liver variceal bleeding

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VARICEAL BLEEDING Gastroesophageal varices develop in 55% of cirrhotic patients 1 www.medicinemcq.com

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Page 1: Liver Variceal Bleeding

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VARICEAL BLEEDING

Gastroesophageal varices develop in 55% of cirrhotic

patients

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Esophageal varices

Superficial veins that lack

support from surrounding tissues

Prominent 2 to 3 cm above the

gastroesophageal junction

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Stomach Next most common site for

varices In continuity with esophageal

varices (i.e., true gastroesophageal varices) or as freestanding gastric varices

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Normal HVPG = 5 mm Hg

Portal hypertension> 5 mm Hg

Esophageal hemorrhageOnly with HVPG > 12 mm Hg

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Ohm's law : P = Q X R

P = Pressure along a vessel Q = Flow R = Resistance to the flow

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Portal pressure

Portal venous inflow X outflow resistance.

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Variceal bleeding Massive hemetemesis

With or without melena Painless

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RISK FACTORS

1. HVPG > 12 mm Hg

2. Large esophageal varices

3. Child-Pugh class C cirrhosis

4. Presence of tense ascites

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“Red signs” Variceal appearance on endoscopy

Red wale marks ○ Longitudinal red streaks on varices

Cherry-red spots ○ Red, discrete, flat spots on varices

Hematocystic spots○ Red, discrete, raised spots)

Diffuse erythema

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Endoscopy Best test to find the cause of upper

GI hemorrhagePatients with varices may bleed from

other gastrointestinal lesions also (e.g., peptic ulcer, gastritis)

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First treatment in variceal bleed

AirwayBreathingCarotid pulse

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Priority First

Protection of airway to prevent aspiration

SecondRestoration of circulating blood

volume Done before diagnostic

endoscopy studies or treatment to stop the bleeding.

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Assess volume status

Heart rate Pulse volume BP – postural hypotension Urine output JVP (CVP) Swan-Ganz pulmonary artery

catheter

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IV fluids Initial

Normal salineFresh frozen plasma - If PT > 3 sec

Avoid over transfusionIncrease portal pressure

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Only after hemodynamically stable

Endoscopy or treatment to prevent further bleeding

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Risk of rebleeding > 60% over 2 years

Greatest risk○Within hours or days after an

acute bleed 50% of variceal bleeding

stops by itself

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Endoscopy To determine the cause of

bleedingAs soon as the patient is

stabilized Variceal ligation

May be performed during the initial endoscopy

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Endoscopic intervention First line of treatment

to control bleeding acutely

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Endoscopic band ligation

Esophageal varices are ligated with endoscopically placed small elastic O-rings

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Complications

1. Esophageal ulceration and stricture

2. Fever

3. Chest pain

4. Mediastinitis

5. Pleural effusions

6. Aspiration

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Esophageal ulcers Seen in most treated patients

Uncomplicated Recurrent bleeding from mucosal

ulcerationIn up to 20%

Esophageal strictures leading to dysphagia15%

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Proton pump inhibitors Most effective

treatment for esophageal ulcer

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Prophylactic banding

Before bleedingNot recommended

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Endoscopic Sclerotherapy Varices are injected with a

sclerosing agent Endoscopic band ligation is

preferred to sclerotherapy

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Complications of sclerotherapy Bacterial peritonitis Esophageal perforation Mediastinitis Brain abscess Spinal cord paralysis Pericarditis

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Pharmacologic therapy Decrease splanchnic blood

flow Reduce portal pressure by

Somatostatin analoguesVasopressin

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Somatostatin Hypothalamic hormone Inhibits the secretion of

vasodilatory peptides from the GIT Short half-life of 2 minutes Reduces renal plasma flow, GFR

and sodium excretion

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Octreotide, lanreotide and vapreotide

Synthetic long-acting analogues of somatostatin

Octreotide is widely used

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Octreotide Half-life of 1.5 hours Direct splanchnic vasoconstrictor Excellent safety profile

No systemic circulatory effectsSide effects are mild hyperglycemia

and abdominal cramping

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Vasopressin - IV infusion Causes generalized

vasoconstriction Diminished blood flow in the portal

venous system Control of bleeding in up to 80% Bleeding recurs in 50 % after the

vasopressin is discontinued

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Short half-life

Vasopressin must be given by continuous intravenous

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Side effects

Cardiac ischemia GIT ischemia Acute renal failure Hyponatremia

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IV nitroglycerin or S/L isosorbide dinitrate

Concurrent use of venodilators enhances the effectiveness and reduces complications

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Terlipressin reduce mortality

in acute variceal bleeding

Synthetic vasopressin analogue

Longer half-life Used in bolus form Fewer side effects

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Terlipressin Vasoconstriction

Splanchnic vasculature No risk to renal function and renal

excretion of sodium More effective and safer than

vasopressin or vasopressin plus nitroglycerin

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Balloon tamponade

When there is failure of vasopressin or endoscopy

Control active bleeding in > 90%

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Serious complications

Esophageal perforation Aspiration pneumonia Rarely asphyxiation

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Sengstaken-Blakemore - triple-lumen or Minnesota-four-lumen

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High risk of aspiration Perform endotracheal

intubation before placing these tubes

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Indication Temporary measure

Active life-threatening hemorrhage

Refractory ○Endoscopic and pharmacologic

therapy

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Rebleeding in up to 50% on deflation of the balloons

Definitive treatment planned for most patientsEndoscopic therapyTIPSOperation

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Transjugular intrahepatic portosystemic shunt (TIPS)

Portal decompression without an operation

Therapy of choice for acute variceal bleeding after failure of drug and

endoscopic therapy

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TIPS - Indication

When endoscopic or drug treatments have failed

Poor surgical risks

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Complications Perforation of the liver capsule

Main early complication Stenosis of the shunt

Main long-term complication Common (50% at 1 year) Presents as further variceal haemorrhage

Hepatic encephalopathy25 % risk

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Primary prevention of variceal bleed

To prevent the first bleeding episode

Only drugNonselective beta-blockers

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Beta 2 receptor blockade Eliminate beta 2 receptor–

mediated vasodilation Unopposed alpha-

adrenergic activitySplanchnic vasoconstrictionReduced portal pressure

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Propranolol, Nadolol or Timolol

Decrease the incidence of bleeding

Prolong survival Continued life long Useful in secondary

prevention also

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Contraindications to β-blockers

Endoscopic band ligation of the varices

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Determinant of survival after a variceal bleed

Hepatic functionMortality rate after a variceal bleed○50% within 6 weeks