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Upper Gastrointestinal Bleeding

Upper gastrointestinal bleeding (UGIB) is a significant and


potentially life-threatening worldwide problem.
Despiteadvances 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 withbleeding from a peptic ulcer and
about 80% of such ulcers stop bleeding. Increasing age
and co-morbidity increasemortality. 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:
ȈPeptic ulcer disease 35 to 50%:
Duodenal ulcer 25%
Gastric ulcer 20%

ȈGastroduodenal erosions 8 to 15%


ȈOesophagitis 5 to 15%
ȈOesophageal varices 5 to 10%
Ȉ'Mallory-Weiss' tears 15%
ȈUpper gastrointestinal malignancy 1%
ȈVascular malformations 5%
ȈRare 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

ȈThe strong association of Helicobacter pylori


(H. pylori) infection with duodenal ulcer is worthy of
specialmention. 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.
ȈNon-steroidal anti-inflammatory drugs (NSAIDS) are the
second most important aetiological factor. They exert
aneffect on cyclooxygenase-1 leading to impaired
resistance of the mucosa to acid.
ȈThe 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 andserosa 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 redblood (hematochezia). Otherwise,
bleeding over time results in anemia, characterized by
lower than normal bloodhemoglobin 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
everyyear 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
figuresdespite 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:


ȈAlcohol abuse
ȈChronic renal failure
ȈNon-steroidal anti-inflammatory use
ȈAge
ȈLow 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:

ȈAge over 60
ȈPresence of signs of shock at admission
ȈCoagulopathy
ȈPulsatile haemorrhage
ȈCardiovascular disease

Assessment- History

ȈIs there abdominal pain?


ȈHistory 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%

ȈAlcohol intake.
ȈPast history of bleeding (haematemesis or melaena) or of
anaemia.
ȈDrug history is important. Drugs such as NSAIDs, aspirin
and corticosteroids are an important cause of
bleeding.Iron and bismuth may mimic melaena.
ȈRetching 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:
ȈPallor and signs of anaemia should be sought
ȈPulse and blood pressure
ȈPostural hypotension may be detected and usually
indicates a blood loss of 20% or more
ȈOther signs of shock:
Cool extremities
Chest pain
Confusion
Delirium

ȈEvidence of dehydration (dry mucosa, sunken eyes, skin


turgor reduced)
ȈStigmata of liver disease may be present (jaundice,
gynaecomastia, ascites, spider naevi, flap etc)
ȈSigns of a tumour may be present (nodular liver,
abdominal mass, lymphadenopathy)
ȈSubcutaneous emphysema and vomiting suggests
Boerhaave's syndrome (oesophageal perforation)
ȈUrine output should be monitored (oliguria is a sign of
shock)

Differential diagnosis

Other conditions which may form part of the differential


diagnosis include:

ȈAbdominal aortic aneurysm


ȈBoerhaave's syndrome
ȈCholecystitis
ȈCoeliac sprue
ȈDengue fever
ȈDisseminated intravascular coagulation
ȈZollinger-Ellison syndrome
ȈVon Willebrand's disease

Laboratory tests
ȈFull blood count
ȈCrossmatch blood (usually between 2 and 6 units
according to rate of active bleeding)
ȈCoagulation profile:
Platelet count
Prothrombin time with activated partial thromboplastin
time and an international normalised ratio (INR)
Fibrinogen level

ȈLiver function tests to detect underlying liver disease


ȈPlasma fibrinogen level
ȈUrea and electrolytes
ȈBUN-to-creatinine ratio (greater than 36 in renal
insufficiency suggests UGIB)
ȈCalcium level should be assessed to detect
hyperparathyroid patients and to monitor the effect of
citrated bloodtransfusions
ȈGastrin levels can identify the rare gastrinomas causing
UGIB

Note:

ȈHaemoglobin is measured serially (4-6 hourly in the first


day) to help assess trend. The requirement for
transfusionis based on initial haemoglobin and a clinical
assessment of shock. Co-morbid conditions such as
advancedcardiovascular disease require transfusion to
help prevent myocardial ischaemia.

ȈA consumptive coagulopathy may occur with UGIB. This


may be associated with thrombocytopenia. A plateletcount
of less than 50 with active bleeding requires platelet
transfusion and fresh frozen plasma to try to make upfor
depleted clotting factors.

ȈCoagulopathy may be a marker also for advanced liver


disease. Low fibrinogen and abnormal liver function
testsmay also indicate liver disease.

Imaging
ȈCXR:

May identify aspiration pneumonia


Pleural effusion
Perforated oesophagus
ȈErect and supine abdominal X ray to exclude perforated
viscus and ileus
ȈCT scan and ultrasound can identify:
Liver disease
Cholecystitis with haemorrhage
Pancreatitis with haemorrhage and pseudocyst
Aortoenteric fistulae

@c Nuclear medicine scans have been used to identify


areas of active haemorrhage
@c 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:


ȈThe extent of blood loss
ȈThe degree of shock

However there are other factors which affect risk of death:


ȈAge: deaths under age 40 years are rare. 30% of patients
over 90 years old with UGIB die as a result of the bleed.
ȈCo-morbidity: complications are more likely with co-
morbid disease.
ȈShock: the presence of signs of shock confers a worse
prognosis.
@c Endoscopic findings: much work has been done on
classifying and identifying endoscopic findings which
correlatewith high risk. For example:
@c 'Mallory-Weiss' tears or clean ulcers have a low risk
of re-bleeding and death.
@c Active bleeding in a shocked patient carries an 80%
risk of re-bleeding or death.
@c 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 bloodproducts if required. As patients with
esophageal varices typically have coagulopathy, plasma
products may have to beadministered. Vital signs are
continuously monitored.Early endoscopy is recommended,
both as a diagnostic and therapeutic approach, as
endoscopic treatment can beperformed through the
endoscope. Therapy depends on the type of lesion
identified, and can include:

Ȉinjection of adrenaline or other sclerotherapy


Ȉelectrocautery
Ȉendoscopic clipping
Ȉor banding of varicesStigmata of high risk include active
bleeding, oozing, visible vessels and red spots. Clots that
are present on the bleedinglesion 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:

ȈProton 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
infusiondepending on the risk of rebleeding.
ȈOctreotide is a somatostatin analog believed to shunt
blood away from the splanchnic circulation. It has found
tobe a useful adjunct in management of both variceal and
non-variceal upper GI hemorrhage. It is the
somatostatinanalog most commonly used in North
America.
ȈTerlipressin is a vasopressin analog most commonly used
in Europe for variceal upper GI hemorrhage.
ȈAntibiotics are prescribed in upper GI bleeds associated
with portal hypertensionIf
Helicobacter pylori
is identified as a contributant to the source of hemorrhage,
then therapy with antibiotics and a PPI issuggested.

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 splenicflexure of the colon. Upper GI
bleeds are considered medical emergencies, and require
admission to hospital for urgentdiagnosis and
management. Due to advances in medications and
endoscopy, upper GI hemorrhage is now usually
treatedwithout 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
amountand 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:
ȈVital signs, in order to determine the severity of bleeding
and the timing of intervention
ȈAbdominal and rectal examination, in order to determine
possible causes of hemorrhage
ȈAssessment for portal hypertension and stigmata of
chronic liver disease in order to determine if the bleeding
isfrom 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
theupper gastrointestinal tract.Patients are usually
stratified into having either variceal or non-variceal
sources of upper GI hemorrhage, as the two havedifferent
treatment algorithms and prognosis.Gastric ulcer in
antrum of stomach with overlying clot. Pathology was
consistent with gastric lymphoma. Reproduced
withpermission of patient

Pathopysiology:
Usually the bacteria called Hpylori is the root cause of
ulcers, they eataway the tissues of the stomach lining where
the inflammation of gastritis hascaused 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 whichwill 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 theesophagus. This can occur with liver
cirrhosis, because blood from the GI tract to the liver
backs up when it has difficultygetting 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 SignsOne 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 redblood (hematochezia).
Otherwise, bleeding over time results in anemia,
characterized by lower than normal bloodhemoglobin and
hematocrit with symptoms like weakness, fatigue, and
fainting.
c

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