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Biomedical subjects

A Marmarou

Publications and source records attributed to A Marmarou.

At least 127 records · Page 7Linked to original sources
PubMed1990

[Test of non-invasive PVI measure with a fiber-optic pressure monitoring device in head injured patients].

At present, method for determining pressure volume status in head injured patients must be obtained via analysis of pressure response to bolus injections into the ventricular catheter system. The concept introduced by Bray of extracting Pressure Volume Index (PVI) measures from analysis of the pulse pressure centroid presents a less invasive technique and provides PVI data continuously. The objective of this study was to test the application of the system which incorporated the Bray concept to PVI measures in head injured patients. The centroid of frequency power spectrum was provided continuously by a computer system linked to the bedside monitor. The computer incorporated the Bray concept for PVI estimation. These values were compared with PVI measured by conventional bolus technique. We tested the system using ICP pulsating wave form delivered from a fiberoptic pressure monitoring system in brain tissue in two different band-width (Narrow band-width: 4-8 Hz, Wide band-width: 4-15 Hz). PVI studies using bolus fluid injection or withdrawal were conducted at least twice a day and usually each study consisted of 3 to 6 injections or withdrawals to obtain a study average PVI. These study average were correlated with the centroid obtained during the same study interval in 17 head injured patients of Glasgow Coma Scale (GCS) 8 or less. The correlation of the centroid and PVI in the wide band-width group was significant (p less than 0.01, r = 0.77), however, in the narrow band-width group, the correlation was not significant (r = 0.07, N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Importance of protein content in the edema fluid for the resolution of brain edema.

This study shows that there is a quantitative relation between the protein content of edema fluid and the rate of fluid clearance. Minimal clearance takes place during the first 3 days in the high albumin group. Thereafter, the majority of the fluid is cleared, and tissue water returns to normal values by 8 days. This appears to support an idea that the rate of clearance is in direct proportion to protein concentration. This also supports the findings of Kuroiwa et al. who showed a direct relation between protein extravasation and the increase of water in extracellular vasogenic edema. However, the rate of clearance does not in fact appear to be linear with time as the greater percentage of protein edema fluid is cleared after 3 days. This may be explained by the observations of Rasmussen and Klatzo and Bodsch and Hossmann who indicate that the composition of the extracellular protein may undergo various changes, similar to fragmentation, hence increasing the number of osmotically active particles so the pre-existing edema would remain stable or slightly increase. In conclusion, this study demonstrates that the infusion model of edema can be applied to the rat for study of resolution dynamics. We have also shown that in this model, there is a proportional relation between protein concentration of the edema fluid and time necessary for clearance.

Albumins↗
PubMed1990

Comparative studies of edema produced by fluid percussion injury with lateral and central modes of injury in cats.

Earlier studies by our laboratories indicated that severe fluid percussion injury in cats results in the development of significant brain edema. In this study we measured the spatial distribution of edema developed after both central and lateral modes of impact with the objective of determining the degree to which the edema volume may contribute to ICP elevation and neurologic deterioration. All animals developed a marked increase in tissue water, particularly in the brainstem. In laterally injured cats, the increase in brainstem water equaled the edema produced supratentorially. Adding the increase of brainstem edema and the edema volume of the supratentorial compartment, we found an average water increase of 1.125 cc in survivors and 2.492 cc in nonsurvivors. This represents a significant volume increase when it is considered that the average PVI of the normal cat is approximately 0.9 cc (6). However, we observed that the PVI was reduced soon after injury and at a time when it has been reported that water content was near normal levels (7). Taking these studies in concert, we believe that the early reduction in PVI is most probably due to vascular swelling. The developing edema further contributes to reductions in PVI, thus setting the stage for elevated ICP and the tissue impaction observed in nonsurvivors.

Animals↗
PubMed1990

Clearance of infusion edema fluid at high and low levels of intracranial pressure.

We found that under conditions of sustained edema production, the rate of edema resolution by the CSF is not appreciably enhanced with lowering of the ICP. Although the entrance of edema fluid into CSF for the high-pressure series was notably slower, the amount of edema remaining in the brain was not appreciably affected. This appears somewhat contradictory to the principle that increasing the bulk flow pressure gradient should increase flow into the CSF. However, simultaneous steady-state measurements of the change in brain tissue pressure for a corresponding change in CSF pressure showed that the two pressures are identical. As a result, when ICP is lowered, the brain tissue pressure follows with no gradient increase. This also suggests that lowering of ICP and the concomitant reduction of tissue pressure may increase the intravascular tissue pressure gradient, which may act to increase the edema production. More work is required to resolve this issue.

Animals↗
PubMed1990

Contribution of brainstem edema to neurophysiologic deterioration in the cat infusion edema model.

These results show that infusion edema produces a significant increase in brainstem tissue water similar to the distribution seen after traumatic injury. The increased brainstem water of 0.24 cc is equivalent to a brainstem volume rise of 7.26% and was sufficient to cause a marked reduction in the PVI and sustained elevation of the ICP. Despite the ICP rise, somatosensory and brainstem potentials are only mildly affected and return to normal within 8 hr. The fact that severe fluid percussion injury results in obliteration of BAER immediately after impact would suggest that the neurologic deterioration seen in the fluid percussion model of injury is due to direct structural damage of the tissue, which was received at the moment of impact, and not to the compressive effect of the developing brainstem edema at levels achieved in these experiments (7.62% swelling). As in other mechanical models, edema results in secondary compression of the tissue and contributes to the general brain swelling, which if unabated could lead to tentorial herniation and death. In these infusion studies, we must conclude that in some cases, mild secondary compression was sufficient to affect other control centers and produce systemic failure at levels of edema that do not result in alteration of evoked potentials. This might explain the deaths of those animals that occurred during the infusion period in which brainstem potentials remained intact.

Animals↗
PubMed1990

In vivo characterization of infusion edema by magnetic resonance imaging.

In vivo measurements of relaxation time profiles were carried out in cats using the infusion model of edema. These profiles were correlated with independent gravimetric measurements of brain water. The results indicated that in vivo determinations of water content by MRI are possible with high spatial resolution.

Animals↗
PubMed1989

Relationship between CT attenuation changes and post-traumatic CSF-CKBB-activity after severe head injury in man.

In order to evaluate if it is practically possible to assess the volume of contused brain tissue from the CT pictures, a comparison has been carried out between the size of the cerebral contusion(s)--as estimated from the CT scans--and the post-traumatic CSF-CKBB activity, in a series of 29 patients with severe head injury. A clearance curve for the elimination of CKBB from the CSF was constructed. The relation between contusion volume and CSF-CKBB-activity was not statistically significant, while the relationships between contusion volume and outcome, and between CSF-CKBB, as estimated at 6 hours after from the clearance curve, and outcome, were.

Adolescent↗
PubMed1989

The importance of protein content in the oedema fluid for the resolution of brain oedema.

The infusion model of oedema is developed in the rat. Unilateral, constant volume, intracerebral infusions of oedema fluid of varying protein (bovine albumin) concentrations are performed. Brain tissue is analyzed for water content using the gravimetric technique. The authors find significant differences in the spatial distribution of brain water in the different infusion groups at 48 and 72 hours post infusion. The control infusate (mock cerebrospinal fluid) clears by 72 hours. However, infusates containing protein (32.5 and 65.0 mg/ml albumin) are not completely cleared until 5 to 8 days post infusion, with the less concentrated solution clearing more rapidly in the area of infusion at 72 and 96 hours post infusion. The data support the hypothesis that the rate of clearance of vasogenic brain oedema is dependent on the amount of extravasated protein.

Albumins↗
PubMed1989

Laser-Doppler assessment of brain microcirculation: effect of systemic alterations.

There is a need for new technical approaches whereby the cerebral microcirculation can be easily and continuously assessed. The objective of this study was to determine whether laser-Doppler (LD) flowmetry can be utilized to assess changes in cerebral cortical blood flow and to determine whether changes in blood perfusion measured by LD flowmetry correlate with simultaneously measured changes in flow measured by H2 clearance in cats or with changes in pial arteriolar diameter measured with a microscope in rabbits equipped with a closed cranial window. In the rabbit experiments a 0.84-mm-diam LD probe was inserted through a cranial window port, and in the cat experiments the probe was fixed adjacent to the H2 probe. The probe was fixed at a distance of 1-2 mm from the cortical surface, where it and its associated electronics detect changes in blood cell velocity and blood volume within a tissue volume of approximately 1 mm3. Volume and velocity are multiplied to provide a flow signal. When cerebral blood flow in cats was decreased by hyperventilation-induced hypocapnia and increased by norepinephrine-induced hypertension, the percent changes in LD flow and H2 clearance flow changed linearly (r = 0.94, slope = 0.97). When arterial PCO2 was increased from 28 to 48 mmHg in the rabbit experiments, the pial arterioles dilated 19 +/- 4% (mean +/- SE) and LD flow increased by 74 +/- 9%, LD flow changes which would be predicted by a third power relationship of diameter to flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Stable xenon versus radiolabeled microsphere cerebral blood flow measurements in baboons.

Regional cerebral blood flow was simultaneously determined using the stable xenon computed tomographic and the radioactive microsphere techniques over a wide range of blood flow rates (less than 10-greater than 300 ml/100 g/min) in 12 baboons under conditions of normocapnia, hypocapnia, and hypercapnia. A total of 31 pairs of determinations were made. After anesthetic and surgical preparation of the baboons, cerebral blood flow was repeatedly determined using the stable xenon technique during saturation with 50% xenon in oxygen. Concurrently, cerebral blood flow was determined before and during xenon administration using 15-microns microspheres. In Group 1 (n = 7), xenon and microsphere determinations were made repeatedly during normocapnia. In Group 2 (n = 5), cerebral blood flow was determined using both techniques in each baboon during hypocapnia (PaCO2 = 20 mm Hg), normocapnia (PaCO2 = 40 mm Hg), and hypercapnia (PaCO2 = 60 mm Hg). Xenon and microsphere values in Group 1 were significantly correlated (r = 0.69, p less than 0.01). In Group 2, values from both techniques also correlated closely across all levels of PaCO2 (r = 0.92, p less than 0.001). No significant differences existed between the slopes or y intercepts of the regression lines for either group and the line of identity. Our data indicate that the stable xenon technique yields cerebral blood flow values that correlate well with values determined using radioactive microspheres across a wide range of cerebral blood flow rates.

Animals↗
PubMed1989

Cerebral blood flow and metabolism in severely head-injured children. Part 1: Relationship with GCS score, outcome, ICP, and PVI.

The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow ("CBF15"), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow as found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume

Adolescent↗
PubMed1989

Cerebral blood flow and metabolism in severely head-injured children. Part 2: Autoregulation.

Autoregulation of cerebral blood flow ("CBF15") was tested in a series of 26 pediatric patients (mean age 13.2 years) with severe head injury (average Glasgow Coma Scale (GCS) score 5.5) in the acute stage. A baseline 133Xe CBF measurement was performed and then repeated, after blood pressure was increased by 29% with intravenous phenylephrine or decreased by 26% with intravenous trimethaphan camsylate. Correlations were made between CBF and clinical condition, outcome, time after injury, intracranial pressure (ICP), and pressure-volume index (PVI) changes, and the site of injury (hemispheres, diencephalon, or brain stem). The site of injury was determined with multimodality evoked potential measurements. Autoregulation was intact in 22 (59%) of 37 measurements. There was no correlation with GCS score, outcome, time after injury, site of injury, or way of testing (decreasing or increasing blood pressure). Autoregulation was statistically significantly more often impaired when CBF was either below normal -2 standard deviations (SD) (reduced flow) or above normal +2 SD (absolute hyperemia). In cases with intact autoregulation, mean ICP decreased from 17.5 to 15.0 mm Hg with higher blood pressure and increased from 19.0 to 21.3 mm Hg with lower blood pressure. When PVI was measured during the blood pressure manipulations, it was found to change in a direction opposite to the ICP change. The consequences of these findings in the management of ICP problems with blood pressure control are discussed.

Adolescent↗
PubMed1988

Spectral analysis of the EEG in craniocerebral trauma.

The objectives of the present study were to evaluate the relationship between the fractional amplitudes of the EEG derived from power spectral analysis (PSA) of the electroencephalogram (EEG) and depth of coma measured clinically with the Glasgow Coma Score, and to assess the accuracy of PSA in predicting long-term outcome. Thirty-two patients rendered unconscious by blunt head injury (mean (GCS = 7) had intermittent EEG recordings daily from 1-10 days post injury. There was a significant correlation between fractional amplitude of the EEG and the GCS. The rate and magnitude of change in the EEG and GCS were also correlated. There were significant differences in PSA parameters between improved and deteriorated patient groups at the termination of monitoring (p = .02) and in the change of PSA parameters over time (p = .02). Using linear discriminant analysis of PSA parameters, the accuracy of outcome prognostication based on the six month outcome was approximately 75%. Accurate classification of outcome was possible in a number of patients in whom there was little or no change in the GCS during the period of monitoring.

Adolescent↗
PubMed1988

Comparison of nurse and computer recording of ICP in head injured patients.

The importance of intracranial pressure monitoring in management and study of the head-injured patient is clearly recognized by the clinician responsible for intensive care. However, in many institutions studies requiring quantitative measures of ICP in head-injured patients are limited by lack of sophisticated computer monitoring equipment. In this study we tested the ability of the nurse to describe ICP course by manual record and compared these results with an on-line computerized ICP monitoring system. The nurse recorded a single "end-hour" value of ICP from the bedside monitor while the computer averaged 720 data samples of ICP during the hour. Our results obtained from five head-injured patients undergoing ICP monitoring showed 55% of the 347 data points had a difference in ICP of 0.01 to 3.0 mm Hg and 38% differed between 3.01 and 6 mm Hg. In comparison, 84% of nurse observations were within 6 mm Hg. Comparison of the temporal course of nurse and computer ICP values combined with the frequency distribution of error data indicates the nurse "end-hour" value is a reasonable estimate of the patient's mean ICP for the entire hour as measured by the computer. Nurses can now ask questions regarding various aspects of a patient's ICP course and compare data with other groups as long as the method of data collection is defined in the same manner.

Computers↗
PubMed1988

Cerebral energy metabolism following fluid-percussion brain injury in cats.

Clinical and experimental evidence suggests that head injury can cause alterations of cerebral energy metabolism. However, the etiology of this metabolic perturbation is not known. The objective of this study was to determine the effect of fluid-percussion trauma on cerebral energy metabolism. Seven ventilated, chloralose-anesthetized cats were subjected to a 3.2-atm fluid-percussion brain injury. Before and for 8 hours after trauma, continuous phosphorus-3 1 magnetic resonance spectrography was obtained to noninvasively monitor tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi) levels. Measurement of cerebral blood flow (CBF) by the radioactive microsphere technique and calculation of oxygen and glucose consumption (CMRO2 and CMRG1) were also performed before trauma as well as 30 minutes and 1, 2, 4, and 8 hours after trauma. The data showed a moderate decrease in tissue pH from 7.04 to 6.89 at 30 minutes following trauma with return to control levels by 3 hours posttrauma. During the 8-hour observation period, CBF, CMRO2, and CMRG1 remained at control levels. Tissue PCr and Pi levels were also unchanged. Fluid-percussion trauma at the 3.2-atm level in ventilated cats causes a moderate and transient decrease in tissue pH that returns to control levels after trauma. No other metabolic changes are seen later than 30 minutes posttrauma. This indicates that a mild metabolic disturbance occurs after trauma in the ventilated animal and quickly returns to normal.

Animals↗
PubMed1988

Effect of posttraumatic hypoventilation on cerebral energy metabolism.

Cerebral energy metabolism was studied in cats subjected to fluid-percussion brain trauma followed immediately by 30 minutes of controlled hypoventilation for the purpose of simulating a more realistic model of human head injury. The cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGl) were measured, with simultaneous phosphorus-31 magnetic resonance spectroscopy quantifications of cerebral tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi). Hypoventilation alone did not produce marked changes in CMRGl, tissue pH, or PCr:Pi ratios. When hypoventilation was combined with trauma, marked alterations in CBF, CMRGl, PCr:Pi ratio, and tissue pH were seen, indicating relative ischemia. The alterations of cerebral energy metabolism produced by combining trauma and hypoventilation are more severe than those caused by fluid-percussion trauma alone, and may provide a more realistic model of human head injury.

Animals↗
PubMed1988

Production and clearance of lactate from brain tissue, cerebrospinal fluid, and serum following experimental brain injury.

Lactate dynamics in the brain, cerebrospinal fluid (CSF), and serum were studied in 20 chloralose-anesthetized cats following fluid-percussion trauma. Brain lactate and brain tissue pH were measured by hydrogen-1 and phophorus-31 magnetic resonance spectroscopy. The CSF, arterial, and cerebrovenous serum lactate levels as well as serum glucose concentration were quantified. In the six sham-operated control animals, brain, CSF, cerebrovenous, and arterial lactate levels as well as brain pH remained at normal values. In the five animals in the mild-trauma group (1.6 atm), brain and CSF lactate levels were moderately elevated, although the brain pH and serum lactate content remained at control values. Severe trauma (3.1 atm) in nine cats produced an 82% increase in the brain lactate index and a reduction in brain tissue pH (7.02 +/- 0.02 to 6.95 +/- 0.02; mean +/- standard error of the mean), indicating brain tissue acidosis caused by excessive lactate accumulation. Brain lactate levels reached a peak 1 1/2 hours after severe trauma, then steadily decreased to normal levels by 8 hours posttrauma. Maximum increases of CSF and arterial lactate levels (from 1.4 +/- 0.2 to 4.1 +/- 0.4 and from 1.6 +/- 0.2 to 4.1 to 0.6 mmol/liter, respectively) were observed 15 minutes after trauma, and the values decreased during the next 2 hours. The response was biphasic, with a secondary rise observed in both CSF and serum lactate levels during the remaining 4 hours of the experiment. The difference between the arterial and venous lactate levels (A-Vlact) gradually increased and reached a peak 2 hours postinjury (from -0.05 +/- 0.10 to -0.41 +/- 0.09 mmol/liter). The results of this study show that the production of lactate in brain tissue, CSF, and blood increased in proportion to the severity of the injury. The observation that lactate levels in blood and CSF are maximum immediately following impact while brain lactate and A-Vlact are gradually increasing suggests that the brain-tissue production of lactate fails to account for the rapid appearance of lactate in CSF and blood. It is speculated that the initial elevation of CSF lactate values reflects the systemic response of trauma, and the secondary rise of CSF lactate levels following severe trauma is due to slow seepage of lactate produced by brain tissue into the CSF space. These studies are the first to describe the temporal profile of brain lactate production and eventual clearance by CSF and blood in fluid-percussion injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗