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Vol. 18. Issue 2.
Pages 403-404 (March - April 2019)
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Vol. 18. Issue 2.
Pages 403-404 (March - April 2019)
DOI: 10.1016/j.aohep.2018.07.002
Open Access
Cerebral autoregulation in a fulminant hepatic failure patient who underwent liver transplantation
Fernando M. Paschoal-Jra,b,
Corresponding author

Corresponding author at: Rua Jaci, 118, Apt. 123, Chácara Inglesa, Sao Paulo 04140-080, Brazil.
, Ricardo C. Nogueiraa, Marcelo de-Lima-Oliveiraa, Eric H. Paschoala,b, Manoel J. Teixeiraa, Luiz A. D’Albuquerquec, Edson Bor-Seng-Shua
a Laboratory for Neurosonology and Cerebral Hemodynamics, Division of Neurological Surgery, Hospital das Clinicas, Sao Paulo University Medical School, Brazil
b Department of Neurology, Federal University of Pará Medical School, Brazil
c Department of Gastroenterology, Sao Paulo University Medical School, Brazil
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Table 1. Performance of systemic and haemodynamic parameters (CBFV and CA) before and after transplantation (tx) liver in FHF.
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Dear Editor,

We report the case of a 47-year-old woman diagnosed with fulminant hepatic failure (FHF). Over a two-week period, the patient had jaundice and Grade 4 encephalopathy associated with coagulopathy and renal failure. On admission, the patient underwent endotracheal intubation and mechanical ventilation, fulfilling the clinical criteria for liver transplantation. The patient underwent urgent liver transplantation and was monitored before and after transplantation by transcranial Doppler (TCD). Norepinephrine was infused to increase the mean arterial blood pressure by approximately 20mmHg in order to calculate static cerebral autoregulation (CA) according to Tiecks et al. [1] Values>0.6 indicate preserved CA. In the case reported, cerebral blood flow (CBF) velocity showed lower values prior to transplant, high values immediately post-transplant, and a tendency to normalize within 48–72h (Fig. 1). Loss of CA was demonstrated before transplant; CA recovery was seen on the 3rd day after transplant. Unexpectedly, deterioration of CA was noted on the 5th day after transplantation, coinciding with hepatic artery thrombosis. The patient underwent liver retransplantation, and restoration of CA occurred 48h later (Table 1).

Fig. 1.

Transcranial Doppler: (A) before liver transplant; (B) 1st day after transplant; and (C) 3rd day after liver transplant; (D) 4th day after transplant; (E) 5th after transplant and (F) 7th after transplant.

Table 1.

Performance of systemic and haemodynamic parameters (CBFV and CA) before and after transplantation (tx) liver in FHF.

  Before tx  1st day after tx  3rd Day after tx  5th Day after tx  7th day after tx and 2nd day after new liver tx 
ABP (mmHg)  108  102  120  107  106 
Heart rate  119  95  73  69  93 
PCO2 (mmHg)  45  34  36.7  36  36.5 
Haemoglobin (g/dl)  11.8  10.8  10.7  12.1  10.8 
Temperature (C)  37  36  36.5  36.1  37 
CBFV MCA maximum (cm/s)  45  145  66  161  63 
CA index MCA maximum (cm/s)  0.25  0.33  0.92  0.30  0.70 

ABP: arterial blood pressure; pCO2: partial pressure of carbon dioxide; CBFV: cerebral blood flow velocity; CA: cerebral autoregulation; MCA: middle cerebral artery.

Cerebral autoregulation refers to the inherent cerebrovascular physiological mechanisms that keep CBF relatively constant despite wide variation in arterial blood pressure levels. These mechanisms act to protect the brain from the harmful effects of oligaemia and hyperaemia due to decreased and increased perfusion pressure, respectively [2–3]. Loss of CA in FHF can be explained by the dysfunction of cerebral arterioles, leading to vasodilation, associated with metabolic derangement and toxic substances released from the necrotic liver [4], but the actual pathophysiological mechanism remains unknown. Both loss of CA and hyperaemia have been considered important factors for the worsening of hepatic encephalopathy, brain swelling, and unfavourable outcomes. The present case raises the possibility that CBF dynamics and CA capacity can be restored shortly after recovery of liver function [4]. TCD can be a useful method for real-time monitoring of FHF patients in terms of CBF velocity and CA. Improvement of CA can be directly associated with recovery of liver function; for this reason, CA may be a marker of liver function, as suggested by this case. Future studies should determine the dynamic behaviour of CA. Such evaluation can help elucidate the pathophysiology of FHF and enable better therapeutic management of patients.

F.P. Tiecks, A.M. Lam, R. Aaslid, D.W. Newell.
Comparison of static and dynamic cerebral autoregulation measurements.
Stroke, 26 (1995), pp. 1014-1019
E. Bor-Seng-Shu, W.S. Kita, E.G. Figueiredo, W.S. Paiva, E.T. Fonoff, M.J. Teixeira, et al.
Cerebral hemodynamics: concepts of clinical importance.
Arq Neuropsiquiatr, 70 (2012), pp. 352-356
E. Bor-Seng-Shu, E.G. Figueiredo, E.T. Fonoff, Y. Fujimoto, R.B. Panerai, M.J. Teixeira.
Decompressive craniectomy and head injury: brain morphometry ICP, cerebral hemodynamics, cerebral microvascular reactivity, and neurochemistry.
Neurosurg Rev, 36 (2013), pp. 361-370
Y. Zheng, A.J. Villamayor, W. Merritt, A. Pustavoitau, A. Latif, R. Bhambhani, et al.
Continuous cerebral blood flow autoregulation monitoring in patients undergoing liver transplantation.
Neurocrit Care, 17 (2012), pp. 77-84
Copyright © 2019. Fundación Clínica Médica Sur, A.C.
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