Gastrointestinal

bleeding describe
every form of
haemorrhage in the
GIT, from the pharynx
to the rectum.
Can be divided into 2
clinical syndromes:- upper GI bleed
(pharynx to ligament
of Treitz)
- lower GI bleed
(ligament of Treitz to
rectum)
2/81

Cause of Bleeding

Relative Frequency

Peptic Ulcer
Oesophagitis
Gastritis/erosions
Duodenitis
Varices
Portal hypertensive
gastropathy
Malignancy
Mallory Weiss tear
Vascular Malformation
Other (e.g. Aortoenteric
fistula)

44
28
26
15
13
7
5
5
3
rare

ACUTE
Haematemesis with or without
malena
Malena with or without hemetemesia
Rarely haematochezia indicating
massive life threatening bleed
CHRONIC
Iron deficiency anemia
Blood loss detected by positive
faecal occult blood test

 RR, HR, and BP can be

used to estimate degree
of blood
loss/hypovolaemia
Class I
Class II
Class III
Class IV
Volume
Loss (ml)

0-750

750-1500

1500-2000

>2000

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
Output
(ml/hr)

>30

20-30

5-15

Anuric

Mental
State

Restless

Anxious

Anxious/co
nfused

Confused/
lethargic

 PC/HPC

Duration, frequency, and volume of bleeding (indicate severity of bleeding)

Nature of bleeding: will point to source
Haematemesis (fresh or coffee ground)/melaena 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
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 abdo pain, bowel symptoms such as diarrhoea 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 consiousness

Pale and clammy
Cool peripheries
Reduced CRT
Tachcardic and thready pulse
Hypotensive with narrow pulse pressure
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, gynacomastia, shifting
dullness/ascites)
Digital rectal examination may reveal melaena, dark
red blood, bright red blood

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 derrangement
NG tube and aspiration (will help differentiate upper from
lower GI bleed)
Organise definitive treatment
(endoscopic/radiological/surgical)

 Patients with low risk ulcers can

be fed promptly, put on oral PPI
therapy.
Patients with ulcers requiring
endoscopic therapy should
receive PPI gtt x 72 hours
Significantly reduces 30 day
rebleeding rate vs placebo (6.7%
vs. 22.5%)
Note: there may not be major
advantage with high dose over nonhigh dose PPI therapy
N Engl J Med 2000;343:310
Arch Intern Med
2010;170:751

 Determine H. pylori status in all

ulcer patients
Discharge patients on PPI (once to
twice daily), duration dictated by
underlying etiology and need for
NSAIDs/aspirin
In patients with cardiovascular
disease on low dose aspirin: restart
as soon as bleeding has resolved
RCT demonstrates increased risk of
rebleeding (10% v 5%) but decreased
30 day mortality (1.3% v 13%)
Ann Intern Med 2010;152:1

 Determine H. pylori status in all

ulcer patients
Discharge patients on PPI (once to
twice daily), duration dictated by
underlying
etiology
and
need for
Not
is
important
Not dying
dying
is more
more
important
NSAIDs/aspirin
than
not
rebleeding
thanwith
not cardiovascular
rebleeding
In patients
disease on low dose aspirin: restart
as soon as bleeding has resolved
RCT demonstrates increased risk of
rebleeding (10% v 5%) but decreased
30 day mortality (1.3% v 13%)
Ann Intern Med 2010;152:1

 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 anastamosis
(opening or dilatation of pre-existing vascular
channels connecting portal and systemic
circulations)
Sites of porto-systemic anastamosis include:
Oesophagus (P= eosophageal branch of L gastric v, S=
oesophageal branch of azygous v)
Umbilicus (P= para-umbilical v, S= infeior epigastric v)
Retroperitoneal (P= right/middle/left colic v, S= renal/suprarenal/gonadal v)
Rectal (P= superior rectal v, S= middle/inferior rectal v)

Furthermore, clotting derrangement in those with

chronic liver disease can worsen bleeding

 Variceal bleed

 Occurs in 1/3 of patients with

cirrhosis
1/3 initial bleeding episodes
are fatal
Among survivors, 1/3 will
rebleed within 6 weeks
Only 1/3 will survive
1 year or more

 Goal: Reduce splanchnic blood flow

Terlipressin only agent shown to
improve control of bleeding and survival
in RCTs and meta-analysis
Not available in US

Vasopressin + nitroglycerine too many

adverse effects
Somatostatin not available in US
Octreotide (somatostatin analogue)
Decreases splanchnic blood flow (variably)
Efficacy is controversial; no proven mortality
benefit
Standard dose: 50 mcg bolus, then 50 mcg/hr
drip for 3-5 days
Gastroenterology 2001;120:946
Cochrane Database Syst Rev
2008;16:CD000193
N Engl J Med 1995;333:555
Am J Gastroenterol 2009;104:617

 Bacterial infection occurs in up to

66% of patients with cirrhosis and
variceal bleed
Negative impact on hemostasis
(endogenous heparinoids)
Prophylactic antibiotics reduces
incidence of bacterial infection,
significantly reduces early
rebleeding
Ceftriaxone 1 g IV QD x 5-7 days
Alt: Norfloxacin 400 mg po BID

Hepatology 2004;39:746
J Korean Med Sci 2006;21:883
Hepatogastroenterology 2004;51:541

 Promptly but with caution

Goal = maintain hemodynamic
stability, Hgb ~7-8, CVP 4-8
mmHg
Avoid excessively rapid
overexpansion of volume; may
increase portal pressure,
greater bleeding

 Should be
performed as
soon as possible
after resuscitation
(within 12 hours)
Endotracheal
intubation
frequently needed
Band ligation is
preferred method
Layer, L. & Jaganmohan, S. & Raju, GS & DuPont, AW (Oct 28 2009).
Esophagus - Band Ligation of Actively Bleeding Gastroesophageal
Varices. The DAVE Project. Retrieved Aug, 2, 2010, from
http://daveproject.org/viewfilms.cfm?film_id=715

TIPSS

Sengstaken-Blakemore Tube

Esophageal
ballon
SB tube

Gastric
ballon

never
exceed
45mmHg.
Volume 200ml

Radiographic confirmation
of the gastric balloons
position -- 30cc air inflate
the gastric balloon
Insufflation of the
esophageal balloon to
35mmHg

 Compression of varices for

not excess 48 hours
Deflate the esophageal
balloon for about 30 mins
every 12 hours
Major complications -aspiration and esophageal
perforation
Control hemorrhage >90%,
but it is temporary

 Bridging procedure buy time

Definite therapeutic
management must be
performed.

 TIPS Transjugular
Intrahepatic
Portosystemic Shunt
Early placement of
shunt (within 24-72hrs)
associated with
improved survival
among high-risk
patients
Preferred treatment for
gastric variceal bleeding
(rule out splenic vein
thrombosis first)
Hepatology 2004;40:793
Hepatology 2008;48:Suppl:373A
N Engl J Med. 2010 Jun 24;362:2370

Fan, C. (Apr 25 2006). Vascular Interventions in

the Abdomen: New Devices and Applications.
The DAVE Project. Retrieved Aug, 2, 2010, from
http://daveproject.org/viewfilms.cfm?
film_id=497

TIPS+embolization of gastric
varices

Surgical porto-systemic shunt (spleno-renal shunt)

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 Bleed
Lower gastrointestinal bleeding is
defined as abnormal hemorrhage into
the lumen of the bowel from a source
distal to the ligament of Treitz.
Originates in the portion of GIT
further down the digestive system
small intestine
--colon
--rectum
--anus

 more common in male > female.

This increase is largely attributable
to the various colonic disorders
commonly associated with aging
(e.g., diverticulosis and
angiodysplasia).
In more than 95% of patients with lower
GI bleeding, the source of hemorrhage is
the colon.

50/81

Lower Gastrointestinal Bleeding in

Percentage of Patients
Adults
Diverticular disease
Diverticulosis/diverticulitis of small
intestine
60%
Diverticulosis/diverticulitis of
colon
Inflammatory bowel diseaseCrohn
disease of small bowel, colon, or
both
13%
Ulcerative colitis
Noninfectious gastroenteritis and
colitis
Benign anorectal
diseasesHemorrhoids
Anal fissure
Fistula-in-ano
NeoplasiaMalignant neoplasia of
small intestine
Malignant neoplasia of colon,
rectum, and anus
Coagulopathy

11%

9%
4%

51/81

Blood on its own or streaking the stool:

Rectum
: polyps or carcinoma, prolapsed
Anus
: Haemorrhoids, Fissure-in-ano, Anal carcinoma.
Stool mixed with blood:
GIT above sigmoid colon.
Sigmoid carcinoma or diverticular disease.
Blood separate from the stool:
Follows defaecation
: Anal condition eg: Haemorrhoids.
Blood is passed by itself
: Rapidly bleeding carcinoma,
inflammatory bowel disease, diverticulitis, or passed down
from high
up in the gut.
Blood is on the surface of the stool: suggest a lesion such
as polyp or carcinoma further proximally either in the
rectum or descending colon
Blood on the toilet paper: Fissure-in-ano, Heamorrhoids.
Loose, black, tarry, foul smelling stool: from the proximal of
DJ flexure
52/81

Bright red/ Fresh blood: Rectum and anus.

Dark blood:
Upper GIT to above rectum.
Drugs eg: iron tablets- appear as greenish
black formed stool.
Discharge apart from blood:-Mucus- irritable bowel syndrome
-Copious mucus- villous adenoma, frank
cancer of the rectum
-Mucus and pus- IBD, diverticular disease
53/81

Normal bowel
Intermittent bouts of
constipation interrupted
by diarrhoea: Carcinoma
or Diverticular disease.
Diarrhoea: Inflammatory
bowel disease or rectal
villous tumour.
Tenesmus: Irritable
bowel syndrome or
abnormal mass of rectum
or anal canal (e.g. CA,
polyps or thrombosed
haemorrhoid)

Causes: Allergic, anal

warts, anal leak of
mucus in haemorrhoid,
excessive used of
liquid paraffin,
generalized disorder.
eg: jaundice, diabetes
mellitus.
During
pregnancy/childbirth:
Fissure-in-ano,
haemorrhoids.
Throbbing, severe pain
occur during defaecation:
54/81

Previous perianal disease

Inflammatory bowel
Laxative agent
disease
Peptic ulcer disease
Anti-parkinson agent
Liver disease
Anti-coagulant therapy
Coagulopathy

History of
malignancy
Familial
Adenomatous
Polyposis

eg: warfarin
NSAIDs-risk factor of
PUD
Low fiber diet
Smoking

55/81

Anaemic
Bruishing/ Purpura
Cachexic
Dehydrated
Jaundice

Perianal Skin
Lesion
Masses
Melaena

Inguinal LN

Confusion

R
E
P
P
U
H
T
D
I
Supraclavicular
Inspection - distension,
E
W
E
LN
scar, prominent vein.
L
E
M I B Cervical LN
Palpation A
- tenderness,
G
mass/ organomegaly
Axillary LN
S
Percussion - shifting
dullness, fluid thrill.
Auscultation hyperactive bowel sound.

56/81

1.
2.
3.
4.

Full Blood Count (FBC)

BUSE
Coagulation profile
Cross-matched (Transfusion)

1. Scintigraphy
-Radioactive test using Technetium-99m
(99mTc)Labelled red cells
-diagnose ongoing bleeding at a rate as
low as 0.1 mL/min
2. Mesenteric angiography
-Can detect bleeding at a rate of more
than 0.5 mL/min.

57/81

3.

Helical CT scan

Abdomen and pelvis

Can also be used when routine workup fails
to determine the cause of active GI bleeding
Multiple criteria are used to establish the
bleeding sites:
-vascular extravasation of the contrast
medium
-contrast enhancement of the bowel wall
-thickening of the bowel wall
-spontaneous hyperdensity of the
peribowel fat
-vascular dilatations with helical CT.
58/81

4.Colonoscopy
Bleeding slowly or who have already
stopped bleeding.
Biopsy

5.Proctosigmoidoscopy
Exclude an anorectal source of
bleeding
6.Oesophagoduodenoscopy (OGDS)
To exclude upper GI bleeding
59/81

7. Double-contrast barium
enema

Elective evaluation of unexplained

lower GI bleeding

Do not use in the acute hemorrhage

phase

8. Small bowel enema

Example of barium enema study

Often
valuable in investigation of long showing
ulcerative colitis of the
term, unexplained lower GI bleeding
colon

60/81

 Common in children
within 1st year of life
Symptoms: abdominal
pain, red-currant-jelly
stool
Signs: palpable mass
at right iliac fossa
Procedure: Barium
enema, laparotomy
61/81

 Adenomatous polyps and

adenomas
Has malignant potential
Morphology:
-polypoid and pedunculated
-dome-shaped and sessile
Histology:
-degree of epithelial
dysplasia is
highly variable
-carcinoma in situ
-early invasive cancer:invasion of tumour cells
through basement
membranemuscularis
mucosasubmucosa

62/81

1.Tubular adenomas
- small pedunculated / sessile lesions
-retain a tubular form similar to normal
colonic
mucosa
-least potential for malignant transformation
2. Villous adenomas
-sessile and frond like lesions
-secrete mucus
-more dysplastic
-greater potential for malignant change
3. Tubulo-villous adenoma
-intermediate between tubular and villous
adenoma
-pedunculated, stalk is covered with normal
epithelium
63/81

Rectal bleeding
Iron deficiency anaemia
Mucus
Hypokalaemia
Tenesmus
Prolapse
Obstructive symptoms
64/81

 Autosomal dominant
defect in APC gene
Mid teen yearshundred / more
adenomatous polyps
Average age of 40colorectal cancer
Symptoms:
-rectal bleeding
-diarrhoea
Gardners syndrome=
+desmoid tumours +
osteomas of mandible
& skull
65/81

 Sigmoidoscopy
Colonoscopy
-gold standard
-visualize, biopsy, remove
-disadvantage: full days bowel preparation
sedation
risk of haemorrhage &
perforation
CT pneumocolon
-elderly / infirm patient
-< invasive & not require sedation.
-bowel preparation
Double contrast barium enema

66/81

 Subtotal colectomy & ileorectal

anastomosis
Panproctocolectomy & ileotomy / ileal
pouch
Follow-up colonoscopies
- an adenomatous polyp is found / a
colorectal
cancer has been treated
-intervals depend on number, size &
pathology of polyps
67/81

 Rare < 50 years old,

Common > 60 years old
Common site- sigmoid
colon, rectum
Clinical features:
-altered bowel habit &
large bowel obstruction
-rectal bleeding
-iron deficiency anaemia
-tenesmus
-perforation
-anorexia & weight loss

68/81

 1 or multiple small mucosal

or submucosal vascular
malformation.
> 60 years old
Common site : ascending
colon and caecum
Malformations consist of
dilated tortuous submucosal
veins
In severe cases, the mucosa
is replaced by massive
dilated deformed vessels
Clinical features:
-acute / chronic rectal
bleeding
-iron deficiency anaemia

69/81

 Colonoscopy
-bright red 0.5-1cm diameter
submucosal
lesion
-small dilated vessels
Mesenteric angiography
Radioactive test using
technetium-99m labeled red cells
70/81

71/81

 colonoscopic diathermy
if patient seriously ill catheter
is placed in the appendix stump
and the colon irrigated
progradely with saline or
water on-table colonoscopy
carried out and site of bleeding
can be confirmed
72/81

 Elderly
Transient ischaemia of a
segment of a large bowel,
followed by sloughing of
mucosa
Common site splenic flexure
Clinical features:
-abdominal pain
-rectal bleeding ( dark red)
-1-3x over 12 hours
Complication- fibrotic sticture
73/81

 M>F
Female- late pregnancy,
puerperium
Supine lithotomy position- 3 ,7,
11 oclock positions
Classification:
1st degree : never prolapse
2nd degree: prolapse during
defaecation but
return spontaneously
3rd degree : remain prolapse but
can be reduced digitally
4th degree
: long-standing
prolapse cannot be
reduced
74/81

Rectal bleeding
Perianal irritation & itching
Mucus leakage
Mild incontinence of flatus
Prolapse
Acute pain
Skin tags at anal margin
75/81

 Longitudinal tear in mucosa & skin of

anal canal
M>F
Common site: midline in posterior anal
margin
Clinical features:
- acute pain during defaecation
- fresh bleeding at defaecation

76/81

 Rare < 40 years old

F>M
Causes:
-Chronic lack of dietary
fibre
-Genetic
Common site: sigmoid colon
Clinical features:
-diverticulosis
(asymptomatic)
-chronic grumbling
diverticular pain (chronic
constipation & episodic
diarrhoea)
77/81

1. Vasoconstrictive agents:
vasopressin
2. Therapeutic embolization:
-Embolic agents: Autologous
clot, Gelfoam, polyvinyl
alcohol, microcoils,
ethanolamine, and
oxidized cellulose
-Selective angiography
3. Endoscopic therapy:
-Diathermy / laser
coagulation
-Short term control of
bleeding during
resuscitation

The bleeding point is

localized, perform a
limited segmental
resection of the small
or large bowel
Poor prognostic
features:
-age over 60 years
-chronic history
-relapse on full
medical treatment
-serious coexisting
medical conditions
-> 4 units of blood

78/81

Mr. TS, 49/ I / gentleman

k/c/o alcoholic liver disease
Child C
Stop alcohol 4 years ago
h/o multiple admission for tapping
Last admission for tapping on
29/5/16
Cell count : 204

 Abdominal discomfort +
distension x 3/7
a/w epigastric pain
Leg swelling
Nausea and vomiting (I
episode: no hemetemesis )
BO x 3 (diarrhea)
Denies bleeding tendency
No fever, no URTI sx or UTI sx

Alert, concious, and GCS full

Looks pale and jaundiced
Vital signs :
BP: 140/95
PR: 78
T: 37
SPO2 : 97% (RA)
GM : 7.9

 P/A : grossly distended, tender

at epigastric area
Pedal edema up to knee
Respiratory : equal air entry,
clear
CVS : S1S2 no murmur
Per rectal : no malena,
brownish stool

 FBC (15/7) HB: 8.5/ TWC :6.9/ PLT :33

RP (15/7) Na: 140/ K: 2.87/ Cl: 99/ urea: 2.3/
creat:69
LFT (15/7) TB: 218/ DB:114/ IB:104/ ALP: 84/
TP: 63/ ALB:25/ GLO: 38/ ALT:15
Coagulation profile : PT: 31.3/ INR:2.98/
APTT:46.9
CK: 63
Amylase: 35
CXR : no pneumonic patches
OGDS (7/12/16) : Forrest 2 esophageal
varices with SRH
OGDS (6/1/16) : Forrest 1 esophageal ulcer
with portal gastropathy

 Treat as Spontaneous Bacterial

Peritonitis
Decompensated Liver Disease

Iv ceftriaxone 2g stat and OD

For diagnostic tapping
T. Thiamine 30 mg OD
T. Pantoprazole 40 mg BD

Diagnostic tapping (15/7/16)

tapped 2.3L
cell count: 6
gram stain: few pus cell
c+s : SFNG
On 16/7/16
still having abdominal discomfort with
distended abdomen.
noted Hb drop from 8.5 5.9
PR done : no malena, brownish stool
no bleeding tendency
transfused 1 pint pack cell
peritoneal tapping done: 2.9L tapped
BP stable during tapping

 On 17/7/2016
Pt c/o dizziness at 1 am, noted BP low but no
bleeding tendency
Then at 5 am, pt had hematemesis and looks
pale
2 pint NS run fast, transfuse 2 pint whole
blood and 2unit FFP
PR: No malena
Tx as UGIB secondary to bleeding esophageal
varices
Urgent OGDS done : forrest 2 esophageal
varices at 30 cm branched into 2 column. No
fundal varices. Portal gastropathy, banded x2
Post 2pint pc tranfusion, Hb: 5.8
transfuse another 1 pint PC

 On 18/7/16
No more hemetemesis
No bleeding tendency
No melena / PR bleed
Hb post tx : 6.7
Transfused another 1 pint pack cell

 19/7/16
Pt comfortable, no active
complaint
Vital sign stable
P/A: soft non tender
Hb post tx: 8.8 (total 4 pint pack
cell)

 20/7/16
Pt was discharge well with no
bleeding tendency
Discharge with T. Ciprofloxacin
500 mg bd x 5/7
Had USG Abdomen appt
(outpatient)

 60 yo Malay gentleman
U/L Decompensated Liver cirrhosis
(Chlids A) secondary to Hepatitis B
(Dx in 1997)
Admitted from gastro clinic dt low HB
5.6 , Plt 34, otherwise no bleeding
tendency
p/w bilateral LL swelling 2/52,
decrease effort tolerance
ass lethargy
Surveillance OGDS done in 2013 ,
normal finding,no varices

 In ward
Total transfuse
3 unit packed cell : HB increase 5.6
8.5
4 unit platelet : Plt increase 34 45

OGDS : OV F3,no SRH

Banded x4
Started on T propanolol
40 mg BD
2/12
Rescope in 3/52

 Discharge plan
1) OGDS appt in 3/52
2) TCA gastro 3/12 with AFP,LFT,RP,FBC,INR
3) Discharge with -T Propranolol 40mg BD
-T Pantoprazole 40mg
OD
- T Tenofovir 30 mg od
- T Lasix 40mg OD
- T Spironolactone
100mg OD
- T BCo2/ Folate/
FeSO4 ll/ll OD