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:

Causes of Portal Hypertension

Prehepatic:

  • Portal vein thrombosis
  • Splenic vein thrombosis
  • Cavernous transformation of the portal vein
  • Splenic arteriovenous fistula
  • Idiopathic tropical splenomegaly

Extrahepatic:

  • Hepatic veins thrombosis (Budd- Chiari disease)
  • Inflammatory/neoplastic infiltration 
  • Caval inferior occlusion (thrombosis, neoplasms)
  • Right ventricular failure
  • Constrictive pericarditis
  • Tricuspid regurgitation

Intrahepatic:

  • Presinusoidal:
    • Hepatic neoplasm
    • Schistosomiasis
    • Viral hepatitis
    • Infiltrative disease: tuberculosis, sarcoidosis, amyloidosis, haemochromatosis
  • Sinusoidal:
    • Cirrhosis: whatever the cause
    • Acute viral or alcoholic hepatitis
    • Fatty liver of pregnancy
  • Post-sinusoidal:
    • Veno-occlusive disease
    • Hyaline sclerosis of central veins

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.

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

References

Escorsell, Angels, Joan Carles García-Pagán, and Jaume Bosch. "Assessment of portal hypertension in humans." Clinics in liver disease 5.3 (2001): 575-589.

de Franchis, Roberto. "Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension." Journal of hepatology 53.4 (2010): 762-768.

A good description of the fluid thrill test can be found at the website of the University of California, San Diego.

Bar-Meir, Simon, Emanuel Lerner, and Harold O. Conn. "Analysis of ascitic fluid in cirrhosis." Digestive diseases and sciences 24.2 (1979): 136-144.

Boyer, Thomas D., Arthur M. Kahn, and Telfer B. Reynolds. "Diagnostic value of ascitic fluid lactic dehydrogenase, protein, and WBC levels." Archives of internal medicine 138.7 (1978): 1103-1105.

Runyon, Bruce A., John C. Hoefs, and Timothy R. Morgan. "Ascitic fluid analysis in malignancy‐related ascites." Hepatology 8.5 (1988): 1104-1109.

Peck-Radosavljevic, Markus, et al. "Austrian consensus on the definition and treatment of portal hypertension and its complications (Billroth II)." Wiener klinische Wochenschrift 125.7-8 (2013): 200-219.

Mirza, Muhammad S., and Guruprasad P. Aithal. "Causes of portal hypertension." Surgery (Oxford) 1.25 (2007): 28-33.

Cichoż-lach, H., et al. "Pathophysiology of portal hypertension." Journal of physiology and pharmacology 59.2 (2008): 231-238.

Petruff, C. A., and S. Chora. "Classification of portal hypertension." Handbook of liver disease. LS Friedman, LS Keeffe EB (eds). Philadelphia, Churchill Livingstone (2004): 264-265.

Menahem, Sasson, and Pesach Shvartzman. "Giant ovarian cyst mimicking ascites." Journal of Family Practice 39.5 (1994): 479-482.

Ronderos-Dumit, Daniel, et al. "Uterine-peritoneal amniotic fluid leakage: an unusual complication of intrauterine shunting." Obstetrics & Gynecology 78.5 (1991): 913-914.

Al-Mandeel, Hazem, and Abeer Qassem. "Urinary ascites secondary to delayed diagnosis of laparoscopic bladder injury." Journal of minimal access surgery 6.2 (2010): 50.

Develing, L., J. F. Hamming, and B. Speelberg. "[Chylous ascites following surgical repair of a ruptured abdominal aortic aneurysm]." Nederlands tijdschrift voor geneeskunde 147.31 (2003): 1513-1516.

Frank, Denis J., et al. "Traumatic rupture of the gallbladder with massive biliary ascites." JAMA 240.3 (1978): 252-253.

Cameron, JOHN L., et al. "Internal pancreatic fistulas: pancreatic ascites and pleural effusions." Annals of surgery 184.5 (1976): 587.