Portal hypertension and ascites

The college loves portal hypertension and ascites. They have asked about these conditions several times (though in the last six years or so it has been neglected). SAQs from past papers include the following:

• Question 5.1 from the second paper of 2010 (list four signs of portal hypertension)
• Question 12.2 from the second paper of 2010 (list four signs of portal hypertension)
• Question 7.3 from the second paper of 2008 (causes of a fluid thrill)
• Question 14 from the second paper of 2001 (information derived from ascitic fluid analysis)

Definition of portal hypertension

According to the Billroth-II guidelines, portal hypertension is defined as an increase in the hepatic venous pressure gradient of greater than 10 mmHg. This is the gradient between the IVC and the portal vein. The normal pressure is ~ 5mmHg; if it rises over 6mmHg portal hypertension is said to be present, and if it rises to over 10mmHg clinical features of portal hypertension can develop. At a hepatic venous pressure gradient in excess of 12mmHg, varices and other complications begin to form.

The  hepatic venous pressure gradient requires a WHVP (wedged hepatic venous pressure) measurement. It requires hepatic vein catheterisation, and you never end up measuring this variable unless you are performing a transjugular venous liver biopsy. The gradient is the difference between the wedged hepatic venous pressure and free (unwedged)  hepatic venous pressure. The wedged pressure approximates the portal venous pressure, in a similar sense as PAWP approximates LA pressure. If the gradient is greater than 10mmHg (i.e. the free hepatic venous pressure is 10mmHg lower than the portal pressure) then there is obviously some sort of obstruction to flow, which defines portal hypertension. One limitation of this technique is that it measures the pressure in the hepatic sinusoids, and so a pre-sinusoidal obstruction to flow (eg. portal vein thrombosis) may not be picked up.

Causes of portal hypertension

A good article by Cichoż-lach et al (2008) and an earlier work by Petruff et al (2004) were the sources for this classification:

Clinical features of portal hypertension

This is fairly straightforward.

• Ascites
• Caput medusae
• Hepatomegaly and splenomegaly
• Haemorrhoids
• Oesophageal varices (and thus haematemesis)

Major complications of portal hypertension include the following:

• Variceal haemorrhage
• Portal hypertensive gastropathy
• Spontaneus bacterial peritonitis
• Hepatorenal syndrome
• Hepatopulmonary syndrome
• Portopulmonary hypertension
• Hepatic hydrothorax
• Splenomegaly
• Hepatic encephalopathy

Conditions which mimic ascites

Question 7.3 from the second paper of 2008 asked about the potential reasons as to why a patient might have a positive  fluid thrill sign. Essentially, the fluid thrill is the transmission of a tap impulse from one side of a tense fluid filled abdomen to the other side. It can therefre only occur if the abdomen is tense and fluid filled. Few conditions can produce such a picture. These are listed below, where possible with links to case reports.

• Giant ovarian cyst (Menahem et al, 1994)
• Massive polyhydramnios (Ronderos-Dumit et al, 1991)
• Bladder rupture (Al-Mandeel et al, 2010)
• Peritoneal dialysis fluid
• Chyle leak post-operatively  (Develing et al, 2003)
• Rupture of gallbladder, "biliary ascites" (Frank et al, 1978)
• Massive pancreatic pseudocyst (Cameron et al, 1976)

Indications for paracentesis

• Diagnostic
  • Ascitic fluid analysis
  • Culture
• Therapeutic
  • Patient discomfort
  • Respiratory compromise due to raised intra-abdominal pressure
  • Abdominal compartment syndrome
  • Infected ascitic fluid (i.e. as source control)
  • Introduction of antibiotics into the ascitic fluid

Information that can be obtained from ascitic fluid analysis

• Appearance - turbidity would be very suspicious for SBP
• Albumin - to calculate serum/ascites albumin gradient
• Amylase/lipase - to consider pancreatitis as the cause of ascites
• LDH (low indicates hepatic cause, whereas >500 suggests malignancy)
• Gram stain - for bacteria
• India ink stain - for hyphae
• ZN stain for acid-fast bacilli (tuberculosis)
• Culture/sensitivities
• Flow cytometry and cell count - RBC/WCC ratio would raise suspicion of SBP
• Cytology - presence of malignant cells
• Alpha-foetoprotein - to investigate for HCC