Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography

Bouma, Gerrit J.; Muizelaar, J. Paul; Stringer, Warren A.; Choi, Sung C.; Fatouros, Panos P.; Young, Harold F.

doi:10.3171/jns.1992.77.3.0360

Cited by 547 publications

(200 citation statements)

References 47 publications

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“…Marion, et al, in 1991, showed that cerebral blood flow was reduced after TBI in the first 12 -24 hours [8]. Bouma, et al, in 1992, showed that there was a 31.4% incidence of ischemia in the first 3.1h +/-2.1h after injury [11]. Chestnut, et al, in 1993, demonstrated that hypotension (BPsys < 90 mmHg) was associated with an increase in morbidity and mortality [3].…”

Section: Discussionmentioning

confidence: 99%

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Palmer¹,

Bader²

2008

TOCCMJ

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Abstract:Introduction: Standard monitoring of severe traumatic brain injury patients (TBI) by intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring fails to recognize episodes of cerebral oxygen desaturation. We found and characterized frequent episodes of desaturation of jugular venous oxygen (SjO2) in the face of normal ICP and CPP.Methods: Fifty six patients with severe TBI had SjO2 and ICP monitors placed. The charts were retrospectively reviewed and all episodes of desaturation were recorded and characterized.Results: Nineteen patients had episodes of desaturation with normal ICP and CPP. The average GCS score was 5.8. 63% of desaturations occurred in the first 24 hours, 17% of desaturations occurred in 24-48 hours, and 20% occurred in 48-72 hours. The depth of desaturation was 50-54% in 50% of instances, 45-49% in 37% of instances, and 40-44% in 13% of instances. The duration of the desaturation episodes was less than 10 minutes in 47%, 10-30 minutes in 17%, 30-60 minutes in 23%, and greater than 50 minutes in 13%. Treatment of the desaturation was elevation of FIO2 in all patients, elevation of pCO2 in 15 patients, volume expansion in 9 patients, pressors in 9 patients, and Propofol in 5 patients. Conclusions:The monitoring of severe TBI patients with ICP and CPP alone is insufficient to recognize cerebral oxygen desaturation episodes in 34% of patients. The monitoring of SjO2 facilitates the recognition and treatment of these episodes.

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Section: Discussionmentioning

confidence: 99%

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Palmer¹,

Bader²

2008

TOCCMJ

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“…This suggests that 2-CA was able to restore CBF only to the normal range early after severe injury. Early posttraumatic hypoperfusion is common in experimental and clinical TBI, and may mediate secondary damage (Yamakami and McIntosh, 1989;Bryan et al, 1995;Bouma et al, 1992); however, the optimal level of CBF early after injury is not known, and changes in metabolic demands are temporally complex. Kelly et al (2000), using a moderate CCI injury level, reported a marked initial increase in CMRglu, followed by metabolic depression by 3 h. Headrick et al (1994) reported that ICV administration of 5 nmol of 2-CA in rats attenuated the loss in phosphorylation potential at 2 to 4 h after fluidpercussion injury.…”

Section: Effect Of 2-chloroadenosine On Cerebral Blood Flow After Tramentioning

confidence: 99%

“…Traumatic brain injury (TBI) acutely reduces cerebral blood flow (CBF) in experimental models and humans (Yamakami and McIntosh, 1989;Bouma et al, 1992). This may mediate secondary damage, since posttraumatic metabolic demands are increased (Hovda et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Effects of Adenosine Receptor Agonists on Cerebral Blood Flow in Uninjured and Traumatically Injured Rat Brain using Continuous Arterial Spin-Labeled Magnetic Resonance Imaging

Kochanek

Hendrich

Jackson

et al. 2005

J Cereb Blood Flow Metab

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Hypoperfusion after traumatic brain injury may exacerbate damage. Adenosine, a vasodilator, regulates cerebral blood flow (CBF). Treatment with adenosine receptor agonists has shown benefit in experimental CNS trauma; however, their effects on CBF after injury remain undefined. We used magnetic resonance imaging to assess CBF in uninjured rats both early and at 24 h after intrahippocampal administration of either the nonselective adenosine receptor agonist 2-chloroadenosine (2-CA, 12 nmol) or the A 2A -receptor agonist 2-p-(2-carboxyethyl)-phenethylamino-5 0 -N-ethylcarbox-amidoadenosine (CGS 21680, 6 nmol). We also assessed the effects of these agents on cerebral metabolic rate for glucose (CMRglu). We then assessed the effect of 2-CA on CBF at 3.5 to 5 h after controlled cortical impact (CCI). Injection of 2-CA into uninjured rat brain produced marked increases in CBF in ipsilateral hippocampus and cortex versus vehicle (Po0.05); CBF increases persisted even at 24 h. Measurement of hippocampal levels of 2-CA showed persistent increases to 24 h. CGS 21680 produced even more marked global increases in CBF than seen with 2-CA (2-6-fold versus vehicle, Po0.05 in 10/12 regions of interest (ROIs)). Neither agonist altered CMRglu versus vehicle. After CCI, 2-CA increased CBF in ipsilateral hippocampal and hemispheric ROIs (Po0.05 versus vehicle), but the response was attenuated at severe injury levels. We report marked increases in CBF after injection of adenosine receptor agonists into uninjured rat brain despite unaltered CMRglu. 2-Chloroadenosine produced enduring increases in CBF in uninjured brain and attenuated posttraumatic hypoperfusion. Future studies of adenosine-related therapies in CNS injury should address the role of CBF.

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“…This is particularly true for studies involving stable xenon CT-CBF measurements [3][4][5] , besides less frequently used single photon emission computerized tomography (SPECT) CBF studies, which simply do not provide any metabolic information.…”

mentioning

confidence: 99%

“…In recent years, however, stable xenon computerized tomography (CT) CBF measurements became available, and a number of studies have emphatically and mistakenly addressed global or regional cere-bral ischemic changes in comatose patients [3][4][5] . The most elementary mistake in all these papers is that ischemia was defined as CBF levels of 18 ml/100 g/ min or less, based on previously reported work addressing ischemic changes at such CBF levels, but in the awake monkey brain 6 .…”

mentioning

confidence: 99%

Expensive cerebral blood flow measurements alone are useless and misinformative in comatose patients: a comprehensive alternative

Cruz

2003

Arq. Neuro-Psiquiatr.

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-Since the first report addressing quantification of cerebral blood flow (CBF), concomitant assessment of cerebral oxygen consumption was also carried out. Over the years, however, some investigators have emphatically and mistakenly addressed cerebral ischemia in comatose patients, on the basis of CBF measurements alone. In contrast, we have repeatedly reported that ischemia in these patients must be precisely evaluated based on CBF-metabolism coupling or uncoupling, rather than CBF alone. Based on these previous findings, we therefore propose a comprehensive alternative approach, namely the evaluation of brain ischemia in comatose patients based on cerebral metabolic parameters, such as cerebral extraction of oxygen or cerebral lactate release, without expensive CBF measurements.KEY WORDS: arteriojugular lactate difference, brain ischemia, cerebral blood flow, cerebral extraction of oxygen, coma.Medidas dispendiosas apenas de fluxo sanguíneo cerebral são inúteis e desinformativas em estados de Medidas dispendiosas apenas de fluxo sanguíneo cerebral são inúteis e desinformativas em estados de Medidas dispendiosas apenas de fluxo sanguíneo cerebral são inúteis e desinformativas em estados de Medidas dispendiosas apenas de fluxo sanguíneo cerebral são inúteis e desinformativas em estados de Medidas dispendiosas apenas de fluxo sanguíneo cerebral são inúteis e desinformativas em estados de coma: uma alternativa abrangente coma: uma alternativa abrangente coma: uma alternativa abrangente coma: uma alternativa abrangente coma: uma alternativa abrangente RESUMO -Desde o primeiro artigo apresentando quantificação de fluxo sanguíneo cerebral (FSC), também se avaliou o consumo cerebral de oxigênio. Todavia, ao longo dos anos, alguns investigadores têm enfaticamente e erroneamente destacado a isquemia cerebral em pacientes comatosos, baseando-se apenas em medidas do FSC. Em contrapartida, temos repetidamente destacado que a avaliação de isquemia cerebral nestes pacientes deve ser baseada no conceito de acoplamento ou desacoplamento entre metabolismo cerebral e FSC, ao invés de alterações no FSC apenas. Baseando-se nestes achados prévios, aqui propomos uma abordagem alternativa e abrangente, a qual envolve a avaliação de isquemia cerebral em pacientes comatosos baseando-se em parâmetros metabólicos cerebrais, tais como a extração cerebral de oxigênio ou a liberação cerebral de lactato, sem medidas dispendiosas de FSC. Since the pioneering work of Kety and Schmidt 1 , addressing quantification of cerebral blood flow (CBF), concomitant assessment of the cerebral metabolic rate of oxygen consumption (CMRO 2 ) was also established. CBF was precisely quantified as the integrated arteriojugular difference of nitrous oxide over approximately 10 minutes (the "height-overarea" method of quantification), whereas CMRO 2 was calculated as the product of CBF and the arteriojugular oxygen content difference (AVDO 2 ). The latter parameter had already been introduced in the pertinent literature by another pioneering work of Gibb...

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Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography

Cited by 547 publications

References 47 publications

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Characterization of the Effects of Adenosine Receptor Agonists on Cerebral Blood Flow in Uninjured and Traumatically Injured Rat Brain using Continuous Arterial Spin-Labeled Magnetic Resonance Imaging

Expensive cerebral blood flow measurements alone are useless and misinformative in comatose patients: a comprehensive alternative

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