Assessment of Portal Hypertension: Understanding Will Improve Treatment

Abstract

To many people it may be disappointing that many uncertainties remain with respect to the assessment of PHT. Only a few findings such as increased WHVPG and varices prove PHT. However, we have gained considerable knowledge. PHT is the consequence of a number of changes which involve the intrahepatic and extrahepatic circulation. Alcohol, viruses and drugs may disturb parenchymal architecture and cause cellular swelling, collagen and fibrin deposition and invasion with inflammatory cells. These processes finally may evolve into cirrhosis. Although in initial stages the parenchymal disturbance per se may account for PHT, increasingly impaired liver function results in metabolic changes which cause altered haemodynamics. Advanced PHT in parenchymal liver disease is the result of the complex interaction between local and systemic changes. The current techniques for the assessment of PHT are helpful for the qualitative aspects: increase in pressure can be assessed directly or indirectly; the portal venous system can be visualized even without arteriography. Gastroscopy remains a standard procedure for diagnosing PHT. Ultrasound-endoscopy is particularly helpful to confirm fundic varices and to assess changes after sclerotherapy. Increasingly, non-invasive methods to quantify PHT have become available such as the Duplex scanner. However, limitations and pitfalls need to be realized. The quantitative assessment remains (as yet?) a technique for research centres. It is obvious that the clinician in general practice can do without most of the more sophisticated techniques which have been discussed here. For the time being, PHT, and particularly variceal bleeding, is most often treated with endoscopic sclerotherapy. For that reason, only in a minority of the cases very detailed studies are required. However, the increasing knowledge opens new perspectives for the treatment and prevention of PHT on various levels. This may be a rather specific treatment of parenchymal liver disease (antivirals, d-penicillamine for Wilson's disease or venesections for haemochromatosis), drugs which may reduce local tissue damage via more general pathways (colchicine, steroids) and drugs which influence flow. Undoubtedly one of these years a more selective blocker of portal venous pressure will become available. Optimal assessment for that type of therapy makes it mandatory to master at least a few more advanced techniques. With respect to noncirrhotic PHT with causes which may vary from congenital or acquired clotting abnormalities to anatomical malformations (oesophageal web) and 'natural healthy herb tea', measures can be taken. It is clear that before treating any of the more rare causes, a proper diagnostic work-up is required.(ABSTRACT TRUNCATED AT 400 WORDS)