Age dependency of regional impedance indices regardless of clinical stage in patients with cirrhosis of the liver.

PURPOSE: To prospectively assess if ageing itself induces modifications of the impedance indices (resistance and pulsatility indexes) of hepatic, splenic, superior mesenteric and renal arteries in patients with liver cirrhosis. MATERIALS AND METHODS: 78 consecutive patients with cirrhosis (41 males, 37 females, Child-Pugh score 7 [range 5 - 12]) were studied by colour-Doppler ultrasound. The resistance index (RI) and pulsatility index (PI) were determined in the main hepatic artery, intraparenchymal branches of hepatic, splenic, and renal arteries, and superior mesenteric artery; clinical data were simultaneously collected. Logistic regression analysis was performed to assess the relative impact of age, severity of liver disease and other relevant variables on the increase of impedance indices. Linear regression analysis was used to identify a coefficient to adjust RIs and PIs to age. RESULTS: Resistance and pulsatility indices of all the vessels studied except of the superior mesenteric artery showed a direct correlation with age (e. g. splenic artery RI: R = 0.520, p < 0.0001), and correlated most strongly with Child-Pugh score (e. g. right renal artery PI: R = 0.462, p < 0.0001). Age was associated independently with increased PI and RI in hepatic, splenic and renal arterial districts. In these vessels, the RI threshold of normality can be adjusted to the decade of age adding a correction of 0.03. CONCLUSION: Ageing itself induces an increase of hepatic, splenic and renal impedance indices in cirrhotic patients. The threshold of normality for these indices in cirrhosis should be adjusted according to the patients' age.

Portal hypertension: pre-primary and primary prophylaxis of variceal bleeding.

In liver cirrhosis, variceal bleeding is the last in a chain of events initiated by the increase in portal pressure (estimated in clinical practice by the hepatic venous pressure gradient). When hepatic venous pressure gradient goes above 10 mmHg the patient is at risk of developing varices, and when hepatic venous pressure gradient reaches 12 mmHg variceal bleeding might develop. Currently, there is not any effective therapy for the prevention of the development of varices. When varices are small, beta-adrenergic blockers might prevent the enlargement of the varices, and may reduce the risk of variceal bleeding. In patients with medium to large varices, beta-blockers are clearly effective in reducing the risk of variceal bleeding. Endoscopic band ligation might be more effective than beta-blockers, but available evidence is still very weak.

New abdominal collaterals at ultrasound: a clue of progression of portal hypertension.

BACKGROUND: Abdominal ultrasound can detect non-invasively the presence of abdominal portal-systemic collaterals in patients with liver cirrhosis. Abdominal portal-systemic collaterals may be protective from the formation and growth of oesophageal varices, but available data are inconclusive. AIM: We aimed at investigating the relationship between abdominal portal-systemic collaterals and variceal formation and growth. METHODS: We studied 126 cirrhotic patients without (n=43) or with small (n=83) oesophageal varices who entered a protocol of serial ultrasonographic and endoscopic examinations for a median of 55 months. Presence and kind of abdominal portal-systemic collaterals was recorded on first ultrasonography and on each control thereafter. RESULTS: At inclusion, abdominal portal-systemic collaterals were found in 19/43 patients without varices and in 23/83 patients with small varices (NS). There was no difference in variceal formation and growth between patients with and without abdominal portal-systemic collaterals at inclusion. However, patients developing new abdominal portal-systemic collaterals during follow-up had a significantly higher rate of variceal formation (56.2% vs. 22.2%; p=0.024) and growth (52.9% vs. 30.6%; p=0.041) compared with patients with unchanged ultrasonography. CONCLUSIONS: Abdominal collaterals are not protective from the formation or growth of oesophageal varices. Conversely, new abdominal portal-systemic collaterals emergence is a non-invasive clue of formation and progression of varices. Therefore, endoscopy is probably indicated whenever new abdominal portal-systemic collaterals are detected in cirrhotic patients.