​Upper Gastrointestinal Bleeding

Acute upper gastrointestinal bleeding (UGIB) is a gastroenterological emergency with a mortality of 6%-13%. Despite changes in management, mortality has not significantly improved over a period of 50 years. Bleeding from the upper gastrointestinal tract (GIT) is about four times as common as bleeding from the lower GIT. It is important to identify patients with a low probability of re-bleeding from patients with a high probability of re-bleeding. The size of the bleeding vessel is important in prognosis. Visible vessels are usually between 0.3 mm and 1.8 mm. Large bleeding vessels cause faster blood loss. Generally, larger vessels are found deeper in the submucosa and serosa and more specifically high in the lesser curve of the stomach and postero-inferiorly in the duodenal bulb.

Aetiology

Endoscopy does not reveal a cause in approximately 20% of patients presenting with apparent acute UGIB. The most common causes are peptic ulcer and oesophago-gastric varicies.

Mallory weiss tear

Portal hypertensive gastropathy

Peptic ulcer

Oesophagitis

Gastritis/erosions

Erosive duodenitis

Varices

Vascular malformation

Malignancy

Rare causes include:

Aortoenteric fistula.

Dieulafoy’s lesion (avascular malformation of the proximal stomach).

Osler-Weber-Rendu syndrome

Angiodysplasia

Haemobilia (bleedingfrom the gallbladder or biliary tree).

Pancreatic pseudocyst and pseudo-aneurysm.

Bleeding diathesis

Pseudoxanthoma elasticum

Gastric antral vascular ectasia.

Ehlers- Danlos syndrome

Uncertainties for UGIB

Peptic Ulcer disease is the most common cause of UGIB. Risk factors for peptic ulcer disease are:

Chronic renal failure

Alcohol abuse

Non-steroidal anti-inflammatory drug (NSAID) use.

Age.

Low socio-economic class.

Although duodenal ulcers are more common than gastric ulcers, both contribute nearly equally to the incidence of UGIB. After an initial bleed the risk factors for re-bleeding, with associated higher mortality, are:

Pulsatile haemorrhage.

Age over 60.

Coagulopathy.

Cardiovascular disease.

Presence of signs of shock at admission.

Reckoning

Bleeding severity can be assessed by:

The extent of blood loss.

The degree of shock.

Initial assessment may provide an indication of the cause of UGIB:

1.Abdominal Pain (Epigastric pain, pain all over abdomen)

2. Bleeding

Coffee-ground vomit: refers to the vomiting of black material which is assumed to be blood; it implies that bleeding has ceased or has been relatively modest.

Haematemesis: bright red haematemesis usually implies active haemorrhage. Patients presenting with haematemesis have a higher mortality than those presenting with melaena alone.

Haematochezia: passage of fresh or altered blood per rectum, usually due to colonic bleeding but occasionally due to profuse upper gastrointestinal or small bowel bleeding.

Melaena: black tarry stools, usually due to acute UGIB but occasionally bleeding from the small bowel or right side of the colon.

3. Loss of blood: shock, syncope, presyncope.

4. Features of underlying cause, eg dyspepsia, weight loss,

5. jaundice Risk factors:

Alcohol intake.

Drug history is important. Drugs such as NSAIDs, aspirin and corticosteroids.

Iron and bismuth may mimic melaena.

6. Retching may precede bleeding with a Mallory-Weiss tear.

7. Past history of bleeding (haematemesis or melaena) or of anaemia.

Check-up

The main aim of examination is to assess blood loss and look for signs of shock. A secondary aim is to look for signs of underlying disease and significant comorbid conditions – for example:

1. Pallor and signs of anaemia should be sought. Pulse and blood pressure.

2. Postural hypotension maybe detected and usually indicates a blood loss of 20% or more. Other signs of shock:

Delirium

Cool extremities

Confusion

Chest pain

3. Subcutaneous emphysema and vomiting suggests Boerhaave’s syndrome (Oesophageal perforation).

4. Signs of a tumour may be present (nodular liver, abdominal mass, lymphadenopathy).

5. Evidence of dehydration (dry mucosa, sunken eyes, skin turgor reduced).

6. Stigmata of liver disease may be present (jaundice, gynaecomastia, Ascites, spider naevi, flap, etc.).

Probes

Endoscopy is the primary diagnostic investigation in patients with acute UGIB:

Endoscopy should be undertaken immediately after resucitation for unstable patients with severe acute UGIB.

Endoscopy should be undertaken within 24 hours of admission for all other patients with UGIB.

Laboratory tests

FBC: haemoglobin is measured serially (4-6 hourly in the first day) to help assess trend. The requirement for transfusion is based on initial haemoglobin and a clinical assessment of shock.

Crossmatch blood (usually between 2 and 6 units according to rate of active bleeding). Cogaulation Profile: Prothrombin time with activated partial thrmoboplastin time and an Internation Normalised Ration (INR) Fibronogen level

A consumptive coagulopathy may occur with UGIB. This may be associated with thrombocytopenia. A platelet count of less than 50 with active bleeding requires platelet transfusion and fresh frozen plasma to try to make up for depleted clotting factors.

Coagulopathy may be a marker also for advanced liver disease. Low fibrinogen and abnormal LFT’s may also indicate liver disease. LFTs to detect underlying liver disease

Gastrin levels can identify the rare gastrinomas causing UGIB.

Renal function tests and electrolytes; BUN-to-creatinine ratio (greater than 36 in renal insufficiency suggests UGIB).

Calcium level should be assessed to detect hyperparathyroid patients and to monitor the effect of citrated blood transfusions.

Imaging

CXR: may identify aspiration pneumonia: pleural effusion perforated oesophagus. Erect and supine abdominal X ray to exclude perforated viscus and ileus.

CT scan and ultrasound can identify: Liver disease.

Cholecystitis with haemorrhage.

Pancreatitis with haemorrhage and pseudocyst.

Aortoenteric fistulae.

Nuclear medicine scans have been used to identify areas of active haemorrhage.

Angiography may be useful if endoscopy fails to identify site of bleeding.

Hospital admission

Consider for admission and early endoscopy (and calculation of full Rockall score) if:

aged ≥60 years (all patients who are aged >70 years should be admitted); or

witnessed haematemesis or haematochezia (suspected continued bleeding); or

haemodynamic disturbance (systolic blood pressure <100 mm Hg, pulse ≥100 beats per minute); or

liver disease or known varices.

Other significant comorbidity (especially cardiac disease, malignancy) should also lower the threshold for admission.

Wellness Program

Resuscitation and initial handling

Shocked patients should receive prompt volume replacement. It has been demonstrated that early and aggressive resuscitation reduces mortality in UGIB.

Correct fluid losses (place two wide-bore cannulae and also send bloods at the same time). Either colloid or crystalloid solutions may be used to achieve volume restoration prior to administering blood products; red cell transfusion should be considered after loss of 30% of the circulating volume.

Transfuse patients with massive bleeding with blood, platelets and clotting factors in line with local protocols for managing massive bleeding. Major haemorrhage protocols should be in place. Decisions on blood transfusion should be based on the full clinical picture;

Platelet transfusions should not be offered to patients who are not actively bleeding and are haemodynamically stable. Platelet transfusions should be offered to patients who are actively bleeding and have a platelet count of less than 50 x 10⁹/litre.

Fresh frozen plasma should be used for patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (INR) or activated partial thromboplastin time greater than 1.5 times normal.

Prothrombin complex concentrate should be used for patients who are taking warfarin and actively bleeding.

Recombinant factor Vlla should not be used except when all other methods have failed.

Handling of non-variceal bleeding

Endoscopy is now the method of choice for controlling active peptic-ulcer related UGIB. Endoscopic therapy should only be delivered to actively bleeding lesions, non-bleeding visible vessels and, when technically possible, to ulcers with an adherent blood clot. Black or red spots or a clean ulcer base with oozing do not merit endoscopic intervention since these lesions have an excellent prognosis without intervention.

Adrenaline (epinephrine) should not be used as monotherapy for the endoscopic treatment of non-variceal UGIB. For the endoscopic treatment of non-variceal UGIB, one of the following should be used:

A mechanical method (eg clips) with or without adrenaline (epinephrine). Thermal coagulation with adrenaline (epinephrine).

Fibrin or thrombin with adrenaline (epinephrine).

Interventional radiology should be offered to unstable patients who re-bleed after endoscopictreatment. Refer urgently for surgery if interventional radiology is not immediately available.

Acid-suppression drugs (PPIs or H₂-receptor antagonists) should not be offered before endoscopy to patients with suspected non-variceal UGIB. PPIs should be offered to patients with non-variceal UGIB and stigmata of recent haemorrhage shown at endoscopy.

Treatment after first or failed endoscopic treatment

Repeat endoscopy, with treatment as appropriate, should be considered for all patients at high risk of re-bleeding, particularly if there is doubt about adequate haemostasis at the first endoscopy.

A repeat endoscopy should be offered to patients who re-bleed with a view to further endoscopic treatment or emergency surgery.

Interventional radiology should be used for unstable patients who re-bleed after endoscopic treatment. Percutaneous angiography may be used to localise the bleeding point and embolisation of the artery using foam and coils to stop bleeding. The benefits of embolisation have to be balanced against the risk of causing ischaemic necrosis of the gastrointestinal tract.

Refer urgently for surgery if interventional radiology is not immediately available.

Management of variceal bleeding

Terlipressin should be offered to patients with suspected variceal bleeding at presentation.

Treatment should be stopped after definitive haemostasis has been achieved, or after five days, unless there is another indication for its use.

Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding.

Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled variceal haemorrhage.

Oesophageal varices:

Band ligation should be used for patients with UGIB from oesophageal varices.

There is sufficient evidence to show that stent insertion is effective for selected patients with oesophageal varices in whom other methods of treatment have failed to control bleeding.

Transjugular intrahepatic portosystemic shunts (TIPS) should be considered if bleeding from oesophageal varices is not controlled by band ligation.

Gastric varices:

Endoscopic injection of N-butyl-2-cyanoacrylate should be offered to patients with UGIB from gastric varices.

TIPS should be offered if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate.

Control of bleeding and prevention of re-bleeding in patients on NSAIDs, aspirin or clopidogrel

Continue low-dose aspirin for secondary prevention of vascular events in patients with UGIB in whom haemostasis has been achieved.

Other NSAIDs (including cyclo-oxygenase 2 (COX-2) inhibitors) should be stopped during the acute phase in patients presenting with UGIB.

Operation and other associated procedures-

Surgical intervention is required when endoscopic techniques fail or are contra-indicated. Clinical judgement is required in all cases. In general, it is recommended:

The particular procedure required depends on a number of factors, not least the site of bleeding. Gastric ulcers are probably best excised. There are few studies comparing the different techniques.

Medical management post-endoscopy care

All patients with a bleeding peptic ulcer should be tested for H. pylori, eg urea breath test or biopsy specimen.

Patients who test positive should receive a one-week course of eradication therapy. This should be followed by three further weeks with ulcer healing treatment.

All therapy can be discontinued after successful healing of peptic ulcers provided patients are not taking NSAIDs.

A negative urea breath test should be confirmed on the initial biopsy specimen taken prior to diagnosis and before any PPI therapy was given.

Important points to be kept in mind

There is evidence to use somatostatin or tranexamic acid routinely in UGIB.

In selected patients (eg variceal haemorrhage) it may be appropriate to use terlipressin or octreotide and, in the case of uncontrolled UGIB in an unstable patient, balloon tamponade may be necessary, eg Sengstaken-Blakemore, Minnesota or Linton-Nachlas tubes.

Patients with an UGIB might need to be admitted to a high-dependency unit or intensive care unit.

Staying on to other medication

Anticoagulants and antiplatelet agents should be stopped during the acute phase and restarted later only if there is a clear indication.

Patients who have healed ulcers and were H. pylori-negative and require aspirin or NSAIDs or COX-2 inhibitors, should be given concomitant PPI.

Selective serotonin reuptake inhibitors (SSRIs) should be used in caution in patients at risk of UGIB or who have had a previous UGIB (especially if other drugs such as aspirin or NSAIDs are used).

Corticosteroids will also need to be used carefully and probably with concomitant PPI in high-risk patients or those on high doses.

Complexities

The complications of UGIB are self-evident. Other complications can arise from treatments administered – for example:

Endoscopy:

Aspiration pneumonia

Perforation.

Complications from coagulation, laser treatments.

Surgery :

Ileus.

Sepsis.

Wound problems.

Salvage surgery for patients who continue to bleed is associated with a high mortality.

Outlook

Elderly patients and people with chronic medical conditions withstand acute UGIB less well and have a higher risk of death. Mortality is about 7% in patients admitted with an UGIB. It is as high as 26% in patients who develop bleeding whilst in hospital having been admitted for another cause

Factors which affect the risk of death include:

Age: deaths under age 40 years are rare. 30% of patients over 90 years old with UGIB die as a result of the bleed.

Comorbidity: complications are more likely with comorbid disease.

Shock: the presence of signs of shock at presentation confers a worse prognosis. Prognosis is also worse with: liver disease, inpatient, continued bleeding after presentation, haematemesis, haematochezia and elevated blood urea.

Endoscopic findings: much work has been done on classifying and identifying endoscopic findings which correlate with high risk – for example:

Mallory-Weiss tears or clean ulcers have a low risk of re-bleeding and death.

Active bleeding in a shocked patient carries an 80% risk of re-bleeding or death. Non-bleeding but visible vessel has a 50% risk of re-bleeding.

The prognosis in liver disease relates significantly to the severity of the liver disease rather than to the magnitude of the haemorrhage.

Obviating UGIB

The most important factor to consider is treatment for H. pylori infection. Eradication of H. pylori reduces the risk of both recurrent ulcers and recurrent haemorrhage.

Primary prophylaxis for acutely ill patients in critical care:

Acid-suppression therapy (H₂-receptor antagonists or PPIs) should be offered for primary prevention of UGIB in acutely ill patients admitted to critical care (using the oral form of the drug if possible).