Definition• UGIB can be defined as bleeding from any site along the gastrointestinal tract (GIT) that is above the ligament of treitz.
Epidemiology• The annual incidence of hospital admissions for UGIB in the United States and Europe is approximately 0.1%, with a mortality rate of about 5-10%.• The mortality rate of patients under 60 years of age in the absence of malignancy or organ failure is < 1%.• The three independent clinical predictions of death in patients hospitalized with UGIB are increasing age, co morbidities and haemodynamic compromise (tachycardia & hypotension)
Aetiology• Common causes 1) Peptic ulcers – most common cause of UGIB – 35-62% of cases 2) Varices (oesophageal & gastric) – 5-30% 3) Mallory-Weiss syndrome – 5-15% 4) Haemorrhagic gastropathy & erosions – 3-11% 5) Erosive oesophagitis – 2-8%
Aetiology (contd)• Uncommon causes; they include Erosive duodenitis, neoplasms, aortoenteric fistulas, vascular lesions[ including hereditary haemorrhagic telengectasias(Osler- Weber-Rendu) and gastric antral vascular ectasia (‘Water- melon stomach’)], Dieulafoy’s lesion (in which an aberrant vessel in the mucosa bleeds from a pinpoint mucosal defect), prolapse gastropathy, haemobilia and hemosuccus pancreaticus.
Clinical Presentation• This bleeding from the GIT can present in 5 ways; a) Haematemesis:- Vomitus of red blood or ‘coffee- grounds’ material. b) Melaena:- Black, tarry foul smelling stool. c) Haematochezia:- Is the passage of bright red or maroon blood from the rectum. d) Occult GIB:- This is identified in the absence of overt bleeding by special examination of the stool (e.g. Guaiac testing) e) Symptoms of blood loss/anaemia:- Light- headedness, syncope, angina or dyspnoea.
Management (contd)• This depends on the following; 1) Age of patient 2) The amount of blood lost 3) Continuing visible blood loss 4) Signs of chronic liver disease on examination 5) Evidence of co morbidity e.g. cardiac failure, ischaemic heart disease and malignant disease. 6) Presence of the classical features of shock.
Quick history• Any of the already mentioned C/P, shock and unconscious.• Hx of epigastric pain or a known PUD patient• Intake of NSAIDS e.g. Asprin• Alcohol binge
• Gastric erosions (black arrows) caused by Ibuprofen as seen on upper endoscopy
Investigations• FBC – especially Hb• S E/U/C – access renal status• Liver function test• Endoscopy (diagnostic) – performed within 24hrs in most patients. - Bleeding site is seen in >80% of cases. i.e. Varices, Mallory-Weiss tear or PUD.
Medical• ABC Resuscitation- for emergency cases, when patient presents with an ongoing blood loss, in shock or unconscious. A- Clear airway Suctioning in cases of haematemesis Left lateral position to avoid aspiration. B- Ensure breathing Oxygen therapy for shocked patients.
Medical (ABCresuscitation contd)C- Circulation Establish one or more intravenous accesses with wide bore cannulae, if bleeding is brisk and massive. - Blood transfusion with fresh whole blood - Colloid (dextran) or crystalloid (N/S) until blood becomes ready. -continue monitoring pulse and BP -avoid circulatory overloadFor continued bleeding - reendoscope
Medical contd(Therapeutic Endoscopy)• This depends on cause;• VARICES: (i) can be injected with a sclerosing agent that produces vessel thrombosis e.g. 5% phenol in almond or arachis oil (ii) Banding Both are said to arrest bleeding in 80% of cases• BLEEDING PUD: (i) Bipolar electrocoagulation (ii) Heater probe (iii) Injection therapy with absolute alcohol, 1:10,000 epinephrine.
Medical contd (DrugTherapy)• In about 20% of cases of bleeding PUD, following use of heater probe, epinephrine or laser therapy they rebleed within 72hrs.• Such cases will require intravenous Omeprazole 80mg bolus followed by infusion 8mg/hr for 72hrs.• This reduces rebleeding rates and need for surgery.
Medical contd (DrugTherapy)• FOR VARICES: Vasoconstrictor therapy with Terlipressin(2mg 6hrly x48hrs then 1mg 4hrly) and Somatostatin infusion (250- 500ug/hr) is helpful. Also Octreotide 50ug bolus and 50ug/hr intravenous infusion x2- 5/7 can control acute bleeding.
Mgt of Varices contd.• Balloon tamponade: with Sengstaken - Blakemore tube is successful in 90% of cases & very useful in first few hrs of bleeding.• Some drawbacks include aspiration pneumonia, oesophageal rupture & mucosal ulceration, which leads to a 5% mortality.
• Esophageal varices filling the lumen of the esophagus as seen
Additional mgt of acutebleeding• Prophylactic antibiotics: e.g. oral or i.v. quinolones – Ciprofloxacin• Nursing – Intensive care nursing & NPO until bleeding stops.• Sucralfate: 1g 6hrly – this reduces oesophageal ulceration following endoscopic therapy.
• Further bleed from a varice will require TIPS (Transjugular intrahepatic portosystemic shunt)- a minimal invasive procedure – done if endoscopic & medical therapy fail.
Surgery• This is indicated when other measures fail or if TIPS is not available. TYPES• a) Oesophageal transection & ligation of the feeding vessels to the bleeding Varices.• b) Portosystemic shunting – but this causes significant encephalopathy Rebleed following treatment can be reduced by giving a non-selective B- blocker e.g. Propranolol
Mgt of Mallory – Weisstears• Bleeding stops spontaneously in 80- 90% of cases & recur in only 0-5% of patients.• Endoscopy therapy is indicated in actively bleeding cases.• Angiographic therapy with intra- arterial infusion of vasopressin or embolization and operative therapy with oversewing of the tear are rarely required.
Prognosis• This depends on; 1) Age: Mortality is < 0.1% for patients < 60yrs but >20% for patients >80yrs. 2) Recurrent haemorrhage increases mortality. 3) Co morbidities increase mortality 4) Melaena is a better prognostic factor than haematemesis 5) Shock increases mortality.
Conclusion• Upper gastrointestinal bleeding can be life threatening seeking immediate medical care for aggressive resuscitation.• Both medical and endoscopic therapy have been shown to significantly improve patient outcomes.
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