Upper gastrointestinal

bleed
Prepared by;
Siti Nazhatul
Raudhah Azurien
Nurul Atiqah
Poncius
Siti Rashidah

History
Mr L, 58 years old, chinese, male came
to the casualty with a chief complain
of;
I. Lower abdominal pain for 2 days
II. Passing out black stool on the day
of admission
III. Coffee ground vomitus on the day of
admission

 Mr L was well until 2 days prior to admission where

he started to felt pain at the lower part of the
abdomen
Site: suprapubic region
Onset: sudden
Character: dull and persistent
Radiation: no radiation to any part of the body
Associated symptom : no associated
Aggravating factor : none
Relieving factor: none
Severity: 3/10

 On the day of admission, after

waking up from sleep, he realised
there is changes in the colour of his
stool.
It was black tarry dark stool.
Foul smelling
The stool was soft
No mucus or fresh blood seen

 after passing the black stool, at

around 8am, he had 1 episode of
vomiting painless, large amount of
coffee ground vomitus.
He was unsure if the vomitus
contains food particles because of its
colour.
The vomitus smells like blood

 Otherwise, he had no shortness of breath,

no palpitation, no dizziness, no weakness of
the limbs, no chest pain, no giddiness, no
fever, no early satiety and no dyspepsia.
He also does not have any decrease in
appetite or any reduce in weight.
He has no comorbidities.
No history of blood transfusion.
He was not on any medication such as
steroids, aspirin, NSAIDS.

 He is a chronic drinker since high school

where he usually drink 4-5 bottles of alcohol
per week and he drank 2 bottles of alcohol
the night before he experienced melena and
haematemesis
He smoked 1 box per day (12 cigarrete)
since 30 years ago.
He is not an intravenous drug user
No history of multiple sex partner
Never had tatoo

Systemic review
Respiratory
System
No shortness of
breath
No wheezing
No hemoptysis
No cough

Cardivascular
System

No
No
No
No

chest pain
dyspnoea
palpitation
ankle swelling

Gastrointestinal
System

Genitourinary
System

No constipation
No diarrhea
bowel habit was
normal-once daily,
soft in consistency
No loss of appetite
No wight loss

No pain during
micturation
No change in color
of urine
No urgency or
incontinence

Nervous System

No LOC
No vertigo
No giddiness
No feeling of
numbness
No blurring of
vision

MSSK
No muscle pain
No joint pain

 No past medical and past surgical history

Family history: Mr L is unsure of any illness
that runs in the family and he was unsure if
there is anyone having the same problem.
Social history: He was divorced 2 years ago.
He has 4 daughters and all of them stay with
his wife. He now stays in Bercham with his
friends. He works as a laundry van driver.

General Examination
Mr L was conscious, alert
and not in pain.
Hand
The palms were moist and
warm
IV cannula on the left
dorsal part of the hand
Capillary refilling time <2
secs
There is no palmar
erythema and no muscle
wasting
No clubbing, no koilonychia
or leukonichia

Head & mouth

The conjunctiva is
pale.
No yellowish
discolouration of the
sclera
Lips were moist and
hydrated
No glossitis, angular
stomatitis

General Examination
No palpable lymph nodes
No neck swelling
No pedal edema
Vital signs
PR : 104 bpm regular rhythm, good volume
RR : 18 breath per min
Temperature : 37 oC
BP : 104/69 mmHg

Abdominal Examination
Inspection
Abdomen is not
distended
Abdomen moves with
respiration
No visible peristalsis
The umbilicus in
inverted and lies in
the midline
No scars visible on the
abdomen
No dilated veins

Palpation
Abdomen is soft
and non tender
No guarding, no
rebound tenderness
the liver is palpable
Spleen is not
palpable
Kidneys are not
ballotable

Abdominal Examination
Percussion
Liver span is about
14cm right
midclavicular line
Resonance traube
space
No shifting dullness

Auscultation
Bowel sounds were
present and normal
No renal bruit

SYSTEMIC EXAMINATION
CARDIOVASCULAR SYSTEM
No chest deformity, no visible median sternotomy
scars, no visible pulsation.
No raised in JVP
No radial-radial delay, radial-femoral delay.
Apex beat is palpable at 5th intercostal space in
the left midclavicular line, no paratsternal heave or
visible thrill.
S1,S2 heard normally.
No murmur.

SYSTEMIC EXAMINATION
RESPIRATORY SYSTEM
1)Shape of the chest is normal (elliptical), AP
diameter is less than tranverse diameter, no
scars, no dilated veins, trachea is in midline and
not shifted, chest movement and expansion is
symmetry.
2)Tactile fremitus is equal on both sides.
3)Percussion is resonance and equal on both
sides.
4)Vesicular breath sound is heard, equal air
entry, no added breath sound such as crackles

SYSTEMIC EXAMINATION
CENTRAL NERVOUS SYSTEM
All are intact.

PROVISIONAL DIAGNOSIS
Upper gastrointestinal bleed

DIFFERENTIAL DIAGNOSIS

Oesophageal varices
Oesophagitis
Peptic ulcer
Carcinoma of stomach

INVESTIGATIONS

FULL BLOOD COUNT

WBC

15.0

0-11.0

Hemoglobin

8.7 g/dl

13.0-18.0

Hematocrit

29.1 %

40-52

MCV

98.5 FL

76.0-96.0

MCH

29.5 PG

27.0-32.0

MCHC

29.9 G/DL

30.0-35.0

RDW

14.9

13.0-14.4

TRBC

2.95

5-6.5

Platelet

175

0-400

Neutrophil

10.54

0-7.0

Lymphocyte

3.13

0-3.0

Monocyte

1.28

2-10

Eosinophil

0.005

0.2-0.5

Basophil

0.045

0.2-0.1

LIVER FUNCTION TEST

RESULT

NORMAL RANGE

Total protein

64

64-83 G/L

Total bilirubin

21.1

1-17 UMOL/L

Alkaline phosphatase

116

40-129 U/L

Albumin

33

35-52 G/L

Aspartate transaminase

85

0-40 U/L

Alanine transaminase

60

0-41U/L

Globulin

31

Haemolysis

No

COAGULATION PROFILES
RESULTS

NORMAL RANGE

Prothrombin time

19.5

12.3-14.3 sec

INR

1.66

Activated partial
thrombin time (APTT)

31.7

28.8-45.3 sec

Oesophagogastroduodenoscopy (OGDS)

Results:
3 columns of grade 2-3 oesophageal
varices
Banding was done
No fundal varices
No blood seen

Other investigation

BUSE
Renal profile
Ultrasound of abdomen
Hepatitis B and C screening

FINAL DIAGNOSIS
UGIB secondary to oesophageal
varices grade 2-3

MANAGEMENT

RESUSCITATION

Secure airway, breathing and circulation

Nil per oral
Obtain IV access
Group and cross match at least 2 units of blood
Administer vitamin K, 10 mg
Antibiotics prophylaxis (IV Rocephine 1gm/day)
Administer IV saline/ packed red cells to
replace blood loss.
Bladder catheterisation performed for
assessment of end organ perfusion.

DEFINITIVE TREATMENT
Endoscopic banding
Vasopressin (IV Telepressin 2mg stat)

UPPER
GASTROINTESTINAL
BLEEDING

 Bleeding of GIT proximal to

ligament of treitz
Ligament of treitz:- a
fibromuscular band which extends
from right crus of diaphragm to
duodenojejunal flexure

ETIOLOGY
NON-VARICEAL BLEEDING
(80% of cases)

VARICEAL BLEEDING
(20% of cases)

1. Peptic ulcer diseases (3050%)

2. Mallory-Weiss tears (15-20%)
3. Gastritis or duodenitis (1015%)
4. Esophagitis (5-10%))
5. Arteriovenous malformations
(5%)
6. Tumours (2%)
7. Others (5%)

1. Gastroesophageal varices
(>90%)
2. Hypertensive portal gastropathy
(<5%)
3. Isolated gastric varices (Rare)

Sabiston Textbook of Surgery,

18th ed

PAIN
1. Peptic ulcer diseases
2. Acute gastric erosion
3. Oesophagitis

NO PAIN
1. Carcinoma of stomach
2. Esophageal varices

1. Mallory-Weiss
tears
2. AV malformations

UPPER GI BLEEDING
PAINFUL
ACUTE

1. Acute
gastric
erosion

CHRONIC

1.
Peptic
ulcers

Gastric ulcer
Pain at Rt HC
++ by eating
--- by vomitting
(loss appetite)
*weight - thin

PAINLESS
HEARTBUR
N

1.
Oesophag
itis

Duodenal
ulcer
Pain at
epigastrium
++ by fasting
--- by food
(hunger pain)
*weight - Fat

ESOPHAG
EAL
VARICES

POLYPS

Due to
portal
hypertensio
n
PRE
Hepatic

STOMACH
CANCER

-Age (elderly)
-Family hx
-Early satiety
-LOW/LOA

HEPATIC

Hepatitis
B&C

POST
Hepatic

Alcohol

COAGULATI
ON

Bleedin
g
disorder
s

Bailey & Loves Short Practice of Surgery,

25th ed

INDICATION FOR
BLOOD TRANSFUSION
1.
2.
3.
4.
5.

Systolic BP <110mmHg
Postural hypotension
Pulse >110/min
Haemoglobin <8g/dL
Angina or cardiovascular disease
with haemoglobin <10g/dL

INDICATION FOR
EMERGENCY SCOPE
1. Vomit blood on the day of admission,
still continue blood in the ward with low
blood pressure
2. After transfuse blood the blood
pressure still low

Peptic Ulcer Disease

Definition
Disruption of the mucosal integrity of the
stomach/ duodenum or both, caused by
local inflammation/ decreased mucosal
resistance/ hyper acidity which leads to a
well-defined mucosal defect (ulcer).
Gastric ulcers are due to decreased
resistance of gastric mucosa. (older
patients)
Duodenal ulcer is predominantly occurs

Etiology
Helicobacter pylori infection.
- Do not invade cells (only mucous membrane)
- Breakdown urea to form ammonia result in
breakdown of mucosal defense.
Non-steroidal anti-inflammatory drugs (eg. Aspirin,
Ibuprofen)
Stress
Cigarette smoking, alcohol, spicy food.

Pathophysiology
Predisposing factors, including H.pylori
infection of mucosa
Acid pepsin attack and/ or breach of
mucosal protection
Acute
inflammation
Destruction of
mucosa
Mucosal
ulceration
Extension through submucosal layers
causing deep ulceration
Erosion of
Perfora
Continue
major
tion
bleeding from
vessel
mucosal
Massive
Periton
surface
Iron
hemorrhage
itis
deficiency
(hematemesis

Granulation
tissue
formed and
attempts at
repair
Chronic
and
relapsing

Duodenal vs Gastric Ulcer

Duodenal Ulcer

Gastric Ulcer

More common
Occur in the 1st part of
duodenum
Fibrosis may lead to
pyloric stenosis.
Can be more than 1
duodenal ulcer at a time.
Ant. Ulcer tends to
perforate & post. Ulcer
tends to bleed.

Less common
Occur near the lesser
curvature.
Fibrosis may lead to hour
class contraction of
stomach.
Large chronic ulcers may
erode posteriorly into
pancreas or into major
vessels such as the
splenic artery.

Cont.
Duodenal ulcer

Gastric ulcer

Pain before meal.

Pain while eating.
Relieved by taking
food, milk.

Relieved by vomiting

Clinical Features
Epigastric pain( described as boring, gnawing
or burning), intermittent and radiates to back
(in case penetrating the pancreas).
May described as indigestion or dyspepsia
Bitter regurgitation : esophageal reflux &
duodenal ulceration
Hematemesis and melaena.

Investigations
H.Pylori testing
Non invasive:
Serology tests to detect IgG antibodies
13C-urea breath test
Stool antigen test

Invasive:
Rapid urease test: during endoscope using CLO test
kits and results received within 3 hours
Biopsy urease test added to a substrate containing
urea and phenol red.
Histology: on Giemsa stain

Cont.
Oesophageal gastro-duodeno scopy (OGDS)
- View the ulcer and take biopsy
- Non malignant ulcer : sharp, punched out
defect, overhanging mucosal border with a
smooth and clean ulcer base.
- Malignant ulcer will be >2cm, bleeds on
touch, irregular margin with slough on the
floor.

Management
1. Control the predisposing or aggravating
causes

Modify diet
Reduce alcohol intake
Quit smoking
Avoid irritant and ulcer-provoking drugs
(aspirin & other NSAIDs),
Avoid stress,
Reduce oesophageal reflux by losing weight
and attention to posture

2. Elimination of proven H. pylori

infection
Triple therapy: consists of two
antibiotics (amoxicillin, clarithromycin,
and/or metronidazole) plus a PPI
(omeprazole, pantoprazole) for 10 to 14
days.

3. Medical treatment
PPI: omeprazole
H2 receptor antagonists (ranitidine,
famotidine and roxatidine)

Gastric Carcinoma
Worldwide, the fourth most
common cancer and the
second most common cause
of death.

Risk Factors
Nurritional
Low fat and
protein
consumption
High salted
meat or fish
High nitrate
consumption

Environmental
& social
Poor drinking
water
Radiation
exposure
Occupational
(coal mining,
rubber or
asbestos
related
Low
socioeconomi
c group
Smoking
Family
history of
gastri cancer

Medical
H. Pylori
infection
Prior gastric
surgery
Gastric
atrophy and
gastritis,
adenomatous
polyps
Blood group
A
Pernicious
anaemia

Signs &
Symptoms
Indigestion
Nausea or vomiting
Dysphagia
Postprandial fullness
Loss of appetite
Melena or pallor from anemia
Hematemesis
Weight loss
Palpable enlarged stomach with succussion splash
Enlarged lymph nodes such as Virchow nodes (ie,
left supraclavicular) and Irish node (anterior axillary)

Spread of Carcinoma Stomach

1.

Direct spread

2.

Lymphatic spread

3.

Spread to supraclavicular lymph

node (Troisiers sign)

Blood-borne metastasis

4.

Penetrates muscularis, mucosa,

adjacent
organs
such
as
pancreas, colon, liver

Spread to liver, lung, bone, brain

Transperitoneal spread

Manifest in peritoneal cavity and

give rise to ascites
Umbilicus nodules (Sister Mary
Josephs Nodule)
Krukenbergs tumor

Investigations
1. Laboratory studies

Full blood count

Tumour markers (CEA and CA 19-9)

2. Diagnostic

Oesophagogastroduodenoscopy with biopsy

X-ray with barium meal

3. Staging

Ultrasound of the abdomen

Liver function test
CT scan of abdomen
Chest X-ray

Management
i) Surgery
depends on the location, size, and locally
invasive characteristics of the tumor.
a) Total gastrectomy
b) Esophagogastrectomy for tumors of the
cardia and gastroesophageal junction
c) Subtotal gastrectomy for tumors of the
distal stomach
d) Lymph node dissection

ii) Chemotherapy
Platinum-based combination chemotherapy:
First-line regimens include epirubicin/cisplatin/5FU.
Ramucirumab for the treatment of advanced
stomach cancer or gastroesophageal (GE)
junction adenocarcinoma in patients with
unresectable or metastatic disease following
therapy with a fluoropyrimidine- or platinumcontaining regimen.

Oesophagitis

 Occurs when acid pepsin refluxes through the

lower oesophageal sphincter onto the
squamous epithelium lining of the
oesophagus.
Risk factors
Obesity
Fatty food
Caffeinated drinks
Alcohol
Drugs such as calcium channel blocker,
antihistamine and anticholinergic

Symptoms
Heartburn (often at night, worsened
by lying flat, initiated by bending,
stooping or heavy lifting)
Bitter taste in the mouth
Dysphagia (long term)

Investigation
Barium swallow and barium meal
Oesophageal ulcer and peptic strictures

Endoscopy
For patients who do not improve on
medical trial, long standing symptoms

Treatment
Proton Pump Inhibitor: Pantoprazole,
Omeprazole

Esophageal Varices
Caused by portal hypertension ( >
10mmHg )
Portal hypertension are caused by:
Liver cirrhosis
Hepatitis
Alcohol

Signs and symptoms

Hematemesis
Melena
Ascites, splenomegaly, spider naevi,
flapping tremor
Anemia symptoms
Fatigue
Dizziness
Pallor
Shortness of breath

Pathophysiology
1. Caused by increased portal vascular
resistance and increased portal flow /
pressure
2. Due to obstruction, collaterals are
formed within systemic circulation
3. The walls of the veins are easily
ruptured if the pressure is high
4. Hematemesis is the most common
presentation

Japanese Classification

Management
General
Secure airway, breathing and circulation
Resuscitation
Administer vitamin K
Short term antibiotic prophylaxis for 7
days

Management
Definitive
Endoscopic scleropathy / banding
Facilities not available give pharmacologic
treatment
Vasopressin / Somatostatin to temporarily reduce portal
pressure and reduce the bleeding

To secure hemostasis, Sengstaken Blackmore tube

can be inserted to achieve temporary hemostasis
Transjugular intra hepatic porto systemic stent
shunt (TIIPS)
Spleen renal shunt
Liver transplant