ascites ss

SURGICAL TREATMENT OF REFRACTORY ASCITES

BYPROF/ GOUDA ELLABBAN

S.C.U. HOSPITAL

• Poor prognostic sign in cirrhotic patients.

• 50% Of cirrhotics develop ascites within 10 years.

• 15% are refractory to standard medical therapy.

• 50% of ascitic patients succumb in 2 years.

Ascites

Ascites

• Most commonly a result of decompensated liver disease.

• Etiology of ascites can be classified on the basis of SAAG (Serum ascites albumin gradient calculated by serum albumin-ascitic albumin.

• Gradient≥ 1.1 indicate portal hypertension related cause

• High gradient≥ 1.1– cirrhosis– congestive heart failure– venoocclusive disease– Budd chiari syndrome– Portal vein thrombosis– Myxedema– Metastatic liver disease

• Low Gradient (<1.1)– Peritoneal

carcinomatosis– pancreatic ascites– Biliary ascites– Nephrotic syndrome– Chylous ascites– Serositis (connective

tissue diseases)– Infection (TB, fungal,

HIV, Whipples ds)

Systemic effects• Preascites stage

– Renal sodium handling is abnormal although no overt retention is noted

– Retention of sodium occurs as a homeostatic mechanism to compensate for increased capacity of splanchnic area

– An impaired ability to excrete free water is noted– Increased total body water relative to sodium

results in dilutional hyponatremia.

Renal function abnormalities• Sodium retention• water retention• renal hypoperfusion• factors responsible for renal dysfunction include

• Extrarenal factors– Renin angiotensin-

aldosterone system– Sympathetic nervous system– Endothelin– Atrial natriuretic peptide

• Intrarenal factors– Arachidonic acid– Nitrous oxide– Kallikrein-kinin system– Adenosine– Renin-angiotensin system

Theories of ascites formation

• Underfill theory• Overfill theory• Peripheral arterial vasodilation theory

Underfill theory

• Loss of intravascular volume secondary to sequestration of ascitic fluid was believed to be a primary event,

• Secondary activation of compensatory pathways such as renin angiotensin resulted in perpetuation of ascites.

• Not accepted as there is evidence indicating expanded plasma volume in cirrhosis

Overflow theory

• Explained ascites as a consequence of sodium and water retention which were considered primary events

Peripheral arterial vasodilation hypothesis

Portal hypertension

Splanchnic arterial vasodilation

Stimulation of Sympathetic nervous system, renin angiotensin and non-osmotic ADH

Sodium and water retention

Normalized effectivearterial blood volume

No ascites

Disease progression

Lack of normalization of EABV

Ascites

Hormonal mechanism

Splanchnic and peripheral vasodilation

Effective plasma volume ↓

Volume receptors ↑

Renin↑

Angiotensin II

Aldosterone

Sympathetic↑ Renal E2↓prostaglandin

Kallikreinkinin

system↓

Natriureticfactor

Increased tubular Na reabsorption

Treatment• Sodium restriction in diet• Diuretics: Potassium sparing, Loop diuretics• Water restriction if hyponatremia (<130meq/l)

occurs• Large volume paracentesis• Peritoneovenous shunts• Saphenoperitonal shunting• Transjugular intrahepatic portosystemic shunt

(TIPS)• Transplantation

Refractory ascites

• Prolonged history of ascites unresponsive to

400 mg of Spironolactone or 30 mg amiloride

plus up-to 120 mg of Furosemide daily for 2

wks

• Patients who can not tolerate diuretics.

Refractory ascitesComplications of medical therapy

•Peritonitis •Malnutrition•Hypovolaemia•Hyponatraemia•Electrolytes imbalance•Reduced renal blood flow•Renal failure

Refractory ascites

Treatment objectives:

• Improve nutritional & electrolyte balance.•Eliminate risk of SBP.•Relieve dyspnea.• Improve mobility.• Increase circulatory blood flow.• Increase renal blood flow & diuresis.•Reduce hospitalization.

Peritoneo-Venous Shunting

Begun in 1970’sTransfer ascitic fluid into

venous circulation

•Hyde Shunt•Holter Valve•LeVeen Shunt•Denver Shunt


Transfer Ascitic Fluid into Venous Circulation

Benefits of Shunting

• Increases blood volume• Retains nutrients & electrolytes• Increase renal blood flow• Increases diuresis • Weight loss & girth reduction


Additional benefits: Cirrhotic ascites*

Increases natriuretic response to diuretics.

Reduces activity of the renin & angiotensin.

Reduces sodium retention.


Wash The shunt with Heparinized Saline


Exposure of Internal Jugular VeinAbdominal IncisionCreation of Subcutaneous TunnelComplete Paracentesis

Partially replacement with SalineTight Peritoneal ClosurePlacement of Venous Catheter in SVCPurse string of IJVSpontaneous Shunt Function


Confirm Placement at Cavo-atrial JunctionMarking Valve Position

Peritoneo-Venous ShuntingPossible complications

Shunt occlusion

Infection

Disseminated intravascular coagulation

Fluid overload

SVC thrombosis

Conclusion

PV Shunting is a minor surgical procedure.Careful selection of patients is mandatory. Despite high rate of blockage (20%) :

EasySafeEffective

A therapeutic option for RA in decompensated cirrhotic patients.


TRANSJAGULAR INTRAHEPATIC

PORTOSYSTEMIC SHUNT (TIPS)

TIPS IN REFRACTORY ASCITESTransjugular portacaval shunt: TIPS

Effective on refractory ascites

More effective than paracentesis in control of ascites

More encephalopathy than paracentesis

Required the control of permeability of shunts

Same survival

Risk of liver failure in Child C patients

Well supported in patients with preserved liver

function.

Venous access through I.J.vein

Insertention of the sheath into the hepatic vein

Puncture of the portal vein

Advancement of the guide wire into the portal vein

Balloon dilatation of shunt tract

Placement of the stent

TIPS : COMPLICATIONS

• Complications related specifically to TIPS procedure.

• Complications related to puncture site.

• Complications related to portosystemic shunting.

• Complications related to transhepatic portal venous canulation and dilatation.

Gouda Ellabban 19/01/07

• Complications related to stenting and the stent.

• Complications related to infection.


Venography shows right hepatic vein

Portography of the portal vein

Balloon dilatation with constriction at the hepatic vein

Complete dilatation of the hepatic parenchyma

Deployment of the stent

TIPS

• Technically feasible

• Complications 9 - 50%

Infection Intraperitoneal Bleeding

Congestive Failure Subcapsular Hematoma

Acute Renal Failure Hemobilia

• Mortality (30 day) 3 - 13%

Saphenoperitoneal shunt (SPS) in the treatment of

refractory ascites


Saphenoperitoneal shunt (SPS)

• SPS plays a major role in the surgery of refractory ascites.

• It allows ascitic fluid to flow back into the circulation when the intra-abdominal pressure rises above venous pressure

• It avoids the insertion of foreign expensive shunt


• It is performed under local anethesiaexposure of long saphenous vein

• It is divided 15 cm distally.

• The proximal cut end of the long saphenous vein was tunneled under the skin towards the abdominal incision.

• Then it is anastomosied to the cut edges of the incision in the peritoneum with continuous suture


Saphenoperitoneal shunt is anindisputably elegant and easy type ofintractable ascites permanentdrainage.

SPS offers all the advantages of PVSshunting without using protheticmaterial. It is safe, effective andsuitable for the mangement ofintractable ascites.

LIVER

TRANSPLANTATION

History of Liver Transplantation

• 1st human liver transplant was performed in 1967

• Between 1967 and 1979 the survival rate was 33%

• By 1979, the use of Cyclosporin- steroid combination doubled the 1 year survival rate

Who needs a liver transplant?

• End-stage cirrhosis• Metabolic disorders• Fulminant hepatic

failure (viral or drug induced)

Organ Procurement

• Uniform Anatomical Gift Act (UAGA) requirements:

Brain Death

Familial consent

Recipient Contraindications

• Has evolved over the past several years• Now generally includes:

– Widespread malignancy– Uncontrolled infection– Severe cardiac/ neurologic disease– Inability to tolerate appropriate

immunosuppression

The Recipients are…..

VERY SICK PATIENTS

The CASE….• 3 surgical phases:

1. Recipient hepatectomy (orthotopic technique)

2. Anhepatic phase

3. Revascularization or Neohepatic Phase

Recipient HepatectomyMobilization of:

suprahepatic vena cava

infrahepatic vena cava

portal triad: portal vein, hepatic artery, bile duct

Extracorporeal Circulation

Veno- veno bypass is established: blood from the femoral and portal vein bypasses the liver via extracorporeal circulation and returns to the heart via RIJ (via CVL)

Anhepatic Phase and Revascularization

• New liver is sutured in place: suprahepatic vena cava, infrahepatic vena cava, portal vein

• Hepatic artery anastomosed just prior to revascularization

• After the hepatic artery anastomosis and reperfusion, the bile duct is connected

THANK YOU

ascites ss

Health & Medicine

etiology of ascites

high gradient

serum albuminascitic

ascitic patients

cirrhotic patients

prof gouda ellabban

poor prognostic sign

standard medical therapy