UGI for MBBS 3 guide to history, examination and acute management

acute management of upper GI bleeding principles

1. APPROACH TO UPPER GI BLEED
Dr.Tim Mutafya
Gen Surg. resident
MBBS III class

2. OVERVIEW
•Definition & Epidemiology
•Classification
•Pathophysiology
•Clinical presentation
•Screening & Diagnosis
•Initial management

3. Definition
Upper GIB is that originating proximal to the ligament of Treitz;
•from the oesophagus, stomach and duodenum

4. EPIDEMIOLOGY
•UGIB is more common than bleeding from the lower GI tract, accounting for 70% of
all gastrointestinal bleeding.
•80% are self-limited.
•Most common source is stomach and proximal duodenum due to peptic ulcer
•Pts on anti platelet therapy has two fold increase in bleed as compared to normal
ones.
•20% of pts of moderate to high risk, who have recurrent bleeding (within 48-72 hrs)
have poor prognosis.
•The mortality rate is 5% to 10% for severe UGI bleed.

5. RISK FACTORS
•Age > 50 years, Male
•Drugs: Use of NSAIDS, antiplatelet
•H-pylori infection
•Excessive alcohol intake
•Excess acid production

6. Classification
•Pathophysiologic
•Anatomic

7. UPPER GI
BLEEDING
VARICEAL
BLEEDING
NON
VARICEAL
BLEEDING
•Esophageal varices
•Gastric varices
Ulcer disease
Esophagitis
Gastritis/erosions
Erosive duodenitis
tumors
Vascular ectasias
Portal Hypertensive
Gastropathy
Mallory weiss tear
Obscure UGIB
Pathophysiologic

8. Anatomical

9. Major causes

10. Esophageal
Varices
Gastric
•Associated with high HPVG > 12mmHg
•About 40% of patients with cirrhosis and in
60% of patients with cirrhosis and ascites.
•Up to 25% of patients with newly diagnosed
varices will bleed within two years.
•80% will stop bleeding spontaneously.
•Can occur with HVPG less than 12mmHg
•High risk
•Not usually associated with cirrhosis
osplenic vein thrombosis
oPancreatitis
opancreatic cancer.

11. Varices
Prehepatic
•Portal venous thrombosis
•Infiltrative tumors
Intrahepatic
•Schistosomiasis
•Liver cirrhosis
•Veno-occlusive disease
Post hepatic
•Budd chiarisyndrome

13. Most frequent cause of upper GI Bleeding
Duodenal Ulcer-gastroduodenalA.
PUD
Gastric ulcer-left gastric A.
PEPTIC ULCER DISEASE
H.PYLORI: NSAIDS:
* involves antrum * gastric ulcers >
common
*duodenal ulcers * 15-45% patients
develop
ulcers on regular use
•As the ulcer burrows deeper into the
gastroduodenal mucosa,weakeningand
necrosis of the arterial wall,development
of a pseudoaneurysm.
•weakened wall ruptures hemorrhage

14. MODIFIED JOHNSON
CLASSIFICATION FOR GASTRIC
ULCER

15. Mallory weiss syndrome / tears
•Mucosal or sub-mucosal lacerations that occur at the
gastro-esophageal junction and usually extend distally
into a hiatal hernia .
•Typically have a history of recent non-bloody vomiting
with excessive retching followed by hematemesis..
•Endoscopy usually reveals a single tear that begins at
the gastro-esophageal junction and extends several
millimeters distally into a hiatal hernia sac/within
cardiac portion of stomach.

16. Haemorragic/Erosive gastritis
•Stress related mucosal injury
•Occur mostly in extremlysick patients
•Major Trauma
•Post Major Surgery
•3
rd
Degree burns
•Major intracranial disease
•Severe medical illness (Ventilator dependence, coagulopathy)
•Significant bleeding probably does not develop unless ulceration occurs.
•Intravenous H
2-receptor antagonist is the treatment of choice. Sucralfate
also effective
•Aspirin and NSAIDS
•Half of the patient who chronically ingest NSAIDS have Erosions. (15 –30%
have Ulcers)
•Most Frequently and severely affected site is gastric antrum.

17. PORTAL GASTROPATHY
•On endoscopic examination mucosa is engorged and
friable.
•Portal hypertensive gastropathy(PHG) is caused by
increased portal venous pressure and severe mucosal
hyperemia that results in ectaticblood vessels in the
proximal gastric body and cardiaand oozing of
blood.
•Less severe grades of PHG appear as a mosaic or
snake skin appearance and are not associated with
bleeding.
•Usually, patients with severe PHG present with chronic
blood loss, but they occasionally can present with
acute bleeding.

18. DIEULAFOY'SLESION
•It is a large (1-to 3-mm) submucosalartery that protrudes
through the mucosa.
•It is not associated with a peptic ulcer, and can cause
massive bleeding.
•It usually is located in the gastric fundus, within 6cm of the
gastroesophagealjunction.
•Dieulafoy'slesion can be difficult to identify at endoscopy
because of the intermittent nature of the bleeding.
•the overlying mucosa may appear normal if the lesion is not
bleeding.

19. GASTRIC ANTRALVASCULAR ECTASIA
•Gastric antralvascular ectasia(GAVE), also described as watermelon
stomach.
•Characterized by rows or stripes of ectaticmucosal blood vessels that
emanate from the pylorus and extend proximally into the antrum .
•Unknown etiology
•Common in older
womenand patients
with ESRD

20. Aortoentericfistula
•The A-E fistula is a communication between the
native abdominal aorta and, most commonly,
the third portion of the duodenum.
•Bleeding is usually acute and massive, with a high
mortality rate(30-100%).
•Often, a self-limited herald bleed occurs hours to
months before a more severe, exsanguinating
bleed.
•The fistula usually forms between three and five
years after graft placement.

21. Presentation

22. 1. Hematemesis
•Vomiting of red blood or coffee-grounds
material when gastric acid converts hemoglobin
into methemoglobin.
Differentiate from :-
Hemoptysis.
Bleeding from Pharynx , nasal passage
USUALLYhematemesisrequiresabucket;BUThaemoptysis
asmallbowl.

23. 2. Melena
•Passage of black tarry stools.
•EBL > 50-100 ml /day will produce melena.
•The black color is caused by Hematin, the
product of oxidation of Hemeby intestinal
and bacterial enzymes.
•10% LGI bleed
•Can be swallowed blood from epistaxis
•Blood for 14 hrsin the GI tract
•Drugs like Oral iron and bismuth mimics
melena.
3. Hematochezia
•It is defined as passage of bright-red or
maroon blood from the rectum.
•Common in bleeding from colon, rectum
and anus.
In case of brisk bleeding in the UGI, bright
red blood may come out unchanged in
the stool.
10% of UGI bleed
Symptoms of blood loss or anemia
•Light headedness, syncope, angina, or dyspnea, palpitations

24. Aetiology Leading history
MalloryWeisstear
Multiple Emesis before hematemesis, alcoholism, retching
Esophageal ulcer
Dysphagia, Odynophagia, GERD
Peptic ulcer
Epigastricpain, NSAID or aspirin use
Stress gastritis
Patient in an ICU, gastrointestinalbleedingoccurring
after admission,respiratoryfailure,multiorganfailure,coagulopathy
Varices, portal
gastropathy
Alcoholism, Cirrhosis of liver
Gastricantral
vascular ectasia
Renal failure, cirrhosis
Malignancy
Recent involuntary weight loss, dysphagia, cachexia,
early satiety
Angiodysplasia
Chronic renal failure, hereditary hemorrhagic
telangiectasia
Aortoentericfistula
Known aortic aneurysm, prior abdominal aortic
aneurysm repair
Clues regardingthe cause of acute UGI bleeding

25. •Pallor , signs of dehydration , Shock
•Icterus
•Clubbing
•Oedema
}Liver disease
Physical Examination

26. Lymphadenopathy
Virchow’s Node
(Troisier’ssign)
Vital signs
Tachycardia
Hypotension
Tachypnea

27. •Ascites •Spider naevi
•Palmar erythema •Dupuytren’scontracture

28. •Leuconychia •Gynecomastia
•Bleeding manifestations•Scars of previous surgery

29. •Splenomegaly
•Caput medusae
•Parotid Swelling
•Fetor hepaticus
•Asterixis
•Testicular atrophy
•Acanthosisnigricans
•Alopecia
•Glossitis
•Loss of Axillary hair
•Loss of Pubic Hair

30. Inspection
Distention , Dilated Veins
Swelling
Visible peristalsis
Palpation
Tenderness
HSM, secondary metastasis
Sister Mary Joseph nodules
Mass
Percussion
Shifting dullness
HSM
Auscultation
Absent Bowel sound
Bruit
Cruveilhier-Baumgartenvenous hum
ABDOMEN EXAMINATION

31. APPROACH TO A PATIENT WITH
UGIB
Immediate Initial Assessment
Stabilization of haemodynamic status
Identify bleed source
Stop active bleed
Treat underlying cause
Prevent recurrence of bleeding

32. Risk assessment & triage
Risk for mortality and
rebleeding.
Categorisedas
low,
intermediate
high risk
Record the GCS
Poo prognostic factors
1.Age over 60
2.Shock(SBP<100mmhg), pulse >100
3.Malignancy or varices as bleeding source.
4.Severe coagulopathy
5.Comorbid medical illness
6.Continued or recurrent bleeding
7.Multi-organ failure

33. Workup
Bloods
•Hematology-FBC, G+ crossmatch
•Biochemistry-U&Es, LFT+ albumin
•Serology-H-pylori, HepB/C,HIV, schistosomiasis
•Coagulation profile
•Stool: occult blood
Imaging
•Esophagogastroduodenoscopy
oTherapeutic and diagnostic
•CXR
•ECG
•AbdominalUSS
•CT Angiography

34. MANAGEMENT OF UGIB
GENERAL MEDICAL
MANAGEMENT
TYPE OF BLEEDING
VARICEAL
BLEEDING
NON VARICEAL
BLEEDING
MEDICAL ENDOTHERAPY
SURGICAL
INERVENTION
PRESSURE
TECHNIQUES

35. AUGIB
RapidAssessment
MonitorHemodynamic Status
FluidResuscitation
Ryle;stubeforGastricLavage
Self Limited Hemorrhage (80%) Continued bleeding (10-25%)
Urgent endoscopy
Recurrent Hemorrhage
Elective Endoscopy
(With in 24 –48 hours)
Definitive Therapy
(If Necessary)
Site not localized Localized
Further Assessment
(Extended EGD,
Radio-isotope
scan,
Arteriography,
Exploratory
Laprotomy)
Definitive
Therapy