1. UGI bleed
Dr Manoj K Ghoda M.D., M.R.C.P.
Consultant Gastroenterologist
Visiting faculty, GCS hospital
mkghoda@yahoo.com
Gujarat gastro group

2. 45 years old male
Referred for UGI endoscopy for “hematemesis”
Vomited blood previous night
Since then he has blood collecting in his mouth
No h/o drug ingestion
No alcohol, no tobacco
Previously diagnosed to have hypertension and on
medication but otherwise fit and well
When confronted with such a case scenario what
should you check?

3. When confronted a patient with
“hematemesis” you should have following
check list
•Is it really hematemesis?
•If it is, is patient stable?
•How bad is hematemesis? What is the
estimated amount of blood loss?
•What could be the lesion?
•Where could be the lesion?
•What could be its blood supply?

4. Is it really hematemesis?
•Vomiting of blood from GI tract is called
hematemesis.
•Apart from UGI tract, blood could be from
respiratory tract, from mouth, and from nose.
•Unless a careful history is taken, wrong
assumption could be made leading to diversion
to a system actually not responsible in the first
place, causing delay in diagnosis and even
death, not to speak of unnecessary expense and
hardship to patient.

5. Is it Hematemesis?.........
Some clinical considerations..
•Bright red blood is less likely to be from upper GI. Consider
epistaxis, hemoptysis or bleeding gums and of course, fictitious
bleeding.
•Frothy blood or blood in lumps is more likely to be from lungs.
•Epistaxis is never a part of hemetemesis. More likely that blood
from epistaxis is swallowed and brought out as hematemesis.
Blood pressure in such cases is very high.
•A small amount of blood, mostly red, after several bouts of
violent retching and non-bloody vomiting, is almost certainly a
Mallory-Weiss tear, and if this is followed by severe chest pain, a
transmural esophageal tear, the “Boerhaave syndrome”.

6. •Blood accumulating in mouth requiring patient to spit it
out is either dental bleed or epistaxis. Dental or gum
disorders may be present in the past.
•Coffee colored or black vomiting is hematemesis, due to
bleeding from upper GI, unless otherwise proved. History
and physical findings of portal hypertension or acid
peptic disease may be present.
This preliminary inquiry will always lead you to the
correct line of investigation and treatment.

8. It always help to check visually...

9. Patient with hematemesis usually requires a bucket;
whereas patient with hemoptysis usually requires a small
bowl
Is it hematemesis?

10. How bad is the bleeding?
…………. Assessing the blood loss.
•Resting pulse and B.P. normal = < 500 ml. blood
loss.
•Resting tachycardia and postural drop of B.P. =
up to 2.0 L loss.
•Shock = > 2.0 l blood loss.

11. What could be the cause of bleeding?
Common causes of UGI bleed in Indian context.
Remember!! Ca esophagus or Ca stomach rarely, if ever,
present with GI bleed. They always have other features of
presentation.
Esophageal Gastric varices are
now one of the commonest
cause of upper GI bleed in
pediatric population
•Peptic ulcer, duodenal or
gastric. Related or unrelated to H.
Pylori.
•NSAID induced mucosal injury,
erosions, and ulcers.
•Esophageal varices are now one
of the commonest cause of
upper GI bleed in India.
•Mallory-Weiss tear.
•Gastric varices.
•Portal hypertensive gastropathy.
•Dieulafoy lesion.

12. Dieulafoy lesion
Varices
Gastric erosions

13. Where could be the lesion?

14. What is the blood supply of the lesion?

15. Could you name these blood vessels ?

16. Blood supply of the lesion
Esophagus:
•Upper esophagus is supplied
from superior and inferior
thyroid arteries.
•Mid-esophagus by the
bronchial, right intercostal
arteries and descending aorta.
•Distal esophagus by left gastric
left inferior phrenic and splenic
arteries.

17. •The venous drainage of upper
esophagus is through the superior
vena cava.
•Mid esophagus through azygous
veins.
•Distal esophagus through portal
vein by means of left and short
gastric veins. Through these veins
there is a porta-systemic
communication.
There is an extensive submucosal
venous anastomotic network
which is very important because
in portal hypertension blood is
diverted from high pressure portal
venous systems to low pressure
systemic circulation via this
network resulting in esophageal
varices.

18. X
X
X
X
X
X
Vascular supply
of stomach
Could you name these blood vessels ?

19. Stomach:
Arterial supply is from celiac artery; through common hepatic, left gastric and
splenic arteries, which form two arterial arcades along lesser curvature and lower
two thirds of greater curvature.
Gastric fundus and left upper aspect of greater curvature are supplied via short
gastric arteries, which arise from the splenic artery.
Greater curvature below fundus is supplied from above by left gastroepiploic artery,
a branch of splenic artery and from below by right gastroepiploic artery, a branch of
gastroduodenal artery and these two usually anastomose.
Lesser curvature is supplied from above by left gastric artery and from below by
right gastric artery or gastroduodenal artery, branches of common hepatic artery.

20. X
X
Duodenum:
Celiac trunk supplies
proximal duodenum via
hepatic artery, from which
arises gastroduodenal
artery, which in turn
branches into superior
pancreaticoduodenal
artery, which gives off
anterior and posterior
branches to duodenum.
Distal duodenum is
supplied by branches the
superior mesenteric artery.
Could you name these blood vessels ?

21. Branches of Common Hepatic Artery?

22. Remember, the celiac trunk has three main branches
1--Left gastric artery (supplies L greater curvature of
stomach)
2--Splenic artery (spleen, pancreas, left greater curve of
stomach)
3--Common hepatic artery (liver, gall bladder, right greater
curvature, head of the pancreas)

23. Clinical presentation of UGI bleed:
•Presentation may be as coffee-brown vomiting known as
hematemesis, or there may be frank red blood.
•Mallory-Weiss tear usually presents with one or more clear vomits
followed by reddish, rather than coffee brown blood.
•Some patients present with dark black, like coal tar, stool known
as melena.
•Some people with massive bleed will have both Hemetemesis and
bleeding PR which is not dark black but red.
•There may be nausea, dizziness, and perspiration related to
hypovolemia and hypotension
•Patients with acid-peptic disease give a history of epigastric pain
for sometime before the illness and there may be history of
analgesic ingestion.
•There may be past history of jaundice, ascites or other features of
chronic liver disease.

24. How will you decide if the patient needs
admission or could be discharged home?

25. Identifying high risk patients.
•When the patient is in shock.
•Patients above the age of 65 years.
•Patients with co-morbid conditions like IHD,
hypertension, diabetes, coagulopathy or chronic liver
disease.
•Where there is simultaneous upper and lower GI
bleeding.
•Previous ulcers/bleed
•Patient having rebleed during the same admission
•On steroids or NSAIDs
•Alcoholic or tobacco smoker
Can you Identifying high risk Doctors ?

26. The Rockall Score for stratifying risk
Variable
0
Score
1 2 3
Age (yrs) < 60 60-79 ≥ 80
Comorbidity No or mild
coexisting
Moderate
coexisting (e.g.,
hypertension)
Severe coexisting
(e.g., CHF)
Life threatening
(e.g., RF)
Hemodynamic
status
No shock
P < 100
Syst BP ≥ 100
P ≥ 100 plus
Sys BP ≥ 100
Hypotension
Diagnosis MW tear, normal
endoscopy with
no blood seen
All other
diagnosis
Malignancy of UGI
tract
Major stigmata
of recent
hemorrhage
None or dark
spot
Blood in UGI tract
Adherent clot,
visible or spurting
vessel
Rockall, Lancet 1996

27. ROCKALL System - Rebleeding
According to Risk Score Category
Rockall et al. Gut 1996;38:316
Rockall score
Cumulativepatientswithrebleeding
Enns RA, W J Gastroenterol, 2006

28. The Glasgow-Blatchford Bleeding Score
• GBS superior to total/clinical
Rockall scores (ROC curves, P<0.05)
• 123 patients (22%) classified as low
risk, with 84 (68%) were managed
as outpatients safely
• Proportion admitted fell (96% to
71%, p<0·00001)
Stanley, Lancet 2008
Score-value
Blood urea (mmol/L)
6.5-7.9 2
8.0-9.9 3
10.0-25.0 4
>25.0 6
Haemoglobin for men (g/L)
120-129 1
100-119 3
<100 6
Haemogolbin for women (g/L)
100-119 1
<100 6
Systolic blood pressure (mmHg)
100-109 1
90-99 2
<90 3
Other markers
Pulse >100/min 1
Presentation with melaena 1
Presentation with syncope 2
Hepatic disease* 2
Cardiac failure** 2
*Known history, or clinical and laboratory evidence, of chronic or acute liver disease.
** Known history, or clinical and echocardiographic evidence, of cardiac failure.
Admission risk markers for
GBS

29. Who could be Discharged from ER?

30. Who can be sent home from the emergency room?
Gralnek, NEJM, 2008
These patients
represent up
to 20-40% of
all patients
presenting with
PUB

31. Investigations:
•CBC with indices.
•Where indicated liver function test and coagulation
profile.
•Renal function tests.
•Endoscopy, once the patient is stable.
•Sonography when portal hypertension is suspected.
•Abdominal angiography in selected cases.

32. Managing UGI bleed:
Some fundamentals:
•Rule of 18; 18 G venflon, 18 F Ryle’s tube, endoscopy in 18 hrs,
•Irrespective of degree of blood loss it is always safer to cross
match at least one unit of PCV to cope with any unexpected
requirement.
•This is a volume loss so..replace volume, use pressure agents
as last resort
•A large bore, 18F, Ryle’s tube is passed and stomach washed
off any blood clots in anticipation of urgent endoscopy.
•Cold saline lavage has no benefit and will cause unnecessary
delay and temperature disturbances. Similarly lavage with
adrenaline, noradrenalin and various “coagulating agents” have
very little to offer.
•If pt has no vomiting, clear fluid is allowed.

33. Resuscitation:
•For small amount of blood loss with normal pulse and
B. P., crystalloids like normal saline etc. are enough.
•For moderate blood loss crystalloids plus colloids like
dextran 70/40 %, hydroxyethyl starch, are required to
maintain B.P. Blood may be required as well, depending
upon the patient’s fitness and previous hemoglobin levels.
•For large blood loss, colloids and crystalloids and blood
are all required, sometimes simultaneously.
•Fluid input is monitored by central venous pressure,
pulse, blood pressure, and hourly urine output and
hemoglobin level. Blood transfusion is given to keep Hb
around 10 Gms.

34. •Pressure agents like dopamine 2.5 to 10 mcg/kg/min,
and dobutamine 2.5 to 10 mcg/kg/min as infusion,
Noradrenalin 3mg. /Hr as infusion may be required, as a
last resort, to maintain peripheral perfusion.

35. •IV Erythromycin and Metochlopromide may be used to
increase forward motility to clear the stomach of clots for
better visualization.
•Somatostatin, 250 mcg bolus and then 250 mcg/ hr as
infusion may be helpful in variceal bleed, and perhaps
bleed of hypertensive gastropathy and ulcer bleed by way
of producing splanchnic vasoconstriction; and is started
while awaiting definitive treatment.
•IV Omeprazole / Pantaprazole is given 40 mg. diluted in
saline, and then 4mg/ hr. and 8mg//hr as infusion
respectively for bleeding ulcers.
•Any disturbance of coagulopathy is corrected using
vitamin K, fresh frozen plasma, platelet infusion and
where appropriate specific clotting factors.

36. •For patients requiring large numbers of blood, i.v.
calcium is supplemented; platelet infusion, one unit for 4
PCV and fresh frozen plasma, 2 units for 4 PCV, are also
required in these circumstances.
•For known or possible cirrhotic, lactulose is given orally
30 ml. Every 2 hours till the diarrhea establishes when
the dose is reduces to produce two stools / day. If oral
lactulose is not possible lactulose enema is given.
•Once the patient is stable, endoscopy is done.

37. Variceal bleeding
Pharmacotherapy consists of
•splanchnic vasoconstrictors (vasopressin and
analogues, somatostatin and analogues,
•nonselective -blockers) and
•venodilators (nitrates)
AASLD PRACTICE GUIDELINES

38. Effect of drugs used for varices
AASLD PRACTICE GUIDELINES

39. Patients with Cirrhosis and an Acute
Episode of Variceal Hemorrhage
Antibiotic prophylaxis
• Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in
any patient with cirrhosis and GI hemorrhage (Class I, Level A).
• Oral norfloxacin (400 mg BID) or intravenous ciprofloxacin (in patients in
whom oral administration is not possible) is the recommended antibiotic
(Class I, Level A).
• In patients with advanced cirrhosis intravenous ceftriaxone (1 g/day) may be
preferable particularly in centers with a high prevalence of quinolone-
resistant organisms (Class I, Level B).
Pharmacological therapy
• Pharmacological therapy (somatostatin or its analogues octreotide and
vapreotide; terlipressin) should be initiated as soon as variceal hemorrhage is
suspected and continued for 3-5 days after diagnosis is confirmed (Class I,
Level A).
AASLD PRACTICE GUIDELINES

40. Interventions
• OGD, performed within 12 hours, should be used to make the
diagnosis and to treat variceal hemorrhage, either with EVL or
sclerotherapy (Class I, Level A).
• Balloon tamponade should be used as a temporizing measure
(maximum 24 hours) in patients with uncontrollable bleeding
for whom a more definitive therapy (e.g., TIPS or endoscopic
therapy) is planned (Class I, Level B).
• TIPS is indicated in patients in whom hemorrhage from
esophageal varices cannot be controlled or in whom bleeding
recurs despite combined pharmacological and endoscopic
therapy (Class I, Level C).
AASLD PRACTICE GUIDELINES

43. Tips

44. Tips

45. PEPTIC ULCER BLEED

46. Overall management
 ABC’s and adequate resuscitation
 Early risk stratification
o pre-endoscopy
o at early endoscopy
Very Low risk patients
 discharge home
All other patients
 admit
High-risk patients
 Endoscopic hemostasis
 Initiate high-dose IV PPI
Consider secondary prophylaxis
 H pylori testing and treating
 NSAID/COX2 use
 ASA use
Low-risk patients
 Initiate daily dose PPI

47. Ulcer bleed
•Adrenalin Injection
•Heater prob
•Hemoclip application

48. THANK YOU
Dr Manoj K Ghoda
Consultant Gastroenterologist
Visiting faculty, GCS hospital
mkghoda@yahoo.com
Gujarat gastro group