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Acute and Chronic Gastrointestinal Bleeding

Acute and Chronic Gastrointestinal Bleeding

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Published by: Marwan M. on Jun 30, 2010
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01/27/2013

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ACUTE AND CHRONIC GASTROINTESTINAL BLEEDING y 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: Age. Evidence of co-morbidity. 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.
1. 2. 3.

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 < 60 60-79 > 79 Age (years)

BP > 100 mmHg Pulse < 100 b.p.m. Comorbidity None Circulation

Endoscopic diagnosis Major SRH

MalloryWeiss tear, no lesion None, or dark spots

BP > 100 BP < 100 mmHg mmHg Pulse > 100 Pulse > 100 b.p.m. b.p.m. Cardiac disease, any other major comorbidity All other Malignancy of the diagnoses upper GI tract -

-

Renal failure, liver failure, disseminated malignancy -

Blood in the upper GI tract, adherent clot or spurting vessel

(b) Rebleed and mortality risk according to Rockall score. Risk score 0 1 2 3 4 5 6 7 8+

5 3 5 11 14 24 33 44 42

0 0 0 3 5 11 17 27 41

BP, blood pressure; GI, gastrointestinal; SRH, stigmata of recent haemorrhage. Emergency Box 6.1 Management of acute gastrointestinal bleeding y History and examination. Note co-morbidity y Monitor the pulse and blood pressure half-hourly. y Take blood for Hb, urea, electrolytes, LFTs, coagulation screen, group and crossmatching (2 units initially) y Establish IV access - 2 large bore i.v. cannulae; central line if brisk bleed y 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 y Oxygen therapy y Urgent endoscopy in shocked patients/liver disease. y Continue to monitor pulse and BP

y y

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 y Organ failure that require blood transfusion. y 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 y Shock. y Suspected varices. y 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:
y y

y

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 preendoscopy 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:
y y y

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:
y y

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:
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. Peptic ulcer disea

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