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