There is increasing evidence that terlipressin is useful in patients with cirrhosis and
hepatorenal syndrome, but there are no data of its use in patients with acute liver
failure (ALF) in whom hepatorenal syndrome is common. Although terlipressin
produces systemic vasoconstriction, it produces cerebral vasodilatation and may
increase cerebral blood flow (CBF). Increased CBF contributes to intracranial
hypertension in patients with ALF. The aim of this study was to evaluate the safety of
terlipressin in patients with ALF with respect to cerebral haemodynamics. Six
successive patients with ALF were electively ventilated for grade IV hepatic
encephalopathy. Patients were monitored invasively and CBF was measured (Kety-
Schmidt technique). Measurements were made before, at 1, 3 hour and 5 hours after
intravenous (single bolus) administration of terlipressin (0.005 mg/kg) )intravenously
(single bolus), median 0.25mg (range 0.2-0.3). There was no significant change in
heart rate, mean arterial pressure or cardiac output. CBF and jugular venous oxygen
saturation both increased significantly at 1 hour (p<0.0=0.016) respectively.
Intracranial pressure increased significantly at 21 hours (p<0=.0.031), returning back
to baseline values at 42 hours. This study shows that administration of terlipressin, at
a dose that did not alter systemic haemodynamicshemodynamics, resulted in
worsening of cerebral hyperemia and intracranial hypertension in patients with ALF
and severe hepatic encephalopathy. These data suggest the need to exercise extreme
caution in the use of terlipressin in these patients in view of its potentially deleterious
consequences on cerebral haemodynamics
