22.02.2017

1. Dr. Sadia Nazneen
22.02.2017, MALDA MEDICAL COLLEGE

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

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

4.  Normal 6-8mm Hg
 In cirrhosis >10mm Hg
 HVPG <12 mm Hg unlikely to develop
variceal bleeding.
 Useful for assessing medical
treatment.

6.  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

8. Portal inflow Systemic outflow Collaterals
Left gastric veins
Short gastric veins
Intercostal,
diaphragmatic and
oesophageal veins
Gastro-
oesophageal
varices
Superior
haemorrhoidal vein
Middle
haemorrhoidal vein
Inferior
haemorrhoidal vein
haemorrhoids
Left portal vein via
falciform ligament
Umbilicus and
abdominal wall
veins
Caput medusa
Liver via lienorenal
ligament
Left renal vein Retroperitoneal
collaterals

9. 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

11.  Splenomegaly
 Oesophageal varices
 Caput medusa.
 Haemorrhoids.
Complications :
 Ascites.
 Spontaneous bacterial peritonitis.
 End-stage renal disease.
 Hepatopulmonary syndrome.
 Encephalopathy

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

13. Assessment of liver function:
 Hypoalbuminaemia.
 ALT & AST are moderately raised.
 Prothrombin time and INR are disturbed.
Blood picture  anaemia, leucopenia,
thrombocytopenia or pancytopenia.

14. Assessment of portal circulation:
Duplex scan or Doppler ultrasound:
 To assess the hepatic artery, hepatic vein
and portal vein.
 Patency of portal vein.

15. Upper GI Endoscopy or
EGD
 To detect
gatroesophageal
varices
 Gold standard for
diagnosing variceal
bleeding

16. Diagnosis of the aetiology of liver disease is
performed by:
 (a) Immunological tests for hepatitis markers.
 Other specific serological markers are alpha foeto
protein, ceruloplasmin,alpha 1 antitrypsin,
antimitochondrial antibodies,and iron studies.
 (b) Liver biopsy.

17. CT ANGIOGRAPHY MR ANGIOGRAPHY

18. 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

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

20.  Prophylaxis – Pharmacotherapy and endoscopic
therapy
 Acute variceal bleeding
 Resuscitaion and pharmacotherapy
 Endoscopic therapy
 Decompressive shunts
 Devascularisation
 Liver transplantation
 Prevention of rebleeding
Level I evidence

21. Pharmacotherapy:
 Non-cardioselective beta blockers
 Endoscopic variceal ligation

23.  Admit patient in ICU
 Fluids and blood products judiciously administered
 Somatostatin or its analogues octreotide or terlipressin
administered 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

24. 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

25. Endoscopic Banding
Occludes venous
channels
Sessions <
sclerotherapy
Same results as
sclerotherapy
Endoscopic
treatment of
choice

28.  Transjugular intrahepatic portosystemic
shunt or (TIPS) is a procedure that involves
the creation of an artificial anastomosis
between 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.

29. Indications forTIPSS:
 Refractory bleeding
 Prior to transplant
 Child C
 Refractory ascites

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

31.  Classification:
Non-selective shunts:
 Total shunts:
Portacaval
Mesocaval
Proximal spleno-renal
 Partial shunts:
 Small diameter porta-caval (Sarfeh)
Selective shunts: Distal spleno renal shunt

32.  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 .

33.  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.

34. Indication:
 EHPVO.
Advantage:
 The incidence of
encephalopathy is less
than after porta caval
shunt.
Disadvantage:
 Less effective In
rebleeding.
 If the splenic vein is less
than 1 cm the anastmosis
is liable to thrombosis.

35. A small diameter
interposition
(8-10 mm) porta – caval
shunt.
Advantage:
 Partially decompress the
portal venous system.
 Hepatic portal flow is
preserved.
Drawback:
 Increasaed incidence of
thrombosis.
 Recurrence of bleeding.

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

37.  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.

39. Devascularisation:
Aim:
Direct disconnection
between the portal
and azygos vein done
by disconnecting the
varices from their
bleeding vessels.
Components:
Splenectomy
Gastric and
oesophageal
devascularisation
Oesophageal
transection

40. 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.

41. 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.

42.  Portal hypertensive gastropathy refers to changes in the
mucosa of the stomach in patients with portal
hypertension
 Most common cause of this is cirrhosis
of 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.

43.  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.

44.  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.

45. THANKYOU.