Upper GI bleeding & it's

management
Background UGIB
• Common medical emergency with associated high morbidity, mortality(6-11%)*
and medical expenditure

• Most commonly presents with haematemesis and/or melena (much less

commonly with haematochezia – 3x higher risk of death*)

• Requires rapid assessment (particularly evaluation of haemodynamic stability)

and then prompt multi-team management

Cameron P, Jelinek G, Kelly AM, Murray L, Brown A. Textbook of Adult Emergency Medicine. 3rd Edition. Churchill Livingston Elsevier 2009
Blood supply to GI tract:
Mostly anterior branch of abdominal artery
Celiac trunk – Foregut
• Left gastic artery
• Splenic artery
• Common hepatic artery

Superior Mesenteric Artery – Midgut

• Inferior pancreaticod uodenal artery jejunal and ileal arteries
• Middle colic artery
• Right colic artery
• Ileocolic artery

Inferior Mesenteric Artery - Hindgut

• sigmoid arteries
• superior rectal artery
• Left colic rtery
Bleeding Manifestations
• Haematemesis = bleeding proximal to Ligament
ofTreitz
• Frank bloody emesis vs coffee ground
• Melena = majority due to bleeding proximal to
Ligament of Treitz, remainder from small bowel or
right side of LI
• Haematochezia = usually in lower GIT bleed, only if
massive UGIB
Gastrointestinal bleeding
• Gastrointestinal bleeding describe every form of
haemorrhage in the GIT, from the pharynx to
the rectum.
• Can be divided into 2 clinical syndromes
• Upper GI bleed (pharynx to ligament of treitz)

Ligament Of Treitz • Lower GI bleed (ligament of Treitz to rectum)

Gastrointestinal bleeding
• Upper GI bleed remains a major medical
problem.
• About 75% of patient presenting to the
emergency room with GI bleeding have an
upper source.
• In-hospital mortality of 5% can be expected.
• The most common cause are peptic ulcer,
erosions, Mallory-Weiss tear & esophageal
varices.
• Haematemesis : vomiting of blood whether fresh
and red or digested and black.
• Coffee ground vomiting : blood clot in the vomitus.
• Hematochezia : passage of bright red blood per
rectum (if the haemorrhage is severe).
Aetiology LOCAL
GENERAL
Oesophagus Stomach • Haemophilia
• Gastric ulcer • Leukemia
• Oesophageal varices • Thrombocytopenia
• Gastric CA
• Oesophageal CA • Anti-coagulant
• Erosive gastritis therapy
• Reflux oesophagitis
• gastric lymphoma
• Mallory-Weiss syndrome
• gastric leiomyoma

Duodenum • Dielafoy’s syndrome

• Duodenal ulcer
• -Duodenitis 7/
8
• -Periampullary tumour 1

• -Aorto-duodenal fistula
Oesophageal varices: Pathophysiology
• Portal venous hypertension Resistance to flow in portal venous system

• Pressure

• Portal systemic shunting

• (Abnormal venous communication between portal system and systemic venous circulation)

• Appearing of large submucosal veins at lower end of

• Oesophagus and gastric fundus

• Haemorrhage due to intra-variceal pressure

Oesophageal varices
• Sudden onset, Painless, Large volume of blood, Dark red

• History of (alcoholic) liver disease

• Physical findings of portal Hypertension

• Ascites, splenomegaly
• Management
• Blood transfusion
• Endoscopic variceal injection with
• Sclerosant or banding.
• Sengstaken tube
Mallory-weiss Tear
Longitudinal tears at the oesophagogastric junction.
• may occur after any event that provokes a sudden rise in intragastric pressure or
gastric prolapse into the esophagus.
Clinical features:
• An episode of haematemesis following retching or vomiting. melaena
• hematochezia syncope abdominal pain.
• Precipitating factors:
• hiatus hernia retching & vomiting straining hiccupping coughing
• blunt abdominal trauma cardiopulmonary resuscitation
• Management:
• Bleeding from MWTs stops spontaneously in 80-90% of patients
• A contact thermal modality, such as multipolar electrocoagulation or heater
probe, with or without epinephrine
• injection, is typically used to treat an actively bleeding
• Epinephrine injection -reduces or stops bleeding via mechanism
vasoconstriction and tamponade
- Endoscopic band ligation, Endoscopic hemoclipping
Peptic ulcer
• Gastric ulcer & duodenal ulcer

• Caused by imbalance between secretion of acid

and pepsin, and mucosal defence mechanism.

Etiology:

-• Helicobacter pylori infection Sign and symptoms

• epigastric pain
• Zollinger-ellison syndrome • haematemesis
• Melaena
• NSAIDs
• heartburn
• others: stress, smoking,alcohol, steroid
12/81
Peptic Ulcer: Pathogenesis
Predisposing factors including H.pylori infection of mucosa

Acid-pepsin attack and/or breach of mucosal protection Acute inflammation

Resolution

Destruction of mucosa

Mucosal ulceration mucosal regeneration

Extension through submucosal & muscular layers causing deep ulceration

Perforation Erosion of major granulation tissue

blood vessel formed & attemps
repair
Peritonitis massive haemorrhage chronic & relapsing
ulceration
Peptic Ulcer
Feature Gastric ulcer Duodenal ulcer

Onset Soon after eating 2-3 hours after eating

Relieving factor Vomiting Eating

Precipitating factor eating Missing a meal, anxiety,

stress

Duration of A few weeks A month or two

attack

14/81
Peptic Ulcer: Complication
• Haemorrhage : posterior duodenal ulcer erode the
gastroduodenal artery lesser curve gastric ulcers
erode the left gastric artery
• Perforation: generalized peritonitis
• signs of peritonitis
• Pyloric obstruction
• Profuse vomiting, LOW, dehydration constipation

15/81
 Peptic Ulcer: Management
• Antacid – aluminium/Mg hydroxide, Mg Trisiclate

• Mucosal protective agents – sucralfate

• Prostaglandin analogues – misoprostol

• H2 receptor antagonist – cimetidine & ranitidine

• Proton pump inhibitor – omeprazole & lansoprazole

• H.pylori eradication- triple therapy :metronidazole,amoxycilin,erythromycin

• Surgery should be done if

-Failed medical treatment
-Vagotomy, gastrectomy, pyloroplasty
Factors Predictive of Upper GI bleed*

• Melena on PR examination (LR 25)

• Blood or coffee ground vomit on NG lavage (LR 9.6) Ratio of blood urea nitrogen

to creatinine >30 (LR 7.5) Self reported history of melena (LR 5.1-5.9)

• Blood clots seen in stool (LR 0.05)

Srygley FD, Gerardo CJ, Tran T, Fisher DA. Does this patient have a severe upper gastrointestinal bleed? JAMA 2012; 307:1072
Assessment and Factors Predictive of a Severe
Bleed
• Aims
• Assess severity of bleed identify potential cause
• Identify co-morbidities that may alter management decisions

• History
• Orthostatic dizziness, confusion, angina, severe palpitations

• Examination
• Tachycardia, orthostatic hypotension or supine hypotension (even worse), cold/clammy peripheries

• Bedside and Laboratory Investigations

• Hb <80 g/L, high Ur:Cr ratio, high red blood found on NG lavage
Mortality/Morbidity Factors
• Advanced age

• Cause of the bleed (particularly varices)

• Presence of shock

• Fresh bright red blood

• Low Hb

• Re-bleed presentation

• Comorbid disease

• Endoscopic findings
Ulcerative or Erosive Disease
• Peptic Ulcer Disease: *Most Common Cause UGIB*
• Idiopathic
• Drug induced Aspirin
• NSAID (approx doubles risk)
• Infectious
• H.pylori, CMV, HSV
• Stress induced ulcer (burns, major trauma, sepsis,
hypotension, HI)
• Zollinger-Ellison Syndrome
Ulcerative or Erosive Disease
• Oesophagitis
• Peptic
• Infectious

• C. albican, CMV, HSV miscellaneous

• Pill induced
• Alendronate tetracycline quinidine KCL
• Aspirin
• Nsaid
Portal Hypertension

• Oesophageal Varices

• Gastric Varices Duodenal Varices

• Portal Hypertensive Gastropathy

• Large amounts of dark venous blood…

Arterial, Venous or Other Vascular
Malformations
• Idiopathic angiomas

• Hereditary haemorrhagic telangectasia

• Dieulafoyǯs Lesion

• Gastric Antral Vascular Ectasia Radiation-induced

telangiectasia Blue rubber bleb nevus syndrome
GIT Tumours

• Traumatic or Post Surgical

• BENIGN: leiomyoma, lipoma, polyps

• MALIGNANT: adenocarcinoma, mesenchymal neoplasm, lymphoma,

Kaposi sarcoma, carcinoid, melanoma, metastatic tumour
General Management
• Supplemental oxygen

• Crystalloid/colloid fluid resuscitation

• +/- Blood transfusion

• Consider correcting coagulopathy (?Benefit vs risk)

• Medical management

• Endoscopic (pretreat with erythromycin) / embolisation /

• Surgical management
Blood Transfusion

• Consider on individual basis (particularly comorbidities) indication:

Hb <70 g/L (except unstable CHD aim Hb > 90 g/L)

• Avoid transfusing patients with suspected variceal bleeding to Hb >10

g/dl (portal P may worsen bleeding)

• One unit FFP for each four units of packed RBC transfused9
Management of UGI bleeding
• Consider reversal of coagulopathy (in those actively bleeding)

• FFP if INR >1.5 or platelets if count <50 x 109/L

• Simultaneous replacement + scope if INR <3

• Delay scope until INR <3 if it is initially higher10

• Consider platelet transfusion if life threatening bleeding and taking antiplatelet agents eg
aspirin or clopidogrel

• If stent or ACS – recommend discuss with cardiologist prior to stopping antiplatelet agent
or transfusing platelets11
Medical Management

• Acid Suppression
• Proton pump inhibitor H2 R antagonists
• Somatostatin Analogue
• Octreotide

• Other
• Terlipressin Antibiotics
• Tranexamic acid
Proton Pump Inhibitor (PPI) / H2 Receptor Antagonist

• PPI (empirically) to all patients with acute UGIB: esomeprazole or pantoprazole:

80mg IV bolus, followed by 8mg/hour IVI (continued for 72 hours)

• Start PPI at presentation (Unknown source of bleeding)

• Once source known (and treated), decision can be made before discharge home

if PPI needs to be continued

Acid Suppression
• Meta analysis (2002): Pharmacotherapies for Non Variceal UGIB :

• PPI (IVI) significantly reduces rate of rebleeding compared to H2 R antagonists or placebo

• H2R antagonists had only modest effects in bleeding gastric ulcers and no longer
recommended:

• Reduced rebleeding by 7.2%

• Reduced surgery by 6.7%

• Reduced mortality by 3.2%

Acid Suppression
• PPIs (oral and IV) have additional benefits: decrease LOHS

• Decreased need for blood transfusion (in those with high risk ulcers treated with

endoscopic therapy)

• May promote haemostasis in other, non ulcer lesions

• However, NO demonstrable effect on all cause mortality

• Asians patients likely benefit best from PPI (related to drug metabolism and

ability to raise intragastric pH)

• PPI may decrease rate rebleeding, LOHS, need for blood transfusion but likely

doesn’t effect mortality

• Oral dose needs to be at least double standard clinical dose

PPI administration

If given PPI pre – endoscopy: reduces high risk stigmata and the need for

endoscopic therapy (OR 0.67)

If given PPI post – endoscopy: reduces risk of requiring surgery, risk of rebleeding

and death in high risk patients (RR 0.43, 0.4, 0.41 respectively)

Lau J, Leung W, Wu J et al. Omeprazole before endoscopy in patients with gastrointestinal bleeding. NEJM 2007; 356:1631- 40.
Leontiadis GI, Sharma VK, Howden CW. Proton pump inhibitor treatment for acute peptic
ulcer bleeding. Cochrane Database Syst Rev 2006;1:CD002094.
Somatostatin Analogue
Octreotide

• In suspected or known cases of variceal bleeding, give octreotide 20-50

mcg bolus followed by 25-50 mcg/hr IVI may also reduce risk of bleeding
due to nonvariceal causes.

• MOA in this setting: reduces splanchnic arterial blood flow (via

vasoconstriction) and portal venous pressure (while still maintaining
systemic BP and cardiac output)
Octreotide Indications

• Suspected or known variceal bleeding controls bleeding in 74-92%

cases comparable to injection sclerotherapy and vasopressin for

bleeding control and survival, however, with less SE18 reduces

reduces rebleeding, blood transfusion requirement and surgery does

NOT reduce mortality significantly (RR 0.80, 95% CI 0.63-1.01)20

Somatostatin Analogue
• Octreotide Indications continued….
• (Some) bleeding peptic ulcers:
• may be reduction in rebleeding
• may be reduction in need for subsequent surgery NO effect on
mortality

• NOT routinely given, consider if high risk (to avoid the

above complications)
• OR delay until emergency endoscopy
Vasopressin Analogue
Terlipressin
• MOA: Synthetic analogue of vasopressin with fewer SE, vasoactive, specificity for
splanchnic vessels causing vasoconstriction and reduction in portal pressure
• In suspected or known cases of variceal bleeding: 2mg bolus IV injection (2mg 6
hourly for 24 hours, then 1mg 6 hourly for 24 hours if bleeding stabilised, then
discontinue)
• 34% relative risk reduction in mortality
• Systematic review has shown insignificant difference between:
• Terlipressin and somatostatin treatment
• Terlipressin and endoscopy therapy
Other Medical Treatments
• Prophylactic antibiotics in patients with cirrhosis + UGIB have been
shown to
• reduce infectious complications
• decreased mortality
• may decrease risk of rebleeding from oesoph varices

• Benefits shown when given both before and after endoscopy.

Tranexamic Acid
• NO role in medical management of UGIB

• A meta analysis of 7 RCTs found in those patients treated with

antiulcer and /or endoscopy for UGIB (the mainstay treatment),
tranexamic acid did not provide any additional beneficial effect

• MOA: Anti fibrinolytic agent which competitively inhibits activation of

plasminogen to plasmin (plasmin degrades fibrin clots)
Management of UGIB
• Careful history and examination important – consider source, assess severity, identify comorbid condition

• Blood transfusion for: ALL patients with acute upper GI bleeding

• PPI role is crucial.

• Evidence PPI in peptic ulcers reduces most things EXCEPT mortality (however high risk patients may have improved

mortality rates if PPI given post endoscopy).

• H2 R antagonists are no longer recommended.

• Patients who present with UGIB and have known cirrhosis should have antibiotics before endoscopy

• Patients with known or suspected gastro - oesophageal variceal bleed should have:

• Octreotide (bolus and then IVI) PLUS antibiotics. Avoid blood transfusing to hb>100 g/L OR

• Terlipressin boluses six hourly PLUS antibiotics. Octreotide remains the therapy of choice18
Thank You