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Julio Cruz

: Excerpta Medica, 1981, pp 140–144 24. Rappaport ZH , Ransohoff J , Hass WK : Cerebral metabolism in head trauma. Prog Neurol Surg 10 : 1 – 13 , 1981 Rappaport ZH, Ransohoff J, Hass WK: Cerebral metabolism in head trauma. Prog Neurol Surg 10: 1–13, 1981 25. Robertson CS , Grossman RG , Goodman JC , et al : The predictive value of cerebral anaerobic metabolism with cerebral infarction after head injury. J Neurosurg 67 : 361 – 368 , 1987 Robertson CS, Grossman RG, Goodman JC

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Julio Cruz

injury. Relationship to intracranial hypertension. J Neurosurg 61 : 241 – 253 , 1984 Obrist WD, Langfitt TW, Jaggi JL, et al: Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg 61: 241–253, 1984 19. Rappaport ZH , Ransohoff J , Hass WK : Cerebral metabolism in head trauma. Prog Neurol Surg 10 : 1 – 13 , 1981 Rappaport ZH, Ransohoff J, Hass WK: Cerebral metabolism in head trauma. Prog Neurol Surg 10: 1–13, 1981 20

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wide-ranging letter. His contributions to the optimization of cerebral metabolism and reducing ICP are well known. Since his return to Brazil, as he notes in his letter, he has published a number of interesting papers, which report remarkably good results in the treatment of the severely head injured. Recently, however, the focus of our research has been somewhat different from that of Dr. Cruz. The data we described came from a multicenter trial for a new drug for head injury and we focused on having 50 investigators follow a reasonably tight protocol in an attempt

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“significant regional differences in both cerebral blood flow (CBF) and metabolism” is just an untrue statement from Drs. Marion and Darby, because in none of the three quoted studies was regional cerebral metabolism evaluated. Although regional CBF may be variable, no less than 100% of previous metabolic studies in acute traumatic coma have shown dramatically reduced cerebral metabolic rate of oxygen consumption (CMRO 2 ), usually 50% to 60% below normal. Thus, low CBF values alone were mistakenly regarded as ischemia in all three quoted papers. The “questioned” normal

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found in Muizelaar and coworkers' 8 study, irrespective of “management.” The claim of “significant regional differences in both cerebral blood flow (CBF) and metabolism” is just an untrue statement from Drs. Marion and Darby, because in none of the three quoted studies was regional cerebral metabolism evaluated. Although regional CBF may be variable, no less than 100% of previous metabolic studies in acute traumatic coma have shown dramatically reduced cerebral metabolic rate of oxygen consumption (CMRO 2 ), usually 50% to 60% below normal. Thus, low CBF values

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Walter D. Obrist, Thomas W. Langfitt, Jurg L. Jaggi, Julio Cruz, and Thomas A. Gennarelli

blood flow (CBF) (p < 0.02, chi-square test). Arteriovenous Oxygen Differences The difference between arterial and jugular venous O 2 content provides a means of assessing the overall balance between cerebral metabolism and blood flow, thereby indicating the presence of global ischemia or hyperemia. This is evident from rearrangement of the Fick equation: AVDO 2 = CMRO 2 /CBF. 27 Thus, when CBF is low relative to the brain's metabolic needs (ischemia), a wide AVDO 2 is obtained. Conversely, when CBF is high relative to metabolism (hyperemia), a

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, the resulting data pertain only to the global effects of hyperventilation. Cruz's conclusions and implicit recommendations for the treatment of severe TBI could be adopted safely only if cerebral metabolism and blood flow were regionally homogeneous after a TBI and if unilateral jugular venous samples were reliably representative of global metabolites. However, most studies of cerebral blood flow (CBF) and metabolism indicate that there are significant regional differences in both. 2, 4, 5 Local variations in CBF are particularly common surrounding contusions or

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, without providing information on regional cerebral metabolism (regional cerebral oxygen consumption or regional cerebral extraction of oxygen). Changes in PaCO 2 were intentionally induced (without clinical indication) in a wide range from 24 to 32 mm Hg, which the authors referred to as “mild hyperventilation.” In contrast, in a recent paper from the same group 7 PaCO 2 levels below 29 mm Hg were regarded as “extreme hyperventilation.” Stable Xe—computerized tomography (CT) rCBF studies lack crucial information regarding comatose patients with acutely injured

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below a level at which the vasculature could be expected to respond. The comments are not aimed at the accuracy of the CBF or cerebral metabolism measurements but at the limitations of their interpretation when CPP is unknown. There is no “misquote” from the article in question. 8 On pages 955 and 956 both citations of the article were in terms of the “lack” of CPP information. The citation stands. The correlation coefficient between blood—ethanol level and Glasgow Outcome Scale (GOS) is 0. This is true both within the Glasgow Coma Scale (GCS) Group 3, within

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suggestive of traumatic vasospasm are unlikely to improve the patients' cerebral metabolism and clinical outcomes, unless cerebral oxygen extraction is abnormally high (which has not been found 4 ). References 1. Cruz J : An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J Neurosurg 82 : 379 – 385 , 1995 Cruz J: An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake. J