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Portal Hypertension

The normal pressure in portal vein is 2-5 mmHg or 10-15 cm saline.Q 

Portal hypertension is defined as portal pressure > 10mmHg or 30 cm saline.Q 

Table 308-3 Classification of Portal Hypertension (Ref. Hari. 18th ed., Pg-2598)
  1. Prehepatic
    1. Portal vein thrombosis
    2. Splenic vein thrombosis
    3. Massive splenomegaly (Banti's syndrome)
  2. Hepatic
    1. Presinusoidal
      1. Schistosomiasis
      2. Congenital hepatic fibrosis
    2. Sinusoidal
      1. Cirrhosis
      2. Alcoholic hepatitis
    3. Postsinusoidal
      1. Hepatic sinusoidal obstruction (venoocclusive syndrome)
  3. Posthepatic
    1. Budd-Chiari syndrome
    2. Inferior vena caval webs
    3. Cardiac causes
      1. Restrictive cardiomyopathy
      2. Constrictive pericarditis
      3. Severe congestive heart failure


Extra Edge

  1. The most common cause of portal hypertension is cirrhosis followed by portal vein obstruction.
  2. PHT is present is 70% cases of cirrhosis of liver
  3. Cirrhosis is present in 90% cases of PHT

Table 308-2 Complications of Cirrhosis (Ref. Hari. 18th ed., Pg - 2597)

  1. Portal hypertension
    1. Gastroesophageal varices
    2. Portal hypertensive gastropathy
    3. Splenomegaly, hypersplenism
    4. Ascites
    5. Spontaneous bacterial peritonitis
  2. Hepatorenal syndrome
    1. Type 1
    2. Type 2
  3. Hepatic encephalopathy
  4. Hepatopulmonary syndrome
  5. Portopulmonary hypertension
  6. Malnutrition
  7. Coagulopathy
    1. Factor deficiency
    2. Fibrinolysis
    3. Thrombocytopenia
  8. Bone disease
    1. Osteopenia
    2. Osteoporosis
    3. Osteomalacia
  9. Hematologic abnormalities
    1. Anemia
    2. Hemolysis
    3. Thrombocytopenia
    4. Neutropenia

Clinical features: The clinical manifestation of portal hypertension include:
  1. Hemorrhage from gastroesophageal varices.
  2. Splenomegaly with hypersplenism
  3. Ascites
1. Upper GI Bleeding
Normally 80% blood to liver is from portal V and 20% by hepatic artery But in cirrhosis major blood supply to liver is by hepatic A

The major sites of collateral involve:
  1. Esophago gastric varicesQ – Left gastric vein and short gastric vein join Q with esophageal vein of caval system.
  2. Hemorrhoids – superior hemorrhoidal vein of portal system to middle and inferior hemorrhoidal vein of the caval system.
  3. Caput medusae – remnants of the umbilical circulation of fetus present in the falciform ligament.
  4. Retroperitoneal space.
  5. Bare area of liver

Extra Edge


Common Causes of hematemesis

  1. Acute gastritis (M/C cause)
  2. Peptic ulcer
  3. Portal hypertension
  4. Mallory’s Weiss syndrome
  5. Stomach cancer.


  1. Fibro-optic esophagoscopy – shows the presence of esophageal varices.
  2. Measurement of portal venous pressure by either percutaneous transhepatic skinny needle catheterization or through transjugular cannulation of the hepatic veins. Wedged hepatic venous pressure is high in sinusoidal and post sinusoidal portal hypertension.
  3. USG abdomenQ – features of portal hypertension such as splenomegaly, collaterals, or portal vein thrombosis can be detected. The size of portal vein can be measured. Normal size is 10 mm.
  4. Portal venogramQ – site and cause of portal venous obstruction can be detected.
Rockall score system:
Rockall risk scoring system is to identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding.

Rockall score in based on
  1. Age
  2. Presence or absence of shock
  3. Comorbidity

Acute bleeding
Patient may have low BP due to hypovolemia than 1st step in the management is to raised the BP. (Hemodynamic stability)

Blood Transfusion should be done to raise the BP (blood for blood)!!!

Treatment to stop acute bleeding
  1. Sclerotherapy
  2. engstaken tube
  3. Octreotide
  4. Vasopressin
  5. Terlipressin
Sclerosing agent
  1. Polidocanol
  2. N butyl – cyanoacrylate (glue injection)
  3. Absolute alcohol/phenol
  4. Ethanolamine maleate
  5. Na tetradecyl SO4

Extra Edge Acetic acid is not use as a sclerosing agent.


  1. B – adrenergic blockers with propranolol or nadolol Q (these are prophylactic drugsQ, not useful in acute bleeding)
  2. They reduce portal pressure through vasodilatory effects on both the splanchnic arterial bed and the portal venous system in combination with reduced cardiac output.
Decompression through portal systemic shunts – trans jugular intrahepatic porto systemic shunt (TIPS).

2. Ascites (Ref. Hari. 18th ed., Pg - 2599)

Patho physiology of ascites:
  1. Decrease albumin  
  2. Increase aldosterone
    1. Due to decrease Renal Blood Flow
    2. Reduce aldosterone metabolism.

Extra Edge


Ascites is the accumulation of excess fluid within the peritoneal cavity. 

  1. The accumulation of ascitic fluid represents a state of total body sodium and water excess.
  2. Therefore dietary salt restriction is the cornerstone of therapy.
  3. Abdominal ultrasound may detect as little as 100 ml of ascitic fluid ultrasound is thus a useful investigation for the diagnosis of minimal ascitis.
  4. Hemorrhagic ascites is diagnosed when RBC count > 10,000 / mm3
    An RBC count of 10,000 / mm3 is the threshold for pink appearance and hemorrhagic ascitis is thus diagnosed when ascitic RBC count is > 10,000 / mm3

Management of Ascites
  1. The first line treatment of ascitis is dietary salt & water restriction.
  2. Diuretic therapy:
    1. Spironolactone., Eplerenone (new aldosterone receptor blocking drug)
    2. Loop diuretics
  3. Paracentesis:
    1. For diagnosis (new onset ascites; suspicion of malignant ascites or spontaneous bacterial peritonitis).
    2. Therapeutic manoeuver (when tense ascites causes significant discomfort or respiratory compromise).
  4. TIPS - Transjugular intrahepatic portosystemic shunts
    Shunts (TIPS) may be used in cases of refractory ascitis in whom recurrent paracentesis is too frequent or poorly tolerated.
Remember this about Ascites
  1. Ascites → Collection of >25 ml of peritoneal fluid
  2. Shifting dullness → Can be demonstrated when ascitic fluid > 500 ml
  3. Ultrasound → Can detect ascitic fluid up to 100 ml.

Extra Edge:


Causes of Chylous Ascites Causes of Mucinous Ascitis
1. Trauma
2. Tumor
3. Tuberculosis
4. Filariasis
5. Congenital anomalies
6. Nephrotic syndrome
1. Pseudomyxoma peritonei
2. Colloid carcinoma stomach with peritoneal implants
3. Colloid carcinoma colon with peritoneal implants
3. Spontaneous or Primary Bacterial Peritonitis (SBP) (Ref. Hari. 18th ed., Pg - 2601)
  1. Peritonitis without an apparent source of infection is k/a SBP.
  2. SBP occurs most commonly in conjunction with cirrhosis of the liver. 
  3. SBP virtually develops in all patients of ascites. 
  4. In a patient in whom a diseased liver and altered portal circulation results in a defect in the usual filtration function.
  5. Fever & Rebound Tenderness are the features.
Microbiology of SBP
  1. Most common organism is E. coli (enteric gram negative bacilli).
  2. Gram positive organisms such as streptococci, enterococci or even pneumococci can be implicated.
Diagnostic criteria of spontaneous bacterial peritonitis
The finding of > 250 PMNs per ml is diagnostic for spontaneous bacterial peritonitis. (Ref. Hari. 18th ed., Pg- 2601)
Treatment of SBP
  1. Third generation cephalosporins cefotaxime
  2. Broad spectrum antibiotics such as penicillin/B lactamase inhibitor or ceftriaxone
  3. Large volume paracentesis should not be done. 
  1. SBP has a high rate of recurrence. Up to 70% of patients experience a recurrence within I year.
  2. Antibiotic prophylaxis reduces the rate of recurrence to < 20%.
  3. Drugs used for prophylaxis are
    1. Ciprofloxacin
    2. Norfloxacin
    3. Trimethoprim sulfamethoxazole.
4. Splenomegaly:
It is the most constant finding is PHT 
In portal hypertension there is massive splenomegaly. At times it may cause hypersplenism which can cause pancytopenia. Other causes of massive splenomegaly are
  1. Chronic malaria
  2. Chronic kala azar
  3. Myelo proliferative disorder
  4. Hairy cell leukemia
  5. Glycogenic storage disease (Gaucher disease)
5. Hepatorenal Syndrome (Ref. Hari. 18th ed., Pg - 2601)
  1. It is a progressive functional renal failure occurring in patients with severe liver disease in the absence of identifiable specific causes of renal dysfunction. 
  2. It is a functional failure i.e. kidney are not functioning is that patient but if they are transplanted in other patient of CRF, they function well!!!.
  3. Pathophysiology: Intense renal vasoconstriction with systemic vasodilatation.
Clinical features:
Worsening azotemia, hyponatremia, progressive oliguria and hypotension are the hallmark of the hepatorenal syndrome. 
Diagnostic criteria for hepato renal syndrome.
  1. Increase in S. creatinine >1.5 or GFR < 40 ml/min
  2. No other cause of renal failure – Shock, Hypotension, nephrotoxic drug.
  3. Proteinuria <500 mg/day & no USG finding suggestive of CKD / obstructive uropathy
  4. No improvement in S. cr/GFR after giving 1.5 liter saline or after withdrawal of diuretic
  1. Urine volume <500 ml/day
  2. Urine sodium <10 meq/lit
  3. S. sodium <130 meq/lit
  4. Urine RBC < 50/HPF
  5. Urine osmolality > plasma osmolality
Diagnosis – All major criteria must be present for diagnosis of HRS. Minor criteria are not necessary for diagnosis but provide supportive evidence.
Treatment: Liver transplantation. (LQ 2012)
6. Hepato Pulmonary Syndrome
  1. It is clinically characterized by triad of exertional dyspnea, platypnea, clubbing and cyanosis. There is orthodeoxia – decrease in PaO2 > 3mmHg when patient move from supine to standing position.Q It is characteristic of hepato pulmonary syndrome. 
  2. The Gold standard for diagnosis is detection of right to left intrapulmonary shunts through dilatations in intrapulmonary vessels by contrast enhanced echocardiography Q or by macro aggregated albumin lung Q perfusion scan.
  3. Treatment – large arterio venous shunts can be embolized.
    1. Liver dysfunctionQ
    2. HypoxemiaQ
    3. Intrapulmonary vascular Q dilatation.
Definitions of orthodeoxia:
Fall in arterial blood oxygen on assuming the upright posture. Usually caused by right-to-left cardiac or vascular shunting with a posturally induced fall in left-sided pressure permitting a corresponding gradient across the shunt.

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