Definitions in upper gastrointestinal (UGI) haemorrhage
UGI haemorrhage: bleeding that arises proximal to the ligament of Treitz i.e. from the oesophagus, stomach or duodenum
Haematemesis: vomiting of blood from the UGI tract
Coffee-ground vomit: vomiting of dark brown granular matter presumed to be digested blood
Melaena: passage of black, tarry stools presumed to be digested blood from the UGI tract
Haematochezia: passage of blood per rectum usually due to a LGI haemorrhage but occasionally due to an UGI haemorrhage with rapid transit time
Aetiology of UGI haemorrhage
Oesophagus
Oesophageal varices
Oesophagitis
Oesophageal carcinoma
Mallory-Weiss tear
Stomach
Gastric ulcer
Gastritis
Gastric carcinoma
Duodenum
Duodenal ulcer
Duodenitis
Other
Thrombocytopenia
Coagulopathy
Aorto-enteric fistula
Pathophysiology of UGI haemorrhage
The commonest cause of UGI haemorrhage is peptic ulcer disease, which may occur in the stomach (gastric ulcer) or duodenum (duodenal ulcer)
Peptic ulcer disease is commonly due to infection with Helicobacter pylori and/or non-steroidal anti-inflammatory drug (NSAID) use
Helicobacter pylori directly disrupts the mucosal barrier and causes inflammation of the gastric and duodenal mucosa
NSAIDs inhibit the enzyme cyclo-oxygenase, reducing the synthesis of prostaglandins which are responsible for stimulating alkaline mucus secretion, thereby exposing the UGI mucosa to damage from gastric acid
Oesophageal varices are dilated porto-systemic anastomotic veins that occur due to portal hypertension secondary to chronic liver disease
History in UGI haemorrhage
Haematemesis
If so what volume? Enough to fill a cup? A bowl? A saucepan?
Coffee-ground vomiting (volume?)
Melaena (volume?)
Haematochezia (volume?)
Abdominal pain
Malignancy red flags
Cachexia
Anorexia
Night sweats
Dysphagia
Dyspnoea
Severity assessment
Light-headedness
Loss of consciousness
Causes assessment
Chronic liver disease
Alcohol misuse
NSAIDs or steroids
Warfarin
Past medical history
Previous GI bleed
Known PUD/varices
Malignancy
Liver disease
Known cardiovascular/respiratory disease (fitness to undergo sedation and/or intubation for endoscopy)
Examination in UGI haemorrhage
Airway
May be compromised by reduced conscious level
Breathing
Kussmaul’s breathing: hyperventilation to compensate for metabolic acidosis manifesting as ‘air hunger’
Circulation
Cold, pale peripheries
Prolonged capillary refill times (CRT >2 s)
Decreased skin turgor
Reduced jugular venous pressure (JVP)
Sunken eyes
Dry lips, mouth and tongue
Tachycardia
Postural hypotension
Absolute hypotension
Disability
Confusion
Reduced conscious level
Exposure
Abdominal examination
Guarding/rigidity
Masses
Per rectum (PR) examination to look for melaena or haematochezia
A score of zero is associated with a predicted mortality of 0.2%
A score of seven is associated with a predicted mortality of 50%
Only patients with a Rockall score of zero can be safely managed as an outpatient; consider for discharge and outpatient follow-up if:
Age <60 years and
No evidence of haemodynamic instability and
No significant co-morbidity and
No witnessed haematemesis or haematochezia
Rockall score ≥1 should not be discharged; consider for admission and early UGI endoscopy if:
Age >60 years or
Haemodynamic instability or
Known chronic liver disease or
Witnessed haematemesis or haematochezia
Initial investigation of UGI haemorrhage
Venous blood gas (VBG) looking for a lactic acidosis indicative of shock
Full blood count (FBC): anaemia may not be apparent initially after acute haemorrhage
Urea & electrolytes (U&Es): deamination of amino acids from digestion of blood proteins may lead to disproportionately elevated urea
Liver function tests (LFTs)
Coagulation
Cross-match
Erect chest radiograph (CXR) looking for pneumoperitoneum indicative of bowel perforation
Further investigation of UGI haemorrhage
UGI endoscopy is the definitive investigation and management
Helicobacter pylori testing for those with peptic ulcer disease
Initial management of UGI haemorrhage
Assess the patient from an ABCDE perspective
Maintain a patent airway: use manoeuvres, adjuncts, supraglottic or definitive airways as indicated and suction any sputum or secretions
Deliver high flow oxygen 15L/min via reservoir mask and titrate to achieve oxygen saturations (SpO2) 94-98% or 88-92% if known to have COPD
Attach monitoring
Pulse oximetry
Non-invasive blood pressure
Three-lead cardiac monitoring
Request 12 lead ECG and portable CXR
Obtain intravenous (IV) access and take bloods and VBG
Fluid resuscitation
Guided by clinical context
Treat shock aggressively
Give boluses of crystalloid 250-500 ml IV and re-assess after each
Aim for permissive hypotension so as not to disrupt any clots that have formed or are in the process of forming
Shock refractory to fluid resuscitation should be considered for referral to critical care for insertion of arterial and central lines and vasoactive drug therapy (vasopressors and/or inotropes)
Transfusion
Be aware that anaemia from haemorrhage will not be apparent initially and will be exacerbated by crystalloid fluid resuscitation
Once ≥30% of circulating volume is lost, red transfusion should be initiated, ideally with fully cross-match blood, or with type specific or even group O rhesus negative (O negative) in an emergency. A trigger of Hb<8 if often used
In variceal bleeding, a transfusion trigger of 7 is reasonable
Transfusion with additional products such as platelets, fresh frozen plasma, cryoprecipitate may be necessary
Activate the major haemorrhage protocol if necessary
Give PCC to anyone actively bleeding on warfarin
Catheter to monitor fluid balance
Antibiotics
Give broad spectrum antibiotics e.g. co-amoxiclav 1.2g TDS iv or tazocin 4.5g iv TDS to all patients with UGI haemorrhage and chronic liver disease. This has been shown to have a significant reduction on mortality
Terlipressin
Give terlipressin 2g iv to all patients with suspected variceal haemorrhage prior to UGI endoscopy
It acts as a splanchnic vasoconstrictor, reducing portal hypertension and the degree of variceal haemorrhage
Contraindicated in patients with cardiovascular disease due to the risk of ischaemia: must have non-ishaemic ECG and be intravascularly replete prior to giving
Prokinetic
Metoclopramide 10mg IV can be given to empty the stomach contents to allow better views at endoscopy
UGI endoscopy
UGI endoscopy is the definitive investigation and management
Techniques include band ligation, clipping, injections of sclerosants and thermal coagulation
Timing depends on pre-endoscopy Rockall score and clinical context; if the patient is unstable and/or has active bleeding then UGI endoscopy should be performed once resuscitation has taken place
If immediate UGI endoscopy is unnecessary, it should be performed within 24 hours
If UGI endoscopy fails to control haemorrhage, arterial embolisation or surgery may be required; the treatment of choice for uncontrolled variceal haemorrhage is transjugular intrahepatic portosystemic shunting (TIPS)
Proton pump inhibitors (PPIs)
Current NICE guidance is NOT to give acid-suppression (PPIs, H2-RA) to patients with suspected non-variceal bleeds prior to endoscopy).
IV PPIs eg omeprazole 40 mg IV should be given following UGI endoscopy in patients found to have peptic ulcer disease
In practice however, this is still commonly given prior to endoscopy
Further management of UGI haemorrhage
Sengstaken-Blakemore tube
In torrential UGI haemorrhage secondary to oesophageal varices consider balloon tamponade via insertion of a Sengstaken-Blakemore tube
The tube is inserted down the oesophagus, the gastric balloon inflated, then pulled back to occlude the gastro-oesophageal junction
The oesophageal balloon is then inflated to tamponade oesophageal varices
Stop aspirin, NSAIDs and anticoagulants
Warfarin may need urgent reversal depending on the international normalised ration (INR)
Eradication therapy for those who test positive for Helicobacter pylori
