1. Gastrointestinal Haemorrhage
Peter Llewellin May 2008
Revised 2017

2. GI bleeding Common presentation to the ED.
Typically male, elderly, patient.
Often stable presentation, but occasionally life threatening bleeds occur.
Upper GI bleeds commoner (100 per 100,000)
Lower GI less common (20 per 100,000)
Mortality related to increased age, co-morbidity, repeated episodes and haemodynamic instability

3. Upper GI Haemorrhage
Defined as bleeding originating above ligament of Trietz
Peptic ulcer bleeding responsible 44% (cf 60% 1983)
Erosive gastritis/oesophagitis ~ %
Mallory Weiss ~ 5-15%
Angiodysplasia (ectasia/AVM) ~ 5-10%
Variceal bleeding ~ 5-10%
Unknown 10-15%

4. Upper GI Haemorrhage -Assessment
ABC – particularly circulation
History – Haematemesis; melaena; haematochezia;
`coffee-ground’ vomit (?)
Abdominal pain; syncope/pre-syncope; angina; confusion, lethargy
Background history – Hepatic disease; Alcohol; PUD; Aortic surgery; NSAID’s; Anti- coagulants;
Examination – CVS; Abdominal (stigmata liver disease + PR exam)

5. Risk stratification Variceal vs. Non-variceal cause of bleed?
25% mortality vs 3-14%
Glasgow-Blatchford score ideal for ED
Identifies low risk cohort potentially suitable for outpatient assessment
Score of 0-1 ; low likelihood of requiring intervention – potential for discharge and outpatient follow up
Modified GB score performs as well (removes ‘other markers’ scores)
Score >6 highly likely (50%) of requiring invasive intervention

6. Management in the ED. Non-variceal UGI Haemorrhage
ABCs
Airway issue uncommon; consider intubation if altered LoC and/or massive bleeding
Circulation – Multiple IV access for significant bleeding, 1 x dedicated volume resuscitation line
Early move to blood products if significant bleeding
If stable, transfusion ONLY if Hb <70-80g/L (<90 if IHD)

7. Management in the ED: Non-variceal UGI Haemorrhage
Adjunctive therapies - Proton-pump inhibitor Evidence for 80mg omeprazole stat, then 8mg/hr for 72hrs in high risk ulcer bleeding only  demonstrated effective in reducing rate of rebleeding and surgery; no effect on mortality Less acute presentations may be suitably managed on 40mg IV bd

8. Management in the ED: Non-variceal UGI Haemorrhage
Definitive therapy of UGI Haemorrhage is early endoscopy
(early defined as 2-24 hrs from presentation).
Preferred to stabilise vital sign parameters prior to endoscopy if possible.
Modern endoscopic treatment for ulcer bleeding is ‘combination therapy’ -> injection with adrenaline followed by thermal therapy
Success rate ~ 95% for ulcer bleeding, nearly 100% for Mallory Weiss/Gastritis bleeding
Surgery rarely required

9. Management in the ED: Variceal UGI Haemorrhage
Variceal bleeding uncommon cause of UGIH, but has dramatically worse prognosis
(25% mortality cf 3-10% all other UGIH).
Likely to be persistent,(only 30% spontaneous cessation) and to re-bleed even if spontaneously ceases (40% at five days).
Mortality more likely due to subsequent liver failure, infection and hepato-renal syndrome (60%) than to bleeding itself. (40% - 4-8%risk of immediate mortality)

10. Management in the ED: Variceal UGI Haemorrhage
Follows the same general principles as for non-variceal haemorrhage, however –
Airway – intubation should be seriously considered early, to prevent aspiration of profuse bleeding and gastric contents  aspiration pneumonia
Circulation – Cautious volume replacement, with early use of blood and coagulation factors aiming systolic 100mmHg.
Avoidance of prolonged hypotension paramount, to prevent subsequent renal/hepatic failure (Beware the patient on propranolol)

11. Management in the ED : Variceal UGI Haemorrhage
Vasoactive medications –act to reduce variceal blood flow therefore improving haemostasis
Terlipressin – long acting derivative of vasopressin.
Administered IV 2mg q4hrly for 48 hrs, then 1mg q4hr.
Has been studied vs. placebo, and shown to have mortality benefit, and reduced blood transfusion requirements. Benefit still present when combined with endoscopy.
Suggestion that terlipressin as effective as banding, but no large trial performed.
Also useful in treatment of hepatorenal syndrome. Success rate at 48hrs 75-80%
Octreotide –.
Octreotide useful when combined with sclerotherapy to reduce bleeding. As monotherapy, benefit doubtful.
Octreotide administered as 50mcg bolus then 50mcg/hr infusion

12. Management in the ED : Variceal UGI Haemorrhage
Antibiotics –
Major cause of mortality in hepatic failure patients is infection rate (35-66% in first 14 days)– therefore prophylactic antibiotics indicated.
Significant absolute reductions (20-30%) in rates of infection noted with these regimes –most commonly studied drugs quinolones (nor-, cipro- floxacin) and ceftriaxone.
Nil difference in oral/IV administration
Easiest to give ceftriaxone 1g IV during initial resuscitation

13. Management in the ED – Variceal UGI Haemorrhage
Definitive therapy 
Endoscopy –Variceal Band Ligation typically used with success in controlling haemorrhage; improved in combination with octreotide infusion.
Balloon tamponade – useful only in non-endoscopy settings.
Nil mortality benefit, but effective at arresting bleeding. However, 50% re-bleed rate on balloon removal, and has significant complication rate.
Useful in non-endoscopy hospitals as ‘bridging’ treatment. Requires operator experience in placement

14. Lower Gastro-intestinal haemorrhage
Less common than UGI haemorrhage, and as general rule, less severe course (mortality 2-4%)
Presents with haematochezia/malaena
10-15% severe haematochezia may come from UGI sources
Main Causes-
Diverticular (20-48%)
Angiodysplasia (10-40%)
Cancer/Polyp (6-20%)
Colitis(inflammatory,infective,ischaemic) (6-20%)
Anorectal (haemorrhoid,fissure,ulcer) (5-14%)

15. Lower Gastrointestinal Haemorrhage
Assessment in the ED follows similar lines as UGIH
Specific features – history of abdominal pain, weight loss, altered bowel habit, previous bleeds, and prior radiotherapy to pelvis.
Examination –focussing upon signs of shock, and localising source of bleeding.
PR in lower GI bleeding ; 40% Rectal Ca. palpable to exam.

16. Management in the ED: Lower GI Haemorrhage
Immediate management in ED
ABC’s
Airway unlikely to be compromised unless exsanguinating bleed with diminished conscious level.
Circulation –resuscitation via two large bore cannulae ml/kg crystalloid as first line with transfusion as required (Hb targets as per UGIH)
Reversal of anticoagulation should be attended
Also – monitor ECG and cardiac performance in this more elderly cohort.

17. Management in the ED: Lower GI Haemorrhage
Most LGI bleeding likely to cease spontaneously (~85%), thus a conservative approach and semi-elective investigation as inpatient is appropriate.
A small number will continue to bleed and progress to haemodynamic instability – this group require emergent investigation whilst resuscitation continues.

18. Management in the ED: Lower GI haemorrhage
Imaging options –in general, these are institute dependent, with no firm international guidelines
Colonoscopy –
Often considered impractical in heavy LGI haemorrhage; however, reported in literature to be 72-86% sensitive in detecting source of bleeding in severe haematochezia.
Can be combined with injection, sclerotherapy or thermal probe techniques to arrest bleeding in virtually all causes of bleeding.
Requires operator technical experience, well resuscitated patient capable of undergoing sedation/anaesthesia, and a “rapid cleansing” of bowel.
’Early’ colonoscopy considered to be within 1st 12 hrs

19. Management in the ED: Lower GI haemorrhage
Radionuclide Imaging – Useful in patients with severe bleeding where a surgical or interventional `target’ is being contemplated. Uses either pertechnetate labelled red cells, or technetium sulphur colloid. Pertechnetate has persistent activity in circulation, allowing repeated images to be taken if required, but needs higher bleeding rate for detection. Technetium sulphur colloid is short lived in circulation(thus necessitating active bleeding), but able to detect bleeding as low as 0.1ml/min.

20. Management in the ED: Lower GI Haemorrhage
CT angiography
Readily available – requires bleeding rate ml/min to identify on scan
Minimally invasive
Quoted sensitivity ~85 % to identify bleeding points
Nil therapeutic option
Interventional angiography
Requires bleeding rates in region mL/Min in order to identify bleeding points, thus sensitivity around 40-70%
Advantages include nil preparation required, and possibility of selective embolisation to control bleeding
(recent series reported 96% success rates, with mesenteric ischaemia rates 16%, mortality 7.4%)

21. Management in the ED: Lower GI Haemorrhage
Surgical intervention – Considered when bleeding causing refractory shock/hypotension AND Not amenable by colonoscopy/angiographic intervention AND Patient is emergency surgical candidate without significant co-morbidities and reasonable quality of life Literature suggests this when transfusion > 6U packed cells. Likelihood of surgery 18-25% if transfusion required for bleeding.

22. Management in the ED: Lower GI Haemorrhage
Ideal if surgeons able to localise the site by pre-operative imaging
`targeted’ segmental colectomy vs. `blind’ subtotal colectomy; mortality rates 8.6% vs %
Re-bleeds more likely in blind surgery up to 33%
Hence, not commonly undertaken

23. Questions?

24. Summary
Risk stratify the upper GI bleeder – do they need inpatient treatment? (Glasgow-Blatchford score)
Decide early on likelihood of variceal vs non-variceal bleeding
Non-variceal – resuscitate, PPI infusion and endoscopy
Variceal – resuscitate, PPI, terlipressin, ceftriaxone and urgent endoscopy
Lower GI – often relatively benign source, and may settle spontaneously.
Early CT angiography and referral for IR if ongoing need for transfusion