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“I’M
THROWING
UP A LOT OF
BLOOD!”
RAWAN ALSULMI
G3
CONTENT
• Introduction
• Definition
• Mode of presentation
• DDx
• Approach to patient with upper GI
bleeding
INTRODUCTION
The gastrointestinal track extend from the mouth to the anus
and divided in to two parts
Upper and lower GIT
By suspensory muscle of duodenum ( ligment of treitz ) at
the duodenojejunal junction
GI BLEEDING
One of the most common cause of
hospital admission specially in elderly
is bleeding , account for 10 %
mortality.
Any bleeding proximal to ligament of
treitz is upper GI bleeding , distal to
the ligament is lower bleeding.
UPPER GI
BLEEDING
MODE OF PRESENTATION
Presentation Description Indication
Hematemesis (50%) Vomiting blood Bright red = significant
bleeding.
Coffee ground = no
active bleeding
Melena (80%) Passage of foul
smelling black stool
Presence in GIT for
more than 14 h
Hematochezia(20%) Bright blood per rectum
Occult bleeding No evidence of visible
blood loss but +ve
microscopic blood
Symptoms of blood
loss or iron
deficiency anemia
Symptoms of anemia Chronic bleeding
APPROACH TO THE PATIENT
WITH UPPER GI BLEEDING
• History
• P/E
• Investigations
HISTORY
Symptoms:
Abdominal pain , Hematemesis , Melena , Hematochezia
Symptoms of blood loss: anemia , syncope , shock
Symptoms of underlying cause : weight loss , dyspepsia
Drug history : NSAIDs , anticoagulant .
Past medical history of chronic liver , renal , cardiac diseases
Past surgical history.
PE
- General :
Level of consciousness
Vitals : HR, BP ,
Sign of shock : cold extremities , tachy ,
hypotension , confusion ,,etc.
Skin change : dry , sunken eye
- Systemic
INVESTIGATIONS
Lab:
• CBC , LFTs
• BUN/creatinine ratio
• Coagulation profile
Imaging
• Endoscopy
• Angiography if the bleeding persist
DIFFERENTIAL DIAGNOSIS
“PAGE ME!”
1.Peptic ulcer 50%
2. Atrioventricular (AV) malformation
3. Gastritis
4. Esophageal varices
5. Mallory-Weiss tear
6. Esophagitis
UNCOMMON CAUSES
• Boerhaave’s syndrome
• Gastric varices
• Upper GI tumours
• Aortoenteric fistulae (AEF)
• Hereditary hemorrhagic telangiectasia (HHT)
• Coagulopathy
CASE
SCENARIOS
CASE 1
An 88-year-old white woman is taking
naproxen for osteoarthritis. She has
noticed mild epigastric discomfort for
several weeks, but has continued the
naproxen because of improvement in joint
symptoms. She suddenly develops
hematemesis and hypotension.
GASTRIC ULCER
CASE 2
A 42-year-old white woman with a history of
alcohol abuse develops nausea and
vomiting without abdominal pain. After
several bouts of retching, she vomits bright
red blood. Physical exam is negative,
without spider angiomata or splenomegaly.
LFTs are normal.
1.MALLORY-WEISS TEAR
Linear mucosal tears at the gastroesophageal junction.
2.BOERHAAVE’S SYNDROME
• Complete transmural (full-thickness) laceration or perforation of the
esophagus, distinct from Mallory-Weiss syndrome, a nontransmural
esophageal tear..
• Perforation is almost always on Left side of Lower esophagus
• Odynophagia and surgical emphysema in the neck
CASE 3
A 76-year-old white man presents with
painless hematemesis and hypotension. He
has no previous GI symptoms but did have
resection of an abdominal aortic aneurysm
12 years previously. EGD shows no
bleeding source in the stomach or
duodenum.
AORTO-ENTERIC FISTULA
CASE 4
A 23-year-old man develops iron-deficiency
anemia and heme-positive stools. His
weight is stable. A few telangiectasias are
present on the lips. Abdominal exam is
negative without hepatosplenomegaly .
Past history of nosebleeds
HEREDITARY HEMORRHAGIC
TELANGIECTASIA (HHT)
(OSLER–WEBER–RENDU SYNDROME)
MANAGEMENT
Aim:
• To stabilize the patient (ABC)
• Identify the source
• Treat the cause accordingly
MANAGEMENT
1- Immediate assessment
2- Stabilization
3- Identify the source of the bleeding
4- Stop the active bleeding
5- Treat the underlying
6- Prevent rebreeding
1- IMMEDIATE
ASSESSMENT
- PE
- Amount of blood loss
ROCKALL
SCORE
ROCKALL SCORE
- Low risk ( 0-2 ) : 80% will resolved
spontaneously
- Intermediate risk (3-5) : hospitalization for
72 hrs.
- High risk (>5): ICU
2- RESUSCITATION
ABC:
Ensure patent airway
Supplemntal O2
IV crystalloid
NG tube
Transfusion
3- LOCALIZATION
NG tube
Blood
EGD
Slow Massive
Angio
Tagged
RBC
No Blood
Suspected GI bleed
Admit , resuscitate ,
stabilize , PPI
Variceal
(cirrhosis )
Non- Variceal
Urgent EGD
Octreotide,Antibiotic
s , nonselective BB
Surgery
PU
Endoscopic
infusion of Epi
Esophagitis
PPI
REFERENCES
• C&K
• BMJ
• Webmed
THANK YOU

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Upper GI bleeding

  • 1. “I’M THROWING UP A LOT OF BLOOD!” RAWAN ALSULMI G3
  • 2. CONTENT • Introduction • Definition • Mode of presentation • DDx • Approach to patient with upper GI bleeding
  • 3. INTRODUCTION The gastrointestinal track extend from the mouth to the anus and divided in to two parts Upper and lower GIT By suspensory muscle of duodenum ( ligment of treitz ) at the duodenojejunal junction
  • 4. GI BLEEDING One of the most common cause of hospital admission specially in elderly is bleeding , account for 10 % mortality. Any bleeding proximal to ligament of treitz is upper GI bleeding , distal to the ligament is lower bleeding.
  • 5.
  • 7. MODE OF PRESENTATION Presentation Description Indication Hematemesis (50%) Vomiting blood Bright red = significant bleeding. Coffee ground = no active bleeding Melena (80%) Passage of foul smelling black stool Presence in GIT for more than 14 h Hematochezia(20%) Bright blood per rectum Occult bleeding No evidence of visible blood loss but +ve microscopic blood Symptoms of blood loss or iron deficiency anemia Symptoms of anemia Chronic bleeding
  • 8. APPROACH TO THE PATIENT WITH UPPER GI BLEEDING • History • P/E • Investigations
  • 9. HISTORY Symptoms: Abdominal pain , Hematemesis , Melena , Hematochezia Symptoms of blood loss: anemia , syncope , shock Symptoms of underlying cause : weight loss , dyspepsia Drug history : NSAIDs , anticoagulant . Past medical history of chronic liver , renal , cardiac diseases Past surgical history.
  • 10. PE - General : Level of consciousness Vitals : HR, BP , Sign of shock : cold extremities , tachy , hypotension , confusion ,,etc. Skin change : dry , sunken eye - Systemic
  • 11. INVESTIGATIONS Lab: • CBC , LFTs • BUN/creatinine ratio • Coagulation profile Imaging • Endoscopy • Angiography if the bleeding persist
  • 12. DIFFERENTIAL DIAGNOSIS “PAGE ME!” 1.Peptic ulcer 50% 2. Atrioventricular (AV) malformation 3. Gastritis 4. Esophageal varices 5. Mallory-Weiss tear 6. Esophagitis
  • 13. UNCOMMON CAUSES • Boerhaave’s syndrome • Gastric varices • Upper GI tumours • Aortoenteric fistulae (AEF) • Hereditary hemorrhagic telangiectasia (HHT) • Coagulopathy
  • 14.
  • 16. CASE 1 An 88-year-old white woman is taking naproxen for osteoarthritis. She has noticed mild epigastric discomfort for several weeks, but has continued the naproxen because of improvement in joint symptoms. She suddenly develops hematemesis and hypotension.
  • 18. CASE 2 A 42-year-old white woman with a history of alcohol abuse develops nausea and vomiting without abdominal pain. After several bouts of retching, she vomits bright red blood. Physical exam is negative, without spider angiomata or splenomegaly. LFTs are normal.
  • 19. 1.MALLORY-WEISS TEAR Linear mucosal tears at the gastroesophageal junction. 2.BOERHAAVE’S SYNDROME • Complete transmural (full-thickness) laceration or perforation of the esophagus, distinct from Mallory-Weiss syndrome, a nontransmural esophageal tear.. • Perforation is almost always on Left side of Lower esophagus • Odynophagia and surgical emphysema in the neck
  • 20.
  • 21. CASE 3 A 76-year-old white man presents with painless hematemesis and hypotension. He has no previous GI symptoms but did have resection of an abdominal aortic aneurysm 12 years previously. EGD shows no bleeding source in the stomach or duodenum.
  • 23. CASE 4 A 23-year-old man develops iron-deficiency anemia and heme-positive stools. His weight is stable. A few telangiectasias are present on the lips. Abdominal exam is negative without hepatosplenomegaly . Past history of nosebleeds
  • 25. MANAGEMENT Aim: • To stabilize the patient (ABC) • Identify the source • Treat the cause accordingly
  • 26. MANAGEMENT 1- Immediate assessment 2- Stabilization 3- Identify the source of the bleeding 4- Stop the active bleeding 5- Treat the underlying 6- Prevent rebreeding
  • 27. 1- IMMEDIATE ASSESSMENT - PE - Amount of blood loss
  • 29. ROCKALL SCORE - Low risk ( 0-2 ) : 80% will resolved spontaneously - Intermediate risk (3-5) : hospitalization for 72 hrs. - High risk (>5): ICU
  • 30. 2- RESUSCITATION ABC: Ensure patent airway Supplemntal O2 IV crystalloid NG tube Transfusion
  • 31. 3- LOCALIZATION NG tube Blood EGD Slow Massive Angio Tagged RBC No Blood
  • 32. Suspected GI bleed Admit , resuscitate , stabilize , PPI Variceal (cirrhosis ) Non- Variceal Urgent EGD Octreotide,Antibiotic s , nonselective BB Surgery PU Endoscopic infusion of Epi Esophagitis PPI
  • 33.

Editor's Notes

  1. anticoagulant although doct caousr per se
  2. high in upper
  3. hx of NSAID use (often with concomitant use of corticosteroids) or past ulcers is common; ingestion of food often transiently improves abdominal pain; coffee-ground emesis and haematemesis are very common
  4. classically, patients note haematemesis following retching or vomiting, but any increase in intra-oesophageal pressure (e.g., from seizures, hiccups, or straining) can cause a tear; some tears develop spontaneously; alcohol use, advanced age, and presence of hiatal hernias are common underlying features Gastric contents enter the mediastinum and pleural cavity, if one were to perform a pleural fluid aspirate; one is likely to aspirate gastric contents!
  5. usually painless and, as such, are often asymptomatic until they cause overt bleeding; associated with cirrhosis, end-stage renal disease, advanced age, and von Willebrand's disease The erosion of the proximal end of a woven aortic graft into the distal duodenum or proximal jejunum can occur many years after the initial surgery. Often the patient will have a smaller herald bleed which is fol- lowed by catastrophic bleeding catastrophic complication of aortic surgery
  6. Patients with HHT usually have low-grade GI blood loss without obvious hematemesis; frequent nosebleeds may occur. The physical finding of small matlike telangiectasias of the mouth, lips, and fingertips points to this autosomal dominant disease and may prevent unnecessary endoscopy.
  7. Score < 3 poor 8 good To detect the high mortality and rebleeding
  8. Reduces portal venous pressure,
  9. 1-Angiodysplasia = associated with vWf 2-Ischemic colitis = abd.pain + ischemic heart disease 3-Investigation of Upper or lower GI bleed: CBC Coagulation factors Endo 4-What are the endoscopic findings that suggest rebreeding?  Clot Visible bleeding Visible Vessels 5-Ranson criteria 6-Analgesia better to be avoided in pancreatitis? Morphine is avoided because it increases sphincter of Oddi pressure and may aggravate pancreatitis. 7-- When we should give antibiotics in pancreatitis ? In Infected necrosis -When CT?  Sign of infection or moderate to sever Ranson. 8-Necrosis, calcification in chronic pancreatic 9-When stare feeding the patient of pancreatitis? After 72 h from presentation if sever give total parental nutrition Or NG tube 10-DDx of pancreatitis: Perforated peptic ulcer why? Epigastria pain , duodenal ulcer radiate to back 11-Chronic pancreatitis complication? Abscess, DM, fat malabsorbtion , chronic diarrhea 12-Infection with streateohrea ? Gardiasis 13- Kerlly B line = horizontal fluid . 14-Non liver disease in ascites ? What is the investigations ? Heart failure: Lab : BNP = not specific may be High in liver in obesity. Chest X ray = cardiomegaly Confirmatory = Eco Renal: Urin output increase early decrees later Uremic : urmic encephalomy , pericarditis , gasstritis . Bleeding tency . Anemia . Neropathy , itching Investigations : kidney function . If normal Bun , do urin analysis 24 h urin collection Urin albumin raio = if the prev need time. Next : GFR 14- 50% of renal function need to be lost . SBP Netrophil 250 Total WBC 500 Dialysis = 100 Acute pancreatitis 2nd high triglycrid= milky Pancritis induced drug : sulpha Thyroglossal vs thyroid = prtrusion of toungue Mediction lead to gynrzlized lyphmo = phtnotoin Hiv and lympha , sle = genrlized lymphodeno