PORTAL HYPERTENSION

-Dr Sunil Kumar .K.P

DEFINITION

o Normal portal pressure is 5-7 mm Hg Pressure more than 10 mmHg is considered as portal hypertension

ANATOMY

o PV is formed by SV and SMV Left gastric vein ,superior pancreatico duodenal vein and pyloric vein

Normal portal blood flow is 1000-1200 ml/min

Normal hepatic arterial blood flow is 400 ml/min

CLASSIFICATION 1.Prehepatic

a) Presinusoidal-- EHPVO 2.Intrahepatic a) Presinusoidal--NCPF,Schistosomiasis b) Sinusoidal--Cirrhosis 3.Post hepatic a)Post sinusoidal-- Hepatic vein obstruction, Constrictive pericarditis

ETIOLOGY

• CIRRHOSIS <50% ETIOLOGY INDIA WEST

Cirrhosis <50% >80%

NCPF 10 – 20% 3 – 5%

EHPVO 30 – 40 % 5 %

ETIOLOGY INDIA WEST

Cirrhosis < 50 % >80%

NCPF 10 – 20 % 3 – 5 %

EHPVO 30 – 40 % 5 %

Budd Chiari syndrome

8 - 26% Rare

NON CIRRHOTIC PORTAL FIBROSIS• Perisinusoidal fibrosis 30 –

40 yr age group Neonatal umbilical sepsis Neonatal peritonitis Umbilical card catheterisation Congenital abnormalities ---- atresia,stenosis of PV Hypercoagulable states -polycythemia rubra vera -myelofibrisis -protein C deficiency - protein S deficiency -antithrombin III -chronic pancreatitis -pancreatic malignancy

LEFT SIDED PORTAL HYPERTENSION

• Seen in isolated splenic vein thrombosis• Causes development of isolated fundic varices

Causes – chronic pancreatitis

pancreatic malignacy hyper coagulable state idiopathic

BUDD CHIARI SYNDROME

• In India incidence is 8 – 26% of all cases of PHT• Type I – Major hepatic vein obstruction• Type II – IVC obstruction above the level of HV• Type III – IVC + HV obstruction Causes – pregnancy related hypercoagulability infection IVC web or web hypercoagulable states

NATURAL HISTIRY OF PHT

EHPVO

CLINICAL FEATURES

1) Gastrointestinal bleeding- 30% of cirrhotics bleed 90% of EHPVO and NCPF bleed stops spontaneously in 50% of cirrhotics

& 90% of EHPVO Rebleeding is more common in first 6

weeks,highest during first 24-48 hrs Mortality is related to Child’s criteria

2) SPLEENOMEGALY

present in all cases of PHT usually mild in cirrhotics moderate in NCPF & EHPVO can present as left hypochondriac pain or

abdominal lump

3) HYPERSPLENISM Leucopenia( WBC <4000/ml) and

thrombocytopenia ( platelets < 1 lakh /ml) Hypersplenism per se doesn’t need any

treatmentSymptomatic hypersplenism –recurrent

sepsis,petechiae,low hb,platelet <50000/ml and WBC < 2000/ml needs surgical intervention

• 3) ASCITIS

Sign of hepatic decompensation

In NCPH transient after bleeding

Clinical examination

- Puddle sign

- Shifting dullness

- Horse shoe dullness

- Fluid thrill

4) HEPATIC ENCEPHALOPATHYSign of hepatic decompensationEarly C/F are alterred sleep pattern & change in

hand writingGrading of encephalopathy Grade I :euphoria,slurred speech, , slurredspeech,depression,change in

sleep pattern Grade II :Drowsy ,inappropriate behaviour Grade III : Excessive sleepines,

arousable,confusion Grade IV :Hepatic coma

4) OBSTRUCTIVE JAUNDICE It is due to extrinisc compression by the

periportal & pericholedochal varices.

INVESTIGATION 1) Hematological- Complete haemogram to look for anemia & to rule out hyeprsplenism 2) BIOCHEMICAL- a) LFT- -To differentiate cirrhosis from NCPF -detect active disease which is a contraindication for surgery -Child classification

b) RFT- done in all patients 3)Coagulation profile- -PT, aPTT, BT, CT - Hypercoagulable work up done in

Buddchiari syndrome, PV thrombosis, left sided PHT

4) Viral markers- -HBsAg, anti HCV in all suspected cases of

cirrhosis - also done in patients with h/o transfusion

• 5) Liver scan – -to differentiate b/w cirrhosis & NC PHT

-degree of liver damage - decreased uptake s/o cirrhosis 6) Liver biopsy- Indications– etiology,to r/o secondary

cirrhosis Contraindication- ascites , coagulopathy Methods- percutaneous, transjugular

6) Upper gastrointestinal endoscopy all suspected or diagnosed cases to document to grade to R/O other causes

STIGMATA OF VARICEAL BLEED ON UGI SCOPY spurt or ooze adherent clot white platelet nipple on varix no other causes

Indicators of bleeding -varices upon varices -cherry red spots - grade IV varices

Endoscopic grading of varices• Grade I –visible on valsalva manoure• Grade II –occupy < 25% of lumen• Grade III -25- 50 % • Grade IV - > 50%( obliterating lumen)

Gastric varices classification

1) Primary- present before est

2) Secondary- develop during or after E S T

Hosking”s classification

Type I OV extending across GE junction

Type II fundic varices which converge to cardia

Type III fundic varices or absence of OV

SARIN”S CLASSIFICATION

a) Gastro esophageal varices( GOV) Type I – most common type,continuation of

esophageal varices Type II – extend upto fundus b) Isolated gastric varices Type I – fundic Type II – isolated ectopic varices

Mathur’s Classification- Type I – lesser curve gastric varices Type II – FGV+EV a) subcardiac – respond to endoscopic

therapy b) diffuse fundal – often requires

surgery Type III – (isolated FGV) a) secondary to SV thrombosis b) part of generalised PHT Type IV – combination of LCGV+FGV+OV Type V – antral varices

RADIOLOGICAL INVESTIGATION1) USG -to establish diagnosis -to differentiate EHPVO from cirrhosis - extent thrombosis of PV, SV - direction if flow - patency of shunt in post shunt surgery

Portovenogrphy indicated only when surgical or radiological

intervention is required approaches –

spleenoportography arterioportogram

transjugular venography umbilical venography spiral CT angiography

MR angiography

MANAGEMENT OF PORTALHYPERTENSION

PHARMACO THERAPY-1) Splanchnic vasoconstriction

a) Betablockers- propranolol,nadolol,carvedilol

b)Vasopressin's- terlipressin,glypressin, ornipressin c)Hormones somatostatin,octriotide,vapreotide

2)Vasodilators -nitroglycerin - isosorbide-5-mononitrate - isosorbide di nitrates - alpha blockers – prazosin

3) Miscellaneous - metaclopramide - calcium channel blockers - angiotensin blockers-losartan

Indication for pharmacotherapy

1) control of acute variceal bleeding2) bleed from portal hypertensive gastropathy3) Primary prophylaxis & prevention of

recurrent of variceal bleed

ENDOSCOPIC THERAPY

1) ENDOSCOPIC SCLEROTHERAPY sodium morrhuate 5% ethanolamine oleate 5% sodium tetradecyl sulphate 1.5 %

polidocanol 1% cyanocrylate glue

absolute alcohol phenol 3% in water phenol 5% in oil

Mechanism of action- inflammation & secondary thrombosis, phenol causes primary

thrombosis

Site of injection

1) Intravariceal-2-3 ml2) Paravariceal – 1-2 ml3) Combined intra and Intravariceal

Schedule of injection - weekly or 3 weekly - in presence of EST ulcer deferred for a

week - follow-up endoscopy every 3 month for 1 year,

6 monthly in 2 nd year , then yearly

Complication of EST 1) Minor- retrosternal pain -fever - transient dysphagia - superficial ulcers 2) Major-oesophageal perforation - mediastinitis - septicemia - ARDS,pneumonitis - bleeding 3)Major(non fatal)-pleural effusion -stricture 4) Miscellaneous- PV thrombosis, splenic abscess - spinal cord paralysis, brain abscess - broncho oesophageal fistula

EVLAdvantages- effective - faster variceal obliteration - less rebleeding - fewer complicationDisadvantages- higher recurrence - not suitable for small varices - expensive

TIPSEfficacy-85-95%Reccurence-20-30%Hepatic encephalopathy-20-30% (refractory 10%)Stent revision-50%Stent migration, haemmorrhage, haemobilia, sepsis RHFNot effective in fundic varices

Indications for TIPS1) Failure of pharmacological, endoscopic

therapy2) Recurrent bleeding3) Refractory ascites4) Hepatorenal syndrome5) Budd Chiari syndrome

Contraindications to TIPS1) Long standing complete PV obstruction2) Right IJV obstruction3) Pre existing septicaemia4) Hypercoagulable state - It is the procedure of choice in patients poor

liver reserve with severe bleed

Surgical Intervention For Portal Hypertension

A. Emergency surgery for acute bleedingB. Elective surgery as primary therapeutic modalityC. Elective surgery as rescue therapy after failure

of endoscopic therapy

Emergency Surgery For Acute BleedingIndicationsa) Continuing or recurrent bleeding after 2

sessions of EST or EVLb) Significant rebleed -fresh blood in RT,

fall in Hb> 2 gm%, hypotension, BP<80mmHg,blood transfusion > 2 ltr

c) Failure of glue injection for fundic varices Procedure of choice in emergency is modified Suigara procedure – trans abdominal gastro – esophageal devascularisation with gastro esophageal stapling

Elective Surgery as Primary Therapy

I. Absolute indication – left sided portal hypertension, ectopic varices ,symptomatic hypersplenism , symptomatic massive splenomegaly , growth retardation, portal biliopathy

II. Relative indications - diffuse fundal gastric varices ( type IIb & III) , failure of glue injection during injection or recurrence after multiple sessions

Elective Surgery As Rescue Therapy

failure of chronic EST significant rebleed in defaulters

TYPES OF SURGERY

A. Decompressive procedure – portosystemic shunts

B. Non decompressive procedure – devascularisation

C. Liver transplantation

Porta Systemic ShuntsTOTA SHUNTS SELECTIVE SHUNTS PARTIAL SHUNTS

1) Porta caval – end to end, side to side

DSRS( Warren shunt ) Small diameter portacaval(Sarfeh shunt)

2) Central splenorenal – proximal , side to side

Coronocaval

3) Mesocaval – cavo mesenteric , mesocaval H graft

Spleenocaval

Porta caval shunts

A. End to side – choice of shunt surgery when medical management fails

B. Side to side – shunt of choice in Budd-Chiari syndrome ( controls ascites & portal hypertension)

Proximal splenorenal shunt(Linton) rebleed 10-19%Encephalopathy 15-19%Mortality 12-38%Not recommended for cirrhotic patients

MESOCAVAL SHUNTS

I. Interposition H graftII. Cavomesenteric shunt – Indication- ectopic varices Budd-Chiari syndrome when SV is not available or not suitable Advantage- Doesn’t interfere future liver transplant

Side to side Splenorenal Shunt Indications - small diameter splenic vein <7 mm - portal biliopathy & ectopic varices ( both GE junction & mesenteric site

to be decompressed)Prerequisite- SV & Renal should be adequately

mobilisedAdvantages – relieves hypersplenism decreases splenic size

Distal Splenorenal Shunt Distal end of splenic vein is anastamosed to

renal vein Decompresses via short gastric vessels Prerequisite- SV should be at least 1 cm Left gastric vein , right and left

gastroepiploic veins and retrogastric collaterals should be ligated .

Low risk of hepatic encephalopathy 0 – 10 %Five year survival is 85 – 90 %

Disadvantages- more complex shunt thrombosis not suitable when SV is thrombosed

(EHPVO) more distance b/w SV & RV early rebleed ContraindicationsIntractable ascitesMassive splenomegalyIn emergency

Corono-caval shunt(Inokuchi)• Left gastric vein is anastamosed to IVC

Partial Shunts(Sarfeh & Rypnis) small diameter graft b/w PV & IVC graft should be at least 50% of the diameter

of PVRebleed 3.3%Encephalopathy 8-16 %

NON SHUNT SURGERYSuiguira Futugawa procedurea) Devascularisation of lower esophagusb) Oesophageal transectionc) Devascularisation of upper half of lesser

curvatured) Splenectomye) Vagotomyf) Pyloroplasty

Advantages low mortality 5% recurrence rate 0.5% rebleed 1.5%Absence of encephalopathy

ComplicationsOesophageal leak 6%Oesophageal stricture 2%

Hassab’s modification extensive gastro-oesophageal

devascularisation with splenectomy without oesophageal transection

Mathur’s modification• Transabdominal approach• Devascularisation of the upper 2/3 rd of

stomach• Transhiatal devascularisation of lower 10 of

oesophagus• Vagus preservation• Pyloric dilation• Stapled oesophageal transection• Floppy Nissen fundoplication• No splenectomy• Splenic artery ligation for hypeersplenism

Complications1. Anastomotic leak2. Dysphagia3. Gastro-oesophageal reflux4. Recurrent haemorrhage5. Intraperitoneal sepsis

Advantages6. No prior PV anatomical investigation7. Easy8. Spleen is preserved

Contraindication1. Congestive gastropathy2. Ectopic varices3. Postsclerotherapy oesophageal ulcer

bleeding

Liver transplant

Reserved for patients with end stage liver disease

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