Upper Gastrointestinal Bleeding
Epidemiology
Duodenal / gastric ulcers: bleeding stops spontaneously in 80% (same in lower GI bleeding);  risk of
rebleeding if atherosclerosis, posterior wall duodenal ulcer, high lesser curve gastric ulcer, vessel visible
in base; 5-6% mortality; 60% GI bleeds are associated with peptic ulcer disease; most common cause of
upper GI bleeding
Oesophageal varices: bleeding stops spontaneously in 20-30%; present in 20% with cirrhosis; grow by
7%/yrea; 10-15% haemorrhage/year; 60% 1 year bleeding recurrence rate; recurrence rate 20-30%; will
usually rebleed unless portal HTN corrected; 15-20% 6/52 mortality per bleed; 25-40% overall mortality;
most common cause of re-bleed in upper GI bleeding
Aetiology
Peptic ulcer disease, ETOH, NSAIDs (2x risk of upper GI bleed), ARDS, burns, CNS disease, cancer, smoking,
aorto-enteric fistula; due to gastritis / oesophagitis / duodenitis in 13%
Pathophysiology
Examination helps determine site of bleeding in 40%; look for signs of chronic liver disease / coagulopathy
Bleeding sites: 25% duodenal ulcer / 25% gastric erosion / 20% gastric ulcer
/ 20% Mallory Weiss
tear / 7-10% oesophageal varices
Peptic ulcer disease 60%; Gastritis / oesophagitis / duodenitis = 13%
Haematemesis: Bleeding proximal to ligament of Treitz; occurs in 50-66% patients with upper GI bleeding;
bright red = severe
Melaena: From upper GI / proximal colon; more liquid = more severe; haematochezia – 10-14% is upper
GI
Mallory-Weiss tear: small tear in mucosa of upper cardia of stomach – in gastro-oesophageal junction;
due to violent vomiting (prior history of vomiting in 50%)  mild haematemesis; brighter blood
Investigation
FOB: false +ive due to raw meat, horseradish; false negative due to vitamin C; remain positive for 2/52
after significant GI bleed
Bloods: Ur:Cr >200 (40% sensitivity, 95% specificity, LR+ 6.4; due to breakdown of Hb protein)
ECG: if shock / anaemia / PMH of IHD
Erect CXR: if significant pain, suspect pulmonary pathology, ?oesophageal rupture
NGT: if unclear history; sensitivity 60%, specificity 75%; presence of fresh blood on aspiration has 
mortality compared to clear
Angiography: can detect bleeding if >0.5ml/min; may be helpful if bleeding / large clots make endoscopy
hard
C: IV fluids, clotting factor replacement, reversal of anticoagulation, platelets if needed, IDC, inotropes
Blood transfusion if: >2L N saline resus; initial Hb <8; significant risk of rebleeding; co-morbidities  ability
to tolerate anaemia
D: treat hepatic encephalopathy
Admit ICU if: variceal bleeding, CV instability, significant co-morbidities, endoscopy features of recent
Haemorrhage
Management
If peptic ulcer disease:
No drugs have been found to be of benefit if acute bleeding is from duodenal ulcer
High dose PPI: 80mg IV omeprazole  8mg/hour INF to maintain gastric pH >6
Pros: Reduces hospital LOS / active bleeding time at endscopy / need for OT
Cons: No effect on transfusion requirement, recurrent bleeding, mortality
Gastroscopy: treatment of choice; identifies source of bleeding in 90%; perform within 12-24 hours if
stable, immediately if unstable; can do injection therapy, thermal devices, laser therapy
Pros:  rebleeding by 60% / mortality by 45% / emergent OT by 65%
Indications for urgent scope: active / recurrent bleeding, bright red blood in vomit, large bleed (>2iu RBC
needed), variceal bleeding
Early discharge after if: non-bleeding Mallory-Weiss tear, clean-based ulcer
OT: emergent OT required in 6-8%
Indications for OT: active bleeding not controlled on endoscopy, recurrent bleeding, perforation, failure
of conservative management, blood transfusion >5iu, refractory shock
Outpatient management: suitable for discharge without scope if: <60yrs, <200ml blood loss, no cardiovascular compromise, no melaena, normal coagulation, no bleeding with 4 hours observation. Organise
outpatient scope.
Management
(cntd)
If variceal bleeding:
Octreotide: somatostatin analogue  splanchnic vasoconstriction; give 50-100mcg (1mcg/kg) bolus  2550mcg/hr (1-4mcg/kg/hr) for 48 hours; as effective as immediate sclerotherapy (in 75-90%); monitor BSL
as causes  glu; alternative is vasopressin
Pros: Reduces active bleeding / transfusion requirement by 1/3
Terlipressin: vasopressin analogue; 2mg Q6h for 1st day  1mg Q6h
Cons: increases afterload so may cause  CO if poor LV function; risk of MI, HTN, peripheral ischaemia
Sengstaken-Blakemore / Minnesota tube: control bleeding in 70-90% (50% recurrence rate on removal
however); use only if emergency endoscopy not available as high risk of complications; insert gastric
balloon 1st with 50ml air  Xray to confirm intragastric  further inflate to 250ml  traction  if still
bleeding, inflate oesophageal balloon to max 40mmHg; use for max 48-72 hours
Indicated if: severe variceal bleeding uncontrolled by other measures (sclerotherapy and vasopressin),
>2L transfusion requirement in 24 hours, Mallory-Weiss tear with ongoing bleeding
Complications: in 25-30%; pulmonary aspiration in 10%; oesophageal perforation; sinusitis; mucosal
ulceration; necrosis of alar cartilage; tracheal compression
Nadolol + ISMN: reduces portal venous p
Banding / sclerotherapy: obliterates bleeding varices in 80-90%
Sclerotherapy: 40% complication rate (eg. Perforation, aspiration, pyrexia, chest pain, ulcers, strictures)
Ligation: as effective as sclerotherapy, with less side effects
Transjugular intrahepatic portal-systemic shunt (TIPS): use if continued bleeding despite ligation; controls
bleeding in 90%; lower mortality and morbidity than portocaval shunt;  1yr mortality by 25% /  risk
of rebleeding by 50% if associated with severe cirrhosis
Contra-indications: encephalopathy, pre-terminal liver failure, portal venous thrombosis, intrahepatic
sepsis, significant cardiac disease
Angiography: if not controlled by endoscopy; embolisation stops bleeding in 80%
OT: partial gastrectomy; oesophageal transection; if failure of endoscopy / failure to visualise / massive
RBC transfusion (>6-8iu/day or >12iu at any time)
Prognosis
Mortality 6-11% (usually due to multi-organ failure and co-morbidities, rather than exsanguination)
Glasgow Blatchford score: <4% need transfusion / need OT / die if: Ur <6.5, Hb >130 (120 in women), SBP
>110, HR <100, no syncope / liver disease / CCF
PUD: Clean base ulcer =
5% risk rebleed, 2% mortality
Active bleeding ulcer = 55% risk rebleed, 11% mortality
Poor prognosis: Hct <30%, SBP <100, red blood in NG/vomit, PMH cirrhosis, ascites
Poor prognostic signs in varices: active bleeding at scope; >2L transfusion requirement; encephalopathy;
abnormal LFT’s
Paediatrics
<2/12: swallowed maternal blood (do Apt test to tell fetal from maternal blood, fetal blood stays pink,
maternal goes brown), stress ulcer, AV malformation, haemorrhagic disease of newborn, coagulopathy
2/12-2yr: gastro / oesophagitis / stress ulcer, toxic ingestion / foreign body, Mallory-Weiss tear, AV
malformation
>2yr: gastro / gastritis / PUD, toxic ingestion / FB, Mallory-Weiss tear, AV malformation, varices (due to
biliary atresia, cystic fibrosis, hepatitis, alpha-1 antitrypsin deficiency), haematopbilia
Nasogastric lavage determines site of bleeding and rate