marinel s. mandapat senior intern. causes of non-variceal ugib
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Marinel S. MandapatSenior Intern
Causes of non-variceal UGIB
Forrest Classificationis a classification of upper gastrointestinal
hemorrhage used for purposes of comparison and in selecting patients for endoscopic treatment
It is instrumental when stratifying patients with upper gastrointestinal hemorrhage into high and low risk categories for mortality.
It is also a significant method of prediction of the risk of rebleeding and very often is used for evaluation of the endoscopic intervention modalities
FORREST CLASSIFICATIONForrest class Type of lesion Risk of
bleedingType I: Active BleedIA Arterial spurting bleeding 100%IB Arterial oozing bleeding 55% (17-100%)Type II: Recent BleedIIA Visible vessel 43% (8-81%)IIB Sentinel clot 22% (14-36%)IIC Hematin covered flat spot 10% (0-13%)Type III: Lesion w/o BleedingIII No stigmata of hemorrhage 5% (0-10%)
Forrest 1a Spurting bleeding
Forrest 1b Non-spurting active bleeding
Forrest 2a Non-bleeding visible vessel
Forrest 2b Non-bleeding ulcer with an adherent clot
Forrest 2c Ulcer with haematin-covered base
Forrest 3 Ulcer with clean base
ENDOSCOPIC MANAGEMENTAdrenaline injection results in haemostasis in up
to100% of patients with bleeding peptic ulcers, probably by a combination of vascular tamponade and vasoconstriction, with a concomitant reduction in re-bleeding rates from 40 to 15%.
The dose of adrenaline required to achieve haemostasis is variable but larger volumes (13–20ml vs. 5–10ml) in high risk patients (Forrest type I or IIa lesions) results in less re-bleeding (15.4% vs. 30.8%).24 Although injection with adrenaline is successful in achieving initial haemostasis, 15-36% of patients rebleed
ENDOSCOPIC MANAGEMENTSclerosants such as ethanol, polidocanol and
ethanolamine are equally effective as adrenaline but carry more risk.
Combination therapy with adrenaline and ethanol may improve haemostasis and shorten hospital stay for patients with spurting haemorrhage.
Repeated daily injection of fibrin glue following treatment with dilute adrenaline in patients with active bleeding or NBVV until the ulcer base is clean or covered is expensive but reduces re-bleeding although not mortality rates.
ENDOSCOPIC MANAGEMENTN-butyl-2-cyanoacrylate (Histoacryl) injection
has been shown to be effective for control of variceal bleeding
More recently, Lee et al demonstrated significantly lower re-bleeding rate for patients with Forrest type Ia lesions treated with Histoacryl compared to injection with hypertonic saline-adrenaline injection. However, there was no overall benefit in the use of Histoacryl with regards to haemostasis rates, emergency surgery or mortality.
ENDOSCOPIC MANAGEMENTIn contrast to injection techniques, thermal
haemostasis is achieved by compression of the artery during heating (coaption) and/or the effect of heat on tissue. The only non-contact thermal techniques currently available are Argon Plasma Coagulation (APC) and laser (Nd:YAG).
APC involves conduction of a high frequency electrical current through a beam of ionized argon gas, resulting in superficial tissue damage and coagulation. A prospective observational study of APC in 254 patients with non-variceal UGIB revealed initial haemostasis rates of 75.9% and re-bleeding rates of 5.7%. The addition of a second haemostasis technique increased successful haemostasis to 99.6%.
ENDOSCOPIC MANAGEMENTBipolar Electrocoagulation (BPE) and Heater
Probe Thermocoagulation (HPT) use thermal. BPE reduces the re-bleeding rate when compared with normal saline injection in high risk bleeding ulcers, and compared to medical therapy when used in combination with adrenaline in Forrest IIb ulcers. Combination therapy with HPT and adrenaline in the treatment of actively bleeding peptic ulcers resulted in haemostasis in up to 98.6%, with re-bleeding in 8.2%, although added benefit is confined to high risk lesions.
When used alone, HPT was not superior to combination treatment with adrenaline and polidocanol in patients with Forrest type I, IIa and IIb ulcers.
ENDOSCOPIC MANAGEMENTMechanical haemostasis with endoloops or
clips, e.g. the Hemoclip (Teleflex Medical, PA), has an increasing role in the control of non-variceal UGIB. Endoclips are deployed on a visible vessel to achieve vascular compression and can achieve homeostasis in up to 100% of cases. Comparative studies suggest lower re-bleeding rates than adrenaline injection, ethanolor saline/adrenaline injection.
ENDOSCOPIC MANAGEMENTEndoscopic band ligation (EBL) is currently
technically easier to use than endoclips and has been shown to be safe and effective for control of small lesions in a small series of acute peptic ulcer bleeding and with bleeding due to Dieulafoy's lesions.
ADHERENT CLOTAdrenaline injectionShaving of the clot with cold guillotineBipolar electrocoagulation of the underlying
ulcer stigmata of recent hemorrhage
ACID SUPPRESSIONIn vitro studies of the effect of gastric pH on
platelet aggregation and coagulation provide the rationale for acid suppression in UGIB.
If gastric pH is maintained above pH6 (by infusional PPI), platelet aggregation is optimized and fibrinolysis relatively inhibited, thereby potentially improving the likelihood of clot stability at an ulcer site.
Acid Neutralizing/Inhibitory DrugsAntacids-rarely used, often used by patients
for symptomatic relief of dyspepsiaH2 receptor antagonists-used for 4-6 weeks
in combination with antibiotics Cimetidine-initial 300 mg qid or 800 mg hs
May have a weak anti-androgenic side effects resulting in reversible gynecomastia and impotence
Ranitidine-300 mg hs Famotidine-40 mg hs Nizatidine-300 mg hs
Acid Neutralizing/Inhibitory DrugsPPIs (e.g. omeprazole, esomeprazole,
lansoprazole, rabeprazole, pantoprazole)-substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H, K-ATPaseRapid onset of action with a max. inhibitory
effect 2-6 h after administration & duration of inhibition up to 72-96h.
Half life ˜18h thus it can take 2-5 days for gastric acid secretion to return to normal levels once these drugs have been discontinued
Cytoprotective AgentsSucralfate-complex sucrose salt in w/c the
hydroxyl groups have been substituted by aluminum hydroxide and sulfateAluminum hydroxide dissociates, leaving the
polar sulfate anion, w/c can bind to positively charged tissue proteins found within the ulcer bed, providing a physico-chemical barrier
May also induce a trophic effect by binding growth factors such as EGF, enhance prostaglandin synthesis, stimulate mucous and bicarbonate secretion, and enhance mucosal defense and repair
Cytoprotective AgentsBismuth-containing preparations-
(e.g.colloidal bismuth subcitrate (CBS) and bismuth subsalicylate (BSS))Ulcer coating; prevention of further
pepsin/HCl-induced damage; binding of pepsin; stimulation of prostaglandins, bicarbonate, and mucous secretion
TreatmentCytoprotective AgentsProstaglandin Analogues (e.g. Misoprostol)
Enhance mucous bicarbonate secretion, stimulate mucosal blood flow, and decrease mucosal cell turnover
Therapeutic dose is 200 µg qid
H. Pylori TherapyTRIPLE THERAPY
1. BSS + Metronidazole + Tetracycline
2. Ranitidine bismuth citrate + Tetracycline + Clarithromycin or Metronidazole
3. Omeprazole (lanzoprazole) + Clarithromycin + Metronidazole or Amoxicillin
2 tabs qid + 250 mg qid + 500 mg qid
400 mg bid + 500 mg bid + 500 mg bid
20 mg bid (30 mg bid) + 250 or 500 mg bid + 500 mg bid or 1 gr bid
QUADRUPLE THERAPY
Omeprazole (lanzoprazole)BSSMetronidazoleTetracycline
20 mg (30 mg) daily2 tabs qid250 mg qid500 mg qid
NSAID-Related Gastric or Duodenal Injury TherapyClinical Setting Recommendation
Active Ulcer NSAID discontinued NSAID continued
H2 receptor antagonist or PPIPPI
Prophylactic Therapy MisoprostolPPISelective COX-2 inhibitor
H. Pylori infection Eradication if active ulcer present or there is a past history of PUD
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