Upper GI bleeds

Symptoms

• The presenting symptom is
  • • Haematemesis in 25%
    • Melaena in 25%
    • Coffee-ground vomiting in 10%
    • Haematochezia in 15%
    • Occult bleeding in 15%
    • Also can present with symptoms of anaemia or of an underlying cancer
    • Can be abdominal pain, syncope, fatigue
• Bleeding can be acute, subacute or chronic. There may be clues in the history.
• Getting symptoms of dyspepsia or reflux is in a way protective – these patients tend to get treatment before deep ulcers develop

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Differential

• Peptic Ulcer Disease (PUD, 38%)
• Varices (8%)
• Gastritis, reflux oesophagitis, duodenitis, haemorrhagic gastropathy or erosions (40%)
• Mallory Weis tear (5%)
• Malignancy (3%)
• Vascular abnormality (2%)
  • • Angiodysplasia / AV malformations
    • Dieulafoy lesion
    • Hereditary haemorrhagic telangiectasia
    • Aortoenteric fistula (if previous aortic aneurysm repair)
    • GAVE (gastric antral vascular ectasia)
• Portal hypertensive gastropathy (4%)
• Other – pseudoxanthoma elasticum, blood dyscrasias, Heyde’s syndrome

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Facts and stats

• Site
  • • Overall, 22% of GI bleeds are lower, 66% upper, the rest undiagnosed
    • In around 20% of patients, apparent upper GI bleed is a lower GI bleed
    • The duodenum is the most common site of bleeding
• Volumes
  • • It only takes 80ml of blood to make melaena, and it takes 14 hours to appear.
    • > 1L upper GI bleed can cause fresh red blood in stool (haematochezia)
    • After an acute bleed, it takes 72 hours for Hb to equilibrate (this is expedited with IV fluid)
• Outcomes
  • • All cause mortality is around 7%, but increases to 25% if the bleed occurs as an inpatient, and up to 40% if it’s a variceal bleed
    • Outcome is most impacted the comorbidity and frailty of the patient, not by the bleed itself
    • 62% of patients are admitted with a GI bleed, however, 38% have the bleed as an inpatient having been admitted for something else
    • Mortality has not improved much over last 50 years (its down a bit) – we’re better at managing but patients older and more comorbid. More patients are anticoagulated today and liver disease is more prevalent
    • Rebleeds are less common today (down to around 10%)
    • Patients often die from aspirations and arrhythmia etc, rather than the bleeding itself

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Acute assessment

• ABCDE assessment
  • • The NEWS score
      • • More sensitive than early Hb drop (which can take an hour).
        • 15 minute observations if actively bleeding
        • Can do lying and standing BP
        • Assess for signs of aspiration and shock
    • Large bore IV access – at least green cannula, white or grey better
    • Bloods: VBG and lab sample – check Hb and lactate
    • Keep patient nil-by-mouth
    • Give bolus 500ml of IV fluid – not enough patients are given crystalloids in audits
    • Consider crossmatching blood / activating major haemorrhage protocol
    • Ensure patient in the right environment – which may be resus
    • Correct calcium and keep patient warm – this will aid clotting
    • If peritonitic – surgical review
    • NG tube not routine – but consider if very high volume bleeding or obstruction
    • Activated charcoal if anticoagulants taken <3 hours before presentation (although there’s a risk of aspiration, so rarely done)
    • Regularly review observations trend
• Ask about
  • • Symptoms and timing
    • Medication use
      • • Anticoagulants (and indication)
        • NSAIDs
          • • Ask specifically about over the counter medications or people don’t mention them
            • The risk of a bleed if taking an NSAID and no PPI is around 1% a year
            • Aspirin might be taken by well people for disease prevention (they should stop – risks outweigh benefits)
        • Bisphosphonates
        • Steroids (and reason) – less relevant
        • Indigestion remedies eg Gaviscon or PPIs
    • ETOH use
    • Liver disease (or risk factors for it), and look for subtle signs of portal hypertension
    • Cancer red flags – weight loss, dysphagia, new reflux
    • Portal vein thrombosis – these patients can have extensive varices, but they don’t have liver disease per say
• Examination
  • • PR exam – essential, look for fresh blood, melaena, can sometimes reveal rectal tumours
    • Signs of chronic liver disease – jaundice, ascites, spider naevi, gynaecomastia, splenomegaly, palmar erythema, bruising, encephalopathy / flap
    • Abdominal exam
    • Consider lying and standing BP if normotensive
• Bloods
  • • Including U&Es, 2x group and save, coagulation including fibrinogen, LFTs, VBG
    • Check for a fall in Hb
    • Platelets might be low in portal hypertension in patients with undiagnosed liver disease
• A note on coffee-ground vomiting
  • • In this scenario, it’s rare to get significant findings on scope
    • Food that has spent a while in the stomach is dark. Often not an upper GI bleed at all
    • Coffee ground vomiting usually indicates stasis – due to obstruction, ileus, gastroparesis, post-op. Could be cancer, sepsis
    • Usually no rush to scope
    • Feel the tummy and low threshold for CT scan.
    • Increased chance of perforation and aspiration when scoping patients with stasis
• If patient unstable after initial fluid resus
  • • Call ITU and endoscopist
    • Do they need to be intubated? Not routine even for large bleeds (risk of pneumonia/aspiration), but consider if
      • • Shock and ongoing haematemesis
        • Severe agitation
        • Low GCS / depressed respiratory status / encephalopathy with airway compromise
    • Determine the likelihood of a variceal bleed – management changes a bit
    • Clarify escalation status
    • Clarify if patient can consent to an OGD and transfusion
    • Consider activating major haemorrhage protocol if haven’t already done so
    • Consider whether the patient needs to be scoped in theatre – and if so, book

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Scoring systems

• The Glasgow-Blatchford Score
  • • Developed in 2000 to predict need for intervention or death
    • Maximum score is 23
    • You need to know
      • • Urea (scores if >6.5)
        • BP (scores if <110)
        • Hb (scores if <130 for men, <120 for women)
        • Heart rate (scores if >100)
        • Symptoms – melaena, syncope
        • Medical history – hepatic disease, HF
    • Only really useful to decide who goes home, not timing of scope
    • If Blatchford 0 or 1:
      • • Very little risk of rebleeding, death within 30 days or hospital intervention
        • Sensitivity 98%, specificity 34%, PPV 96.6%
        • 30 day mortality 0.4%
        • Consider home with outpatient scope
    • There’s an argument that a score of 0 doesn’t need a scope at all. Around 16% of patients score 0.
    • If score > 1, often admit
    • If score > 5, high risk of intervention (and if >6, 50% risk of needing one)
    • Issues
      • • Not validated for inpatient bleeds
        • Not accurate if patient has low Hb chronically and some renal impairment
• ABC score
  • • Age, bloods, comorbidities – predicts 30 day mortality
• Rockall score
  • • Can do pre-scope, but best to do this post scope once diagnosis made
    • Assesses threat to life (but not as good at GBS)

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Medications – to give, withhold, avoid and reverse

• PPI
  • • Most guidance suggests always giving a PPI pre-scope (but some guidelines still advise against it)
    • In a moderate/severe bleed pre-OGD – give 80 mg pantoprazole IV (sometimes followed by infusion 8mg/hour for 72 hrs, but most clinicians don’t bother)
    • No impact on mortality but does downgrade what’s seen at endoscopy and therefore reduces requirement for endoscopic interventions
    • Also reduces length of stay. Might reduce risk of rebleeding (jury out)
    • If giving, it must not delay the scope
• Prokinetic
  • • Give erythromycin 250mg IV at one-hour pre-endoscopy in selected patients if severe/ongoing bleeding (clears blood)
    • Alternative is metoclopramide
• Anticoagulants
  • • Hold (including prophylactic LMWH)
    • Usually discuss with haematology if considering reversal agents. More here
    • Warfarin
      • • If unstable – give low dose vitamin K and PCC (beriplex or Octaplex, FFP if not available) though they do increase risk of VTE
        • Endoscopic outcomes in patients with normal and therapeutic INR are similar (though probably more at risk if INR > 3.5), so don’t worry too much if INR is around 2.5
        • Vitamin K will take 2-4 hours to work
        • Consider the indication for warfarin
    • DOAC
      • • Find out which, and when the last dose was given
        • Consider PCC for severe bleeding
        • Consider reversal agent if life threatening
• Antiplatelets
  • • Ascertain the indication and tailor plan to individual risk
    • Aspirin can often continue (though hold off if still bleeding post scope)
• Tranexamic acid
  • • Usually avoid
    • Only rarely used if big bleed, malignant bleed or iatrogenic bleed (but can be harmful in variceal bleeds, and can be associated with clots)
    • No evidence of benefit
    • May be associated with VTE and seizures
• If cirrhotic, high INR and not anticoagulated – give 10mg IV vitamin K for 3 days
• Consider blood, FFP, cryoprecipitate, platelets – see below
• Consider terlipressin and antibiotics in variceal bleeds – see below

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Targets

• Systolic > 100
  • • Hartman’s is best. Give early
    • Don’t give more than necessary (restrictive fluid resuscitation)
• Hb >70 (>80 if history of Ischaemic Heart Disease)
  • • Only transfuse to these parameters
    • Care not to over-transfuse, especially in variceal bleeds
    • Excessive transfusion is associated with rebleeding and increased mortality. Audits suggest we still overtransfuse often
    • If active bleeding/exsanguination you can transfuse at much higher Hb as this won’t reflect how much blood is lost – if you see blood, replace blood
• Platelets >50
  • • If <50, give 1-2 pools
• Give FFP (12mg/kg) if INR > 1.5 or fibrinogen < 1g/L
  • • If fibrinogen remains <1.5 despite FFP, give cryoprecipitate as well
    • However, be aware that INR does not accurately reflect haemostatic status in chronic liver disease
    • FFP may not correct coagulopathy, and can lead to volume overload / worsening of portal hypertension (European guidelines avoid FFP)
    • Consider checking the TEG (thromboelastogram, may be available in ICU). This recommends whether a patient needs FFP, cryoprecipitate, TXA, platelets or nothing

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 The scope (OGD)

• The timing
  • • Consider appropriateness and urgency of scopes
    • Scopes can be emergent (< 6 hours), urgent (<12 hours), early (<24 hours) or delayed (>24 hours)
    • Ideally all admitted patient should be scoped within 24 hours
    • Only reason to scope bleeding patients urgently is persistent haemodynamic instability
    • Do not use history of anticoagulant use or INR to guide timing
    • Most critical incidents in GI bleeds occur when patients get scoped prior to proper resuscitation
    • Best time is 12-24 hours – this provides time for other medical issues to be managed and is associated with the best outcomes
    • Stabilise patient first – don’t scope too early, but also don’t delay. Scoping too early or too late increases mortality (U shaped curve)
    • Clotting should be corrected first ideally or it limits endoscopic interventions
    • Glasgow Blatchford Score of >6 suggests the need for a more urgent scope. Score > 12 suggests they need ICU (but don’t use the score in isolation to decide)
    • 80% of GI bleeds settle with good conservative management. Rarely a patient remains unstable and is scoped more urgently (sometimes tubed and in theatre).
    • If unstable despite resuscitation – scope within 2 hours. If this occurs overnight it will be in theatre, without the best kit, and with theatre nurses not endoscopy ones, so it’s a last resort.
    • Gastroenterology may come in overnight to scope
      • • Haemodynamically unstable patients with active high-volume bleeds
        • Complete obstruction with a foreign body
        • Variceal bleeds
        • Sigmoid volvulus
        • Rebleeds
• Preparation
  • • Adequate access and monitoring
    • Bloods products available and Hb result up to date
    • Fasted
    • Airway support
    • Prokinetic given
    • Consented
• Endoscopic interventions – use at least two, or three if major bleed
  • • Adrenaline injection – cheap, easy and effective
    • Thermal injection (diathermy)
    • Endoclips are effective
    • APC (argon plasma coagulation) / lasers
    • Haemospray / endoclot (adjunct, buys time, not a long-term fix)
    • Variceal banding (for oesophageal varices)
    • Glue injection (for gastric varices)
    • Haemostatic forceps
    • Traditional endoscopic therapies don’t work for cancer (haemospray useful however)
    • If bleeding continues – over the scope clips, powder. If endoscopy failed, consider IR/surgery
• Afterwards
  • • Check OGD report for pathology, interventions and follow up plan
    • Forrest classification of peptic ulcers
      • • Spurting, oozing, visible vessel, adherent clot, dot, clean base
        • 1A is worst (spurting), 3 is no clot / no vessel
        • A dynamic classification that directs management
        • Forest 2c or 3 – no endoscopic therapy needed
        • Forest 2b – clot removal and treat (usually inject epinephrine – and use enough)
        • Forest 2a – monotherapy +/- dilute epinephrine
        • Forest 1a/b – combination therapy
    • Find out therapy given during scope
      • • And was it successful?
        • Should be two therapies in significant bleeds
        • Often forest 2b ulcers with adherent clot not treated (in around 30%) – they should be
        • Much higher rates of rebleeding if ulcers not treated endoscopically
    • Clarify the plan regarding eating and drinking, PPI, rescope, antithrombotics, h. pylori testing, rebleeds
    • Do Rockall score after OGD
      • • Need to know age, shock, comorbidities, diagnosis, major stigmata of recent haemorrrhage
        • > 7 need HDU monitoring, >8 mortality is > 40%
    • If no site of bleeding identified
      • • Consider capsule endoscopy for small bowel bleeds if stable
        • Consider CT angio if unstable
    • Sometimes best to talk to Interventional Radiology if a rebleed looks possible – especially if unstable at presentation, posterior duodenal wall ulcer, large ulcer >2cm or large visible vessel, or uncertain about effectiveness of endoscopic treatment

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Other interventions

• Sengstaken Blakemore tube
  • • Temporising measure in an intubated patient
    • 80-90% effective
    • They need definitive therapy in the next 24 hours, risk of pressure necrosis
    • Inject water into gastric balloon but never inflate oesophageal balloon.
    • Never apply lots of traction – just tape to patient face
    • Do under endoscopic guidance not blind (inflating balloons in oesophagus or lung can cause serious damage)
• Danis stent
  • • Alternative for oesophageal varices
    • Can be left in for longer than a Sengstaken Blakemore tube, often for 7 days
• TIPSS – more below
• Embolisation via IR
  • • Comparable outcomes to surgery
    • Useful if failed to manage endoscopically
    • Most commonly used in bleeding duodenal ulcers
    • May need to transfer to another hospital
    • High success rates but risk of stomach ischaemia
• Surgery
  • • Last resort. Risk of perforation
    • Can overstitch an ulcer or ligate a feeding vessel. Not used for varices
    • Consider if
      • • Aged <60, continued bleeding requiring > 8 units or 2 rebleeds
        • Aged >60, or those with IHD, and continued bleeding requiring 4 units or 1 rebleed plus further hypovolaemic/fresh haematemesis or Hb drop >3g in 48 hours
• Video capsules which can sense blood – not advised currently

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UGIB if known liver disease or varices

• If it’s a liver patient, it’s a variceal bleed until proven otherwise (60% of all known cirrhotics have varices, and 2/3 of those with varices will bleed at some stage)
• Look for subtle signs of portal hypertension – thrombocytopenia, elevated MCV, low albumin, splenomegaly
• Mortality higher (15-40%)
• There are non-cirrhotic causes of varices, but these patients are much lower risk
• Location can be a clue to aetiology. Varices more often oesophageal in cirrhosis. In pancreatitis or portal vein thrombosis they tend to be gastric
• Do ECG – terlipressin can cause coronary artery vasoconstriction and is contraindicated if coronary artery disease
• Management tips
  • • Manage in resus or HDU until scope
    • Make sure airway secure – often need intubation. Consider intubation if agitated, active haematemesis, encephalopathic
    • Crossmatch 2-4 units of blood. Transfuse if exsanguinating or Hb <70. Target Hb 70-90. Over-transfusing makes outcomes worse
    • Correct coagulopathy
    • Order OGD but still resuscitate first as with any bleed (always scope within 12 hours)
    • Give Terlipressin – or discuss with hepatology first
      • • Dose is 2mg IV early, pre-OGD and then 1-2mg QDS afterwards and often for 5 days (or perhaps stop much earlier, following haemostasis)
        • Contraindications: untreated IHD – in which case consider Octreotide 50mcg IV in 5ml saline instead, followed by infusion (but this doesn’t work particularly well)
        • Caution in peripheral vascular disease, hyponatraemia, arrhythmias, uncontrolled hypertension
        • Can cause ischaemic gut (stop if abdominal pain) or MI
        • Can be very effective
    • Give co-amoxiclav 2g IV (ciprofloxacin if penicillin allergic) early and continue for 3 days post bleeding (some advocate stopping following haemostasis). Good evidence that it reduces mortality
    • PPI not required unless ulcer (might increase risk of SBP)
    • Anticipate widespread hepatic decompensation afterwards
• Interventions
  • • Banding is better than sclerotherapy and has fewer complications
    • You can glue gastric varices (which are more difficult to diagnose and treat). Small risk of emboli and strokes.
    • Risk of injecting varices – glue embolization, ulceration, bleeding
• If bleeding not controlled
  • • Consider rescue TIPSS
      • • Catheter from jugular vein to hepatic vein, connection made to hepatic portal vein
        • Increases risk of encephalopathy and can precipitate heart failure
        • Check cardiac function and grade of encephalopathy first (any encephalopathy is a contraindication)
        • Used in very high risk patients or when endoscopic therapy fails
        • May be underused
    • Consider a bridge
      • • Balloon tamponade with Sengstaken Blakemore tube in intubated patients
        • Danis Stent
• Once bleeding controlled – risk stratify based on Childs Pugh and endoscopic findings
  • • Low risk – banding and drugs
    • High risk – pre-emptive TIPSS as soon as possible
    • Very high risk – banding and drugs
• Risk of rebleeding at 12 months is 60% without additional therapy
  • • Start betablockers and uptitrate (propranolol 40mg – 80mg BD, aim heart rate < 60)
    • May need further banding in a varices eradication programme

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After scoped upper GI bleeds (but during the same admission)

• Diet and fluids
  • • Usually start clear fluids 1-hour post OGD and no bleeding, light diet after 6 hours. Aim to feed everyone < 24 hours post scope, especially if confident in endoscopic haemostasis
    • Reduces length of stay. Doesn’t change rebleed rate or mortality
    • If difficult bleed or high risk of rebleed, often keep NBM for a bit longer initially
• Aspirin and DAPT (dual antiplatelets)
  • • Withhold aspirin if for primary prophylaxis
    • Continue aspirin for secondary prevention as discontinuation is associated with 3-fold increase risk of CV or cerebrovascular events, often in first 7-10 days. But check with endoscopist/cardiology
      • • If aspirin for secondary prophylaxis and low risk endoscopic findings (flat pigmented spot, clean based ulcer ie Forrest 3) – often continue along with other antiplatelets
        • If secondary prophylaxis and high-risk endoscopic findings (active bleeding, visible ulcer, adherent clot), continue/restart aspirin, consider 2^nd look endoscopy, restart 2^nd antiplatelet agent within 5 days but check with cardiology
        • If recent stent, generally start low dose aspirin immediately with PPI if rebleeding risk is low
    • Aspirin doubles risk of rebleeding but significantly reduces mortality (as many patients die of other problems, not bleeds)
    • Drug eluting stents need to be on DAPT for 1 year and bare metal stents for 1 month
    • Stopping DAPT gives a 40% risk of an acute ischaemic event
    • Sometimes stop clopidogrel for 5 days if severe bleed, but always discuss with cardiology
• Restart anticoagulation (unless variceal bleed) after discussion with specialist
  • • Warfarin often started 7 days later, but check OGD report
    • Note that DOACs have a quick onset compared to warfarin
    • Consider checking CHADSVASC and HASBLED to help guide decisions
    • Might discuss with haematology
• PPI
  • • Do not give for variceal bleeds
    • All other patients with active bleeding on OGD should have a PPI (high dose, oral or IV equally effective)
    • Best option is probably twice daily PPI omeprazole (40mg BD) for 5 days, then OD for 4 -6 weeks
    • Previously pantoprazole infusions were advised if a major ulcer – 80mg stat then 8mg/hr for 72 hours, but not any evidence this is better
    • Reduces risk of rebleeding but does not affect mortality
• LMWH
  • • Can start prophylactic LMWH 24 hours after OGD if no bleeding, or > 48 hours if high risk of rebleed
• Iron – start after bleed treated. Oral or IV (latter better if rapid nortmalisation needed)

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Rebleeds

• Mortality is 4 x higher
• First discuss with gastro / endoscopy
• Then might discuss with Interventional Radiology (IR) for embolization – especially if endoscopist doesn’t feel any further intervention would be of benefit
• Consider CT angio if non-variceal (85% sensitive, 92% specific). Usually part of the IR protocol.
• If variceal – Sengstaken tube first and then consider TIPSS
• If non-variceal – consider rescope, IR or rarely surgery
• If oesophageal bleed – focus on scope. No role for IR/surgery
• If stomach bleed – surgery an option but IR comes with risks, not ideal
• If duodenal bleed – interventions by IR can be very effective

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Follow up after discharge

• H Pylori eradication
  • • Only after scope and if told to (usually if CLO test positive)
    • Sometimes given empirically (eg for duodenal ulcer) rather than testing for it (in the heat of battle, testing might be forgotten, or impacted by prior PPI)
    • Regime is 7 days of twice daily PPI + amoxicillin + clarithromycin/metronidazole
    • If penicillin allergic – PPI + clarithromycin + metronidazole.
    • Continue PPI for 8 weeks
    • Can do urease breath test at 6-8 weeks to confirm H Pylori eradication (off PPI for 2 weeks).
    • Usually need to a breath test later if H pylori negative during endoscopy (as CLO test low sensitivity in acute bleed)
• Rescoping
  • • Gastric ulcers will need repeat OGD at 6-8 weeks to exclude malignancy/confirm healing. 2% are malignant.
    • Most duodenal ulcers don’t need rescopes
• If no cause of an ulcer is found – long term PPI
• Follow up for variceal bleeds
  • • Consider betablocker eg carvedilol (reduces risk of rebleed by 40%) once patient stable
    • Consider rebanding varices every 2-4 weeks until gone
    • 3 yearly surveillance scopes
    • Consider referral for liver transplant (without, mortality is 25% at 1 year)
    • No PPI required

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Notes on rare causes

• GAVE (Gastric Antral Vascular Ectasia, or ‘Watermelon Stomach)
  • • Dilated mucosal capillaries in the antrum arranged in longitudinal stripes
    • Often associated with cirrhosis or systemic sclerosis
• Heyde’s syndrome
  • • Gastrointestinal bleeding from angiodysplasia in the presence of aortic stenosis
    • It is caused by cleavage of Von Willebrand factor (vWF) due to high shear stress forces from aortic valvular stenosis. This results in Von Willebrand disease type IIA (acquired)
• Dieulafoy’s Lesion
  • • A large submucosal artery that erodes through the gastric mucosa (often at the lesser curvature) without a primary ulcer. Can cause a sudden, massive haemorrhage
• Hepatic Arterioportal Fistula, or Aortoenteric Fistula
• Hemosuccus Pancreaticus
  • • Bleeding into the pancreatic duct, usually secondary to chronic pancreatitis, a pancreatic pseudocyst, or a splenic artery pseudoaneurysm
• Gastric Amyloidosis
• Gastrointestinal Stromal Tumors (GISTs), metastases and rare neoplasms
• Infections