Upper GI Bleed Flashcards
What is the aetiology of upper GI bleeding? (UGIB)
Peptic ulceration
- Most common cause
- Possibly from erosion into the gastroduodenal artery that runs close to the posterior wall of the 1st part of the duodenum
- SEE SPECIFIC DECKS FOR ULCERATION
Gastro-oesophageal varices
- Second most common/clinically important cause
Other causes:
- Oesophagitis, gastritis/erosions
- Mallory-Weiss tear
- Malignancy
- Vascular malformation, bleeding diathesis etc.
How do you clinically assess UGIB?
(ABCDE in acute)
Bleeding:
- Haematemesis = bright red blood, implies active bleed
- Coffee-ground vomit = black material assumed to be clotted blood, implies bleeding has ceased/has been modest
- Melaena = black tarry stools, usually due to UGIB, sometimes from ascending colon; DONT FORGET TO DO A PR
- Signs of shock = poor prognosis
Look for signs of cause:
- Dyspepsia, weight loss, jaundice etc
- Alcohol and drug Hx
- Hx retching
How do you investigate UGIB?
Bloods:
- FBC - every 4-6hrs on 1st day to assess trend and need for transfusion; MCV
- Xmatch - 2-6units
- Clotting - to assess need for FFP/Plts; assess for liver disease
- LFTs
- U+E
Immediate endoscopy post stabilisation/resuscitation for unstable bleeds and within 24hrs for all other bleeds
- c.20% will not have an identifiable cause here
Imaging:
- CXR -?aspiration pneumonia, perforated oesophagus
- CT +/- angiography - to look for other pathologies or identify bleeding site if not found on endoscopy
What is the Rockall score?
A score used to predict risk of death or re-bleeding following UGIB
- <2 is low risk, excellent prognosis
- > 8 = high mortality
Age:
- <60yrs = 0
- 60-79yrs = 1
- > 80yrs = 2
Shock: SBP +HR
- > 100mmHg + <100bpm = 0
- > 100bpm = 1
- <100mmHg = 2
Comorbidity:
- Nil major = 0
- Heart failure, IHD = 1
- Renal/liver failure = 2
- Metastatic disease = 3
Diagnosis:
- Mallory-Weiss tear/none = 0
- All other = 1
- UGI malignancy = 2
Bleeding on OGD:
- Nil recent = 0
- Recent = 2
Scores >3 need discussion with endoscopist, on call surg +/- interventional radiology
What basic care is needed for managing all UGIBs?
ABCDE approach
Full monitoring of obs
2x wide bore cannulae
Fluids
- Large volumes of crystalloid and colloid may be needed
- May include blood depending on extent of bleed
Oxygen:
- Sats depending
IV Vit K +/- FFP +/- Plts:
- If INR prolonged
Vasoactive drugs
- If required
HDU/ICU admission
- For massive haemorrhage
What are oesophageal varices and what causes them?
Veins that make up the junction between the portal and systemic venous system
- Tend to be found in the distal oesophagus +/- proximal stomach (isolated ones also possible in distal stomach and intestines)
Majority of patients have chronic liver disease
They are prone to bleeding and make up 5-10% of all UGIBs
- Size of varices and tendency to bleed related to portal pressure, which in turn is related to the severity of the liver disease
- Other factors affecting coagulation also evidently affect bleeding i.e. malnourishment, alcohol intake, NSAIDs etc
Other causes:
- Portal vein thrombosis or obstruction
- Acute hepatitis
- Schistosomiasis
- Compression i.e. from tumour
- Budd-Chiari syndrome
- Constrictive pericarditis
How do bleeding varices present?
Haematemesis
Melaena
Abdo pain
Features of liver disease including confusion secondary to encephalopathy
Hypotension, tachycardia, low urine output, pallor, low GCS - in severe bleeds
How do you manage bleeding varices specifically?
Terlipressin
- Should be offered to all with suspected variceal bleeds
- Is an analogue of vasopressin and thus is a vasoactive agent
Prophylactic Abx
- e.g. ciprofloxacin
- Offered to all at presentation
- Reduces all cause mortality for those presenting with variceal bleed secondary to chronic liver disease
Balloon tube tamponade
- With a Sengstaken-Blakemore tube
- Only as a temporary salvage treatment for uncontrolled haemorrhage
- Inserted into oesophagus and pulled up against the varices to tamponade the bleed
Band ligation:
- Endoscopy and banding for all who are eligible
TIPS:
- If bleed not controlled by ligation
How can you prevent variceal haemorrhage?
Varices with a high risk of bleeding = non-selective betablockers +/- prophylactic banding if large
3yrly endoscopy in those with cirrhosis to screen for problems
Once bleeding has occurred, re-bleeds are common with 1/3 being fatal
What is a Mallory-Weiss tear?
UGIB occurring following prolonged or forceful episode of retching, vomiting, coughing, straining
- <10% of UGIBs
- Can sometimes be a single vomit
- Tears usually in just below the gastro-oesophageal junction on the lesser curvature of the stomach
Often associated with excessive alcohol intake or other conditions that predispose people to vomiting:
- Gastroenteritis
- Hyperemesis gravidarum
- Bulimia
- Renal disease
- Raised ICP
- Biliary disease and hepatitis
- Migraines
- Medications e.g. chemotherapy
- GI obstruction
How do you manage a Mallory-Weiss tear?
In the same way as all UGIBs
- Endoscopic treatment is rarely needed to control ongoing bleeding as tears heal rapidly
Manage underlying cause of vomiting as required
- Antiemetics may be of use
What is the Glasgow-Blatchford score?
Another scoring system for UGIB:
- Does not use subjective variables or require OGD
- Reliant on other blood markers
Urea: (mmol/L)
- 6.5-8 = 2
- 8-10 = 3
- 10-25 = 4
- > 25 = 6
Hb: (g/dL)
- 12-12.9 = 1
- 10-11.9 = 3
- <10 = 6
Systolic BP: (mmHg)
- 100-109 = 1
- 90-99 = 2
- <99 = 3
Other markers:
- Pulse >100 = 1
- Presentation with melaena = 1
- Presentation with syncope = 2
- Hepatic disease = 2
- Cardiac failure = 2
> 6 score = needs intervention
What is Boerhaave’s syndrome?
Refers to oesophageal rupture - needs to be excluded in cases of UGIB
Why is urea raised in UGIB?
As ingested blood is broken down and absorbed in the GIT
The absorbed haemoglobin contains no residues of isoleucine and due to the sequential nature of protein assembly, the relative deficiency in this amino acid blocks conversion of Hb breakdown into proteins (as would be done with other ingested proteins from eating animal meats etc)
Consequently, the built up amino acids have to be converted to urea instead and serum urea rises
Also, hypovolaemia due to blood loss will also aggravate the AKI (hypoperfusion/pre-renal) and impair urea excretion
