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Prepared by
OUTLINE 
2 
 Introduction 
 Definition 
 Epidemology 
 classificationCause and risk factors 
 Aproach to patients with acute GI bleeding 
 Management
Introduction 
3 Figure 23.2 
The principal function 
of GIT is to provide the 
body with a continuous 
supply of nutrients, water 
and electrolytes.
Introduction…. 
Histology of the Alimentary Canal 
 From esophagus to the anal canal the walls of the GIT 
4 
have the same four layers 
From the lumen outward they are the 
1. Mucosa, 
2. Submucosa, 
3. Muscularis externa, and 
4. Serosa 
 Each layer has a predominant tissue type and a 
specific digestive function
Introduction…Blood Supply to Digestive System 
 The blood vessels of the GI-system are part of a more extensive system 
5 
called the splanchric circulation. 
 splanchnic BF =1000 ml/min 
 It includes the blood flow through the GIT itself plus through the spleen, 
pancreas and the liver. 
 All of the blood that courses through the gut, spleen and pancreas then 
flows immediately into the liver by way of the portal vein. 
 In the liver, blood passes through million of liver sinusoids and finally 
leaver the liver by way of the hepatic veins that empty into the inferior 
venacava of the general circulation.
Blood Supply to GIT (cont’d) 
6
Gastrointestinal Bleeding: 
7 
Bleeding from the gastrointestinal (GI) tract may present 
in five ways. 
 Hematemesis is vomitus of red blood or "coffee-grounds" 
material. 
 Melena is black, tarry, foul-smelling stool. 
 Hematochezia is the passage of bright red or maroon 
blood from the rectum. 
 Occult GI bleeding (GIB) may be identified in the 
absence of overt bleeding by a fecal occult blood test or 
the presence of iron deficiency. 
 Finally, patients may present only with symptoms of 
blood loss or anemia such as lightheadedness, 
syncope, angina, or dyspnea.
Classification of GI Bleeding 
8 
 UGIB  blood loss proximal to ligament of 
Treitz(DJ flexure) 
 LGIB blood loss distal to ligament of Treitz 
(DJ flexure) 
 Ligament of treize…. 
 Upper GI bleeding 4x more common 
than lower GI bleeding
Suspencery ligament of doudenum 
or ligament of tertz 
9
UGIB 
10 
 Upper GI bleeding refers to bleeding from 
oesophagus, stomach, duodenum. 
 Can be: 
Variceal bleeding 
Non-variceal bleeding
Sources of Gastrointestinal 
Bleeding 
11 
Upper Gastrointestinal Sources of Bleeding 
 The annual incidence of hospital admissions for upper 
GIB (UGIB) in the United States and Europe is 0.1%, 
with a mortality rate of 5–10%. 
 Patients rarely die from exsanguination; rather, they die 
due to decompensation from other underlying illnesses. 
 The mortality rate for patients <60 years in the absence 
of major concurrent illness is <1%. 
 Independent predictors of rebleeding and death in 
patients hospitalized with UGIB include increasing age, 
comorbidities, and hemodynamic compromise 
(tachycardia or hypotension).
Sources of bleeding in patients hospitalized for upper gi 
bleeding 
12 
Sources of Bleeding Proportion of Patients, % 
Ulcers 31–67 
Varices 6–39 
Mallory-Weiss tears 2–8 
Gastroduodenal erosions 2–18 
Erosive esophagitis 1–13 
Neoplasm 2–8 
Vascular ectasias 0–6
13 
 Peptic ulcers are the most common cause of 
UGIB, accounting for up to 50% of cases; an 
increasing proportion is due to nonsteroidal anti-inflammatory 
drugs (NSAIDs), with the prevalence 
of Helicobacter pylori decreasing. 
 Mallory-Weiss tears account for 5–10% of cases. 
 The proportion of patients bleeding from varices 
varies widely from 5 to 40%, depending on the 
population. 
 Hemorrhagic or erosive gastropathy (e.g., due to 
NSAIDs or alcohol) and erosive esophagitis often 
cause mild UGIB, but major bleeding is rare.
14 
PUD (DU & GU) 
 Are break in the gastric or duodenal mucosa 
that arises when the normal factors are impaired 
or overwhelmed by acid or pepsin 
Erosive Gastritis 
 Because this process is superficial, it is a relatively 
unusual cause of severe gastrointestinal bleeding (< 
5% of cases).
MW TEAR (LACERATION) 
15 
 Classically, Mallory-Weiss tears are mucosal lacerations at the 
GEJ or in the cardia of the stomach 
 associated with repeated retching or vomiting 
 another important cause of nonvariceal UGIB. 
 acute UGIB secondary to Mallory-Weiss tears bleeding 
episodes are self-limited.
ESOPHAGITIS 
16 
 Is a common medical condition, 
 usually caused by gastroesophageal reflux. 
 Less frequent causes include 
 infectious esophagitis (in patients whoare immunocompromised), 
 radiation esophagitis, and 
 esophagitis from direct erosive effects of medication or corrosive 
agents.
VASCULAR ECTASIAS 
17 
 Vascular ectasias, also referred to as “angiomas,” “arteriovenous 
malformations,” and “angiodysplasia,” are another source of 
acute and chronic nonvariceal UGIB 
 Abnormal communication 
 The severity of bleeding can also range from trivial to severe 
 Vascular ectasias are associated with chronic renal insufficiency 
or failure; valvular heart disease, specifically aortic stenosis; and 
congestive heart failure.
Varices 
18 
 There is communication between the intra-abdominal 
splanchnic circulation and the systemic venous circulation 
through the esophagus. 
 When portal venous blood flow into the liver is impeded by 
cirrhosis or other causes, the resultant portal hypertension 
induces the formation of collateral bypass channels. 
 The increased pressure in the esophageal plexus produces 
dilated tortuous vessels called varices. 
 Variceal rupture produces massive hemorrhage into the lumen. 
 produce no symptoms until they rupture
LGIB 
19 
 Lower GI bleed refers to bleeding arising distal to 
the ligament of Treitz (DJ flexure) 
 Although this includes jejunum and ileum bleeding 
from these sites is rare. 
 Vast majority of lower GI bleeding arises from 
colon/rectum/anus 
 over 90% of cases arise from the colon
CAUSES OF Acute LGIB 
Majorcauses 
 Diverticulosis(40%) 
 Colitis 
 IBD 
 Ischemia 
 Infection 
 Angiodysplasia 
(avm)(30%) 
 Neoplasia 
 Anorectal 
 Hemorrhoids 
 Fissure 
20
Causes... 
21 
Causes of Colon 
bleeding 
Causes of 
Rectal bleeding 
Causes of Anal 
bleeding 
Diverticular 
Disease 
Polyps Haemorrhoids 
Polyps Malignancy Fissure 
Malignancy Proctitis Malignancy 
Colitis
IBD 
22 
 Chronic inflammation of the colon. 
 ulcerative colitis & Crohn disease 
 is characterized by severe inflammation and 
ulceration of the colon and rectum 
 Patients with inflammatory bowel disease 
(especially ulcerative colitis) often have 
diarrhea with variable amounts of 
hematochezia
Differentiation of Upper from Lower Gib 
 Hematemesis indicates an upper GI source of bleeding 
23 
(above the ligament of Treitz). 
 Melena indicates that blood has been present in the GI 
tract for at least 14 h (and as long as 3–5 days). 
 The more proximal the bleeding site, the more likely 
melena will occur. 
 Hematochezia usually represents a lower GI source of 
bleeding, although an upper GI lesion may bleed so briskly 
that blood does not remain in the bowel long enough for 
melena to develop. 
 When hematochezia is the presenting symptom of UGIB, it 
is associated with hemodynamic instability and dropping 
hemoglobin.
24 
 Bleeding lesions of the small bowel may present as 
melena or hematochezia. 
 Other clues to UGIB include hyperactive bowel sounds 
and an elevated blood urea nitrogen level (due to volume 
depletion and blood proteins absorbed in the small 
intestine). 
 A nonbloody nasogastric aspirate may be seen in up to 
18% of patients with UGIB—usually from a duodenal 
source. 
 Even a bile-stained appearance does not exclude a 
bleeding postpyloric lesion because reports of bile in the 
aspirate are incorrect in 50% of cases. 
 Testing of aspirates that are not grossly bloody for occult 
blood is not useful.
 Obscure GIB is defined as persistent or recurrent 
bleeding for which no source has been identified 
by routine endoscopic and contrast x-ray studies; 
it may be overt (melena, hematochezia) or occult 
(iron-deficiency anemia). 
 Current guidelines suggest angiography as the 
initial test for massive obscure bleeding, and 
video capsule endoscopy, which allows 
examination of the entire small intestine, for all 
others. 
25 
GIB of Obscure Origin
26 
 Push enteroscopy, with a specially designed 
enteroscope or a pediatric colonoscope to inspect 
the entire duodenum and part of the jejunum, also 
may be considered as an initial evaluation. 
 A systematic review of 14 trials comparing push 
enteroscopy to capsule revealed "clinically 
significant findings" in 26% and 56% of patients, 
respectively. 
 However, in contrast to enteroscopy, lack of 
control of the capsule prevents its manipulation 
and full visualization of the intestine; in addition, 
tissue cannot be sampled and therapy cannot be 
applied.
Clinical Presantation : 
27 
 Hematemesis 
 Melena 
 Hematochezia 
 Syncope 
 Dyspepsia 
 Epigastric pain 
 Heartburn 
 Diffuse abdominal pain 
 Dysphagia 
 Weight loss 
 Jaundice
Approach to the Patient: 
Gastrointestinal Bleeding 
28 
 History 
 Physical examination 
 Lab investigation
APROACH TO PATIENT………….. Con’t 
29 
 History: 
• Abdominal pain 
• Haematamesis 
• Haematochezia 
• Melaena 
• Features of blood loss: shock, syncope, 
anemia 
• Features of underlying cause: dyspepsia, 
jaundice, weight loss
30 
o Drug history: NSAIDs, Aspirin, anticoagulants, 
o History of epistaxis or hemoptysis to rule out the GI 
source of bleeding. 
o Past medical :previous episodes of upper 
gastrointestinal bleedin; coronary artery disease; 
chronic renal or liver disease; 
o Past surgical: previous abdominal surgery
Approach 
Cont….. 
31 
Physical Examination : 
• General examination and systemic examinations 
• VITALS: 
Pulse = Feable pulse 
BP = Orthostatic Hypotension 
• SIGNS of shock: 
Cold extremeties, Tachycardia, Hypotension 
Chest pain, Confusion, Delirium, Oliguria, and etc.
32 
SKIN changes: 
Cirrhosis – Palmer erythema, spider nevi 
Bleeding disorders – Purpura /Echymosis, 
Haemarthrosis, Muscle hematoma. 
• Signs of dehydration (dry mucosa, sunken eyes, skin 
turgor reduced). 
• Signs of a tumour may be present (nodular liver, 
abdominal mass, lymphadenopathy, and etc. 
• DRE : fresh blood, occult blood, bloody diarrhea 
• Respiratory, CVS, CNS  For comorbid diseases
Lab Diagnosis : 
33 
CBC with Platelet Count, and Differential 
 A complete blood count (CBC) is necessary to 
assess the level of blood loss. 
 CBC should be checked frequently(q4-6h) during 
the first day. 
Hemoglobin Value, Type and Crossmatch Blood 
 The patient should be crossmatched for 2-6 units, 
based on the rate of active bleeding. 
 The hemoglobin level should be monitored serially 
in order to follow the trend. 
 An unstable Hb level may signify ongoing 
hemorrhage requiring further intervention.
34 
 LFT- to detect underlying liver disease 
 The BUN-to- creatinine ratio increases with 
upper gastrointestinal bleeding (UGIB). 
A ratio of greater than 36 in a patient without 
renal insufficiency is suggestive of UGIB. 
 The patient's prothrombin time (PT), activated 
partial thromboplastin time, should be checked 
to document the presence of a coagulopathy
Endoscopy 
35 
• Initial diagnostic examination for all patients 
presumed to have UGIB. 
• Endoscopy should be performed immediately 
after endotracheal intubation (if indicated), 
hemodynamic stabilization, and adequate 
monitoring in an intensive care unit (ICU) setting 
have been achieved.
36 
Endoscopy
Imaging 
37 
• CHEST X-RAY-Chest radiographs should be 
ordered to exclude aspiration pneumonia, 
effusion, and esophageal perforation. 
• Abdominal X-RAY- erect and supine films should 
be ordered to exclude perforated viscous and 
ileus.
Angiography 
: 
38 
 Angiography may be useful if bleeding persists 
and endoscopy fails to identify a bleeding site. 
 Angiography along with transcatheter arterial 
embolization (TAE) should be considered for all 
patients with a known source of arterial UGIB that 
does not respond to endoscopic management, 
with active bleeding and a negative endoscopy. 
 In cases of aortoenteric fistula, angiography 
requires active bleeding (1 mL/min) to be 
diagnostic.
Nasogastric 
Lavage 
39 
 A nasogastric tube is an important diagnostic tool. 
 This procedure may confirm recent bleeding 
(coffee ground appearance), possible active 
bleeding (red blood in the aspirate that does not 
clear), or a lack of blood in the stomach (active 
bleeding less likely but does not exclude an upper 
GI lesion).
40
41 
BENEFITS OF LAVAGE : 
1. Better visualization during endoscopy 
2. Give crude estimation of rapidity of bleeding 
3. Prevent the development of Porto systemic 
encephalopathy in cirrhosis 
4. Increases PH of stomach, and hence, decreases clot 
desolation due to gastric acid dilution 
5. Tube placement can reduce the patient's need to vomit 
 During gastric lavage use saline and not use large volume 
of to avoid water intoxication. 
 Gastric lavage should be done in alert and cooperative 
patient to avoid bronco-pulmonary aspiration
Risk Stratification: Rockall 
Score 
 Identifies patients at risk of adverse outcome 
following acute upper GI bleed 
Variable Score 0 Score 1 Score 2 Score 3 
Age <60 60-79 >80 - 
Shock Nil HR >100 SBP <100 - 
Co-morbidity Nil major - IHD/CCF/major morbidity Renal failure/liver failure 
Diagnosis Mallory Weiss tear All other diagnoses GI malignancy - 
Endoscopic Findings None - Blood, adherent clot, 
spurting vessel 
 Score <3 carries good prognosis 
 Score >8 carries high risk of mortality 
-
Management 
43 
Priorities are: 
1. Stabilize the patient: protect airway, 
restore circulation. 
2. Identify the source of bleeding. 
3. Definitive treatment of the cause.
Emegency Resuscitation 
Takes priority over determining the 
diagnosis/cause 
 ABC (main focus is ‘C’) 
 Oxygen: 15L Non-rebreath mask 
 2 large bore cannulae into both ante-cubital 
fossae 
Take bloods at same time for FBC, U&E, 
LFT, Clotting, X match 6Units 
 Catheterise
45 
 IVF initially then blood as soon as available 
(depending on urgency: O-, Group specific, fully 
X-matched) 
 Monitor response to resuscitation frequently 
(HR, BP, urine output, level of consciousness, 
peripheral temperature, CRT) 
 Stop anti-coagulants and correct any clotting 
derrangement 
 NG tube and aspiration (will help differentiate 
upper from lower GI bleed) 
 Organise definitive treatment 
(endoscopic/radiological/surgical)
Management (Non-variceal) 
 Emergency resuscitation as already described 
 Endoscopy 
Urgent (within 24hrs) – diagnostic and 
therepeutic 
Treatment administered if active 
bleeding, visible vessel, adherent blood 
clot 
Treatment options include injection 
(adrenaline), coagulation, clipping 
If re-bleeds then arrange urgent repeat 
endoscopy.
47 
 Pharmacology 
PPI (infusion) – pH >6 stabilises clots and 
reduces risk of re-bleeding following 
endoscopic haemostasis 
If H pylori positive then for eradication 
therapy 
Stop 
NSAIDs/aspirin/clopidogrel/warfarin/steroids 
if safe to do so (risk:benefit analysis)
Management (Non-variceal) 
 Surgery 
 Reserved for patients with failed medical management 
(ongoing bleeding despite 2x endoscopy) 
 Nature of operation depends on cause of bleeding (most 
commonly performed in context of bleeding peptic ulcer: 
DU>GU) 
 E.g. Under-running of ulcer (bleeding DU), wedge excision 
of bleeding lesion (e.g. GU), partial/total gastrectomy 
(malignancy)
Variceal Bleeds 
 Suspect if upper GI bleed in patient with history of 
chronic liver disease/cirrhosis or stigmata on clinical 
examination 
 Liver Cirrhosis results in portal hypertension and 
development of porto-systemic anastamosis 
(opening or dilatation of pre-existing vascular 
channels connecting portal and systemic 
circulations)
50 
 Sites of porto-systemic anastamosis include: 
 Oesophagus 
(P= eosophageal branch of L gastric v, S= oesophageal 
branch of azygous v) 
Umbilicus 
(P= para-umbilical v, S= infeior epigastric v) 
 Retroperitoneal 
(P= right/middle/left colic v, S= renal/supra-renal/gonadal 
v) 
 Rectal 
 (P= superior rectal v, S= middle/inferior rectal v) 
 Furthermore, clotting derrangement in those with chronic liver 
disease can worsen bleeding
Management of Variceal bleeds 
Emergency resuscitation as already described 
 Drugs 
Somatostatin/octreotide – vasoconstricts splanchnic 
circulation and reduces pressure in portal system 
Terlipressin – vasoconstricts splanchnic circulation 
and reduces pressure in portal system 
Propanolol – used only in context of primary 
prevention (in those found to have varices to reduce 
risk of first bleed) 
 Endoscopy 
Band ligation 
 Injection sclerotherapy
52 
 Balloon tamponade – sengstaken-blakemore tube 
 Rarely used now and usually only as temporary measure if failed 
endoscopic management 
 Radiological procedure – used if failed medical/endoscopic Mx 
 Selective catheterisation and embolisation of vessels feeding the 
varices 
 TIPSS procedure: transjugular intrahepatic porto-systemic shunt 
 shunt between hepatic vein and portal vein branch to reduce 
portal pressure and bleeding from varices): performed if failed 
medical and endoscopic management 
 Can worsen hepatic encephalopathy 
 Surgical 
 Surgical porto-systemic shunts (often spleno-renal) 
 Liver transplantation (patients often given TIPP/surgical shunt 
whilst awaiting this)
Sengstaken-Blakemore 
Tube 
TIPSS
Variceal Bleed: Prognosis 
 Prognosis closely related to severity of underlying chronic liver disease 
(Childs-Pugh grading) 
 Child-Pugh classification grades severity of liver disease into A,B,C based 
on degree of ascites, encephalopathy, bilirubin, albumin, INR 
 Mortality 32% Childs A, 46% Childs B, 79% Childs C
Management-lower GI 
BLEEDING 
 Emergency resuscitation as already described 
 Pharmacological 
 Stop NSAIDS/anti-platelets/anti-coagulants if safe 
 Endoscopic 
 15% of patients with severe acute PR bleeding will have an upper 
GI source!) 
 Colonoscopy – diagnostic and therepeutic (injection, diathermy, 
clipping)
Management 
 Radiological 
 CT angiogram – diagnostic only (non-invasive) 
 Determines site and cause of bleeding 
 Mesenteric Angiogram – diagnostic and therepeutic 
(but invasive) 
 Determines site of bleeding and allows embolisation of 
bleeding vessel 
 Can result in colonic ischaemia
Management 
 Surgical – Last resort in management as very 
difficult to determine bleeding point at 
laparotomy 
 Segmental colectomy – where site of bleeding is 
known 
 Subtotal colectomy – where site of bleeding unclear 
 Beware of small bowel bleeding – always 
embarassing when bleeding continues after large 
bowel removed!
Management Flow Chart for 
Severe lower GI bleeding 
Resuscitate 
Endoscopy (to exclude upper GI cause for severe PR bleeding) 
Colonoscopy (to identify site and cause of 
bleeding and to treat bleeding by 
injection/diathermy/clipping) – often 
unsuccesful as blood obscures views 
CT angiogram (to identify 
site and cause of 
bleeding) 
Mesenteric angiogram (to identify 
site of bleeding and treat 
bleeding by embolisation of 
vessel) 
Surgery
Management 
 As 85% of lower GI bleeds will settle 
spontaneously the interventions mentioned on 
previous slide are reserved for: 
 Severe/Life threatening bleeds 
 In the 85% where bleeding settles spontaneously 
OPD investigation is required to determine 
underlying cause: 
 Endoscopy: flexible sigmoidoscopy, colonoscopy 
 Barium enema
REFERENCE 
60 
 Harrison principles of intrnal medicine 18th edi. 
 Kumar .clinical medicine 8th edit. 
 On line search
61 
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ACUTE GI BLEEDING

  • 2. OUTLINE 2  Introduction  Definition  Epidemology  classificationCause and risk factors  Aproach to patients with acute GI bleeding  Management
  • 3. Introduction 3 Figure 23.2 The principal function of GIT is to provide the body with a continuous supply of nutrients, water and electrolytes.
  • 4. Introduction…. Histology of the Alimentary Canal  From esophagus to the anal canal the walls of the GIT 4 have the same four layers From the lumen outward they are the 1. Mucosa, 2. Submucosa, 3. Muscularis externa, and 4. Serosa  Each layer has a predominant tissue type and a specific digestive function
  • 5. Introduction…Blood Supply to Digestive System  The blood vessels of the GI-system are part of a more extensive system 5 called the splanchric circulation.  splanchnic BF =1000 ml/min  It includes the blood flow through the GIT itself plus through the spleen, pancreas and the liver.  All of the blood that courses through the gut, spleen and pancreas then flows immediately into the liver by way of the portal vein.  In the liver, blood passes through million of liver sinusoids and finally leaver the liver by way of the hepatic veins that empty into the inferior venacava of the general circulation.
  • 6. Blood Supply to GIT (cont’d) 6
  • 7. Gastrointestinal Bleeding: 7 Bleeding from the gastrointestinal (GI) tract may present in five ways.  Hematemesis is vomitus of red blood or "coffee-grounds" material.  Melena is black, tarry, foul-smelling stool.  Hematochezia is the passage of bright red or maroon blood from the rectum.  Occult GI bleeding (GIB) may be identified in the absence of overt bleeding by a fecal occult blood test or the presence of iron deficiency.  Finally, patients may present only with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea.
  • 8. Classification of GI Bleeding 8  UGIB  blood loss proximal to ligament of Treitz(DJ flexure)  LGIB blood loss distal to ligament of Treitz (DJ flexure)  Ligament of treize….  Upper GI bleeding 4x more common than lower GI bleeding
  • 9. Suspencery ligament of doudenum or ligament of tertz 9
  • 10. UGIB 10  Upper GI bleeding refers to bleeding from oesophagus, stomach, duodenum.  Can be: Variceal bleeding Non-variceal bleeding
  • 11. Sources of Gastrointestinal Bleeding 11 Upper Gastrointestinal Sources of Bleeding  The annual incidence of hospital admissions for upper GIB (UGIB) in the United States and Europe is 0.1%, with a mortality rate of 5–10%.  Patients rarely die from exsanguination; rather, they die due to decompensation from other underlying illnesses.  The mortality rate for patients <60 years in the absence of major concurrent illness is <1%.  Independent predictors of rebleeding and death in patients hospitalized with UGIB include increasing age, comorbidities, and hemodynamic compromise (tachycardia or hypotension).
  • 12. Sources of bleeding in patients hospitalized for upper gi bleeding 12 Sources of Bleeding Proportion of Patients, % Ulcers 31–67 Varices 6–39 Mallory-Weiss tears 2–8 Gastroduodenal erosions 2–18 Erosive esophagitis 1–13 Neoplasm 2–8 Vascular ectasias 0–6
  • 13. 13  Peptic ulcers are the most common cause of UGIB, accounting for up to 50% of cases; an increasing proportion is due to nonsteroidal anti-inflammatory drugs (NSAIDs), with the prevalence of Helicobacter pylori decreasing.  Mallory-Weiss tears account for 5–10% of cases.  The proportion of patients bleeding from varices varies widely from 5 to 40%, depending on the population.  Hemorrhagic or erosive gastropathy (e.g., due to NSAIDs or alcohol) and erosive esophagitis often cause mild UGIB, but major bleeding is rare.
  • 14. 14 PUD (DU & GU)  Are break in the gastric or duodenal mucosa that arises when the normal factors are impaired or overwhelmed by acid or pepsin Erosive Gastritis  Because this process is superficial, it is a relatively unusual cause of severe gastrointestinal bleeding (< 5% of cases).
  • 15. MW TEAR (LACERATION) 15  Classically, Mallory-Weiss tears are mucosal lacerations at the GEJ or in the cardia of the stomach  associated with repeated retching or vomiting  another important cause of nonvariceal UGIB.  acute UGIB secondary to Mallory-Weiss tears bleeding episodes are self-limited.
  • 16. ESOPHAGITIS 16  Is a common medical condition,  usually caused by gastroesophageal reflux.  Less frequent causes include  infectious esophagitis (in patients whoare immunocompromised),  radiation esophagitis, and  esophagitis from direct erosive effects of medication or corrosive agents.
  • 17. VASCULAR ECTASIAS 17  Vascular ectasias, also referred to as “angiomas,” “arteriovenous malformations,” and “angiodysplasia,” are another source of acute and chronic nonvariceal UGIB  Abnormal communication  The severity of bleeding can also range from trivial to severe  Vascular ectasias are associated with chronic renal insufficiency or failure; valvular heart disease, specifically aortic stenosis; and congestive heart failure.
  • 18. Varices 18  There is communication between the intra-abdominal splanchnic circulation and the systemic venous circulation through the esophagus.  When portal venous blood flow into the liver is impeded by cirrhosis or other causes, the resultant portal hypertension induces the formation of collateral bypass channels.  The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.  Variceal rupture produces massive hemorrhage into the lumen.  produce no symptoms until they rupture
  • 19. LGIB 19  Lower GI bleed refers to bleeding arising distal to the ligament of Treitz (DJ flexure)  Although this includes jejunum and ileum bleeding from these sites is rare.  Vast majority of lower GI bleeding arises from colon/rectum/anus  over 90% of cases arise from the colon
  • 20. CAUSES OF Acute LGIB Majorcauses  Diverticulosis(40%)  Colitis  IBD  Ischemia  Infection  Angiodysplasia (avm)(30%)  Neoplasia  Anorectal  Hemorrhoids  Fissure 20
  • 21. Causes... 21 Causes of Colon bleeding Causes of Rectal bleeding Causes of Anal bleeding Diverticular Disease Polyps Haemorrhoids Polyps Malignancy Fissure Malignancy Proctitis Malignancy Colitis
  • 22. IBD 22  Chronic inflammation of the colon.  ulcerative colitis & Crohn disease  is characterized by severe inflammation and ulceration of the colon and rectum  Patients with inflammatory bowel disease (especially ulcerative colitis) often have diarrhea with variable amounts of hematochezia
  • 23. Differentiation of Upper from Lower Gib  Hematemesis indicates an upper GI source of bleeding 23 (above the ligament of Treitz).  Melena indicates that blood has been present in the GI tract for at least 14 h (and as long as 3–5 days).  The more proximal the bleeding site, the more likely melena will occur.  Hematochezia usually represents a lower GI source of bleeding, although an upper GI lesion may bleed so briskly that blood does not remain in the bowel long enough for melena to develop.  When hematochezia is the presenting symptom of UGIB, it is associated with hemodynamic instability and dropping hemoglobin.
  • 24. 24  Bleeding lesions of the small bowel may present as melena or hematochezia.  Other clues to UGIB include hyperactive bowel sounds and an elevated blood urea nitrogen level (due to volume depletion and blood proteins absorbed in the small intestine).  A nonbloody nasogastric aspirate may be seen in up to 18% of patients with UGIB—usually from a duodenal source.  Even a bile-stained appearance does not exclude a bleeding postpyloric lesion because reports of bile in the aspirate are incorrect in 50% of cases.  Testing of aspirates that are not grossly bloody for occult blood is not useful.
  • 25.  Obscure GIB is defined as persistent or recurrent bleeding for which no source has been identified by routine endoscopic and contrast x-ray studies; it may be overt (melena, hematochezia) or occult (iron-deficiency anemia).  Current guidelines suggest angiography as the initial test for massive obscure bleeding, and video capsule endoscopy, which allows examination of the entire small intestine, for all others. 25 GIB of Obscure Origin
  • 26. 26  Push enteroscopy, with a specially designed enteroscope or a pediatric colonoscope to inspect the entire duodenum and part of the jejunum, also may be considered as an initial evaluation.  A systematic review of 14 trials comparing push enteroscopy to capsule revealed "clinically significant findings" in 26% and 56% of patients, respectively.  However, in contrast to enteroscopy, lack of control of the capsule prevents its manipulation and full visualization of the intestine; in addition, tissue cannot be sampled and therapy cannot be applied.
  • 27. Clinical Presantation : 27  Hematemesis  Melena  Hematochezia  Syncope  Dyspepsia  Epigastric pain  Heartburn  Diffuse abdominal pain  Dysphagia  Weight loss  Jaundice
  • 28. Approach to the Patient: Gastrointestinal Bleeding 28  History  Physical examination  Lab investigation
  • 29. APROACH TO PATIENT………….. Con’t 29  History: • Abdominal pain • Haematamesis • Haematochezia • Melaena • Features of blood loss: shock, syncope, anemia • Features of underlying cause: dyspepsia, jaundice, weight loss
  • 30. 30 o Drug history: NSAIDs, Aspirin, anticoagulants, o History of epistaxis or hemoptysis to rule out the GI source of bleeding. o Past medical :previous episodes of upper gastrointestinal bleedin; coronary artery disease; chronic renal or liver disease; o Past surgical: previous abdominal surgery
  • 31. Approach Cont….. 31 Physical Examination : • General examination and systemic examinations • VITALS: Pulse = Feable pulse BP = Orthostatic Hypotension • SIGNS of shock: Cold extremeties, Tachycardia, Hypotension Chest pain, Confusion, Delirium, Oliguria, and etc.
  • 32. 32 SKIN changes: Cirrhosis – Palmer erythema, spider nevi Bleeding disorders – Purpura /Echymosis, Haemarthrosis, Muscle hematoma. • Signs of dehydration (dry mucosa, sunken eyes, skin turgor reduced). • Signs of a tumour may be present (nodular liver, abdominal mass, lymphadenopathy, and etc. • DRE : fresh blood, occult blood, bloody diarrhea • Respiratory, CVS, CNS  For comorbid diseases
  • 33. Lab Diagnosis : 33 CBC with Platelet Count, and Differential  A complete blood count (CBC) is necessary to assess the level of blood loss.  CBC should be checked frequently(q4-6h) during the first day. Hemoglobin Value, Type and Crossmatch Blood  The patient should be crossmatched for 2-6 units, based on the rate of active bleeding.  The hemoglobin level should be monitored serially in order to follow the trend.  An unstable Hb level may signify ongoing hemorrhage requiring further intervention.
  • 34. 34  LFT- to detect underlying liver disease  The BUN-to- creatinine ratio increases with upper gastrointestinal bleeding (UGIB). A ratio of greater than 36 in a patient without renal insufficiency is suggestive of UGIB.  The patient's prothrombin time (PT), activated partial thromboplastin time, should be checked to document the presence of a coagulopathy
  • 35. Endoscopy 35 • Initial diagnostic examination for all patients presumed to have UGIB. • Endoscopy should be performed immediately after endotracheal intubation (if indicated), hemodynamic stabilization, and adequate monitoring in an intensive care unit (ICU) setting have been achieved.
  • 37. Imaging 37 • CHEST X-RAY-Chest radiographs should be ordered to exclude aspiration pneumonia, effusion, and esophageal perforation. • Abdominal X-RAY- erect and supine films should be ordered to exclude perforated viscous and ileus.
  • 38. Angiography : 38  Angiography may be useful if bleeding persists and endoscopy fails to identify a bleeding site.  Angiography along with transcatheter arterial embolization (TAE) should be considered for all patients with a known source of arterial UGIB that does not respond to endoscopic management, with active bleeding and a negative endoscopy.  In cases of aortoenteric fistula, angiography requires active bleeding (1 mL/min) to be diagnostic.
  • 39. Nasogastric Lavage 39  A nasogastric tube is an important diagnostic tool.  This procedure may confirm recent bleeding (coffee ground appearance), possible active bleeding (red blood in the aspirate that does not clear), or a lack of blood in the stomach (active bleeding less likely but does not exclude an upper GI lesion).
  • 40. 40
  • 41. 41 BENEFITS OF LAVAGE : 1. Better visualization during endoscopy 2. Give crude estimation of rapidity of bleeding 3. Prevent the development of Porto systemic encephalopathy in cirrhosis 4. Increases PH of stomach, and hence, decreases clot desolation due to gastric acid dilution 5. Tube placement can reduce the patient's need to vomit  During gastric lavage use saline and not use large volume of to avoid water intoxication.  Gastric lavage should be done in alert and cooperative patient to avoid bronco-pulmonary aspiration
  • 42. Risk Stratification: Rockall Score  Identifies patients at risk of adverse outcome following acute upper GI bleed Variable Score 0 Score 1 Score 2 Score 3 Age <60 60-79 >80 - Shock Nil HR >100 SBP <100 - Co-morbidity Nil major - IHD/CCF/major morbidity Renal failure/liver failure Diagnosis Mallory Weiss tear All other diagnoses GI malignancy - Endoscopic Findings None - Blood, adherent clot, spurting vessel  Score <3 carries good prognosis  Score >8 carries high risk of mortality -
  • 43. Management 43 Priorities are: 1. Stabilize the patient: protect airway, restore circulation. 2. Identify the source of bleeding. 3. Definitive treatment of the cause.
  • 44. Emegency Resuscitation Takes priority over determining the diagnosis/cause  ABC (main focus is ‘C’)  Oxygen: 15L Non-rebreath mask  2 large bore cannulae into both ante-cubital fossae Take bloods at same time for FBC, U&E, LFT, Clotting, X match 6Units  Catheterise
  • 45. 45  IVF initially then blood as soon as available (depending on urgency: O-, Group specific, fully X-matched)  Monitor response to resuscitation frequently (HR, BP, urine output, level of consciousness, peripheral temperature, CRT)  Stop anti-coagulants and correct any clotting derrangement  NG tube and aspiration (will help differentiate upper from lower GI bleed)  Organise definitive treatment (endoscopic/radiological/surgical)
  • 46. Management (Non-variceal)  Emergency resuscitation as already described  Endoscopy Urgent (within 24hrs) – diagnostic and therepeutic Treatment administered if active bleeding, visible vessel, adherent blood clot Treatment options include injection (adrenaline), coagulation, clipping If re-bleeds then arrange urgent repeat endoscopy.
  • 47. 47  Pharmacology PPI (infusion) – pH >6 stabilises clots and reduces risk of re-bleeding following endoscopic haemostasis If H pylori positive then for eradication therapy Stop NSAIDs/aspirin/clopidogrel/warfarin/steroids if safe to do so (risk:benefit analysis)
  • 48. Management (Non-variceal)  Surgery  Reserved for patients with failed medical management (ongoing bleeding despite 2x endoscopy)  Nature of operation depends on cause of bleeding (most commonly performed in context of bleeding peptic ulcer: DU>GU)  E.g. Under-running of ulcer (bleeding DU), wedge excision of bleeding lesion (e.g. GU), partial/total gastrectomy (malignancy)
  • 49. Variceal Bleeds  Suspect if upper GI bleed in patient with history of chronic liver disease/cirrhosis or stigmata on clinical examination  Liver Cirrhosis results in portal hypertension and development of porto-systemic anastamosis (opening or dilatation of pre-existing vascular channels connecting portal and systemic circulations)
  • 50. 50  Sites of porto-systemic anastamosis include:  Oesophagus (P= eosophageal branch of L gastric v, S= oesophageal branch of azygous v) Umbilicus (P= para-umbilical v, S= infeior epigastric v)  Retroperitoneal (P= right/middle/left colic v, S= renal/supra-renal/gonadal v)  Rectal  (P= superior rectal v, S= middle/inferior rectal v)  Furthermore, clotting derrangement in those with chronic liver disease can worsen bleeding
  • 51. Management of Variceal bleeds Emergency resuscitation as already described  Drugs Somatostatin/octreotide – vasoconstricts splanchnic circulation and reduces pressure in portal system Terlipressin – vasoconstricts splanchnic circulation and reduces pressure in portal system Propanolol – used only in context of primary prevention (in those found to have varices to reduce risk of first bleed)  Endoscopy Band ligation  Injection sclerotherapy
  • 52. 52  Balloon tamponade – sengstaken-blakemore tube  Rarely used now and usually only as temporary measure if failed endoscopic management  Radiological procedure – used if failed medical/endoscopic Mx  Selective catheterisation and embolisation of vessels feeding the varices  TIPSS procedure: transjugular intrahepatic porto-systemic shunt  shunt between hepatic vein and portal vein branch to reduce portal pressure and bleeding from varices): performed if failed medical and endoscopic management  Can worsen hepatic encephalopathy  Surgical  Surgical porto-systemic shunts (often spleno-renal)  Liver transplantation (patients often given TIPP/surgical shunt whilst awaiting this)
  • 54. Variceal Bleed: Prognosis  Prognosis closely related to severity of underlying chronic liver disease (Childs-Pugh grading)  Child-Pugh classification grades severity of liver disease into A,B,C based on degree of ascites, encephalopathy, bilirubin, albumin, INR  Mortality 32% Childs A, 46% Childs B, 79% Childs C
  • 55. Management-lower GI BLEEDING  Emergency resuscitation as already described  Pharmacological  Stop NSAIDS/anti-platelets/anti-coagulants if safe  Endoscopic  15% of patients with severe acute PR bleeding will have an upper GI source!)  Colonoscopy – diagnostic and therepeutic (injection, diathermy, clipping)
  • 56. Management  Radiological  CT angiogram – diagnostic only (non-invasive)  Determines site and cause of bleeding  Mesenteric Angiogram – diagnostic and therepeutic (but invasive)  Determines site of bleeding and allows embolisation of bleeding vessel  Can result in colonic ischaemia
  • 57. Management  Surgical – Last resort in management as very difficult to determine bleeding point at laparotomy  Segmental colectomy – where site of bleeding is known  Subtotal colectomy – where site of bleeding unclear  Beware of small bowel bleeding – always embarassing when bleeding continues after large bowel removed!
  • 58. Management Flow Chart for Severe lower GI bleeding Resuscitate Endoscopy (to exclude upper GI cause for severe PR bleeding) Colonoscopy (to identify site and cause of bleeding and to treat bleeding by injection/diathermy/clipping) – often unsuccesful as blood obscures views CT angiogram (to identify site and cause of bleeding) Mesenteric angiogram (to identify site of bleeding and treat bleeding by embolisation of vessel) Surgery
  • 59. Management  As 85% of lower GI bleeds will settle spontaneously the interventions mentioned on previous slide are reserved for:  Severe/Life threatening bleeds  In the 85% where bleeding settles spontaneously OPD investigation is required to determine underlying cause:  Endoscopy: flexible sigmoidoscopy, colonoscopy  Barium enema
  • 60. REFERENCE 60  Harrison principles of intrnal medicine 18th edi.  Kumar .clinical medicine 8th edit.  On line search