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Upper GI Bleed James Peerless April 2011.

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Presentation on theme: "Upper GI Bleed James Peerless April 2011."— Presentation transcript:

1 Upper GI Bleed James Peerless April 2011

2 Introduction Incidence of 100/100 000 population per year (UK & USA)
>80% occur as acute admissions ‘Hospital-acquired’ Critically ill patients Prolonged NG tube Drug Rx Associated with high rate of mortality and long ICU stay Critically ill patients (stress ulcers, mechanical ventilation, coagulopathy, splanchnic hypoperfusion  mucosal ischaemia)

3 Objectives Definitions Anatomy Sources of Bleeding Presentation
Assessment Management

4 Definitions Upper GI Tract The oral cavity, pharynx, oesophagus, stomach & proximal duodenum Haematemesis The act of vomitting blood; swallowed or that arisen from the bleeding within the upper GI tract Melaena Black discoloured faeces due to the presence of partly-digested blood from the upper GI tract

5 Anatomy Coeliac trunk Left gastric a. Splenic a. Hepatic a.
Left gastro-epiploic a. Right gastric a. Right gastro-epiploic a.

6 Azygous v. Portal v. L + R gastric vv.

7 Causes Upper GI Bleed GU DU Ca Oe Varices M-W Tear Oeso-phagitis
Gastri-tis GU/DU 50% MW 5-10 Varices 10-20 Bleeding from the nasopharynx should not be excluded (especially if considering endoscopy/ SB tube) Aortic fistula

8 Dieulafoy’s ulcer

9 Varices Secondary to portal hypertension
Dilated collateral veins formed at G-Oe junction These portosystemic anastomoses are superficial and prone to rupture High pressure veins in a hyperdynamic circulation 80% caused by ALD Portal hypertension and subsequent variceal bleed is a complication of chronic liver disease Portal vein receives most blood from splenic and superior mesenteric veins. Pre-hepatic: portal vein thrombosis Hepatic: cirrhosis, schistosoiasis Post-hepatic: Budd-Chiari syndrome, right heart failure As portal pressure rises, the venous system dilates and collaterals are formed. Formed at G-Oe junction, rectum, left renal vein, abdominal wall (caput medusae) Portal hypertension is a complication of cirrhosis and is the etiological factor behind gastroesophageal varices and subsequent bleeding. Portal hypertension generates reversal of portal venous flow (hepatofugal), which diverts venous blood in a cephalic direction through the left gastric vein to the venous plexus of the esophagus. There- fore, portal hypertensive varices are more common in the lower third of the esopha- gus, especially at the gastroesophageal junction.

10 Presentation Active bleeding History of haematemesis Melaena
Shock/hypotension/collapse Anaemia Bleeding cannot be seen (unlike in other trauma calls) – and therefore management is guided almost totally on clinical and physiological signs

11 Acute Management Supportive Corrective Resuscitation
A B C History & Examination Recruit help Investigations Continuous monitoring Blood products Correction of coagulopathy Medical Balloon tamponade Endoscopy Surgical Early volume replacement Multidisciplinary involvement, major haemorrhage protocol Cyp, arterial line, catheter Vit. K, FFP, Platelets PPI

12 Assessment Acute Assessment History & Examination Is the airway safe?
Is the patient at risk of further events? PUD Recent vomitting Stigmata of chronic liver disease (bruising, liver flap, spaider naevi, caput medusae, gynaecomastia, palmar erythema, ascites) Variceal bleeds are more likely to have airway compromise due to the volume of blood (& associated encephalopathy)

13 Identifying Risk Rockall Score

14 Predictors of Mortality
Rockall Criteria Predictors of Mortality Age Co-morbidity Diagnosis SRH Re-bleed Allows us to stratify the risk according to five clinical criteria. Risk is assessed using five clinical criteria Organ failure Adds up to a score which predicts risk of rebleed and mortality

15 Rockall Score 1 2 3 Age <60 60-79 >80 Shock No shock HR >100
1 2 3 Age <60 60-79 >80 Shock No shock HR >100 HR >100, SBP <100 Comorbidity Cardiac failure, ischaemic heart disease Renal failure, liver failure, disseminated malignancy Diagnosis Mallory Weiss, no lesion, no stigmata of recent haemorrhage All other diagnoses Malignancy of upper gastrointestinal tract SRH (Endoscopy) None, or dark spot Fresh blood, adherent clot, visible or spurting vessel

16 Mortality Rates 1 2 3 4 5 6 7 8+ Total (%) 4.9 9.5 11.4 15.0 17.9 15.3
1 2 3 4 5 6 7 8+ Total (%) 4.9 9.5 11.4 15.0 17.9 15.3 10.6 9.0 6.4 Re-bleed (%) 3.4 5.3 11.2 14.1 24.1 32.9 43.8 41.8 Death (non re-bleed) (%) 0.3 2.0 3.5 8.1 14.9 28.1 Death (re-bleed) (%) 10.0 15.8 22.9 33.3 43.4 52.5 Death (total) (%) 0.2 2.9 10.8 17.3 27.0 41.1 Rockall TA, Logan RF, Devlin HB, Northfield TC (1996) Risk assessment after acute upper gastrointestinal haemorrhage. Gut 38:316 – 21

17 Scoring Systems Rockall Score Forrest Classification
Active haemorrhage Signs of recent haemorrhage Lesions without active bleeding Glasgow-Blatchford Score Scored on Hb, urea, BP, presentation/comorbidities (no endoscopy) Forrest classification – used in endoscopy for comparison of at-risk patients after endoscopy GBS – new scoring system which is a quick way of triaging which patients are likely to need medical intervention

18 Management Pathway Resuscitation Suspicion of Variceal Bleeding?
No: Endoscopy <24h Conservative Management Yes: Endoscopy <4h Endoscopy

19 Oesophagogastroduodenoscopy
Offers diagnostic information and opportunity for therapeutic intervention Scoping within 24 hours has a proven reduction in rebleed, mortality and length of admission For ulcers: Adrenaline injection (temporary efect) Diathermy/haemocoagulation Endocscopic clips Ulcers: Endoscopic therapeutic options are epinephrine injection, heat treatment/dia- thermy, endoscopic clips, and argon plasma coagulation

20 Variceal Bleeding Endoscopy is the definitive treatment of choice for variceal bleed ETT Vasopressin analogue Affect splanchnic vasoconstriction reduce hepatic portal pressure gradient ET Sclerotherapy Glue (lung, spleen embolism) Adrenaline (vasoconstriction and tamponade) Heat Band ligation Sengstaken-Blakemore tube (200mL balloon + oesophageal balloon) Linton-Nachlas tube (600mL balloon)

21 Vasopressin/somatostatin
Drugs & Secondary MX Drugs Vasopressin/somatostatin Anti-biotics PPI Vitamin K

22 Sengstaken-Blakemore Tube
First described in 1950 (not usedas much now due to better identification of liver disease, and pharmacological management acutely. Useful tool (if skilled to use it) for massive haemorrhage, and perhaps buys you time before implementing a more permanent management plan. High risk of rebleeding following deflation of the tube (~50%) Patients should ideally be intubated before insertion. Inserted orall or nasally gastric balloon should be inflated with 150 – 200 ml of air, water or con- trast, and traction applied and maintained The esophageal balloon is not routinely inflated as concerns exist regarding pressure necrosis.

23 Sengstaken-Blakemore Tube

24 Linton-Nachlas Tube an alternative for effective control of gastric varices. This tube has a larger gastric balloon (600 ml) which provides tamponade throughout the gastric fundus.

25 TIPSS Transjugular Intrahepatic Portosystemic Shunt
Radiologically guided stent Drilled through the liver and connects the portal and hepatic vein Available in specialised units Complications Thrombosis (10%) Bleeding Infarction transjugular intrahepatic portosystemic shunt (TIPSS), is a radiologically guided insertion of a self-expanding metallic stent into the liver parenchyma via the inter- nal jugular vein, to connect the portal and hepatic veins. This technique is indicated as a rescue therapy in patients with uncontrollable acute variceal bleeding who have failed conventional endoscopic therapy, or for recurrent bleeding in patients intoler- ant to standard medical treatments. In patients with a hepatic venous pressure gra- dient 20 mmHg TIPSS has been shown to reduce early re-bleeding risk and 6- week mortality [47]. The main complications of TIPSS include stent failure, either due to thrombosis or intimal hyperplasia, and worsening encephalopathy. Stent thrombosis occurs in 10 % of cases [48], generally within the first 24 h post-inser- tion. Blockage can be identified with Doppler ultrasound and released with repeat radiological catheterization. Procedural related complications such as intra-perito- neal bleeding, hepatic infarction, and formation of biliar y-venous or arterio-venous fistulas are rare.

26 Summary Hidden clinical picture Supportive and Corrective Management
Endoscopic therapy mainstay of treatment Risk of rebleeding remains high – keep monitoring the patient!

27 The End

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