Background Information
Definition
Upper vs lower GI bleed is an anatomical definition:
- Upper GI bleed: bleeding that originates from a source proximal to the ligament of Treitz (duodenal-jejunal ligament)
- Lower GI bleed: source distal to the ligament of Treitz
Aetiology
Upper and lower GI bleeding causes (adults mainly): [Ref1][Ref2][Ref3]
| Upper GI bleeding | Lower GI bleeding | |
|---|---|---|
| Important causes |
|
|
| Rarer causes |
|
|
| Shared causes |
|
|
Be aware of some causes that may mimic GI bleeding: [Ref]
- Iron supplements cause stools to appear like melena
- Certain food (e.g. beet root) causes stool to turn red
Some paediatric-specific causes of GI bleeding:
| Necrotising enterocolitis | In premature neonates
|
| Meckel’s diverticulum | In <2 y/o
|
| Intussusception | In 6-18 m/o
|
| Inflammatory bowel disease (ulcerative colitis > Crohn’s disease) | In adolescents |
Clinical Features
Presentation of upper vs lower GI bleeding: [Ref1][Ref2]
| Upper GI bleeding | Lower GI bleeding |
|---|---|
Common presentation:
Rarely, severe upper GI bleeding can cause haematochezia |
Presents as haematochezia (passage of fresh blood per rectum)
|
Non-specific features of bleeding:
- Tachycardia
- Orthostatic hypotension
- Pre-syncope
Assessment
Risk Assessment
BSG recommends using the Oakland score, key components:
- Age and sex
- Heart rate and systolic BP
- Haemoglobin
- Any previous lower GI bleeding?
- Findings on digital rectal examination?
Do not mix up the scoring systems for GI bleeds:
- Upper GI bleed: Glasgow-Blatchford score (pre-endoscopy) and Rockall score (post-endoscopy)
- Lower GI bleed: Oakland score
Work-Up
A standard work-up for acute GI bleed would include:
- CBC, U&E, LFT
- Coagulation tests – PT/INR, APTT
- Blood type and crossmatch
Main non-specific biochemical findings in GI bleed:
- ↓ Haemoglobin (but may be normal initially in acute bleeding)
- Acute bleeding gives a normocytic normochromic anaemia
- Chronic bleeding gives a microcytic hypochromic anaemia (iron deficiency)
- ↑ Urea with normal creatinine
- Mechanism (“protein meal”): digested blood → ↑ protein absorption → ↑ hepatic urea production → disproportionate rise in urea
- This classic pattern is only seen in upper GI bleeding, as blood is usually NOT digested in lower GI bleeding (so there is no increased protein absorption)
Management
If self-terminating bleed (Oakland score ≤8), with no other indications for admission → discharge for urgent outpatient investigation
Initial Management
A-E approach:
- Gain IV access and start IV fluid resuscitation
- Transfuse and reverse anticoagulation accordingly (see below)
Transfusion Thresholds
Various transfusion thresholds:
| Component | Cut-off |
|---|---|
| Whole blood | Haemoglobin <70 g/L |
| Platelet | Platelet count <50 x 109 /L + actively bleeding |
| Fresh frozen plasma | PTProthrombin time (or INR) or APTTActivated partial thromboplastin time >1.5x normal |
| Cryoprecipitate | Fibrinogen level <1.5 g/L despite fresh frozen plasma |
| Recombinant factor VIIa | Only considered if all other methods have failed |
Anticoagulation Reversal
| Anticoagulant | Reversal agent |
|---|---|
| Heparin | Protamine sulfate (fully effective for UFHUnfractionated heparin, but only partial reversal for LMWHLow molecular weight heparin) |
| Warfarin | Prothrombin complex concentrate PCC (preferred to FFP) is the most vital reversal agent as it allows for rapid correction of vitamin-K dependent clotting factors. Vitamin K has a delayed onset of action and is not effective for immediate hemostasis in acute bleeding. However, it should be administered intravenously as an adjunct to sustain reversal and allow endogenous synthesis of clotting factors. (only consider fresh frozen plasma as 2nd line) + IV vitamin K |
| Dabigatran | Idarucizumab |
| Apixaban and rivaroxaban | Andexanet alfa |
There is no reversal agent for edoxaban (which is also a DOAC).
There are no reversal agents for antiplatelets (e.g. aspirin, clopidogrel). If patients take antiplatelet → withhold them.
Definitive Management
After initial resuscitation:
- Haemodynamically unstable → CT angiography
- If bleeding source identified → catheter angiography + embolisation
- If no bleeding source can be identified → consider upper endoscopy to exclude upper GI bleeding
- Stable → colonoscopy (diagnostic and therapeutic)
Last resort: emergency laparotomy