ABC of intensive care: neurological support.
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Biomedical subjects
Publications and source records attributed to P J Andrews.
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Using single slice two-dimensional spectroscopic imaging (SI), nine acute head injury patients and six controls have been successfully scanned. The problems presented by the need for ITU monitoring of these patients during MR scanning was overcome using MR compatible monitoring equipment. In previous studies of head injury which used proton spectroscopy, single voxel localisation procedures have meant that the spatial extent of the spectral data has been limited. With spectral data from a whole axial slice, we have been able to identify NAA abnormalities in regions remote to any T2 visible lesions. This suggests that SI (of NAA in particular) will be useful for the diagnosis of diffuse axonal injury.
OBJECTIVE: To investigate the role of the endothelin system in pressure autoregulation of cerebral blood flow (CBF) in rats. DESIGN: We tested pressure autoregulation by increasing cerebral perfusion pressure (CPP; mean arterial pressure-intracranial pressure) with norepinephrine (0.08 microgram.kg-1.min-1 for 30 min) twice in ten anesthetized normocapnic rats. The first test was performed without (control test) and the second test after administration of the combined endothelin ETA/B receptor antagonist, bosentan, i.v. (30 mg/kg; drug test). CBF was measured by the hydrogen clearance technique. RESULTS: During the control test, norepinephrine infusion increased CPP by 21 +/- 2 (23 +/- 2%) mmHg (mean +/- SEM; p < 0.001) and CBF by 3.6 +/- 3.1 (6 +/- 8%) ml/100 g/min (p = 0.5, Fig. 1); during the drug test, norepinephrine infusion increased CPP by 18 +/- 1 (20 +/- 2%) mmHg (p < 0.001) and CBF by 15.8 +/- 4.1 (46 +/- 13%) ml/100 g/min (p = 0.004). Mean arterial pressure was not affected by bosentan infusion (p = 0.2). PaCO2 levels were stable during the tests (40.2 +/- 1.4 mmHg). CONCLUSIONS: The endothelin system is involved in cerebral pressure autoregulation in a rodent model in vivo. The role of this system under pathophysiologic conditions such as subarachnoid hemorrhage, where basal vascular tone and its regulation may be altered, remains to be defined.
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Fibreoptic jugular bulb oximetry has been validated for use in the care of severely head-injured patients. We compared bench and fibreoptic methods of measuring jugular bulb oxyhaemoglobin saturation (SjO2) in 33 patients undergoing cardiac surgery both during cardiopulmonary bypass (CPB) and in the early postoperative period. After insertion of a fibreoptic reflectance oximetry catheter into the jugular bulb, it was calibrated against a bench oximeter. Comparisons were made while on CPB (n = 60) and in the postoperative period for up to 18 h (n = 215). There was negligible bias throughout. There were wide limits of agreements (mean difference +/- 2SD) between the two methods during operation (-20.29% to 18.05%), whereas after operation the limits of agreement were far narrower (-6.39% and 7.45%). Measurement of SjO2 by the fibreoptic method compared poorly with bench oximetry during CPB but there was good agreement between the two methods in the early postoperative period.
We studied 15 patients undergoing cardiac surgery involving hypothermic cardiopulmonary bypass (CPB). Cerebral arteriovenous difference in oxygen content (AVDO2) was significantly less during CPB and for up to 18 h after operation compared with pre-CPB values (P < 0.05). There were no significant changes in mean jugular bulb oxyhaemoglobin saturation (SjvO2), cerebral arteriovenous difference in lactate content or lactate-oxygen index (LOI). SjVO2 and arterial carbon dioxide tension (PaCO2) (P = 0.005) were positively correlated as were AVDO2 and haemoglobin concentration (P = 0.012). AVDO2 and PaCO2 (P = 0.007) were negatively correlated as were LOI and arterial oxyhaemoglobin saturation (P = 0.037). There were no significant correlations between mean arterial pressure and any of the variables. SjVO2 and AVDO2 may require correction for changes in PaCO2 and haemoglobin concentration before relating these variables to cerebral outcome.
OBJECTIVE: Secondary intracranial hypertension has been linked to leukocytosis. We examined our data bank containing physiologic recordings and outcome data of severely head injured patients to investigate the relationship between delayed increases in intracranial pressure (ICP), defined as occurring after a 12-hr period of normal ICP values, and leukocytosis. DESIGN: A retrospective study of observational data. SETTING: Regional neurosurgical unit and intensive care unit. PATIENTS: Sixty-four patients suffered increased ICP >20 mm Hg. Thirty-five patients fulfilled selection criteria for delayed increases in ICP (group 1). Twenty-nine patients with increased ICP with no preceding or intervening periods of normal ICP were selected as a comparison group (group 2). MEASUREMENTS AND MAIN RESULTS: Comparison of 12-month outcome revealed that 11% of group 1 patients died, with 49% remaining severely disabled, in contrast to group 2, where 35% of patients died and 14% were left severely disabled (p = .021). The pattern of outcome was independent of monitoring time, or injury severity. Regression modeling was performed for prediction of delayed increase in ICP. Of 46 patients with an initial increase then decrease in leukocyte count in the first 48 hrs, 65% experienced delayed increases in ICP, as compared with 18% of the 11 patients without this pattern p = .01 1). CONCLUSIONS: Patients with delayed increases have a significantly different pattern of outcome. Change in leukocyte count from admission to day 2 is a significant predictor of such a delayed increase.
OBJECTIVE: We examined the accuracy and repeatability of an intracranial pressure (ICP) monitor (Codman MicroSensor; Johnson & Johnson Professional, Inc., Raynham, MA) in a nonmagnetic environment and during magnetic resonance imaging (MRI). The resulting image artifact generation was calculated. ICP monitoring is essential in management of severe head injury, but few ICP monitoring devices are compatible with use in an MRI scanner. The use of MRI to assess head injury is increasing, and developing safe methods of continuously monitoring ICP may improve patient care. METHODS: A water manometer was used as the standard for comparison. We assessed pressure readings from the ICP monitor in a nonmagnetic environment using a standard and a long connector cable between the pressure transducer and display unit. This long cable permitted testing during MRI sequences because the display unit could be distanced from the magnet. Accuracy was determined during T2-weighted imaging, proton spectroscopy, and diffusion-weighted imaging, and artifact generation was assessed. RESULTS: We found a high degree of accuracy for repeated measurements over a clinical pressure range using both standard and long connector cables outside the MRI room. During MRI scanning, the ICP monitor was accurate during T2 and proton spectroscopy sequences. Accuracy during diffusion-weighted imaging, however, was clinically unacceptable. This ICP monitor creates a reduction in signal-to-noise ratio in the received signal during T2-weighted imaging and proton spectroscopic imaging, with the obtained images still radiologically interpretable. CONCLUSION: The Codman ICP monitor is sufficiently accurate and free of artifact generation to be used during most clinical MRI applications. This could enhance patient monitoring and safety.
OBJECTIVES: Prediction of patient outcome can be useful as an aid to clinical decision making, to explore possible biological mechanisms, and as part of the clinical audit process. Many studies have constructed predictive models for survival after traumatic brain injury, but these have often used expensive, time consuming, or highly specialised measurements. The aim of this study was to develop a simple easy to use model involving only variables which are rapidly and easily clinically achievable in routine practice. METHODS: All consecutive patients admitted to a regional trauma centre with moderate or severe head injury were enrolled in the study. Basic demographic, injury, and CT characteristics were recorded. Patient survival at 1 year was used to construct a simple predictive model which was then validated on a very similar patient group. RESULTS: 372 patients were included in the study, of whom 365 (98%) were followed up for survival at 1 year. Multiple logistic regression resulted in a model containing age (p<0.001), Glasgow coma scale score (p<0.001), injury severity score (p<0.001), pupil reactivity (p=0.004), and presence of haematoma on CT (p=0.004) as independently significant predictors of survival. The model was validated on an independent set of 520 patients, showing good discrimination and adequate calibration, but with a tendency to be pessimistic about very severely injured patients. It is presented as an easy to use nomogram. CONCLUSIONS: All five variables have previously been shown to be related to survival. All variables in the model are clinically simple and easy to measure rapidly in a centre with access to 24 hour CT, resulting in a model that is both well validated and clinically useful.
OBJECTIVES: To assess the prognostic value of summary measures of secondary physiological insult in addition to baseline clinical variables for patients with traumatic brain injury. METHODS: A series of 110 patients with traumatic brain injury had data on intracranial pressure (ICP), arterial blood pressure (ABP), cerebral perfusion pressure (CPP), arterial O2 saturation (SaO2), temperature in degrees C (Temp), and heart rate in beats/min (HRT) monitored and recorded every minute. Secondary insults were defined according to the Edinburgh University secondary insult grading system. The prognostic value of summary measures of these secondary insults was assessed by adding them to a prognostic model for survival at 1 year after controlling for baseline clinical variables using a previously validated model. RESULTS: Of the eight secondary insults measured, only ICP added significantly to the prediction of survival in the first 72 hours after injury. The particular type of summary measure did not seem to influence the results. After the addition of ICP to the model, none of the other secondary insult measures could improve the predictive power of the model significantly. CONCLUSIONS: Early intracranial hypertension is confirmed as a sign of poor prognosis in patients with traumatic brain injury, even after controlling for baseline clinical variables. The value or otherwise of treating such secondary insults, however, can only be definitively established in the context of prospective randomised controlled trials. The specific pathophysiological evolution of secondary insults is still the subject of much research, and a clear understanding will be necessary before the development of specific treatments is feasible.
Neuron specific enolase (NSE) and protein S-100 have previously been described as markers of brain injury. We aimed to discover whether concentrations of either were raised in arterial and jugular venous serum after traumatic brain injury, and whether serum profiles were related to injury severity and neurological outcome. We recruited 22 patients with a traumatic brain injury who were admitted to the intensive care unit. Paired arterial and jugular venous blood samples were taken on admission, and at 24, 48 and 96 hrs after injury. Samples were analysed for NSE and S-100 by RIA. Concentrations of both NSE and S-100 were increased above controls--mean NSE concentration was highest on admission, whilst mean S-100 peaked at 24 hours after injury. There was a small, but significant difference between jugular venous and arterial concentrations of S-100 (p = 0.022). High NSE and S-100 concentrations were significantly related to poor neurological outcome (p = 0.004 and p < 0.001 respectively). Both serum NSE and S-100 may be of some value in helping to predict outcome after a traumatic brain injury.
Adhesion molecules have an important role in leukocyte migration into tissue after injury. We hypothesised that changes in ICAM-1 and L-selectin expression after traumatic brain injury would result in altered serum concentrations of these molecules, which would be related to injury severity and outcome. We investigated arterial and jugular venous concentrations of ICAM-1 and L-selectin in 22 patients. The Glasgow Coma Score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken at designated times after brain injury: on admission, at 24 hours, 48 hours and 96 hours. Glasgow Outcome Scores at 6 months were obtained. Mean serum concentrations of ICAM-1 were normal on admission, but became significantly increased by 96 hours (p = 0.018). Mean L-selectin concentrations wre markedly below controls at all time points (p < 0.001). There were no significant differences between jugular venous and arterial concentrations of either ICAM-1 or L-selectin. Serum ICAM-1 was significantly related to neurological outcome (p < 0.001) and to the Glasgow Coma Score (p < 0.001). These changes in adhesion molecules expression may be important in the pathophysiology of secondary injury. The highly significant relationship between serum ICAM-1 and neurological outcome suggests that drugs which antagonize adhesion molecule activity may improve outcome after traumatic brain injury.
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Diaspirin cross-linked haemoglobin (DCLHb) is a new oxygen carrying blood substitute with vasoactive properties. Vasoactive properties may be mediated via high affinity binding of nitric oxide by the haem moiety. Using a rodent model of head injury combined with ischaemia, we studied the effects of DCLHb on cerebral blood flow (CBF) and intracranial pressure (ICP). Twenty anaesthetized rats were allocated randomly to receive treatment with DCLHb 400 mg kg-1 i.v. or placebo (oncotically matched plasma protein substitute 4.5% i.v.). To produce diffusely increased ICP, after a severe weight drop injury, all animals underwent a 30-min period of bilateral carotid ligation combined with a period of induced hypotension. After reperfusion, DCLHb or placebo was infused and the animals instrumented for measurement of intraventricular ICP and CBF in the region of the sensorimotor cortex using the hydrogen clearance technique. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP) (CPP = MAP - ICP) and CBF were measured 4 h after injury in all animals. DCLHb significantly reduced ICP from mean 13 (SEM 2) to 3 (1) mm Hg (P < 0.001), increased CPP from 52 (8) to 95 (6) mm Hg (P < 0.001) and increased CBF from 21 (2) to 29 (2) ml 100 g-1 min-1 (P = 0.032). We conclude that DCLHb improved CPP without a reduction in CBF in a rodent model of post-traumatic brain swelling.
Twenty-two patients undergoing coronary artery bypass surgery underwent postoperative measurement and recording of jugular venous oxyhaemoglobin saturation (SjO2) with desaturation defined as a value of less than 50% for 5 min or longer. Fifteen of the 22 patients monitored experienced desaturations. An average of four episodes were experienced by those 15 patients (range 1-14). The mean duration of a single episode was 46 (range 5-212) min whilst mean total duration of desaturation was 175 (range 5-570) min. The mean duration of desaturation in the 15 patients, expressed as a percentage of monitored time, was 21.1% (range 0.58%-61.96%). SjO2 desaturation, possibly indicating cerebral hypoperfusion, occurs in the early post-operative period following cardiac surgery.
UNLABELLED: Adhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. IMPLICATIONS: This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful.
UNLABELLED: Reductions in cerebral venous oxyhemoglobin saturation (SjO2) occur during the rewarming phase of hypothermic cardiopulmonary bypass (CPB). We prospectively investigated the effects of propofol on these reductions in SjO2 (SjO2 <50%). Fiberoptic jugular bulb catheters were inserted in 30 patients undergoing coronary artery bypass grafting. Patients were randomly allocated to a test or control group. Test group patients (n = 15) received a propofol IV infusion titrated to electroencephalographic burst suppression during CPB. No significant differences in SjO2 <50% were found between the groups either by blood sampling and bench oximetry or fiberoptic oximetry. The arteriovenous difference in lactate concentration became negative in 59 of 120 samples. Propofol was associated with an increased incidence of hypotension (mean arterial pressure <50 mm Hg) (P = 0.023), an increased requirement for vasoconstrictor therapy (P = 0.025), and increases in the lactate oxygen index (P < 0.01). Propofol, when administered in doses that produce electroencephalographic burst suppression, does not attenuate the frequency or extent of reductions of SjO2 below 50% during rewarming from hypothermic CPB. However, it is associated with arterial hypotension and an increase in cerebral anaerobic metabolism. IMPLICATIONS: Reductions in cerebral venous oxyhemoglobin saturation during the rewarming phase of cardiopulmonary bypass may be related to brain injury. When administered in doses sufficient to produce electroencephalographic burst suppression, propofol did not attenuate the frequency or extent of such reductions in cerebral venous oxyhemoglobin saturation.