Significant Change In Intracranial Pressure Research Articles

Hypertonic Saline Solution versus Mannitol in Children with Intracranial Hypertension: A Systematic Review and Meta-Analysis (P11-7.002)

<h3>Objective:</h3> We aimed to perform a systematic review and meta-analysis on the efficacy of hypertonic saline (HS) versus mannitol (MAN), as hyperosmolar agents, in children with elevated intracranial pressure. <h3>Background:</h3> Hyperosmolar therapy may reduce intracranial hypertension (IH) and act as a lifesaving method in critically ill patients with IH. There is no established superiority of either HS or MAN, the most frequently used agents, in pediatric patients. <h3>Design/Methods:</h3> PubMed, Embase, and Cochrane databases were searched for studies and abstracts published up to October 1st, 2022. Studies were excluded if boluses of HS or MAN were held in patients undergoing elective procedures. The outcomes of interest were mortality; changes in intracranial pressure (ICP); and changes in cerebral perfusion pressure (CPP). <h3>Results:</h3> Six studies with 819 patients were included. The mean patient age ranged from 9 months to 13.5 years. Mortality was not significantly different between the HS (15.6%) and the MAN (21.6%) groups (risk ratio [RR] 0.66; 95% confidence interval [CI] 0.44,0.99; p=0.05). There were also no significant changes in ICP (standardized mean difference −0.25; 95% CI −0.90,0.40; p=0.45) or CPP (standardized mean difference 0.20; 95% CI −0.29,0.68; p=0.42) between patients treated with HS or MAN. <h3>Conclusions:</h3> In this meta-analysis including 819 children with elevated intracranial pressure, there was no difference in mortality, ICP, or CPP between patients treated with HS or MAN. <b>Disclosure:</b> Mr. Menegaz de Almeida has nothing to disclose. Miss Oliveira has nothing to disclose. Miss Viana has nothing to disclose. Dr. Araujo has nothing to disclose. Ms. Oliveira has nothing to disclose. Ms. Dantas has nothing to disclose. Ms. Rodrigues has nothing to disclose. Miss Silva has nothing to disclose. Miss Cordeiro Rocha has nothing to disclose. Dr. Campello Jorge has nothing to disclose. Ms. Godoi has nothing to disclose. Mrs. Reis Marques has nothing to disclose. Mrs. Garcia has nothing to disclose. Miss Barreiros has nothing to disclose. Miss Toguchi has nothing to disclose. Mr. Dos Santos-Bezerra has nothing to disclose. Dr. Polverini has nothing to disclose.

Selective Cerebrospinal Fluid Hypothermia: Bioengineering Development and In Vivo Study of an Intraventricular Cooling Device (V-COOL)

Hypothermia is a promising therapeutic strategy for severe vasospasm and other types of non-thrombotic cerebral ischemia, but its clinical application is limited by significant systemic side effects. We aimed to develop an intraventricular device for the controlled cooling of the cerebrospinal fluid, to produce a targeted hypothermia in the affected cerebral hemisphere with a minimal effect on systemic temperature. An intraventricular cooling device (acronym: V-COOL) was developed by in silico modelling, in vitro testing, and in vivo proof-of-concept application in healthy Wistar rats (n = 42). Cerebral cortical temperature, rectal temperature, and intracranial pressure were monitored at increasing flow rate (0.2 to 0.8 mL/min) and duration of application (10 to 60 min). Survival, neurological outcome, and MRI volumetric analysis of the ventricular system were assessed during the first 24 h. The V-COOL prototyping was designed to minimize extra-cranial heat transfer and intra-cranial pressure load. In vivo application of the V-COOL device produced a flow rate-dependent decrease in cerebral cortical temperature, without affecting systemic temperature. The target degree of cerebral cooling (− 3.0 °C) was obtained in 4.48 min at the flow rate of 0.4 mL/min, without significant changes in intracranial pressure. Survival and neurological outcome at 24 h showed no significant difference compared to sham-treated rats. MRI study showed a transient dilation of the ventricular system (+ 38%) in a subset of animals. The V-COOL technology provides an effective, rapid, selective, and safe cerebral cooling to a clinically relevant degree of − 3.0 °C.

Evaluation of cerebral hemodynamics by transcranial Doppler ultrasonography and its correlation with intracranial pressure in an animal model of intracranial hypertension.

Transcranial Doppler has been tested in the evaluation of cerebral hemodynamics as a non-invasive assessment of intracranial pressure (ICP), but there is controversy in the literature about its actual benefit and usefulness in this situation. To investigate cerebral blood flow assessed by Doppler technique and correlate with the variations of the ICP in the acute phase of intracranial hypertension in an animal model. An experimental animal model of intracranial hypertension was used. The experiment consisted of two groups of animals in which intracranial balloons were implanted and inflated with 4 mL (A) and 7 mL (B) for controlled simulation of different volumes of hematoma. The values of ICP and Doppler parameters (systolic [FVs], diastolic [FVd], and mean [FVm] cerebral blood flow velocities and pulsatility index [PI]) were collected during the entire procedure (before and during hematoma simulations and venous hypertonic saline infusion intervention). Comparisons between Doppler parameters and ICP monitoring were performed. Twenty pigs were studied, 10 in group A and 10 in group B. A significant correlation between PI and ICP was obtained, especially shortly after abrupt elevation of ICP. There was no correlation between ICP and FVs, FVd or FVm separately. There was also no significant change in ICP after intravenous infusion of hypertonic saline solution. These results demonstrate the potential of PI as a parameter for the evaluation of patients with suspected ICP elevation.

Intracranial Pressure During the Development of Renovascular Hypertension.

[Figure: see text].

Changes in intracranial pressure and pulse wave amplitude during postural shifts

Monitoring of intracranial pressure (ICP) and ICP pulse wave amplitude (PWA) is an integrated part of neurosurgery. An increase in ICP usually leads to an increase in PWA. These findings have yet to be replicated during the positional shift from supine to upright, where we only know that ICP decreases. Our main aim is to clarify whether the positional shift also results in a change in pulse wave amplitude. Our database was retrospectively reviewed for subjects having had a standardized investigation of positional ICP. In all subjects, mean ICP and PWA were determined with both an automatic and a manual method and compared using Student's t test. Finally, ICP and PWA were tested for correlation in both in supine and upright position. The study included 29 subjects. A significant change in ICP (Δ14.1mmHg, p < 0.01) and no significant change in PWA (Δ0.4mmHg, p = 0.06) were found. Furthermore, a linear correlation between ICP and PWA was found in both supine and upright positions (p < 0.01). We found that during the positional shift from supine to upright, ICP is reduced while PWA remains unaffected. This indicates that the pressure-volume curve is shifted downward according to a hydrostatic pressure offset, while the slope of the curve does not change. In addition, the correlation between ICP and PWA in both supine and upright position validates the previous research on the matter.

A preliminary exploration of acute intracranial pressure-cerebrospinal fluid production relationships in experimental hydrocephalus.

CONTEXT:By occluding the fourth ventricle simultaneously obtaining telemetric data on intracranial pressure (ICP) and cerebrospinal fluid (CSF) production, the authors of this study investigate a variety of physiologic parameters in cases of experimental hydrocephalus.AIMS:The aim of this study is to provide a new context on the disrupted homeostasis in hydrocephalus and guide toward improved treatment based on multiple physiological parameters.MATERIALS AND METHODS:Hydrocephalus was induced in ten 21-day-old Sprague–Dawley rats by blocking the flow of CSF to the fourth ventricle with kaolin. Ten days post induction, when physical signs of ventriculomegaly reached Evan's ratio (ER) of ≥0.46, CSF flow and ICP were measured while manipulating body position (0°, 45°, 90°) and heart rate.RESULTS:In hydrocephalic animals (ER ≥0.46), we found a near-steady average acute ICP (13.638 ± 2.331) compared to age-matched controls (ER <0.30) (13.068 ± 8.781), whose ICP fluctuated with the position. Hydrocephalic and controls exhibited an insignificant degree of parabolic shifts in CSF production when body position was changed from prone to 90° and again when moved back to the prone position, a trend more noteworthy in controls (P = 0.1322 and 0.2772). A Pearson's Correlation found CSF production and ICP to be correlated at baseline 0° posture (P = 0.05) in the control group, but not the hydrocephalic group. Weight appeared to play a role when animals were held at 90°. No significant changes in ICP or CSF flow patterns were observed when the heart rate was increased within either group.CONCLUSIONS:These preliminary findings suggest that our standard assumptions of posture-dependent changes in ICP created using data from physiologic data may be inaccurate in the hydrocephalic patient, and thus describe a need to further explore these relationships.

Dynamic assessment of cerebral blood flow and intracranial pressure during inversion table tilt using ultrasonography

ContextInversion tables are used as treatment for back pain, but there is a lack of agreement on systemic effects of inversion. ObjectiveTo assess intracranial pressure (ICP) and cerebral blood flow using ultrasonography during inversion table tilt. MethodsOptic nerve sheath diameter (ONSD), heart rate (HR), blood pressure, internal carotid artery (ICA) and middle cerebral artery (MCA) blood flow of participants were measured in 3 positions: supine before inversion, during inversion with head down, and supine post-inversion. ONSD was evaluated with ocular ultrasonography and blood flow (ICA and MCA) with Doppler ultrasonography. ResultsThe ONSD changed significantly between the supine position, at 3 min of inversion, and after returning to supine position (all P < .001). The post-inversion HR was less than pre-inversion (P = .03) and 3-min inversion HR (P = .003). There were significant changes in ICA and MCA flow caused by inversion, which affected blood flow velocity, resistance, and pulsatility index (all P ≤ .005). ConclusionInversion caused significant changes in ICP and blood flow. Thus, increased chance of complications may exist when using inversion as a therapeutic tool or during surgical procedures in patients with previous history of elevated ICP. These results demonstrate that inversion therapy should be used with caution.

The Effects of Resistance Exercise on Intracranial Pressure

IntroductionOne of the primary health concerns faced by NASA astronauts on board the International Space Station is a decline in visual acuity. It is believed that increases in intracranial pressure (ICP) due to resistive exercise performed on the station's Advanced Resistive Exercise Device (ARED) may contribute to Spaceflight Associated Neuro‐Ocular Syndrome (SANS), also referred to as the Visual Impairment and Intracranial Pressure (VIIP) syndrome. In a manner similar to low level Valsalva exertion, it is hypothesized that ICP would increase during low level resistance exercise.MethodsSix healthy subjects (4 male, 2 female, age: 27 ± 10 years, weight: 77 ± 15 kg) were recruited to perform low‐level resistance exercises in both the seated and supine positions. A Cerebral Cochlear Fluid Pressure analyzer (CCFP) was used to noninvasively measure ICP by assessing tympanic membrane displacement (Vm) in the inner ear following an auditory stimulus. Increased values of Vm correspond to a decrease in ICP. After a 10‐minute acclimation period, a baseline measurement was taken with the subject at rest in the seated position. ICP was then measured during randomized, isometric, overhead shoulder holds with weights of 0lbs, 2lbs, and 5lbs (per hand). This procedure was then repeated in the supine position. ICP was also measured in the 15‐degree head down tilt (HDT) position following a 10‐minute acclimation period. Significant differences between groups were determined at p&lt;0.05 using a Student's T‐test.ResultsThe relative changes in Vm with increased loading by position are shown in Figure 1. Vm decreased by 40% ± 15% (p=0.001) in the HDT position as compared to the supine baseline, showing a predicted, reliable increase in ICP for positional changes. In the seated position, displacement increased slightly from baseline (12% ± 63%, p=0.412) for all subjects across all weight levels, indicating a statistically nonsignificant decrease in ICP. Measurements in the supine position were more consistent, with decreasing Vm (3% ± 3%, p=0.563) for all subjects across all weight levels, indicating a nonsignificant increase in ICP.DiscussionContrary to our hypothesis, measured data showed no significant change in ICP during low level resistance exercise in either the seated or supine positions. Based on these results, resistance exercise may not be the primary contributing factor to the development of SANS in astronauts. This study will form the basis of future investigation into the effects of exercise and ICP in different such as gender, age, and clinical populations. Sensitivity of the CCFP to motion and pulse artifacts will also be addressed to reduce variability between subjects.Support or Funding InformationSupported by NASA grant NNX13AJ12GThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The course of intracranial pressure after antipyretic therapy in acute brain injury.

The present study was performed to evaluate intracranial pressure (ICP) variations after antipyretic therapy and their relationship to ICP at baseline (ICPbas) in acute brain injury (ABI) patients. We completed a retrospective analysis on data derived from 2 previously published prospective observational studies. The first study involved 32 ABI patients and was performed to elucidate the cerebral and hemodynamic effects of intravenous (IV) paracetamol. The second study involved 30 ABI patients and was performed to investigate cerebral and hemodynamic effects of intramuscular IM diclofenac sodium (DCF). Overall patient population was divided into 2 groups: 1) group A (G-A) when ICPbas was ≤15 mmHg; and 2) group B (G-B) when ICPbas was >15 mmHg. The main objective was to evaluate if ICPbas affects the time course of ICP after antipyretics administration. Data from 62 ABI patients were analyzed. We failed to observe a significant change in ICP after antipyretic treatment in the overall group of patients (P<inf>1</inf>=0.486). A significant difference, however, was found between the two groups (P<inf>2</inf><0.001). We observed that in the G-A, ICP increased in response to antipyretic administration, whereas in the G-B, ICP decreased. These opposite responses are reflected in the statistically significant interaction (P<inf>3</inf><0.001). Variation in ICP after antipyretic therapy is influenced by ICPbas. Specifically, patients with ICPbas≤15 mmHg showed a significant increase in ICP after antipyretic therapy, while a significant reduction in ICP was observed in patients with ICPbas>15 mmHg.

A Systematic Review of Alpha-2 Agonists for Sedation in Mechanically Ventilated Neurocritical Care Patients.

The use of sedative medications is commonplace in intensive care units (ICUs) and an invaluable clinical tool for the intensive care physician. Sedation for critically ill, mechanically ventilated patients provides an opportunity to reduce anxiety, discomfort as well as ventilator intolerance and dyssynchrony. Alpha-2 agonists in particular have become increasingly popular for use in the neurocritical care population due to their proposed effectiveness in facilitating examinations and procedures as well as reducing the need for adjunctive agents. However, there is a paucity of literature to assess the safety of their use in the neurocritically ill patients, a population that presents unique sensitivities and considerations for management of global and cerebral hemodynamics, agitation and facilitation of neurological assessments. This review assesses the safety and efficacy of alpha-2 agonists for non-procedural sedation in critically ill brain-injured patients on mechanical ventilation. In June 2016, we searched the EMBASE, MEDLINE and CENTRAL Cochrane Databases for randomized controlled trials, prospective and retrospective cohort studies examining neurocritically ill adult patients aged 18 years and older who are on mechanical ventilation and receiving alpha-2 agonists for non-procedural sedation. Primary outcomes of interest include mean arterial pressure (MAP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). Secondary outcomes include adverse events, duration of mechanical ventilation, 30-day mortality, ICU length of stay, incidence of delirium, and quality of sedation. We identified 17 studies for inclusion, all reporting on dexmedetomidine use, only 7 of which reported on our primary outcomes of interest. We found mixed results with regard to statistically significant changes in ICP, CPP, and MAP but did not find evidence of severe hemodynamic disturbances. However, the studies are notably limited by lack of reporting on sedative and hemodynamic adjuncts. Based on the limited available data, dexmedetomidine does not appear to result in severe, uncompensated hemodynamic disturbances (cerebral or systemic). The validation of an effective and safe agent with reporting of dosing strategy, sedation protocol use, co-interventions administered, and a priori defined adverse events is recommended.

Positive End-Expiratory Pressure as a Factor Influencing Cerebral Perfusion Pressure (an experimental study)

Objective: to evaluate the effect of positive end-expiratory pressure (PEEP) on cerebral perfusion pressure (CPP) in intracranial hypertension in an experiment using a biological model. Materials and methods. The experiment was carried out on 10 pigs aged 2 months and weighing 17—20 kg. The experimental animals were anesthetized. The authors monitored the following parameters: invasive arterial and central venous pressures, intracranial pressure (ICP), and peak inspiratory pressure. ICP was simulated with a subdurally placed balloon. During mechanical ventilation (MV), PEEP was gradually increased up to 5, 10, 15, and 20 cm H2O. Results. PEEP elevation during MV was accompanied by a progressive rise in intrathoracic pressure and a reduction in mean blood pressure. When PEEP was increased, there was a significant rise in ICP in the intact brain and basic subcompensated intracranial hypertension; no statistically significant change in ICP was observed in decompensated intracranial hypertension. The safe PEEP with regard to CPP was determined by the severity of basic intracranial distention (it was 15 cm H2O in the intact brain and 10 cm H2O in subcompensated hypertension); PEEP exerted no significant effect on CPP in decompensated intracranial hypertension. Conclusion. The effect of PEEP on CPP is determined by not only the value of PEEP, but also by the severity of brain damage. Key words: positive end-expiratory pressure, intracranial pressure, cerebral perfusion pressure.

Changes in plasma phenylalanine, isoleucine, leucine, and valine are associated with significant changes in intracranial pressure and jugular venous oxygen saturation in patients with severe traumatic brain injury

Changes in plasma aromatic amino acids (AAA=phenylalanine, tryptophan, tyrosine) and branched chain amino acids (BCAA=isoleucine, leucine, valine) levels possibly influencing intracranial pressure (ICP) and cerebral oxygen consumption (SjvO(2)) were investigated in 19 sedated patients up to 14days following severe traumatic brain injury (TBI). Compared to 44 healthy volunteers, jugular venous plasma BCAA were significantly decreased by 35% (p<0.001) while AAA were markedly increased in TBI patients by 19% (p<0.001). The BCAA to AAA ratio was significantly decreased by 55% (p<0.001) which persisted during the entire study period. Elevated plasma phenylalanine was associated with decreased ICP and increased SjvO(2), while higher plasma isoleucine and leucine levels were associated with increased ICP and higher plasma leucine and valine were linked to decreased SjvO(2). The amount of enterally administered amino acids was associated with significantly increased plasma levels with the exception of phenylalanine. Contrary to the initial assumption that elevated AAA and decreased BCAA levels are detrimental, increased plasma phenylalanine levels were associated with beneficial signs in terms of decreased ICP and reduced cerebral oxygen consumption reflected by increased SjvO(2); concomitantly, elevated plasma isoleucine and leucine levels were associated with increased ICP while leucine and valine were associated with decreased SjvO(2) following severe TBI, respectively. The impact of enteral nutrition on this observed pattern must be examined prospectively to determine if higher amounts of phenylalanine should be administered to promote beneficial effects on brain metabolism and if normalization of plasma BCAA levels is without cerebral side effects.

The effect of nursing interventions on the intracranial pressure in paediatric traumatic brain injury

The aim of this research was to investigate the effect of five selected intensive care nursing interventions on the intracranial pressure (ICP) of moderate to severe traumatic brain-injured children in intensive care. The physiological effects of many nursing interventions in paediatric intensive care (PIC) are not known. This results in the lack of an evidence base for many PIC nursing practices. Prospective observational cohort study conducted over 3 years in a single tertiary referral paediatric intensive care unit (PICU) in the North West of England. Five selected commonly performed nursing interventions were studied: endotracheal suctioning and manual ventilation (ETSMV), turning via a log-rolling (LR) approach, eye care, oral care and washing. These were studied in the first 72 h after injury. A total of 25 children with moderate to severe traumatic brain injury and intraparenchymal ICP monitoring in intensive care (aged 2-17 years) were enrolled. Both ETSMV and LR were associated with clinically and statistically significant changes in ICP from baseline to maximal ICP (p = 0·001 ETSMV; p = < 0·001 LR) and from maximal post-ICP (p = < 0·001 ETSMV; p = < 0.001 LR). Eye care, oral care or washing did not cause any clinically significant change in ICP from baseline. After decompressive craniectomy, none of the interventions caused significant changes in ICP. Only two of the five nursing interventions, endotracheal suctioning and LR, caused intracranial hypertension in moderate to severe traumatic brain-injured children, and after craniectomy, no care interventions caused any significant change in ICP. Knowledge about the physiological effects of many intensive care nursing interventions is lacking and this is magnified in paediatrics. This study provides a significant addition to the evidence base in this area and allows intensive care nurses to plan, implement and evaluate more effectively their nursing care for brain-injured children.

Increase in cerebral aerobic metabolism by normobaric hyperoxia after traumatic brain injury

Traumatic brain injury (TBI) is associated with depressed aerobic metabolism and mitochondrial dysfunction. Normobaric hyperoxia (NBH) has been suggested as a treatment for TBI, but studies in humans have produced equivocal results. In this study the authors used brain tissue O(2) tension measurement, cerebral microdialysis, and near-infrared spectroscopy to study the effects of NBH after TBI. They investigated the effects on cellular and mitochondrial redox states measured by the brain tissue lactate/pyruvate ratio (LPR) and the change in oxidized cytochrome c oxidase (CCO) concentration, respectively. The authors studied 8 adults with TBI within the first 48 hours postinjury. Inspired oxygen percentage at normobaric pressure was increased from baseline to 60% for 60 minutes and then to 100% for 60 minutes before being returned to baseline for 30 minutes. The results are presented as the median with the interquartile range in parentheses. During the 100% inspired oxygen percentage phase, brain tissue O2 tension increased by 7.2 kPa (range 4.5-9.6 kPa) (p < 0.0001), microdialysate lactate concentration decreased by 0.26 mmol/L (range 0.0-0.45 mmol/L) (p = 0.01), microdialysate LPR decreased by 1.6 (range 1.0-2.3) (p = 0.02), and change in oxidized CCO concentration increased by 0.21 mumol/L (0.13-0.38 micromol/L) (p = 0.0003). There were no significant changes in intracranial pressure or arterial or microdialysate glucose concentration. The change in oxidized CCO concentration correlated with changes in brain tissue O(2) tension (r(s)= 0.57, p = 0.005) and in LPR (r(s)= -0.53, p = 0.006). The authors have demonstrated oxidation in cerebral cellular and mitochondrial redox states during NBH in adults with TBI. These findings are consistent with increased aerobic metabolism and suggest that NBH has the potential to improve outcome after TBI. Further studies are warranted.

Changes in cerebrovascular response during brain hypothermia after traumatic brain injury.

Transcranial Doppler sonography (TCD) provides a rapid and noninvasive assessment of cerebral hemodynamics after traumatic brain injury. This study evaluates the change of cerebrovascular response at the rewarming stage of brain hypothermia using TCD. Seventeen patients who had suffered from closed brain injury were investigated with daily TCD recordings and the changes in flow velocities were evaluated to determine whether they reflected the temperature during brain hypothermia. All patients who had treated brain hypothermia underwent continuous monitoring of SjO2, mean arterial blood pressure, and intracranial pressure (ICP). No significant changes in ICP and cerebral perfusion pressure (CPP) were recorded in all cases. Of 17 patients, 5 had a significant increase in SjO2 > 75% or more, retrospectively, with a robust increase in flow velocities of the middle cerebral artery (P < .01) at the rewarming stage. These cases marked a decrease in pulsatility index (P < .05) concomitant with an increase in SjO2 values. The CT scan revealed acute brain swelling in these cases. These data suggest cerebral vasoactivity could be altered at the rewarming stage. Hypothermia runs a risk of hyperemia at the rewarming stage, which induced a decrease in cerebral vasoresistance.

Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury.

Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. Prospective study. Neurosurgical intensive care unit A total of 42 patients with severe head injuries. Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 +/- 0.32 to 0.71 +/- 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (> or =5 mm Hg) in the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.

Brain-stem auditory evoked potential monitoring in experimental diffuse brain injury.

The time course of brain-stem auditory evoked potential (BAEP) changes was investigated using an impact-acceleration trauma model in 23 spontaneously breathing rats. Intracranial pressure (ICP), arterial blood pressure and respiratory rate were monitored. The experiments were terminated at four hours after trauma. No significant changes in intracranial pressure (ICP) occurred following the impact. After a short increase, blood pressure returned to baseline values within 5 min. Transient apnea was not followed by prolonged respiratory depression. Diffuse closed head injury (CHI) did not result in general, unidirectional changes of peak latencies or amplitudes of auditory evoked responses. Most BAEP changes developed slowly reaching a maximum at 1 to 4 hours after the injury. In the absence of ICP changes, this pattern reflects secondary ischemia in sensitive brain-stem areas rather than direct traumatic lesions or hypoxia due to respiratory depression.

Effect of passive range of motion on intracranial pressure in neurosurgical patients

Purpose: A prospective patient study was done to evaluate the effect of passive range of motion (PROM) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in neurosurgical patients. Materials and Methods: Twelve adult patients admitted to the neurological-neurosurgical intensive care unit of a community teaching hospital were enrolled in the study. The study patients all required ICP monitoring and they underwent a total of 20 PROM sessions. Six patients (10 PROM sessions) were mechanically ventilated, and six patients (10 PROM sessions) were breathing spontaneously. Mean arterial pressure (MAP), heart rate (HR), respiratory rate (RR), and ICP were measured at baseline and at 1-minute intervals during the physical therapy session. CPP was calculated as the difference between MAP and ICP. Results: No significant changes were detected in MAP, ICP, HR, or RR during the study period. Calculated CPP remained unchanged. Mean duration of PROM intervention was 7 ± 1 minute. Mean Glasgow Coma Scale (GCS) for mechanically ventilated patients was 7 ± 1.3 and for spontaneously breathing patients 13 ± 0.8. Conclusion: PROM results in no significant changes in ICP or CPP in stable, neurosurgical patients in the absence of intracranial hypertension.

Effects of rocuronium and vecuronium on intracranial pressure, mean arterial pressure and heart rate in neurosurgical patients

We have evaluated the effects of a single bolus dose of rocuronium 0.6 mg kg-1 (group 1, n = 10) or vecuronium 0.1 mg kg-1 (group 2, n = 10) on intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and heart rate (HR) in 20 neurosurgical patients undergoing mechanical ventilation of the lungs during continuous sedation with sufentanil and midazolam. Before and after neuromuscular block using twice the ED90 of the blockers, ICP, MAP, CPP and HR were recorded continuously for 15 min. Treatment caused no significant changes in ICP, CPP or MAP and there was no evidence of histamine release. Mean maximum block in the rocuronium group was slightly less than that in the vecuronium group (95.9 (3.1)% vs 100%; ns) The difference between the two groups in onset time (rocuronium 142 (62) s, vecuronium 192 (64) s; P = 0.04) was significant. Patients in the rocuronium group showed a slight (7(4)%) but significant (P = 0.003) increase in heart rate.

The effect of suxamethonium on intracranial pressure and cerebral perfusion pressure in patients with severe head injuries following blunt trauma

Eleven adult patients with severe head injuries caused by blunt trauma, (Glasgow Coma Score of eight or less after resuscitation), were studied while being mechanically ventilated and sedated in the intensive care unit (ICU). In a double blind randomized cross over trial each patient received a bolus of suxamethonium (1 mg kg−1) or an equal volume of saline (0.02 mL kg−1) before planned physiotherapy. Intracranial pressure (ICP) and mean arterial pressure (MAP) were measured continuously for 10 min after each injection. There were no significant changes in intracranial pressure or cerebral perfusion pressure (CPP) following the administration of suxamethonium or saline. Suxamethonium appears to be a safe drug to use on sedated persons with severe head injuries following blunt trauma.