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APPROACH TO UPPER GI BLEED
Dr. Tim Mutafya
Gen Surg. resident
MBBS III class
OVERVIEW
 Definition & Epidemiology
 Classification
 Pathophysiology
 Clinical presentation
 Screening & Diagnosis
 Initial management
Definition
Upper GIB is that originating proximal to the ligament of Treitz;
 from the oesophagus, stomach and duodenum
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.
RISK FACTORS
 Age > 50 years, Male
 Drugs: Use of NSAIDS, antiplatelet
 H-pylori infection
 Excessive alcohol intake
 Excess acid production
Classification
 Pathophysiologic
 Anatomic
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
Anatomical
Major causes
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 12 mm Hg
 High risk
 Not usually associated with cirrhosis
o splenic vein thrombosis
o Pancreatitis
o pancreatic cancer.
Varices
Prehepatic
 Portal venous thrombosis
 Infiltrative tumors
Intrahepatic
 Schistosomiasis
 Liver cirrhosis
 Veno-occlusive disease
Post hepatic
 Budd chiari syndrome
UGI for MBBS 3 guide to history, examination and acute management
Most frequent cause of upper GI Bleeding
Duodenal Ulcer-gastroduodenal A.
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,weakening and
necrosis of the arterial wall,development
of a pseudoaneurysm.
 weakened wall ruptures hemorrhage
MODIFIED JOHNSON
CLASSIFICATION FOR GASTRIC
ULCER
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.
Haemorragic/Erosive gastritis
 Stress related mucosal injury
 Occur mostly in extremly sick patients
 Major Trauma
 Post Major Surgery
 3rd Degree burns
 Major intracranial disease
 Severe medical illness (Ventilator dependence, coagulopathy)
 Significant bleeding probably does not develop unless ulceration occurs.
 Intravenous H2-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.
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 ectatic blood vessels in the
proximal gastric body and cardia and 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.
DIEULAFOY'S LESION
 It is a large (1- to 3-mm) submucosal artery 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 6 cm of the
gastroesophageal junction.
 Dieulafoy's lesion 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.
GASTRIC ANTRAL VASCULAR ECTASIA
 Gastric antral vascular ectasia (GAVE), also described as watermelon
stomach.
 Characterized by rows or stripes of ectatic mucosal blood vessels that
emanate from the pylorus and extend proximally into the antrum .
 Unknown etiology
 Common in older
women and patients
with ESRD
Aortoenteric fistula
 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.
Presentation
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
USUALLY hematemesis requires a bucket; BUT haemoptysis
a small bowl.
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 Heme by intestinal
and bacterial enzymes.
 10% LGI bleed
 Can be swallowed blood from epistaxis
 Blood for 14 hrs in 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
Aetiology Leading history
MalloryWeiss tear Multiple Emesis before hematemesis, alcoholism, retching
Esophageal ulcer Dysphagia, Odynophagia, GERD
Peptic ulcer Epigastric pain, NSAID or aspirin use
Stress gastritis Patient in an ICU, gastrointestinal bleeding occurring
after admission,respiratory failure,multiorgan failure,coagulopathy
Varices, portal
gastropathy
Alcoholism, Cirrhosis of liver
Gastric antral
vascular ectasia
Renal failure, cirrhosis
Malignancy Recent involuntary weight loss, dysphagia, cachexia,
early satiety
Angiodysplasia Chronic renal failure, hereditary hemorrhagic
telangiectasia
Aortoenteric fistula Known aortic aneurysm, prior abdominal aortic
aneurysm repair
Clues regarding the cause of acute UGI bleeding
 Pallor , signs of dehydration , Shock
 Icterus
 Clubbing
 Oedema
}Liver disease
Physical Examination
Lymphadenopathy
Virchows Node
(Troisiers sign)
Vital signs
Tachycardia
Hypotension
Tachypnea
 Ascites  Spider naevi
 Palmar erythema  Dupuytrens contracture
 Leuconychia  Gynecomastia
 Bleeding manifestations  Scars of previous surgery
 Splenomegaly
 Caput medusae
 Parotid Swelling
 Fetor hepaticus
 Asterixis
 Testicular atrophy
 Acanthosis nigricans
 Alopecia
 Glossitis
 Loss of Axillary hair
 Loss of Pubic Hair
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-Baumgarten venous hum
ABDOMEN EXAMINATION
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
Risk assessment & triage
Risk for mortality and
rebleeding.
Categorised as
 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
Workup
Bloods
 Hematology - FBC, G+ crossmatch
 Biochemistry- U&Es, LFT+ albumin
 Serology - H-pylori, Hep B/C,HIV, schistosomiasis
 Coagulation profile
 Stool: occult blood
Imaging
 Esophagogastroduodenoscopy
o Therapeutic and diagnostic
 CXR
 ECG
 Abdominal USS
 CT Angiography
MANAGEMENT OF UGIB
GENERAL MEDICAL
MANAGEMENT
TYPE OF BLEEDING
VARICEAL
BLEEDING
NON VARICEAL
BLEEDING
MEDICAL ENDOTHERAPY
SURGICAL
INERVENTION
PRESSURE
TECHNIQUES
AUGIB
Rapid Assessment
Monitor Hemodynamic Status
Fluid Resuscitation
Ryle;s tube for Gastric Lavage
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 Definitive
UGI for MBBS 3 guide to history, examination and acute management
UGI for MBBS 3 guide to history, examination and acute management

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YIHENEW CHALLIE LIYEW

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

  • 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
  • 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
  • 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 12 mm Hg High risk Not usually associated with cirrhosis o splenic vein thrombosis o Pancreatitis o pancreatic cancer.
  • 11. Varices Prehepatic Portal venous thrombosis Infiltrative tumors Intrahepatic Schistosomiasis Liver cirrhosis Veno-occlusive disease Post hepatic Budd chiari syndrome
  • 13. Most frequent cause of upper GI Bleeding Duodenal Ulcer-gastroduodenal A. 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,weakening and necrosis of the arterial wall,development of a pseudoaneurysm. weakened wall ruptures hemorrhage
  • 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 extremly sick patients Major Trauma Post Major Surgery 3rd Degree burns Major intracranial disease Severe medical illness (Ventilator dependence, coagulopathy) Significant bleeding probably does not develop unless ulceration occurs. Intravenous H2-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 ectatic blood vessels in the proximal gastric body and cardia and 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'S LESION It is a large (1- to 3-mm) submucosal artery 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 6 cm of the gastroesophageal junction. Dieulafoy's lesion 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 ANTRAL VASCULAR ECTASIA Gastric antral vascular ectasia (GAVE), also described as watermelon stomach. Characterized by rows or stripes of ectatic mucosal blood vessels that emanate from the pylorus and extend proximally into the antrum . Unknown etiology Common in older women and patients with ESRD
  • 20. Aortoenteric fistula 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.
  • 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 USUALLY hematemesis requires a bucket; BUT haemoptysis a small bowl.
  • 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 Heme by intestinal and bacterial enzymes. 10% LGI bleed Can be swallowed blood from epistaxis Blood for 14 hrs in 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 MalloryWeiss tear Multiple Emesis before hematemesis, alcoholism, retching Esophageal ulcer Dysphagia, Odynophagia, GERD Peptic ulcer Epigastric pain, NSAID or aspirin use Stress gastritis Patient in an ICU, gastrointestinal bleeding occurring after admission,respiratory failure,multiorgan failure,coagulopathy Varices, portal gastropathy Alcoholism, Cirrhosis of liver Gastric antral vascular ectasia Renal failure, cirrhosis Malignancy Recent involuntary weight loss, dysphagia, cachexia, early satiety Angiodysplasia Chronic renal failure, hereditary hemorrhagic telangiectasia Aortoenteric fistula Known aortic aneurysm, prior abdominal aortic aneurysm repair Clues regarding the cause of acute UGI bleeding
  • 25. Pallor , signs of dehydration , Shock Icterus Clubbing Oedema }Liver disease Physical Examination
  • 26. Lymphadenopathy Virchows Node (Troisiers sign) Vital signs Tachycardia Hypotension Tachypnea
  • 27. Ascites Spider naevi Palmar erythema Dupuytrens contracture
  • 28. Leuconychia Gynecomastia Bleeding manifestations Scars of previous surgery
  • 29. Splenomegaly Caput medusae Parotid Swelling Fetor hepaticus Asterixis Testicular atrophy Acanthosis nigricans 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-Baumgarten venous 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. Categorised as 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, Hep B/C,HIV, schistosomiasis Coagulation profile Stool: occult blood Imaging Esophagogastroduodenoscopy o Therapeutic and diagnostic CXR ECG Abdominal USS 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 Rapid Assessment Monitor Hemodynamic Status Fluid Resuscitation Ryle;s tube for Gastric Lavage 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 Definitive