2Introduction Incidence of 100/100 000 population per year (UK & USA) >80% occur as acute admissions‘Hospital-acquired’Critically ill patientsProlonged NG tubeDrug RxAssociated with high rate of mortality and long ICU stayCritically ill patients (stress ulcers, mechanical ventilation, coagulopathy, splanchnic hypoperfusion mucosal ischaemia)
3Objectives Definitions Anatomy Sources of Bleeding Presentation AssessmentManagement
4DefinitionsUpper GI Tract The oral cavity, pharynx, oesophagus, stomach & proximal duodenumHaematemesisThe act of vomitting blood; swallowed or that arisen from the bleeding within the upper GI tractMelaenaBlack discoloured faeces due to the presence of partly-digested blood from the upper GI tract
5Anatomy Coeliac trunk Left gastric a. Splenic a. Hepatic a. Left gastro-epiploic a.Right gastric a.Right gastro-epiploic a.
7Causes Upper GI Bleed GU DU Ca Oe Varices M-W Tear Oeso-phagitis Gastri-tisGU/DU 50%MW 5-10Varices 10-20Bleeding from the nasopharynx should not be excluded (especially if considering endoscopy/ SB tube)Aortic fistula
9Varices Secondary to portal hypertension Dilated collateral veins formed at G-Oe junctionThese portosystemic anastomoses are superficial and prone to ruptureHigh pressure veins in a hyperdynamic circulation80% caused by ALDPortal hypertension and subsequent variceal bleed is a complication of chronic liver diseasePortal vein receives most blood from splenic and superior mesenteric veins.Pre-hepatic: portal vein thrombosisHepatic: cirrhosis, schistosoiasisPost-hepatic: Budd-Chiari syndrome, right heart failureAs 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.
10Presentation Active bleeding History of haematemesis Melaena Shock/hypotension/collapseAnaemiaBleeding cannot be seen (unlike in other trauma calls) – and therefore management is guided almost totally on clinical and physiological signs
11Acute Management Supportive Corrective Resuscitation A B CHistory & ExaminationRecruit helpInvestigationsContinuous monitoringBlood productsCorrection of coagulopathyMedicalBalloon tamponadeEndoscopySurgicalEarly volume replacementMultidisciplinary involvement, major haemorrhage protocolCyp, arterial line, catheterVit. K, FFP, PlateletsPPI
12Assessment Acute Assessment History & Examination Is the airway safe? Is the patient at risk of further events?PUDRecent vomittingStigmata 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)
14Predictors of Mortality Rockall CriteriaPredictors of MortalityAgeCo-morbidityDiagnosisSRHRe-bleedAllows us to stratify the risk according to five clinical criteria.Risk is assessed using five clinical criteriaOrgan failureAdds up to a score which predicts risk of rebleed and mortality
15Rockall Score 1 2 3 Age <60 60-79 >80 Shock No shock HR >100 123Age<6060-79>80ShockNo shockHR >100HR >100, SBP <100ComorbidityCardiac failure, ischaemic heart diseaseRenal failure, liver failure, disseminated malignancyDiagnosisMallory Weiss, no lesion, no stigmata of recent haemorrhageAll other diagnosesMalignancy of upper gastrointestinal tractSRH (Endoscopy)None, or dark spotFresh blood, adherent clot, visible or spurting vessel
17Scoring Systems Rockall Score Forrest Classification Active haemorrhageSigns of recent haemorrhageLesions without active bleedingGlasgow-Blatchford ScoreScored on Hb, urea, BP, presentation/comorbidities (no endoscopy)Forrest classification – used in endoscopy for comparison of at-risk patients after endoscopyGBS – new scoring system which is a quick way of triaging which patients are likely to need medical intervention
19Oesophagogastroduodenoscopy Offers diagnostic information and opportunity for therapeutic interventionScoping within 24 hours has a proven reduction in rebleed, mortality and length of admissionFor ulcers:Adrenaline injection (temporary efect)Diathermy/haemocoagulationEndocscopic clipsUlcers: Endoscopic therapeutic options are epinephrine injection, heat treatment/dia- thermy, endoscopic clips, and argon plasma coagulation
20Variceal BleedingEndoscopy is the definitive treatment of choice for variceal bleedETTVasopressin analogueAffect splanchnic vasoconstrictionreduce hepatic portal pressure gradientETSclerotherapyGlue (lung, spleen embolism)Adrenaline (vasoconstriction and tamponade)HeatBand ligationSengstaken-Blakemore tube (200mL balloon + oesophageal balloon)Linton-Nachlas tube (600mL balloon)
21Vasopressin/somatostatin Drugs & Secondary MXDrugsVasopressin/somatostatinAnti-bioticsPPIVitamin K
22Sengstaken-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 nasallygastric balloon should be inflated with 150 – 200 ml of air, water or con- trast, and traction applied and maintainedThe esophageal balloon is not routinely inflated as concerns exist regarding pressure necrosis.
24Linton-Nachlas Tubean alternative for effective control of gastric varices.This tube has a larger gastric balloon (600 ml) which provides tamponade throughout the gastric fundus.
25TIPSS Transjugular Intrahepatic Portosystemic Shunt Radiologically guided stentDrilled through the liver and connects the portal and hepatic veinAvailable in specialised unitsComplicationsThrombosis (10%)BleedingInfarctiontransjugular 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 . 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 , 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.
26Summary Hidden clinical picture Supportive and Corrective Management Endoscopic therapy mainstay of treatmentRisk of rebleeding remains high – keep monitoring the patient!