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Dr. Sadia Nazneen 22.02.2017, MALDA MEDICAL COLLEGE

VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION

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Page 1: VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION

Dr. Sadia Nazneen22.02.2017, MALDA MEDICAL COLLEGE

Page 2: VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION

Gasatroesophageal varices > 90% Hypertensive portal gastropathy <5% Isolated gastric varices – rare.

Page 3: VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION

Portal hypertension is defined as a hepatic venous pressure gradient equal to or greater than 10 mm of Hg.

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Normal 6-8mm Hg In cirrhosis >10mm Hg HVPG <12 mm Hg unlikely to develop

variceal bleeding. Useful for assessing medical

treatment.

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Block to portal flow increased portal pressure

Splanchnic vascular bed response : (a) Initial increased vasoconstrictor and decreased

vasodialator response intrahepatic response

(b)Secondarily vasodialator response dominates with increase in splanchnic inflow

Collaterals develop. Plasma volume expansion Systemic

hyperdynamic circulation

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Portal inflow Systemic outflow Collaterals

Left gastric veinsShort gastric veins

Intercostal, diaphragmatic and oesophageal veins

Gastro-oesophagealvarices

Superior haemorrhoidal vein

Middle haemorrhoidal veinInferior haemorrhoidal vein

haemorrhoids

Left portal vein via falciform ligament

Umbilicus and abdominal wall veins

Caput medusa

Liver via lienorenalligament

Left renal vein Retroperitoneal collaterals

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Pre hepatic: Portal vein thrombosis Splenic vein thrombosis Congenital thrombosis of Portal vein Arteriovenous fistula

Intra hepatic: Primary biliary cirrhosis Cirrhosis Infiltrative liver disease Congenital hepatic fibrosis Polycystic liver disease Veno – occlusive disease

Post hepatic: Budd – Chiari syndrome Inferior vena cava webs or thrombosis Congenital heart failure Constrictive pericarditis Tricuspid valve diseases

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Splenomegaly Oesophageal varices Caput medusa. Haemorrhoids.

Complications : Ascites. Spontaneous bacterial peritonitis. End-stage renal disease. Hepatopulmonary syndrome. Encephalopathy

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Assessment of the liver function. Assessment of the portal circulation. Upper GI endoscopy.

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Assessment of liver function: Hypoalbuminaemia. ALT & AST are moderately raised. Prothrombin time and INR are disturbed.

Blood picture anaemia, leucopenia, thrombocytopenia or pancytopenia.

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Assessment of portal circulation:

Duplex scan or Doppler ultrasound:

To assess the hepatic artery, hepatic vein and portal vein.

Patency of portal vein.

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Upper GI Endoscopy or EGD

To detect gatroesophagealvarices

Gold standard for diagnosing varicealbleeding

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Diagnosis of the aetiology of liver disease is performed by:

(a) Immunological tests for hepatitis markers.

Other specific serological markers are alpha foetoprotein, ceruloplasmin,alpha 1 antitrypsin, antimitochondrial antibodies,and iron studies.

(b) Liver biopsy.

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CT ANGIOGRAPHY MR ANGIOGRAPHY

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Points

1 2 3

Bilirubin (mg/dL) < 2 2 – 3 > 3

Albumin (g/dL) > 3.5 2.8 – 3.5 < 2.8

Prothrombin time (seconds)

1 – 3 4 – 6 > 6

Ascites None Slight Moderate

Encephalopathy None Minimal Advanced

Grade A, 5-6 points; Grade B, 7-9 points; Grade C, 10-15 points

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Score = 0.957 × loge creatinine (mg/dL) + 0.378 × loge bilirubin (mg/dL) + 1.120 loge INR

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Prophylaxis – Pharmacotherapy and endoscopic therapy

Acute variceal bleedingResuscitaion and pharmacotherapy Endoscopic therapyDecompressive shuntsDevascularisation Liver transplantation

Prevention of rebleedingLevel I evidence

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Pharmacotherapy: Non-cardioselective beta blockers

Endoscopic variceal ligation

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Admit patient in ICU

Fluids and blood products judiciously administered

Somatostatin or its analogues octreotide or terlipressinadministered and continued for 3-5 days

Non-selective beta blockers like propanol or nadolol

Current recommendation is to administer an antibiotic prophylaxis upto 7days, specifically a fluoroquinolones.

Initial bolus 100 microgram continuous infusion of 25 microgram / h for 24 hrs.

Dose 20-60 mg bid

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Sclerotherapy

Intra- or Para- Variceal.

1-3 ml sclerosant

(ethanolamine oleate).

Multiple sessions (2 weekly).

Control bleeding in 80-95 %.

About 50% rebleed.

Intravariceal

Paravariceal

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Endoscopic BandingOccludes venous

channels

Sessions <

sclerotherapy

Same results as

sclerotherapy

Endoscopic

treatment of

choice

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Transjugular intrahepatic portosystemicshunt or (TIPS) is a procedure that involves the creation of an artificial anastomosisbetween the hepatic and portal veins under fluoroscopic guidance with the use of a covered stent, shunting away blood from the hepatic sinusoids and relieving portal pressure.

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Indications for TIPSS: Refractory bleeding Prior to transplant Child C Refractory ascites

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Porta – systemic shunts. Non Shunt surgery – Devascularisation. Liver transplantation.

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Classification:

Non-selective shunts: Total shunts:

PortacavalMesocavalProximal spleno-renal

Partial shunts: Small diameter porta-caval (Sarfeh)

Selective shunts: Distal spleno renal shunt

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Portal blood is completely redirected into IVC below the liver.

Two types: end to side and side to side

Side to side shunt is useful in preventing portal hypertension in Budd – Chiari syndrome .

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Anastomosis of the side of the SMV to the proximal end of the divided IVC, for control of portal hypertension;

The incidence of thrombosis is high.

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Indication: EHPVO.Advantage: The incidence of

encephalopathy is less than after porta cavalshunt.

Disadvantage: Less effective In

rebleeding. If the splenic vein is less

than 1 cm the anastmosisis liable to thrombosis.

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A small diameter interposition

(8-10 mm) porta – cavalshunt.Advantage: Partially decompress the

portal venous system. Hepatic portal flow is

preserved.Drawback: Increasaed incidence of

thrombosis. Recurrence of bleeding.

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Types :•The distal splenorenal shunt (Dean Warren shunt)•Inokuchi splenocaval shunt (IMV to IVC)•Interposition shunts with the left gastric vein to IVC

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An anastomosis of the splenic vein and the left renal vein, created to lower portal hypertension

Merits:•The incidence of encephalopathy is low •Liver functions remain normal.

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Devascularisation:Aim: Direct disconnection between the portal and azygos vein done by disconnecting the varices from their bleeding vessels.Components:SplenectomyGastric and oesophagealdevascularisationOesophagealtransection

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Good-risk patients—Child’s A patients or MELD less than 10.

Pharmacotherapy +/- Banding If they rebleed or have failure to obliterate

their varices banding, they may be a candidate for decompression with TIPS or DSRS.

Indeterminate patients—Child’s B or MELD 10–16. Majority of patients Initial treatment is with endoscopic banding

and a beta-blocker. Subsequent treatment depends on the course

of their liver disease.

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End-stage liver disease—Child’s C or MELD greater than16.

Liver transplantation

Patients with any of the above scenarios, who also have advanced liver disease, are candidates for liver transplantation, possibly using TIPS as a bridge.

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Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension

Most common cause of this is cirrhosisof the liver.

Investigations: Endoscopy Treatment: Medications: o Non-selective beta blockers (such as propranolol and nadolol)o Octreotide Procedural:o Argon plasma coagulation.o TIPS.o Cryotherapy.

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Most commonly found in patients with portal hypertension. Gastric varices may also be found in patients with

thrombosis of the splenic vein.

Clinical features: Hematemesis, melena, shock

Treatment: Injecting cyanoacrylate glue, TIPS. Intravenous octreotide Splenectomy Liver transplantation.

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Variceal bleeding has high morbidity and mortality rate.

Endoscopy is both diagnostic and therapeutic. Beta blockers and EVL are first line of treatment. TIPSS and DSRS are used as bridge to Liver

Transplant. Liver transplant though last resort may be

curative.

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THANK YOU.