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Keywords:

  • cerebral vasoconstriction;
  • cerebrovascular reactivity;
  • cirrhosis;
  • portal hypertension;
  • transcranial Doppler ultrasonography

Abstract

Background & Aims

Factors other than elevated levels of ammonia may be implicated in hepatic encephalopathy (HE) pathophysiology, including abnormal cerebral haemodynamics. Transcranial Doppler ultrasonography (TCD) evaluates cerebrovascular structural integrity and reactivity, through pulsatility index (PI) and breath-holding index (BHI) respectively. The aim of this study was to evaluate cerebral haemodynamics by TCD in patients with compensated and decompensated cirrhosis, and patients with and without HE.

Methods

We studied 90 subjects by TCD measuring PI and BHI in the middle cerebral artery: 30 with cirrhosis and no HE, 30 with cirrhosis and low-grade HE and 30 healthy subjects. Critical flicker frequency, psychometric hepatic encephalopathy score and West-Haven criteria were performed to assess MHE and HE respectively.

Results

Pulsatility index increased in decompensated cirrhotics (Child ≥ 7) when compared with compensated cirrhotics and healthy subjects [median (IQR) 1.07 (0.95–1.21) vs 0.90 (0.83–1.05) vs 0.87 (0.78–0.96); P < 0.001]. A reverse relationship was observed for BHI among the three groups [0.82 (0.45–1.11) vs 1.20 (0.82–1.52) vs 1.28 (1.06–1.68); P < 0.001]. Similar findings were observed in decompensation [model for end-stage liver disease (MELD) score ≥14]. Patients with HE showed higher PI and lower BHI [1.05 (1.00–1.16) and 0.89 (0.59–1.15)], when compared with patients without HE [0.96 (0.83–1.13) and 1.00 (0.60–1.53)] or controls [0.87 (0.78–0.96) and 1.28 (1.06–1.68)] (P < 0.001 for PI, and P = 0.007 for BHI). In multivariate regression models, only PI predicted HE, but it was outperformed by MELD-sodium and tumour necrosis factor-alpha.

Conclusions

These results indicate that cerebral haemodynamics are altered in patients with cirrhosis, in relation to severity of disease and HE. Findings on impaired PI and BHI suggest that structural vascular damage and loss of vascular autoregulation are implicated in the pathophysiology of HE.