ACUTE AND CHRONIC GASTROINTESTINAL BLEEDING

 Acute upper gastrointestinal bleeding

The cardinal features are haematemesis (the vomiting of blood) and melaena (the
passage of black tarry stools; the black colour due to blood altered by passage through
the gut). Melaena can occur with bleeding from any lesion proximal to the right
colon. Following a bleed from the upper GI tract, unaltered blood can appear per
rectum, but the bleeding must be massive and is almost always accompanied by
shock. The passage of dark blood and clots without shock is always due to lower GI
bleeding.
Aetiology
Peptic ulceration is the commonest cause of serious and life-threatening G.I bleeding.
Drugs. Aspirin and NSAIDs can produce ulcers and erosions. These agents are also
responsible for GI haemorrhage from both duodenal and gastric ulcers, particularly in
the elderly. Corticosteroids in the usual therapeutic doses probably have no influence
on GI haemorrhage. Anticoagulants do not cause acute GI haemorrhage per se but
bleeding from any cause is greater if the patient is anticoagulated.
Clinical approach to the patient
All cases with a recent (i.e. within 48 hours) significant GI bleed should be seen in
hospital. In many, no immediate treatment is required as there has been only a small
amount of blood loss. Approximately 85% of patients stop bleeding spontaneously
within 48 hours.
Scoring systems have been developed to assess the risk of rebleeding or death
(Rockall score which is based on clinical and endoscopy findings) and need for
intervention (Blatchford uses the level of plasma urea, haemoglobin and clinical
markers but not endoscopic findings) such as transfusion or endoscopic therapy.
.
The following factors affect the risk of rebleeding and death:

1. Age.
2. Evidence of co-morbidity.
3. Presence of the classical clinical features of shock (pallor, cold peripheries,
tachycardia and low blood pressure).
4. Endoscopic diagnosis.
5. Ulcer with active bleeding or endoscopic stigmata of recent bleeding.
6. Clinical signs of chronic liver disease, bleeding associated with liver disease is
often severe and recurrent if it is from varices.

Splenomegaly suggests portal hypertension but its absence does not rule out
oesophageal varices.
Immediate management (see emergency box)
Stop NSAIDs, aspirin and warfarin if patients are taking them.
Patients should be managed in high-dependency beds. Oxygen should be given by
face mask and the patient should be kept NPO until endoscopy has been performed.
Blood volume
Table 6-7. Risk assessment in non-variceal upper gastrointestinal haemorrhage
(a) Rockall risk assessment score

Variable Score
  0 1 2 3

Age (years) < 60 60-79 > 79 -

Circulation BP > 100 BP > 100 BP < 100 mmHg -

mmHg mmHg

  Pulse < 100 Pulse > 100 Pulse > 100 b.p.m.  
b.p.m. b.p.m.

Comorbidity None - Cardiac disease, any Renal failure, liver

other major failure, disseminated
comorbidity malignancy

Endoscopic Mallory- All other Malignancy of the -

diagnosis Weiss tear, diagnoses upper GI tract
no lesion

Major SRH None, or - Blood in the upper GI -

dark spots tract, adherent clot or
spurting vessel

(b) Rebleed and mortality risk

according to Rockall score.

Risk score

0 5 0

1 3 0

2 5 0

3 11 3
4 14 5

5 24 11

6 33 17

7 44 27

8+ 42 41

BP, blood pressure; GI, gastrointestinal; SRH, stigmata of recent

haemorrhage.
Emergency Box 6.1 Management of acute gastrointestinal
bleeding
 History and examination. Note co-morbidity
 Monitor the pulse and blood pressure half-hourly.
 Take blood for Hb, urea, electrolytes, LFTs, coagulation
screen, group and crossmatching (2 units initially)
 Establish IV access - 2 large bore i.v. cannulae; central line
if brisk bleed
 Give blood transfusion/colloid if necessary. Indications for
blood transfusion are:
o (a) SHOCK (pallor, cold nose, systolic BP < 100
mmHg, pulse > 100 b.p.m.)
o (b) Hb < 10 g/dL in patients with recent or active
bleeding
 Oxygen therapy
 Urgent endoscopy in shocked patients/liver disease.
 Continue to monitor pulse and BP
 Re-endoscope for continued bleeding/hypovolaemia.
 Surgery if bleeding persists.

The major principle is to rapidly restore the blood volume to normal. This can be
best achieved by transfusion of red cell concentrates via one or more large-bore
intravenous cannulae; plasma expanders or 0.9% saline is given until the blood
becomes available.
Transfusion must be monitored to avoid overload leading to heart failure. The
pulse rate and venous pressure are the best guides to adequacy of transfusion. A
CVP line is inserted for patients with
 Organ failure that require blood transfusion.
 Severe hypotension.
Hb levels are generally a poor indicator of the need to transfuse because anaemia
does not develop immediately as haemodilution has not taken place. However, if the
Hb is less than 10 g/dL and the patient has either bled recently or is actively
bleeding, transfusion is usually necessary. In most patients the bleeding stops, albeit
temporarily, so that further assessment can be made.
Endoscopy
Endoscopy should be performed within 24 hours in patients with significant bleeds.
Patients with Rockall scores of 0 or 1 may be candidates for immediate discharge and
outpatient endoscopy the following day.
After adequate resuscitation, urgent endoscopy should be performed in patients with
 Shock.
 Suspected varices.
 Continued bleeding.
Endoscopy can detect the cause of the haemorrhage in 80% or more of cases. In
patients with a peptic ulcer, if the stigmata of a recent bleed are seen (i.e. a spurting
artery, active oozing, fresh or organized blood clot or black spots) the patient is more
likely to rebleed. Calculation of the postendoscopy Rockall score gives an indication
of the risk of rebleeding and death.
At first endoscopy:

 Varices should be treated, usually with banding.

 Bleeding ulcers and those with stigmata of recent bleeding should be
treated with two haemostatic methods, usually injection with epinephrine
and thermal coagulation (with heater probe, bipolar probe, laser or
endoscopic clipping because dual therapy is clearly more effective than
monotherapy in reducing rebleeding.
 Antral biopsies should be taken to look for H. pylori. A positive biopsy
urease test is valid, but a negative test is not reliable. If the urease test is
negative, gastric histology should always be performed.

The above procedures reduce the incidence of rebleeding, although they do not
significantly improve mortality.
Drug therapy
After diagnosis at endoscopy, intravenous omeprazole 80 mg followed by infusion
8 mg/h for 72 hours should be given to all ulcer patients as it reduces rebleeding
rates and the need for surgery. PPI therapy has no effect on mortality. H2-receptor
antagonists are of no value.
Uncontrolled or repeat bleeding
Endoscopy should be repeated to assess the bleeding site and to treat, if possible.
Surgery is necessary if bleeding is persistent and/or uncontrollable and should aim
primarily to control the haemorrhage.
Discharge policy
1. The patient's age.
2. Diagnosis on endoscopy.
3. Co-morbidity.
4. The presence or absence of shock.
5. The availability of support in the community should be taken into
consideration. In general, all patients who are haemodynamically stable and
have no stigmata of recent haemorrhage on endoscopy (Rockall Score pre-
endoscopy 0, post-endoscopy ≤ 1) can be discharged from hospital within 24
 hours. All shocked patients and patients with co-morbidity need inpatient
observation.
Specific conditions
1. Chronic peptic ulcer.
Eradication therapy. A PPI is continued for 4 weeks to ensure ulcer healing. Give
long-term acid suppression if eradication is not possible. If bleeding is not controlled,
surgery with ligation is indicated to control haemorrhage.
2. Gastric carcinoma.
Most of these patients do not have large bleeds.
3. Oesophageal varices.
4. Mallory-Weiss tear.
This is a linear mucosal tear occurring at the EG junction and produced by a sudden
increase in intra-abdominal pressure. It often occurs after a bout of coughing or
retching and is classically seen after alcoholic 'dry heaves'. There may be no
antecedent history of retching. Most bleeds are minor and discharge is usual within 24
hours. The haemorrhage may be large but most patients stop spontaneously. Early
endoscopy confirms diagnosis and allows therapy if necessary. Surgery with
oversewing of the tear is rarely needed.
5. Bleeding after percutaneous coronary intervention (PCI).
This occurs in 2% of patients undergoing PCI (who are on antiplatelet therapy), and
has a high mortality of 5-10%. Urgent endoscopy should be performed with
appropriate therapy. A proton pump inhibitor should be given IV. Management is
difficult as cessation of antiplatelet therapy has a high risk of acute stent thrombosis
and also an associated high mortality. Using a risk assessment score is a reasonable
approach is to stop all antiplatelet therapy in high risk patients but continue in low
risk ones.
Prognosis
The mortality has not changed from 5-12% over the years. Early therapeutic
endoscopy has not so far reduced the mortality, although rebleeding episodes are
reduced.
Acute lower gastrointestinal bleeding
Massive bleeding is rare and usually due to diverticular disease or ischaemic colitis.
Common causes of small bleeds are haemorrhoids and anal fissures.
Management
Most of them start and stop spontaneously. The few patients who continue bleeding
and are haemo-dynamically unstable need resuscitation using the same principles as
for upper GI bleeding. Surgery is rarely required.
A diagnosis is made using the history, examination including rectal examination and
the following investigations as appropriate:

 Proctoscopy.
 Flexible sigmoidoscopy or colonoscopy.
 Angiography - vascular abnormality (e.g. angiodysplasia).

Isolated episodes of rectal bleeding in the young (< 45 years) usually only require
rectal examination and flexible sigmoidoscopy because the probability of a significant
proximal lesion is very low unless there is a strong family history of colorectal
cancer at a young age.
Chronic gastrointestinal bleeding
Usually present with iron-deficiency anaemia (IDA).
Chronic blood loss producing IDA in all men and all women after the menopause is
always due to bleeding from the GI tract. The primary concern is to exclude cancer,
particularly of the stomach or right colon, and coeliac disease. Occult blood tests are
unhelpful.
Diagnosis
Chronic blood loss can occur with any lesion of the GI tract that produces acute
bleeding. However, oesophageal varices usually bleed obviously and rarely present as
chronic blood loss. Hookworm is the most common world-wide cause of chronic
GI blood loss.
History and examination may indicate the most likely site of the bleeding, but if no
clue is available it is usual to investigate both the upper and lower GI tract
endoscopically at the same session ('top and tail').
Upper gastrointestinal endoscopy is usually performed first. Duodenal biopsies
should always be taken to exclude coeliac disease which is a recognized cause of iron
deficiency. Colonoscopy follows and any lesion should be biopsied or removed,
though it is not safe to assume that colonic polyps are the cause of chronic blood loss.
Unprepared CT scanning is a reasonable test to look for colon cancer in frail
patients; it can be used on the rare occasions if colonoscopy fails to reach the caecum.
Box 6.4 Measurement of faecal occult blood
This is frequently performed unnecessarily. It is only of value in:

 Premenopausal women - if a history of menorrhagia is

uncertain and the cause of IDA is unclear
 Mass population screening for large bowel malignancy
Advantages: cheap and easy to perform
Disadvantages: high false-positive rate, leading to
unnecessary investigations

If gastroscopy, colonoscopy and duodenal biopsy have not revealed the cause,
investigation of the small bowel is probably only justified if the anaemia is
transfusion-dependent. The diagnostic yield of small bowel follow-through in this
situation is very low. Video capsule endoscopy is the diagnostic investigation of
choice if endoscopy fails to reveal the cause, but has no therapeutic ability.
If these investigations fail to show the cause, coeliac axis and mesenteric
angiography may be performed, although the yield is low.
Treatment
Causes of upper G.I bleeding:
.Peptic ulcer disease (50%) .I
II. Variceal bleeding (10-20%).
III. Hemorrhagic gastropathy and erosions (15-20%).
IV. Mallory-Weiss tear syndrome (5-10%).
V. Reflux esophagitis (2-5%).
VI. Gastric carcinoma & gastric varices.
VII. Hereditary telangiectasia.
VIII. Pseudoxanthoma elasticum.
IX. Blood dyscrasias.
X. Portal gastropathy.
 XI. Aortic graft surgery with fistula.
XII. Dieulafoy gastric vascular abnormality.

Causes of lower G.I bleeding:

1. Anal fissures and hemorrhoids are common.

2. Colitis (Crohn's disease, ulcerative and infective colitis usually associated with
diarrhea).
3. Colon cancer.(carcinoma of the right colon usually gives occult bleeding.
4. Diverticula.
5. Polyps (small bleeds but frequent).
6. Solitary rectal ulcer.
7. Ischemic colitis.
8. Angiodysplasia.
9. Meckel's diverticulum.