Upper Gastrointestinal Bleeding

Upper gastrointestinal bleeding (UGIB) is a significant and potentially life-threatening worldwide problem. Despite
advances in diagnosis and treatment, mortality and morbidity have remained constant. Bleeding from the upper
gastrointestinal tract (GIT) is about 4 times as common as bleeding from the lower GIT. Typically patients present with
bleeding from a peptic ulcer and about 80% of such ulcers stop bleeding. Increasing age and co-morbidity increase
mortality. It is important to identify patients with a low probability of re-bleeding from patients with a high probability of
re-bleeding.
Etiology

A cause is found in 80% of cases. Approximate percentages given.

Note the predominance of peptic ulcer disease:
• Peptic ulcer disease 35 to 50%:
○ Duodenal ulcer 25%
○ Gastric ulcer 20%
• Gastroduodenal erosions 8 to 15%
• Oesophagitis 5 to 15%
• Oesophageal varices 5 to 10%
• 'Mallory-Weiss' tears 15%
• Upper gastrointestinal malignancy 1%
• Vascular malformations 5%
• Rare causes - less than 5%:
○ Dieulafoy's lesion (a vascular malformation of the proximal stomach)
○ Angiodysplasia
○ Haemobilia (bleeding from the gallbladder or biliary tree)
○ Pancreatic pseudocyst and pseudo-aneurysm
○ Aortoenteric fistula
○ Bleeding diathesis
○ Ehlers-Danlos syndrome
○ Pseudoxanthoma elasticum
○ Gastric antral vascular ectasia
○ Rendu-Osler-Weber syndrome
• The strong association of Helicobacter pylori (H. pylori) infection with duodenal ulcer is worthy of special
mention. The organism disrupts the mucosal barrier and causes inflammation in the gastric and duodenal mucosae.
Eradication reduces the risk of both recurrent ulcers and recurrent haemorrhage.
• Non-steroidal anti-inflammatory drugs (NSAIDS) are the second most important aetiological factor. They exert an
effect on cyclooxygenase-1 leading to impaired resistance of the mucosa to acid.
• 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.
Symptoms and Signs

One of the symptoms of upper GI bleeding is vomiting of blood (hematemesis). If the blood travels through the GI tract,
the stool may appear tarry and black (melena) because of digested blood, though the stool can still be stained with red
blood (hematochezia). Otherwise, bleeding over time results in anemia, characterized by lower than normal blood
hemoglobin and hematocrit with symptoms like weakness, fatigue, and fainting.
Epidemiology

The incidence of UGIB is between 47 and 116 per 100,000 population. There are about 2,500 admissions to hospital every
year in the United Kingdom for UGIB. Incidence is highest in areas of low socioeconomic status.
Risk factors for upper gastrointestinal bleeding
An aging population with associated conditions and a worse prognosis has helped maintain constant mortality figures
despite advances in treatment. Mortality is about 7% in patients admitted because of bleeding but some three times higher
amongst those developing UGIB whilst in hospital. Peptic ulcer disease is the most common cause of UGIB. Risk factors
for peptic ulcer disease are:
• Alcohol abuse
• Chronic renal failure
• Non-steroidal anti-inflammatory 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:
• Age over 60
• Presence of signs of shock at admission
• Coagulopathy
• Pulsatile haemorrhage
• Cardiovascular disease
Assessment- History
• Is there abdominal pain?
• History of other gastrointestinal symptoms should be sought. The symptoms in order of frequency are:
○ Haematemesis including coffee-ground emesis: 40 to 50%
○ Melaena: 70 to 80%
○ Haematochezia (red or maroon stool): 15 to 20%
○ Syncope: 14%
○ Presyncope: 43%
○ Dyspepsia:18%
○ Epigastric pain: 41%
○ Diffuse abdominal pain:10%
○ Weight loss: 12%
○ Jaundice: 5%
• Alcohol intake.
• Past history of bleeding (haematemesis or melaena) or of anaemia.
• Drug history is important. Drugs such as NSAIDs, aspirin and corticosteroids are an important cause of bleeding.
Iron and bismuth may mimic melaena.
• Retching may precede bleeding with a 'Mallory-Weiss' tear.
Examination
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 co-morbid conditions. For example:
• Pallor and signs of anaemia should be sought
• Pulse and blood pressure
• Postural hypotension may be detected and usually indicates a blood loss of 20% or more
 • Other signs of shock:
○ Cool extremities
○ Chest pain
○ Confusion
○ Delirium
• Evidence of dehydration (dry mucosa, sunken eyes, skin turgor reduced)
• Stigmata of liver disease may be present (jaundice, gynaecomastia, ascites, spider naevi, flap etc)
• Signs of a tumour may be present (nodular liver, abdominal mass, lymphadenopathy)
• Subcutaneous emphysema and vomiting suggests Boerhaave's syndrome (oesophageal perforation)
• Urine output should be monitored (oliguria is a sign of shock)
Differential diagnosis
Other conditions which may form part of the differential diagnosis include:
• Abdominal aortic aneurysm
• Boerhaave's syndrome
• Cholecystitis
• Coeliac sprue
• Dengue fever
• Disseminated intravascular coagulation
• Zollinger-Ellison syndrome
• Von Willebrand's disease
Laboratory tests
• Full blood count
• Crossmatch blood (usually between 2 and 6 units according to rate of active bleeding)
• Coagulation profile:
○ Platelet count
○ Prothrombin time with activated partial thromboplastin time and an international normalised ratio (INR)
○ Fibrinogen level
• Liver function tests to detect underlying liver disease
• Plasma fibrinogen level
• Urea 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
• Gastrin levels can identify the rare gastrinomas causing UGIB
Note:
• 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. Co-morbid conditions such as advanced
cardiovascular disease require transfusion to help prevent myocardial ischaemia.
• 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 liver function tests
may also indicate liver disease.
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
Assessment of bleeding severity and re-bleeding
Bleeding severity can be assessed by:
• The extent of blood loss
• The degree of shock
However there are other factors which affect risk of death:
• Age: deaths under age 40 years are rare. 30% of patients over 90 years old with UGIB die as a result of the bleed.
• Co-morbidity: complications are more likely with co-morbid disease.
• Shock: the presence of signs of shock confers a worse prognosis.
• 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.
Treatment:
Endoscopic image of small gastric ulcer with visible vessel
Emergency treatment for upper GI bleeds includes aggressive replacement of volume with intravenous solutions, and blood
products if required. As patients with esophageal varices typically have coagulopathy, plasma products may have to be
administered. Vital signs are continuously monitored.
Early endoscopy is recommended, both as a diagnostic and therapeutic approach, as endoscopic treatment can be
performed through the endoscope. Therapy depends on the type of lesion identified, and can include:
• injection of adrenaline or other sclerotherapy
• electrocautery
• endoscopic clipping
• or banding of varices
Stigmata of high risk include active bleeding, oozing, visible vessels and red spots. Clots that are present on the bleeding
lesion are usually removed in order to determine the underlying pathology, and to determine the risk for rebleeding.
Same ulcer seen after endoscopic clipping
Pharmacotherapy includes the following:
• Proton pump inhibitors (PPIs), which reduce gastric acid production and accelerate healing of certain gastric,
duodenal and esophageal sources of hemorrhage. These can be administered orally or intravenously as an infusion
depending on the risk of rebleeding.
• Octreotide is a somatostatin analog believed to shunt blood away from the splanchnic circulation. It has found to
be a useful adjunct in management of both variceal and non-variceal upper GI hemorrhage. It is the somatostatin
analog most commonly used in North America.
• Terlipressin is a vasopressin analog most commonly used in Europe for variceal upper GI hemorrhage.
 • Antibiotics are prescribed in upper GI bleeds associated with portal hypertension
If Helicobacter pylori is identified as a contributant to the source of hemorrhage, then therapy with antibiotics and a PPI is
suggested.

Upper Gastrointestinal Bleeding

Upper gastrointestinal (GI) bleeding refers to hemorrhage in the upper gastrointestinal tract. The anatomic cut-off for upper
GI bleeding is the ligament of Treitz, which connects the fourth portion of the duodenum to the diaphragm near the splenic
flexure of the colon. Upper GI bleeds are considered medical emergencies, and require admission to hospital for urgent
diagnosis and management. Due to advances in medications and endoscopy, upper GI hemorrhage is now usually treated
without surgery.
Clinical presentation Patients with upper GI hemorrhage often present with hematemesis, coffee ground vomiting, melena,
or hematochezia (maroon coloured stool) if the hemorrhage is severe. The presentation of bleeding depends on the amount
and location of hemorrhage.
Patients may also present with complications of anemia, including chest pain, syncope, fatigue and shortness of breath.
The physical examination performed by the physician concentrates on the following things:
• Vital signs, in order to determine the severity of bleeding and the timing of intervention
• Abdominal and rectal examination, in order to determine possible causes of hemorrhage
• Assessment for portal hypertension and stigmata of chronic liver disease in order to determine if the bleeding is
from a variceal source.
Laboratory findings include anemia, coagulopathy, and an elevated BUN-to-creatinine ratio.
Causes: There are many causes for upper GI hemorrhage. Causes are usually anatomically divided into their location in the
upper gastrointestinal tract.
Patients are usually stratified into having either variceal or non-variceal sources of upper GI hemorrhage, as the two have
different treatment algorithms and prognosis.

Gastric ulcer in antrum of stomach with overlying clot. Pathology was consistent with gastric lymphoma. Reproduced with
permission of patient
Pathopysiology: Usually the bacteria called Hpylori is the root cause of ulcers, they eat
away the tissues of the stomach lining where the inflammation of gastritis has
caused a weakened area of the tissue.
Gastrointestinal bleeding is a diagnosis commonly managed by gastroenterologists. Given the length of the digestive tract,
there are many causes for GI bleeding. It can be divided into upper GI bleeding and lower GI bleeding, the former of which
will be discussed here.
Causes
Upper GI bleeding originates in the GI tract from the mouth to the ligament of Treitz where the duodenum, the first part of
the small intestine, ends. Bleeding from the esophagus may occur from esophageal varices, dilation of the veins in the
esophagus. This can occur with liver cirrhosis, because blood from the GI tract to the liver backs up when it has difficulty
getting through the liver. For the stomach and duodenum, bleeding in these areas can often occur from tumors and ulcers,
the latter of which can be due to certain medications (e.g., nonsteroidal anti-inflammatory drugs) or the bacterium
Helicobacter pylori. These causes do not comprise a complete list but do represent common causes.
Symptoms and Signs
One of the symptoms of upper GI bleeding is vomiting of blood (hematemesis). If the blood travels through the GI tract,
the stool may appear tarry and black (melena) because of digested blood, though the stool can still be stained with red
blood (hematochezia). Otherwise, bleeding over time results in anemia, characterized by lower than normal blood
hemoglobin and hematocrit with symptoms like weakness, fatigue, and fainting.