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GI BLEEDING
Dr Anoop V
JR EM
SSIM S
• Upper and lower gastrointestinal bleeding (GIB)
are defined based on their location relative to
the ligament of Treitz in the terminal duodenum
• Esophagus, stomach, and duodenum origin
bleeds are upper and all others are lower.
• Upper GIB (UGIB) mortality rates have remained
constant at about 15% over the past 2 decades despite
advances in medical therapy, intensive care unit (ICU)
management, endoscopy, and surgery.
• The lower GIB (LGIB) mortality rate is approximately
4%.
• Despite diagnostic advances for all ages, the source of
GIB is not identified in nearly 15% of patients.
• The characteristics of the GIB, age of the
patient, and social factors can all help
determine the cause.
• UGIB can routinely manifest as
I. bloody or coffee-ground–like vomit termed
hematemesis or as
II. dark, tarry stools termed melena.
ADULT PEDIATRICS
OLDER
1) PUD
2) ESOPHAGITIS
3) GASTRITIS
YOUNGER
1) MALLORY WEISS
TEAR
2) GI VARICES
3) GASTROPATHY
1) GASTRIC/DUODENAL ULCER
2) ESOPHAGITIS
3) GASTRITIS
4) ESOPHAGEAL VARICES
5) MALLORY WEISS TEAR
• LGIB usually produces bright red or maroon
blood per rectum,termed hematochezia
• Classified according to pathophysiologic cause
a) Inflammatory
b) Vascular
c) Oncologic
d) Traumatic
e) Iatrogenic
• Anorectal sources, such as hemorrhoids, are
the most common causes of LGIB in all age
groups
ADULTS
1) COLONIC DIVERTICULA
2) ANGIODYSPLASIA
3) COLITIS DUE TO
• ISCHEMIA
• INFECTION
• INFLAMMATORY BOWEL
DISEASE
CHILDREN
1) ANORECTAL FISSURES
2) INFECTIOUS COLITIS
3) INTUSUSCEPTION
4) MECKEL DIVERTICULAM
• Death from exsanguination resulting from GIB
is rare.
• However, there are two causes of GIB that
may rapidly cause death if not recognized and
mitigated,
a) esophageal varices
b) aortoenteric fistula.
• Esophageal- varices which typically arises from
portal hypertension usually caused by
alcoholic cirrhosis, is the single most common
source of massive UGIB and has a mortality
rate of 30%.
• Aorto-enteric fistula is a rare but rapidly fatal
cause of GIB, with the mortality of an
untreated fistula of nearly 100%.
• Epistaxis, dental bleeding, or red food coloring
can mimic the appearance of hematemesis
• Bismuth-containing medications and iron
supplements can create melanotic-appearing (but
guaiac-negative) stools
• Vaginal bleeding, gross hematuria, and red foods
(eg, beets) can all be mistaken for hematochezia
• The history centres on the GI tract and on the
timing, quantity, and appearance of the
bleeding.
• Reviewing the patient’s vital signs, appearance
of the stool, and basic laboratory studies will
help identify the bleeding source and guide
treatment
Symptoms
• A useful starting point is to determine the
a) time of onset,
b) duration of symptoms, and
c) relevant supporting historical facts.
• weakness,
• shortness of breath,
• angina,
• orthostatic dizziness, > 800 ml blood loss
• confusion,
• palpitations,
• cool extremities
• The context of the bleeding can help explain its cause
• if a patient complains of bright red blood per rectum after
several days of constipation and straining, that presentation
suggests an anorectal source.
• a patient with hematemesis after several earlier episodes
of retching would lead one to suspect an esophageal tear.
• a patient with easy bruising and recurrent gingival bleeding
might suggest an underlying coagulopathy.
Relevant Medical History
• note whether a patient has had similar bleeding
before and the location of the causative lesion
• identification of relevant comorbid diseases helps
risk stratify these patients in the context of their
bleed. Patients with GIB and a history of coronary
artery disease, congestive heart failure, liver
disease, or diabetes have a higher mortality and
therefore may require earlier or more extensive
interventions
.
• A review of the patient’s medications should pay
particular attention to gastrotoxic substances,
anticoagulants, and anti platelet drugs
• Alcohol abuse is associated with gastritis and
peptic ulcerdisease. It can also result in cirrhosis,
portal hypertension and,ultimately, esophageal
variceal bleeding
• Smoking cigarettes results in slower healing and
greater recurrence of ulcers
SIGNS
• Pulse- tachycardia indicates shock
• Temperature- cool extremities – hypovolemic
shock
• BP- hypotension – shock
• Pallor
a) Stable patient – sub acute or chronic
b) Unstable patient – massive blood loss
• Icterus – UGIB from varices
• General examination
Mental status is evaluated for signs of poor cerebral perfusion
spider angioma , palmar erythema – UGIB from variceal indices
Ecchymoses or petechiae suggest a coagulopathy
ABDOMEN
Tenderness on palpation may be seen in PUD
Severe diffuse tenderness on examination warrants
a) Bowel ischemia
b) Mech obstruction
c) Ileus
d) Bowel perforation
hepatomegaly, ascites, or caput medusae.- portal HTN
Hyperactive bowel sounds- Non specific but can indicate UGIB
Investigations
1) Occult blood and Guanic testing
H2O2 + guainic paper containing stool = blue
(positive)
• makes use of the pseudoperoxidase activity
found in hemoglobin.
False positive Guanic negative
Red meet
Vitamin c
Turnip
Iron
Bismuth
2) Blood investigations
• Hemoglobin, RFT, platelet and coagulation should
be sent
Hemoglobin
• The hemoglobin level does not immediately decline in
the setting of an acute bleed, because whole blood is
lost.
• Changes in hemoglobin levels are typically seen after
24 hours, when there is hemodilution from shifting
extravascular fluids and intravenous (IV) hydration with
crystalloid
• acute hemoglobin levels less than 10 g/dL have been positively
correlated with higher rates of rebleeding and mortality
• Indications of blood transfusion
1) Hb less than 7 or 8 mg/dl
2) Experiencing vigorous blood loss
3) Resuscitation beyond 2L of crystalloids due to unstable vitals
• An even lower threshold for transfusion is indicated in older adults
and those with significant comorbidities, such as coronary artery
disease.
2) RFT
• Absorption of digested blood breakdown
products into the circulatory system from the gut
causes elevation of BUN levels.
• The BUN level can also be elevated from prerenal
azotemia in the setting of hypovolemia.
• A BUN-to-creatinine ratio greater than 36 when
the patient does not have renal failure has a
sensitivity of 90% in predicting GIB
3) Coagulopathy
• Coagulation studies, particularly
prothrombin time, becomes especially
important in patients with liver disease or
those taking therapeutic anticoagulants such
as warfarin.
4) Other labs
• Rarely used in patients with GIB
• Electrolyte abnormalities may be present in patients
with repeated or prolonged episodes of vomiting or
diarrhea.
• Leukocytosis often is present because of the stress
response to acute blood loss and should not be
considered to represent underlying infection unless
other indications of infection are present.
• The serum lactate level is elevated when circulatory
shock is present or, much less commonly, from gut
ischemia, if that is the cause of the GI blood loss
• Blood is sent to the blood bank for a type and
screen if the patient is stable and for cross
matching if blood loss is brisk or the patient is
hemodynamically unstable or has significant
comorbidities,especially heart disease.
• If the patient is highly unstable, transfusion of
non–cross matched blood may be necessary.
ECG
• Because GIB and its subsequent anemia can
reduce the oxygen carrying capacity of blood,
patients should be screened for signs of
myocardial ischemia
• Electrocardiographic findings consistent with
myocardial ischemia likely represent demand
ischemia rather than coronary thrombosis and
are treated with restoration of adequate
circulatory volume, including blood, if needed
Imaging
• Emergent imaging of the chest or abdomen in
the ED setting is rarely indicated in the patient
with acute GIB.
• Abdominal plain radiographs are of no value
for patients with GIB, except in the rare case
where bowel obstruction is strongly
suspected.
• When endoscopy is not possible or cannot
locate the hemorrhage source, CT
angiography (CTA) is the principle diagnostic
imaging tool and has the benefit of allowing
for therapeutic options via embolization.
• angiography has a high complication rate,
including acute renal failure, contrast
reactions,and bowel infarction
Diagnostic alogrithm
• The initial assessment should assess the patient’s
general appearance, vital signs, and volume
status
• If the patient is unstable, resuscitation begins
with the immediate placement of two large-bore
IV catheters (18 gauge or larger) or central
venous catheter placement and crystalloid
infusion, with the aim of establishing and
maintaining adequate tissue perfusion.
• End points of adequate resuscitation would
include
a) evidence of adequate perfusion of skin,
b) urine output greater than 1 mL/kg/hr,
c) normal mental status.
• The second decision point involves use of the
history and physical examination findings to
determine if the patient has UGIB or LGIB.
• These details will help risk-stratify the GIB
patient further and establish the differential
diagnosis. Once the presumptive origin of the
bleed has been determined, the emergency
clinician should consider the anticipated
hospital course of the patient.
• The third decision point relies on the severity
of the UGIB or LGIB to determine the ED
management and disposition
management
• Rapid identification of the bleeding source (ie,
upper vs. lower GI tract), risk stratification,
resuscitation, consultation, and disposition are
the integral elements
• Massive bleeding, active hematemesis,
hypoxia, severe tachypnea, and/or altered
mental status may mandate tracheal
intubation for protection and to supplement
tissue oxygenationof this process.
Resuscitation
• Hemodynamic instability and estimated
volume loss should guide initial resuscitation
efforts.
• Patients should be placed on pulse oximetry
and should receive supplemental oxygen with
prompt crystalloid resuscitation through two
peripheral, large-bore IV catheters.
• Cardiac telemetry should be initiated because
demand ischemia and myocardial infarction
may occur in patients with significant GIB
Blood transfusion
• Blood transfusion is immediately indicated in
patients with GIB who have a hemoglobin level
acutely less than 7 to 8 g/dL, are experiencing
vigorous blood loss, or require further resuscitation
beyond 2 L of crystalloid to maintain a systolic
blood pressure in the range of 100 mm Hg.
• Factors such as age, comorbidities (eg, ischemic
heart disease, peripheral vascular disease, heart
failure), baseline hemoglobin and hematocrit levels,
and evidence of cardiac, renal, or cerebral
hypoperfusion should be considered when
determining transfusion quantity
Nasogastric tube placement and
lavage
• NG tube placement with aspiration or
gastric lavage is not indicated for the
evaluation of GIB
• NG tube placement is not a benign
procedure and has been associated with
complications, including pain, aspiration,
pneumothorax, pharyngeal or esophageal
perforation, and gastric lesions
Sengstaken blakemore tube
• A bedside balloon tamponade should only be
considered in exsanguinating patients with
likely variceal bleeding when endoscopy is not
immediately available.
• Complications are common and significant, but
tube placement is indicated in the appropriate
patient population due to the high mortality
of uncontrolled bleeding.
• Insertion of these tubes is a rarely performed
procedure
Pharmacologic agents
• Proton pump inhibitor (PPI) infusions have
long been a staple of acute GIB therapy,
but evidence has contradicted their
necessity in the emergent setting.
• A recent systematic review has found no
evidence to suggest that PPI therapy
affects clinically important outcomes such
as mortality, rebleeding, or subsequent
surgery
• The infusion of high-dose PPIs before
endoscopy has been proven to accelerate
the resolution of signs of bleeding in ulcers
and reduce the need for endoscopic
sclerotherapy and thermocoagulation
• IV dosing of an 80-mg bolus of omeprazole,
followed by 8 mg/hr by continuous IV
infusion for 3 days
• Somatostatin and octreotide, synthetic
analogues, are splanchnic vasoconstrictors that
reduce portal hypertension and the risk of
persistent bleeding, rebleeding, and
transfusion requirements in patients with
variceal bleeding
• Octreotide should be empirically administered
to patients presenting with an acute GIB and
history of significant liver disease, variceal
bleeding, or alcoholism or with abnormal liver
function tests.
• Octreotide is given as a 50-µg bolus
followed by 50 µg/hr continuous IV
infusion
Definitive treatment
• Endoscopy
Upper endoscopy is the most effective
diagnostic and therapeutic intervention for
UGIB, achieving hemostasis in greater than
90% of cases
• Endoscopic treatments include injection
therapy (eg, saline, vasoconstrictors,
sclerosing agents, tissue adhesives, or a
combination), thermal therapy with the use
of contact methods, such as multipolar
electrocoagulation and heater probe, or
noncontact methods
• Urgent colonoscopy has variable diagnostic
value for the identification of a bleeding
source in LGIB. Lesion visualization is
maximized by bowel preparation with
polyethylene glycol
Disposition
• Currently no well-validated clinical decision
rules for Disposition of GIB patients
• Several risk scoring systems, including the
Blatchford and Rockall systems, can aid
emergency clinicians in stratifying UGIB
patients into low- and high-risk
• High-risk UGIB patients require admission for inpatient
monitoring, assessment, and consultation for definitive
diagnosis and treatment
• Patients at low risk for recurrent or worsening UGI
bleed can be discharged to home if they meet all the
following criteria: no significant comorbid diseases (eg,
ischemic heart disease, congestive heart failure,
hepatic disease); normal vital signs; normal or trace
positive results on stool guaiac testing; normal
hemoglobin and hematocrit levels; good support
systems; proper understanding of signs and symptoms
of significant bleeding; immediate access to emergent
care; and arranged follow-up within 24 hours
• There are no clear guidelines on risk stratification
for the outpatient management of LGIB patients,
other than clear iden-tification of a local anal
source of the bleeding, such as a hemor-rhoid or
fissure.
• Most LGIB patients, therefore, are hospitalized or
placed in an observation unit for further
evaluation. Lower GI bleeding not clearly due to
hemorrhoids, fissure, or proctitis may require
nuclear medicine imaging or coloscopy

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GI BLEEDING

  • 1. GI BLEEDING Dr Anoop V JR EM SSIM S
  • 2. • Upper and lower gastrointestinal bleeding (GIB) are defined based on their location relative to the ligament of Treitz in the terminal duodenum • Esophagus, stomach, and duodenum origin bleeds are upper and all others are lower.
  • 3.
  • 4. • Upper GIB (UGIB) mortality rates have remained constant at about 15% over the past 2 decades despite advances in medical therapy, intensive care unit (ICU) management, endoscopy, and surgery. • The lower GIB (LGIB) mortality rate is approximately 4%. • Despite diagnostic advances for all ages, the source of GIB is not identified in nearly 15% of patients.
  • 5. • The characteristics of the GIB, age of the patient, and social factors can all help determine the cause.
  • 6. • UGIB can routinely manifest as I. bloody or coffee-ground–like vomit termed hematemesis or as II. dark, tarry stools termed melena.
  • 7. ADULT PEDIATRICS OLDER 1) PUD 2) ESOPHAGITIS 3) GASTRITIS YOUNGER 1) MALLORY WEISS TEAR 2) GI VARICES 3) GASTROPATHY 1) GASTRIC/DUODENAL ULCER 2) ESOPHAGITIS 3) GASTRITIS 4) ESOPHAGEAL VARICES 5) MALLORY WEISS TEAR
  • 8. • LGIB usually produces bright red or maroon blood per rectum,termed hematochezia • Classified according to pathophysiologic cause a) Inflammatory b) Vascular c) Oncologic d) Traumatic e) Iatrogenic
  • 9. • Anorectal sources, such as hemorrhoids, are the most common causes of LGIB in all age groups ADULTS 1) COLONIC DIVERTICULA 2) ANGIODYSPLASIA 3) COLITIS DUE TO • ISCHEMIA • INFECTION • INFLAMMATORY BOWEL DISEASE CHILDREN 1) ANORECTAL FISSURES 2) INFECTIOUS COLITIS 3) INTUSUSCEPTION 4) MECKEL DIVERTICULAM
  • 10. • Death from exsanguination resulting from GIB is rare. • However, there are two causes of GIB that may rapidly cause death if not recognized and mitigated, a) esophageal varices b) aortoenteric fistula.
  • 11. • Esophageal- varices which typically arises from portal hypertension usually caused by alcoholic cirrhosis, is the single most common source of massive UGIB and has a mortality rate of 30%. • Aorto-enteric fistula is a rare but rapidly fatal cause of GIB, with the mortality of an untreated fistula of nearly 100%.
  • 12. • Epistaxis, dental bleeding, or red food coloring can mimic the appearance of hematemesis • Bismuth-containing medications and iron supplements can create melanotic-appearing (but guaiac-negative) stools • Vaginal bleeding, gross hematuria, and red foods (eg, beets) can all be mistaken for hematochezia
  • 13. • The history centres on the GI tract and on the timing, quantity, and appearance of the bleeding. • Reviewing the patient’s vital signs, appearance of the stool, and basic laboratory studies will help identify the bleeding source and guide treatment
  • 14. Symptoms • A useful starting point is to determine the a) time of onset, b) duration of symptoms, and c) relevant supporting historical facts.
  • 15. • weakness, • shortness of breath, • angina, • orthostatic dizziness, > 800 ml blood loss • confusion, • palpitations, • cool extremities
  • 16. • The context of the bleeding can help explain its cause • if a patient complains of bright red blood per rectum after several days of constipation and straining, that presentation suggests an anorectal source. • a patient with hematemesis after several earlier episodes of retching would lead one to suspect an esophageal tear. • a patient with easy bruising and recurrent gingival bleeding might suggest an underlying coagulopathy.
  • 17. Relevant Medical History • note whether a patient has had similar bleeding before and the location of the causative lesion • identification of relevant comorbid diseases helps risk stratify these patients in the context of their bleed. Patients with GIB and a history of coronary artery disease, congestive heart failure, liver disease, or diabetes have a higher mortality and therefore may require earlier or more extensive interventions .
  • 18. • A review of the patient’s medications should pay particular attention to gastrotoxic substances, anticoagulants, and anti platelet drugs • Alcohol abuse is associated with gastritis and peptic ulcerdisease. It can also result in cirrhosis, portal hypertension and,ultimately, esophageal variceal bleeding • Smoking cigarettes results in slower healing and greater recurrence of ulcers
  • 19. SIGNS • Pulse- tachycardia indicates shock • Temperature- cool extremities – hypovolemic shock • BP- hypotension – shock • Pallor a) Stable patient – sub acute or chronic b) Unstable patient – massive blood loss • Icterus – UGIB from varices
  • 20. • General examination Mental status is evaluated for signs of poor cerebral perfusion spider angioma , palmar erythema – UGIB from variceal indices Ecchymoses or petechiae suggest a coagulopathy ABDOMEN Tenderness on palpation may be seen in PUD Severe diffuse tenderness on examination warrants a) Bowel ischemia b) Mech obstruction c) Ileus d) Bowel perforation hepatomegaly, ascites, or caput medusae.- portal HTN Hyperactive bowel sounds- Non specific but can indicate UGIB
  • 21. Investigations 1) Occult blood and Guanic testing H2O2 + guainic paper containing stool = blue (positive) • makes use of the pseudoperoxidase activity found in hemoglobin. False positive Guanic negative Red meet Vitamin c Turnip Iron Bismuth
  • 22. 2) Blood investigations • Hemoglobin, RFT, platelet and coagulation should be sent Hemoglobin • The hemoglobin level does not immediately decline in the setting of an acute bleed, because whole blood is lost. • Changes in hemoglobin levels are typically seen after 24 hours, when there is hemodilution from shifting extravascular fluids and intravenous (IV) hydration with crystalloid
  • 23. • acute hemoglobin levels less than 10 g/dL have been positively correlated with higher rates of rebleeding and mortality • Indications of blood transfusion 1) Hb less than 7 or 8 mg/dl 2) Experiencing vigorous blood loss 3) Resuscitation beyond 2L of crystalloids due to unstable vitals • An even lower threshold for transfusion is indicated in older adults and those with significant comorbidities, such as coronary artery disease.
  • 24. 2) RFT • Absorption of digested blood breakdown products into the circulatory system from the gut causes elevation of BUN levels. • The BUN level can also be elevated from prerenal azotemia in the setting of hypovolemia. • A BUN-to-creatinine ratio greater than 36 when the patient does not have renal failure has a sensitivity of 90% in predicting GIB
  • 25. 3) Coagulopathy • Coagulation studies, particularly prothrombin time, becomes especially important in patients with liver disease or those taking therapeutic anticoagulants such as warfarin.
  • 26. 4) Other labs • Rarely used in patients with GIB • Electrolyte abnormalities may be present in patients with repeated or prolonged episodes of vomiting or diarrhea. • Leukocytosis often is present because of the stress response to acute blood loss and should not be considered to represent underlying infection unless other indications of infection are present. • The serum lactate level is elevated when circulatory shock is present or, much less commonly, from gut ischemia, if that is the cause of the GI blood loss
  • 27. • Blood is sent to the blood bank for a type and screen if the patient is stable and for cross matching if blood loss is brisk or the patient is hemodynamically unstable or has significant comorbidities,especially heart disease. • If the patient is highly unstable, transfusion of non–cross matched blood may be necessary.
  • 28. ECG • Because GIB and its subsequent anemia can reduce the oxygen carrying capacity of blood, patients should be screened for signs of myocardial ischemia • Electrocardiographic findings consistent with myocardial ischemia likely represent demand ischemia rather than coronary thrombosis and are treated with restoration of adequate circulatory volume, including blood, if needed
  • 29. Imaging • Emergent imaging of the chest or abdomen in the ED setting is rarely indicated in the patient with acute GIB. • Abdominal plain radiographs are of no value for patients with GIB, except in the rare case where bowel obstruction is strongly suspected.
  • 30. • When endoscopy is not possible or cannot locate the hemorrhage source, CT angiography (CTA) is the principle diagnostic imaging tool and has the benefit of allowing for therapeutic options via embolization. • angiography has a high complication rate, including acute renal failure, contrast reactions,and bowel infarction
  • 31. Diagnostic alogrithm • The initial assessment should assess the patient’s general appearance, vital signs, and volume status • If the patient is unstable, resuscitation begins with the immediate placement of two large-bore IV catheters (18 gauge or larger) or central venous catheter placement and crystalloid infusion, with the aim of establishing and maintaining adequate tissue perfusion.
  • 32. • End points of adequate resuscitation would include a) evidence of adequate perfusion of skin, b) urine output greater than 1 mL/kg/hr, c) normal mental status.
  • 33. • The second decision point involves use of the history and physical examination findings to determine if the patient has UGIB or LGIB. • These details will help risk-stratify the GIB patient further and establish the differential diagnosis. Once the presumptive origin of the bleed has been determined, the emergency clinician should consider the anticipated hospital course of the patient.
  • 34. • The third decision point relies on the severity of the UGIB or LGIB to determine the ED management and disposition
  • 35. management • Rapid identification of the bleeding source (ie, upper vs. lower GI tract), risk stratification, resuscitation, consultation, and disposition are the integral elements • Massive bleeding, active hematemesis, hypoxia, severe tachypnea, and/or altered mental status may mandate tracheal intubation for protection and to supplement tissue oxygenationof this process.
  • 36. Resuscitation • Hemodynamic instability and estimated volume loss should guide initial resuscitation efforts. • Patients should be placed on pulse oximetry and should receive supplemental oxygen with prompt crystalloid resuscitation through two peripheral, large-bore IV catheters. • Cardiac telemetry should be initiated because demand ischemia and myocardial infarction may occur in patients with significant GIB
  • 37. Blood transfusion • Blood transfusion is immediately indicated in patients with GIB who have a hemoglobin level acutely less than 7 to 8 g/dL, are experiencing vigorous blood loss, or require further resuscitation beyond 2 L of crystalloid to maintain a systolic blood pressure in the range of 100 mm Hg. • Factors such as age, comorbidities (eg, ischemic heart disease, peripheral vascular disease, heart failure), baseline hemoglobin and hematocrit levels, and evidence of cardiac, renal, or cerebral hypoperfusion should be considered when determining transfusion quantity
  • 38. Nasogastric tube placement and lavage • NG tube placement with aspiration or gastric lavage is not indicated for the evaluation of GIB • NG tube placement is not a benign procedure and has been associated with complications, including pain, aspiration, pneumothorax, pharyngeal or esophageal perforation, and gastric lesions
  • 39. Sengstaken blakemore tube • A bedside balloon tamponade should only be considered in exsanguinating patients with likely variceal bleeding when endoscopy is not immediately available. • Complications are common and significant, but tube placement is indicated in the appropriate patient population due to the high mortality of uncontrolled bleeding. • Insertion of these tubes is a rarely performed procedure
  • 40.
  • 41. Pharmacologic agents • Proton pump inhibitor (PPI) infusions have long been a staple of acute GIB therapy, but evidence has contradicted their necessity in the emergent setting. • A recent systematic review has found no evidence to suggest that PPI therapy affects clinically important outcomes such as mortality, rebleeding, or subsequent surgery
  • 42. • The infusion of high-dose PPIs before endoscopy has been proven to accelerate the resolution of signs of bleeding in ulcers and reduce the need for endoscopic sclerotherapy and thermocoagulation • IV dosing of an 80-mg bolus of omeprazole, followed by 8 mg/hr by continuous IV infusion for 3 days
  • 43. • Somatostatin and octreotide, synthetic analogues, are splanchnic vasoconstrictors that reduce portal hypertension and the risk of persistent bleeding, rebleeding, and transfusion requirements in patients with variceal bleeding • Octreotide should be empirically administered to patients presenting with an acute GIB and history of significant liver disease, variceal bleeding, or alcoholism or with abnormal liver function tests.
  • 44. • Octreotide is given as a 50-µg bolus followed by 50 µg/hr continuous IV infusion
  • 45. Definitive treatment • Endoscopy Upper endoscopy is the most effective diagnostic and therapeutic intervention for UGIB, achieving hemostasis in greater than 90% of cases
  • 46. • Endoscopic treatments include injection therapy (eg, saline, vasoconstrictors, sclerosing agents, tissue adhesives, or a combination), thermal therapy with the use of contact methods, such as multipolar electrocoagulation and heater probe, or noncontact methods
  • 47. • Urgent colonoscopy has variable diagnostic value for the identification of a bleeding source in LGIB. Lesion visualization is maximized by bowel preparation with polyethylene glycol
  • 48. Disposition • Currently no well-validated clinical decision rules for Disposition of GIB patients • Several risk scoring systems, including the Blatchford and Rockall systems, can aid emergency clinicians in stratifying UGIB patients into low- and high-risk
  • 49.
  • 50.
  • 51. • High-risk UGIB patients require admission for inpatient monitoring, assessment, and consultation for definitive diagnosis and treatment • Patients at low risk for recurrent or worsening UGI bleed can be discharged to home if they meet all the following criteria: no significant comorbid diseases (eg, ischemic heart disease, congestive heart failure, hepatic disease); normal vital signs; normal or trace positive results on stool guaiac testing; normal hemoglobin and hematocrit levels; good support systems; proper understanding of signs and symptoms of significant bleeding; immediate access to emergent care; and arranged follow-up within 24 hours
  • 52. • There are no clear guidelines on risk stratification for the outpatient management of LGIB patients, other than clear iden-tification of a local anal source of the bleeding, such as a hemor-rhoid or fissure. • Most LGIB patients, therefore, are hospitalized or placed in an observation unit for further evaluation. Lower GI bleeding not clearly due to hemorrhoids, fissure, or proctitis may require nuclear medicine imaging or coloscopy