Elsevier

Clinical Imaging

Volume 34, Issue 5, September–October 2010, Pages 327-331
Clinical Imaging

Cerebral pulsatility index by transcranial Doppler sonography predicts the prognosis of patients with fulminant hepatic failure

https://doi.org/10.1016/j.clinimag.2009.09.006Get rights and content

Abstract

Aim

Cerebral hemodynamic derangement is well known in patients with fulminant hepatic failure. The advent of transcranial Doppler sonography (TCD) enabled noninvasive observation of cerebral hemodynamics. To evaluate its clinical usefulness, we examined longitudinal cerebral hemodynamic parameters in patients with fulminant hepatic failure and severe acute hepatitis.

Methods

The six subjects were four patients with fulminant hepatic failure, one with severe acute hepatitis and one with severe acute exacerbation on chronic hepatitis. The pulsatility indices of the right middle cerebral artery were used as parameters of cerebral hemodynamics.

Results

The pulsatility indices of the two patients with a deteriorating course had elevated to >1.00, whereas those of the two patients undergoing recovery were within normal limits, as well as of the patients with acute hepatitis or acute exacerbation on chronic hepatitis.

Conclusion

Cerebral pulsatility measured by TCD may be a real-time and useful tool to assess and monitor patients with fulminant hepatic failure.

Introduction

Acute liver failure rapidly develops cerebral dysfunction including hepatic encephalopathy and cerebral edema. Cerebral edema is reported to occur in more than 80% of patients with hepatic fulminant failure, which is associated with a high mortality rate [1]. However, to evaluate intracranial pressure (ICP), the direct implanting of ICP monitoring devices is involved, which carries a risk of hemorrhage [2]. Recently, transcranial Doppler sonography (TCD) as one of the neuromonitoring systems has become available to help evaluate intracranial disease. TCD is a noninvasive and bedside procedure, which was validated for the measurement of cerebral blood flow [3], [4], [5], [6]. We have reported that patients with liver cirrhosis have a higher vascular resistance according to the severity of liver diseases and hepatic encephalopathy [7]. Furthermore, patients with fulminant hepatic failure have been reported to have a cerebral hypoperfusion pattern and an increased pulsatility index [8], [9]. TCD monitoring is less invasive and safer than direct ICP monitoring. In this paper, we have reported that TCD is useful to assess the severity and predict the prognosis of patients with fulminant hepatic failure.

Section snippets

Patients

The present study included four consecutive patients with fulminant hepatic failure, one patient with acute hepatitis and one patient with acute exacerbation of chronic hepatitis, who were admitted to our hospital. Severe acute hepatitis and severe acute exacerbation of chronic hepatitis were defined as having a prothrombin time <40% and no distinct hepatic encephalopathy. None of the patients in this study were hypoglycemic or treated with sedatives before the appearance of hepatic

Results

The clinical courses of the six patients (Cases 1–4: fulminant hepatic failure; Cases 5 and 6: severe acute hepatitis) are shown in Fig. 2, Fig. 3, Fig. 4. Among the four patients with fulminant hepatic failure, two patients (Cases 1 and 2) died (Fig. 2) and two were successfully treated (Fig. 3). Among the recovered patients, one patient (Case 3) underwent transplant on the third day after admission. The standard value (mean±2 S.D.) of the pulsatility index from 25 healthy controls was

Discussion

Cerebral autoregulation is due to the reactive dilatation or constriction of cerebral resistance vessels as a response to alterations in cerebral perfusion pressure. Within a wide range of arterial blood pressure values, cerebral blood flow is kept constant. But in fulminant hepatic failure, cerebral autoregulation is upset by neurotoxins, resulting in cerebral edema and intracranial hypertension. Straus et al. [9] and Larsen et al. [10] showed that cerebral autoregulation was absent in

References (13)

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