Esophageal Disorders

Esophageal Disorders
 Motility
 Anatomic &
Structural
 Reflux
 Infectious
 Neoplastic
 Miscellaneous
 Esophageal Anatomy
Upper Esophageal
Sphincter (UES)

Esophageal Body 18 to 24 cm
(cervical & thoracic)

Lower Esophageal
Sphincter (LES)
 Normal Phases of Swallowing
 Voluntary
 oropharyngeal phase – bolus is voluntarily
moved into the pharynx
 Involuntary
 UES relaxation
 peristalsis (aboral movement)
 LES relaxation
Esophageal Motility
Disorders
 Motility Disorders
 Upper esophageal  Primary disorders
 UES disorders  achalasia
 neuromuscular disorders  diffuse esophageal spasm
 Esophageal body  nutcracker esophagus
 achalasia  nonspecific esophageal
 diffuse esophageal spasm dysmotility
 nutcracker esophagus  Secondary disorders
 nonspecific esophageal  severe esophagitis
dysmotility  scleroderma
 LES  diabetes
 achalasia  Parkinson’s
 hypertensive LES  stroke
Diagnostic
Bariumesophagram
Esophageal manometry
Endoscopy
Normal Manometry
 Motility Disorders
Based on Manometry
 Achalasia
– Inadequate LES relaxation
 Diffuse Esophageal Spasm
– Uncoordinated contraction
 Nutcracker Esophagus
– Hypercontraction
 Ineffective Esophageal Motility
– Hypocontraction
Achalasia
 Achalasia
 first clinically recognized esophageal
motility disorder
 described in 1672, treated with
whale bone bougie
 term coined in 1929
 epidemiology
 1-2 per 200,000 population
 usually presents between ages
25 to 60
 male=female
 Caucasians > others
 average symptom duration at
diagnosis: 2-5 years
 Pathophysiology
 Degeneration of NO producing inhibitory neurons
 loss of ganglionic cells in the myenteric plexus (distal
to proximal)
 vagal fiber degeneration
 underlying cause: unknown
 autoimmune? (antibodies to myenteric neurons in
50% of patients)
 that affect relaxation of LES
 Basal LES pressure rises
 Clinical Presentation
 clinical presentation
 solid dysphagia 90-100% (75% also with
dysphagia to liquids)
 post-prandial regurgitation 60-90%
 chest pain 33-50%
 pyrosis 25-45%
 weight loss
 nocturnal cough and recurrent aspiration
Diagnostic
 plain film (air-fluid level, wide mediastinum,
absent gastric bubble, pulmonary infiltrates)
 barium esophagram (dilated esophagus with
taper at LES) Bird peak
 good screening test (95% accurate)
 endoscopy (rule out GE junction tumors, esp.
age>60)
 esophageal manometry (absent peristalsis, 
LES relaxation, & resting LES >45 mmHg)
Treatment of Achalasia
 Goals
 reduce LES pressure and
 increase emptying
 Nitrates and Calcium Channel
Blockers
 Isosorbide dinitrate
Reduces LES Pressure 66% for 90 min
 Nifedipine
Reduces LES pressure 30-40% for > 60 minutes

 50-70% initial response; <50% at 1 year

 limitations: tachyphylaxis and side-effects
 Pneumatic Dilatation
 Balloon dilatation to 300 psi
 disrupt circular muscle
 60-95% initial success; 60% at 5 years
 recent series suggest 20-40% will require
re-dilation
 Success increases with repeat dilatations
 risk of perforation 1-13% (usually 3-5%);
death 0.2-0.4%
 Businasi
 POEM
 Surgical Treatment
 surgical myotomy
(open or minimally-
invasive)
 >90% initial response;
85% at 10 years; 70%
at 20 years (85% at 5
years with min. inv.
techniques)
 <1% mortality; <10%
major morbidity
 10-25% acutely develop
reflux, up to 52%
develop late reflux
Spastic Motility Disorders of the
Esophagus
 Spastic Motility Disorders of the
Esophagus
 Diffuse Esophageal Spasm
 Nutcracker Esophagus
 Hypertensive LES
 Nonspecific Esophageal Dysmotility
 Epidemiology
 Any age (mean 40 yrs)
 Female > Male
 Clinical Presentation
 Dysphagia to solids and liquids
 intermittent and non-progressive
 present in 30-60%, more prevalent in DES (in most studies)
 Chest Pain
 constant % across the different disorders (80-90%)
 swallowing is not necessarily impaired
 can mimic cardiac chest pain
 Pyrosis (20%) and IBS symptoms (>50%)
 Symptoms and Manometry correlate
poorly
 Diffuse Esophageal Spasm

 frequent non-peristaltic
contractions
 simultaneous onset
(or too rapid
propagation) of
contractions in two
or more recording
leads
 occur with >30% of
wet swallows (up to
10% may be seen in
“normals”)
 Nutcracker Esophagus
 high pressure peristaltic
contractions
 avg pressure in 10
wet swallows is >180
mm Hg
 33% have long duration
contractions (>6 sec)
 may inter-convert with
DES
 Nonspecific
Hypertensive Esophageal
LES Dysmotility
 abnormal motility
 high LES pattern
pressure  fits in no other
 >45 mm Hg category
 normal  non-peristalsis in
20-30% of wet
peristalsis
swallows
 often overlaps  low pressure
with other waves (<30 mm
motility disorders Hg)
 prolonged
contractions
 Diagnosis of Spastic Motility
Disorders of the Esophagus
 Manometry
 Barium Esophagram
 Endoscopy
 PH monitoring
 Spastic Motility Disorders
of the Esophagus

 treatment
 reassurance
 nitrates, anticholinergics, hydralazine - all
unproven
 calcium channel blockers - too few data with
negative controlled studies in chest pain
 psychotropic drugs – trazodone, imipramine and
setraline effective in controlled studies
 dilation - anecdotal reports, probable placebo
effect
 Hypomotilty Disorders
 primary (idiopathic)
 aging produces gradual decrease in contraction
strength
 reflux patients have varying degrees of hypomotility
 more common in patients with atypical reflux
symptoms
 usually persists after reflux therapy
 defined as
 low contraction wave pressures (<30 mm Hg)
 incomplete peristalsis in 30% or > of wet
swallows
 Hypomotilty Disorders
 secondary
 scleroderma
 in >75% of patients
 progressive, resulting in aperistalsis in smooth-muscle region
 incompetent LES with reflux
 other “connective tissue diseases”
 CREST
 polymyositis & dermatomyositis
 diabetes
 60% with neuropathy have abnormal motility on testing (most
asx)
 other
 hypothyroidism, alcoholism, amyloidosis
 GERD
 36-77% of all Americans experience
 GERD
 – 7% have daily GERD symptoms
 – 14-20% weekly symptoms
 – 15-50% monthly
 Symptoms include: heartburn, acid
 regurgitation, water brash, dysphagia,
 atypical symptoms (asthma, globus,
 laryngitis, cough, throat clearing)
 Pathophysiology
 Lower esophageal sphincter dysfunction
 Delayed gastric emptying
 Esophageal dysmotility
 +/- hiatal hernia
 Repetitive mucosal injury / esophagitis
 Barrett’s Esophagus
 Medical Treatment
 Lifestyle modifications
– avoid coffee, fatty foods, smoking;
lose weight, raise head of bed,
eliminate late night meals
 Acid suppressin via PPI’s
 Indications for Surgery
 Failed medical management
 Need for lifelong medical therapy
 Hiatal hernia
 Atypical symptoms with (+) pH probe
 Complications
 – Barrett’s esophagus (5-15% develop
BE)
 – Erosive esophagitis
 Surgical Treatment
 Pre-operative evaluation
 – Esophagram
 – EGD
 – Manometry (resting LES >5, length
>2cm)
 – 24-hr esophageal pH monitoring
 Surgical Treatment
 Laparoscopic Nissen Fundoplication
 Goals of antireflux surgery:
 – Recreate Angle of His
 – Reconstitute LES with wrap
GASTROESOPHAGEAL
REFLUX DISEASE.

.
 Definitions of Reflux
 Clinical manifestations of reflux of stomach & duodenal
contents into the esophagus.
 Characterized by any combination of symptoms,
radiologic, endoscopic, or pathologic changes.
 In its milder forms, is common.
 Its most severe forms is uncommon but life-threatening.
 GERD is preferable to "reflux esophagitis“
 GERD may be associated with a sliding HH, but
"symptomatic HH" is an anatomic entity & not the
underlying pathophysiology in GERD.
 PATHOGENESIS.

 The most common event :

 Transient relaxation of the LES unassociated with
swallowing or the distention of the esophagus.
 2 abnormalities:
 A LES with very low tone & pressure.
 Inappropriate relaxation of a normally competent
sphincter.
 Acid within the esophagus is cleared less well by
patients with GERD than by normal subjects, although
the manometric tracings in both groups seem identical.
 PATHOGENESIS:
 Pregnancy:
From increased abdominal pressure by the fetus.
Diminished LES strength caused by increased
estrogen & progesterone.
 Weight gain also aggravate reflux through an
unknown mechanism.
 Resection of the lower esophageal area for cancer
or myotomy for achalasia.
 It is especially severe in progressive systemic
sclerosis.
 PATHOGENESIS.

 Although HH may be associated with reflux, its

presence is much less important, as it is present in a
large percentage of normal subjects.
 It is not necessary to spend time to find a HH with
most patients with GERD.
 Focus should be on the symptoms of reflux.
 SYMPTOMS.

Heartburn, the most common.

Vary from mild burning to chronic, severe markedly limiting
a patient's lifestyle

Regurgitation of gastric contents, either into the mouth or

into the respiratory tree: nocturnal wheezing, coughing,
hoarseness, a need to clear the throat repeatedly, or a
sensation of deep pressure at the base of the neck.
 SYMPTOMS.

Dysphagia is often present.

When severe, may indicate stricture,but even if mild &
must be carefully sought.
 Dysphagia is for solids, usually overcome by swallowing
repeatedly or by washing the bolus down with water.
Many are aware of the location of each solid as it travels
down the esophagus.
 SYMPTOMS.
 Blood loss may result from esophageal erosions &
shallow ulcer
 Some have very few other clinical manifestations &
discovered by endoscopy during evaluation of occult
GIB.
 Alcohol abuse produce severe erosive esophagitis
with bleeding.
 DIAGNOSIS.

 History &clinical manifestations are the most important .

 Objective testing quantify the extent & severity.
 In the majority, diagnosed by typical symptoms & the
response to therapy.
 Diagnostic evaluation becomes important when
symptoms are atypical &/or do not respond to therapy.
 Diagnosis include:
1. Documenting reflux.
2.Linking reflux to symptoms.
3. Assessing the effect of reflux on eso mucosa.
 ASSESSING THE EFFECT OF REFLUX ON THE
ESOPHAGEAL MUCOSA.

 A barium swallow detects gross changes, as stricture or

ulcer, but misses shallow ulcerations - erosions, detected
by OGD.
 On OGD only lesions such as erosions & ulcerations
should be taken as proof of esophageal damage, as
erythema, edema, or friability, are subject to wide
interobserver variation.
 In 50% with moderate - severe symptoms, the mucosa
appears absolutely normal, but a biopsy may demonstrate
histologic changes(NERD).
 The LA Classification system
– Grade A reflux esophagitis
Grade A: One (or more) mucosal break, no longer than 5 mm,
that does not extend between the tops of two
mucosal folds.

Stomach
 The LA Classification system
– Grade B reflux esophagitis
Grade B: One (or more) mucosal break, more than 5 mm long,
that does not extend between the tops of two mucosal
folds.

Stomach
 The LA Classification system
– Grade C reflux esophagitis
Grade C: One (or more) mucosal break that is continuous between
the tops of two or more mucosal folds, but which involves
less than 75% of the circumference.

Stomach
 The LA Classification system
– Grade D reflux esophagitis
Grade D: One (or more) mucosal break that involves at least
75% of the esophageal circumference.

Stomach
 APPROACH TO THE PATIENT

 Endoscopy indicated if:

Hematemesis is present.
Prolonged & not respond to empiric treatment.
Systemic manifestations, as weight loss, anemia.
Occult blood–positive stool are present.
 APPROACH TO THE PATIENT
 After first evaluation, it may be appropriate to begin
empiric therapy
 If the response to therapy is poor, esophageal pH
monitoring can confirm the diagnosis.
 At the same time, esophageal manometry may be
performed to estimate LES pressure & to determine
the presence or absence of peristaltic waves.
 If dysphagia is present, a barium swallow is
appropriate, Uncommonly, reflux, stricture or a deep
ulcer seen, which leads to immediate endoscopy for
more complete evaluation.
COMPLICATIONS.
 1.ESOPHAGEAL STRICTURE.
 Only a few develop strictures.
 Usually at the lower end, but sometimes migrating over
years to the mid or higher.
 Cause is Circumferential ulceration.
 If reflux can be controlled, these strictures may disappear.
 Dysphagia is the clinical hallmark.
 The dysphagia tends to be constant ,slowly progressive,
causing the patient to alter the type of food taken.
 ESOPHAGEAL STRICTURE.

 Most easily evaluated by barium swallow.

 Sometimes the extent of the strictured area is
overestimated unless the esophagus below the stricture
can be fully distended by barium.
 For mild strictures, the ingestion of barium-soaked bread
or a bolus can draw attention to slight luminal narrowing
where the bolus is impacted.
 Endoscopy with biopsy &/or brush cytology is required to
make certain that the stricture is benign.
 2.ESOPHAGEAL ULCER.
 The presence of an ulcer can be suspected on a
barium swallow & confirmed endoscopically.
 Characteristically produce severe & unrelenting pain,
often with radiation of the pain to the back.
 Brisk hemorrhage may be caused by erosion of an
esophageal artery.
 The ulcer usually is in columnar (Barrett's)
epithelium.
3.BARRETT'S ESOPHAGUS (COLUMNAR
EPITHELIUM).

 The presence on biopsy of specialized columnar

epithelium with goblet cells in the esophagus.

 In some patients with chronic reflux esophagitis,

the healing epithelium replaced with a specialized
columnar epithelium with intestinal metaplasia

 The junctional zone between squamous &

columnar (Barrett's) epithelium can progress
upwards over years.
 BARRETT'S ESOPHAGUS (COLUMNAR
EPITHELIUM).
 Identified endoscopically as salmon-pink (gastric-
appearing) mucosa above the lower esophageal
sphincter.
 Barrett's epithelium is often found at & below mid-
esophageal strictures & around deep esophageal ulcers.
 Barrett's epithelium is a marker for severe reflux & a
precursor to adenocarcinoma of the esophagus.
 4.PULMONARY ASPIRATION.
 Into the larynx & tracheobronchial tree.
 Produces mild laryngeal or respiratory symptoms or
hoarseness or intense respiratory stridor.
 The gastric contents do not have to reach the larynx,as acid
in the esophagus can cause closure of small bronchi by a
vagal reflex.
 Or volatile HCL can reach upper airways.
 Wheezing, hoarseness, or coughing occur.
 Dual esophageal pH monitoring with pH probes in both the
lower & upper esophagus can help.
 Treatment of reflux followed by disappearance of
pulmonary symptoms may confirm the relationship.
 Possible extraesophageal
manifestations of GERD
 Asthma
 Sinusitis
 Dental erosions
 Reflux laryngitis
 Vocal cord ulcers
 Subglottal/tracheal stenosis
 Laryngospasm

Jailwala & Shaker 2000; Richter 2000; Ulualp et al 1999

 Symptoms of Reflux in Infants
 Regurgitation – emesis &weight loss
 Esophagitis - chest pain, irritability, feeding problems,
anemia, hematemesis, stricture causing obstruction
 Neurobehavioral - infant “spells” (seizure-like events),
Sandifer syndrome (opisthotonos & other abnormal
posturing)
 Respiratory symptoms - chronic or recurrent pneumonia,
wheezing (especially intractable asthma), apnea
(especially obstructive), cyanotic episodes, stridor, cough,
hiccups, hoarseness
 Complex respiratory disease-reflux interactions -
esophageal atresia, TEF, cystic fibrosis.
Endoscpic management of GERD:

Endoscopic Baloon dilatation of esophageal stricture.

Endoscopic photodynamic therapy, laser, or multipolar
electrocoagulation ablasion of Barret esophagus
Endoscopic Radiofrequency application to LES
Laproscopic funduplication.
Endoscopic antireflux stents
Endoscopic therapies – the Stretta
procedure

Step 1

Step 2

Step 3
Endoscopic therapies – gastroplication

A B

C D
Hiatal Hernia
 Pathophysiology & Classification
 Type I - sliding
 Type II -
paraesophageal
 Type III - para and
sliding component
 Type IV - other
viscera involved
 Clinical Presentation
 postprandial fullness (63%),
 Reflux (31%),
 Dysphagia (34%),
 Bleeding (24%)
 Regurgitation/vomiting (36%)
 Dyspnea (11%)
Work Up
 Surgical Treatment
 Effective repair includes:
– Excision of hernia sac
– Reduction of hernia contents
– Repair of crural defect
 – Fundoplication, gastropexy, PEG,
esophageal lengthening (Collis
gastroplasty)
 Gastroenteritis
 Inflammation of stomach or intestines
 Inhibits nutrient absorption and excessive H2O and
electrolyte loss
 Bacterial
 Viral
 Parasites
 Poisoning by microbial toxins
 food borne intoxication
 Signs and Symptoms:
 General features: diarrhea, loss of appetite, abdominal
cramps, nausea, vomiting and possibly fever
 Dysentery
 Typically self Limiting

 Enteric fevers
 Systemic with severe headache, high fever, abscesses,
intestinal rupture, shock and death
 Epidemiology
 Occurs worldwide
 Oral to fecal route of transmission
 Water common reservoir
 Overcrowding & poor sanitation are risk factors
 Animals may be source of infection
 Prevention
 Hand washing
 Proper food handling and complete cooking
 Pasteurization of milk and juices
 Adequate sanitation
 Safe water supplies

 Treatment
 Rapid replacement of fluids and electrolytes
 Anti-nausea medication
 Antimicrobials may be used in severe cases
 Bacterial Gastroenteritis

 3 groups of gram negative bacteria account for

most bacterial intestinal infections:
 Vibrio cholerae (Cholera)
 Enterics (Salmonella, Shigella, E. coli)
 Campylobacter jejuni
 Cholera
 Causative agent: Vibrio cholerae
 High infectious dose
 Bacteria sensitive to stomach acid
 Adheres to small intestine and multiply
 Bacteria don’t enter cells
 Cholera toxin
 Potent exotoxin
 Causes intestinal cells
to rapidly pump out
electrolytes
 Passive osmotic H2O
loss follows
 Metabolic acidosis
 Shock
 Heavy loss of fluid
 “rice-water stool”
 Up to 20L of fluids lost per day

 May discharge 1 million bacteria per ml of feces

 Untreated cases potentially fatal

 Fluid/electrolyte replacement
 Tetracycline reduces toxin production
 Shigellosis
 Causative Agent: Shigella sp.
 S. dysenteriae, S. flexneri, S. boydii, S. sonnei
 Low infecting dose
 Bacteria not sensitive to stomach acid
 Characterized by fever and dysentery
•Infects cells of large intestine and
initiates intense inflammatory
response

•Dead cells slough off

•Produces areas covered with
pus and blood
 All species produce enterotoxin and type III
secretion systems
 S. dysenteriae produces powerful endotoxin
 shiga-toxin
 Ciprofloxacin, rifampin or azithromycin may reduce
duration and infectivity
 Traveler’s Diarrhea
 Causative Agent: Escherichia coli
 Multiple antigenic strains (O, H, K)
 Virulent strains have fimbriae, adhesions and
multiple toxins

 Enterotoxigenic E. coli
 Enterotoxins
 Type III secretion system
 Typically self limiting
 Enterohemorrhagic E. coli
 O157:H7
 Produce potent Shiga-like toxins and type III secretion
systems

 Antimicrobials cause increase in toxin production

 Salmonellosis and Typhoid Fever
 Causative agent: Salmonella enterica
 2000 strains (serotypes)
 Typhimurium and Enteritidis commonly cause
Salmonellosis
 Typhi and Paratyphi cause Typhoid Fever
 Common intestinal
flora of many animals
 Contaminated animal
products are reservoir
 Reptiles,
eggs and
undercooked
poultry
•Virulent strains tolerate stomach
acid and pass to intestines

•Toxin induces phagocytosis in

intestinal cells

•Pathogen reproduces inside

phagosome killing host cell

•Bacteria (Typhi) may pass

through intestinal cells into
bloodstream
 Typhoid fever is an
enteric fever
 Macrophages carry
bacteria to liver, spleen,
bone marrow and
gallbladder
 Treated with ciprofloxacin
or ampicillin
 Surgical removal of
gallbladder
 Campylobacteriosis
 Causative agent: Campylobacter jejuni
 Leading cause of bacterial diarrhea in United States
 Estimated 1million cases annually with ~100 deaths
 Associated with poultry
 Low infecting dose
 Virulent strains possess adhesions, cytotoxins
and endotoxin
 Induce endocytosis in cells of intestine and initiate
inflammation and bleeding lesions
 Non-motile mutants are avirulent

 Severe cases treated with ciprofloxacin or

azithromycin
 Guillain-Barré Syndrome
 Tingling of the feet leads to progressive paralysis of the
legs, arms and rest of the body
 40% of cases preceded by campylobacteriosis
 May be associated with autoimmune response
 80% recover completely; 5% mortality with treatment
 Viral Gastroenteritis
 Common causative agents:
 Rotaviruses and Noroviruses
 Both naked RNA viruses

Star-like Noroviruses

Wheel -like Rotaviruses

 Epidemology
 Infect intestinal cells causing cell death
 Typically self-limiting
 Norovirus epidemics cause 90% of cases
 Rotaviruses responsible for 50% infant cases
of serious diarrhea
 600,000 worldwide annual fatalities
 Oral vaccine available
 Bacterial Food Intoxication
 Staphylococcus aureus
 Halotolerent; grows well in foods at room temp
 Associated with cafeterias and social functions
 5 heat stable enterotoxins:
 1000 for up to 30 min
 Stimulate muscle contractions, nausea and intense
vomiting, diarrhea and cramping
 Acute and self limiting
 symptoms begin 4-6 hrs after consumption and
end within 24 hrs
 Botulism
 Causative agent:
 Clostridium botulinum
 Obligate anaerobic, Gram +, spore forming bacillus
 Produce 7 different neurotoxins
 One of most deadly toxins known
 Signs & Symptoms
 Dizziness, dry mouth, blurred vision
 Abdominal symptoms include pain, nausea,
vomiting and diarrhea or constipation
 Progressive paralysis
 Paralysisof respiratory muscles most common
cause of death
 3 forms of botulism:
 Food-borne botulism – progressive paralysis of
all voluntary muscles due to toxin production

 Wound botulism – similar symptoms

 Infant botulism – bacteria grow in the intestines,

producing non-specific symptoms
 “floppy baby syndrome”
 Epidemiology
 Food borne botulism
 Commercial sterilization
 Toxin destroyed by heating foods

 Wound botulism
 deep crushing wounds

 Infant botulism
 Inhalationor ingestion of spores
 Commonly associated with honey
or juices
 Prevention
 Proper sterilization and sealing of canned food
 No honey or unpasteurized juices for infants!!

 Treatment
 Antitoxin
 Gastric washing and surgical removal of tissues
 Artificial respiration may be required
 Anti-microbials given to kill bacteria in infant and wound
botulism
INFLAMMATORY
BOWEL DISEASE
 CROHN’S DISEASE-
DEFINITION
 Chronic Inflammatory Bowel Disease
(IBD)
 Unknown Aetiology
 Characterised by
1. Focal
2. Asymmetrical
3. Transmural
4. Occasionally granulomatous
inflammation
 CROHN’S DISEASE-
EPIDEMIOLOGY
 Incidence: 9.56 per 100,0001
 Prevalence: 115,000 in the UK
 Age of onset: 2 peaks 1) 15-30 Y (more
common)
2) 60-80 Y
 Female: Male 1.8:1 Children this is
reversed!

 Risk Factors2
 Mycobacterium paratuberculosis, Pseudomonas spp. &
Listeria spp.
 ↑TNF-alpha
 High-fat diets
 Genetic mutations

1) Steed H, Walsh S, Reynolds N; Crohn's disease incidence in NHS Tayside. Scott Med J. 2010 Aug;55(3):22-5
2) Rangasamy P et al; Crohn Disease, Medscape, Jun 2011
 CROHN’S DISEASE-
SYMPTOMS
• Abdominal pain, cramping or swelling
• Anaemia
• Fever
• Gastrointestinal bleeding
• Joint pain
• Malabsorption
• Persistent or recurrent diarrhoea
• Stomach ulcers
• Vomiting
• Weight loss
 CROHN’S DISEASE- ON
EXAMINATION
 General ill health- weight loss & dehydrated

 Hypotension, tachycardia and pyrexia

 Abdominal tenderness or distension, palpable
masses.
 Anal and perianal lesions (abscesses, fistulae)
 Mouth Ulcers

 Extra-intestinal manifestations of Crohn’s ......

CROHN’S DISEASE- EXTRA
INTESTINAL
 Investigations
 Bloods
 FBC, CRP, LFTs
 Stool culture and microscopy
 anti-S. cerevisiae antibodies Perinuclear
antineutrophil cytoplasmic antibody (p-ANCA)
(UC>CD)
 Abdo Xray
 Ileocolonscopy and biopsy from the terminal
ileum as well as the affected sites
 Small bowel follow through
 If upper GI symptoms- Upper GI endoscopy
 If lower GI symptoms- Flexible
sigmoidoscopy/EUA
 CROHN’S DISEASE-
MANAGEMENT
 First presentation (NICE guidelines)
1. Glucocorticoids
1. Prednisolone, Methylprednisolone IV
hydrocortisone
2. Budesonide
3. 5-ASA

 +/- ADD ON Azathioprine or

Mercaptopurine
 CROHN’S DISEASE-
MANAGEMENT
 Maintaining Remission (NICE guidelines)

 Offer Azathioprine or Mercaptopurine as

Monotherapy

 Methotrixate

 Surgery- if limited to distal ileum (weighing out

the risk Vs benefits) and for complications...
 Ulcerative Colitis- Definition
 Chronic Inflammatory
Bowel Disease
 Unknown etiology

 Only Large Colon

 Classification:
 Distal Disease
 More extensive disease
 Pancolitis
Ulcerative Colitis
Epidemiology
 More common than Crohn’s
 Incidence: 10 per 100,000
 Prevalence 240 per 100,000 in the UK
 Age of onset: 2 peaks 1) 15-25 Y (more common)
2) 55-65 Y
 Male:Female= 1:1
 Idiopathic: autoimmune condition triggered by
colonic bacteria  inflammation
 Genetic component: sibling of an individual who
has IBD 17-35 x more risk of development
 Risk of UC decreased in smokers
1) Ulcerative Colitis; NICE Clinical Guideline (Jun 2013)
 Ulcerative Colitis- Symptoms
 Bloody diarrhoea
 Abdominal Pain
 Tenesmus
 Systemic symptoms: malaise, fever,
weightless
 Ulcerative Colitis- On
examination
 Unwell, pale, febrile, dehydrated
 Abdo pain and tenderness .. +
distension
 TOXIC MEGACOLON

 Worrying signs: Tachycardia, anaemia

and fever

 Extra- intestinal disease...

 Ulcerative Colitis- Extra-
intestinal
 Aphthous ulcers
 Ocular manifestations 5%
 Episcleritis
 Anterior uveitis
 Acute arthropathy affecting the large joints 26%
 Sacroiliitis
 Ankylosing Spondylitis 3%
 Deramatology 19%
 Pyoderma gangrenosum
 Erythema nodosum
 Primary Sclerosing Cholangitis
Ulcerative Colitis- Investigations
 Bloods: FBC, LFTs, U+Es, CRP
 Serology- pANCA Vs. ASCA
 Stool cultures

 Imaging
 Abdo x-ray- acute setting
 Barium enema- can show mucosal structure

 Flexible Sigmoidoscopy and Biopsy- for

diagnosis
Ulcerative Colitis- Management

a) Topical aminosalicylate a) PO Aminosalicylate - If no improvement 72 hrs

alone (suppository or
enema
b) ?ADD PO
aminosalicylate to a topical
aminosalicylate OR
c) consider an PO
aminosalicylate alone
- High induction despite IV Hydrocortisone
dose of an OR
b) ?ADD topical -Symptoms worsen to
Aminosalicylate OR pancolitis:
PO beclometasone
dipropionate a) ADD IV Ciclosporin to IV
steroids
Ulcerative Colitis- Management
 Indications for Surgery:
 Unresponsive to medical treatment
 Significantly affecting quality of life
 Growth retardation in Children
 Life-threatening complications...

 Bleeding
 Toxic Megacolon
 Impending perforation
 Carcinoma
SUMMARY
SUMMARY: CROHN’S VS. UC
Symptoms of Crohn's Symptoms of Ulcerative
Disease Colitis

• Abdominal pain, cramping or •Bloody diarrhoea

swelling •Abdominal pain or discomfort
•Anaemia •Anaemia caused by severe
•Fever bleeding
•Gastrointestinal bleeding •Dehydration
•Joint pain •Fatigue
•Malabsorption •Fever
•Persistent or recurrent •Joint pain
diarrhoea •Loss of appetite
•Stomach ulcers •Malabsorption
•Vomiting •Rectal bleeding
•Weight loss •Urgent bowel movements
•Weight loss
SUMMARY: CROHN’S VS. UC
SUMMARY- CROHN’S VS. UC
SUMMARY: CROHN’S VS. UC
1/7/2019 LDLT 5th case 126