” Content ”

Subject page

1 Nausea and vomiting. 3

2 GERD. 10

3 Peptic Ulcer. 23

4 Esophageal motility disorders. 30

5 GI Bleeding. 38

6 Ulcerative Colitis . 51

7 Crohn’s disease. 63

8 Mesenteric Ischemia. 78

9 Diverticular disease of the colon 85

10 Portal Hypertension. 91

11 Pancreatitis. 99

12 Vascular liver disease.

13 Billiary disease.

14 Chronic hepatitis.
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Nausea and Vomiting

Definition:
• Nausea: is the unpleasant feeling of the need to vomit. usually felt in the
throat or epigastrium, associated with autonomic symptoms (pallor, cold
sweat, salivation, tachycardia).
• Vomiting is the forceful oral expulsion of gastric contents via retroperistalsis
(Abdominal effects).

What is it?
• Primitive defense mechanism against ingested toxins mediated via: Higher
centers: sight, smell, taste.
• Controlled by integrated Chemoreceptor trigger zone and vomiting center in
the medulla and pons (floor of 4th ventricle).
• Specific neurotransmitters are involved.

CAUSES OF NAUSEA/VOMITING:
‐ Acute gastroenteritis. ‐ Myocardial infarction.
‐ Acute gastritis. ‐ Peritonitis.
‐ Gastric retention. ‐ Cancer therapy.
‐ Peptic ulcer. ‐ Drug withdrawal.
‐ Bulimia. ‐ Urinary tract infection.
‐ Acute obstruction. ‐ Neurological emergency.
‐ Early pregnancy. ‐ Electrolyte disturbance as
‐ Drug toxicity. Hypercalcemia.
‐ Psychogenesis vomiting. ‐ Positional changes (motionsickness).

Brain stem Vomiting center

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What are the main neurotransmitters in the pathophysiology of

nausea?
• Acetylcholine (M1).
• Dopamine (D2).
• Histamine (H1).
• Serotonin (5HT3).
Other neurotransmitter:
• Gamma-Aminobutyric acid (GABA).
• Substance P (Neurokinin 1 Receptor/NK1).
• Cannabinoid type 1 (CB1).
• Endogenous opioids.

Main Receptors in the CTZ Zone:

• Dopamine (D2)
• Serotonin (5-HT3)
• Substance P (Neurokinin 1 Receptor (NK1)
• Cannabinoid type 1 (CB1)

Neural pathways project from the CTZ to the nucleustractus solitarius and the
reticular formation of the medulla oblongata, which is the location of the
vomiting center (VC).

CTZ Zone:
• Most medications that induce nausea affect the chemoreceptor trigger zone.
• In addition, biochemical changes and electrolyte abnormalities.
• Treatment should focus on agents that affect dopamine and serotonin.

Gastrointestinal Tract:
• In the stomach, there are pits and glands that have enterochromaffin cells.
• This cells have chemoreceptors that release serotonin and dopamine which
activates the vomiting center via the vagus nerve (CN X).
• There are also mechanoreceptors trigger by constipation/obstruction, gastric
stasis, or infections which also activate the vomiting center.

Labyrinth and Vestibular Nucleus:

• Inside the labyrinth is the vestibule, which is important for balance.
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• Abnormalities trigger the vestibular cochlear nerve (VIII) which goes to the brain
stem to an area called Vestibular Nuclei located in the Pons.
• Vestibular Nuclei have receptors for Histamine (H1) and Acetylcholine
(Muscarinic receptors ), which ultimately activates the vomiting center to triggers
the vomiting reflex.
• Triggers: motion sickness, Benign paroxysmal positionalvertigo, tumors,
medications (opioids), infection (e.g Meniere's disease).
• Treatment should focus on agents that affect histamine and acetylcholine.

Medications that often cause nausea and vomiting:

1. Cancer chemotherapy e.g. cisplatin. 6. Metformin.

7. Anti-parkinsonians e.g., bromcryptine, L-DOPA
2. Analgesics e.g. opiates, NSAIDs.
8. Anti-convulsants e.g., phenytoin,
3. Anti-arrythmics e.g. digoxin, carbamazepine
quinidine 9. Anti-hypertensives.
10. Theophylline.
4. Antibiotics e.g. erythromycin 11. Anesthetic agents.
5. Oral contraceptives

Assessment
Assessment history
• Establish whether the resident is vomiting
• Description of the vomiting
• What precipitates nausea and vomiting?
• Is there a pattern?
• What eases the nausea and vomiting?
• Check for constipation
Nausea and Vomiting Key Historical
Questions
• How long?
• Relationship to meals?
• Contents of vomitus?
• Associated symptoms
• Pain in chest or abdomen, fever, myalgia, diarrhea, vertigo, dizziness,
headache, focal neurological symptoms, jaundice, weight loss

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• Diabetes?
• When was last menstrual period?
Nausea and Vomiting Key Physical
Findings
• Vital signs. • Abdominal exam.
• Cardiopulmonary exam. • Neurological exam including
• Rectal exam. fundus exam (papilledema).
Laboratory studies guided by history
and physical
• Electrolytes, glucose, BUN/ • Liver Function Tests.
Creatinine. • Pregnancy test.
• Calcium, albumin, total serum • Urinalysis.
proteins. • Serum lipase? amylase.
• Complete blood count (CBC).
Radiology studies guided by history
and physical
• Plain abdominal films.
• Abdominal ultrasonography.
• CT if pain is key feature.
• Head CT or MRI if severe headache, papilledema, marked hypertension,
altered mental status, or focal neurological findings.
Endoscopic examination
• Upper GI endoscopy: to separate high duodenal obstruction from peptic
ulcers or gastroparesis.

Treatment of nausea and vomiting

◼ General guidelines include:
1. Identify and treat underlying cause, whenever possible.
2. Identify contributing factors.

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3. Provide temporary symptomatic relief of the symptoms.

4. Use preventive measures when vomiting is likely to occur (e.g. cancer
chemotherapy, parenteral opiate administration).
5. Treat complications regardless of cause e.g., replace salt, water, potassium
losses.

Treatment
Non-pharmacological therapy
• Correct reversible causes.
• Environmental factors: fresh air, absence of offensive smells
• Ingest non-odourous foods, eat slowly small amounts frequently.
• Avoid lying flat before and after meals.
• Avoidance of emetogenic smells and foods.
Oral care
• Maintaining good mouth care is important part of management.
• Water and toothpaste.
• Small soft brush.
• Soaking dentures in weak non-toxic solution.
• Artificial saliva e.g. oral balance.
Pharmacological management
If cause is gastrointestinal If cause is affected by If cause is intracranial with
(poor gastric emptying) use of: psychological issues: pressure related to tumor:
‐ Prokinetic agent. ‐ Diazepam. ‐ Dexamethasone.
‐ Metoclopramide. ‐ Alprazolam. ‐ Haloperidol.
‐ Domperidone. ‐ Lorazepam. ‐ Cyclazine.

Drugs with anti- emetic properties and known mechanisms

• Antihistamines, e.g., meclizine (miclizigo) esp. for vestibular disorders
• Anticholinergics, e.g., scopolamine (Transderm Scop, Donnatal) esp. for
vestibular and GI disorders
• Dopamine antagonists, e.g. metoclopramide (primperan) or prochlorperazine
(emedrotec) esp. for GI disorders
• Selective serotonin-3 (5HT3) RAs, e.g. odansetron (Zofran),
granisetron (emetovoid) to prevent chemotherapy induced
nausea/vomiting

Complications of Vomiting:
• Nutritional.
• Adults: weight loss.
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• Kids: failure to gain.

• Cutaneous: petechia, purpura.
• Orophayngeal: (dental, sore throat).
• Esophagitis/ esophageal hematoma.
• GE Junction (MW) tears rupture.
• Metabolic electrolyte, acid-base disturbance, water loss(dehydration).
• Renal, prerenal azotemia, ATN, hypokalemic nephropathy.

Summary:
‐ Nausea and vomiting are features of many GI and non-GI diseases.
‐ Regardless of its cause, treatment of nausea and vomiting should initially
focus on replacing volume and electrolyte deficits. Later on, nutritional
deficitsmust be addressed.
‐ Nausea and vomiting can cause several life-threatening GI and non-GI
complications.
‐ Elucidation of the cause is often possible, and treatment of the underlying
cause will usually be successful.
‐ Effective symptomatic therapies for nausea and vomiting are available
when the cause is unclear or when the treatment of the underlying cause
takes time to work.
‐ Nausea and vomiting can occur independently.
‐ Important to identify and treat reversible causes.
‐ There is Pharmacological and non- pharmacological therapies.

MCQ

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MCQ
◼ which of the following is accessible to emetogenic stimuli in
blood or CSF, rich in D2receptors and opioid receptors?
a) Chemoreceptors Trigger Zone (CTZ).
b) CNS/ Vestibular system.
c) Vagal and spinal afferent nerves from GIT.
d) Limbic system.
◼ which of the following is associated with motion sickness?
a) Chemoreceptors Trigger Zone (CTZ).
b) CNS / Vestibular system.
c) Vagal and spinal afferent nerves from GIT.
d) Limbic system.
◼ Serotonin 5-HT3 Antagonist are used for:
a) Chemotherapy induced N/V.
b) Post operative.
c) Radiation therapy.
d) a and c.
e) all of the above.
◼ Which of the following require dose adjustment for hepatic
dysfunction:
a) Ondansetron (zofran).
b) Granisetron.
c) Dolaseetron.
d) Palonosetron.
e) All of the above.
◼ Which area of the brain is responsible for control of chemically
induced vomiting?
a) Vomiting center
b) Medulla
c) Cerebral cortex
d) Chemoreceptor Trigger Zone

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◼ Which of the following dose not require dose adjustment for renal
dysfunction
a) Ondansetron (zofran).
b) Granisetron.
c) Dolaseetron.
d) D) Palonosetron.
e) All of the above.
◼ A patient who is about to undergo there 3rd cycle of
chemotherapy develops sever nausea and vomiting one night
prior to her next round of chemotherapy. which of the following is
the best description of the type of nausea and vomiting this
patient is experiencing:
a) Acute CINV.
b) Delayed CINV.
c) Anticipatory nausea and vomiting.
d) Breakthrough nausea and vomiting.
◼ Which of the following medication would be considered first line
in the prevention of nausea and vomiting related to motion
sickness?
a) Cetirizine.
b) Ginger.
c) Scopalamine.
d) Ondansetron.

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Gastroesophageal reflux disease (GERD)

Definitions
2007:
Reflux of gastric content to Cause troublesome symptoms or
complications

2015:
Troublesome symptoms sufficient to:
• -Impair individual's quality of life
• -Cause injury
• -Cause complications
That result from the retrograde flow of gastric contents
Into the esophagus, oropharynx, and/or respiratory tract.

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Types
o Physiological: in neonates.
o Functional: after heavy meals.
o Pathological: primary or secondry.

pathological
1ry 2ry
Reflux of gastric contents into A case in which an underlying
esophagus (GERD) condition may predispose to acid
reflux. eg: asthma,any cause of
increase IAP

Factors leads to reflux:

o Gastric contents.
o Functional disorders. creates reflux
o Anatomical disorders.

o Gastric acid pocket

o Psychological disorders
o Genetics AGGREVATES REFLUX
o Acid hypersensetivity

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o ACID(HCL)
o PEPSIN
Gastric contents:
o FOOD
o BILE

o anatomical site of LES

Anatomical o HAITAL HERNIA
disorders: o GASTRIC SHAPE

o length,pressure,relaxation, of LES
o ESOPHAGEAL CLEANING
Functional
o GASTRIC EMPTYINg
disorders:
o BILE REFLUX

Gastric acid
pocket:

o -Heavy meals
o -Medications: Motility inhibition
o - Nocturnal DGE(delayed gastric emptying)
Others: o -Diseases: DM
o - Obesity
o - Smoking
o -Stress

◼ Q/Role of LES in preventing GERD?

A/ length,pressure,relaxation, and anatomical site

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Presentation
troublesome
• Classic(Esophageal) symptoms. • Extra-esophageal
• Esophageal complications . symptoms(complications).
• Quality of the life complications

classic symptoms:
1) heartburn (not related to severity of the disease).

2) Regurgitation

3) water brush

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Esophageal complications:
1-Erosive Complications Bleeding
• Erosive esophagitis is initial step of esophageal complications
• Can cause bleeding but usually mild
• LA classification(los angelos):

2-Stricture Complications Dysphagia

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3-Barrett’s esophagitis Cancer

◼ Barrett’s esophagus is defined as an esophagus in which any

portion of the normal distal squamous epithelial lining has
been replaced by metaplastic columnar epithelium,
which is clearly visible endoscopically (≥1 cm) above the
GOJ (gastroesophageal junction) and confirmed
histopathologically from esophageal biopsies.

◼ BE is diagnosed in 7% to 10% of individuals with chronic

GERD and is estimated to be present in 1% to 2% of the
general adult population. The incidence of EAC
(esophageal adenocarcinoma) continues to be among the
fastest rising incidence cancers in the Western population.

◼ BE, a premalignant condition for esophageal

adenocarcinoma (EAC) about 0.3%
BE progresses to invasive EAC through stages of intestinal
metaplasia (nondysplastic BE [NDBE]), low-grade
dysplasia (LGD), to high-grade dysplasia (HGD), to
intramucosal carcinoma, and finally to invasive EAC.

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RISK FACTORS OF BE:

◼ The known risk factors of BE include the following:
1. Chronic (>5 years) GERD symptoms
2. Advancing age (>50 years)
3. Male gender
4. Tobacco usage
5. Central obesity
6. Caucasian race
7. first-degree relatives of BE.
◼ Alcohol consumption does not increase risk of BE

Screening for BE:

• Men:
▪ Chronic (>5 years) symptoms GERD.
▪ Two or more risk factors for BE or EAC:
- Age >50 years.
- Caucasian.
- Presence of central obesity.
- Current or past history of smoking.
- Confirmed family history of BE or EAC.
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• FEMALES:
Given the substantially lower risk of EAC with chronic GER
symptoms, screening for BE in females is not recommended.
• General population:
-Screening of the general population is not recommended.
Extraesophageal complications:
1. Pulmonary problems:
• Asthma.
• Chronic bronchitis.
• Pulmonary fibrosis.
• Aspiration pneumonia.
• Sleep apnea.
• Chronic cough.
2. ENT:
• laryngitis Is The Most Common ENT Complication.
hoarseness of voice (10% Of Persons ).
• otitis, Sinusitis, Pharyngitis, Vocal Cord Granulomas .
• subglottal Stenosis.
• laryngeal Cancer.
3. Atypical Noncardiac Chest Pain (60% Of Case).
4. Dental problems:
• Dental erosions
Quality of life complications:
• 75% of patients with GERD reported that their symptoms affected sleep.
• 40% stated that nighttime heartburn impaired daily functioning the
following day.
• Unable to enjoy meals.
• Reduced overall productivity.
• Altered social well-being.
• Altered emotional well-being.

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Diagnosis
• Start treatment with: life style modification and PPI
before meals (Drug of choice). e.g: ILAPRAZOLE-
DEXALANSOPRAZOLE-ESOMEPRZOLE-PANTOPRAZOLE-
RABEPRAZOLE-LANSOPRAZOLE-OMEPRAZOLE
Clinically proven
• Standard dose: Once/ twice e daily For 8 weeks
(typical symptoms)
-Improvement : Stepdown
-If no improvement : Switch the drug
-If no improvement after switching : investigations
• In case of Dysphagia.
• Stricture or hiatus hernia may be the cause.
Radiological
• There’s no role of US or CT as they cannot capture
study.
tubes.
(barium
swallow
study)

• Test of choice for initial assessment.

• Differentiate between:
Endooscopy.
-EROSIVE OR NON-EROSIVE.
-GARDING OF DISEASE.
-ASSESSMENT OF THE CARDIA.
-EXCLUSION OF COMPLICATIONS.
MOST specific test.
Esophageal PH- Indications:
impedance test. -NERD.(non erosive reflux disease).
-normal endoscopy.
-pre-operative.
Esophageal
Manomtery.

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Indications of investigations:

PERSISTENT RECURRENT
SYMPTOMS. SYMPTOMS.

ALARMING SYMPTOMS:
‐ Age > 55 years
‐ Dysphagia
ATYPICAL ‐ Odynophagia
SYMPTOMS. ‐ Iron deficiency anemia
‐ Weight loss
‐ Hemorrhage (including melena
or coffee round emesis)

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Treatment
• Treatment of GERD:
1. life style modification and PPI before meals (Drug of choice).
e.g: ILAPRAZOLE-DEXALANSOPRAZOLE-ESOMEPRZOLE-PANTOPRAZOLE-
RABEPRAZOLE-LANSOPRAZOLE-OMEPRAZOLE
Standard dose: Once/ twice e daily For 8 weeks
-Improvement : Stepdown
-If no improvement : Switch the drug

2. Other Medications:
-Antacids : locally.
-H2- blocker: H2 receptors.
-Prokinetics : gastric emptying.
-Digestant.

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• Treatment of complications:
1. Erosive complications:
-PPI is main treatment.
-sometimes need intervention, endoscopic hemostasis.
-Rarely need more than endoscopic treatment as surgery.

2. Stricture:
-endoscopic dilatation.
-self-expandable stents.
-surgical esophageal replacement.

3.BE:
Patients with BE should receive once-daily PPI therapy. Routine use of
twice-daily dosing is notrecommended, unless necessitated
because of poor control of reflux symptoms or esophagitis.
Chemoprevention
Therapy: Asprin or NSAIDs should not be routinely prescribed to patients with
BE as an antineoplastic strategy.Similarly, other putative
chemopreventive agents currently lack sufficient evidence and should
not be administered routinely

1-Endoscopic mucosal resection(EMR):

• Patients with nodularity in the BE segment should undergo
endoscopic mucosal resection of the nodular lesion(s) as the
initial diagnostic and therapeutic maneuver,Histologic
assessment of the EMR specimen should guide further
therapy.
• In subjects with EMR specimens demonstrating HGD (high
grade dysplasiaL, or IMC (intra-mucosal carcinoma),
Endoscopic
endoscopic ablative therapy of the remaining BE should be
therapy: performed.
2- Endoscopic ablative:
• Endoscopic ablative therapies should not be routinely applied
to patients with nondysplastic BE because of their low risk of
progression to EAC.
• Endoscopic eradication therapy is the procedure of choice for
patients with confirmed LGD (low grade dysplasia), and
confirmed HGD.
Surgery.

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Peptic Ulcer Disease

Incidence
• High due to NSAIDs ( at most of patients ).

Definition
• An ulcer is defined as disruption of the mucosal integrity of the stomach
and/or duodenum leading to a local defect or excavation due to active
inflammation.

Peptic Ulcers:
• Gastric & Duodenal

Symptoms of peptic ulcer

Pain in epigastric area (acute mostly ‘may be chronic /
burning sensation / mostly referred to back).

PUD Demographics
Higher prevalence in developing countries:
H. Pylori is sometimes associated with socioeconomic status and poor hygiene
In the US:
• Lifetime prevalence is 0%.
• PUD affects million annually.
• Hospitalization rate is pts per 100,000 cases.
• Mortality rate has decreased dramatically in the past 20 years.
• approximately 1 death per 100,000 cases.

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Comparing Duodenal and Gastric Ulcers:

DUODENAL GASTRIC
4x as common as
gastric sites
most common in common in late middle
middle age age
peak 30-50 years incidence increases with age
Male to female ratio 4:1 Male to female ratio 2:1
more common in
More common in patients
patients with blood
with blood group A
group O
H. pylori infection Less related to H. pylori
Common up to 95% (80%)

◼ Q: The least place that can develop malignancy at the git is

small intestine,why?
• Answer: due to high count of lymphoid tissue ( high immunity ).

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• GUS (Gastric Ulcers) can represent a malignancy.

• Benign GUS are most often found distal to the junction between the antrum
and the acid secretory mucosa.

Etiology:
• Additional aggressive factors include smoking, ethanol, bile acids, aspirin,
steroids, and stress.
• NSAIDs act as COX inhibitor decreaseing of PG low
protection of gastrointestinal mucosa.
• Important protective factors are mucus, bicarbonate, mucosal blood flow,
prostaglandins, hydrophobic layer, and epithelial renewal.
• Increased risk when older than 50 d/t decrease protection.
• When an imbalance occurs, PUD might develop.

Pathophysiology
• H. pylori infection - virtually always associated with a chronic active
gastritis.

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Symptoms:
• Pain:
Site:epigastric area Onset:mainly acute but may be chronic
Character: gnawing, aching, or burning Radiation: to the back.

- Duodenal ulcers: occurs 1-3 hours after a meal and may awaken patient from
sleep. Pain is relieved by food, antacids, or vomiting.

-Gastric ulcers: food may exacerbate the pain while vomiting relieves it.

• Nausea, vomiting, belching, dyspepsia, bloating, chest discomfort, anorexia,

hematemesis, &/or melena may also occur. (Important investigations
mainly upper endoscopy).
• nausea, vomiting, & weight loss more common with Gastric ulcers.

Signs:
• May be absent
• Epigastric tenderness.
• Signs of complications if present

Complications:
• Perforation & Penetration into pancreas, liver and retro-peritoneal space.
• Peritonitis.
• Bowel obstruction, Gastric outflow obstruction, & Pyloric stenosis.
• Bleeding--occurs in 25% to 33% of cases and accounts for 25% of ulcer deaths.
• Gastric CARCINOMA.

Differential Diagnosis
‐ Neoplasm of the stomach. ‐ Acute Cholecystitis.
‐ Acute Pancreatitis. ‐ Gastritis.
‐ Pancreatic cancer. ‐ GERD.
‐ Peptic ulcer . ‐ MI ( mostly inferior ) —not
‐ Non-ulcer dyspepsia (also to be missed if having
called functional. chest pain ( character
‐ dyspepsia). help with diagnosis).
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 Diagnostic Plan
◼ Stool: for fecal occult blood.
◼ Labs: CBC (R/O bleeding), liver function test, amylase, and lipase.
◼ H. Pylori can be diagnosed by urea breath test, blood test, stool
antigen assays(standard), & rapid urease test on a biopsy
sample.
◼ Upper Gl Endoscopy: Any pt >50 yo with new onset of symptoms
or those with alarm markings including anemia, weight loss, or Gl
bleeding.
◼ Preferred diagnostic test b/c its highly sensitive for dx of ulcers and
allows for biopsy to rule out malignancy and rapid urease tests for
testing for H. Pylori.

Treatment Plan: H. Pylori

Medications: Triple therapy for 14 days is considered the

treatment of choice.

• Proton Pump Inhibitor + clarithromycin and amoxicillin.

• Omeprazole (Prilosec): 20 mg PO bid for 14 d OR
• Lansoprazole (Prevacid): 30 mg PO bid for 14 d OR
• Rabeprazole (Aciphex): 20 mg PO bid for 14 d OR
• Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
• Clarithromycin (Biaxin): 500 mg PO bid for 14 and
• Amoxicillin (Amoxil): 1 g PO bid for 14 d
• OR ( FLUROCONAZOLE or METRONIDAZOLE ) FOR 10 DAYS IN CASES OF
RESISTANCE + NANAZOXIDE AS ALTERNATIVE.
◼ Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN (penicilin).
◼ In the setting of an active ulcer, continue qd proton pump inhibitor therapy for
additional 2 weeks.
• Goal: complete elimination of H. Pylori. Once achieved reinfection rates are
low. Compliance!

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 Treatment Plan: Not H. Pylori
• Medications: treat with Proton Pump Inhibitors or H2 receptor antagonists to
assist ulcer healing.
‐ H2 blocker: Tagament, Pepcid, Axid, or Zantac for up to 8 weeks.
‐ PPI: Prilosec, Prevacid, Nexium, Protonix, or Aciphex for 4-8 weeks.
• Lifestyle Changes:
- Discontinue NSAIDs and use Acetaminophen for pain control if possible.
- Acid suppression—Antacids.
- Smoking cessation.
- No dietary restrictions unless certain foods are associated with problems.
- Alcohol in moderation:
➢ Men under 65: 2 drinks/day.
➢ Men over 65 and all women: 1 drink/day.
- Stress reduction.
• Surgery:
People who do not respond to medication, or who develop
complications surgery is done:
• Vagotomy - cutting the vagus nerve to interrupt messages sent from the
brain to the stomach to reducing acid secretion.
• a Antrectomy - remove the lower part of the stomach (antrum), which
produces a hormone that stimulates the stomach to secrete digestive juices.
A vagotomy is usually done in conjunction with an antrectomy.
• a Pyloroplasty - the opening into the duodenum and small intestine
(pylorus) are enlarged, enabling contents to pass more freely from the
stomach. May be performed along with a vagotomy.

Prevention
Consider prophylactic therapy for the following patients:
• Pts with NSAID-induced ulcers who require daily NSAID therapy.
• Pts older than 60 years.
• Pts with a history of PUD or a complication such as Gl bleeding.
• Pts taking steroids or anticoagulants or patients with significant comorbid
medical illnesses.

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 Prophylactic regimens that have been shown to dramatically
reduce the risk of NSAID-induced gastric and duodenal ulcers
include the use of a prostaglandin analogue or a proton pump
inhibitor.
• Misoprostol (Cytotec) 100-200 mcg PO 4 times per day.
• Omeprazole (Prilosec) 20-40 mg PO every day.
• Lansoprazole (Prevacid) 15-30 mg PO every day.

Evaluation/FoIIow-up/Referrals
H. Pylori Positive: retesting for tx efficacy
• Urea breath test—no sooner than 4 weeks after therapy to avoid false
negative results
• Stool antigen test—an 8 week interval must be allowed after therapy.

H. Pylori Negative: evaluate symptoms after one month.

Patients
who are controlled should cont. 2-4 more weeks.
If symptoms persist then refer to specialist for additional
diagnostic testing.

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 Esophageal motility disorders

Normal Phases of Swallowing:

• Voluntary:
- Oropharyngeal phase bolus is voluntarily
moved into the pharynx.
• Involuntary:
- UES relaxation.
- peristalsis (aboral movement) .
- LES relaxation .
• Between swallows
- UES prevents air entering the esophagus during inspiration and prevents .
esophagopharyngeal reflux .
- LES prevents gastroesophageal reflux.
- peristaltic and non-peristaltic contractions in response to stimuli.
- capacity for retrograde movement (belch, vomiting) and decompression.

Motility Disorders :

• Upper esophageal • Primary disorders

o UES disorders o achalasia
o neuromuscular disorders o diffuse esophageal spasm.
• Esophageal body o nutcracker esophagus
o achalasia o nonspecific esophageal
o diffuse esophageal spasm. o dysmotility
o nutcracker esophagus • Secondary disorders
o nonspecific esophageal o severe esophagitis
o dysmotility o scleroderma
• LES o diabetes
o Achalasia o Parkinson's
o hypertensive LES

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 Diagnostic tools:
• Cineradiology or video fluoroscopy (MBS).
• barium esophagogram.
• esophageal manometry.
• endoscopy.

Upper Esophageal Motility Disorders

• Pharyngoesophageal neuromuscular disorders:
‐ stroke.
‐ Parkinson's.
‐ poliomyelitis.
‐ ALS.
‐ multiple sclerosis.
‐ diabetes.
‐ myasthenia gravis.
‐ dermatomyositis and polymyositis.
• Upper esophageal sphincter (cricopharyngeal) dysfunction .

Symptoms: oropharyngeal dysphagia (transfer dysphagia):

- patients complain of difficulty swallowing.
- tracheal aspiration may cause symptoms.

UES Disorders
• Cricopharyngeal hypertension:
o elevated UES resting tone.
o poorly understood (reflex due to acid reflux or distension)
• Cricopharyngeal achalasia:
o incomplete UES relaxation during swallow
o may be related to Zenker's diverticula in some patients.

Clinical manifestations:
o localizes as upper (cervical) dysphagia.
o within seconds of swallowing
o coughing, choking, immediate regurgitation, or nasal regurgitation.

Diagnosis: swallow evaluation & modified barium swallow

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 Motility Disorders of the Body & LES
• Disorders:
o Achalasia.
o diffuse esophageal spasm (DES).
o nutcracker esophagus.
o hypertensive LES.
o nonspecific esophageal dysmotility:
▪ hypomotility.
▪ Hypermotility.

symptoms: usually dysphagia (intermittent and occurring

with liquids & solids).
diagnostic tests:
o barium esophagogram.
o endoscopy.
o esophageal manometry.

Achalasia:
• It’s a dual disorder:
o LES fails to appropriately relax.
o resistance to flow into stomach.
o not spasm or LES but an increased basal LES pressure
often seen (55-90%).
o loss of peristalsis in distal 2/3 esophagus.
Epidemiology:
o 1-2: 200,000 of people .
o Age: 25 to 60.
o Sex: equal.
o Caucasians > others.

Pathology:
o loss of ganglionic cells in the myenteric plexus (distal to proximal).
o vagal fiber degeneration.
o Underlying cause:

32
 o unknown..autoimmune? (antibodies to myenteric neurons in 50% of
patients)

Clinical presentation:
o solid dysphagia 90-100% (75% also with dysphagia to liquids).
o post-prandial regurgitation 60-90%.
o chest pain 33-50%.
o pyrosis 25-45%.
o weight loss.
o nocturnal cough and recurrent aspiration.

Diagnosis:
o plain film (air-fluid level, wide mediastinum, absent gastric bubble,
pulmonary infiltrates).
o barium esophagogram (dilated esophagus with taper at LES) good
screening test (95% accurate).
o endoscopy (rule out GE junction tumors, esp. age>60).
o esophageal manometry (absent peristalsis, LES relaxation, & resting
LES >45 mmHg).

Treatment:=> Reduce LES pressure and increase emptying

o Nitrates and calcium channel blockers:
▪ 50-70% initial response; at 1 year.
▪ limitations: tachyphylaxis and side-effects.
o Botulinum toxin (prevents ACH release at NM junction):
▪ 90% initial response; 60% at I year.
o Pneumatic dilation (disrupt circular muscle):
▪ 60-95% initial success; 60% at 5 years.
▪ recent series suggest 20-40% will require re-dilation.
▪ risk of perforation 1-13% (usually 3-5%); death 0.2-0.4%.
o Surgical myotomy (open or minimally invasive):
▪ >90% initial response; 85% at IO years; 70% at 20 years (85% at 5.
▪ years with min. inv. techniques).
▪ <1% mortality; <IO% major morbidity.
▪ 10-25% acutely develop reflux, up to 52% develop late reflux.

33
 Spastic Motility Disorders of the Esophagus
Epidemiology:
o any age (mean age 40).
o female > male.

Symptoms:
o dysphagia to solids and liquids:
▪ intermittent and non-progressive.
▪ present in 30-60%, more prevalent in DES (in most studies).
o chest pain:
▪ constant % across the different disorders (80-90%).
▪ swallowing is not necessarily impaired.
▪ can mimic cardiac chest pain.
o pyrosis (20%) and IBS symptoms (>50%).
o symptoms and manometry correlate poorly.

Approaches:
• "lumper" approach:
-normal.
-achalasia.
-spastic motility disorder.
• "splitter" approach (radiology and manometry):
-diffuse esophageal spasm.
- nutcracker esophagus.
-hypertensive LES.
-nonspecific esophageal dysmotility.
• "splitting" has not resulted in a clinical benefit.

Diffuse Esophageal Spasm

• frequent non-peristaltic contractions:
o simultaneous onset (or too rapid propagation) of
contractions in two or more recording leads.
o occur with of wet swallows (up to 10% may be seen in
"normals").

34
 Nutcracker Esophagus
• high pressure peristaltic contractions
o avg pressure in 10 wet swallows is >180 mm Hg.
• 33% have long duration contractions (>6 sec)
• may inter-convert with DES(Distal esophageal spasm).

Non specific esophageal

Hypertesnsive LES
dysmotility
• abnormal motility pattern
• high LES pressure >45 mm Hg. • fits in no other category
• normal peristalsis o — non-peristalsis in 20-30% of
• often overlaps with another wet swallows
motilityNdisorders o low pressure waves (<30 mHg)
o prolonged contractions

Diagnosis:
o Manometry.
o barium esophagogram.
o Endoscopy.
o pH monitoring.

Treatment:
o Reassurance.
o nitrates, anticholinergics, hydralazine - all unproven.
o calcium channel blockers - too few data with negative controlled studies
in chest pain.
o psychotropic drugs — trazodone, imipramine and sertraline effective
in controlled studies.
o dilation - anecdotal reports, probable placebo effect.

35
 Hypomotility Disorders:-
• Primary (idiopathic)
o aging produces gradual decrease in contraction strength.
o reflux patients have varying degrees of hypomotility.
▪ more common in patients with atypical reflux symptoms
▪ usually persists after reflux therapy.
o Defined as
▪ low contraction wave pressures (<30 mm Hg).
▪ incomplete peristalsis in 30% or > of wet swallows.
• Secondary
o Scleroderma:
▪ in >75% of patients.
▪ progressive, resulting in aperistalsis in smooth muscle region.
▪ incompetent LES with reflux.
o other "connective tissue diseases":
▪ CREST.
▪ polymyositis & dermatomyositis.
o diabetes:
▪ 60% with neuropathy have abnormal motility on testing (most asx).
o Other:
▪ hypothyroidism, alcoholism, amyloidosis.

Nonischemic Chest Pain

• remains poorly understood (functional chest pain)
• enthusiastic investigation finds numerous associations in studies.
o psychiatric disorders :(depression, panic, or anxiety disorder...)
o esophageal disorders :(GERD, motility disorders...)
o musculoskeletal disorders.
o cardiac disease (microvascular, MVP, tachyarrhythmias...)
• GERD is by far the most common, diagnosable, esophageal cause.
o 50-60% of patients have heartburn or acid regurgitation symptoms
o 50% have abnormal esophageal pH studies (not always correlating to
sxs)
o very low incidence of endoscopic findings
o "PPI Test" may be the best and most cost-effective approach.

36
 • A small subset of patients with non-GERD NCCP display a variety of
esophageal motility disorders.
o symptoms and motility findings correlate poorly.
o esophageal hypersensitivity/hyperalgesia may explain the symptoms.

37
 Practical Approach to Acute
Gastrointestinal Bleeding

GI Bleeding:
• Maybe classified into :
o Upper GI bleeding (proximal to DJ flexure)
▪ Variceal bleeding
▪ Non-variceal bleeding
o Lower GI bleeding (distal to DJ flexure)
• Upper GI bleeding 4x more common than lower GI bleeding
• Emergency resuscitation same for upper and lower GI bleeds

Emergency Resuscitation
Takes priority over determining the diagnosis/cause.
➢ ABC (main focus is ‘C’)
➢ Oxygen: 15L Non-rebreath mask
➢ 2 large bore cannulae into both ante-cubital fossae
➢ Take bloods at same time for FBC, U&E, LFT, Clotting, X match 6Units
➢ Catheterise
➢ IVF initially then blood as soon as available (depending on urgency: O-,
Group specific, fully X-matched)
➢ Monitor response to resuscitation frequently (HR, BP, urine output, level
of consciousness, peripheral temperature, CRT)
➢ Stop anti-coagulants and correct any clotting derangement
➢ NG tube and aspiration (will help differentiate upper from lower GI bleed)
➢ Organise definitive treatment (endoscopic/radiological/surgical)

38
 Estimating Degree of Blood Loss
RR, HR, and BP can be used to estimate degree of blood loss/hypovolemia
Class I Class II Class III Class IV

Volume 0-750 750-1500 1500-2000 >2000

Loss
(ml)
Loss 0-15 15-30 30-40 >40
(%)
RR 14-20 20-30 30-40 >40

HR <100 >100 >120 >140

BP Unchanged Unchanged Reduced Reduced

Urine >30 20-30 5-15 Anuric

Output
(ml/hr)
Mental Restless Anxious Anxious/confused Confused/
State lethargic

Assessment of acute Gastrointestinal Bleeding

Aim of history and examination is 3 fold:
• 1. Identify likely source – upper vs lower – and potential cause .
• 2. Determine severity of bleeding.
• 3. Identify precipitants (e.g. Drugs).
• PC/HPC
• Duration, frequency, and volume of bleeding (indicate
severity of bleeding).
• Nature of bleeding: will point to source.
History • Hematemesis (fresh or coffee ground)/melena suggest
upper GI bleed. (Note a very brisk upper GI bleed can
present with dark or bright red blood PR).
• PR Dark red blood suggests colon.
• PR Bright red blood suggests rectum, anus.

39
 • If PR bleeding, is blood being passed alone or with bowel
opening (if alone suggests heavier bleeding).
• If with bowel opening is blood mixed with the stool
(colonic), coating the stool (colonic/rectal), in the toilet
water (anal), on wiping (anal).
• Ask about associated upper or lower GI symptoms that
may point to underlying cause.
• E.g. Upper abdominal pain/dyspeptic symptoms suggest
upper GI cause such as peptic ulcer.
• E.g. 2. Lower abdominal pain, bowel symptoms such as
diarrhea or a background of change in bowel habit suggest
lower GI cause e.g. Colitis, cancer.
• Previous episodes of bleeding and cause.
• PMH
• History of any diseases that can result in GI bleeding, e.g.
Peptic ulcer disease, diverticular disease, liver
disease/cirrhosis.
• Bleeding disorders e.g. haemophilia.
• DH
• Anti-platelets or anti-coagulants can exacerbate bleeding.
• NSAIDs and steroids may point to PUD.
• SH
• Alcoholics at risk of liver disease and possible variceal
bleeding as a result.
• Smokers at risk of peptic ulcer disease.
• Reduced level of consciousness.
• Pale and clammy.
• Cool peripheries.
• Reduced CRT.
• Tachycardic and thready pulse.
• Hypotensive with narrow pulse pressure.
Examination • Tenderness on abdominal examination may point to underlying
cause e.g. Epigastric → peptic ulcer.
• Stigmata of chronic liver disease (palmer erythema,
leukonychia, dupuytrens contracture, liver flap, jaundice,
spider naevi, gynaecomastia, shifting dullness/ascites).
• Digital rectal examination may reveal melena, dark red blood,
bright red blood.

40
 Upper GI bleed
• Upper GI bleeding refers to bleeding from oesophagus, stomach, duodenum
(i.e. Proximal to ligament of treitz).
• Bleeding from jejunum/ileum is not common.

Presentation
• Acute Upper GI bleeding presents as:
o Hematemesis (vomiting of fresh blood)
o Coffee ground vomit (partially digested blood)
o Melena (black tarry stools PR)
• If bleeding very brisk and severe then can present with red blood PR!
• If bleeding very slow and occult then can present with iron deficiency
anaemia

Causes
Cause of Bleeding Relative Frequency

Peptic Ulcer 44

Oesophagitis 28

Gastritis/erosions 26

Duodenitis 15

Varices 13

Portal hypertensive gastropathy 7

Malignancy 5

Mallory Weiss tear 5

Vascular Malformation 3

Other (e.g. Aortoenteric fistula) Rare

41
 Risk Stratification: Rockall Score
• Identifies patients at risk of adverse outcome following acute upper GI bleed
Variable Score 0 Score 1 Score 2 Score 3

Age <60 60-79 >80 -

Shock Nil HR >100 SBP <100 -

Co- Nil major - IHD/CCF/major Renal

morbidity morbidity failure/liver
failure

Diagnosis Mallory All other GI malignancy -

Weiss tear diagnoses

Endoscopic None - Blood, -

Findings adherent clot,
spurting vessel
• Score <3 carries good prognosis
• Score >8 carries high risk of mortality

Management (Non-variceal)
Emergency resuscitation as already described
Endoscopy
• Urgent OGD (within 24hrs) – diagnostic and therapeutic
o Treatment administered if active bleeding, visible vessel, adherent blood
clot
o Treatment options include injection (adrenaline), coagulation, clipping
• If re-bleeds then arrange urgent repeat OGD.
Pharmacological
• PPI (infusion) – pH >6 stabilises clots and reduces risk of re-bleeding
following endoscopic haemostasis
• Tranexamic acid (anti-fibrinolytic) – maybe of benefit (more studies needed)
• If H pylori positive then for eradication therapy
• Stop NSAIDs/aspirin/clopidogrel/warfarin/steroids if safe to do so (risk:
benefit analysis)

42
 Surgery
• Reserved for patients with failed medical management (ongoing bleeding
despite 2x OGD)
• Nature of operation depends on cause of bleeding (most commonly
performed in context of bleeding peptic ulcer: DU>GU)
• E.g. Under-running of ulcer (bleeding DU), wedge excision of bleeding lesion
(e.g. GU), partial/total gastrectomy (malignancy)

Variceal Bleeds
• Suspect if upper GI bleed in patient with history of chronic liver
disease/cirrhosis or stigmata on clinical examination.
• Liver Cirrhosis results in portal hypertension and development of porto-
systemic anastomosis (opening or dilatation of pre-existing vascular channels
connecting portal and systemic circulations).
• Sites of porto-systemic anastomosis include:
o Oesophagus (P= oesophageal branch of L gastric v, S= oesophageal
branch of azygous v).
o Umbilicus (P= para-umbilical v, S= inferior epigastric v).
o Retroperitoneal (P= right/middle/left colic v, S= renal/supra-
renal/gonadal v).
o Rectal (P= superior rectal v, S= middle/inferior rectal v).
• Furthermore, clotting derangement in those with chronic liver disease can
worsen bleeding.
Management of Variceal bleeds
Emergency resuscitation as already described
Pharmacological
• Somatostatin/octreotide – vasoconstricts splanchnic circulation and
reduces pressure in portal system.
• Terlipressin – vasoconstricts splanchnic circulation and reduces pressure in
portal system.
• Propanolol – used only in context of primary prevention (in those found to
have varices to reduce risk of first bleed).
Endoscopy
• Band ligation.
• Injection sclerotherapy.
43
 Balloon tamponade – sengstaken-blakemore tube
• Rarely used now and usually only as temporary measure if failed endoscopic
management
Radiological procedure – used if failed medical/endoscopic Mx
• Selective catheterisation and embolization of vessels feeding the varices
• TIPSS procedure: Transjugular intrahepatic porto-systemic shunt
o Shunt between hepatic vein and portal vein branch to reduce portal
pressure and bleeding from varices): performed if failed medical and
endoscopic management
o Can worsen hepatic encephalopathy
Surgery
• Surgical porto-systemic shunts (often spleno-renal).
• Liver transplantation (patients often given TIPP/surgical shunt whilst awaiting
this).

44
 Variceal Bleed: Prognosis
• Prognosis closely related to severity of underlying chronic liver disease
(Childs-Pugh grading).
• Child-Pugh classification grades severity of liver disease into A,B,C based on
degree of ascites, encephalopathy, bilirubin, albumin, INR.

• Mortality 32% Childs A, 46% Childs B, 79% Childs C.

Lower GI bleeding
• Lower GI bleed refers to bleeding arising distal to the ligament of Treitz
(DJ flexure)
• Although this includes jejunum and ileum bleeding from these sites is rare
(<5%)
• Vast majority of lower GI bleeding arises from colon/rectum/anus.

Presentation
• Lower GI Bleeding presents as:
o Dark red blood PR – more proximal bleeding point (e.g. Distal small
bowel, colon)
o Bright red blood PR – more distal bleeding point (e.g. rectum, anus)
• PR blood maybe:
o mixed or separate from the stool.
o If separate from the stool it may be noticed in the toilet water or on
wiping.
o Passed with motion or a lone.
45
 • If blood mixed with stool (as opposed to separate from it) suggests more
proximal bleeding.
• If bleeding very slow and occult, then can present with iron deficiency
anemia.

Causes:
Colon Rectum Anus

Diverticular Disease Polyps Haemorrhoids

Polyps Malignancy Fissure
Malignancy Proctitis Malignancy
Colitis
Angiodysplasia
Management:
 Emergency resuscitation as already described.
• Pharmacological
o Stop NSAIDS/anti-platelets/anti-coagulants if safe.
o Tranexamic acid.
• Endoscopic
o OGD (15% of patients with severe acute PR bleeding will have an
upper GI source!).
o Colonoscopy – diagnostic and therapeutic (injection, diathermy,
clipping).
• Radiological
o CT angiogram – diagnostic only (non-invasive).
o Determines site and cause of bleeding.
o Mesenteric Angiogram – diagnostic and therapeutic (but invasive).
o Determines site of bleeding and allows embolization of bleeding
vessel.
o Can result in colonic ischaemia.
o Nuclear Scintigraphy – technetium labelled red blood cells:
diagnostic only.
o Determines site of bleeding only (not cause).

46
 • Surgical
o Last resort in management as very difficult to determine bleeding
point at laparotomy.
o Segmental colectomy – where site of bleeding is known.
o Subtotal colectomy – where site of bleeding unclear.
o Beware of small bowel bleeding – always embarrassing when
bleeding continues after large bowel removed!

Management Flow Chart for Severe lower GI bleeding:

Resuscitate

OGD (to exclude upper GI cause for severe PR bleeding

Colonoscopy (to identify site and cause of bleeding and to treat

bleeding by injection/diathermy/clipping) – often unsuccessful as
blood obscures views.

CT angiogram
(To identify site and Mesenteric angiogram (to
identify
cause of bleeding) site of bleeding and treat
bleeding.
by embolization of vessel)

Surgery

47
 • As 85% of lower GI bleeds will settle spontaneously the interventions
mentioned on previous slide are reserved for:
o Severe/Life threatening bleeds
• In the 85% where bleeding settles spontaneously OPD investigation is
required to determine underlying cause:
o Endoscopy: flexible sigmoidoscopy, colonoscopy
o Barium enema

Iron Deficiency Anaemia

Definition
o Insufficient iron in the body for haemopoiesis
o Decrease Hb and MCV
o Decreased serum iron and Ferritin.
o Increased TIBC and serum transferrin

48
 Causes: -
• Chronic Blood loss
o Think Chronic bleeding (often occult) from
GI tract in men and post-menopausal
 Increased Iron females (pre-menopause menorrhagia
demand most common cause) e.g. Colonic polyp or
cancer, gastric/duodenal ulcer, or
malignancy.
o Chronic hemolysis
❖ Pregnancy
o Diet lacking in iron.
 Insufficient
o Vegans – plant-based iron poorly absorbed
Iron intake
compared to meat-based iron.

❖ small intestinal disease e.g. Crohn’s, coeliac

 Malabsorption
disease
of iron
❖ Lack of vitamin C (important for iron absorption)

• In adults >50yrs of age the most common cause of Iron deficiency anemia is
chronic occult GI bleeding
• In females <50yrs most common cause is blood loss during menses with
inadequate replacement
• In developing world intestinal parasitic infection causing chronic blood loss
from the GI tract is the most common cause of iron deficiency anaemia (rare in
developed world)

Investigation
• To confirm iron deficiency anemia
o Hb, MCV, Ferritin, transferrin, TIBC.
o Rarely bone marrow aspirate (gold standard but invasive: rarely
performed).

• OGD and colonoscopy

o Perform in males and post-menopausal females.

49
 o In pre-menopausal females' menorrhagia is most common cause
and often OGD/colonoscopy not required unless other symptoms
warrant it (e.g. dyspepsia, dysphagia, PR bleeding, change in bowel
habit, family history etc.)

o Note that iron deficiency anemia the only sign of an occult GI

malignancy.

50
 Ulcerative Colitis
Definition:
• IBD: Immune mediated chronic intestinal conditions.
• Ulcerative colitis : Mucosal ulceration in Colon.
• Chron’s disease : Transmural inflammation (Ileitis, ileocolitis, colitis ).

CAUSES OF Ulcerative colitis:

Unknown but may be:
• Immunologic.
• Infection.
• Genetics (Run in families).
Chron’s Ulcerative colitis
• Psychological.
• Diet and smoking.
• Drugs as NSAIDS.
• Others.

Manifestations
Intestinal manifestations
1. Abdominal cramping.
2. Frequent bowel movements : Diarrhea may be bloody or bleeding per rectum.
3. Weight loss.
Extra intestinal manifestations
General Skeletal
1. Fever and tachycardia in severe disease 1. Ankylosing spondylitis : Arthritis in
2. DVT/ PE, intracranial, intraocular joints of spine.
thromboembolic events. 2. Colitic arthritis : Arthritis present with IBD
3. Hepatobiliary complications : primary 3. Sacroiliitis : Arthritis of sacroiliac joint
Sclerosing cholangitis. 4. Osteopenia, osteoarthritis.
4. Renal stone. 5. Avascular necrosis is the death of bone
5. UTI due to fistula. tissue due to a lack of blood supply.

Skin Ocular
1. Uveitis and Episcleritis.
1. Pyoderma gangrenosum.
2. Blurred vision.
2. Erythema nodosum.
3. Eye pain.
3. Sweet syndrome.
4. Photophobia with ocular involvement.

51
Pyoderma gangrenosum Erythema nodosum Sweet syndrome

Differential Diagnosis of IBD

1. Chronic infectious colitis.
2. Ischemic colitis.
3. Diverticulitis.
4. Irritable Bowel Syndrome (in case of bloody diarrhea).
5. Small Bowel Bacterial Overgrowth.
6. Crohn's Disease.
7. Colon Cancer.

Differential Diagnosis of IBD

Perianal lesions common;
Crohn's Disease Frank (rectal) bleeding less common than in UC.

Sudden onset; pathogens present in stool

Infectious colitis Pain may be a predominant feature.

Irritable bowel Meets Rome II criteria for irritable bowel syndrome .

syndrome ‫الدكتور مشرحهاش و قال هتبقو تاخدوها بعد كدا‬
Affects older age groups
Sudden onset, often painful
Ischemic colitis
Other vascular disease often present:
As coronary or intracranial atherosclerosis
Pseudomembranous Recent antibiotic use
colitis Clostridium difficile toxin detectable in stool

52
 Ulcerative colitis Chron’s disease

Frequent small-volume
Diarrhea accompanied by abdominal
Diarrhea diarrhea with urgency
pain and malnutrition
Predominantly bloody diarrhea
Abdominal pain Not present Present
Abdominal mass Not present Present

Perianal lesions Not present Present

Diffuse superficial Discontinuous transmural

colonic inflammation asymmetric lesions
Mainly involving ileum (Terminal part)
Involvement of rectum,
and right-sided colon
but this can be patchy

Shallow erosions and ulcers Cobblestone appearance

Endoscopic and
radiological

Cobblestone

Spontaneous bleeding Longitudinal ulcer

No fissures (Superficial only) Deep fissures

Diffuse inflammation in
Granulomatous inflammation
mucosa or submucosa
Histopathological
Fissures or aphthous ulcers can be
Crypt architecture distortion
seen; often transmural inflammation

Serological Antineutrophil cytoplasmic Anti-Saccharomyces cerevisiae ASCA

markers antibodies (ANCA) other antibodies to microbial antigens

53
 IBD IBS
Less common More common
Epidemiology
Age : 20-30 and 60-70 (bimodal) Prevalence decreased with age.
(UK)
Equally common in male & female Male : Female = 1 : 2
3 groups
Diarrhea. bloody stools. crampy
1. Diarrhea predominant
abdominal pain. fever, weight loss.
2. Constipation predominant
Symptoms fatigue
3. Alternating diarrhea and
Associated with non-gut problems
Constipation
May be Abdominal cramps or Bloating
Blood tests - abnormal Blood tests – normal
Investigations (anemia. raised inflammatory markers)
Colonoscopy and biopsy inflammation Colonoscopy and biopsy - normal

Symptomatic treatment :
• Dietary modification.
• Anti—inflammatory agents
• Antidiarrheal agents
Treatment • immunosuppressive agents
• Anti-spasmodic
• Steroids
• Stool bulking agents
• Anti-depressants
A long-term condition requiring Can affect quality of life but not life
continuous monitoring threatening.

Prognosis Surgery is required in some patients Surgery is never indicated

Increased risk of colorectal cancer No increased risk of colorectal cancer

compared to the normal population

DIAGNOSIS
• UC and CD are generally diagnosed using clinical endoscopic, and histologic
criteria.
• No single finding is absolutely diagnostic for one disease or the other.
• Approximately 20% of patients have a clinical picture that falls between
CD and UC the are said to have Indeterminate colitis.

54
 inflammatory bowel disease
GENERAL
Current Diagnostic Tools for Initial IBD Diagnosis

• History and Physical • Barium Enema

Exam=clinical suspicion • WCE=Wireless Capsule Endoscopy
• Stool studies • EUS=Endoscopic Ultrasound
• Colonoscopy • Pelvic MRI Enterography
• Serology studies • CT Enterography
• Small Bowel Series/SBFT • PET Scan
• WBC Scanning

Common Bloodwork in diagnosing IBD

• C-Reactive Protein Inflammation reflects inflammatory disease activity

initially Can be used as a marker to treatment response
• pANCA= Anti-neutrophil cytoplasmic antibody with perinuclear staining
• ASCA= anti-saccharomyces cerevisiae

Differentiating type of IBD

LaB TEST SENSITIVITY SPECIFICITY TYPE IBD

+ PAN CA 50-65% 85-92% UC
+ ASCA 55-61% • 88-95% CROHN'S
+pANCA&
44-57% 81-97% UC
ASCA -
-pANCA&
38-56% 94-970/0 CROHN'S
ASCA

55
 Etiological
Pathogen Evaluation
Viruses
Stool PCR
Adenovirus ,astrovirus, norovirus,
Tissue biopsy with CMV antigen staining
rotavirus sapovirus ,CMV
Bacteria
Salmonella , shigella, yersinia Stool culture
enterohemorrhagic, E.coli , Stool PCR for toxin genes
campylobacter, Aeromonas
Mycobacteria Tissue acid fast bacilli staining tissue
Tuberculosis culture
Fungi Blood culture tissue biopsy culture
Histoplasma, Coccidioides serology
Protozoa Immunoassay serology
Giardia cryptosporidium,
E.histolytica
Helminths Stool ova and parasite with microscopic
Strongyloid stercoralis , Schistosoma exam

Radiological
Barium Enema Findings In Inflammatory Bowel Disease

56
 Endoscopic findings :

• Endoscopic Severity: UC

Treatment
Goals so treatment:
• Resolution of acute inflammatory processes
• Resolution of complications
• Alleviation of extraintestinal manifestations
• Maintenance of remission

1- Non-pharmacological therapy:
• Avoid antidiarrheal meds, anticholinergics, opiates and NSAIDs.
• Address diet case-by-case.
• Vit D and Ca supplementations in all pts on steroids.
• Surgery case by case
57
 2- Pharmacological treatment:
➢ Corticosteroids
• Severe IBD with hospitalization should be
treated with IV steroids for rapid symptom relief.
• Not a long-term solution
• Convert IV to PO then taper off advised
• Steroid dependence occurs in 28% pts.
• Should be used in combination with AZA/
6-MP +/- cyclosporine for severe IBD symptoms
➢ Cyclosporine
• IV dosing effective for induction of remission in severe UC
• Little efficacy for maintenance of remission
• No data on mucosal healing
• Nephrotoxicity, seizures rare SE
➢ Mesalamines: 5-ASA/Aminosalicylates
• •Aminosalicylates has been the mainstay of
therapy because of its anti-inflammatory activities.
• 50-70% response in high doses for UC.
• Some mucosal healing found.
• Excellent safety profile.
• Not always beneficial. Be quick to move on if patient is not seeing benefit.
• No fistula closure benefits to treatment found.
➢ Different formulations have been released and are thought to target
specific regions of the bowel in oral and rectal formulations:
Sulfasalazine and — Are primarily released in the colon
Balsalazide — Folic acid supplement advised with sulfasalazine
Dipentum and Asacol — Releases in the distal ileum and colon
Pentasa — Releases in the distal colon
Rowasa — Primarily effective in the distal colon and rectum

➢ Thiopurines : Azathioprine/ 6-MP (mercaptopurine)

• up to 6-12 weeks until effective
• Has been shown beneficial in both induction and
• maintenance of remission
• NOT as beneficial a 5-ASA for UC
• Not as many trials for data with UC as with CD
58
 • Some chance of fistula closure with use
• Must monitor CBC and LFTs with use
• Bone marrow suppression
• Liver toxicity possible
➢ Methotrexate
• Used with patients who are allergic or
unresponsive to trial of Thiopurines (6-MP or AZA) at adequate dosing.
• Has been shown to induce and maintain remission.
• Little data to prove fistula closure on this drug
• 1mg Folate supplementation advised
• Monitor CBC and LFTs
— Bone marrow suppression
— Risk of hypersensitivity pneumonitis
— Liver toxicity.

3- Biologic therapy with UC

• Infliximab approved for moderate-severe Ulcerative Colitis
who have had inadequate response to steroids and AZA.
Best results in overall sx reduction and healing with remission for UC.
• Future therapies : Visilizumab, MLN-02, Natalizumab

• Biologic Therapy —vs — Conventional Therapy in IBD

Conventional therapy Biologic therapy

Aimed at symptom relief 25-50% remission sx 1 month

Reduces hospitalizations Reduces hospitalizations

Doesn't reduce long term surgery rates Lowers surgery rates

Doesn't maintain mucosal healing Maintains long term mucosal healing

Fistula closures more often

4- IBD Surgery Treatment

Ulcerative Colitis Surgery Indications

59
 absolute indications: relative indication:
1. Hemorrhage 1. Chronic intractability
2. Perforation 2. Steroid dependency
3. Cancer or dysplasia 3. Growth retardation
4. Systemic complications
4. Unresponsive acute sx associated with UC

Surgery types with UC

• IPAA = Ileal pouch-anal anastomosis.
— Gold standard as "cure" but not without its own complications :
‐ Incontinence, diarrhea, sexual dysfunction, decreased fertility, pouchitis,
cuffitis
• Conventional Ileostomy (Brooke).
• Continent ileostomy (Koch pouch).
• Ileorectal anastomosis.

MCQ

◼ Which of the following is the most common cause of

ulcerative colitis-related mortality?
1. Colonic adenocarcinoma
2. Toxic megacolon
3. Perforated colon
4. Colonic infarction
5. Severe rectal bleeding
◼ Symptoms of ulcerative colitis can include
1. Diarrhea
2. Rectal bleeding
3. Abdominal pain
4. Nausea and vomiting
5. Joint pain
◼ Ulcerative colitis can be cured by
1.Antibiotics
2.Surgery
60
 3.5 ASA
4.Corticoisteroids
5.Biological therapy
◼ What causes ulcerative colitis
1.Intestinal viruses
2.Unknown
3.Contaminated food
4.Intestinal parasites
5.Smoking
◼ Complications of ulcerative colitis can be limited to
1. Colon
2. colon and intestine
3. colon and liver and biliary tree
4. Colon and joints
5. Joints alone
◼ Ulcerative colitis is related to what similar condition
1. Indigestion
2. Acid reflux disease
3. Crohn's disease
4. Celiac disease
5. Diverticulosis
◼ A patient is admitted with ulcerative colitis. In the
physician's notes, it is stated that the patientls barium
enema results showed the patient has colitis that starts
in the rectum and extends into the sigmoid and
descending colon. what type of ulcerative colitis? *
1.Right-sided colitis
2.Proctosigmoiditis
3.Ulcerative rocotitis
4.Left-sided colitis
5.pancolitis
◼ A patient is newly diagnosed with mild ulcerative colitis.
What type of anti-inflammatory medication is typically
prescribed as first-line treatment for this condition?
1.5-Aminosa licylates (Sulfasa lazine)
61
 2.Immunomodulators (Adalimumab)
3.Corticosteroids(Prednisone)
4.Immunosu ressors (Azathioprine)
5.Biological therapy
◼ Which of the following statements about pathology of
Ulcerative colitis (UC) is false?
1. Limited to mucosa & superficial submucosa
2. Cobblestone mucosa
3. Crypt architecture of colon is preserved
4. Basal suggests chronicity
5. Cryptitis and crypt atrophy

◼ Which of the following about investigative features of

Ulcerative colitis (UC) is false ?
1.CRP levels may rise in active disease
2.Orosomucoid levels may rise in active disease
3.Leukocytosis is a specific indicator of disease activity
4.Proctitis or proctosigmoiditis rarely cause rise in CRP
5.Stool calprotectin is high

Short questions
◼ Give an account on DD of UC?
◼ How to investigate a case of UC?

62
 CRHONS DISEASE

Definition:
• Crohn’s disease (CD): is a chronic relapsing inflammatory
condition usually with flare-ups alternating with periods of
remission, and an increasing disease severity and incidence of
complications as time goes on.
• It can affect any part of the gastrointestinal tract from the mouth
to the anus.
Incidence:
• Sex: - Female : Male = 1.2 : 1
• Age: - Biomodal age distribution 20-40Y / 60-80Y
• Jews more affected than non-Jews

Typical Sites Patients Affected

Ileocaecal 45%

Colon 25%
Terminal Ileum 20%
Extensive Small Bowel 5%
Others 5%

63
 Pathology:

• It is characterized by patchy transmural

inflammation.

• The chronic inflammatory process leads of

thickening of the bowel wall and can cause
a narrowed lumen.

• In early CD there are prominent lymphoid

follicles followed by aphthoid ulceration.
Later these progresses to larger deep
fissuring ulcers separated by normal
looking mucosa (cobble-stoning), fibrosis,
structuring and fistulation. These changes
are often segmentally distributed (skip
lesions).

Aetiology:
• Unknown. But may be due to interaction between:
1. Genetic Predisposition.
2. Environmental Factors.
3. Subsequent reactions of immune system.

64
Genetic Factors
• There are 3 mutations on the CARD15 gene on Chromosome 16 that
are associated with some forms of CD. The risk of developing CD in
increased forty-fold if homozygous for all three mutations.
• The mutations appear to alter monocyte recognition of the constituent
flora of the gut. It is possible that functional defects in CARD15 prevent
innate immunity from balancing resistance to the microbes in the gut in
CD patients, leading to uncontrolled inflammation and mucosal damage.
• However the CARD15 mutations only account for 20-30% of cases of
CD and CD is not found in oriental populations who have the
mutations. Therefore this gene is not necessary for CD.
• It is likely that there are other susceptibility genes that influence how
the immune system interacts with the gut flora which may be
discovered in the future. Putative loci have been mapped to
chromosome 12 (IBD2), 6 (IBD3) and 14 (IBD4).
Environmental Factors
➢ A wide range of environmental factors have been found to play a
role:
• Smoking – Patients with CD are more likely to have been smokers
and smoking may worsen CD and increase the risk of
relapse/surgical intervention.
• Diet – Active CD may improve when a normal diet is changed to a
liquid formula diet.
• Bacterial infection – There is some evidence implicating E.coli,
M.paratuberculosis, the measles virus and L. monocytogenesin the
pathogenesis of CD. This data is controversial and requires further
research to clarify.
• Drugs – the oral contraceptive pill has been linked
epidemiologically with CD.
‐ Relapse may be precipitated by NSAIDs.
65
Immune response
• Both the potential genetics underlying CD and the
environmental and host factors surrounding the patient may
be considered as initiating factors for CD, but the exact
etiology is unknown.
• What is known is that mucosal immunity is dysregulated in
CD leading to a prolonged inflammatory response in the gut.
• In CD, a dominant CD4 Th1 reaction is induced. This diagram shows
its mechanism:

Adhesins ( ) are important in assisting the migration of

leukocytes through endothelial cells to the area

Clinical features of Crohn’s Disease:

• The clinical presentation can be very variable depending upon
the site and predominant pathology of that site.

66
 • Major symptoms include:
‐ Diarrhoea (can be bloody with colonic involvement, or
steatorrhoea in small bowel disease).
‐ Abdominal pain
‐ Weight loss
‐ Constitutional symptoms such as malaise, anorexia,
nausea, vomiting and a low-grade fever.

➢ Hey You!!!!!!!! If you need things more complicated : 15% of

patients have no gastrointestinal symptoms at all!

But if you need it easier, the following shows:

The clinical presentations in different sites
• Patients present with pain and/or tender mass
in right iliac fossa with or without diarrhea and
weight loss.
• The nature of the pain can distinguish
between the underlying pathology:
Ileocecal (45%) &
constant pain with fever suggests inflammation
terminal ileum
and abscess; fibrosis/stricture formation has
(20%)
more generalised, intermittent colicky pain with
signs of bowel obstruction.
• CD here can sometimes present as an
emergency with acute right iliac fossa pain
which mimics appendicitis.
• Symptoms such as diarrhoea (mucous/blood),
sense of urgency and occasionally abdominal
Crohns Colitis
pain/malaise.
(25%)
• Similar to ulcerative colitis but less blood in the
diarrhoea.

67
 • Extra-intestinal features are more common in
CD of the colon than CD of the small bowel.
• Very rare.
• The former presents with upper abdominal pain
Gastroduodenal & or dyspepsia with anorexia, nausea and weight
oral (5%) loss.
• The latter presents with mouth ulcers or
induration
• Presents with typical pain, diarrhoea and weight loss
Extensive small in addition to features of malabsorption (e.g.
bowel (5%) steatorrhoea) and anaemia.Due to the malabsorption,
undernutrition is frequently a problem

Complications of CD
1. Perianal complication
• Characterised by perianal pain and/or discharge. It’s due to
fistula, fissure or abscess formation and can be confirmed by
examination. It is not as painful as it looks but sedation is often
needed for sigmoidoscopy.
• Pneumaturia (air bubbles in the urine) and faeculent vaginial
discharge
2. Intestinal Complications
i. Anal and perianal complications
a. Fissure in ano or fistula in d. Perianal or ischiorectal
ano. abscess.
b. Haemorrhoids. e. Anorectal fistulae.
c. Skin tags.
ii. Undernutrition Caused by
a.Reduced food intake. c. Increased protein loss
b. Malabsorption. from inflamed bowel.
d. Increased metabolic
demands of being sick.

68
 iii. Short bowel syndrome:
Develops when extensive bowel resection leads to excessive
malabsorption of fluids, electrolytes and nutrients.
iv. Cancer:
a. With Crohn’s colitis, there is a increased risk of colorectal
carcinoma.
b. There is an small increased risk of rarer small intestinal and anal
cancers occurring in cites of prolonged inflammation.
3. Extra-intestinal complications
There are many systemic associations and complications of CD, most
affecting the liver and biliary tree, joints, skin and eyes:
a) Sclerosing Cholangitis –
occurs in a small
proportion of patients. The
pathogenesis is unknown
and the condition is
characterised by an
inflammatory obliterative
fibrosis of the biliary tree (the white in the diagram->). It
progresses slowly and a liver transplant is the only cure.
b) Ankylosing spondylitis – affects about
5% of patients with Crohn’s colitis. The
patient presents with back pain and
stiffness and the diagnosis can come
years before the CD.
c) Erythema nodosum – occurs in ~8%
of Crohn’s colitis patients when
disease is active. Hot, red tender
nodules appear on the arms and legs
and subside after a few days.

69
 d) Pyoderma gangrenosum – occurs in
~2% of CD patients, starting as a
small pustule, then developing into a
painful, enlarging ulcer, most
commonly on the leg.

e) Others:
i. Episcleritis and uveitis (occuring
in 5% of patients with active disease),
ii. Osteoporosis (as a consequence of chronic inflammation,
malabsortion and treatment with corticosteroids)
iii. Arthropathy.
Diagnosis Crohn’s Disease:

a. Colonoscopy, terminal
ileoscopy & biopsy: These
allow direct visualisation and
allows for a biopsy of the
mucosa to be taken. This is
central to macroscopic and
microscopic diagnosis.
• Radiology and b. Barium follow-through – findings
imaging consistent with Crohn’s
include an
asymmetrical alteration
in mucosal pattern with
deep ulceration and
areas of narrowing or
stricturing.
c. Ultrasound & CT scanning: Can help
define thickness of the bowel and
70
 mesentery and can be
useful to evaluate
disease progress &
chart fistula formation.

a. Haematology: Anaemia
platelet count
ESR suggests an inflammatory bowel
condition.
• Blood tests b. Biochemistry:
C-reactive protein
serum albumin suggests active CD.

‐ Liver biochemistry may be abnormal.

a. Faecal calprotectin: provides accurate

marker of inflammatory activity. Calprotectin
is a neutrophil-derived cytosolic protein that is
resistant to bacterial degradation if present in
the stools provides an accurate index of
• Stool cultures
intestinal inflammatory activity. It is not
routinely available but has the potential to be
a simple, cheap, non-invasive marker.
b. Stool cultures should be done to rule out
infection as a differential diagnosis.

Differential Diagnosis:
Depending site and pathology.
• Acute ileitis: - Yersinia infections.
- appendicitis.
• Bloody diarrhea: (as it sometimes is with colonic CD),
71
 a) Ulcerative colitis.
b) Infective colitis.
c) Colorectal cancer.
d) ischemia or Iatrogenic causes (NSAIDs or antibiotics).

• Abdominal pain, diarrhoea and weight loss

a) Ulcerative colitis.
b) Infective colitis and other forms of colitis.
c) Cancer (of pancreas, colorectal, small bowel lymphomas or
endocrine tumours).
d) Ischaemia coeliac disease and irritable bowel disease.
Management:
•Dietary advice and
• Management is best if a MDT approach is
nutritional support:
adopted, including physicians, surgeons,
including vitamin
specialist nurses, dieticians and
supplementation to counsellors.
counter-act any • Treatment depends upon the disease activity
deficiencies that develop and site but should also be tailored to the
Medical Management clinical presentation and underlying
pathology. The aim in to induce and
• Anti-diarrhoeals maintain remission.
a) Loperamide, • Risk factors outlined earlier (such as
b) Codeine phosphate smoking) should be avoided.
or co-phenotrope. • Full explanation and psychosocial support
c) If the diarrhoea is should be given to the patient as CD is a
lifelong chronic condition and this may not
due to bile acid
be fully understood by the patient at the time
malabsorption, then of diagnosis.
this can be treated • Patient education is very important.
with colestyramine.
• Likely to be beneficial in
inducing remission:
a) Corticosteroids (oral).

72
 b) Aminosalicylates.
c) (azathioprine /mercaptopurine – trade off between
benefits and harms).
d) Methotrexate.
e) Infliximab.
• Likely to maintain remission:
a) Smoking cessation.
b) (Unknown if the following are effective: enteral nutrition, fish oil,
probiotics).

Surgical management
• Indications of Surgery
a) Perforation. e) Abscess (intra-abdo and
b) Haemorrhage (emergency) perianal).
c) For small-bowel f) Fistulas and inflammation
obstruction, unresponsive to medical
d) Crohn's colitis. therapy.
➢ In small bowel CD –
resection with end-to-end anastomosis. •Approximately 80% of
The benefits of strictureplasty to widen a patients with CD will
narrowed lumen are unknown at this time. require surgery at some
➢ In colonic CD – point.
segmental and subtotal colectomy: •The principle of surgery is
1. In a segmental colectomy the part of to conserve as much
the colon affected is removed and an bowel as possible as 60%
end-to-end anastomosis created in of patients need further
remaining colon. surgery.
2. In a subtotal colectomy the ileum is •Surgery is not curative.
sewn/stapled to the sigmoid colon.

73
 Prognosis:
• Mortality
a) The cumulative mortality is approximately twice that of the
general population.
b) Death is primarily due to sepsis, pulmonary embolism and
complications of the surgery or immunosuppressive agents used
as treatments.
• Morbidity
a) The pattern of CD is a lifelong duration with periods of active
disease alternating with periods of remission. The disease
causes significant disability with only 75% of patients being fully
capable of work in the first year of disease and 15% of patients
unable to work after 5-10years of the disease.
b) People with CD are also more at risk of developing certain
cancers and other complications as mentioned under the
clinical features section of this module.
Summary:
• Crohn’s disease is a chronic inflammatory condition of the
gastrointestinal tract characterised by transmural inflammation,
skip lesions and fistula formation.
• It is a recurring condition alternating between active disease and
remission. The disease is more common in males and in the west.
• It is caused by an interaction between genetic susceptibility,
environmental factors and the host immune system.
• The clinical presentation and subsequent treatments depend
upon the site of inflammation and the type of pathology
underlying it. For example, the most common site is the
ileocaecal area which presents typically with pain and/or tender
mass in right iliac fossa with or without diarrhoea and weight loss.
On the other hand oral CD presents with mouth ulcers and
induration.
74
 • Treatment involves a multi-disciplinary team and working closely
with the patient is very important.
• Drug therapies include aminosalicalates, oral corticosteroids ,
Infliximab and Methotrexate.
• Surgical options include small bowel resection or
segmental/subtotal colectomy.

Questions
Epidemiology
True or false.
A). Crohn’s disease effects only the small bowel.
B). Crohn’s disease has a bimodal age distribution.
C). The incidence is decreasing.

ANSWERS
A.FALSE – it can affect any part of the gastrointestinal system
from the mouth to the anus.
B.TRUE – it has two age peaks, one at 20 – 40 years of age, the
other at 60 – 80 years of age
C.FALSE – The incidence is increasing

Pathology
Fill in the blank.
1). Crohn’s disease is characterised by t_______ inflammation.
2). The discontinuous nature of the disease is see as s___ l______.
3). Deep fissuring ulcers separated by normal looking mucosa is
known as c_______ s________.
ANSWERS:
1.Transmural.

75
 2.Skip lesion.
3.Cobble Stoning.
Aetiology & Pathogenesis
Which of the following statements is true:
1. CD is genetically determined.
2. Smoking is a protective factor in the development of CD
3. CD is the result of a complex interaction between genetic
susceptibility, environmental factors and the patients immune
system.
4. The gene suspected to be involved in CD is called CARD16 on
Chromosome 15.
5. In CD a CD4 Th1 immune response is initiated.
6. In CD the gut epithelium has a decreased permeability.

ANSWERS:
1. FALSE – it is a combination of genetics, environmental factors
and immunity.
2. FALSE – Smoking is a risk factor for CD.
3. TRUE.
4. FALSE – It is the CARD15 gene on Chromosome 16!
5. TRUE.
6. FALSE – There is an increased permeability which allows antigens
into the tissues.

76
1 - C; 2 - B; 3 - A; 4 - E; 5 - D
Diagnosis & Management
Fill in the blanks:
1). F________ C_________ although not routinely available, is a good,
cheap, noninvasive marker of disease activity
2). Approximately ___% of patients will require some form of surgery during
the course of their CD.
3). The drugs most commonly used to induce remission are
aminosalicalates, c_________________ (oral), Infliximab and
M_____________.
4). The surgery most applicable for small bowel CD is r_____________
whereas for colonic involvement the most suitable surgical options are
segmental or subtotal c___________.
ANSWERS
1. Faecal Calprotectin
2. 80%
3. corticosteroids (oral), Methotrexate.
4. Resection, colectomy

77
 Mesenteric ischemia

Types of ischemia:
• Acute mesenteric ischemia.
• Chronic mesenteric ischemia.

1- Acute mesenteric ischemia (AMI)

Is a syndrome caused by inadequate blood flow through mesenteric
vessels, resulting in ischemia and eventual gangrene of the bowel wall.
CLASSIFICATION OF (AMI):
I. ARTERIAL:
1- Non occlusive mesenteric ischemia (NOMI)
2- Occlusive mesenteric arterial ischemia:
a- Acute mesenteric arterial embolism (AMAE).
b- Acute mesenteric arterial thrombosis (AMAT).
II. VENOUS:
Mesenteric venous thrombosis (MVT).
Pathophysiology:
• Insufficient blood perfusion of the small bowel and colon.
Whether the occlusion is arterial or venous, hemorrhagic
infarction leading to perforation is thecommon pathologic
pathway.
• Damage to the affected bowel portion may rangefrom reversible
ischemia to transmural infarction with necrosis and perforation.
• As the ischemia persists, the mucosal barrier becomes disrupted,
and bacteria, toxins, and vasoactive substances are released into
the systemic circulation. This can cause death fromseptic shock,
cardiac failure, or multisystem organ failure before bowel
necrosis actually occurs.
• Bowel necrosis can occur in 8-12 hours from the onset of symptoms.

78
 Causes of acute mesentric ischemia
Acute Non occlusive Mesenteric
Acute mesenteric
mesenteric mesenteric venous
arterial
arterial ischemia thrombosis
thrombosis
embolism
1-pre-existing
visceral 1. NOMI is 1-
1-Mural thrombi precipitated by a Hypercoagulability.
after myocardial atherosclerosis severe reduction in
infarction. 2-Tumor causing
2-Atrial thrombi 2-complication of mesenteric
venous
associated with arterial aneurysm perfusion, with
secondary arterial compression or
mitral stenosis spasm from such hypercoagulability
and atrial 3-dissection
causes as cardiac (paraneoplastic
fibrillation. failure, septic syndrome)
4-trauma
shock, hypovolemia.
3-Vegetative 3-Infection, usually
5-thromboangiitis
endocarditis intra-abdominal.
obliterans
(septic emboli). 2. Potent
vasopressors in 4-Venous
6-inflammatory
critically ill patients. congestion from
4-Thrombi formed bowel disease
cirrhosis (portal
at the site of (IBD)
3. Vasoactive drugs hypertension).
atheromatous
plaques. as cocaine.
5-Increased intra-
abdominal pressure
from
pneumoperitoneum
during laparoscopic
surgery.

6-Pancreatitis.

79
 C/P of acute mesentric ischemia:
Acute mesenteric arterial embolism (AMAE)
acute mesenteric arterial embolism (AMAE; ie, embolic AMI) typically
has the most abrupt and painful presentation as a consequence of
the rapid onset ofocclusion and the inability to form additional
collateral circulation. It has beendescribed as abdominal apoplexy
and is sometimes referred to as a “bowel attack”.
Often, vomiting and diarrhea (gut emptying) are observed.

Acute mesenteric arterial thrombosis

‐ A patient with AMAT presents with severe abdominal pain.. The pain
is diffuse, and the patient may report frank blood in the stool.
Symptoms worsen over time.
‐ Typically, these patients typically have a history of atherosclerotic
disease at other sites, such as coronary artery disease (CAD).
Nonocclusive mesenteric ischemia (NOMI)
‐ Nonocclusive mesenteric ischemia (NOMI) occurs more frequently
in older patients. Patients with acute respiratory failure or severe
hypotension fromcardiogenic or septic shock, or else they are taking
vasopressive drugs.
‐ Symptoms typically develop over several days, and patients may
haveexperienced a prodrome consisting of malaise and vague
abdominal discomfort. They may become hypotensive and
tachycardic, with loosebloody stool.
Mesenteric venous thrombosis
‐ Acute or subacute abdominal pain syndrome related to
involvement of the small intestine rather than the colon.
‐ Many patients have a history of one or more of risk factors for
hypercoagulability.

80
 • Fever, hypotension, tachycardia, tachypnea, and
altered mental statusare observed.
• Early in the course of AMI, in the absence of
peritonitis, physical signs are few and nonspecific.
• Tenderness is minimal to non-existent. The
Physical
abdomen may be distended.
examination
• Peritoneal signs develop late, when infarction with
necrosis or perforation occurs. Tenderness
becomes severe and may indicate the location of
the infarcted bowel segment.
• Bowel sounds range from hyperactive to absent.
• Bowel necrosis necessitating bowel resection.
• Sepsis and septic shock.
Complications
• Multiple organ dysfunction syndrome (MODS).
• Death.
1- Basic:
• Complete blood count (CBC).
• Prothrombin time (PT).
• Activated partial thromboplastin time (aPTT).
• International normalized ratio (INR).
• Chemistry studies that may show metabolic
Investigations acidosis, increased amylase levels, or
increased lactate dehydrogenase (LDH) levels.
2- Diagnosis:
• Ultrasonography (U/S):
‐ Ultrasonography and Duplex US is highly
specific (92-100%), but its sensitivity(70-
89%) does not match that of angiography.

81
 • Plain abdominal
radiography:
Patients demonstrated
focally edematous bowel
wall (thumbprinting) or
pneumatosis intestinalis.
nonspecific and include
ileus, small-bowel
obstruction, edematous or
thickened bowel walls.

• CT and angiography:
‐ Conventional Angiography: Angiography has been the standard
for diagnosis and preoperative planning.
‐ CT findings with a specificity greater than 95% for AMI include
SMA or SMV thrombosis, intestinal pneumatosis, portal venous
gas, lack of bowel-wall enhancement, and ischemia of other
organs.
‐ Abdominal CTA is considered by many to be the diagnostic test of
choice if the index of suspicion for MVT is high.
• MRI & MRA.
‐ It is particularly effective for evaluating MVT.
3- To detect the cause :
1- Echocardiography.
2- ECG.
3- Thrombophilia screen.

Treatment:
• Initial Resuscitation and Stabilization.
• All cases of mesenteric ischemia with signs of peritonitis or possible
bowel infarction, regardless of etiology, generally warrant immediate
surgical intervention for the resection of ischemic or necrotic
intestines.
• ACUTE MESENTERIC ARTERIAL EMBOLISM papaverine
infusion , surgical embolectomy and intra-abdominal thrombolysis

82
• ACUTE MESENTERIC ARTERIAL THROMBOSIS papaverine
infusion and arterial reconstruction
• NON-OCCLUSIVE MESENTERIC ISCHEMIA Papaverine
infusion
• MESENTERIC VENOUS THROMBOSIS anticoagulation with
warfarin or heparin, either alone or combined with surgery

2- CHRONIC MESENTERIC ISCHEMIA

Is a condition in which plaque build up in the major arteries including
celiac and superior mesenteric arteries which supply the small
intestine.
Causes and risk factors:
• Causes: atherosclerosis.
• Risk factors: old age > 60 yrs , diabetes , smoking & high
cholesterol levels.
Clinical picture:
• Severe abdominal pain, 15 up to 60 minute after eating and lasting
for 90 minutes.
• Weight loss. • Flatulence.
• Nausea and vomiting. • Constipation.
• Fear to food due to recurrent pain.

83
 Investigations:

Treatment:
• Angioplasty and stenting.
• Bypass surgery.
• Lifestyle changes
‐ Decreasing the risk of atherosclerosis.
‐ Quitting smoking.
‐ Controlling blood sugars in people with diabetes.
‐ Lowering cholesterol levels.
‐ Lowering high blood pressure.
‐ Taking anti-platelet medications, such as aspirin and
clopidogrel (Plavix).

84
 Diverticulosis
Diverticulosis occurs when small, bulging
pouches (diverticula) develop in your digestive
tract.
EPIDEMIOLOGY:
• Overall prevalence - 12% to 49%.
• Increases with age.
• < 10% in those younger than 40 years.
• > 50% to 66% of patients 80 years.
• As common in men and women .
• Men - higher incidence of diverticular bleeding .
• Women - more episodes of obstruction or stricture .
✓ Disease of Western civilization:
‐ Extraordinarily rare in rural Africa and Asia.
‐ Highest prevalence rates united States,Europe, andAustralia.
‐ Increase with urbanization.

Factors That Influence the Risk for Diverticulosis

Increased Risk Decreased Risk
• Increasing age.
• Dietary meat intake. • High dietary fiber intake.
• Living in Western countries (e.g., • Living in predominantly rural
United States,Western Europe, Asian or African countries
Australia). (e.g. Kenya, Jordan, Thailand).
• Connective tissue diseases.

85
 Pseudodiverticula

Conspicuously absent from the

portion of colon between the two
antimesenteric taenia.

Location:
• In Western countries- left colon – 90% -- sigmoid | 15% have right-sided.
• InAsian countries- right-sided.

Spectrum
UNCOMPLICATED DIVERTICULOSIS COMPLICATED DIVERTICULOSIS
• ASYMPTOMATIC DIVERTICULOSIS. (A) DIVERTICULITIS:
• SYMPTOMATIC UNCOMPLICATED • UNCOMPLICATED DIVERTICULITIS
DIVERTICULAR DISEASE. - localized phlegmon.
• COMPLICATED DIVERTICULITIS
- abscess, free perforation with
peritonitis,fistula or obstruction.
(b) Bleeding.

Hinchey Classification of Colonic Diverticular

Perforation
I
• Confined pericolic abscess.

II
• Distant abscess (retroperitoneal or pelvic).

III • Generalized peritonitis caused by rupture of a pericolic or pelvic

abscess (not communicating with the colonic lumen because of
obliteration of the diverticular neck by inflammation).

• Fecal peritonitis caused by free perforation of a diverticulum

IV (communicating with the colonic lumen).

86
 Diagnosis
Plain Films • abnormal in 30% to 50%.
• only water- soluble contrast enemas, such as
Gastrografin, should be used.
• A gentle, single-contrast study should be
Contrast performed and terminated once findings of
Enema diverticulitis are discovered.
Examinations • Findings -- extravasated contrast material with or
without the outlining of an abscess cavity, an
intramural sinus tract, or a fistula.
• Diagnostic procedure of choice for acutediverticulitis
Because diverticulitis is mainly an extraluminal
disease.
Computed • CT criteria for diverticulitis-presence of diverticula
Tomography with pericolic infiltration of fatty tissue (often
appearing as fat stranding),thickening of the colon
wall and formation of abscesses.
• Suspected acute diverticulitis - endoscopy generally
Endoscopy
is avoided (risk of perforation, either from the
instrument itself or from air insufflation).
• Once the acute phase has passed (one to three
months later), a colonoscopy should be electively
performed to exclude competing diagnoses,
particularly neoplasia.

Treatment:
1-Uncomplicated diverticulitis:
(A) Outpatient management – When?
• Mild symptoms.
• No peritoneal signs.
• The ability to take oral fluids.
• Supportive home network.
• These patients should be treated with a clear liquid diet and antibiotics.

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 • Mixed aerobic and anaerobic organism( Escherichia coli, Streptococcus
species, and Bacteroides fragilis ).

(B) Hospitalization- When?

• Elderly.
• Immunosuppressed.
• Severe comorbidities.
• High fever / significant leukocytosis.
• Bowel rest /Intravenous fluid.
• Broad-spectrum intravenous antibiotics should be started.
• If improvement continues, patients may be discharged, but they
should complete a seven- to 10-day course of oral antibiotics.
• Failure to improve with conservative medical therapy warrants a
diligent search for complications, consideration of alternative
diagnoses, and surgical consultation.

2- COMPLICATED DIVERTICULITIS:
• (A) Abscesses:
Small pericolic abscesses (Hinchey stage I).
‐ Noninterventional management- with broad- spectrum antibiotics and
bowel rest.
‐ Continued of abscesses should be considered only in stable patients
who demonstrate unequivocal improvements in pain, fever,
tenderness, and leukocytosis over the first few days of therapy.
‐ Percutaneous catheter drainage.
Hinchey stage II- surgery
• Single operation (resection with primary anastomosis) have become the
preferred surgical approaches.
• Two-stage management - Hartmann procedure.
• CT-guided percutaneous drainage of abdominal abscesses has
assumed a prominent complementary role to surgery.
• It often eliminates the need for a multiple- stage surgical procedure with
colostomy.
Hinchey stages III or IV
• Surgical emergency requires urgentoperative intervention.

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 • (B) Fistula:
• Fewer than 5% of patients.
• Single-stage operative resection with fistula closure and primary
anastomosis could be performed in 75% of patients.
• (C) Obstruction
Obstruction can accompany diverticulardisease either acutely or chronically.

DIVERTICULAR HEMORRHAGE
• Most common identifiable cause of significant lower gastrointestinal bleeding
(30% to 40% of cases).
• Western patients/ Asian patients - right- sided.
• Intimal thickening and medial thinning of the vasa recta as it coursed over the
dome of the diverticulum.
• Segmental weakening of the artery, thus predisposing to its rupture.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated in lower
intestinal, and specifically diverticular, bleeding.

CLINICAL FEATURES:
• Abrupt, painless hematochezia.
• Arterial, the volume of blood usually is moderate or large.
• Patients often pass red or maroon clots; melena is unusual.
• Neither a positive fecal occult blood test nor iron- deficiency anemia should be
attributed to diverticular hemorrhage.
• Bleeding ceases spontaneously in 70% to 80% of patients.
• Rebleeding rates range from 22% to 38%.

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 DIAGNOSIS AND TREATMENT
• Resuscitation
• If bleeding is massive or if the patient remains unstable after attempted
resuscitation, early angiography to attempt bleeding localization and
surgical consultation should be obtained.
• A stable patient with suspected active or recent diverticular bleeding should
undergo bowel preparation for a colonoscopy.
• If diverticula are found but bleeding has stopped and no other colonic
causes are found, a presumptive diagnosis of diverticular hemorrhage is
made and the patient should be instructed to avoid NSAIDs and
anticoagulants, if possible.
• As noted, most patients with diverticular hemorrhage do not rebleed.
• The endoscopic identification of active bleeding.
• Stigmata of recent hemorrhage stigmata—visible vessel or adherent clot
within a diverticulum.
• The use of epinephrine injection alone or in combination with other therapies
such as heater probe coagulation, bipolar coagulation endoclips,fibrin
sealant,and band ligation .

• If endoscopic therapy is not effective or durable, localizing the site

facilitates directed therapy with angiography or segmental surgical resection.
• When active bleeding is present but colonoscopy fails to allow localization or
treatment of a bleeding source, further evaluation with nuclear scintigraphy
(tagged red blood cell scan) or angiography can be undertaken.

• Surgery for lower intestinal bleeding usually is avoided unless endoscopic or

angiographic therapies are unavailable or fail.

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 Portal hypertension

Portal vein anatomy:

• The portal vein is formed in front of IVC and behind the neck of the
pancreas ( at the level of 2nd lumber vertebra ) by union of the splenic
& SMV.
• It is 7-8 cm in length & contains no valves.
• It courses in the lesser omentum posterior to both the common
hepatic artery & common bile duct.

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 Causes of portal hypertension
A) Pre-hepatic (portal vein obstruction):
1- congenital atresia or stenosis.
2- thrombosis of portal vein.
3- thrombosis of splenic vein.
4- Extrinsic compression (e.g , tumor).
B) Intra-hepatic:
1- liver cirrhosis →sinusoidal & post-sinusoidal.
2- bilharzial periportal fibrosis →obstruction is pre-sinusoidal.
• causes of portal hypertension in cirrhotic patients:
Causes of portal
-Diminution of the total vascular bed by obliteration,
hypertension :
distortion, & compression of sinusoids.
due to Increased
-Compression of the tiny radicals of portal & hepatic veins
resistance to
by excessive fibrosis.
flow:
-Development of multiple arteriovenous shunts between
the branches of the hepatic artery & portal vein.
C) Post-hepatic causes:
1- Budd-Chiari syndrome ( hepatic vein thrombosis ) >
prominent ascites hepatomegaly & abdominal pain.
2- Veno-occlusive disease.
3- Cardiac disease:
• constrictive pericarditis.
• valvular heart disease.
right heart failure
Causes of A) Arterial-portal venous fistula.
portal B) Increased splenic flow:
hypertension 1- Banti's syndrome
due to ( liver disease secondary to splenic disease,
Increased result from cirrhosis & other hepatic
portal disorders)
blood flow: 2- Splenomegaly (e.g tropical splenomegaly,hematologic
diseases).

Sequelae & Clinical picture:

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 1- Porto-systemic collaterals:
-In normal conditions > collapsed.
-In portal hypertension > engorged > divert blood away from the portal circulation.
❖ The important sites of these collaterals:
a) At the lower end of oesophagus:
▪ Between Oesophageal tributaries of Lt gastric vein (portal) - Oesophageal
tributaries of hemiazygous vein (systemic).
b) Around the umbilicus:
▪ Para umbilical vein (portal) - Superior & inferior epigastric veins (systemic).
c) Lower rectum & analcanal:
▪ Superior rectal vein (portal) - Middle & Inferior rectal veins (systemic)
d) At the back of the colon:
▪ Rt & Lt colic veins (portal) - Rt & Lt renal veins (systemic)
e) Retroperitoneum:
▪ Tributaries of superior & inferior mesentric veins { Retzius } (portal) - Posterior
abdominal & subdiaphragmatic veins (systemic)

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 2- Splenomegaly:
➢ The most constant physical finding.
➢ In 80% of patients regardless the cause.
-In Bilharzial cases : at 1st due to reticuloendothelial hyperplasia
due to absorption of bilharsial toxins.
-With progress of portal hypertension-- > due to congestion.
3- Congestion of the whole GIT:
Leads to anorexia, dyspepsia, indigestion, and malabsorption.
4- Bleeding varices.
5-Ascites (multifactorial):
-Portal hypertension alone cannot cause ascites.
-Hypoalbuminaemia > below 3 gm/100 ml.
-Salt &water retention > high level of aldosterone,oestrogens & anti-duretic
hormone.
-Increased lymphatic transudation from liver surface.

Investigations

-Hypoalbuminaemia.
(The liver is the only site of albumin synthesis).
Assessment of -ALT & AST are moderately raised.
liver function -Prothrombin time and concentration are
tests disturbed.
(This test is the most sensitive liver function).

-Fibreoptic upper endoscopy

-Barium swallow can visualize varices in
Detection of 90% of cases.
esophageal o They appear as multiple, smooth, rounded filling
varices o defects (honey-comb appearance)
-Duplex scan can show dilated portal vein

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 and collaterals.
-Blood picture :
anaemia, leucopenia, thrombocytopenia or
pancytopenia.
Detection of -Bone marrow examination : hypercellularity.
splenic -Radioactive isotope studies :
sequestration and using the patients own RBCs tagged with 51Cr
hypersplenism --> diminished half life of RBCs & increased
radioactivity over the spleen.

-Immunological tests for hepatitis

Diagnosis of the markers.
aetiology of liver -Liver biopsy after assessment of
disease prothrombin time and concentration.

Management of oesophageal varices:

1-Admission: The patient should be admitted to hospital.

2-Resuscitation:
- A wide bore cannula is inserted.
- A blood sample is taken.
- Restoration of blood volume should be rapid.
- Overexpansion of the circulation should be avoided.
- Morphine and Pethidine are contraindicated.

3-Correct coagulopathy : Vitamin K is administered intravenously.

4-Prevent encephalopathy :
- Repeated enemas.
- Oral lactulose “ This is a disaccharide sugar, fermented by the intestinal flora lactic -
acid combines with ammonia” .
- Neomycin 0.5 gm every 4 hours can reduce the bacterial flora.

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 5- Sclerotherapy :
- Intra- or Para- Variceal.
- 1-3 ml sclerosant (ethanolamine oleate).
- Occludes venous channels.
- Multiple sessions (2 weekly).
- Control bleeding in 80-95%.
- About 50% rebleed.
- 30% complication rate..
Complications of Sclerotherapy :
LOCAL : Ulceration , Stricture , Retrosternal discomfort for few days , Perforation.
SYSTEMIC : Fever, Pneumonitis , CNS.
6- Endoscopic Banding :
- Occludes venous channels.
- Sessions < sclerotherapy.
- Same results as sclerotherapy.
- ↓ complications vs sclerotherapy.
- Endoscopic treatment of choice.
7- Vasopressin:
- vasoconstriction of the splanchnic circulation.
Disadvantages :
- colicky abdominal pains, & diarrhoea.
- anginal pains, so it is contraindicated in the elderly.
- Produce temporary control of bleeding in about 80% of cases.
- To prolong its action it is combined with glycine .
8- Somatostatin:
- lower the intravariceal pressure without significant side effects.
- Initial bolus 100 microgram continuous infusion of 25 microgram / h for 24 hs.
9- Beta blocker :
-reduce bleeding by reduce cardiac output.
-Does 20-60 mg bid 25% in HR.
-Reduces 40% of bleeding episodes.
Does not reduce mortality.

10- Balloon tamponade by Sengestaken or Linton tube :

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 ‐ The gastric balloon is inflated first by 200 ml of air, and pulled upwards to press the
gastric fundus.
‐ If bleeding continues, the oesophageal balloon is inflated.
‐ The pressure in the oesophageal balloon should not exceed 40 mm Hg.
‐ This therapy is effective in controlling bleeding in 80-90% of cases.
Disadvantages :
‐ Discomfort to the patient.
‐ -The patient cannot swallow his saliva
‐ -Liability to cause oesophageal ulceration or
stricture.
‐ -Once the tube is deflated, there is liability to
rebleeding in 60-80% of patients.
‐ “Balloon tamponade is only used as a temporary
measure before sclerotherapy or surgery.”
11- Emergency surgery :
‐ If all the previous measures fail to stop bleeding, surgery is recommended by
Trans-jugular Intra-hepatic Porto- Systemic Shunt (TIPSS).
‐ If the general condition of the patient is satisfactory splenectomy, portoazygos
disconnection and stapling of the oesophagus..
‐ If the patient is not very fit stapling alone can be performed.
‐ Does not reduce mortality.
◼ Indications of TIPSS :
‐ Refractory bleeding.
‐ Prior to transplant.
‐ Child C.
‐ Refractory ascites.
◼ Main early complications of TIPSS :
Perforation of liver capsule which cause massive haemorrhage.

12- Treatment of patients with history of bleeding oesophageal varices:

1- Repeated sclerotherapy until the varices are obliterated is the first choice.
2- Elective surgery is mainly indicated if sclerotherapy failed to stop recurrent
attacks of bleeding provided that they are fit.

13- Total shunt operations :

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 “The idea of these operations is to lower the portal pressure by shunting the
portal blood away from the liver”:
a-Porta-caval operation :
very efficient in lowering the portal pressure so no bleeding occurs from the varices.
disadvantages:
Deprives the liver of portal blood flow →
accelerates the onset of liver failure.
Recurrent hepatic encephalopathy in 30- 50%
of patients.
b-Proximal spleno-renal shunt:
◼ indicated if the portal vein is thrombosed or
if splenectomy is indicated due to
hypersplenism.
◼ The incidence of encephalopathy is less than after porta caval shunt.
◼ it is less effective In preventing further bleeding.
◼ If the splenic vein is less than 1 cm the anastmosis is liable to thrombosis.
c-Mesocaval (Drapanas shunt):
◼ insertion of a a synthetic graft as dacron, or autogenic vein between the
superior mesenteric vein and inferior vena cava.
◼ The incidence of thrombosis is high.
d- Selective shunt (Warren shunt):
◼ The Rt and Lt gastric vessels are ligated.
◼ The proximal end of splenic vein is ligated while the distal end is anastomosed
to the left renal vein.
◼ The short gastric veins are preserved and will selectively decompress the lower
end of the oesophagus.
◼ The incidence of encephalopathy is low, and the liver functions remain normal.
e- Porta azygos disconnection operations:
◼ There are many techniques for performing devascularization.
Hassab Khairy operation:
splenectomy & ligation of the Rt and Lt gastric vessels, the short gastric
vessels and the vascular arcade along the greater curvature of the stomach
leaving only the right gastroepiploic vessels.

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 Pancreatitis

Definition: Pancreatic inflammatory Disease .

◼ May be classified into: acute and chronic pancreatitis.

Acute pancreatitis:
Acute inflammatory process of the pancreas that can range from mild
interstitial pancreatitis to severe necrotizing pancreatitis.
• The most common GI disease requiring acute admission to hospital.
• An unpredictable and potentially lethal disease.
Etiology:
• Gallstones (45%) = biliary pancreatitis = gallstone pancreatitis .
• Alcohol abuse (20 %) .
• Idiopathic 10-30 % .
• Medication:
(azathioprine, sulfonamides, tetracycline, valproic acid, thiazide,
estrogens) .
• Endoscopic retrograde cholangiopancreatography (ERCP) = PostERCP
pancreatitis.
• Others : Hypercalcemia. hypertriglyceridemia, infections, Genetic
mutations. -autoimmune pancreatitis, trauma ( blunt or
postoperative).
Diagnosis:
• Symptoms :
Abdominal pain; the major symptom:
◼ Constant and steady
◼ Epigastric , left upper quadrant or peri umbilical, referred to
the back.
◼ Increased on supine position, Decreased by sitting and leaning
forwards.
◼ Vary from mild to severe.
◼ Associated with nausea, vomiting and abdominal distention
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 • General Examination:
◼ Low grade fever, tachycardia, hypotension or even shock
(exudation of blood and plasma protein into retroperitoneal space with
hypovolemia).
◼ Left pleural effusion.
(Reduced breath sounds and stony dull chest percussion suggest a pleural
effusion).
◼ Jaundice.

• Local abdominal examination

◼ Abdominal tenderness with distention.
◼ May be voluntary guarding or rigidity.
◼ Abdominal ecchymoses around umbilicus (Cullen's
sign) and in both flanks (Turner’s sign) → indicate
severe necrotizing pancreatitis with hemoperitoneum .
◼ Diminished or absent bowel sounds if ileus (due to chemical
peritonitis).
• Laboratory investigations :
◼ Elevated Serum amylase and or serum lipase
(s. amylase return to normal even with continuous inflammation after
2-3 days, but serum lipase remains elevated for 7-14 days ).
◼ Leukocytosis, hyperglycemia, hypocalcemia, hypertriglyceridemia.
◼ Increased serum bilirubin and ALP.
◼ High ALT and AST may indicate biliary etiology.
◼ High LDH , low serum albumin & high hematocrit > 44%
(hemoconcentration) indicate more severe disease with poor
prognosis.
• Imaging investigations :
◼ Abdominal ultrasound : to evaluate the gall bladder for stones.
◼ Contrast enhanced CT : for detailed evaluation of
pancreas and surrounding structures ( necrosis ,
collections , pseudocyst , tumors , vascular
thromboses).
◼ MRCP : for noninvasive evaluation of pancreatico-

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 biliary ductal system ( small stones).
◼ EUS : for better visualization of pancreatico-biliary ductal
system and pancreatic parenchyma.
Criteria for diagnosis of acute pancreatitis
The diagnosis of acute pancreatitis isbased on the fulfilment of
two of three criteria:
(1) Upper abdominal pain.
(2) Elevated serum amylase or lipase (or
both) of at least three times the upper
limit of normal .
(3) Findings consistent with acute pancreatitis on imaging
(contrast enhanced CT [CECT], MRI, or abdominal ultrasound).
Complications
• Local complications:
1- The most frequent local complications associated with acute
pancreatitis are pancreatic or peripancreatic fluid
collection.
2- pancreatic pseudocyst.
3- gastric outlet dysfunction.
4- splenic or portal vein thrombosis.
• Pancreatic collection:
1- Interstitial pancreatitis :
◼ Contain a homogeneous liquid content.
◼ Collections resolve spontaneously over time.
◼ If these collections persist beyond 4 weeks after onset of acute
pancreatitis, they are referred to as pancreatic pseudocysts .
2- Necrotizing pancreatitis:
◼ Contain variable amounts of fluid and necrotic debris.
◼ Necrosis can involve the pancreatic parenchyma alone but is
often accompanied by the presence of peripancreatic necrosis.
◼ When acute necrotic collections mature and
encapsulate, usually after 4 weeks, they are referred to
as walled-off necrosis.
• Systemic complications :
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 1- Pulmonary : ARDS , respiratory failure.
2- Cardiovascular : shock.
3- Renal: Renal failure.
4- CNS : psychosis , fat embolism and encephalopathy.
5- Hematological : DIC.
6- Gastrointestinal : bleeding.

• Classification according to severity

◼ Mild: no local or systemic complications .
◼ Moderate : local complications or systemic complications, and in
the absence of persistent organ failure.
◼ Severe : persistent single or multiple organ failure, which is
associated mortality rates between 20% and 40%

◼ .

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 Differential diagnosis of acute severe upper abdominal pain:
1) Perforated peptic ulcer.
2) Acute cholecystitis.
3) Acute intestinal obstruction .
4) Mesenteric vascular occlus.ion.
5) Acute myocardial infarction.
6) Pneumonia.
7) DKA.

Treatment
◼ Symptom control.
◼ Fluid replacement .
◼ Early enteral feeding .
◼ Close observation
◼ Antibiotics as needed.
◼ Intervention in certain circumstances
◼ Fluid resuscitation
• Rate : Intravenous fluid therapy with 5–10 mL/kg per h
• Type : Ringer's lactate solution should be the preferred
choice.
◼ Pain treatment and Nutrition:

• Analgesic (NSAIDs ,Opioid , epidural

anesthesia) according to degree of
pain.
• Enteral tube feeding and early oral
feeding should be initiated after 48
hours.
◼ Role of ERCP and antibiotics in treatment

• ERCP is only indicated in patients with biliary

pancreatitis and concomitant cholangitis •
◼ Antibiotics: only in confirmed or clinically suspected secondary
infection .

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 ◼ Management of local complications

The majority of patients with sterile ( with no secondary

infection ) pancreatic or peripancreatic necrosis and fluid
collections as well as pancreatic pseudocyst can be
treated conservatively because most of them will resolve
spontaneously over time .

◼ Interventional treatment

1) Infected necrotizing pancreatitis:

• Secondary infection of peripancreatic necrosis
nearly always requires invasive intervention.
• Step-up treatment:
- Broad-spectrum antibiotic therapy.
- Percutaneous catheter drainage.
- Endoscopic drainage.
- Minimally invasive necrosectomy.

2) Pancreatic pseudocyst
• Indicated if pancreatic pseudocyst causes gastric
outlet obstruction or refractory pain or larger than 6
cm in diameter.
• Treatment by either Endoscopic or surgical drainage.

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 Prevention of recurrence:
◼ Approximately 20% of patients with acute
pancreatitis develop recurrent attacks of
pancreatitis. After mild biliary pancreatitis,
cholecystectomy during the same hospital
admission is strongly advised to prevent disease
recurrences.
◼ Other important risk factors for recurrence of acute
pancreatitis, as well as for progression to chronic
pancreatitis, are alcohol consumption and
smoking. Alcohol abstinence after the first disease
episode protects against recurrence of disease.

105