UPPER GI BLEEDING
Dr. Atul Sharma
FCCCM Exam Student 2023
OUTLINE
• Introduction
• Aetiology
• Presentation
• Resuscitation
• Diagnosis
1. History
2. Clinical
examination
3. investigations
• Treatment
• Complications
• Follow up
• Prognosis
• conclusion
INTRODUCTION
• Bleeding of GIT proximal to ligament of treitz.
• Ligament of treitz- a fibromuscular band which extends from
right crus of diaphragm to duodenojejunal flexure.
Presents as:
• Haematemesis,, malena, hematochezia or occult blood.
• Malena can present with loss of 50-60ml of blood.
• May be acute or chronic
• 100 cases per 100,000 person per year.
• Accounts for 3-5% of all hospitalizations
• The incidence is 2- fold greater in males but death rate is similar
in both sexes.
• Overall mortality from acute bleeding is 20% .
• Mortality & morbidity increases as age advances (>60 yrs)
AETIOLOGY (COMMON CAUSES)
1. Peptic ulcer disease
≥ 50% of cases
• Duodenal ulcer
• Gastric ulcer
• Stomal ulcer
AETIOLOGY (COMMON CAUSES)
2. Erosive gastritis,
esophagitis, duodenitis
15-30% of cases
Common causative factors are:
ETOH [alcohol], ASA, NSAID’S,STEROIDS.
AETIOLOGY (COMMON CAUSES)
3. Esophageal and gastric varices
10-20% of cases
caused by portal hypertension
AETIOLOGY (COMMON CAUSES)
4. Mallory- Weiss syndrome
• 5% of cases
• Characterized by longitudinal mucosal tear in the
cardioesophageal region.
• Result from repeated vomitting or retching.
• Common in male alcoholic patients
AETIOLOGY
Less common
• Oesophagitis
• Malignant gastric tumor
• Benign gastric tumors
• Oesophageal ulcer
• Oesophageal tumors
• A-V malformations
Rare
• Duodenal tumous
• Pancreatic tumors
• Arterial aneurysm
• Blood dyscrasia
• Hereditary telangiectasia
• Haemobilia
MALIGNANCY
• In 3% of cases presentation is with upper GI bleeding
• Gastric cancer
• Oesophageal cancer
CLINICAL PRESENTATION
A. Chronic upper GI bleeding
• Anemia.
• Weakness.
• Fatigueness.
• Pt :looks pale.
• Malena.
• Occult blood positive.
B. Acute upper GI bleeding
• Presents as emergency with hemetemesis or malena.
• Hypovolaemia:
i. Mild: no significant hypovolaemia.
ii. Moderate: hypovolaemia which responds to volume
replacement.
iii. Severe: hypovolaemia with continued active major
bleeding making resuscitation difficult even with blood
transfusions.
These patients are difficult to manage.
Patients will show all signs of shock.
Note: all patients should be examined for stigmata of CLD.
• H/O drugs (NSAIDS).
• H/O ulcers.
• H/O alcohol abuse.
RESUSCITATION
Initial management has 4 primary goals:
1. Quick assessment with attention to hemodynamic status
2. Appropriate resuscitation (ABC) & monitoring
3. Identify major source of bleeding
4. Specific therapeutic intervention.
RESUSCITATION (GENERAL MEASURES)
• Airway cleared of clot.
• Oxygen inhalation.
• Maintain IV line with at least 2 wide bore
cannulae
• Sample to blood bank for cross matching.
• Class I + II hemorrhage replace with
crystalloid.
• Class III + IV hemorrhage replace with
crystalloid & blood.
• Pass NG tube for diagnostic & therapeutic
purpose.
• Catheterize the patient.
• Sedation may be needed.
SEVERITY
Estimated Fluid and Blood Losses in Shock
Class 1 Class 2 Class 3 Class 4
Blood Loss,
mL
Up to 750 750-1500 1500-2000 >2000
Blood Loss,%
blood volume
Up to 15% 15-30% 30-40% >40%
Pulse Rate,
bpm
<100 >100 >120 >140
Blood
Pressure
Normal Normal Decreased Decreased
Respiratory
Rate
Normal or
Increased
Decreased Decreased Decreased
Urine
Output,
mL/h
14-20 20-30 30-40 >35
CNS/Mental
Status
Slightly
anxious
Mildly
anxious
Anxious,
confused
Confused,
lethargic
Fluid
Replacement,
3-for-1 rule
Crystalloid Crystalloid
Crystalloid
and blood
Crystalloid
and blood
SPECIFIC MEASURES
• If stable following resuscitation, proceed for upper GI
endoscopy.
• Endoscopy ideally done within 4-24 hrs.
• If patient could not be stabilized, an emergency laparatomy
may be necessary.
DIAGNOSIS
History of:
• Epigastric pain or retrosternal burning
• hematemesis, melena, or hematochezia.
• Vomiting, weight loss, alteration of bowel habits.
• Aortic graft surgery
• Use of ASA, NSAID’S, steroids, alcohol addiction
DIAGNOSIS
Physical examination
• Vital signs may show hypotension &
tachycardia.
• Cool, clammy skin.
• Petechiael hemorrhage & purpura seen in
coagulopathy.
• Signs of chronic liver disease.
• Proper abdominal & rectal examination.
INVESTIGATIONS
• Upper GI endoscopy.
• Arteriography.
• Barium swallow
• Ultrasound
• Lab investigations
ENDOSCOPY
• Most important investigation
• For diagnosis & intervention
• Establishes diagnosis in 90% of patients
• Can be repeated more than once.
ARTERIOGRAPHY
• In pts who bleeds contineously & site can not be
identified.
• Has accuracy of 50-90%.
• Accuracy is increased if there is active bleeding
during investigation.
• Demonstrates bleeding of 0.5-1.0ml/min
• With technetium-labelled RBC, 0.1-0.5ml/min
• Embolisation may be done at same time
BARIUM SWALLOW / MEAL
• Used when endoscopy is not available
• Double contrast study is ideal
• May show varices, esophagitis, peptic ulcers, gastric tumors
etc
ABDOMINAL ULTRASOUND SCAN
• To assess both liver architecture and portal circulation
• More widely available than Arteriography
• Should be performed before more invasive procedures
LAB INVESTIGATIONS
• CBC
• Electrolytes
• Glucose
• Coagulation studies
• Liver function studies
• Blood grouping and cross-match
LAB INVESTIGATIONS
• CBC, urea/creatinine, S/Electrolytes, ABGs.
• ed urea/ creatinine in upper GI bleeding.
• Iron deficiency anemia in chronic blood loss.
TREATMENT ( PEPTIC ULCER
DISEASE)
At endoscopy
• 10ml epinephrine at ulcer base
• Thermal treatment with bipolar diathermy
• Laser photocoagulation
• Rebleed is treated similarly
• A second rebleed is treated by surgery
Post endoscopy treatment
• Continuous intravenous infusion of Octretide (somatostatin
analogue)
• Proton pump inhibitors
• H. pylori treatment may be required.
SURGERY- PUD
Surgical options are:
• Truncal vagotomy & drainage
• Highly selective vagotomy
• Partial gastrectomy
SURGERY - PUD
Indications for surgery are:
• Exsanguinating hemorrhage
• Visible spurting arterial bleed
• Concomitant perforation
• Pts >60 yrs, who rebleed once or need 4 units at resuscitation
or 8 units in 48 hrs
• Younger pts requiring 8 units at initial resuscitation or 12
units in 48 hrs
• Rare blood group
TREATMENT
GASTRIC EROSIONS / STRESS
ULCERS
• Treatment of underlying cause
• Intraluminal antacids
• IV proton pump inhibitors
• Bleeding usually subsides in 24-48 hrs
TREATMENT
ESOPHAGEAL VARICES
1. Endoscopic sclerotherapy
• Repeated at 3 weeks interval then 3 monthly until varices
disappear
• Some sclerosing agents are ethanolamine
oleate, sodium morrhuate, 3% tetradecyl
sulphate, absolute alcohol
2. Rubber band ligation
3. Vasoconstriction therapy (octreotide, vasopressin,
propranolol)
4. Balloon tamponade: if above measures fail
Modified Sengstaken- Blakemoore tube
Minnesota tube, Linton tube, Foley catheter
• Balloon tamponade applied for 12 hrs
• Stop bleeding in 80% of cases
• Must be followed by surgery as bleeding is likely to recur after
removal.
SURGERY – ESOPHAGEAL
VARICES
• TIPS: in refractory bleed
Shunt established between portal vein & Rt or
middle hepatic vein
• Stapling transection of esophagus at CEJ
• Distal splenorenal shunt
• Portosystemic shunts
• Spleenectomy in hypersplenism
• Liver transplantation
TREATMENT
• Mallory- weiss
observe
if persist, suture mucosal tear
• Esophagitis
Observe
• Benign gastric tumors
Excise
• Dieulafoy’s lesion
Endoscopic electrocoagulation, sclerotherapy
COMPLICATIONS
• Of presenting problem
• Of resuscitative measures
• Of underlying disease
• Of treatment
COMPLICATIONS OF
MASSIVE HEMORRHAGE
• Hemorrhagic shock
• Acute renal shut down
• MODS
• Death
COMPLICATIONS OF
RESUSCITATION
• Fluid overload
• Pulmonary edema
• CCF
• Blood transfusion reaction
• Cardiac arrest
• Hypothermia
• Esophageal perforation
COMPLICATIONS OF
UNDERLYING DISEASES
• Rebleed in PUD & varices
• Gastric outlet obstruction in PUD
• Progressive CLD causing portal hypertension, ascites &
coagulopathies
COMPLICATIONS OF
DEFINITIVE SURGERY
• PUD
Early & late dumping
gastric tumors
Iron deficiency anemia
• Bypass procedures for portal hypertension
mucosal ulceration
Hepatic encephalopathy
FOLLOW-UP
• To monitor progress of non- surgical treatment
• To prepare pts for elective definitive surgery
• To look out for, and treat complications of surgery
PROGNOSIS
Depends upon
ROCKALL scoring system
this includes :
• The state / time of presentation of pt
• energetic resuscitation
• underlying disease
• Co morbidities
ROCKALL SCORING SYSTEM
ADVERSE PROGNOSTIC FACTORS
CONCLUSION
• Upper GI bleeding is not uncommon & may be life
threatening.
• Prompt intervention could be life saving.
• It require multidisciplinary approach.
• Definitive treatment depends upon the final diagnosis.
THANK YOU

uppergi.ppt

  • 1.
    UPPER GI BLEEDING Dr.Atul Sharma FCCCM Exam Student 2023
  • 2.
    OUTLINE • Introduction • Aetiology •Presentation • Resuscitation • Diagnosis 1. History 2. Clinical examination 3. investigations • Treatment • Complications • Follow up • Prognosis • conclusion
  • 3.
    INTRODUCTION • Bleeding ofGIT proximal to ligament of treitz. • Ligament of treitz- a fibromuscular band which extends from right crus of diaphragm to duodenojejunal flexure.
  • 4.
    Presents as: • Haematemesis,,malena, hematochezia or occult blood. • Malena can present with loss of 50-60ml of blood. • May be acute or chronic • 100 cases per 100,000 person per year.
  • 5.
    • Accounts for3-5% of all hospitalizations • The incidence is 2- fold greater in males but death rate is similar in both sexes. • Overall mortality from acute bleeding is 20% . • Mortality & morbidity increases as age advances (>60 yrs)
  • 6.
    AETIOLOGY (COMMON CAUSES) 1.Peptic ulcer disease ≥ 50% of cases • Duodenal ulcer • Gastric ulcer • Stomal ulcer
  • 7.
    AETIOLOGY (COMMON CAUSES) 2.Erosive gastritis, esophagitis, duodenitis 15-30% of cases Common causative factors are: ETOH [alcohol], ASA, NSAID’S,STEROIDS.
  • 8.
    AETIOLOGY (COMMON CAUSES) 3.Esophageal and gastric varices 10-20% of cases caused by portal hypertension
  • 9.
    AETIOLOGY (COMMON CAUSES) 4.Mallory- Weiss syndrome • 5% of cases • Characterized by longitudinal mucosal tear in the cardioesophageal region. • Result from repeated vomitting or retching. • Common in male alcoholic patients
  • 10.
    AETIOLOGY Less common • Oesophagitis •Malignant gastric tumor • Benign gastric tumors • Oesophageal ulcer • Oesophageal tumors • A-V malformations Rare • Duodenal tumous • Pancreatic tumors • Arterial aneurysm • Blood dyscrasia • Hereditary telangiectasia • Haemobilia
  • 11.
    MALIGNANCY • In 3%of cases presentation is with upper GI bleeding • Gastric cancer • Oesophageal cancer
  • 12.
    CLINICAL PRESENTATION A. Chronicupper GI bleeding • Anemia. • Weakness. • Fatigueness. • Pt :looks pale. • Malena. • Occult blood positive.
  • 13.
    B. Acute upperGI bleeding • Presents as emergency with hemetemesis or malena. • Hypovolaemia: i. Mild: no significant hypovolaemia. ii. Moderate: hypovolaemia which responds to volume replacement. iii. Severe: hypovolaemia with continued active major bleeding making resuscitation difficult even with blood transfusions. These patients are difficult to manage. Patients will show all signs of shock.
  • 14.
    Note: all patientsshould be examined for stigmata of CLD. • H/O drugs (NSAIDS). • H/O ulcers. • H/O alcohol abuse.
  • 15.
    RESUSCITATION Initial management has4 primary goals: 1. Quick assessment with attention to hemodynamic status 2. Appropriate resuscitation (ABC) & monitoring 3. Identify major source of bleeding 4. Specific therapeutic intervention.
  • 16.
    RESUSCITATION (GENERAL MEASURES) •Airway cleared of clot. • Oxygen inhalation. • Maintain IV line with at least 2 wide bore cannulae • Sample to blood bank for cross matching. • Class I + II hemorrhage replace with crystalloid. • Class III + IV hemorrhage replace with crystalloid & blood. • Pass NG tube for diagnostic & therapeutic purpose. • Catheterize the patient. • Sedation may be needed.
  • 17.
    SEVERITY Estimated Fluid andBlood Losses in Shock Class 1 Class 2 Class 3 Class 4 Blood Loss, mL Up to 750 750-1500 1500-2000 >2000 Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40% Pulse Rate, bpm <100 >100 >120 >140 Blood Pressure Normal Normal Decreased Decreased Respiratory Rate Normal or Increased Decreased Decreased Decreased Urine Output, mL/h 14-20 20-30 30-40 >35 CNS/Mental Status Slightly anxious Mildly anxious Anxious, confused Confused, lethargic Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood
  • 18.
    SPECIFIC MEASURES • Ifstable following resuscitation, proceed for upper GI endoscopy. • Endoscopy ideally done within 4-24 hrs. • If patient could not be stabilized, an emergency laparatomy may be necessary.
  • 19.
    DIAGNOSIS History of: • Epigastricpain or retrosternal burning • hematemesis, melena, or hematochezia. • Vomiting, weight loss, alteration of bowel habits. • Aortic graft surgery • Use of ASA, NSAID’S, steroids, alcohol addiction
  • 20.
    DIAGNOSIS Physical examination • Vitalsigns may show hypotension & tachycardia. • Cool, clammy skin. • Petechiael hemorrhage & purpura seen in coagulopathy. • Signs of chronic liver disease. • Proper abdominal & rectal examination.
  • 21.
    INVESTIGATIONS • Upper GIendoscopy. • Arteriography. • Barium swallow • Ultrasound • Lab investigations
  • 22.
    ENDOSCOPY • Most importantinvestigation • For diagnosis & intervention • Establishes diagnosis in 90% of patients • Can be repeated more than once.
  • 23.
    ARTERIOGRAPHY • In ptswho bleeds contineously & site can not be identified. • Has accuracy of 50-90%. • Accuracy is increased if there is active bleeding during investigation. • Demonstrates bleeding of 0.5-1.0ml/min • With technetium-labelled RBC, 0.1-0.5ml/min • Embolisation may be done at same time
  • 24.
    BARIUM SWALLOW /MEAL • Used when endoscopy is not available • Double contrast study is ideal • May show varices, esophagitis, peptic ulcers, gastric tumors etc
  • 25.
    ABDOMINAL ULTRASOUND SCAN •To assess both liver architecture and portal circulation • More widely available than Arteriography • Should be performed before more invasive procedures
  • 26.
    LAB INVESTIGATIONS • CBC •Electrolytes • Glucose • Coagulation studies • Liver function studies • Blood grouping and cross-match
  • 27.
    LAB INVESTIGATIONS • CBC,urea/creatinine, S/Electrolytes, ABGs. • ed urea/ creatinine in upper GI bleeding. • Iron deficiency anemia in chronic blood loss.
  • 28.
    TREATMENT ( PEPTICULCER DISEASE) At endoscopy • 10ml epinephrine at ulcer base • Thermal treatment with bipolar diathermy • Laser photocoagulation • Rebleed is treated similarly • A second rebleed is treated by surgery
  • 29.
    Post endoscopy treatment •Continuous intravenous infusion of Octretide (somatostatin analogue) • Proton pump inhibitors • H. pylori treatment may be required.
  • 30.
    SURGERY- PUD Surgical optionsare: • Truncal vagotomy & drainage • Highly selective vagotomy • Partial gastrectomy
  • 31.
    SURGERY - PUD Indicationsfor surgery are: • Exsanguinating hemorrhage • Visible spurting arterial bleed • Concomitant perforation • Pts >60 yrs, who rebleed once or need 4 units at resuscitation or 8 units in 48 hrs • Younger pts requiring 8 units at initial resuscitation or 12 units in 48 hrs • Rare blood group
  • 32.
    TREATMENT GASTRIC EROSIONS /STRESS ULCERS • Treatment of underlying cause • Intraluminal antacids • IV proton pump inhibitors • Bleeding usually subsides in 24-48 hrs
  • 33.
    TREATMENT ESOPHAGEAL VARICES 1. Endoscopicsclerotherapy • Repeated at 3 weeks interval then 3 monthly until varices disappear • Some sclerosing agents are ethanolamine oleate, sodium morrhuate, 3% tetradecyl sulphate, absolute alcohol 2. Rubber band ligation 3. Vasoconstriction therapy (octreotide, vasopressin, propranolol)
  • 34.
    4. Balloon tamponade:if above measures fail Modified Sengstaken- Blakemoore tube Minnesota tube, Linton tube, Foley catheter • Balloon tamponade applied for 12 hrs • Stop bleeding in 80% of cases • Must be followed by surgery as bleeding is likely to recur after removal.
  • 35.
    SURGERY – ESOPHAGEAL VARICES •TIPS: in refractory bleed Shunt established between portal vein & Rt or middle hepatic vein • Stapling transection of esophagus at CEJ • Distal splenorenal shunt • Portosystemic shunts • Spleenectomy in hypersplenism • Liver transplantation
  • 36.
    TREATMENT • Mallory- weiss observe ifpersist, suture mucosal tear • Esophagitis Observe • Benign gastric tumors Excise • Dieulafoy’s lesion Endoscopic electrocoagulation, sclerotherapy
  • 37.
    COMPLICATIONS • Of presentingproblem • Of resuscitative measures • Of underlying disease • Of treatment
  • 38.
    COMPLICATIONS OF MASSIVE HEMORRHAGE •Hemorrhagic shock • Acute renal shut down • MODS • Death
  • 39.
    COMPLICATIONS OF RESUSCITATION • Fluidoverload • Pulmonary edema • CCF • Blood transfusion reaction • Cardiac arrest • Hypothermia • Esophageal perforation
  • 40.
    COMPLICATIONS OF UNDERLYING DISEASES •Rebleed in PUD & varices • Gastric outlet obstruction in PUD • Progressive CLD causing portal hypertension, ascites & coagulopathies
  • 41.
    COMPLICATIONS OF DEFINITIVE SURGERY •PUD Early & late dumping gastric tumors Iron deficiency anemia • Bypass procedures for portal hypertension mucosal ulceration Hepatic encephalopathy
  • 42.
    FOLLOW-UP • To monitorprogress of non- surgical treatment • To prepare pts for elective definitive surgery • To look out for, and treat complications of surgery
  • 43.
    PROGNOSIS Depends upon ROCKALL scoringsystem this includes : • The state / time of presentation of pt • energetic resuscitation • underlying disease • Co morbidities
  • 44.
  • 45.
  • 46.
    CONCLUSION • Upper GIbleeding is not uncommon & may be life threatening. • Prompt intervention could be life saving. • It require multidisciplinary approach. • Definitive treatment depends upon the final diagnosis.
  • 47.