What Undergraduates should know Prof SM Chandramohan Prof and HOD Department of Surgical Gastroenterology and Center of Excellence for Upper GI Surgery Madras Medical College and Rajiv Gandhi Government General Hospital ID: 933438
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UPPER GASTROINTESTINAL BLEEDINGWhat Undergraduates should know ?
Prof SM
Chandramohan
Prof and HOD
Department of Surgical Gastroenterology and
Center of Excellence for Upper GI Surgery
Madras Medical College and
Rajiv Gandhi Government General Hospital
Chennai
Slide2Can download this presentation from
www.esoindia.org
Prof SM
Chandramohan
Prof and HOD
Department of Surgical Gastroenterology and
Center of Excellence for Upper GI Surgery
Madras Medical College and
Rajiv Gandhi Government General Hospital
Chennai
Slide3Slide4Slide5Slide6DEFINITION
CAUSES
EVALUATION
TREATMENT
PLAN OF THE TALK
Slide7DEFINITION
CAUSES
EVALUATION
TREATMENT
PLAN OF THE TALK
MEDICAL
ENDOSCOPIC
SURGICAL
Slide8DEFINITION
Any bleeding from
The gastrointestinalTract above the
Level of
ligament of
Treitz
is upper GI Bleeding
Slide9DEFINITIONS
Acute
GI bleed< 3 days durationhemodynamic instability
requires blood transfusion
Overt vs. occult
overt = visible blood (melena, bright red blood, coffee grounds)
occult = only detected by lab tests
Slide10Slide11COMMON CAUSES OF UGI BLEED
CAUSE
%
Peptic Ulcer
38%
Varix
16%
Tumor
7%
MW
Tear
4%
Erosions
4%
Esophagitis
13%
Slide12NSAID
(1)
the risk of gastric ulceration is increased to a greater extent than that of duodenal ulceration
(2) the risk of bleeding varies with the individual NSAID; for example, the relative risk of bleeding is greatest with
piroxicam
and less with ibuprofen
(3) the risk of bleeding is dose dependent
-age greater than 75 years,
-history of heart disease,
-history of peptic ulcer
- history of previous gastrointestinal bleeding
RISK FACTORS
Slide13AIRWAY
BREATHING
CIRCULATION
A
B
C
Slide14Examination
Tell tale signs…
Chronic Liver DiseasePortal Hypertension
Slide15Slide16Slide17Slide18ExaminationNot to miss……..
Haemodynamic
stabilitySigns of coagulation dysfunctionSigns of Liver cell failurePR
Slide19Slide20Slide21Bleeding PR
Slide22As he comes………….Resuscitate and Examine
Simultaneously…….
Slide23Form a team……….Wide bore IV line……
preferably central line
(take samples at the same time)Naso gastric tubeUrinary CatheterALERT OTHERS IN TEAM…….
Slide24Blood Sample for
Blood Group
Haemogram including plateletsCoagulation profileLiver function testRenal functionMarkers
Slide25Blood Sample
TRY NOT TO TAKE SAMPLES
FREQUENTLYExcept for serial evaluation
Slide26WHICH TUBE AND WHY?
Slide27Naso Gastric Tube orSenstaken
tube?
Slide28ROLE OF NASOGASTRIC TUBE
10 % of UGIB presents as LGIB
Red
blood
vs
c
offee grounds
NGT
clears the gastric field for endoscopic
visualization
prevent
aspiration of gastric content
Slide29Slide30EndoscopyWhen to do?
What is Possible?
When not to do???
Slide31EndoscopyOne stop Shop
Diagnose
AssessTreatReassess
Slide32ENDOSCOPIC EVALUATION
If Hemodynamically stable
Identify Bleeding site
Delineate cause
Allow endotherapy
Slide33Slide34Slide35ENDOSCOPIC MANAGEMENT
VARICEAL
NONVARICEAL
Slide36ENDOSCOPIC VARICEAL LIGATIONA rubber band is placed over the varix which
then undergoes thrombosis,sloughing,fibrosis.
Slide37Slide38Slide39Slide40ENDOSCOPIC SCLEROTHERAPY
Involves injecting a
sclerosant
Intravariceal
/
perivariceal
Common
sclerosants
Ethanolamine oleateAbsolute alcoholSodium morrhuate
Sodium
tetradecylHypertonic saline
Polidocanol
Slide41Slide42GLUE THERAPY
Cyanoacrylate
is a glue that is injected intoGastric varicesActs by forming a Cast over the varix on contact
with blood
Slide43Slide44Endoclip
Slide45DEFINITIVE MANAGEMENT OF NON VARICEAL BLEED
HIGH RISK
ULCER
FOR
BLEED
SRH/LARGE ULCER >2 cm
ULCERS IN
POSTERIOR WALL
BULB-GDA
ULCERS IN THE HIGH LESSER CURVE - LGA
Slide46Endoscopic Management
Non-Variceal - Modalities
Injection Therapy
(a) Adrenaline
(b) Sclerosants
Thermal Therapy
(a) Monopolar
(b) Bicap
(c) Heater Probe
(d) Argon Plasma Coagulation
(e) Laser
Mechanical Therapy
(a) Haemoclips
Slide47Endoscopic Management
Bleeding Peptic Ulcer - Stigmata
1a – Spurting vessel
1b – Oozing from a vessel
2 – Clot in the ulcer base
3 – Ulcer without bleed
Forrest
Classification
Slide48Slide49Slide50Slide51SECOND LOOK ENDOSCOPY
It is repeat endoscopy 24 hours after initial
Endoscopic hemostasis
INDICATIONS
1 Incomplete first endoscopic examination due
to blood obscuring the field
2 Patients with clinically significant
rebleeding
Slide52WHEN TO CALL IT AS
FAILED ENDOTHERAPY?
Slide53SURGICAL MANAGEMENT OF UGI BLEEDING
The Need
Only in Select Situations
Slide54Role of Surgery
5-10% of UGI Bleed Mortality
3% to
14
%
Slide55Slide56TV Vs H.PYLORI Eradication
40% to 70% of patients with a bleeding duodenal ulcers- positive for
H. pylori
Slide57Bleeding Gastric Ulcer
Simple excision alone -
rebleed in 20% of patients10% incidence of malignancy
Slide58Surgical options- Variceal bleeding
Shunt
Or Devascularisation
Slide59Less Common Causes of UGIB
Slide60MALLORY WEISS TEARS
Managed with
1 Hemoclips2 MPEC Probes
3 PPI
Slide61Mallory-Weiss TearsAngiographic embolization – in cases of failed endoscopic therapy
High gastrotomy and suturing of the mucosal tear – failure of all methodes
Slide62DIEULAFOY’S LESION
large
submucosal artery that protrudes through mucosa
at the gastric
fundus
.
bleeding can
be massive
Endoscopic Doppler USG can
help
localizeEndoscopic
hemostasis
-injection therapy , Thermal probe, clips.
Slide63Dieulafouy’s lesion
Slide64DIEULAFOY'S LESIONFailed endoscopic therapy - angiographic coil embolization
Surgical intervention - prior endoscopic tattooing
Gastrotomy - bleeding source can be oversewn Partial gastrectomy - the bleeding point not identified
Slide65GASTRIC ANTRAL VASCULAR ECTASIA-GAVE
rows
of
ectatic
mucosalVessels
(WATERMELON
STOMACH)
most
patients present with persistent, iron deficiency anemia from continued occult blood loss.
It is managed with1 APC-argon Plasma coagulation2 MPECMultiple sessions may be needed to eradicate
the lesions.
Slide66PP
PRE APC
PP
POST APC
Slide67Slide68Slide69Gastric Antral Vascular Ectasia
Endoscopic therapy - successful in up to 90% of patients
Failure of endoscopic therapy - antrectomy
Slide70SEVERE PORTAL HYPERTENSIVEGASTROPATHY
May present with acute or
chronic bleed.
No role for endoscopic
management.
Managed with B Blockers, TIPS,
Surgical Porto
Caval
shunt,
Liver transplantation.
Slide71HEMOBILIA
The diagnosis can be confirmed
By Side viewing ScopyOngoing or Recurrent bleed isTreated with
angioembolization
CAUSES-HEMOBILIA
Liver
trauma
Liver biopsy
ERCP/PTC/TIPS
HCC,
CHOLANGIOCARCINOMABiliary parasite infestations
Slide72HEMOSUCCUS PANCREATICUS
The diagnosis can be made
by Side viewing scopyManagement is by angioembolization
CAUSES-HEMOSUCCUS PANCREATICUS
Acute pancreatitis/chronic pancreatitis
Pancreatic pseudocyst
Pancreatic cancer
ERCP manipulation of PD
Rupture of
splenic
artery pseudoaneurysm into PD
Slide73ANGIOEMBOLIZATION
Slide74STRESS GASTRITISSurgery - rarely indicated
Vagotomy and pyloroplasty, with oversewing of the hemorrhage, or near-total gastrectomy - mortality rates as high as 60%
Slide75MalignancyEndoscopic therapy - successful in controlling hemorrhage, the rebleeding rate is high
Standard cancer operations - indicated when possible
Palliative wedge resections – to control bleed
Slide76Aortoenteric Fistula
Ligation of the aorta proximal to the graft
Removal of the infected prosthesisExtra-anatomic bypassDefect in the duodenum - small and can be repaired primarilyTypically, patients with bleeding from an aortoenteric fistula will present first with a “sentinel bleed.”
Slide77MORTALITY
7% to 10%.
The mortality has decreased only minimally during the last 30 years, despite the introduction of endoscopic therapy that reduces the rate of
rebleeding
.
increasing percentage of UGIB occurring in the elderly
frequent use of antiplatelet medications or anticoagulants
frequent comorbid conditions.
Slide78Conclusion