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Dr. Ashok Jaisingani
   The hepatic portal circulation carries blood from
    GI tract (i.e. from the distil esophagus to anorectal
    junction) to the liver.
   Porto – systemic anastomosis occurs in junctional
    areas of venous drainage.
   Portal venous blood drain into liver venous
    sinusoids and hence in to the hepatic veins.
   Portal hypertension develop when there is
    elevation of portal pressure is greater than 12
    mmHg, while normal portal pressure is 5 –
    10mmHg.
   As portal hypertension produce no symptoms it is
    usually diagnosed following presentation with
    decompensated        chronic      liver     disease
    encephalopathy, ascites or variceal bleeding.
 Pre – Hepatic:
  1- Congenital portal atresia
  2- Portal vein thrombosis (Neonatal sepsis)
  3- Phlebitis of portal vein (abdominal infection)
  4- Trauma or thrombosed porto – caval shunt.
 Hepatic:
  1- Cirrhosis (alcoholic most frequently)
  2- Chronic Active hepatitis
  3- Parasitic diseases (Schiatosomiasis)
 Post – Hepatic:
  1- Budd – Chiari syndrome (Hepatic venous thrombosis)
  2- Constrictive pericarditis
  3- Tricuspid valve incompetence
 Decrease or reverse portal blood flow to the liver promote
  the development of the portosystemic anastomosis
  between the portal system and systemic circulation.
  1- Left gastric vein into the esophageal veins at gastro-
  esophageal junction – esophageal and gastric varices.
  2- Superior rectal vein into inferior rectal vein at lower
  rectum rectal varices.
  3- Obliterated umbilical vein into epigastric vein – capute
  medusae.
 Esophageal and gastric varices may bleed torrentially
 Liver cell dysfunction/liver failure occurs in hepatic and
  post – hepatic causes
 Splenomegaly (hypersplenism may be result)
 The child – pug classification use to asses the severity.
Conditions           Point – 1   Point – 2   Point - 3

Bilirubin (µmol/L)   <34         34 – 51     >51

Albumin (g/L)        >35         28 – 35     <28

PT (sec)             <3          3 – 10      >10

Ascites              None        Moderate    Moderate – severe

Encephalopathy       None        Moderate    Moderate – severe
   Many investigations may be used at different time
    in portal hypertension such as
   1- FBC, Urea & electrolytes and clotting
   2- Screening tests for the causes of the cirrhosis
   3- CT & ultrasound scan to assess liver
    morphology, diagnose Portal hypertension and
    assess cause.
   4- Transabdominal Doppler ultrasound to assess
    blood flow in the portal vein and hepatic artery.
   Gastroscopy in acute variceal bleeding
 General resuscitation
 Anti – coagulation for Budd – Chiari syndrome
 Treatment of hepatic cause
 Treatment Of Chronic Complication such as Esophageal gastric
  varices:
 1- Beta – blocker (propranolol or nadolol), reduce portal venous
  pressure.
 2- Repeated injection sclerotherapy or variceal ligation
 3- Elective porto – systemic shunt (spleno – renal anastomosis)
 4- Liver transplant may be considered for treatment if associated with
  severe liver diseases.
 Rectal Varices: Injection sclerotherapy
 Symptomatic splenomegaly: laparoscopic or open splenectomy.
 Ascites: Oral spironolactone, in cases of ascites, paracentesis may be
  required with IV albumin replacement.
 Hemorrhage from the varices is acute
  complication of the portal hypertension.
 Mortality rate of first variceal bleed established
  portal hypertension is 30%.
  Causes & Features:
 Typical variceal bleeding is rapid in onset, copious
  dark blood with little mixing with food.
 Feature of established portal hypertension e.g.
  capute medusae
 Feature of developing hepatic encephalopathy
  (ingested blood provide an extremely rich meal)
   Established large caliber IV access, give crystalloid fluid up
    to 1000 mL, if tachycardic or hypotensive.
   Only use O - ve blood if the patient is in extremis,
    otherwise wait for cross – match blood.
   Catheterize and place on fluid balance chart if hypotensive.
   Send blood for FBC, HB conc. WCC, U&E, Na, K, LFT,
    albumin and clotting.
   Always consider HDU, variceal bleeding can deteriorate
    extremely rapidly.
   Monitor pulse rate, BP and urinary output.
   Insertion Of sangstaken Blackmore gastro-esophageal tube
    may be a life saving resuscitation manure, usually only
    inserted without prior gastroscopy if the patient known to
    have varices and has life – threatening bleeding.
   Blood transfusion
   Correct coagulopathy
   Esophageal      balloon     tamponade      (sangstaken
    Blackmore tube)
   Drug therapy (vasopressin or octreotide)
   Endoscopic sclerotherapy or banding
   Assess portal vein patency (Doppler ultrasound or CT)
   Transjuglar intrahepatic portosystemic stent shunt
    Surgery:
   Portosystemic shunts
   Esophageal transection
   Splenectomy and gastric devescularization.

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2 portal hypertension

  • 2. The hepatic portal circulation carries blood from GI tract (i.e. from the distil esophagus to anorectal junction) to the liver.  Porto – systemic anastomosis occurs in junctional areas of venous drainage.  Portal venous blood drain into liver venous sinusoids and hence in to the hepatic veins.
  • 3. Portal hypertension develop when there is elevation of portal pressure is greater than 12 mmHg, while normal portal pressure is 5 – 10mmHg.  As portal hypertension produce no symptoms it is usually diagnosed following presentation with decompensated chronic liver disease encephalopathy, ascites or variceal bleeding.
  • 4.  Pre – Hepatic: 1- Congenital portal atresia 2- Portal vein thrombosis (Neonatal sepsis) 3- Phlebitis of portal vein (abdominal infection) 4- Trauma or thrombosed porto – caval shunt.  Hepatic: 1- Cirrhosis (alcoholic most frequently) 2- Chronic Active hepatitis 3- Parasitic diseases (Schiatosomiasis)  Post – Hepatic: 1- Budd – Chiari syndrome (Hepatic venous thrombosis) 2- Constrictive pericarditis 3- Tricuspid valve incompetence
  • 5.  Decrease or reverse portal blood flow to the liver promote the development of the portosystemic anastomosis between the portal system and systemic circulation. 1- Left gastric vein into the esophageal veins at gastro- esophageal junction – esophageal and gastric varices. 2- Superior rectal vein into inferior rectal vein at lower rectum rectal varices. 3- Obliterated umbilical vein into epigastric vein – capute medusae.  Esophageal and gastric varices may bleed torrentially  Liver cell dysfunction/liver failure occurs in hepatic and post – hepatic causes  Splenomegaly (hypersplenism may be result)  The child – pug classification use to asses the severity.
  • 6. Conditions Point – 1 Point – 2 Point - 3 Bilirubin (µmol/L) <34 34 – 51 >51 Albumin (g/L) >35 28 – 35 <28 PT (sec) <3 3 – 10 >10 Ascites None Moderate Moderate – severe Encephalopathy None Moderate Moderate – severe
  • 7. Many investigations may be used at different time in portal hypertension such as  1- FBC, Urea & electrolytes and clotting  2- Screening tests for the causes of the cirrhosis  3- CT & ultrasound scan to assess liver morphology, diagnose Portal hypertension and assess cause.  4- Transabdominal Doppler ultrasound to assess blood flow in the portal vein and hepatic artery.  Gastroscopy in acute variceal bleeding
  • 8.  General resuscitation  Anti – coagulation for Budd – Chiari syndrome  Treatment of hepatic cause  Treatment Of Chronic Complication such as Esophageal gastric varices: 1- Beta – blocker (propranolol or nadolol), reduce portal venous pressure. 2- Repeated injection sclerotherapy or variceal ligation 3- Elective porto – systemic shunt (spleno – renal anastomosis) 4- Liver transplant may be considered for treatment if associated with severe liver diseases.  Rectal Varices: Injection sclerotherapy  Symptomatic splenomegaly: laparoscopic or open splenectomy.  Ascites: Oral spironolactone, in cases of ascites, paracentesis may be required with IV albumin replacement.
  • 9.  Hemorrhage from the varices is acute complication of the portal hypertension.  Mortality rate of first variceal bleed established portal hypertension is 30%. Causes & Features:  Typical variceal bleeding is rapid in onset, copious dark blood with little mixing with food.  Feature of established portal hypertension e.g. capute medusae  Feature of developing hepatic encephalopathy (ingested blood provide an extremely rich meal)
  • 10. Established large caliber IV access, give crystalloid fluid up to 1000 mL, if tachycardic or hypotensive.  Only use O - ve blood if the patient is in extremis, otherwise wait for cross – match blood.  Catheterize and place on fluid balance chart if hypotensive.  Send blood for FBC, HB conc. WCC, U&E, Na, K, LFT, albumin and clotting.  Always consider HDU, variceal bleeding can deteriorate extremely rapidly.  Monitor pulse rate, BP and urinary output.  Insertion Of sangstaken Blackmore gastro-esophageal tube may be a life saving resuscitation manure, usually only inserted without prior gastroscopy if the patient known to have varices and has life – threatening bleeding.
  • 11. Blood transfusion  Correct coagulopathy  Esophageal balloon tamponade (sangstaken Blackmore tube)  Drug therapy (vasopressin or octreotide)  Endoscopic sclerotherapy or banding  Assess portal vein patency (Doppler ultrasound or CT)  Transjuglar intrahepatic portosystemic stent shunt Surgery:  Portosystemic shunts  Esophageal transection  Splenectomy and gastric devescularization.