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1.
2. INTRODUCTION
• 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)
LIGAMENT OF
TREITZ
2/81
8. Clinical presentation
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
9. Estimating Degree of Blood
Loss
• 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/confu
sed
Confused/
lethargic
10. History in patients with GI bleeding
– 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
11. Examination in patients with GI bleeding
• 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
12. Emegency 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 derrangement
• NG tube and aspiration (will help differentiate upper from
lower GI bleed)
• Organise definitive treatment
(endoscopic/radiological/surgical)
13. Nonvariceal UGIB –
Post-endoscopy
management
• 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 non-
high dose PPI therapy
N Engl J Med 2000;343:310
Arch Intern Med 2010;170:751
14. Nonvariceal UGIB –
Post-endoscopy
management
• 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
15. Nonvariceal UGIB –
Post-endoscopy
management
• 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
Not dying is more important
than not rebleeding
17. 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 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/supra-
renal/gonadal v)
• Rectal (P= superior rectal v, S= middle/inferior rectal v)
• Furthermore, clotting derrangement in those with
chronic liver disease can worsen bleeding
19. Variceal Bleeding
• 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
21. asoconstrictor therapy
• 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
22. ntibiotics
• 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
23. esuscitation
• 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
24. ndoscopy
• 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
37. Tamponade Tube
Sengstaken-Blakemore (S-B) tube
Radiographic confirmation
of the gastric balloon’s
position -- 30cc air inflate
the gastric balloon
Insufflation of the
esophageal balloon to
35mmHg
38. • 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
40. ternative/Rescue
therapies
• 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)
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
Hepatology 2004;40:793
Hepatology 2008;48:Suppl:373A
N Engl J Med. 2010 Jun 24;362:2370
43. 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
44.
45.
46.
47. Lower GI bleed
• 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
48. 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.
51. Lower Gastrointestinal Bleeding in Adults Percentage of Patients
•Diverticular disease
Diverticulosis/diverticulitis of small
intestine
•Diverticulosis/diverticulitis of colon
60%
•Inflammatory bowel diseaseCrohn disease
of small bowel, colon, or both
•Ulcerative colitis
•Noninfectious gastroenteritis and colitis
13%
•Benign anorectal diseasesHemorrhoids
•Anal fissure
•Fistula-in-ano
11%
•NeoplasiaMalignant neoplasia of small
intestine
•Malignant neoplasia of colon, rectum, and
anus
9%
Coagulopathy 4%
Arteriovenous malformations (AVMs) 3%
TOTAL 100%
Source: Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal
bleeding. Surg Res Commun. 1996;18:113-20.[9]
51/81
52. HISTORY TAKING:
RECTAL BLEEDING
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
53. 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
HISTORY TAKING:
COLOUR OF
BLOOD/DISCHARGE
53/81
54. 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)
HISTORY TAKING
ALTER BOWEL HABIT
ANAL PAIN
ITCHINESS
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: Fissure-
in-ano.
54/81
55. •Previous perianal disease
•Inflammatory bowel
disease
•Peptic ulcer disease
•Liver disease
•Coagulopathy
HISTORY TAKING
• Laxative agent
• Anti-parkinson agent
• Anti-coagulant therapy eg:
warfarin
• NSAID’s-risk factor of PUD
• Low fiber diet
• Smoking
PREVIOUS HISTORY
•History of malignancy
•Familial Adenomatous
Polyposis
FAMILY HISTORY
DRUGS HISTORY
SOCIAL HISTORY
55/81
57. INVESTIGATION
1. Full Blood Count (FBC)
2. BUSE
3. Coagulation profile
4. 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.
LABORATORY
IMAGING
57/81
58. IMAGING
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
59. IMAGING
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
60. IMAGING
7. Double-contrast barium enema
• Elective evaluation of unexplained lower GI
bleeding
• Do not use in the acute hemorrhage phase
8. Small bowel enema
• Often valuable in investigation of long-term,
unexplained lower GI bleeding
Example of barium enema study
showing ulcerative colitis of the colon
60/81
61. INTUSSUSCEPTION
• 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
62. Colorectal polyps
• 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
membrane→muscularis 62/81
63. TYPES OF COLORECTAL
POLYPS
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
67. MANAGEMENT
• 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
68. ADENOCARCINOMA OF
COLON & RECTUM
• 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
69. ANGIODYSPLASIA
• 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
70. INVESTIGATION
• Colonoscopy
-bright red 0.5-1cm diameter
submucosal
lesion
-small dilated vessels
• Mesenteric angiography
• Radioactive test using technetium-
99m –labeled red cells
70/81
72. MANAGEMENT
• 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
73. ISCHAEMIC COLITIS
• 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
74. HAEMORRHOIDS
• M > F
• Female- late pregnancy,
puerperium
• Supine lithotomy position- 3 ,7,
11 o’clock 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
76. ANAL FISSURE
• 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
77. DIVERTICULAR DISEASE
• 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 77/81
78. MANAGEMENT
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
transfusion required
MEDICAL SURGICAL
78/81
79.
80. • 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
81. presentation
• 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
82. Physical examination
• Alert, concious, and GCS full
• Looks pale and jaundiced
• Vital signs :
• BP: 140/95
• PR: 78
• T: 37
• SPO2 : 97% (RA)
• GM : 7.9
83. • 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
86. Management
• Iv ceftriaxone 2g stat and OD
• For diagnostic tapping
• T. Thiamine 30 mg OD
• T. Pantoprazole 40 mg BD
87. Progress in ward
• 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
88. • 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
89. • 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
90. • 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)
91. • 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)
92.
93. • 60 yo Malay gentleman
• U/L Decompensated Liver cirrhosis
(Chlid’s 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
94. • 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
95. • 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