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Inflammatory Bowel Disease
Speaker
Dr Pooja Pandey
Surgery PG Resident -1st Year
Department of general surgery
MIMS,Barabanki
Moderator
Dr A.K.Srivastava
Professor
Department of general surgery
MIMS , Barabanki
‘Inflammatory bowel disease’ is reserved for conditions characterised
by the presence of idiopathic intestinal inflammation increase (i.e.
Ulcerative colitis [UC] Crohn’s disease [CD].
Introduction
Ulcerative colitis
 UC is a disease of the rectum and colon with extraintestinal manifestations.
 The incidence is 10 per 100 000 per year in the UK
 Prevalence of 160 per 100 000 population. UC affects men and women equally in
early life, although it is said to be more common in males in later life.
 It is most commonly diagnosed between the ages of 20 and 40.
Aetiology
 Unknown.
 There is clearly a genetic contribution, as 10–20% of patients have a first-degree relative with
inflammatory bowel disease.
 Patients with severe colitis have a reduction in the number of anaerobic bacteria and in the
variability of bacterial strains in the colon, but no causative link with any specific organism has
been identified.
 Unlike CD, smoking seems to have a protective effect in UC and has even been the basis of
therapeutic trials of nicotine
Pathology
 In virtually all cases the disease starts in the rectum and extends proximally in continuity.
 Colonic inflammation is diffuse, confluent and superficial, primarily affecting the mucosa and
superficial submucosa.
 ‘Pseudopolyposis’ occurs in almost one-quarter of cases.
 Stricturing in UC is very unusual (unlike CD) and should prompt urgent assessment because
of the possibility of coexisting carcinoma.
 A small proportion of patients develop irregular mucosal swellings (dysplasia associated
lesions or mass [DALMs]), which are highly predictive of coexisting carcinoma
Inflammatory bowel disease – Ulcerative colitis
• N n n
 Histological examination reveals an increase in inflammatory cells in the lamina
propria and the crypts of Lieberkuhn and there are ‘crypt abscesses’.
 There is depletion of goblet cell mucin. With time, precancerous changes can
develop (dysplasia).
 High-grade dysplasia is regarded as an indication for surgery as 40% of
colectomy specimens in which highgrade dysplasia was detected will have
evidence of a colorectal cancer.
Symptoms
Proctitis
Colitis is almost always associated with bloody diarrhoea and urgency.
 Rectal bleeding, tenesmus and mucous discharge.
Severe and/or extensive colitis may result in anaemia, hypoproteinaemia and
electrolyte disturbances.
Pain is unusual.
Extraintestinal manifestations are to occur.
Extensive colitis is also associated with systemic illness, characterised by
malaise, loss of appetite, and fever.
Symptoms contd…
Classification of colitis severity
The assessment of severity of UC is determined by frequency of bowel action and the
presence of systemic signs of illness:
●● Mild disease is characterized by < 4 stools daily, with or without bleeding. There
are no systemic signs of toxicity.
●● Moderate disease corresponds to >4 stools daily, but with few signs of systemic
illness. There may be mild anaemia. Abdominal pain may occur. Inflammatory
markers, including erythrocyte sedimentation rate and C-reactive protein, are often
raised.
●● Severe disease corresponds to >6 bloody stools a day and evidence of systemic
illness, with fever, tachycardia, anaemia and raised inflammatory markers.
Hypoalbuminaemia is common and an ominous finding.
●● Fulminant disease is associated with > 10 bowel movements daily, fever,
tachycardia, continuous bleeding, anaemia, hypoalbuminaemia, abdominal
tenderness and distension, the need for blood transfusion and, in the most severe
cases, progressive colonic dilation (‘toxic megacolon’).
Extraintestinal manifestations
 15% of patients
 Large joint polyarthropathy, affecting knees, ankles, elbows and wrists.
 Sacroiliitis and ankylosing spondylitis are 20 times more common in patients
with UC than the general population and are associated with the HLA-B27
genotype.
 Sclerosing cholangitis is associated with UC and can progress to cirrhosis and
hepatocellular failure.
 Patients with UC and sclerosing cholangitis are also at a significantly greater
risk of development of large bowel cancer.
 Cholangiocarcinoma is an extremely rare association and its frequency is not
influenced by colectomy.
 The skin lesions erythema nodosum and pyoderma gangrenosum are associated
with UC and both normally resolve with good colitis control.
 The eyes can also be affected by uveitis and episcleritis.
Extraintestinal manifestations contd..
Acute colitis
Approximately 5% of patients present with severe acute (fulminant) colitis.
Plain abdominal radiograph of a colon with a diameter of more than 6 cm .
A reduction in stool frequency is not always a sign of improvement in patients with severe
UC, and a falling stool frequency, abdominal distension and abdominal pain (resulting from
progression of the inflammatory process through the colonic wall) are strongly suggestive of
disintegrative colitis and impending perforation.
Cancer risk in colitis
 The risk of cancer in ulcerative colitis increases with duration of disease. At 10 years from
diagnosis it is approximately 1%, increasing to 10–15% at 20 years and 20% at 30 years.
 Patients with pancolitis (defined as the presence of inflammation proximal to the splenic
flexure) of more than ten years duration should be entered into screening programmes in
order to detect clinically silent dysplasia, which is predictive of increased cancer risk.
 The value of screening programmes remains somewhat controversial, however, with most UC
patients who develop cancer (approximately 3.5% of all patients) presenting with their
tumours in-between attendances for screening colonoscopy
Investigations
ENDOSCOPY AND BIOPSY
Rigid/flexible sigmoidoscopy can detect proctitis in the clinic; the mucosa is
hyperaemic and bleeds on touch.
Purulent exudate.
Where there has been remission and relapse, there may be regenerative mucosal
nodules or pseudopolyps.
Later, tiny ulcers may be seen that appear to coalesce.
Colonoscopy and biopsy has a key role in diagnosis and management:
1 to establish the extent of inflammation, although colonoscopy
is contraindicated in severe acute colitis because of the risk of colonic
perforation.
2 to distinguish between UC and Crohn’s colitis (although
this can be exceptionally difficult.
3 to monitor the response to treatment.
4 to assess longstanding cases for malignant change.
RADIOLOGY
A plain abdominal film - toxic megacolon.
Barium enema has largely been replaced by CT.
Macroscopic Ulceratice colitis Crohn’s disease
Distribution Colon/rectum Anywhere in the gastrointestinal
tract
Rectum Always involved Often spared
Perianal disease rare Common
Fistula formation rare Common
Stricture rare Common
Microscopic
Layers involved Mucosa/submucosa Full thickness
Granulomas No Common
Fissuring No Common
Crypt abscesses Common rare
BACTERIOLOGY
A stool specimen should be sent for microbiological analysis when UC is suspected,
in order to exclude infective colitides, notably Campylobacter, which may be very
difficult to distinguish from acute severe UC.
Clostridium difficile colitis may need to be considered in populations at risk of this
disease.
Treatment
MEDICAL TREATMENT
Medical therapy is based on anti-inflammatory agents. The 5-aminosalicylic acid (5-
ASA) derivatives can be given topically (per rectum) or systemically.
They can be used long term as maintenance therapy
 Corticosteroids are the mainstay of treatment for ‘flareups’, either topically or systemically,
and have a widespread anti-inflammatory action.
 The immunosuppressive drugs azathioprine and cyclosporin can be used to maintain
remission and as ‘steroid-sparing’ agents.
 The monoclonal antibodies infliximab and adalimumab both act against
antitumour necrosis factor alpha, which has a central role in inflammatory cascades.
 Most recently, vedolizumab, which blocks integrins, has been used as ‘rescue therapy’
for severe colitis, to try and avoid emergency colectomy.
MEDICAL TREATMENT contd…
INDICATIONS FOR SURGERY
The greatest likelihood of a patient with UC requiring surgery is during the first
year after diagnosis.
The overall risk of colectomy is 20%.
Indications for surgery in UC are:
●● severe or fulminating disease failing to respond to medical therapy;
●● chronic disease with anaemia, frequent stools, urgency and tenesmus;
●● steroid-dependent disease – here, the disease is not severe but remission
cannot be maintained without substantial doses of steroids; inability of the
patient to tolerate medical therapy required to control the disease (steroid
psychosis or other side effects, azathioprine-induced pancreatitis), such that
remission cannot be maintained;
●● neoplastic change: patients who have severe dysplasia or carcinoma on
review colonoscopy.
●● extraintestinal manifestations.
●● rarely, severe haemorrhage or stenosis causing obstruction.
Indications for surgery in UC are contd…:
OPERATIVE TREATMENT FOR UC
Emergency In the emergency situation, (or for a patient who is malnourished or
on steroids), the ‘first aid’ procedure is a subtotal colectomy and end ileostomy
Elective surgery The indications for elective surgery include:
1 Failure of medical therapy/steroid dependence
2 Growth retardation in the young
3 Extraintestinal disease (polyarthropathy and pyoderma gangrenosum respond to
colectomy)
4 Malignant change.
In the elective setting four operations are available – all of these can be
successfully performed laparoscopically in experienced hands:
1 subtotal colectomy and ileostomy (as in an emergency)
2 proctocolectomy and permanent end ileostomy
3 restorative proctocolectomy with ileoanal pouch
4 subtotal colectomy and ileorectal anastomosis.
 CD is characterised by a chronic full-thickness inflammatory process that can
affect any part of the gastrointestinal tract from the lips to the anal margin.
 It is slightly more common in women than in men, and is most commonly diagnosed
between the ages of 25 and 40 years.
Crohn’s disease
 There is a second peak of incidence around the age of 70 years.
 In those countries with high prevalence of CD, the groups with the highest
prevalence seem to be Caucasian, notably American Whites and Northern
Europeans, whereas it is less common, even in high prevalence countries, in
those originating from Central Europe and less prevalent still in those originating
from South America, Asia and Africa.
Incidence and prevalence
The aetiology of CD is incompletely understood but is thought to involve
a complex interplay of genetic and environmental factors
Aetiology
A wide variety of foods have been implicated, in particular a diet high in refined
foodstuffs, but none conclusively.
An association with high levels of sanitation in childhood has been suggested.
 Smoking increases the relative risk of CD three-fold and is certainly an
exacerbating factor after diagnosis, contrary to the protective effect seen in
ulcerative colitis (UC).
The NOD2/ CARD15 gene has excited particular interest as variants of this gene have
been shown to have strong associations with CD
Aetiology contd…
 Depends on pattern of disease.
 Occasionally, CD presents acutely with ileal inflammation and symptoms
and signs resembling those of acute appendicitis, or even with free perforation of
the small intestine, resulting in a local or diffuse peritonitis.
 CD may present with fulminant colitis but this is considerably less common
than in UC.
 Colonic CD presents with symptoms of colitis and proctitis as described for UC
Clinical presentation
 The rectal mucosa is often spared in CD and may feel normal on rectal
examination.
 If it is involved, however, it will feel thickened, nodular and irregular.
 Perianal disease is frequently associated with dense, fibrous stricturing at
the anorectal junction. Incontinence may develop as a result of destruction
of the anal sphincter musculature because of inflammation, abscess
formation, fibrotic change and repeated episodes of surgical drainage. In
severe cases, the perineum may become densely fibrotic, rigid and
covered with multiple discharging openings (watering-can perineum).
Clinical presentation contd…
Extraintestinal manifestations of Crohn’s disease
Related to disease activity
 Erythema nodosum
 Pyoderma gangreosum
 Arthropathy
 Eye complications (iritis/uveitis)
 Aphthous ulcer
 Amyloidosis
Unrelated to disease activity
 Gall stone
 Renal calculi
 Primary sclerosing cholangitis
 Chronic active hepatitis
 Sacroilitis
Investigations
LABORATORY
 A full blood count should be performed, as anaemia is common
and usually multifactorial.
 Fall in serum albumin, magnesium, zinc and selenium.
 Acute phase protein measurements (C-reactive protein and orosomucoid) and
the erythrocyte sedimentation rate may correlate with disease activity.
 Finding an elevated concentration in the stools of calprotectin, a specific marker
of inflammation.
ENDOSCOPY
Upper gastrointestinal symptoms may require upper gastrointestinal endoscopy,
which may reveal deep longitudinal ulcers and cobblestoning of mucosa in the
duodenum, stomach or, rarely, in the oesophagus.
IMAGING
 Ultrasound can demonstrate inflamed and thickened bowel loops, as well as fluid
collections and abscesses.
 The small intestine is traditionally imaged by a small bowel enema
 This is performed by instilling contrast into the small bowel via a nasoduodenal tube,
and will show up areas of stricturing and prestenotic dilatation.
 The involved areas tend to be narrowed, irregular and, sometimes, when a length of
terminal ileum is involved, there may be the ‘string sign’ of Kantor
 Computed tomography (CT) scans with oral contrast are widely used in the
investigation of abdominal symptoms and can demonstrate fistulae, intra-
abdominal abscesses and bowel thickening or dilatation.
 Magnetic resonance imaging (MRI) is useful in assessing complex
perianal disease and, more recently, has been shown to be an excellent
method for investigating the small bowel.
 MR enterography (oral contrast) or enteroclysis (contrast administered via
nasoduodenal tube) is particularly effective at demonstrating small bowel
stricturing
Treatment
MEDICAL TREATMENT
 Steroids are the traditional method for inducing remission in CD, and
remain important when rapid remission is required.
 They induce remission in 70–80% of cases with moderate to severe
disease.
Immunomodulatory agents
 Azathioprine is used for its additive and steroid-sparing effects and
currently represents standard maintenance therapy.
 Cyclosporin also acts by inhibiting cell-mediated immunity. Short-course
intravenous cyclosporin treatment is associated with 80% remission;
however, there is relapse after completion of treatment in many cases
 Infliximab, a murine chimeric monoclonal antibody, was the first available monoclonal
antibody for the treatment of CD. This needs to be administered as an intravenous infusion
and is typically given every 8 weeks for maintenance of remission.
 Adalimumab, an entirely human monoclonal antibody, is an alternative to infliximab. This is
administered subcutaneously every 1–2 weeks, depending on response, and most patients
can self-administer this agent.
 Third-generation monoclonal antibody therapies include integrin antibodies vedulizumab
and etrolizumab. Both prevent leucocyte migration preferentially in the gastrointestinal
tract and may therefore have fewer side effects than the earlier monoclonal antibodies,
although they are both currently in limited use.
Monoclonal antibody
 Patients with moderate nutritional impairment will require nutritional
supplementation and severely malnourished patients may require enteral tube or
even intravenous feeding.
 Anaemia, hypoproteinaemia and electrolyte, vitamin and metabolic bone
problems must all be addressed.
 Elemental diet or parenteral nutrition can induce remission in up to 80% of
patients, an effect comparable to steroids.
Nutitional support
INDICATIONS FOR SURGERY
 Surgical resection will not cure CD. Surgery therefore focuses on managing
the complications of the disease.
 As many of these indications for surgery may be relative, joint management
by an aggressive physician and a conservative surgeon is ideal
Complications or manifestations of CD for which surgery is usually
appropriate include the following:
●● recurrent intestinal obstruction;
●● persistent or, less commonly, massive acute bleeding;
●● free perforation of the bowel;
●● failure of medical therapy;
●● steroid dependent disease;
●● intestinal fistula;
●● perianal disease (abscess, fistula, stenosis);
●● malignant change (notably in the colon and less commonly
as a complication of small bowel disease).
TOP-DOWN APPROACH TO
MANAGEMENT OF CROHN’S DISEASE
Traditionally, active Crohn’s disease is treated in a ‘step-up’ approach where newer, more
aggressive therapies are added only when more established and less toxic therapies have
failed.
Thus, active ileocolic CD may be treated initially with a thiopurine, adding steroids and then a
monoclonal antibody only if and when required.
Some centres instead advocate a top-down approach, where rapid remission is obtained by
initiating therapy with a monoclonal antibody agent (unless contraindicated), often in
combination with thiopurine.
A range of operations is performed for CD, depending on the pattern of disease
– the most common are outlined below:
●● Ileocaecal resection is the usual procedure for terminal ileal disease, with a
primary anastomosis between the ileum and the ascending or transverse
colon, depending on the extent of the disease.
●● Segmental resection of short segments of small or large bowel strictures
can be performed.
●● Colectomy and ileorectal anastomosis may be undertaken for colonic CD
with rectal sparing and a normal anus.
●● Subtotal colectomy and ileostomy for Crohn’s colitis accounts for 8% of
such procedures for acute colonic disease.
Temporary loop ileostomy. This can be used either in patients with acute distal
CD, allowing remission and later restoration of continuity, or in patients with
severe perianal or rectal disease.
●● Proctectomy and proctocolectomy. Many patients with severe anal disease
failing to respond to medical treatment will eventually require a permanent
colostomy. When this occurs in a setting of severe colonic disease,
proctocolectomy and permanent ileostomy may be required.
●● Strictureplasty. Strictured areas of CD can be treated by strictureplasty, a
local widening procedure, to avoid small bowel resection and is thus an
important bowel sparing technique .
Strictureplasty is particularly useful for the treatment of fibrostenotic disease,
when there is little or no active inflammation in the involved segment. Multiple
strictureplasties can be performed and strictureplasty can be combined with
resection
Questions
Q1)Difference between ulcerative colitis and crohn’s
disease ?
Q2)What are the extraintestinal manifestations ?
Q3)How will you approach to a patient having pain while
defaecation , altered bowel movement and intermittent
per rectal bleeding ?
Q4) What is the treatment of inflammatory
bowel disease?
Q5) write in brief about the surgical
approaches of ulcerative colitis ?
Thank you

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Inflammatory bowel disease

  • 1. Inflammatory Bowel Disease Speaker Dr Pooja Pandey Surgery PG Resident -1st Year Department of general surgery MIMS,Barabanki Moderator Dr A.K.Srivastava Professor Department of general surgery MIMS , Barabanki
  • 2. ‘Inflammatory bowel disease’ is reserved for conditions characterised by the presence of idiopathic intestinal inflammation increase (i.e. Ulcerative colitis [UC] Crohn’s disease [CD]. Introduction
  • 3. Ulcerative colitis  UC is a disease of the rectum and colon with extraintestinal manifestations.  The incidence is 10 per 100 000 per year in the UK  Prevalence of 160 per 100 000 population. UC affects men and women equally in early life, although it is said to be more common in males in later life.  It is most commonly diagnosed between the ages of 20 and 40.
  • 4. Aetiology  Unknown.  There is clearly a genetic contribution, as 10–20% of patients have a first-degree relative with inflammatory bowel disease.  Patients with severe colitis have a reduction in the number of anaerobic bacteria and in the variability of bacterial strains in the colon, but no causative link with any specific organism has been identified.  Unlike CD, smoking seems to have a protective effect in UC and has even been the basis of therapeutic trials of nicotine
  • 5. Pathology  In virtually all cases the disease starts in the rectum and extends proximally in continuity.  Colonic inflammation is diffuse, confluent and superficial, primarily affecting the mucosa and superficial submucosa.  ‘Pseudopolyposis’ occurs in almost one-quarter of cases.  Stricturing in UC is very unusual (unlike CD) and should prompt urgent assessment because of the possibility of coexisting carcinoma.  A small proportion of patients develop irregular mucosal swellings (dysplasia associated lesions or mass [DALMs]), which are highly predictive of coexisting carcinoma
  • 6. Inflammatory bowel disease – Ulcerative colitis • N n n
  • 7.  Histological examination reveals an increase in inflammatory cells in the lamina propria and the crypts of Lieberkuhn and there are ‘crypt abscesses’.  There is depletion of goblet cell mucin. With time, precancerous changes can develop (dysplasia).  High-grade dysplasia is regarded as an indication for surgery as 40% of colectomy specimens in which highgrade dysplasia was detected will have evidence of a colorectal cancer.
  • 8. Symptoms Proctitis Colitis is almost always associated with bloody diarrhoea and urgency.  Rectal bleeding, tenesmus and mucous discharge. Severe and/or extensive colitis may result in anaemia, hypoproteinaemia and electrolyte disturbances.
  • 9. Pain is unusual. Extraintestinal manifestations are to occur. Extensive colitis is also associated with systemic illness, characterised by malaise, loss of appetite, and fever. Symptoms contd…
  • 10. Classification of colitis severity The assessment of severity of UC is determined by frequency of bowel action and the presence of systemic signs of illness: ●● Mild disease is characterized by < 4 stools daily, with or without bleeding. There are no systemic signs of toxicity. ●● Moderate disease corresponds to >4 stools daily, but with few signs of systemic illness. There may be mild anaemia. Abdominal pain may occur. Inflammatory markers, including erythrocyte sedimentation rate and C-reactive protein, are often raised.
  • 11. ●● Severe disease corresponds to >6 bloody stools a day and evidence of systemic illness, with fever, tachycardia, anaemia and raised inflammatory markers. Hypoalbuminaemia is common and an ominous finding. ●● Fulminant disease is associated with > 10 bowel movements daily, fever, tachycardia, continuous bleeding, anaemia, hypoalbuminaemia, abdominal tenderness and distension, the need for blood transfusion and, in the most severe cases, progressive colonic dilation (‘toxic megacolon’).
  • 12. Extraintestinal manifestations  15% of patients  Large joint polyarthropathy, affecting knees, ankles, elbows and wrists.  Sacroiliitis and ankylosing spondylitis are 20 times more common in patients with UC than the general population and are associated with the HLA-B27 genotype.  Sclerosing cholangitis is associated with UC and can progress to cirrhosis and hepatocellular failure.  Patients with UC and sclerosing cholangitis are also at a significantly greater risk of development of large bowel cancer.
  • 13.  Cholangiocarcinoma is an extremely rare association and its frequency is not influenced by colectomy.  The skin lesions erythema nodosum and pyoderma gangrenosum are associated with UC and both normally resolve with good colitis control.  The eyes can also be affected by uveitis and episcleritis. Extraintestinal manifestations contd..
  • 14. Acute colitis Approximately 5% of patients present with severe acute (fulminant) colitis. Plain abdominal radiograph of a colon with a diameter of more than 6 cm . A reduction in stool frequency is not always a sign of improvement in patients with severe UC, and a falling stool frequency, abdominal distension and abdominal pain (resulting from progression of the inflammatory process through the colonic wall) are strongly suggestive of disintegrative colitis and impending perforation.
  • 15. Cancer risk in colitis  The risk of cancer in ulcerative colitis increases with duration of disease. At 10 years from diagnosis it is approximately 1%, increasing to 10–15% at 20 years and 20% at 30 years.  Patients with pancolitis (defined as the presence of inflammation proximal to the splenic flexure) of more than ten years duration should be entered into screening programmes in order to detect clinically silent dysplasia, which is predictive of increased cancer risk.  The value of screening programmes remains somewhat controversial, however, with most UC patients who develop cancer (approximately 3.5% of all patients) presenting with their tumours in-between attendances for screening colonoscopy
  • 16.
  • 17. Investigations ENDOSCOPY AND BIOPSY Rigid/flexible sigmoidoscopy can detect proctitis in the clinic; the mucosa is hyperaemic and bleeds on touch. Purulent exudate. Where there has been remission and relapse, there may be regenerative mucosal nodules or pseudopolyps. Later, tiny ulcers may be seen that appear to coalesce.
  • 18. Colonoscopy and biopsy has a key role in diagnosis and management: 1 to establish the extent of inflammation, although colonoscopy is contraindicated in severe acute colitis because of the risk of colonic perforation. 2 to distinguish between UC and Crohn’s colitis (although this can be exceptionally difficult. 3 to monitor the response to treatment. 4 to assess longstanding cases for malignant change.
  • 19. RADIOLOGY A plain abdominal film - toxic megacolon. Barium enema has largely been replaced by CT.
  • 20.
  • 21. Macroscopic Ulceratice colitis Crohn’s disease Distribution Colon/rectum Anywhere in the gastrointestinal tract Rectum Always involved Often spared Perianal disease rare Common Fistula formation rare Common Stricture rare Common Microscopic Layers involved Mucosa/submucosa Full thickness Granulomas No Common Fissuring No Common Crypt abscesses Common rare
  • 22. BACTERIOLOGY A stool specimen should be sent for microbiological analysis when UC is suspected, in order to exclude infective colitides, notably Campylobacter, which may be very difficult to distinguish from acute severe UC. Clostridium difficile colitis may need to be considered in populations at risk of this disease.
  • 23. Treatment MEDICAL TREATMENT Medical therapy is based on anti-inflammatory agents. The 5-aminosalicylic acid (5- ASA) derivatives can be given topically (per rectum) or systemically. They can be used long term as maintenance therapy
  • 24.  Corticosteroids are the mainstay of treatment for ‘flareups’, either topically or systemically, and have a widespread anti-inflammatory action.  The immunosuppressive drugs azathioprine and cyclosporin can be used to maintain remission and as ‘steroid-sparing’ agents.  The monoclonal antibodies infliximab and adalimumab both act against antitumour necrosis factor alpha, which has a central role in inflammatory cascades.  Most recently, vedolizumab, which blocks integrins, has been used as ‘rescue therapy’ for severe colitis, to try and avoid emergency colectomy. MEDICAL TREATMENT contd…
  • 25. INDICATIONS FOR SURGERY The greatest likelihood of a patient with UC requiring surgery is during the first year after diagnosis. The overall risk of colectomy is 20%.
  • 26. Indications for surgery in UC are: ●● severe or fulminating disease failing to respond to medical therapy; ●● chronic disease with anaemia, frequent stools, urgency and tenesmus; ●● steroid-dependent disease – here, the disease is not severe but remission cannot be maintained without substantial doses of steroids; inability of the patient to tolerate medical therapy required to control the disease (steroid psychosis or other side effects, azathioprine-induced pancreatitis), such that remission cannot be maintained;
  • 27. ●● neoplastic change: patients who have severe dysplasia or carcinoma on review colonoscopy. ●● extraintestinal manifestations. ●● rarely, severe haemorrhage or stenosis causing obstruction. Indications for surgery in UC are contd…:
  • 28. OPERATIVE TREATMENT FOR UC Emergency In the emergency situation, (or for a patient who is malnourished or on steroids), the ‘first aid’ procedure is a subtotal colectomy and end ileostomy
  • 29. Elective surgery The indications for elective surgery include: 1 Failure of medical therapy/steroid dependence 2 Growth retardation in the young 3 Extraintestinal disease (polyarthropathy and pyoderma gangrenosum respond to colectomy) 4 Malignant change.
  • 30. In the elective setting four operations are available – all of these can be successfully performed laparoscopically in experienced hands: 1 subtotal colectomy and ileostomy (as in an emergency) 2 proctocolectomy and permanent end ileostomy 3 restorative proctocolectomy with ileoanal pouch 4 subtotal colectomy and ileorectal anastomosis.
  • 31.
  • 32.  CD is characterised by a chronic full-thickness inflammatory process that can affect any part of the gastrointestinal tract from the lips to the anal margin.  It is slightly more common in women than in men, and is most commonly diagnosed between the ages of 25 and 40 years. Crohn’s disease
  • 33.  There is a second peak of incidence around the age of 70 years.  In those countries with high prevalence of CD, the groups with the highest prevalence seem to be Caucasian, notably American Whites and Northern Europeans, whereas it is less common, even in high prevalence countries, in those originating from Central Europe and less prevalent still in those originating from South America, Asia and Africa. Incidence and prevalence
  • 34.
  • 35. The aetiology of CD is incompletely understood but is thought to involve a complex interplay of genetic and environmental factors Aetiology
  • 36. A wide variety of foods have been implicated, in particular a diet high in refined foodstuffs, but none conclusively. An association with high levels of sanitation in childhood has been suggested.  Smoking increases the relative risk of CD three-fold and is certainly an exacerbating factor after diagnosis, contrary to the protective effect seen in ulcerative colitis (UC). The NOD2/ CARD15 gene has excited particular interest as variants of this gene have been shown to have strong associations with CD Aetiology contd…
  • 37.  Depends on pattern of disease.  Occasionally, CD presents acutely with ileal inflammation and symptoms and signs resembling those of acute appendicitis, or even with free perforation of the small intestine, resulting in a local or diffuse peritonitis.  CD may present with fulminant colitis but this is considerably less common than in UC.  Colonic CD presents with symptoms of colitis and proctitis as described for UC Clinical presentation
  • 38.  The rectal mucosa is often spared in CD and may feel normal on rectal examination.  If it is involved, however, it will feel thickened, nodular and irregular.  Perianal disease is frequently associated with dense, fibrous stricturing at the anorectal junction. Incontinence may develop as a result of destruction of the anal sphincter musculature because of inflammation, abscess formation, fibrotic change and repeated episodes of surgical drainage. In severe cases, the perineum may become densely fibrotic, rigid and covered with multiple discharging openings (watering-can perineum). Clinical presentation contd…
  • 39. Extraintestinal manifestations of Crohn’s disease Related to disease activity  Erythema nodosum  Pyoderma gangreosum  Arthropathy  Eye complications (iritis/uveitis)  Aphthous ulcer  Amyloidosis Unrelated to disease activity  Gall stone  Renal calculi  Primary sclerosing cholangitis  Chronic active hepatitis  Sacroilitis
  • 40. Investigations LABORATORY  A full blood count should be performed, as anaemia is common and usually multifactorial.  Fall in serum albumin, magnesium, zinc and selenium.  Acute phase protein measurements (C-reactive protein and orosomucoid) and the erythrocyte sedimentation rate may correlate with disease activity.  Finding an elevated concentration in the stools of calprotectin, a specific marker of inflammation.
  • 41. ENDOSCOPY Upper gastrointestinal symptoms may require upper gastrointestinal endoscopy, which may reveal deep longitudinal ulcers and cobblestoning of mucosa in the duodenum, stomach or, rarely, in the oesophagus.
  • 42. IMAGING  Ultrasound can demonstrate inflamed and thickened bowel loops, as well as fluid collections and abscesses.  The small intestine is traditionally imaged by a small bowel enema  This is performed by instilling contrast into the small bowel via a nasoduodenal tube, and will show up areas of stricturing and prestenotic dilatation.  The involved areas tend to be narrowed, irregular and, sometimes, when a length of terminal ileum is involved, there may be the ‘string sign’ of Kantor
  • 43.  Computed tomography (CT) scans with oral contrast are widely used in the investigation of abdominal symptoms and can demonstrate fistulae, intra- abdominal abscesses and bowel thickening or dilatation.  Magnetic resonance imaging (MRI) is useful in assessing complex perianal disease and, more recently, has been shown to be an excellent method for investigating the small bowel.  MR enterography (oral contrast) or enteroclysis (contrast administered via nasoduodenal tube) is particularly effective at demonstrating small bowel stricturing
  • 44.
  • 45. Treatment MEDICAL TREATMENT  Steroids are the traditional method for inducing remission in CD, and remain important when rapid remission is required.  They induce remission in 70–80% of cases with moderate to severe disease.
  • 46. Immunomodulatory agents  Azathioprine is used for its additive and steroid-sparing effects and currently represents standard maintenance therapy.  Cyclosporin also acts by inhibiting cell-mediated immunity. Short-course intravenous cyclosporin treatment is associated with 80% remission; however, there is relapse after completion of treatment in many cases
  • 47.  Infliximab, a murine chimeric monoclonal antibody, was the first available monoclonal antibody for the treatment of CD. This needs to be administered as an intravenous infusion and is typically given every 8 weeks for maintenance of remission.  Adalimumab, an entirely human monoclonal antibody, is an alternative to infliximab. This is administered subcutaneously every 1–2 weeks, depending on response, and most patients can self-administer this agent.  Third-generation monoclonal antibody therapies include integrin antibodies vedulizumab and etrolizumab. Both prevent leucocyte migration preferentially in the gastrointestinal tract and may therefore have fewer side effects than the earlier monoclonal antibodies, although they are both currently in limited use. Monoclonal antibody
  • 48.  Patients with moderate nutritional impairment will require nutritional supplementation and severely malnourished patients may require enteral tube or even intravenous feeding.  Anaemia, hypoproteinaemia and electrolyte, vitamin and metabolic bone problems must all be addressed.  Elemental diet or parenteral nutrition can induce remission in up to 80% of patients, an effect comparable to steroids. Nutitional support
  • 49. INDICATIONS FOR SURGERY  Surgical resection will not cure CD. Surgery therefore focuses on managing the complications of the disease.  As many of these indications for surgery may be relative, joint management by an aggressive physician and a conservative surgeon is ideal
  • 50. Complications or manifestations of CD for which surgery is usually appropriate include the following: ●● recurrent intestinal obstruction; ●● persistent or, less commonly, massive acute bleeding; ●● free perforation of the bowel; ●● failure of medical therapy; ●● steroid dependent disease; ●● intestinal fistula; ●● perianal disease (abscess, fistula, stenosis); ●● malignant change (notably in the colon and less commonly as a complication of small bowel disease).
  • 51. TOP-DOWN APPROACH TO MANAGEMENT OF CROHN’S DISEASE Traditionally, active Crohn’s disease is treated in a ‘step-up’ approach where newer, more aggressive therapies are added only when more established and less toxic therapies have failed. Thus, active ileocolic CD may be treated initially with a thiopurine, adding steroids and then a monoclonal antibody only if and when required. Some centres instead advocate a top-down approach, where rapid remission is obtained by initiating therapy with a monoclonal antibody agent (unless contraindicated), often in combination with thiopurine.
  • 52. A range of operations is performed for CD, depending on the pattern of disease – the most common are outlined below: ●● Ileocaecal resection is the usual procedure for terminal ileal disease, with a primary anastomosis between the ileum and the ascending or transverse colon, depending on the extent of the disease. ●● Segmental resection of short segments of small or large bowel strictures can be performed. ●● Colectomy and ileorectal anastomosis may be undertaken for colonic CD with rectal sparing and a normal anus. ●● Subtotal colectomy and ileostomy for Crohn’s colitis accounts for 8% of such procedures for acute colonic disease.
  • 53. Temporary loop ileostomy. This can be used either in patients with acute distal CD, allowing remission and later restoration of continuity, or in patients with severe perianal or rectal disease. ●● Proctectomy and proctocolectomy. Many patients with severe anal disease failing to respond to medical treatment will eventually require a permanent colostomy. When this occurs in a setting of severe colonic disease, proctocolectomy and permanent ileostomy may be required.
  • 54. ●● Strictureplasty. Strictured areas of CD can be treated by strictureplasty, a local widening procedure, to avoid small bowel resection and is thus an important bowel sparing technique . Strictureplasty is particularly useful for the treatment of fibrostenotic disease, when there is little or no active inflammation in the involved segment. Multiple strictureplasties can be performed and strictureplasty can be combined with resection
  • 55.
  • 56. Questions Q1)Difference between ulcerative colitis and crohn’s disease ? Q2)What are the extraintestinal manifestations ? Q3)How will you approach to a patient having pain while defaecation , altered bowel movement and intermittent per rectal bleeding ?
  • 57. Q4) What is the treatment of inflammatory bowel disease? Q5) write in brief about the surgical approaches of ulcerative colitis ?

Editor's Notes

  1. Dysplasia – abnormal development of cell . Polyp from mucous membrane Pseudopolyp- from granulation tissue
  2. Is a gland found in the intestinal epithelium lining the small and large intestine (colon) Digestive enzymes- peptidase,sucrose,maltase,lactase and lipase .
  3. Rectal – proctitis - inflammation of lining of the rectum Tenesmus- spurious feeling of need to evacuate bowel with little or no stool passed
  4. This is a very significant finding, suggestive of disintegrative colitis, and an indication for emergency surgery if colonic perforation is to be avoided.
  5. Erythema nodosum acute nodular erythematous eruption limited to extensor aspect of the lower leg . Pyoderma is ulcerative cutaneous condition of uncertain etiology .
  6. Intensive medical treatment leads to remission in 70% but the remainder require urgent surgery Toxic dilatation should be suspected in patients who develop severe abdominal pain and confirmed by the presence on a plain
  7. Effective treatment of UC requires a multidisciplinary approach to management. This involves the gastroenterologist, nurses, nutritionist, enterostomal therapists and, occasionally, clinical psychologists and social workers as well as the surgeon. They act as inhibitors of the cyclo-oxygenase enzyme system and are formulated to protect the aspirin-related drug from degradation before reaching the colon.
  8. A full blood count should be performed, as anaemia is common and usually multifactorial. It may result from the anaemia of chronic disease, or from iron deficiency as a result of blood loss or malabsorption. Vitamin B12 deficiency may occur as a consequence of terminal ileal disease or resection. Folate deficiency may also result from diffuse small bowel disease or Active inflammatory disease is usually associated with a fall in serum albumin, magnesium, zinc and selenium. Acute phase protein measurements (C-reactive protein and orosomucoid) and the erythrocyte sedimentation rate may correlate with disease activity. Finding an elevated concentration in the stools of calprotectin, a specific marker of inflammation, may support a diagnosis of CD in patients with new onset of persistent gastrointestinal symptoms. It can also be used to monitor disease activity in the long-term management of established CD. may support a diagnosis of CD in patients with new onset of persistent gastrointestinal symptoms. It can also be used to monitor disease activity in the long-term management of established CD.
  9. Immunomodulatory agents Azathioprine is used for its additive and steroid-sparing effects and currently represents standard maintenance therapy. It is a purine analogue, which is metabolised to 6-mercaptopurine (6-MP) and works by inhibiting cell-mediated immune responses. 6-MP may be given directly for the same effects. Approximately 10% of people have deficient thiopurine methyltransferase (TPMT) and 1 in 300 people have no enzyme activity, causing inefficient metabolism of 6-MP. The resulting supra-pharmacological concentrations may cause severe adverse effects such as myelosuppression. Testing TPMT activity is usually undertaken before commencing treatment. Cyclosporin also acts by inhibiting cell-mediated immunity. Short-course intravenous cyclosporin treatment is associated with 80% remission; however, there is relapse after completion of treatment in many cases