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Pressure Reactivity as a Guide for Cerebral Perfusion Pressure

Neurosurgical Forum: Letters to the Editor To The Editor Carl-Henrik Nordström , M.D., Ph.D. Lund University Hospital, Lund, Sweden 196 198 I read with interest the article by Howells, et al. (Howells T, Elf K, Jones PA et al: Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma. J Neurosurg 102: 311–317, February 2005). In this paper, the authors describe their retrospective analysis of patients with severe brain trauma and compare outcome results

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Hyperacute measurement of intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, and laser Doppler flowmetry, before and during removal of traumatic acute subdural hematoma

Bon H. Verweij, J. Paul Muizelaar, and Federico C. Vinas

Object. The poor prognosis for traumatic acute subdural hematoma (ASDH) might be due to underlying primary brain damage, ischemia, or both. Ischemia in ASDH is likely caused by increased intracranial pressure (ICP) leading to decreased cerebral perfusion pressure (CPP), but the degree to which these phenomena occur is unknown. The authors report data obtained before and during removal of ASDH in five cases.

Methods. Five patients who underwent emergency evacuation of ASDH were monitored. In all patients, without delaying treatment, a separate surgical team (including the senior author) placed an ICP monitor and a jugular bulb catheter, and in two patients a laser Doppler probe was placed.

The ICP prior to removing the bone flap in the five patients was 85, 85, 50, 59, and greater than 40 mm Hg, resulting in CPPs of 25, 3, 25, 56, and less than 50 mm Hg, respectively. Removing the bone flap as well as opening the dura and removing the blood clot produced a significant decrease in ICP and an increase in CPP. Jugular venous oxygen saturation (SjvO2) increased in four patients and decreased in the other during removal of the hematoma. Laser Doppler flow also increased, to 217% and 211% compared with preevacuation flow.

Conclusions. Intracranial pressure is higher than previously suspected and CPP is very low in patients with ASDH. Removal of the bone flap yielded a significant reduction in ICP, which was further decreased by opening the dura and evacuating the hematoma. The SjvO2 as well as laser Doppler flow increased in all patients but one immediately after removal of the hematoma.

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Experience with Althesin in the management of persistently raised ICP following severe head injury

Ross Bullock, James R. van Dellen, Derek Campbell, Ian Osborn, and S. Gustav Reinach

Althesin infusion. Postmortem examinations were carried out in all patients who died. The outcome of the survivors was evaluated according to the Glasgow Outcome Scale.10 Case notes and intensive care unit charts were studied retrospectively, and ICP and cerebral perfusion pressure (CPP) data were statistically analyzed independently. Statistical Procedures An IBM 4331 computer was used together with the BMDP package ‡ to analyze the data. Since the continuous variables did not seem to be normally distributed and the sample sizes when two groups were

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The effect of cold-induced brain edema on cerebrospinal fluid formation rate

K. Gwan Go, Gerald M. Hochwald, Lenie Koster-Otte, Annie K. van Zanten, and Mysore Gandhi

decrease in pressure was not statistically significant (p > 0.05). As a result of the cold lesion, there was a significant increase in mean ventricular pressure, which rose from 2.0 ± 0.8 to 15.6 ± 3.6 mm Hg (p < 0.001). Because of the increase in ventricular pressure and no change in arterial pressure, there was a decrease in cerebral perfusion pressure of 9.9 ± 2.0% (p < 0.02). In those cats in which the cold-induced edema occupied most of the hemisphere, water content in cortex was 85.7 ± 1.1% and in subcortical white matter 79.7 ± 1.4%. In the contralateral

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Experimental cerebral oligemia and ischemia produced by intracranial hypertension

Part 2: Brain morphology

Lawrence F. Marshall, David I. Graham, Felix Durity, Robert Lounsbury, Frank Welsh, and Thomas W. Langfitt

significant factors in the genesis of the ischemic damage in many of these patients, it has been tempting to attribute at least some of it to a reduced cerebral perfusion pressure (CPP) secondary to elevated ICP. Miller and Myers 15 found that up to 14 minutes of circulatory arrest could be tolerated by adult monkeys without any morphological evidence of brain damage. When the period of circulatory arrest was increased beyond 15 minutes, ischemic cell changes were observed in the brain stem but not in the more traditionally vulnerable areas of the brain. Hemispheric

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Cerebrospinal fluid lactate and lactate/pyruvate ratios in hydrocephalus

James E. Raisis, Glenn W. Kindt, John E. McGillicuddy, and Carole A. Miller

T he status of cerebral metabolism in hydrocephalus has not been thoroughly investigated. Previous experiments have demonstrated that a moderate increase in intracranial pressure (ICP) may significantly reduce cerebral blood flow due to a decrease in the cerebral perfusion pressure (CPP). 6, 8, 15 In the presence of a decreased CPP there is a shift from aerobic to anaerobic metabolism. 5, 7, 15 The anaerobic metabolism results in a rise in the lactate and lactate/pyruvate (L/P) ratio in brain tissue and the cerebrospinal fluid (CSF). 4, 9, 12, 16 Granholm

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Effects of increased ICP on brain phosphocreatine and lactate determined by simultaneous 1H and 31P NMR spectroscopy

Leslie N. Sutton, Alan C. McLaughlin, William Kemp, M. D. Schnall, Byung-Ku Cho, Thomas W. Langfitt, and Britton Chance

I t is now well established that autoregulation of cerebral blood flow (CBF) occurs when cerebral perfusion pressure (CPP) is decreased by means of an induced rise in cerebrospinal fluid (CSF) pressure. 2, 7 Cortical blood flow, measured by the clearance of radioactive xenon, is generally maintained at normal values until the effective perfusion pressure is lowered to between 30 and 50 mm Hg; however, significant decreases in CBF have been recorded even at moderately reduced CPP's in the range of 110 to 72 mm Hg. 2 Ultimately, compromise of CBF results in

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Catecholamine response to a gradual increase of intracranial pressure

Johan van Loon, Bharati Shivalkar, Chris Plets, Jan Goffin, T. Budya Tjandra-Maga, and Wim Flameng

induce brain death by increasing the ICP gradually and to study concomitant plasma catecholamine levels, showing the relationship between ICP, cerebral perfusion pressure (CPP), and the rise of circulating epinephrine and norepinephrine levels. These observations are of great clinical relevance since most donor hearts for transplantation are from brain-dead patients who have suffered progressive intracranial hypertension. Posttransplant cardiac failure may be due to, among other factors, a catecholamine excess causing myocardial lesions before excision of the donor

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Cerebral blood flow regulation during experimental brain compression

J. Douglas Miller, Albert E. Stanek, and Thomas W. Langfitt

Hg. This difference between MAP and ICP was held to represent cerebral perfusion pressure (CPP). If autoregulation was impaired, irrespective of the cause of impairment, so that a change in MAP caused a corresponding change in CBF, then a subsequent increase in ICP also caused an immediate reduction in CBF. It was concluded that, with this experimental model, maintenance of CBF during increased ICP is a form of autoregulation closely related to the mechanism by which constant CBF is preserved during changes of MAP. 10, 28 Furthermore, with the CSF infusion

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Experimental neurogenic pulmonary edema

Part 1: The role of systemic hypertension

Julian T. Hoff, Merry Nishimura, Jose Garcia-Uria, and Sandra Miranda

, stable cerebral perfusion pressure (CPP). The infusion volume never exceeded 45 cc/kg/30 min, an amount shown previously to have no effect upon the development of experimental NPE. 19 One group of 13 cats served as normal controls, with no infusion of fluid into the lateral ventricle; their ICP was maintained at normal levels throughout the 3½-hour anesthetic period. A second group of nine cats served as Cushing response control animals; their ICP was elevated gradually (at 1 mm Hg/sec) by an intraventricular infusion of mock CSF to a level of 140 mm Hg, which was