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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
Non variceal gi bleed
AETIOLOGY
PEPTIC ULCER
MALIGNANCY
MALLORY
WEISS TEAR
OESOPAGITIS
EROSIONS
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
NSAID ASPIRINS
HELICOBACTER
PYLORI
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
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
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
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
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)
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
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
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
Non variceal gi bleed
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
• Variceal bleed
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
leed
asoconstrictor therapy
ntibiotics
esuscitation
U level care
ndoscopy
ternative/Rescue therapies
eta blockade
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
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
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
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
Sengstaken-Blakemore Tube
TIPSS
Available in MMH
S-B tube
SB tube
Gastric
ballon
Esophageal
ballon
never
exceed
45mmHg.
Volume 200ml
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
• 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.
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
TIPS+embolization of gastric varices
Surgical porto-systemic shunt (spleno-renal shunt)
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 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
 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.
Types of LGIB
50/81
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
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
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
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
•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
PHYSICAL EXAMINATION:
LOWER GI BLEED
 Anaemic
 Bruishing/ Purpura
 Cachexic
 Dehydrated
 Jaundice
 Inspection - distension, scar,
prominent vein.
 Palpation - tenderness, mass/
organomegaly
 Percussion - shifting dullness,
fluid thrill.
 Auscultation - hyperactive
bowel sound.
 Perianal Skin Lesion
 Masses
 Melaena
 Supraclavicular LN
 Cervical LN
 Axillary LN
 Inguinal LN
 Confusion ( Shock, liver
failure….)
 Neurological Deficit
GENERAL INSPECTION
ABDOMEN
RECTAL
LYMPH NODES
CNS
56/81
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
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
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
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
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
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
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
SIGN AND SYMPTOM
• Rectal bleeding
• Iron deficiency anaemia
• Mucus
• Hypokalaemia
• Tenesmus
• Prolapse
• Obstructive symptoms
64/81
FAMILIAL ADENOMATOUS
POLYPOSIS
• Autosomal dominant
defect in APC gene
• Mid teen years- hundred
/ more adenomatous
polyps
• Average age of 40-
colorectal cancer
• Symptoms:
-rectal bleeding
-diarrhoea
• Gardner’s syndrome=
+desmoid tumours +
osteomas of mandible &
skull 65/81
INVESTIGATION
• Sigmoidoscopy
• Colonoscopy
-gold standard
-visualize, biopsy, remove
-disadvantage: full day’s bowel preparation
sedation
risk of haemorrhage &
perforation
• CT pneumocolon
-elderly / infirm patient
-< invasive & not require sedation.
-bowel preparation
• Double contrast barium enema
66/81
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
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
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
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
71/81
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
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
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
HAEMORRHOIDS: SIGNS &
SYMPTOMS
• Rectal bleeding
• Perianal irritation & itching
• Mucus leakage
• Mild incontinence of flatus
• Prolapse
• Acute pain
• Skin tags at anal margin
75/81
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
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
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
• 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
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
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
• 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
Investigation
• 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
Diagnosis
• Treat as Spontaneous Bacterial
Peritonitis
• Decompensated Liver Disease
Management
• Iv ceftriaxone 2g stat and OD
• For diagnostic tapping
• T. Thiamine 30 mg OD
• T. Pantoprazole 40 mg BD
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
• 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
(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
• 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
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3255739dwe43ew234eds34ew96-GI-Bleed-ppt.ppt

  • 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
  • 3.
  • 6. 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
  • 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
  • 20. leed asoconstrictor therapy ntibiotics esuscitation U level care ndoscopy ternative/Rescue therapies eta blockade
  • 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
  • 28.
  • 29.
  • 30.
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  • 32.
  • 33.
  • 34.
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  • 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
  • 39. • Bridging procedure buy time Definite therapeutic management must be performed.
  • 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
  • 42. Surgical porto-systemic shunt (spleno-renal shunt)
  • 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.
  • 50. 50/81
  • 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
  • 56. PHYSICAL EXAMINATION: LOWER GI BLEED  Anaemic  Bruishing/ Purpura  Cachexic  Dehydrated  Jaundice  Inspection - distension, scar, prominent vein.  Palpation - tenderness, mass/ organomegaly  Percussion - shifting dullness, fluid thrill.  Auscultation - hyperactive bowel sound.  Perianal Skin Lesion  Masses  Melaena  Supraclavicular LN  Cervical LN  Axillary LN  Inguinal LN  Confusion ( Shock, liver failure….)  Neurological Deficit GENERAL INSPECTION ABDOMEN RECTAL LYMPH NODES CNS 56/81
  • 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
  • 64. SIGN AND SYMPTOM • Rectal bleeding • Iron deficiency anaemia • Mucus • Hypokalaemia • Tenesmus • Prolapse • Obstructive symptoms 64/81
  • 65. FAMILIAL ADENOMATOUS POLYPOSIS • Autosomal dominant defect in APC gene • Mid teen years- hundred / more adenomatous polyps • Average age of 40- colorectal cancer • Symptoms: -rectal bleeding -diarrhoea • Gardner’s syndrome= +desmoid tumours + osteomas of mandible & skull 65/81
  • 66. INVESTIGATION • Sigmoidoscopy • Colonoscopy -gold standard -visualize, biopsy, remove -disadvantage: full day’s bowel preparation sedation risk of haemorrhage & perforation • CT pneumocolon -elderly / infirm patient -< invasive & not require sedation. -bowel preparation • Double contrast barium enema 66/81
  • 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
  • 71. 71/81
  • 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
  • 75. HAEMORRHOIDS: SIGNS & SYMPTOMS • Rectal bleeding • Perianal irritation & itching • Mucus leakage • Mild incontinence of flatus • Prolapse • Acute pain • Skin tags at anal margin 75/81
  • 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
  • 84. Investigation • 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
  • 85. Diagnosis • Treat as Spontaneous Bacterial Peritonitis • Decompensated Liver Disease
  • 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