Neurological complications after orthotopic liver transplantation

Clinical Medicine 5 and Veneto Regional Reference Centre for Hepatic Diseases, University of Padova, Padova, Italy.
Digestive and Liver Disease (Impact Factor: 2.96). 09/2007; 39(8):740-7. DOI: 10.1016/j.dld.2007.05.004
Source: PubMed


The number of orthotopic liver transplantation performed each year is increasing due to increased safety and logistic facilities. Therefore, the importance of reducing adverse events is progressively growing.
To review present knowledge on the neurological complications of orthotopic liver transplantation.
The epidemiology, the clinical features and the pathophysiology of the neurological complications of orthotopic liver transplants, resulting from a systematic review of the literature in the last 25 years, are summarized.
The review highlights that a relevant variety of neurological adverse events can occur in patients undergoing orthotopic liver transplantation. The knowledge of neurological complications of orthotopic liver transplantation is important for transplantation teams to reduce their prevalence and improve their management. In addition, the likelihood of neurological adverse effects provides evidence for the need of a careful cognitive and neurological work up of patients in the orthotopic liver transplantation waiting list, in order to recognize and interpret neurological dysfunction occurring after orthotopic liver transplantation.

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    • "Cerebral thromboembolism could also induced by liver transplantation surgery due to peri-operative detachment of arterial emboli from carotid or intracranial arteries or paradoxical emboli of thrombotic material from deep leg [11]. Thus, we could differentiate our case from those occurred after liver transplantation by prominent air embolic signal (Fig. 2). "
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    Korean journal of anesthesiology 08/2014; 67(2):139-43. DOI:10.4097/kjae.2014.67.2.139
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    • "Signed informed consent was obtained from all participants. The diagnosis of MHE was based on spectral EEG features and on psychometric hepatic encephalopathy score (PHES; Amodio et al. 2007; Weissenborn et al. 2001). Cirrhotic patients were qualified as having MHE if either PHES or EEG were abnormal (Ferenci et al. 2002). "
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    Metabolic Brain Disease 03/2014; 29(4). DOI:10.1007/s11011-014-9529-0 · 2.64 Impact Factor
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    • "Some clues for a progress in the understanding of this syndrome regard the changes occurring into the brain due to ammonia (Butterworth 2003; Haussinger 2006; Norenberg et al. 2007) and body ammonia trafficking (Olde Damink et al. 2002a, b; Romero-Gomez et al. 2006). In addition, new features of brain-liver interaction are appearing on the horizon and are worthy of consideration: a detrimental influence of HCV virus on cognitive function and wellbeing (Forton et al. 2001), either related to the virus per se or to systemic or brain inflammatory response; the influence of liver transplantation and immunosuppressive agents on the brain (Amodio et al. 2007); the renewed interest for nutrition, microelements deficiency, notably—but not only—thiamine; and the consequences of alcohol misuse (Butterworth 1995; Kalaitzakis et al. 2007). Treatment for hepatic encephalopathy is still based, somewhat empirically, on our concepts of the pathogenesis of the syndrome and so primarily on methods to Fig. 1 The Morgagni's Book of Medicine where liver cirrhosis and a possible case of HE are described. "

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