scholarly journals Monitoring cerebral blood flow: A useful clinical tool in acute liver failure?

2005 ◽  
Vol 11 (11) ◽  
pp. 1320-1322 ◽  
Author(s):  
Andres T. Blei
2004 ◽  
Vol 19 (3/4) ◽  
pp. 177-194 ◽  
Author(s):  
Javier Vaquero ◽  
Chuhan Chung ◽  
Andres T. Blei

1998 ◽  
Vol 28 (2) ◽  
pp. 199-203 ◽  
Author(s):  
Gitte Strauss ◽  
Bent Adel Hansen ◽  
Gitte Moos Knudsen ◽  
Fin Stolze Larsen

2004 ◽  
Vol 41 (4) ◽  
pp. 613-620 ◽  
Author(s):  
Rajiv Jalan ◽  
Steven W.M. Olde Damink ◽  
Peter C. Hayes ◽  
Nicolaas E.P. Deutz ◽  
Alistair Lee

2017 ◽  
Vol 7 ◽  
pp. S32-S33
Author(s):  
Anna Czarnecka ◽  
Krzysztof Jasinski ◽  
Radoslaw Jazwiec ◽  
Wojciech Hilgier ◽  
Anna Gajos-Draus ◽  
...  

2000 ◽  
Vol 14 (suppl d) ◽  
pp. 105D-111D ◽  
Author(s):  
Fin Stolze Larsen ◽  
Bent Adel Hansen ◽  
Andres T Blei

Acute liver failure (ALF) is a devastating disease leading to multiorgan dysfunction. The most dramatic impact of ALF is on the brain, as hepatic encephalopathy and intracranial hypertension (IH) develop. IH is associated with systemic hemodynamic instability, alterations in the regulation of cerebral blood flow and the development of cerebral edema. This review focuses on the pathophysiology of IH with special emphasis on cerebral blood flow and the development of cerebral edema. Based on these considerations, both traditional and new treatments for the management of IH in the future are discussed.


Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 272-279 ◽  
Author(s):  
P Javlé ◽  
J Yates ◽  
H G Kynaston ◽  
K F Parsons ◽  
S A Jenkins

Background—Massive liver necrosis, characteristic of acute liver failure, may affect hepatosplanchnic haemodynamics, and contribute to the alterations in renal haemodynamics and function.Aims—To investigate the relation between hepatosplanchnic haemodynamics, including portal systemic shunting, and renal blood flow and function in rats with acute liver failure.Methods—Liver failure was induced in male Wistar rats by intraperitoneal injection of 1.1 g/kg ofd(+)-galactosamine hydrochloride. The parameters assessed included: systemic, hepatosplanchnic, and renal blood flow (57Co microsphere method); portal-systemic shunting and intrarenal shunting (consecutive intrasplenic, intraportal, or renal arterial injections of 99mTc methylene diphosphonate and99mTc albumin microspheres); arterial blood pressure and portal pressure; renal function; and liver function (liver function tests and 14C aminopyrine breath test).Results—Progressive liver dysfuntion was accompanied by the development of a hyperdynamic circulation, a highly significant decrease in renal blood flow and function, and an increase in intrarenal shunting 36, 42, and 48 hours after administration of d-galactosamine. The alterations in renal blood flow and function were accompanied by significant increases in portal pressure, portal venous inflow, and intrahepatic portal systemic shunting in galactosamine treated rats compared with controls. There was a significant correlation between changes in renal blood flow and changes in portal pressure, intrahepatic portal systemic shunting, and deterioration in liver function (r=0.8, p<0.0001).Conclusions—The results of this study suggest that both increased intrahepatic portal systemic shunting and hepatocyte impairment may contribute to alterations in renal haemodynamics and function.


2007 ◽  
Vol 28 (5) ◽  
pp. 916-926 ◽  
Author(s):  
Thomas J Dethloff ◽  
Gitte Moos Knudsen ◽  
Fin Stolze Larsen

Patients with acute liver failure (ALF) display impairment of cerebral blood flow (CBF) autoregulation, which may contribute to the development of fatal intracranial hypertension, but the pathophysiological mechanism remains unclear. In this study, we examined whether loss of liver mass causes impairment of CBF autoregulation. Four rat models were chosen, each representing different aspects of ALF: galactosamine (GIN) intoxication represented liver necrosis, 90% hepatectomy (PH×90) represented reduction in liver mass, portacaval anastomosis (PCA) represented shunting of blood/toxins into the systemic circulation thus mimicking intrahepatic shunting in ALF, PCA + NH3 provided information about the additional effects of hyperammonemia Rats were intubated and sedated with pentobarbital. We measured CBF with laser Doppler, intracranial pressure (ICP) was measured in the fossa posterior and registered with a pressure transducer, brain water was measured using the wet-to-dry method, and cerebral glutamine/glutamate was measured enzymatically. The CBF autoregulatory index in both the GIN and PH×90 groups differed significantly from the control group. Conversely, CBF autoregulation was intact in the PCA and PCA + NH3 groups despite high arterial ammonia, high cerebral glutamine concentration, and increased CBF and ICP. Increased water content of the brainstem or cerebellum was not associated with defective CBF autoregulation. In conclusion, impairment of CBF autoregulation is not caused by brain edema/high ICP. Nor does portacaval shunting or hyperammonemia impair autoregulation. Rather, massive liver necrosis and reduced liver mass are associated with loss of CBF autoregulation.


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