Variceal Bleeding FFH Med-2

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    Varicose veins that develop in the esophagous as a result of

    elevated pressure in the venous system of the abdomen.

    Upper G.I. Bleeding is a Medical Emergency associated with high mortality.

    80-90% bleed from esophageal varices & not from other sources.

    Overall mortality of first bleed is 50% mainly due to patientsdying before they reach hospital.

    50-70% patients experience a re-bleeding episode during

    hospitalisation.

    At least, a third will re-bleed within 6 weeks of discharge fromhospital.

    No more than third will survive beyond one year.

    Introduction

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    Esophageal Varices

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    Varices in the distal esophagus as viewed through an endoscope

    Esophageal Varices

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    About 30% cirrhotic patients with demonstrable varices manifest

    bleed.

    Almost all bleeding episodes occur within 2 years of initialobservation.

    Once bleeding occurs 40-50% cirrhotic patients die within 6months.

    There is an 80% incidence of re-bleeding once patient bleedsfrom varices.

    Mortality seen with every re-bleeding is about 60%.

    Every re-bleeding even if treated successfully requires a lot ofhospital resources, especially blood.

    Facts & Figures

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    Causes of Portal Hypertension

    Liver Cirrhosis (alcoholic, biliary, posthepatitis)

    Non-cirrhotic portal fibrosis/ Portal

    hypertension

    Schistosomiasis

    Budd-Chiari Syndrome

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    1stDegree Varices

    2ndDegree Varices

    3rdDegree Varices

    Predictors of Bleeding in EV

    - Size

    - Red Spots

    - Child Pugh Score

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    EMERGENCY MANAGEMENT OF UPPER G.I. BLEEDING

    AT FAMILY PHYSICIANS CLINIC

    MINOR BLEEDING

    (BP Stable, Pulse < 100/min)

    History of past bleeding attacks,

    jaundice/NSAIDs, other

    medications

    Inject Octreotide 50 mcg* i.v. stat

    at the site of visit

    No further bleeding

    Patient remains stable

    Consult G.I. Specialist/Hospital for

    further evaluation & Endoscopy

    MAJOR BLEEDING

    Hypotensive Shock, Patient Collapse

    Maintain i.v. line with

    Normal Saline & Plasma

    Expanders

    Inject Octreotide 50 mcg stat i.v.AND START

    I.V. infusion of Sandostatin

    25 mcg/hour

    HOW?

    (Add 3 ampoules of 100 mcg

    Sandostatin in 500 c.c.

    dextrose/water 5% in 12 hours)

    URGENTLY SHIFT PATIENT

    TO HOSPITAL

    * Sandostatin (Octreotide) is available as (a) 0.05 mg injection (50 mcg ampoule) (b) 0.1 mg injection (100 mcg ampoules)

    For further Specialized Management please refer a Gastroenterologist

    Note:

    Upper G.I. Bleeding may present with

    Vomiting of fresh blood

    Black color loose stools

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    Prevention

    - Beta blockers and nitrates

    Acute variceal bleeding

    - Vasopressin

    - Vasopressin Analogue

    - Somatostatin

    - Somatostatin Analogue

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    Acts by decreasing portal pressure by

    constricting splanchnic blood vessels

    LIMITATIONS

    - Short half life

    - Systemic vasoconstriction

    - MI and mesenteric Ischaemia

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    Same mode of action as vasopressin

    Longer half life

    Fewer side effects

    LIMITATIONS

    - Less effective in controlling active bleeding andpreventing re-bleeding

    - No reduction in transfusion requirements- Should be use with trans-dermal Nitroglycerineto counter cardiac side effects

    (Hepatology 1993, vol.18, p 61-65)

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    Contrindicated in IHD

    (Management of Portal Hypertension and Budd Chiari Syndrome,

    Andrew K Burroughs)

    ECG and BP must be monitored

    Can only be used when ICU facilities are

    available

    (Terlipressin package insert)

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    Acts by selectively reducing hepatic blood flow

    and wedge hepatic venous pressure

    LIMITATIONS

    - Shorter half life

    - Necessitates continuous IV infusion

    - Rebound bleeding

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    Same pharmacologic effects as Somatostatin

    Much longer half life

    Significantly reduces intra-variceal pressure

    Decreases the inflow of blood to the portalsystem

    Increased selectivity

    Potency greater than that of Somatostatin

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    Advantages of Sandostatin (Octreotide)

    Longer plasma half-life

    (about 1-2 hours)

    Longer duration of action

    S.C. injection which can be

    self-administered by the patient

    More potent

    More selective

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    USES AND BENEFITS

    Sandostatinis effective in control of acute variceal bleeding

    at 24 hours and stops variceal haemorrhage in 80% of

    patients.

    Sandostatinis equally effective as endoscopic therapy in

    mild, moderate and severe disease.

    Sclerotherapy is not available at all centres and depends

    upon the technical expertise.

    Sandostatinwhen used prior to sclerotherapy produces an

    effective Holding & prevents re-bleeding during the first 4

    hours especially when used with sclerotherapy.

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    Sandostatinis more effective than other modalities in theemergent control of active variceal bleeding.

    Sandostatinreduces the transfusion requirements as

    compared to other pharmacological treatment modalities i.e

    1 unit versus 3 units within 48 hours.

    Sandostatinhas an excellent safety profile than other

    treatments. It is well tolerated & has fewer side effects.

    Due to absence of systemic circulatory effects Sandostatin

    can be used without special monitoring.

    USES AND BENEFITS

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    A recent meta-analysis evaluated 13 randomized trials ofoctreotide v/s several alternative interventions for varicealhemorrhage[21] These 13 trials included a total of 1077 patients(numbers ranged from 40 to 199 total patients per trial). Theendpoints analyzed involved assessments made at the end of therecorded follow-up, rather than at arbitrary times during the firstfew hours of hospitalization. The primary endpoints were:

    Total rebleeding

    Mortality

    Complications

    This study defined lack of control of bleeding as any episode of

    rebleeding during the follow-up period It defined major complications as hypertension or hypotension,

    cardiac or intestinal ischemia, arrhythmias, pneumonia, pulmonaryedema, or any side effect that required termination of treatment

    Corley DA, Cello JP, Adkisson W, et al. Octreotide for acute esophageal variceal

    bleeding: a meta-analysis. Gastroenterology. 2001;120:946-954.

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    Meta-analysis demonstrated that most studies favor octreotide vs alternative

    therapy (vasopressin/terlipressin, placebo/no therapy, and sclerotherapy) for

    the control of bleeding in acute variceal hemorrhage

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    0

    10

    20

    30

    40

    50

    60

    70

    80

    90

    100

    Octreotide

    Vaso/Terli

    Sclero/Band

    Placebo

    Balloon

    Major

    Any

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    Octreotide was associated with fewer Major Complicationthan vasopressin/ Terlipressin

    A trend towards Morality benefitespecially against

    Balloon or Vasopressin Comparable in efficacyto Emergency Sclerotherapy and

    comparable or better than other modalities. Mostcommon dosage regime in studies was 2550 g IV for48- 120 hours

    Addition of Octreotideto Sclerotherapy producedsignificant better initial bleeding control and Rebleedingrates and small survival advantage compared withvasopressin/Terlipressin

    (Gastroenterology 2001, 120, p 946-954)

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    50 mcg intravenous as bolus in case of acute bleeding

    Maintain i.v. line and start

    50 mcg per hour for 5 days by continous i.v. infusion

    Emergency therapy required at Family Physicians Clinic

    for a patient with projectile bloody vomiting reports

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    Conclusion

    At present, available clinical evidence suggests that, because of

    its efficacy & lack of major side effects Sandostatin most closely

    fulfil the requirements of the ideal vasoactive drugfor the

    control of acute variceal bleeding.