis of Diverticulitis
 Clinically, diagnosis can be made with typical history
and examination

 Radiographic confirmation is often performed

 Rules out other causes of an acute abdomen
 Determines severity of the diverticulitis
Treatment of Diverticulitis
 Complicated diverticulitis = Presence of
macroperforation, obstruction, abscess, or fistula

 Uncomplicated diverticulitis = Absence of the above

complications
Uncomplicated diverticulitis
 Bowel rest or restriction
 Clear liquids or NPO for 2-3 days
 Then advance diet

 Antibiotics
Uncomplicated diverticulitis
 Antibiotics
 Coverage of fecal flora
 Gram negative rods, anaerobes

 Common regimens
 Cipro + Flagyl x 10 days
 Augmentin or Unsayn x 10 days
Uncomplicated diverticulitis
 Monitoring clinical course
 Pain should gradually improve several days
(decrescendo)
 Normalization of temperature
 Tolerance of po intake

 If symptoms deteriorate or fail to improve with 3 days,

then Surgery consult
Uncomplicated diverticulitis
 After resolution of attack  high fiber diet with
supplemental fiber
Uncomplicated diverticulitis
 Follow-up: Colonoscopy in 4-6 weeks

 Flexible sigmoidoscopy and BE reasonable alternative

 Purpose
 Exclude neoplasm
 Evaluate extent of the diverticulosis
Prognosis after resolution
 30-40% of patients will remain asymptomatic

 30-40% of pts will have episodic abdominal cramps

without frank diverticulitis

 20-30% of pts will have a second attack

Prognosis after resolution
 Second attack
 Risk of recurrent attacks is high (>50%)

 Some studies suggest a higher rate (60%) of

complications (abscess, fistulas, etc) in a second attack
and a higher mortality rate (2x compared to initial
attack)

 After a second attack  elective surgery

Prognosis after resolution
 Some argue in the elderly recurrent attacks can be
managed with medications

 Some argue elective surgery should be considered after

a first attack in
 Young patients under 40-50 years of age
 Immunosuppressed
Complicated Diverticulitis
 Peritonitis
 Resuscitation
 Antibiotics
 Ampicillin + Gentamycin + Metronidazole
 Imipenem/cilastin
 Zosyn
 Emergency exploration
 Mortality 6% purulent peritonitis and 35% fecal
peritonitis
Complicated Diverticulitis: Abscess
 Occurs in 16% of patients with acute diverticulitis

 Percutaneous drainage followed by single stage surgery

in 60-80% of patients
Complicated Diverticulitis: Abscess
 CT guided drain
 Leave in until drain output less than 10 mL in 24 hours

 May take up to 30 days

 Catheter sinograms helpful to show persistent

communication between abcess and bowel
Complicated Diverticulitis: Abscess
 Small abscesses too small to drain percutaneously (<
1cm) can be treated with antibiotics alone

 These pts behave like uncomplicated diverticulitis and

may not require surgery
Complicated Diverticulitis: Fistulas
Complicated Diverticulitis: Fistulas
 Occurs in up to 80% of cases requiring surgery
 Major types
 Colovesical fistula 65%
 Colovaginal 25%
 Coloenteric, colouterine 10%
Complicated Diverticulitis: Fistulas
- Symptoms
 Passage of gas and stool from the affected organ

 Colovesical fistula:
 pneumaturia, dysuria, fecaluria

 50% of patients can have diarrhea and passage of urine

per rectum
Complicated Diverticulitis: Fistulas
 Diagnosis
 CT: thickened bladder with associated colonic
diverticuli adjacent and air in the bladder
 BE: direct visualization of fistula track only occurs in 20-
26% of cases
 Flexible sigmoidoscopy is low yield (0-3%)
 Some argue cystoscopy helpful
Complicated Diverticulitis:
Treatment of Fistulas
 Surgery
 Resection of affected colon (origin of the fistula)
 Fistula tract can be “pinched off” most of the time
 Suture closure for larger defects
 Foley left in 7-10 days
Surgical Treatment of Diverticulitis
 Elective single stage resection is ideal, ~6 weeks after
episode

 Two stage procedure (Hartmann procedure)

Surgical Treatment of Diverticulitis
 Two stage procedure (Hartmann procedure)

 Sigmoid resection
 Colostomy
 Rectal stump
 3 months later  colostomy takedown and colorectal
anastomosis
Common Anorectal desease
 Benign Anal Rectal Disease

 Anatomy of the anal canal and perianal spaces

 Benign Anal Rectal Disease
 Abscess and Fistula
 Fissure
 Hemorrhoids
 Retrorectal Space

Waldeyer’s Fascia

Supralevator Space

Levator Ani Muscle

Deep Postanal Space

Superficial Postanal
Space
 ANAL CANAL

Peritoneum
Supralevator
Levator Ani m. Space

Puborectalis m.
Ischioanal Space
Deep External
Sphincter m.
Intersphincteric
Space
Internal
Sphincter m.
Perianal Space
Transverse Septum
 ANAL CANAL

Column of
Anal Morgagni
Transitional
Zone Dentate Line

Anal Crypt

Anal Gland

Anoderm
 Patient complaints
Anal Pain
Bleeding
Drainage
Time course

Fissure Hemorrhoid Abscess

Knifelike pain with BM
Acute or Chronic Generally Acute
Passing Glass Brick, Throbing
Bleeding itching burning Minimal bleeding
Pain with BM:minutes to hours
Sudden swelling, +/- pain Pain Swelling over large
Blood on toilet paper
Prolapse area not associated with BM
No drainage
Difficulty with hygiene +/-Purulent Drainage
Small tag or “hemorrhoid”
Pain rarely knifelike Rapid increase in size
Soooo Angry
Hemorrhoids
 Classification
 1st degree
 Painless bleeding
 2nd degree
 Prolapse on defecation
 Spontaneous reduction
 bleeding
 3rd degree
 prolapse
 Manual reduction
 bleeding
 4th degree
 Irreducible
 bleeding
Internal
 Internal hemorrhoids are those that occur inside
the rectum.
 As this area lacks pain receptors, internal
hemorrhoids are usually not painful and most
people are not aware that they have them.
 Internal hemorrhoids, may bleed when irritated.
 Untreated internal hemorrhoids can lead to two
severe forms of hemorrhoids: prolapsed and
strangulated hemorrhoids.
Internal
 Prolapsed hemorrhoids are internal
hemorrhoids that are so distended that they are
pushed outside of the anus.
 If the anal sphincter muscle goes into spasm and
traps a prolapsed hemorrhoid outside of the anal
opening, the supply of blood is cut off, and the
hemorrhoid becomes a strangulated
hemorrhoid.
Clinical Manifestations
 The most common symptoms associated with
enlarged, abnormal hemorrhoids are prolapsed and
bleeding. The bright red bleeding and prolepses
usually occur at time of defecation
Objective Assessment
 Observing external hemorrhoids and palpating
internal hemorrhoids on examination
 Bleeding and constipation are signs of cancer of the
rectum, all patients with these symptoms should have
a thorough examination to rule out cancer
Medical Management
 local treatments such
- warm sitz baths, using a bidet,
- cold compress
- topical analgesic (such as Nupercainal)
- medicated creams (such as Anusol) during the early
stages of a hemorrhoid flare-up will also provide
relief and may stave off further development and
irritation.
 Keep the area clean and dry, with some lubrication
provided by hemorrhoidal creams.
 Suppositories are of little help since all of the
symptoms come from the external tissues and not in
the rectum where the suppository is placed.
Medical Management
 Rubber band ligation: elastic bands are applied
onto an internal hemorrhoid to cut off its blood
supply. Within several days, the withered
hemorrhoid is sloughed off during normal bowel
movement.
 Hemorrhoidolysis/Galvanic Electrotherapy:
desiccation of the hemorrhoid by electrical
current.
 Sclerotherapy (injection therapy): sclerosant or
hardening agent is injected into hemorrhoids. This
causes the vein walls to collapse and the
hemorrhoids to shrivel up.
Medical Management
 Cryosurgery: a frozen tip of a cryoprobe is used to
destroy hemorrhoidal tissues. Rarely used
anymore because of side effects
 Laser, infrared or BICAP coagulation: laser,
infrared beam, or electricity is used to cauterize
the affected tissues. Lasers are now much less
popular.
 Hemorrhoidectomy: a true surgical procedure to
excise and remove hemorrhoids.
Medical Management
 Stapled Hemorrhoidectomy: Also called the procedure
for prolapse and hemorrhoids, it is designed to resect soft
tissue proximal to the dentate line, which disrupts the
blood flow to the hemorrhoids. It is generally less painful
than complete removal of hemorrhoids and also allows for
faster recovery times. It's meant for hemorrhoids that fall
out or bleed and is not helpful for painful outside
conditions.
 Enema: This Practice is only used to clean the rectum in
some cases and only done by an M.D. Water is injected into
the rectum and then flushed out cleaning the area.
 Doppler Guided Hemorrhoidal Artery Ligation : The
only evidence based surgery for all grades of hemorrhoids.
It does not involve cutting tissues or even a stay at the
hospital; patients are usually back to work on the same day.
Best treatment for bleeding piles, as the bleeding stops
immediately.
Rubber band ligation Stapled Hemorrhoidectomy
Diseases with similar symptoms
 Symptoms associated with rectal cancer, anal fissure,
anal abscess, anal fistula, and other diseases may be
similar to those produced by hemorrhoids and may be
reduced by the topical analgesic, so it is important to
have the Doctor examine the patient.
 Anorectal Abscess
Etiology
 Cryptoglandular abscess
 Most common
 Infection in the glands at the dentate line
 Other causes
 Crohn’s and Ulcerative Colitis
 Tuberculosis and Actinomycoses
 Malignancy
 Foreign Bodies, Prostate Surgery or Radiation
 Pubic bone

Right anterior Left anterior

Right Left

Right posterior Left posterior

Tailbone
 Abscess Classification

 Four Types Based on Space Involved

 Perianal - 19-54%
Most
 Intersphincteric - 20-40% Common

 Ischioanal - 40-60%
 Supralevator 2% or less Rare
Supralevator
Abscess

Intersphincteric
Abscess

Ischioanal Abscess
Perianal Abscess
HORSESHOE ABSCESS

Supralevator
Space

Intersphincteric
Space

Ischioanal Space
 Anorectal Abscess
Treatment of Perianal and
Ischiorectal Abscesses
 Diagnosis - usually straightforward
 Erythema and Pain over affected area
 Fluctuance
 Treatment
 Incision and Drainage
 +/- Excision of small amount of overlying skin
 Initial packing for hemostasis
 Drainage catheter (Pezzer) or pack wound
 Attention to good hygiene and control blood sugar
 Antibiotics if immunocompromised, obese or
diabetic
Small Radial incision
Short distance from anus – feel for soft spot
Place drain and trim – avoids packing
Follow up in 7-10 days to remove drain
Peri anal abscess - ? Antibiotics
 Not usually indicated if there is adequate drainage
 Indicated for patients with:
 Obesity
 Diabetes
 Imunocompromised
 Extensive large abscess or recurrent abscess
 Fistula-in-Ano

 Definition
 abnormal connection between two epithelial
surfaces.
 Classification:
 Parks: Defines fistula by course of tract
 Goodsall’s rule
 Diagnosis
 Treatment
 Goals
 Options
 Fistula-in-Ano
Goodsall’s Rule
Posterior

Anterior
Fistula in ano
Fistula in ano: Surgical disease
 Refer to Colon and Rectal Surgeon or General
Surgeon
 Reassure patient – rarely cancer, most do not
need a colostomy
 If suspect Crohns
 Gain control of perianal sepsis
 Then complete full workup and staging
 Goals of therapy
 Get rid of the fistula/connection
 Preserve continence
 Fissure in Ano
Pathogenesis
 Acute fissure results from trauma to the anal
canal most commonly from a large fecal bolus
 Secondary changes of chronic fissure include
 Sentinel pile or skin tag at the distal end
 Hypertrophied anal papilla-swelling, edema and
fibrosis near the dentate line
 Fibrosis of the internal sphincter at the base
Fissure with Sentinel Tag
Fissure with Sentinel Tag
 Fissure in Ano
Symptoms
 Pain is the main symptom
 Sharp, cutting or tearing during defecation
 Duration is few minutes to hours
 Bleeding – bright red and scant
 Skin Tag
 Mucous discharge resulting in itching
 Fissure in Ano
Diagnosis
 Diagnosis often made on history alone
 Inspection – gently spread the buttocks and the
fissure becomes apparent
 Triad of chronic anal fissure
 Sentinel pile
 Hypertrophied anal papilla
 Anal ulcer
 Fissure in Ano
Differential Diagnosis
 Intersphincteric abscess
 Pruritus Ani
 Fissure from inflammatory bowel disease
 Carcinoma of the anus
 Infectious Perianal conditions
 Leukemic infiltration
 Acute Fissure in Ano
Treatment
 Increase dietary fiber
 Local anesthetic to prevent spasm
 Nitroglycerin or Nifedepine Ointment
 Not commercially available
 Must be mixed by pharmacist
 Warm tub soaks
 4-6 weeks of treatment
 Chronic Fissure in Ano
Surgical Treatment

 Indicated on Chronic non-healing anal fissure and

fissure that is refractory to medical therapy
 Lateral Internal Sphincterotomy
 Forces the muscle to relax

 V-Y Anoplasty flap

 Allow coverage of fissure with healthy tissue