This presentation covered most common gastrointestinal disease like GERD, PUD, Dyspepsia, IBS & IBD.

1. Earlydiagnosis&treatmentofmostcommon
GastrointestinalDisease

2. Introduction
 Gastrointestinal (GI) diseases are a source
of substantial morbidity, mortality, and cost.
 Diagnosis and management of GI disorders
has been recognized as very important, and
it has been suggested that they have all the
available resources in order to ensure high
standard of care for their patients.

3. Common GI
Disease
GERD
PUD
Dyspepsia
 IBS
IBD

4. GERD
Gastroesophageal reflux disease (GERD) is a
consequence of the failure of the normal anti-
reflux barrier to protect against frequent and
abnormal amounts of gastroesophageal
reflux.
Common in western countries due to obesity.
(BMI ≥ 30) (M:F= 1:1)
Ref: Sleisenger & Fordtran's Gastrointestinal and Liver Disease 9th
Edition, Page-705

5.  Community based study- a defined
area of Dhaka city.
 Door to door survey among 1600
adults aged 18 years and above.
 Validated Questionnaire.
 Total population included 1417.
 Prevalence was 18%.
Ref: Shahed .MD Thesis. BSMMU 2005.
Prevalence of
GERD in
Bangladesh

6. Pathophysiology
Gastro-oesophageal reflux disease develops
when the oesophageal mucosa is exposed to
gastroduodenal contents for prolonged
periods of time, resulting in symptoms and,
in a proportion of cases, oesophagitis.
Occasional episodes of gastro-oesophageal
reflux are common in healthy individuals.
GERD affects 30% of the general population.
Ref- Davidsons Principles and Practice of Medicine 23rd Edition, Page:
791

7. Classic Reflux symptoms:
Heartburn: Occurring after meals, aggravated by
rich food, lying down, nocturnal heartburn
Regurgitation of acidic fluids.
Dysphagia
Clinical
features
Ref: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 9th Edition,
Page- 713 & 714

8. Factors That
Can
Aggravate
GERD
 Diet – Caffeine, fatty/spicy foods,
chocolate, coffee, peppermint, citrus,
alcohol.
 Position/Activity – Bending, straining.
 External Pressure – pregnancy, tight
clothing.

9. 1. Haemorrhage, Ulcers and Perforations.
2. Strictures.
3. Barrett’s oesophagus.
(Columnar lined)
Complications
Ref: Sleisenger & Fordtran's Gastrointestinal and Liver Disease 9th
Edition, Page- 720

10. Columnar lined oesophagus.
Present in 10% GERD patients.
Higher risk of adenocarcinoma.
Should be treated with long term PPI.
Regular surveillance.
Barrett’s
oesophagus

11. Alarm symptoms: Dysphagia, Chest pain,
Weight loss, Upper abdominal mass, G.I.
bleeding.
No response to empiric treatment.
Diagnosis uncertain.
When to
investigate

12. Investigation
 Upper GI endoscopy.
 Barium esophagography.
 Esophageal pH or combined esophageal
pH-impedance testing.
Ref- Current Medical Diagnosis and Treatment 2015, Page: 591

13. Differential
Diagnosis
 Peptic ulcer disease.
 Dyspepsia.
 Coronary artery disease.
Ref- Harrison's Principles of Internal Medicine 18th, Page: 2434

14. How is GERD
treated?
►Lifestyle Changes
►Medications
►Surgery

15. Lifestyle
Changes
►If you smoke - stop.
►Do not drink alcohol.
►Lose weight if needed.
►Eat small meals.
►Wear loose-fitting clothes.
►Avoid lying down for 2-3 hours after a meal.
►Raise the head of your bed 6 to 8 inches by putting blocks of wood
under the bedposts-just using extra pillows will not help.

16. Medications
►Antacids
►Foaming agents
Potassium
Bicarbonate +
Sodium Alginate
►H2 blockers
Cimetidine.
Famotidine
Nizatidine
Ranitidine
►Prokinetics
• Bethanechol
• Metoclopramide
• Domperidone
►Proton pump
inhibitors
• Rabeprazole
• Esomeprazole
• Pantoprazole
• Lansoprazole
• Omeprazole

17. Proton pump inhibitors are the drugs of choice.
PPIs reduce gastric acid secretion up to 90%.
PPIs inhibit meal-stimulated and nocturnal
acid secretion to a significantly greater degree
than H2RAs.
Controlled studies and a large meta analysis
report showing complete healing of even severe
ulcerative esophagitis after eight weeks in
more than 80% of patients taking PPIs
compared with 51% on H2RAs.
Acid
suppressing
agents
Ref: Sleisenger & Fordtran's Gastrointestinal and Liver Disease 9th Edition,
Page- 723 & Kumar & Clark's Clinical Medicine, 7th Edition Page: 252

18. Surgery
Nissen Fundoplication

19. The term ‘Peptic ulcer’ refers
to an ulcer in the lower
oesophagus, stomach or
duodenum, in the jejunum
after surgical anastomosis to
the stomach or, rarely, in the
ileum adjacent to a Meckel’s
diverticulum.
PEPTIC ULCER
DISEASE
Ref- Davidsons Principles and Practice of Medicine 23rd Edition,
Page: 798

20. Epidemiology
Incidence:
Annual Incidence of Peptic Ulcer 0.1-0.3%.
Prevalance:
In Western countries
0.12- 1.5 percent (population based)
1- 6 percent (H pylori positive subjects)
In BANGLADESH:
Point prevalence: Around 15% (1985 data)

21. Etiology
1. H.pylori
2. NSAIDs
3. Other risk factors
 Genetics
 Smoke cigarettes
 Psychological
 Other drugs (non-NSAID)
H.pylori

22. Sites of peptic
ulcers
 Gastric ulcers.
 Duodenal ulcers.
 Other sites are
Lower end of Oesophagus.
Stomal Ulcer.
Ulcer at Meckels Diverticulum.

23. Prevalence OF
H. pylori &
Relation with
PUD
 Now H pylori is reduced to 50 to 75% people in USA and
Europe
 BUT remains high in Asia.
 In BANGLADESH 90% adults and 84% children are H. Pylori
positive
 Only 10 to 15 percent of patients with H. pylori infection
develop ulcer disease.
 H. pylori was absent in almost 30 percent of patients with
an endoscopically documented duodenal ulcer.

24. Duodenal ulcer:
 Most common form of
peptic ulcer.
 Usually located in the
proximal duodenum.
 Multiple ulcers or ulcers
distal to the second
portion of duodenum
raise possibility of
Zollinger-Ellison
syndrome.
Gastric ulcer:
 Less common than
duodenal ulcer in absence
of non steroidal anti-
inflammatory drugs
(NSAIDs).
 Commonly located along
lesser curvature of the
antrum.
Types of
Peptic Ulcer
Ref- Davidsons Principles and Practice of Medicine 23rd Edition,
Page: 798

25. ClinicalFeatures
 Asymptomatic
 Upper abdominal pain
 Feeling fullness after food
 Belching, or feeling bloated after eating
 Heartburn or acid reflux
 Nausea
 Vomiting (may be blood: Hematemesis)
 Black- tarry stools (Melaena)

26. Investigations
 To diagnose peptic ulcer disease
 Upper GI Endoscopy
 Imaging (Now rarely practiced)
• To establish the etiology-
• Test for Helicobacter pylori
• Assessment of NSAID use
• Additional assessment

27. TestforH.pylori
NON INVASIVE
 FAECAL ANTIGEN TEST
 UREA BREATH TEST
 ANTIBODY TEST
INVASIVE
 RAPID UREASE TEST (CLO)
 HISTOLOGY
 CULTURE

28.  Non ulcer dyspepsia.
 Drug-induced dyspepsia.
 Celiac disease.
 Gastric malignancy.
 Chronic pancreatitis.
 Gallstone disease.
 Oesophagitis.
 IHD.
Differential
diagnosis
of PUD

29. Complications
 Bleeding
 Perforation
 Acute pancreatitis
 Acute cholecystitis or choledocholithiasis
 Gastric outlet obstruction

30. Treatment
 General measures: Cigarette smoking, aspirin and
NSAIDs should be avoided.
 Drug treatment:
A. Acid-Antisecretory Agents:
 Proton pump inhibitors.
 H2-receptor antagonists.
 B. Agents Enhancing Mucosal Defenses:
 Bismuth, misoprostol and antacids.
 C. H pylori Eradication Therapy:
Ref- Current Medical Diagnosis and Treatment 2015,
Page: 609-610

31. Indication of
H. pylori
eradication
 Peptic ulcer.
 Extranodal marginal-zone lymphomas of MALT type.
 Family history of gastric cancer.
 Previous resection for gastric cancer.
 H. pylori-positive dyspepsia.
 Long-term NSAID or low-dose aspirin users.
 Chronic (> 1 yr) PPI users.
 Extragastric disorders:
 Unexplained vitamin B12 deficiency*
 Idiopathic thrombocytopenic purpura*
 Iron deficiency anaemia*
*If H. pylori-positive on testing.
Definite
Ref- Davidsons Principles and Practice of Medicine 23rd Edition,
Page: 800

32. Not indicated
Gastro-oesophageal reflux disease.
Asymptomatic people without gastric
cancer risk factors.
Ref- Davidsons Principles and Practice of Medicine 23rd Edition,
Page: 800
Indication of
H. pylori
eradication

33. TREATMENT
REGIMENS FOR
H. pylori
• Triple therapy
• Quadruple therapy
• Sequential therapy

34. Ref- Current Medical Diagnosis and Treatment 2015, Page: 611

35. Sequential therapy: Duration 5+5 days
Drugs in Initial 5 days Drugs in subsequent 5 days In drug resistance
PPI (twice daily)
and amoxicillin
(1 g twice daily)
PPI (twice daily) + clarithromycin (500 mg twice daily)
+ tinidazole / Metronidazole
(500 mg twice daily)
With penicillin allergy or
high Clarithromycin
resistance:
(>15 percent)
Levofloxacin (250 mg twice
daily) may be used

36. Surgical
Treatment
 Indications for surgery in peptic ulcer:
 Emergency:
 • Perforation
 • Haemorrhage
 Elective:
 • Gastric outflow obstruction.
 • Persistent ulceration despite adequate medical
 therapy.
 • Recurrent ulcer following gastric surgery.
Ref- Davidsons Principles and Practice of Medicine
23rd Edition, Page: 800

37. Dyspepsia
 Dyspepsia describes symptoms as
discomfort, bloating & nausea, which are
thought to originate from upper
gastrointestinal tract.

38. Overview
Dyspepsia affects 20-40% of adults annually.
7-40% prevalence based on population studies.
50% self medicate.
10-25% will seek medical attention.
Quality of life impaired; more absent work
days.

39. Etiology of
Dyspepsia
A. Food:
Overeating.
Eating too quickly.
Eating high-fat foods.
Eating during stressful situations.
Drinking too much alcohol or coffee.

40. B. Medications:
Nonsteroidal anti-inflammatory drugs (NSAIDs)
including Aspirin.
Antibiotics (metronidazole, macrolides).
Diabetes drugs (metformin, alpha-glucosidase
inhibitors(acarbose, miglitol), amylin
analogs[Pramlintide], GLP- 1 receptor
antagonists [Exinatide, Liraglutide]).
Antihypertensive medications (ACE inhibitors,
ARBs).
Cholesterol-lowering agents (niacin, fibrates).
Etiology of
Dyspepsia

41. C. Functional Dyspepsia:
 Most common cause of chronic dyspepsia.
 Three-fourths of patients have no obvious organic
cause.
 Symptoms may arise from a complex interaction of :
 Gastric delayed emptying.
 Impaired accommodation to food.
 Psychosocial stressors.
Etiology of
Dyspepsia

42. Rome III
Diagnostic
Criteria for
Functional
Dyspepsia
At least 3 months, with onset at least 6 months
previously, of 1 or more of the following:
Bothersome postprandial fullness.
Early satiation.
Epigastric pain.
Epigastric burning.
No evidence of structural disease (including at
upper endoscopy) that is likely to explain the
symptoms.

43. Differential
Diagnosis

45. Treatment
of Functional
Dyspepsia
1. General Measures:
 Most patients have mild, intermittent
symptoms that respond to reassurance and
lifestyle changes. Alcohol and caffeine should
be reduced or discontinued.
 Patients with postprandial symptoms should
be instructed to consume small, low-fat meals.
 A food diary, in which patients record their
food intake, symptoms, and daily events, may
reveal dietary or psychosocial precipitants of
pain.

46. 2. Pharmacologic Agents:
 Acid suppression therapy for 4-8 weeks with
oral proton pump inhibitors (Esomeprazole,
Rabeprazole, Pantoprazole, dexlansoprazole,
lansoprazole) or H2 blockers (Cimetidine,
Ranitidine, Famotidin).
 Simethicone.
 Motility agents like Domperidone,
Erythromicin.
Treatment
of Functional
Dyspepsia

47. 3. H. pylori eradication therapy
Meta-analyses have suggested that a
small number of patients with
functional dyspepsia (less than 10%)
derive benefit from H. Pylori
eradication therapy. Therefore,
patients with functional dyspepsia
should be tested and treated for H
pylori as recommended above.
Treatment of
Functional
Dyspepsia

48. Irritable
bowel
syndrome

• Irritable Bowel Syndrome is not a disease. It's a
functional disorder, which means that the
bowel simply does not work as it should.
• (IBS) is a common disorder that affects the
large intestine (colon).
• (IBS) commonly causes cramping,
abdominal pain, bloating, gas, diarrhea
and constipation.
4
8

49. What does the
colon do in
IBS?
The contraction of the colon muscles and the
movement of its contents is controlled by nerves,
hormones, and impulses in the colon muscles.
These contractions move the contents inside the
colon toward the rectum.
During this passage, water and nutrients are
absorbed into the body, and what is left over is
Stool.
4
9

50. CONT..
 A few times each day contractions push the stool
down the colon, resulting in a bowel Movement.
 However, if the muscles of the colon do not contract in
the right way, the contents inside the colon do not
move correctly.
 Resulting in abdominal pain, cramps,-
constipation, a sense of incomplete stool
movement, or diarrhea.
5
0
What does the
colon do in
IBS?

51. 5
1

52. Causes of IBS
10
1. Abnormal gastrointestinal (GI) tract movements.
2. A change in the nervous system communication
between the GI and brain.
3. Sensory and motor disorders of the colon.
4. Dietary allergies or food sensitivities.
5. Neurotransmitter imbalance“(decreased
serotonin levels).
6. Stress

53. PATHOPHYSI
OLOGY
5
3
IBS pathophysiology is not clear. Many theories have been
put forward , but the exact cause of IBS is still uncertain.
1. Alteration in GI motility : alteration in frequency and
irregularity of luminal contractions.
2. Visceral hypersensitivity : increased sensation in
response to stimuli.
3. Brain gut axis : alteration in communications
between enteric nervous system and CNS.
4. Post infectious :about 10% of IBS cases are triggered
by an acute gastroenteritis infection.
5. Genetics

54. Symptoms of
IBS
 Pain, distension or abdominal discomfort and
Bloating.
 Abnormal bowel habits with periods of
constipation and/or diarrhea.
 Sensation of incomplete bowel movement.
 Mucus in the stool.
5
4

55. Types of
IBS
IBS can be subdivided into:
Constipation-predominant : The person tends to
alternate constipation with normal stools.
Symptoms of abdominal cramping or aching are
commonly triggered by eating.
Diarrhea-predominant : The person tends to
experience diarrhea first thing in the morning or
after eating. The need to go to the toilet is
typically urgent and cannot be delayed.
14

56. 5
6

57. Diagnosis
of IBS
5
7
Rome criteria
The most important are abdominal pain and
discomfort lasting at least 12 weeks, though the
weeks don't have to occur consecutively
You also need to have at least two of the following:

58.  A change in the frequency or consistency of stool.
For example patient may change from having one- normal
formed stool every day to three or more loose stools daily, or
may have only one hard stool every three to four days.
 Straining, urgency or a feeling that patient can't empty bowels
completely.
 Mucus in stool.
 Bloating or abdominal distension.
5
8

59. Additional
tests
Flexible sigmoidoscopy:
This test examines the lower part of the colon
(sigmoid) with a flexible, lighted tube.
5
9

60. Computerized tomography (CT) scan
 CT scans produce cross-sectional X-ray images of
internal organs.
6
0
Additional
tests

61. Colonoscopy :
20
Additional
tests

62. 6
2
Management
The goals of treatment are symptom
relief and improved quality of life.
Treating IBS can be challenging because
symptoms often are recurrent and
resistant to therapy.
Positive patient-physician interaction is
associated with fewer return visits for
IBS.

63. DIETARY
MODIFICATION
6
3
 Avoid food that trigger symptoms (such as gases
forming foods as lentils , legumes , and beans )
 Low FODMAP diet ( Fermentable Oligo Di Mono-
saccharides And Polyols) : are short chain carbohydrates
that are poorly absorbed in small intestine.
 Fiber supplementation : May improve symptoms of
constipation.

64. PHARMACOLOGICAL
THERAPIES
Antispasmodics :
Dicyclomine, hyoscine N-butylbromide,
clidinium ,peppermint oil, mebeverine.
Tricyclic antidepressants :
Imipramine , amitriptyline , nortriptyline.
Selective serotonin reuptake inhibitors (SSRIS):
Fluoxetine, sertraline , paroxetine , citalopram,
escitalopram.
Probiotics : Improvement in global symptoms
24

65. Drugs for IBS-C
Laxatives : Psyllium.
Chloride channel activators: Lubiprostone.
Serotonin agonists: Tegaserod , mosapride.
Guanylate cyclase -C agonists : Linaclotide.
Antibiotics : Rifaximin
Antimotility agents : Loperamide
Serotonin antagonists : Alosetron , cilansetron
25
Drugs for IBS-D
PHARMACOLOGICAL
THERAPIES

66. IBD
 Inflammatory Bowel Disease (IBD) consist of
Ucerative colitis and Crohn’s disease.
 Protracted relapsing and remitting course
persisting several years.
 They have many similarities and sometimes
difficult to differentiate.
 Ulcerative colitis only involves the colon while
Crohn’s disease can involve any part of the
gastrointestinal tract.

67. PATHOPHYSIOLOGY
 Environmental and genetic components
 In both, the intestinal wall is infiltrated with
acute and chronic inflammatory cells
 Important differences between them in the
distribution of
 lesions and
 histological features

68. COMPARISON OF
ULCERATIVE
COLITISAND
CROHN’S
DISEASE

69. COMMON PATTERNS OFDISEASE
DISTRIBUTION INIBD

70. AssessmentOf
DiseaseSeverity
In
Ulcerative
Colitis

71. ClinicalFeaturesof
Ulcerativecolitis
 Rectal bleeding with passage of mucus and bloody
diarrhoea accompanied by tenesmus
 First attack is usually severe than relapses and
remissions
 Provokating facors for a relapse
 Emotional stress
 intercurrent infection
 Gastroenteritis
 antibiotics or NSAID therapy may all.

72.  Some pass small volume fluid stools
others pass pellety stools due to constipation.
 In severe cases
 Anorexia
 Malaise
 weight loss and abdominal pain occur
 the patient is toxic, with fever, tachycardia and signs of
peritoneal inflammation
ClinicalFeatures
ofUlcerative
colitis

73. ClinicalFeatures
ofCrohn’sdisease
 The major symptoms are
 Abdominal pain
 Diarrhoea and
 weight loss
 Diarrhoea usually watery and does not contain blood or
mucus.
 Weight loss because they avoid food due to pain and
Malabsorption
 Subacute or even acute intestinal obstruction (Ileal Crohn’s)
 Some patients present with features of fat, protein or
vitamin deficiencies.

74.  May present as an identical manner to ulcerative
colitis, but
 Rectal sparing and the presence of perianal
disease favour a diagnosis of Crohn’s disease.
 Symptoms may be of both small bowel and colon
 A few patients present with
 isolated perianal disease
 vomiting from jejunal strictures or
 severe oral ulceration
ClinicalFeatures
ofCrohn’s
disease

75.  Physical examination often reveals
 weight loss
 anaemia with glossitis and angular stomatitis.
 There is abdominal tenderness, most
(over the inflamed area)
 Abdominal mass may be palpable due to-matted
thick loops or intra-abdominal abscess
 Perianal skin tags, fissures or fistulae are found in
at least 50% of patients
ClinicalFeatures
ofCrohn’s
disease

76. CONDITIONS
WHICHCANMIMIC
IBD

77. Complications
Life-threatening colonic inflammation
In both ulcerative colitis and Crohn’s colitis
In most extreme cases
 colon dilates (toxic megacolon)
 bacterial toxins pass freely across the diseased
mucosa into the portal and then systemic
circulation
This arises most commonly during the first
attack of colitis

78. Complications
 Abdominal X-ray showing
transverse colon is dilated
more than 6 cm.
 There is a high risk of colonic
perforation
 Can occur in the absence of
toxic megacolon.

79. Complications
 Haemorrhage
 Fistulae
 These are specific to Crohn’s disease
 Enteroenteric fistulae can cause diarrhoea
and malabsorption due to blind loop
syndrome.
 Enterovesical fistulation causes recurrent
urinary infections and pneumaturia.
 An enterovaginal fistula causes a faeculent
vaginal discharge.
 Fistulation from the bowel may also cause
perianal or ischiorectal abscesses,
fissures and fistulae.

80. Complications
Cancer (More in Ulcerative Colitis)
 Risk increases with the duration and extent of
uncontrolled colonic inflammation
 Oral mesalazine and other treatment modalities
reduces the risk of dysplasia and neoplasia in
ulcerative colitis.

81. Complications
Extra-intestinal complications
Extra-intestinal complications are
common may dominate the clinical
picture
May occur during relapse of intestinal
disease or unrelated to intestinal
disease activity

82. Complications

83. Investigations
 Full blood count : Anaemia resulting from bleeding
or malabsorption of iron, folic acid or vitamin B12.
 Serum albumin: Decrease level -as a consequence
of protein-losing enteropathy, inflammatory
disease or poor nutrition.
 The ESR and CRP: Increase level in exacerbations
and in response to abscess formation.
 Faecal calproctectin:

84. Investigations
 Microbiology
At initial presentation
 stool microscopy and culture
 examination for Clostridium difficile
toxin
 ova and cysts of parasite
 blood cultures and serological tests
During acute flares
 Three separate stool samples should
be sent to maximise sensitivity

85. Investigations
 Endoscopy
Ileocolonoscopy of patients with
 Diarrhoea plus raised inflammatory
markers or
 Alarm features: weight loss, rectal
bleeding and anaemia
In ulcerative colitis, there is
 Loss of vascular pattern
 Granularity, friability and contact bleeding
 with or without ulceration

86. Investigations

87. Investigations
 Colonoscopy In Crohn’s disease
 patchy inflammation
 discrete, deep ulcers
 strictures and perianal disease (fissures, fistulae and
skin tags)
 often with rectal sparing.
 Wireless capsule endoscopy useful for small
bowel inflammation (avoid in presence of
strictures)
 Enteroscopy (Double/Single Bolloon or Push)
are used to make a histological diagnosis

88. Investigations
Radiology
 Barium enema is a less sensitive investigation than
colonoscopy in patients with colitis .
 CT colonogram (where colonoscopy is incomplete)
 Barium follow-through demonstrates affected areas of
the bowel as narrowed and ulcerated, often with multiple
strictures.
 MRI enterography (replaced Barium Enenma): can detect
extraintestinal manifestations and assess pelvic and
perianal involvement

89. Investigations
 Plain abdominal X-ray is essential in severe
active disease
 Small bowel Crohn’s disease
 evidence of intestinal obstruction or
 displacement of bowel loops by a mass
 Ultrasound: very powerful tool to detect
 small bowel inflammation and stricture formation
 it is rather operator-dependent
 CT is limited to screening for complications:
 perforation or abscess formation

90. Management
Optimal management depends on
establishing a multidisciplinary team based
approach involving:
 Physicians
 Surgeons
 Radiologists
 Nurse specialists and
 Dietitians.

91. Management
 Both ulcerative colitis and Crohn’s disease are
life-long conditions and have important
psychosocial implications:
 Specialist nurses.
 Counsellors and
 Patient support groups have key roles in education,
reassurance and coping.

92. Management
The key aims of medical therapy are to:
 Treat acute attacks (induce remission)
 Prevent relapses (maintain remission)
 Prevent bowel damage
 Detect dysplasia and prevent carcinoma
 Select appropriate patients for surgery.

93. ManagementU
lcerativeColitis
 Active proctitis
 For Ulcerative Colitis
mesalazine suppository 1 g ( for Proctitis)
oral 5-aminosalicylate (5-ASA) therapy
 Topical corticosteroids are less effective
 In resistant disease systemic corticosteroids or
immunosuppressant

94. Management
Ulcerative
Colitis
 Active left-sided or extensive ulcerative colitis.
 In mild to moderately active cases, the combination of a
once daily oral and a topical 5-ASA preparation (‘top and
tail approach’) is usually effective.
 In patients who do not respond to this approach within
2–4 weeks, oral prednisolone (40 mg daily, tapered by 5
mg/week over an 8-week total course) is indicated.
 Corticosteroids should never be used for maintenance
therapy. At the first signs of corticosteroid resistance
(lack of efficacy) or in patients who require high
corticosteroid doses to maintain control,
immunosuppressive therapy with a thiopurine should
be introduced.

95. Management
Ulcerative
Colitis
 Severe ulcerative colitis.
 Patients who fail to respond to maximal oral
therapy and those who present with acute
severe disease
 Topical and oral aminosalicylates have no role
 Response to therapy is judged over the first 3
days.
 Considered for medical rescue therapy with
 ciclosporin (intravenous infusion or oral) or
 infliximab (5 mg/kg), which, in approximately 60%
of cases, can avoid the need for urgent colectomy.

96. Management-
Ulcerative
Colitis
Urgent colectomy is required:
 Patients who develop colonic dilatation (> 6 cm),
 those whose clinical and laboratory measurements
deteriorate and
 those who do not respond after 7–10 days maximal
medical.
 Subtotal colectomy can also be performed
laparoscopically, given sufficient local
expertise.

97. Management-Ulcerative Colitis

98. Management
Ulcerative
Colitis
 Maintenance of remission.
 Life-long maintenance therapy is
recommended for all patients with left-sided or
extensive disease but is not necessary in those
with proctitis.
 Once-daily oral 5-aminosalicylates are the preferred
first-line agents.
 Patients who frequently relapse despite
aminosalicylate drugs should be treated with
thiopurines.

99. ManagementCrohn’s
disease
 Principles of treatment.
 Crohn’s disease is a progressive condition may
result in stricture or fistula formation if
suboptimally treated
 It is therefore important to agree long-term
treatment goals with the patient;
 To induce remission and then maintain corticosteroid-
free remission with a normal quality of life.
 Treatment should focus on monitoring the patient
carefully for evidence of disease activity and
complications and
 Ensuring that mucosal healing is achieved.

100.  Induction of remission.
 Corticosteroids remain the mainstay of treatment.
Drug of first choice is budesonide, (90% first-
pass metabolism & very little systemic toxicity).
9 mg once daily for 6 weeks, with a gradual reduction
 If no response within 2 weeks,
prednisolone, 40 mg daily, reducing by 5 mg/week over
8 weeks,.
 Calcium and vitamin D supplements
Management
Crohn’sdisease

101.  As an alternative to corticosteroid therapy,
enteral nutrition with either an elemental
(constituent amino acids) or polymeric (liquid
protein) diet may induce remission.
 It is particularly effective in children, in whom
equal efficacy to corticosteroids has been
demonstrated, and in extensive ileal disease in
adults. As well as resting the gut and providing
excellent nutritional support, it also has a
direct anti-inflammatory effect.
Management
Crohn’sdisease

102.  Some patients with severe colonic disease
require admission to hospital for intravenous
corticosteroids.
 In severe ileal or panenteric disease, induction
therapy with an anti-TNF agent is appropriate,
provided that acute perforating complications,
such as abscess, have not occurred.
Management
Crohn’sdisease

103.  Maintenance therapy.
 Immunosuppressive treatment
thiopurines (azathioprine and
mercaptopurine)
methotrexate: orally and once weeklyis also.
 Combination therapy with an
immunosuppressant and an anti-TNF antibody
is the most effective strategy but costs are high
and there is an increased risk of serious
adverse effects.
Management
Crohn’sdisease

104.  Careful monitoring of disease is the key to
maintaining sustained remission and
preventing the accumulation of bowel damage
in Crohn’s disease.
 Cigarette smokers should be strongly
counselled to stop smoking at every possible
opportunity.
Management
Crohn’sdisease

105.  Fistulae and perianal disease.
 Fistulae may develop in relation to active Crohn’s
disease and are often associated with sepsis. The first
step is to define the site by imaging (usually MRI of the
pelvis).
 Surgical exploration by an examination under
anaesthetic is usually then required, to delineate the
anatomy and drain abscesses.
 Seton sutures can be inserted through fistula tracts to
ensure adequate drainage and to prevent future sepsis.
Corticosteroids are ineffective.
Management
Crohn’sdisease

106.  For simple perianal disease, metronidazole
and/or ciprofloxacin are first-line therapies.
Thiopurines can be used in chronic disease but
do not usually result in fistula healing.
 Infliximab and adalimumab can heal fistulae
and perianal disease in many patients and are
indicated when the measures described above
have been ineffective.
Management
Crohn’sdisease

107. Surgical
Management
Ulcerative colitis
 Up to 60% of patients with extensive ulcerative colitis
eventually require surgery.
 Surgery involves removal of the entire colon and rectum,
and cures the patient. One third of those with pancolitis
undergo colectomy within 5 years of diagnosis.
 The choice of procedure is either panproctocolectomy
with ileostomy, or proctocolectomy with ileal–anal
pouch anastomosis.

108. Surgical
Management
Crohn’s disease
 The indications for surgery are similar to those for
ulcerative colitis.
 Operations are often necessary to deal with fistulae,
abscesses and perianal disease, and may also be
required to relieve small or large bowel obstruction.
 In contrast to ulcerative colitis, surgery is not curative
and disease recurrence is the rule.
 Antibiotics are effective in the short term only.

109. Surgical
Management
 Obstructing or fistulating small bowel disease
may require resection of affected tissue.
 Patients who have localised segments of
Crohn’s colitis may be managed by segmental
resection and/or multiple stricturoplasties, in
which the stricture is not resected but instead
incised in its longitudinal axis and sutured
transversely.

110. IBDinspecial
circumstances
Childhood
 Chronic ill health in childhood or adolescent
IBD may result in
 growth failure,
 metabolic bone disease and
 delayed puberty.
 Treatment is similar to that described for adults
and may require corticosteroids,
immunosuppressive drugs, biological agents
and surgery.

111. IBDinspecial
circumstances
Pregnancy
 A women’s ability to become pregnant is
adversely affected by active IBDDuring
pregnancy.
 The rule of thirds applies – roughly
 one-third of women improve,
 one-third get worse and
 one third remain stable with active disease.
 In the post-partum period, these changes
sometimes reverse spontaneously.

112. IBDinspecial
circumstances
Metabolic bone disease
 Patients with IBD are prone to developing
osteoporosis due to effects of chronic
inflammation, corticosteroids, weight loss,
malnutrition and malabsorption.
 Osteomalacia can also occur in Crohn’s disease
that is complicated by malabsorption, but is
less common than osteoporosis

113. Microscopic
colitis
 Microscopic colitis, which comprises two related
conditions,
 lymphocytic colitis and
 collagenous colitis,
 Cause is unknown.
 The presentation is with watery diarrhoea.
 The colonoscopic appearances are normal but
histological examination of biopsies shows a range of
abnormalities.