There may be differences to the approach in some of the different pathologies. A particular differentiation is variceal vs non-variceal. Specialist gastroenterology input will form an important part of both management advice and specific interventions.
Resuscitation This may be part of the assessment of acutely unwell patients i.e. A to E approach Specific points to consider for massive UGIB include:
I&V may be needed to protect airway when there is associated neurological compromise
Large bore IV access should be obtained
Massive transfusion protocols may need activation
Balloon tamponade may be part of resuscitation in variceal haemorrhage
Transfusion A resuscitative approach to transfusion should be used in massive bleeding i.e. massive transfusion protocols. In other scenarios, a restrictive approach is advised. Thresholds:
Hb - 7 g/DL
Platelets - 50 x 10^9/L
INR - 1.5
Fibrinogen - 1 g/L
Importantly a restrictive Hb target (7) shows better outcomes:
Lower transfusion rates
2008 UK wide audit - rebleeding was more common in patients requiring transfusion. However, this is clearly not relevant for patients with massive upper GI bleed who should be managed using a massive transfusion approach.
FFP is recommended for correction of coagulopathy in bleeding. PCC should be used to correct patients on warfarin who are actively bleeding.
Prokinetic Administration of prokinetics may aid gastric emptying, benefiting endoscopy. One study suggested erythromycin translated into some better outcomes.
Antacid Antacid therapy doesn’t appear to make an outcome difference if given pre-endoscopy. However, there is evidence that it improves visualisation of any bleeding point at endoscopy. Alongside the intuitive sense to treat the underlying problem, many clinicians would commence an antacid if there is going to be any sort of delay to endoscopy. PPI is recommended post endoscopy in patients with PUD - given IV. Those with high risk features at endoscopy benefit from a high dose therapy regime - 80mg bolus with 8mg/hr for 72hr. PPIs appear to be better than H2RBs
Antiplatelets Aspirin for secondary prevention should be continued in patients with upper GI bleeding (assuming control of bleeding has been achieved). The benefits of this continued effect appear to outweigh any increased bleeding risks (there is a threefold increase in cardiovascular events in those whom it is stopped). Patients at high risk of cardiovascular events on other antiplatelet agents (e.g. clopidogrel) should have specialist discussion. Other agents (e.g. NSAIDs) should be stopped.
Immediately in unstable patients with severe UGIB, after resuscitation. Within 24h for other patients admitted with UGIB.
Some risk factors that suggest need for urgent endoscopy:
Major transfusion (>4 units)
As well as identification of the source of bleeding, intervention may be possible via the endoscope: PUD:
Subsequent management is dependent on findings and may involve:
H. Pylori treatment
84-172/100,000 adult/year Upper GIB is about 4 times as common as a lower source. Mortality: Presents with UGIB - 7% Bleeding as IP - 30%
Variceal bleeding is recognised as a specific subset of upper GI bleeding. This arises from varices, high pressure venous vessels that are connected to the portal venous system. The high resistance to blood flow within a cirrhotic liver increases portal venous pressure and leads to venous dilatation. This ongoing resistance to flow can result in the blood flow utilising other means of reaching the systemic circulation, termed portosystemic shunts, a major route being those found in the oesophagus. These dilate as there is an increase in blood flow and pressure beyond what these vessels are able to cope with. Subsequent bleeds can therefore occur under not insignificant pressure (because of the portal hypertension) and blood loss can be rapid.
It is important to note that variceal bleeding can be a precipitant for other cirrhosis complications e.g. encephalopathy.
The general principles will be much the same as those described above. High consideration to management of coagulation must be an especially important feature of the resuscitation of these patients given the common association with the underlying disease. Key specific features include:
Terlipressin Terlipressin is a splanchnic vasoconstrictor that reduces portal blood flow and thus can improve variceal bleeding. It should be started in patients with suspected variceal GI bleeding. The dose is 2mg IV 4 times a day for up to 5 days or until haemostasis is achieved. Octreotide (a long acting somatostatin analogue) is an alternative here. The BSG guidance makes a strong recommendation for this noting a relative risk reduction in all cause mortality of 34%.
Antibiotics IV antibiotics are also recommended to be given routinely in suspected variceal bleeding as prophylaxis. These patients have a high risk of concomitant bacterial infection and standardised antibiotic administration reduces mortality, length of stay and rebleeding rates. The evidence favours IV over the oral route here. The choice of antibiotic will usually be led by local policy e.g. ceftriaxone.
Endoscopy This will often be the diagnostic component as well as the major therapeutic option. Endoscopy will usually reveal the characteristic tortuous vessels, although intense bleeding can make it challenging. Band treatment (ligation) suggests better outcomes compared to sclerotherapy.
Balloon Tamponade This is a last resort when unable to control bleeding through other means. A specially designed tube (Sengstaken-Blakemore) is inserted into the oesophagus and into the stomach. With inflation the pressure effect will hopefully allow a tamponading effect and stop ongoing haemorrhage. The initial pressure is directed through a gastric balloon with traction then being applied to try and tamponade vessels passing up from the stomach. If this fails, tamponade can be tried using the esophageal balloon. It is not without its complications, including oesophageal rupture, especially if used when unfamiliar with it.
TIPS TIPS stands for transjugular intrahepatic portosystemic shunt. This involves the vascular bypassing of the highly resistant, cirrhotic liver. The improved flow allows reduction in portal pressure and reduces variceal bleeding, especially in refractory cases. However, the loss of the metabolic activity of the liver on portal blood means a high delivery of adverse products to the circulation and there is a high rate of encephalopathy. As such it is primarily used as a last resort therapy in the acute setting, although it does have a role in refractory ascites or varices in the elective setting too. Other shunt procedures are also potential options.
About 50% of patients will have varices at the time that their cirrhosis is diagnosed. In addition, about ⅓ of those with varices will develop a bleeding complication at some point. This is increased to between 60-70% of those with decompensated cirrhosis. Overall it is the cause of 5-10% of all UGIB.
Mortality is closely relates to
Severity of liver disease
Severity of bleeding
Coagulopathy, such as that related to liver disease, will also worsen outcome. Risk of death is highest in the first few days after a bleed, then slowly decreases. Rebleed rates can be as high as 70% and associated with worse outcomes.
Beta blockers may be used a preventative therapy in those at moderate to high risk of bleeding or as secondary prevention.
NICE. Acute upper gastrointestinal bleed in over 16s: management. CG141. 2012. Available at https://www.nice.org.uk/guidance/cg141 [link]
Tripathi D et al. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. 2015. Gut. Available at: http://gut.bmj.com/content/early/2015/05/12/gutjnl-2015-309262.full.pdf+html [link]