Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage

Schulz, Mette Katrine; Wang, Lars Peter; Tange, Mogens; Bjerre, Per

doi:10.3171/jns.2000.93.5.0808

Cited by 191 publications

(134 citation statements)

References 15 publications

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“…As an indicator of a severe brain injury, the L=P was elevated to values well above the presumed normal value of 20 (Reinstrup et al, 2000;Schulz et al, 2000). The L=P decreased over time and had significantly decreased at 24 h of treatment without significant difference between the PG-G and Plac-G.…”

Section: Discussionmentioning

confidence: 88%

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Olivecrona

Rodling-Wahlström

Naredi

et al. 2009

Journal of Neurotrauma

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Prostacyclin (PGI 2 ) is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation. In trauma the balance between PGI 2 and thromboxane A 2 (TXA 2 ) is shifted towards TXA 2 . Externally provided PGI 2 would, from a theoretical and experimental point of view, improve the microcirculation in injured brain tissue. This study is a prospective consecutive double-blinded randomized study on the effect of PGI 2 versus placebo in severe traumatic brain injury (sTBI). All patients with sTBI were eligible. Inclusion criteria: verified sTBI, Glasgow Coma Score (GCS) at intubation and sedation of 8, age 15-70 years, a first-recorded cerebral perfusion pressure (CPP) of !10 mm Hg, and arrival within 24 h of trauma. All subjects received an intracranial pressure (ICP) measuring device, bilateral intracerebral microdialysis catheters, and a microdialysis catheter in the abdominal subcutaneous adipose tissue. Subjects were treated according to an ICP-targeted therapy based on the Lund concept. 48 patients (mean age of 35.5 years and a median GCS of 6 [3-8]) were included. We found no significant effect of prostacyclin (epoprostenol, Flolan) on either the lactate-pyruvate ratio (L=P) at 24 h or the brain glucose levels. There was no significant difference in clinical outcome between the two groups. The median Glasgow Outcome Score (GOS) at 3 months was 4, and mortality was 12.5%. The favorable outcome (GOS 4-5) was 52%. The initial L=P did not prognosticate for outcome. Thus our results indicate that there is no effect of PGI 2 at a dose of 0.5 ng=kg=min on brain L=P, brain glucose levels, or outcome at 3 months.

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Section: Discussionmentioning

confidence: 88%

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Olivecrona

Rodling-Wahlström

Naredi

et al. 2009

Journal of Neurotrauma

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“…The neurotoxic effects of widespread subarachnoid blood associated with transient cerebral ischemia cause diffuse cortical damage that occurs immediately after the hemorrhage (Doczi, 1985;Doczi et al 1986;Enblad et al, 1996;Gotoh et al, 1984;Hutchinson et al, 2000;Jackowski et al, 1990;Nilsson et al, 1996Nilsson et al, , 1999Persson et al, 1996;Sarrafzadeh et al, 1998Sarrafzadeh et al, , 2002Saveland et al, 1996;Schulz et al, 2000;Staub et al, 2000;Untemberg et al, 2001). This damage results from the interaction of numerous pathophysiologic factors where presumably, the blood itself and/or active substances derived in part from the degradation of the extravasated blood are centrally involved.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, bedside intracerebral microdialysis monitoring of patients with SAH exhibiting signs of delayed ischemia revealed dramatic changes in extracellular concentrations of excitatory amino acids, including glucose, piruvate, lactate, glycerol, and glutamate, confirming that these characteristic metabolic changes occur during vasospasm (Unterberg et al, 2001;Zouh et al, 1996). Moreover, a correlation between EAA concentrations and patient clinical status has been demonstrated Hutchinson et al, 2000;Inage et al, 2000;Nilsson et al, 1996Nilsson et al, , 1999Persson et al, 1996;Sarrafzadeh et al, 1998Sarrafzadeh et al, , 2002Saveland et al, 1996;Schulz et al, 2000;Staub et al, 2000).…”

Section: Introduction Dmentioning

confidence: 95%

“…Data collected in both clinical and experimental settings have reported remarkable changes in levels of lactate, glycerol, glutamate, and aspartate, in addition to changes in the lactate/piruvate ratio. These levels are in turn, affected by ischemic deterioration, with changes in metabolite levels varying with respect to substance, location, and time Hutchinson et al, 2000;Inage et al, 2000;Nilsson et al, 1996Nilsson et al, , 1999Persson et al, 1996;Sarrafzadeh et al, 1998Sarrafzadeh et al, , 2002Saveland et al, 1996;Schulz et al, 2000;Staub et al, 2000;Untemberg et al, 2001). …”

Section: Effects Of Fbm After Experimentalmentioning

confidence: 99%

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NMDA Receptor Antagonist Felbamate Reduces Behavioral Deficits and Blood–Brain Barrier Permeability Changes after Experimental Subarachnoid Hemorrhage in the Rat

Germanò

Caffo

Angileri

et al. 2007

Journal of Neurotrauma

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“…Por otra parte, si comparamos estos resultados con el estudio de Shultz et al 31 , en donde estos autores determinaron los niveles de lactato e índice LP durante episodios de isquemia en pacientes con hemorragia subaracnoidea (Tabla 4), observamos que éstos fueron mucho más elevados que en nuestra serie de pacientes en la que se estudió un perfil metabólico más heterogéneo. El hecho de que nuestros valores de lactato sean más elevados que en el grupo de pacientes no traumáticos, pero mucho más bajos que el grupo en el que solamente se estudia el patrón isquémico sugiere que existen alteraciones más moderadas en los niveles de lactato que no cursan con hipoxia pero que pueden ser características en el contexto de un TCE.…”

Section: Niveles De Lactato E íNdice Lpunclassified

¿Es el lactato un buen indicador de hipoxia tisular? Resultados de un estudio piloto en 21 pacientes con un traumatismo craneoencefálico

et al. 2010

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SummaryLactate and the lactate-pyruvate index (LPI) are two hypoxia markers widely used to detect brain tissue hypoxia in patients with acute traumatic brain injury. These two markers have a more complex behavior than expected as they can be abnormally high in circumstan¿Es el lactato un buen indicador de hipoxia tisular? Resultados de un estudio piloto en 21 pacientes con un traumatismo craneoencefálico ces with no detectable brain hypoxia. This condition must be considered in the differential diagnosis because it also reflects an alteration of brain energy metabolism.Objectives. 1. To describe cerebral energy metabolism characteristics observed in the acute phase of traumatic brain injury (TBI) based on two traditional indicators of anaerobic metabolism: lactate and LPI, 2. To determine the concordance between these two biomarkers in order to classify the incidence of anaerobic metabolism and 3. To classify the different types of metabolic abnormalities found in patients with moderate and severe TBI using both lactate and LPI.Materials and methods. Twenty-one patients were randomly selected from a cohort of moderate or severe TBI patients admitted to the neurotraumatology intensive care unit. All of them who underwent both cerebral microdialysis and brain tissue oxygen monitoring (PtiO 2 ). We analyzed the levels of lactate and the LPI for every microvial within the first 96 hours after head trauma. These data were correlated with PtiO 2 values.Results. Lactate levels and the LPI were respectively increased during 49,5% and 38,4% of the monitoring time. The incidence and behavior of high levels of both markers were extremely heterogeneous. The concordance between these two biomarkers to determine episodes of dysfucntional metabolism was very weak (Kappa Index=0,29; IC 95%: 0,24-0,34). Based on the levels of lactate and the LPI, we defined four metabolic patterns: I: L>2,5 mmol/L and LPR>25; II: L>2,5 mmol/L and LPR≤ 25; III: L≤ 2,5 mmol/L and LPR≤ 25; IV: L≤ 2,5 mmol/L and LPR>25). In more than 80% of cases in which lactate or LPI were increased, PtiO 2 values were within the normal range (PtiO 2 > 15mmHg).Conclusions. Increased lactate and LPI were frequent findings after acute TBI and in most cases they were not related to episodes of brain tissue hypoxia. Furthermore, the concordance between both biomarkers to classify metabolic dysfunction was weak. LPI and lactate should not be used indistinctly in everyday clinical practice because of the weak correlation between these two markers, the difficulty in their interpretation and the heterogeneous and complex nature of the pathophysiology. Other differential diagnoses apart from tissue hypoxia should always be considered when high lactate and/or LPI are detected in the acute injured brain.KEY WORDS: Brain hypoxia. Lactate. Lactate-pyruvate index. Microdialysis. Traumatic brain injury. Anaerobic metabolism.

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Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage

Cited by 191 publications

References 15 publications

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

Prostacyclin Treatment in Severe Traumatic Brain Injury: A Microdialysis and Outcome Study

NMDA Receptor Antagonist Felbamate Reduces Behavioral Deficits and Blood–Brain Barrier Permeability Changes after Experimental Subarachnoid Hemorrhage in the Rat

¿Es el lactato un buen indicador de hipoxia tisular? Resultados de un estudio piloto en 21 pacientes con un traumatismo craneoencefálico

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