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Upper Gastrointestinal Bleeding. Dr Bernard Stacey Consultant Gastroenterologist. Variceal Known varices Signs of chronic liver disease Prolonged INR Low platelets (Alcohol history). Non-variceal NSAID use Preceding dyspeptic symptoms M-W tear history. Upper GI bleeding.
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Upper Gastrointestinal Bleeding Dr Bernard Stacey Consultant Gastroenterologist
Variceal Known varices Signs of chronic liver disease Prolonged INR Low platelets (Alcohol history) Non-variceal NSAID use Preceding dyspeptic symptoms M-W tear history Upper GI bleeding
Lower GI bleeding • Previous history of similar events • Bright red PR bleed • Dark red PR bleed • Unless massive upper GI bleed • Normal urea
Trials investiging a raised urea as a predictor of UGIB v LGIB (or no bleed) • USA 6, Europe 6, Japan 4, SA 1 • Twice as many retrospective trials • 1729 patients • Sensitivities 54 – 95% • Specificities 27 – 100% • 10 trials in favour, 2 against
OGD findings Varices DU/GU/pyloric ulcer Gastritis (NSAIDs) Oesophageal ulcer Normal Cancers Oesophagitis Dielafoy Miscellaneous
Acute Resuscitation A B C not “OGD”
Acute Resuscitation • Airway protection • Breathing (oxygenation) • Circulation (BP, postural drop) • N/Saline, blood • (FFP) • (Platelets)
Acute Resuscitation (2) Endoscopy • Allows direct visualisation • Heater probe, endoclips • Injection with adrenaline, ethanolamine • Band ligation • Rebleed rate = 15 – 20%
On Call Endoscopist • Aim for OGD within 24 hours of admission • Endoscopy at night if: • Severe haemodynamic upset (pulse, BP) • Varices • Otherwise endoscope next morning • Discussion of management
Variceal bleeding • Venous bleeding • Usually an associated coagulopathy • Drug administration recommended as early as possible (before endoscopic therapy) • Combination therapy better than drugs or endoscopy alone
Risk of Bleeding • Portal pressure - circadian change • Highest pressures at night • risk with: • severity of liver disease • variceal size • red markings on varix • pressure over 12 mmHg
Pharmacological treatment • Similar effectiveness to sclerotherapy • Terlipressin (Glypressin) - Synthetic vasopressin • bolus administration but may need nitrates if angina provoked • Beneficial effects temporary so endoscopy still necessary • Antibiotics (cefotaxime)
blockers • Propranolol, nadolol • Lower risk of rebleeding by 40% • Lower mortality by 20% • Splanchnic haemodynamics unpredictable • Not an acute drug
Non-variceal bleeding • Endoscopy is the key to effective treatment • Proton pump inhibitors / H2 receptor antagonists not effective in stopping active bleeding • But: clot stabilisation
The Vessel • Artery protruding above ulcer floor: 33% • Clot protruding above ulcer floor: 65% • not simply an acute excess acid problem • Aneurysm formation in 51% • true 42% false 58%
Proton Pump Inhibitors • Actively bleeding ulcers / visible vessel adrenaline injection + thermocoagulation IV omeprazole or Placebo 120120 8 (6.7%) Rebleeding 27 (22.5%) 5 In first 3 days 24 3 Surgery 9 5 Died 12
Tranexamic acid • Used as pro-coagulant in other settings • cardiac surgery • ENT • menorrhagia • Complications • Anecdotal use for portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE)
Think of underlying conditions: MI Pneumonia GI obstruction
Recurrence rates Duodenal ulcer • Without eradication: 80% in 1 year • With eradication: 5% in 1 year
Arterial Physical measures Excess acid not the main acute problem IV drugs after OGD (but before also helps) Venous Lower pressures involved Associated coagulopathy Combination therapy best outcome IV drugs before and after OGD Arterial (ulcer) v Venous (variceal) bleeding Acute ‘ABC’ resuscitation
Summary • Basic ‘ABC’ resuscitation is imperative • Remember coagulopathy and synthetic vasopressin in variceal bleeds • Inform endoscopist • At night if unstable • Early the next morning if stable • Early surgical involvement • Acid suppression and eradication regimes