TO THE SOUL OF MY DAD

1. 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

2. 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
1) Presinusoidal :
1. Schistosomiasis
2. Myeloproliferative
3. Primary biliary cirrhosis
4. Sarcoid
5. Arsenic ,Vinyl chloride
6. Firopolycystic disease
7. Ideopathic P.HTN
2) Sinusoidal:
1. Cirrhosis
2. Chronic active hepatitis
3. Partial nodular transfusion
D.Increased hepatic blood flow:
Tropical splenmegally
Hematological disease with massive splenomegally
Hepatorenal A/V fistula
PORTAL VEIN THROMBOSIS:
1. Abdominal sepsis—omphalitis ,pancreatitis, umbilical sepsis ,portal sepsis
2. Collagen vascular disease, inflammatory bowel disease
3. Cirrhosis ,retroperitoneal fibrosis
4. Hepatocellular carcinoma
5. Myeloproliferative syndromes ,PNH
6. Compression or invasion of portal vein by tumor
7. Sclerotherapy
8. Hypercoagulable--Factor V leide deficiency ,protein C deficiency
9. Pregnancy
10. Trauma
Liver cirrhosis is the cause of 80% of cases.

3. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
With presinusoidal P.HTN , due to blocked portal vein or narrowing of the smaller intrahepatic
portal vein branches, the WHVP is normal.
P.HTN in cirrhosis may be:
a. Sinusoidal (( high WHVP + HPVG ))
b. Pruning of portal vein branches
c. Narrowing of sinusoids due to :
 Hepatocyte enlargement
 Collagen deposition in the space of disse
 Distortion of intrahepatic vasculature by fibrosis / nodule formation
WHAT ARE THE SYMPTOMS OF PORTAL HTN?
The onset may not always be associated with specific symptoms .the main symptoms and
complications of PORTAL HTN include:
1. GIT bleeding----black tarry stools or blood in the stools ,hematemsis
2. Ascites
3. Encephalopathy ,confusion ,forgetfulness
4. Bleeding tendency----peteichea , ecchymosis
CLINICAL SIGNS:
 Signs may be related to the underlying cause or complication of P.HTN.
 The spleen is usually palpable ,may be very large in young patients with :
1. Extrahepatic portal block
2. Small ,shrunken livers
 Prominent abdominal wall veins are often found with P.HTN
 Veins radiating away from the umbilicus are a valuable sign as they indicate that
the block is distal to the main portal vein branches. They disappears if P.V.
thrombosed.
 With extrahepatic portal vein block ,there are no abdominal wall collaterals .
 Collaterals may occur at the site of surgical scar and indicate only a high portal
pressure.
 Prominent abdominal wall veins result on the side of an ileofemoral block ;or with
IVC obstruction " when they are bilateral and visible over the back".
 Budd chiarri syndrome----Hepatomegally ,Ascitis ,Signs of IVC obstruction
The sudden development of umbilical collaterals in patients with cirrhosis suggests
an acute hepatic vein block ; inferior vena caval collaterals suggest a blocked cava.
A venous hum ;loudest during inspiration ; Heard over large upper abdominal
collaterals (( Cruveilheir --Baumarten syndrome )). There may be accompanying
thrill
HOW IS PORTAL HTN TREATED?
Most causes can't be treated. Treatment focuses on preventing or managing
complications especially bleeding from the varices.

4. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
RICESVA
od to systemicolHTN portal vein and return bseen to decompress the-----VARICES
circulation.
Varices in the oesophagus tend to develop in cirrhosis when HPVG rises> 12 mmHg.
They are seen when the pressure gradient B/W portal veins and hepatic veins > 12mmHg.

5. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
The portal –hepatic venous pressure gradient is obtained by hepatic venous
catheterization and with measurement of the difference between the wedged
hepatic venous pressure (( which approximates the sinusoidal and portal pressures
in cirrhosis and the free hepatic venous pressure)).
Oesophageal varices----important collateral in P. HTN
90% Oesophagus ,10% gastric area
Oesophageal varices are dilatation of normal submucosal oesophageal veins which
extend 10—15cm below gastroes-ophageal junction.
Bleeding can be slow oozing or sudden sever.
Bleeding occurs nearly always from the lower 5cm of the oesophagus.
CLINICAL PRESENTATION:
 Hematemsis
 Melena
 Hematochezia
 Upper GIT bleeding can be:
1. Bleeding varices.
2. Portal hypertensive gastropathy.
The severity depends on the amount and rapidity of blood loss.
CONSEQUENCES OF PORTAL HTN:
Increased P.V.P----distends the veins proximal to the block and spleen enlarges
Capillary pressure raises in the organs drained by the obstructed V.

6. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Fluid exudation and lymph flow both increase.
Small anastomoses connecting the portal and systemic circulation may enlarge (( often
markedly )) because of the increased portal pressure and allow portal blood to pass
directly into the systemic circulation.
Patients with cirrhosis tend to have a high cardiac output ,and increased splanchanic blood
flow may maintain an elevated portal HTN despite the development of large anastomoses.
There are three main types of anastomosis:
1. Gastro –oesophageal junction:
Veins at the oesophagogastric junction shunt blood from the left gastric and short
gastric veins into the inferior oesophageal plexus and onto the superior vena cava
via the azygous system.
Varices are dilated(( submucosal veins projecting into the lumen of oesophagus
and stomach)).
2. Venous channels from retroperitoneal visera may communicate directly with
systemic veins on the posterior abdominal wall.
3. The obliterated umbilical vein and paraumbilical veins may open up, allowing
blood to pass from the left branch of the portal vein to the umbilicus and thence
into abdominal –wall veins.
Anterior abdominal wall collaterals also occurs where adhesions exists between
abdominal viscera and parietal peritoneum or at ileostomy or colostomy site.
Localized varices in colon may be related to previous operation.
When hepatic veins are occlude "budd chiarri syndrome" ;collaterals open up
within the liver ; blood tends to be diverted through the caudate lobe whose short
hepatic veins drain directly into the inferior vena cava.
A varix explodes as a result of:
1. Increased pressure
2. Increased size
3. Thinning of its wall
Sites of bleeding:
1. Oesophageal varices
2. Gastric varices
3. Portal HTN gastropathy
4. Sclero-therapy ulcer
5. Peptic ulcer
6. Oesophageal erosions
7. Gastric erosions
May be more sever because of high IVP.
Seen in Alcoholics and NSAIDS ingestion.
8. Rectal varices

7. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
IS THERE A RISK FACTORS FOR BLEEDING VARICES?
1.LOCATION OF VARICES:
Distal oesophagus ,stomach ,rectum
Gastroesophageal junction have the thinnest coat of supporting tissue.
It is most likely to rupture and bleed.
The varices in the gastric fundus bleed frequently.
Gastric varices are classified according to their location.
A. Varices in different continuity with esophagus along the lesser and greater curves of the
stomach ((gastroesophageal varices --GOV)) type 1 & 2
B. Isolated gastric varices in the fundus occur less frequently than GOV (( 10% Vx 90%))
Bleeding from isolated gastric varices in the fundus occurred much more frequently than others.
RISK FACTORS FOR RECURRENT VARICEAL BLEEDING
2.SIZE OF VARICES:
Small increase in the vessel radius result in large increase in wall tension.
F1 small straight varices
F2 enlarged tortuous varices that occupy < 1/3 of lumen
F3 large coil –shaped varices that occupy > 1/3 of lumen
Causes of hematemsis:
1. Peptic ulcer disease
2. Erosive gastritis due to hypergastrinemia , alcohol intake
Hypergastrinemia occurs due to defective metabolism by cirrhotic liver.
REBLEEDING > 6 WEEKS(LATE)REBLEEDING < 6 WEEKS(EARLY)ITEM
noyesAge >60 year
noyesSeverity if initial bleed
Anemia / blood pr low
noyesRenal failure
yesyesSeverity of hepatic failure
yesyesascites
yesnothepatoma
yesnoalcoholism
noyesActive bleeding on endoscopy
yesyesIncreased varices size
Not knownyesRed signs
Not knownyesPlatelet clot on varix
nounclearPortal pressure

8. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
3.APPEARANCE OF VARICES:
 Red wale marks
 Cherry red spots
 Hematocystic spots
 Diffuse erythema
4.CLINICAL FEATURES:
 Degree of liver dysfunction
 H/O previous variceal bleed
5.VARICEAL PRESSURE:
By endoscopic gauge
013 mmHg≥
9%13 ----14
17%>14---- <15
50%>15----<16
72%>16
MANAGEMENT:
Investigation-----
CBP , coagulation profile , RFT ,electrolytes ,BUN ,LFT ,blood group ,Cx matching
When portal HTN is suspected ,endoscopy should be done to look for
oesophageal and gastric varices.
Increased risk of bleeding:
1) Large varices---5 mm in diameter
2) Blue varices
3) Have red wheals
 P.HTN gastropathy causes chronic anemia or frank bleeding .
 Red spots similar to petechiae , particularly over antrum and fundus.
 Diagnostic endoscopy is mandatory as identification of the source of
bleeding and directly influence therapy.
 If it is delayed for 24 hours, it may be impossible to identify the source
of bleeding.
 Early endoscopy always identify source of bleeding after few hours.
Delirium tremens ----------------------------------controlled by Chloromethiazole

9. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Bleeding varices------ definitive if there is :
A. A venous { non pulsatile spurt } ; A venous ooze a varix
B. A white fibrin –platelet plug on the varix
C. Adherent blood clot ---rare
In cirrhotic patients ,there is gastric varices 10% and non variceal source 30%.
The major detrminent of subsequent mortality depends on:
A. The severity of bleeding
B. Pugh childs grading
A 10% B 25% C 50%
In patient with splenomegally or prominent abdominal wall veins ,but no varices ,P.HTN
can be confirmed by direct measurement of portal pressure by
1. Splenic puncture
2. Transhepatic cannulation of portal vein branch
Liver biopsy helpful but can be normal in:
A. Ideopathic portal HTN
B. Extrahepatic portal venous obstruction
Portography -----to detect the site of block to portal flow
Abdominal uss and CTscan
Doppler USS give information about the direction of flow.

10. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Catheterization of hepatic vein with venography.
You should asses RFT , evidence of infection –CXR ,U C/S , BLOOD CULTURE
INVESTIGATIONS:
CBC
LFT
USS ABDOMEN –asctes, splenomegally ,liver cirrhosis
Detection of oesophgeal varices:
Fibroptic endoscopy
Barium swallow
Duplex scan
Liver biopsy/ hepatitis marker
Portal venography (( prior to surgery ))
CLIP SCORING SYSTEM:
Child –Pugh stage Score
A 0
B 1
C 2
Tumor morphology :
Uninodular with extention ≤ 50% 0
Multinodular with extention ≤ 50% 1
Massive or extention > 50% 2
Alpha feto protein:
<400 0
≥400 1
Portal vein thrombosis;
NO 0
YES 1
TREATMENT :
1. Ensure clear airway
2. I.V. line ---central or peripheral (( large bore venous canula )).
3. Replacement of loss –Blood cross matching
After restoring the systolic pressure to 80—90 mmHg ;Packed cells should be given to
maintain HB 10 g/dl and the urine output 40ml/hr or more.
Monitor CVP ---I.V.ringer lactate
Fresh frozen plasma given to maintain and correct the effect of large transfusion of stored
blood .
Fresh frozen plasma If P.T. prolonged or platelet count < 50000/ml

11. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Platelet transfusion if massive transfusion or thrombocytopenia
VIT K 10 mg should be given.
4. Lactulose and mg sulphate to decrease encephalopathy
5. Na containing fluid should be avoided
6. Insert Foleys catheter
7. Arrest the haemorrhage:
A. Black moor stengstaken tube---gastric and oesophageal ballon
Balloon tamponade
If the patient uncooperative or comatosed ,intubation is the solution.
Bleeding is controlled in 90% of cases.
If the bleeding is continuing ,the cause is:
a. Incorrect placement
b. Presence of coagulopathy
c. Wrong diagnosis about source of bleeding
It should not be maintained for more than 12 hours
Temporary measures is done until definitive therapy planned.
1. Linton tube(( gastric balloon ---alternative ))
Aspiration of gastric and oesophageal content
Inflation of gastric then oesophageal balloon
Not more than 24 hrs
2. VASOACTIVE DRUGS—splanchnic arteriolar vasoconstrictors
A. VASPRESSIN :
20U in 200ml fluid over 20 min---0.2 -0.4U/min for 24-48hr
C/I--- coronary artery vasospasm ,so give glyceryl nitrate" infusion or patch "
Systolic pressure should be maintained at 100mmHg or more.
Morphin is contraindicated.
Once is hemostasis stabilized ,urgent endoscopy is done with sclerotherapy
(( ethanolamine oleate)) injected into varices.
B. Glypressin 2mg/6hr/24---48hr
C. Somatostatin 250 microgm/hr for 2 ---5 days
D. Octeotide 5o microgm /hr for 2 –5 days
They don’t alter hospital mortality.
3. Operation :
Emergency operation is avoided because of higher mortality but if sclerotherapy is
failed ,there is no alternative.
Types:
Devascularization or transaction
Portosystemic shunting
4. General measures to:
A. Encephalopathy ----neomycin ,lactulose ,mg sulphate
B. Correction of clotting defect ---VIT K injection& prevention of rebleeding
C. Endoscopic therapy:
5% Ethanolamine ,1% polidocanal
Sclerotherapy is the mainstay of acute management of bleeding varices.
Oesophageal ---- inject into the varix or along side it.
Gastric -tissue adhesive(( Bucrylate)) , polymerizes in contact with bloodRepeated
sclerotherapy with regular check.
Single session of sclerotherapy 65% affective
Two session of sclerotherapy 85% affective

12. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
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No more than two sclerotherapy sessions should be used in 5 days.
This is to minimize oesophageal complications.
1. Mediastinitis
2. Deep oesophageal ulceration
3. Oesophageal stenosis
D. Devascularization and transection operation
A surgical procure that removes the bleeding varices. .This procedure done when a
TIPS or surgical shunt is no possible or is unsuccessful in controlling the bleeding.
Upper 1/3 of stomach and lower part of oesophagus are devascularized.
Gastroeosophageal junction is transected and reanastomosis by ((stapling gun)).
E. Portosystemic shunt
TIPS ---transjugular intrahepatic portosystemic stent shunt
To achive shunting with out surgery.
It is very affective.
It has higher thrombosis rate within 12 hours.
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
2. Hepatic encephalopathy:
Lactulose
Twicw daily cleaning enema
3. Infection due to:
Enteric organism causing septicemia
Spontaneous bacterial peritonitis
Cephalosporin I.V. is the antibiotic of choice.
Nephrotoxic antibiotics should be avoided .

13. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
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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
Repeated sclerotherapy decrease 50% + reduce mortality
Drug therapy ----more convinent and cheaper
B—BLOCKER
 Decrease cardiac output ----decrease variceal flow
 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.

14. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
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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.

15. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
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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

16. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
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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