PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015 PORTAL HTN PHYSIOLOGY: Portal vein flow 900 --- 1200 ml/min. Hepatic arterial flow 500 --- 700 ml /min. Normal pressure 8---12 (( cmH2o))------ 5 –10 mmHg. Pressure = flow(( rarely due to increase flow AV fistula and splenomegally x resistance(( )). PORTAL HTN--- an increase in resting portal venous pressure > 12 mmHg. PORTAL HTN results from: A. Increased resistance to portal flow B. Increased portal flow measurement of hepatic venous pressure are useful for determining the site of resistance . The hepatic venous pressure gradient is the difference between the wedged hepatic venous pressure and free hepatic venous pressure. DEFINITION: Portal HTN is an increase in the blood pressure within the portal venous system . Normally the veins come from the stomach ,intestine ,spleen and pancrease ,merge into the portal veins. If the vessels in the liver are blocked ,it is hard for the blood to flow causing pressure in the portal system. When the pressure becomes too high ,the blood backs up and finds other ways to flow back to the heart ,where it is pumped to the lungs ,where it gets rid of waste products and picks up oxygen . The blood travel to the veins in the oesophagus ,in the skin of the abdomen , and the veins of the rectum to get around the blockages in the liver. It is Product of portal flow volume and resistance to out flow from the portal vein. The hydrostatic pressure is more than 5 mmHg , results initially from obstruction to portal venous out flow. WHAT IS THE CAUSE? The most common symptom is cirrhosis. PRE SINUOIDAL------ portal vein thrombosis Portal fibrosis Infiltrative lesions SINUSOIDAL -------------cirrhosis POST SINUSOIDAL ------ budd chiari syndrome Venoocclusive lesions In cirrhosis, 1.There is increased resistance to out flow through distorted hepatic sinusoids 2.Enhanced portal flow due to splanchnic arteriolar dilatation
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PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
PORTAL HTN
PHYSIOLOGY:
Portal vein flow 900 --- 1200 ml/min.
Hepatic arterial flow 500 --- 700 ml /min.
Normal pressure 8---12 (( cmH2o))------ 5 –10 mmHg.
Pressure = flow(( rarely due to increase flow AV fistula and splenomegally x resistance(( )).
PORTAL HTN--- an increase in resting portal venous pressure > 12 mmHg.
PORTAL HTN results from:
A. Increased resistance to portal flow
B. Increased portal flow
measurement of hepatic venous pressure are useful for determining the site of resistance . The
hepatic venous pressure gradient is the difference between the wedged hepatic venous pressure and
free hepatic venous pressure.
DEFINITION:
Portal HTN is an increase in the blood pressure within the portal venous system . Normally
the veins come from the stomach ,intestine ,spleen and pancrease ,merge into the portal
veins. If the vessels in the liver are blocked ,it is hard for the blood to flow causing pressure
in the portal system.
When the pressure becomes too high ,the blood backs up and finds other ways to flow
back to the heart ,where it is pumped to the lungs ,where it gets rid of waste products and
picks up oxygen .
The blood travel to the veins in the oesophagus ,in the skin of the abdomen , and the veins
of the rectum to get around the blockages in the liver.
It is Product of portal flow volume and resistance to out flow from the portal vein.
The hydrostatic pressure is more than 5 mmHg , results initially from obstruction to portal
venous out flow.
WHAT IS THE CAUSE?
The most common symptom is cirrhosis.
PRE SINUOIDAL------ portal vein thrombosis
Portal fibrosis
Infiltrative lesions
SINUSOIDAL -------------cirrhosis
POST SINUSOIDAL ------ budd chiari syndrome
Venoocclusive lesions
In cirrhosis,
1.There is increased resistance to out flow through distorted hepatic
sinusoids
2.Enhanced portal flow due to splanchnic arteriolar dilatation
PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
CAUSES OF PORTAL HTN: A.EXTRAHEPATIC OBSTRUCTION OF PORTAL VEIN AND ITS BRANCHES:---- 1. Postal vein thrombosis 2. Splenic vein thrombosis B. HEPATIC VENOUS OUTFLOW OBSTRUCTION:----- 1. Suprahepatic ----
i. Budd chiarri syndrome ii. Constrictive
iii. Right heart failure 2.Smaller hepatic vein and venules--- A. Veno-occlusive disease
i. Pyrrlizidine alkaloids ii. Radiation
iii. Anti leukemic drugs B. Sclerosing hyaline necrosis C. Hepatic causes: There may be presinusoidal and sinusoidal resistance to flow
If transplantation is contemplated ,abdominal surgery should be avoided.
Portacaval ---- end to end ,side to side Mesocaval Proximal splenorenal Distal splenorenal
PORTOCAVAL---portal vein is patent with good liver function.
It is very effective in lowering portal pressure.
Disadvantage ---high incidence of encephalopathy
MESOCAVAL---- used when portal vein is thrombosed.
PROXIMAL SOLENORENAL---less encephalopathy .It is less effective in preventing
further bleeding.
DISTAL SPLENORENAL ----SELECTIVE SHUNT
Right and left gastric vessels are ligated ,the distal splenic vein is jointed to renal
vein and short gastric veins are preserved.
Low incidence of encephalopathy , liver function remains normal
TRANSJUGUKAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
F. Splenectomy :
It is only effective in sectorial HTN (( LT side portal HTN)) that occurs after
pancreatitis leads to splenic vein thrombosis---fundal varices
THE MAJOR COMPLICATIONS OF VARICEAL BLEEDING: Which may lead to multiorgan failure and cause death
1. PNEUMONIA: Especially during endoscopy or placement of balloon tamponade tube Tracheal intubation should be used if patient comatosed. Pulse oximetry is mandatory ,even in absence of pneumonia As hypoxemia is common ,sepsis ,shock ,massive transfusion
3. Infection due to: Enteric organism causing septicemia Spontaneous bacterial peritonitis Cephalosporin I.V. is the antibiotic of choice. Nephrotoxic antibiotics should be avoided .
PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
As soon as infection is suspected ,it should be treated. 4. Water / electrolyte imbalance:
With ascitis and development of renal failure Saline solutions should be avoided. Aim ---maintain an adequate circulating volume & avoid volume overload. Ascites should be treated. Electrolyte abnormalities should be corrected.
5. Under nutrition: Nutrition should be strated as soon as possible within 24 hrs wether enteral or parenteral according to the renal function and bleeding.
REBLEEDING:
Rebleeding is the most frequent in 1st 6 weeks,accounting for 20—30% of deaths during
follow up. Patients who survived the first bleed from oesophageal varices are at significant
risk of recurrent haemorrhage: 70% of patients will experience recurrent haemorrhage and
about a third of further bleeding episodes are fatal.
Up to fifty percent of recurrent haemorrhage occurs within the first 6 weeks after the
index bleed.
The risk of re-bleeding is highest during the first five days, decreases slowly over the first 6
weeks, and becomes virtually equal to that before the index bleed after the sixth week.
Risk factors predictive of re-bleeding include the degree of hepatic decompensation, age greater than 60, severity of initial bleed, renal insufficiency, level of portal pressure, size of varices, active bleeding at the time of initial endoscopy and the presence of hepatoma.
All therapy decrease rebleeding and choice depends on:
1. Individual circumstances
2. Severity of liver disease
3. Feasibility of different methods of treatment
Portal systemic shunts decrease 10% + not proloning survival
Allowing unopposed α vasoconstriction of splanchanic arterioles.
Acts directly on collaterals feeding the varices.
Decrease portal pressure with increase intra hepatic resistance.
Appears that lowering the hepatic vein pressure gradient to < 80%.
Pretreatment values at 3 months reduce risk of rebleeding.
Decrease rebleeding 50% and lowers the mortality.
Portal hypotensive effect may be enhanced by isosorbide mononitrate.
affective to reduce bleeding and anemia in gastropathy.
In trials ,comparing scleropathy with B blockers ,((higher risk patients were
included)) ,there were no differences in survival /rebleeding rates.
No advantage occurred by combinig B blocker withsclerotherapy.
PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
CLINICAL POINTS: HVPG—hepatic venous pressure gradient should be reduced to 12mmHg or below to eliminate the risk of bleeding. 1ry prevention with B blocker show reduction in bleeding from varices and portal hypertensive gastropathy and decrease in mortality. B blocker should be given to patients with varices at risk. 1ry prevention with scleropathy /surgical shunts ,it have shown no overall benefit and increased mortality.
Prognosis in patients with esophageal varices Approximately 30% of patients with esophagieal varices will bleed within the first year after diagnosis. The mortality resulting from bleeding episodes depends on the severity of the underlying liver disease The mortality resulting from any bleeding episode may range from < 10% in well- compensated cirrhotic patients with Child–Pugh grade A to > 70% in those in the advanced Child–Pugh C cirrhotic stage. The risk of re-bleeding is high, reaching 80% within 1 year Patients with a hepatic venous pressure gradient > 20 mmHg within 24 h of variceal hemorrhage, in comparison with those with lower pressure, are at higher risk for recurrent bleeding within the first week of admission, or of failure to control bleeding (83% vs. 29%) and have a higher 1-year mortality rate (64% vs. 20%) Approximately 60% of untreated patients develop “late rebleeding '” within 1–2 years of the index hemorrhage
TIPS:
Transjugular intrahepatic portosystemic shunt:
This procure involving placing a stent in the middle of the liver. The stent connects the hepatic
vein with the portal vein.
PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
DSRS---distal splenorenal shunt:
WHAT TESTS ARE REQUIRED BEFORE THE TIPS AND DSRS PROCEDURES?
Before receiving either of these procures ,the following tests may be performaed to
determine the extent and severity of the condition.
1. Evaluation of the medical history
2. Physical examination
3. Blood tests
4. Angiogram
5. Ultrasound
6. Endoscopy
7. Chest x ray
8. ECG
9. Keep plasma ready for O.T.
WHAT HAPPENS IN TIPS?
A radiologist makes a tunnel through the liver with a needle ,connecting the portal vein to
one of the hepatic veins . A metal stent often covered with a thin plastic material ,is placed
in this tunnel to keep the tunnel open.
The procedure reroutes blood flow in the liver and reduces pressure in all abnormal veins
,not only in the stomach and oesophagus ,burt also in the bowel and the liver
This not surgery , The radiologist performs the procedure within the vessels under X –ray
guidance. This process lasts one to three hours ,but you should expect to stay in the
hospital over night after the procedure.
HOW SUCCESSFUL IS THE TIPS PROCEDURE?
It controls bleeding immediately in 90% of patients.
20% of cases develop rebleeding due to narrowing of the shunt
COMPLICATIONS OF TIPS:
1. Shunt narrowing /occlusion within the 1st year
Follow up UU examinations are performed frequently
The signs of occlusion include increased ascites and rebleeding.
Treatment ---by radiologist who re-expand the shunt with a ballon or
repeats the procedure to place a new stent
2. Encephalopathy ----can occur with sever liver disease
It can become worse when blood flow to the liver is reduced by TIPS which
may result in toxic substances reaching the brain without being metabolise
1st by the liver.
Treated by diet ,medications ,or occluding the shunt
PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD SASI 2015
WHAT HAPPENS IN THE DSRS PROCEDURE?
DSRS--- a surgical procedure during which the splenic vein is detached from
the portal vein and connected to the renal vein. .This selectively reduces
the pressure in the varices and control the bleeding. It is done only in
patients with good liver function.
HOW SUCCESSFUL IS THE DSRS SURGERY ?
It controls the bleeing in 90% of patients with the highest risk of rebleeding
occurring in the first month. It provides good long term control of bleeding.
COMPLICATIONS OF DSRS?
Ascites can occur.
FOLLOW UP:
10 days after hospital discharge , patient should follow hepatologist to
evaluate the progress .Lab work will be done at this time.
6 weeks after TIPS , 3 months ,USS should be to check the shunt.
Angiogram is done if USS indicates a problem.
6 weeks after DSRS ,3 months, USS should be done to check the shunt.
12 months after either procedures , USS to be done to check shunt.
If the shunt is working well every 6 months after the 1st year of follow up
appointements ,have an USS ,lab work and visit the doctor