This patient, a 52-year-old male, presented to the emergency room after vomiting coffee ground material and blood clots during bowel movements that morning. He briefly lost consciousness. The emergency case is acute upper gastrointestinal bleeding. The patient is presenting with hematemesis (vomiting blood) and melena (black tarry stool), which are signs of a bleed in the upper GI tract. The most probable cause is esophageal varices, given that esophageal varices are the most common cause of acute UGI bleeding in Egypt, accounting for around 55% of cases. Immediate resuscitation efforts are needed to stabilize the patient, including IV access, fluid resuscitation, blood

1. THEME CASE
DISCUSSION
Gastroenterology
DR Abdelrahman A.Mokhtar

2. Case scenario
A 52 years old male from Talkha , DK
presented to ER complaining of vomiting of
blood about 1 cup of coffee ground material
with 2 clotts during abolution this morning ,
His wife told that he suffered a momentary
fainting attack when he tried to complete his
abolution , so
She kept him at bed until the ambulance
came and brought him to the Emergency
room.

3. What is the Emergency Case ?????
What is the possible presentation of this case????
What is the most probable cause of such a condition ?

4. Don’t forget about mimics:
WHAT IS THE EMERGENCY CASE ?????

5. WHAT IS THE POSSIBLE
PRESENTATION OF ACUTE UGIB ????

6. WHAT IS THE MOST PROBABLE CAUSE
OF SUCH A CONDITION ?

7. ACUTE UGI BLEEDING
ETIOLOGY (EGYPT)
Esophageal varices 55%
Acute gastric erosions 15%
Chronic DU
Chronic GU
Esphagitis & erosions
Mallory Weiss tears
Duodenitis
Gastric cancer
Coagulopathies

8. What is the Sequence of events?
IN THE ER

9. Rapid History
Rapid Examination
IN THE ER
Investigation
Resuscitation
Stabilization
Initial assessment

10. TARGETS OF INITIAL ASSESSMENT
• Severity of the attack …….Immediate ( first aid ) management.
• The most probable cause………Long term plan.
• Comorbidities…………..Prognosis

11. Hematemsis , hematochezia ?
Altered digested ,Fresh bright blood ?
Clotts ?
 Associated symptoms ( compromised
perfusion to vital organs e.g disturbed
sensorium , chest pain , …etc.

12. Vital signs.
Postural changes ( role of 20 ).
Shock:
Massive hemorrhage: shock (supine hypotension) 20-25%
loss of vascular volume
Submassive hemorrhage: orthostatic hypotension 15-20%
loss of vascular volume
Trivial hemorrhage: No change in vital signs < 15% loss
of vascular volume

13. Hemoglobin & Hct changes.
Hypoperfusion to vital organs :
ECG ischemic changes?????
Prerenal azotemia , oliguria.

14.  Present History : ???Other orificial or subcutaneous bleeding???

16. CAUSES OF MORTALITY IN PATIENTS WITH PEPTIC ULCER
BLEEDING
Most common causes of non-bleeding mortality:
Terminal malignancy (34%)
Multiorgan failure (24%)
Pulmonary disease (24%)
Cardiac disease (14%)
Comorbid illness rather than actual bleeding, is the major
cause of death.
Am J Gastroenterol 2010;105:84

17. Resuscitation

18.  Principles of resuscitation ( ABC )
 Ryle tube insertion.
 Blood transfusion.
 Cirrhotic Coagulopathy.
RESUSCITATION

19. Airway and Breathing
 Administer oxygen if saturation is low.
If applying an oxygen mask, keep in mind if he has another episode of
hematemesis you will need to take this off immediately, to reduce the chance of aspiration .
Circulation
This patient is hemodynamically unstable and therefore requires several
interventions including:
 Large-bore IV access (x2)
 Blood tests – FBC, U&Es, LFTs, clotting, group and cross match blood
 IV fluids (crystalloids)
 Blood transfusion – to replace blood lost due to haemorrhage
 Strict fluid balance (including catheterisation to measure urine output accurately)
 Correction of any identified clotting abnormalities may be required with vitamin K,
FFP and platelets .
ABC
Principles of resuscitation ( ABC )

20. Gastric lavage
 Indicative of a UGIB , but may be negative in 15% of cases with
UGIB.
 Clears the gastric contents to aid visualization
 Removes bright red blood, coffee ground material, and clots from
the stomach to avoid HE.
The patient’s level of consciousness must be taken into
consideration during this procedure; a patient with a diminished gag
reflex may require airway support with endotracheal intubation.
.
RYLE TUBE
Ryle tube insertion.

21. GENERAL PRINCIPLES OF TRANSFUSION IN UGIB EMERGENCIES
Hemodynamic instability: Transfuse regardless of hemoglobin
level
Shock index: A shock index (HR/SBP) of >1 should trigger
consideration for massive transfusion
Don’t trust the Hb: Hemoglobin often lags behind bleeding, so
trend it by repeating the hemoglobin in an hour or two.
Consider clinical factors: Pre syncopal patient, high volume
blood loss or brisk bleeding should trigger consideration for red
cell transfusion.
Be flexible: Lower your threshold to transfuse in patients with
co-morbidities such as coronary artery disease or coagulopathy.
Portal bleeding: Restitution of blood volume may be associated
with recurrence of portal bleeding.
Blood transfusion.

22. DONOT TRUST HGB

23. WHAT IS MY TARGET HGB ?
The hemoglobin target should be > 7 g/dL (>70 g/L) in
nearly all cases
Exceptions include:
Massive bleed with hemodynamic instability.
Acute coronary syndrome (target hemoglobin > 8 g/dL or >80 g/L).
Don't transfuse to a high hemoglobin to “tank up” the patient.
Massive transfusion protocol (MTP): For severe instability (e.g. vasopressor
dependence) consider activation of a massive transfusion protocol .
Blood transfusion.

24. Blood transfusion.

25. Portal bleeding:
Variceal bleeding is
from a venous source,
so any fluid will
increase the central
venous pressure and
directly promote
bleeding .
These patients often
live at a low blood
pressure (e.g. 80-90
mm systolic), so
borderline
hypotension is
preferable to large-
volume resuscitation.

26. When in doubt, try to avoid massive transfusion in patients with variceal
hemorrhage. This can rapidly devolve into a vicious cycle which promotes
ongoing bleeding and worsening coagulopathy

27. Best case scenario:
• Profound anemia (e.g.
hemoglobin <5 g/dL or <50
g/L) in a patient who is
hemodynamically stable and
minimally symptomatic implies
a chronic bleed, with little risk
of rapid deterioration. These
patients have been bleeding for
days, meanwhile
• gradually retaining volume to
compensate (isovolemic
anemia).
• The only immediate danger to
these patients is iatrogenic: if
given blood too rapidly they will
develop volume overload. Ideal
management isn't to slam in
several units of blood, but
rather to provide
• gradual transfusion (often in
combination with diuresis).
Intermediate scenarios:
• Many patients will present
with moderate anemia (e.g.
hemoglobin
• 6-7 g/dL or 60-70 g/L)
and hemodynamic stability.
In this case, it can be
helpful to
• determine the patient's
response to blood
transfusion. A unit of
packed cells should
• increase hemoglobin by
~1 g/dL (~10 g/L).
Failure to respond
appropriately to
transfusion implies
ongoing bleeding.
Worst case scenario:
• Normal hemoglobin
with hemodynamic
instability is worrisome
for
• severe bleed.
Hemoglobin takes time
to fall in response to
bleeding,
• so normal hemoglobin
plus shock implies a
very active bleed.
DON'T FORGET WE ARE TREATING
PATIENT NOT TREATING LAB
Take home message

28. CIRRHOTIC
COAGULOPATHY
Most cirrhotics are in a state of rebalanced hemostasis, due
to similar reductions in pro- and anti-coagulant
proteins. This often yields a normal overall clotting
tendency.
INR measures the level of clotting factors only, not the
overall balance of coagulation. To determine the balance of
enzymatic coagulation, thromboelastography (TEG) is
needed.
Responding to an elevated INR by transfusing FFP is a
misguided practice which should be abandoned.
 Cirrhotics rarely have true enzymatic hypocoagulability, so
they generally do not benefit from FFP.

29.  Trying to “correct” the INR with fresh frozen plasma is a classic mistake. This is
rarely benefecial. Studies in cirrhosis have shown that administration of FFP
generally doesn't improve coagulation.
 Giving platelets can be helpful if the platelet count is <50,000. Unfortunately platelets
are often consumed rapidly, making this a short-lived intervention.
 Many patients with cirrhosis develop hyperfibrinolysis, which causes ongoing
degradation of their fibrinogen. Hyperfibrinolysis is suggested by the presence of a
low fibrinogen level.
 For bleeding cirrhotic patients with a low fibrinogen consider:
• Cryoprecipitate transfusion to increase the fibrinogen level over ~150 mg/dL
(~1.5g/L)
• Tranexamic acid to prevent ongoing fibrinolysis.
CIRRHOTIC
COAGULOPATHY

30.  The general strategy of repleting blood factors individually
to target a roughly “euboxic” coagulation panel should be
questioned. It is possible that focusing on the overall
balance of coagulation and fibrinolysis, rather than
individually normalizing each component, may allow for a
more flexible and effective approach.
CIRRHOTIC COAGULOPATHY

31. CONSIDER THROMBOELASTOGRAPHY (TEG)
TO TEST ENZYMATIC COAGULATION
Recently TEG has
emerged as a more
integrative
approach which
explores both
clotting factors
and cellular
interactions.
This involves
monitoring
thrombosis and
thrombolysis
within a sample of
whole blood .

32. For now, the following approach may be reasonable:
CIRRHOTIC COAGULOPATHY

33. RISK
STRATIFICATION
( pre & post endoscopy)

34. Risk assessment scores for all patients with acute upper
gastrointestinal bleeding:
 Use the Blatchford score on first assessment to help
inform management decisions.
 Use the Rockall score after endoscopy to assess the
patient’s risk of re-bleeding and death.
Patients who re-bleed have a high mortality rate.
RISK STRATIFICATION

36. The GBS is used in EDs to stratify risk and
determine the best treatment options.
Patients with a GBS of zero may not require any
intervention and could potentially be discharged
from the ED.
Patients with scores from one to five are at risk and
should be admitted to the hospital for further
evaluation and management.
High-risk patients with a score of six or more are
admitted for immediate intervention to stop
the bleeding.
THE BLATCHFORD SCORE
GBS—A risk
stratification tool

37. A score of less than 3 is
associated with a good
prognosis, while a score of
greater than 8 is associated
with a high risk of death.
ROCKALL SCORE

40. TREATMENT

41. Resuscitate then
Endoscopate
ENDOSCOPY
NICE guidelines recommend offering
endoscopy to unstable patients with severe
acute upper gastrointestinal bleeding
immediately after resuscitation.
All other patients with UGIB should be
offered endoscopy within 24 hours of
admission.

42. Endoscopy
One stop Shop
Diagnose
Assess
Treat
Reassess

43. VASOACTIVE TREATMENT

44. VASOACTIVE TREATMENT

45. Balloon tamponade as abridge

46. TO STOP VARICEAL BLEEDING

47. ENDOSOPY

48. PPI
Proton pump inhibitors-
its use is widely adopted and is mandatory in all UGIB.
PPIs are the only drugs that can maintain a gastric pH >6 and thus
prevent fibrinolysis of clot
In patients initially treated with a bolus infusion of omeprazole/
pantaprazole 80 mg followed by a continuous infusion 8mg/hr ,and
the need for endoscopic therapy has reduced.
PPI+ Endotherapy shown the best results in terms of rebleeding,
morbidity and mortality.

49.  MONITORING FOR REBLEEDING .
 RESUME ORAL FEEDING .
 DISCHARGE & 2ry prophylaxis .
AFTER CONTROL OF BLEEDING

50. Early feeding (within 4 hrs ) with a regular semi solid diet in
conscious patients after successful variceal ligation for esophageal
varices is safe, provides better nutrition and results in lower
incidence of infections in bleeders compared to delayed feeding.
ORAL FEEDING

51. To clinically monitor for possible rebleeding you should order
the following:
 Check vital signs hourly
 Re-examine the patient after 4 hours
 Monitor the color of stool.
 Monitor the patient appetite.
 Perform daily blood tests
– FBC, U&Es, LFTs
MONITORING FOR REBLEEDING
Clinical signs
associated with
rebleeding include:
Tachycardia
Reduced urine
output
New haematemesis
and/or melaena
Hypotension (late
sign)

52. 2RY PROPHYLAXIS