Is crystalloid co-loading necessary to prevent spinal hypotension during elective cesarean delivery? A randomized double-blind trial.

BACKGROUND: Hypotension is common during spinal anesthesia for cesarean delivery. Preventive strategies include fluid loading and phenylephrine. We hypothesized that if prophylactic phenylephrine infusion is used, omission of fluid loading would be non-inferior to fluid co-loading in maintaining cardiac output. We assumed that if there was a difference, the increase in cardiac output would be greater in the no-loading than in the co-loading group. METHODS: Term pregnant women scheduled for elective cesarean delivery were randomized to receive 1 L crystalloid co-loading or maintenance fluids only. Phenylephrine was titrated to maintain blood pressure. Changes in cardiac output following spinal anesthesia were the primary outcome. The study was powered as a non-inferiority trial, allowing the no-loading arm to have a 50% greater change in cardiac output. Heart rate, dose of phenylephrine, occurrence of nausea and vomiting, Apgar scores and neonatal acid base status were secondary outcomes. RESULTS: Data from 63 women were analyzed. In contrast to our hypothesis, there was 33% less increase in cardiac output with no loading (ratio 0.67, 95% CI 0.15 to 1.36), and 60% greater reduction of cardiac output with no loading (ratio 1.6, 95% CI 1.0 to 2.7). Total dose of phenylephrine was higher in the no-loading group. There may be a less favorable neonatal acid base status without volume loading. CONCLUSION: Omission of crystalloid co-loading leads to a decrease in cardiac output which has a potentially unfavorable impact on neonatal acid base status. We conclude that crystalloid co-loading may be useful in the presence of phenylephrine infusion.

Pressure Reactivity-Based Optimal Cerebral Perfusion Pressure in a Traumatic Brain Injury Cohort.

OBJECTIVES: Retrospective data from patients with severe traumatic brain injury (TBI) indicate that deviation from the continuously calculated pressure reactivity-based "optimal" cerebral perfusion pressure (CPPopt) is associated with worse patient outcome. The objective of this study was to assess the relationship between prospectively collected CPPopt data and patient outcome after TBI. METHODS: We prospectively collected intracranial pressure (ICP) monitoring data from 231 patients with severe TBI at Addenbrooke's Hospital, UK. Uncleaned arterial blood pressure and ICP signals were recording using ICM+® software on dedicated bedside computers. CPPopt was determined using an automatic curve fitting procedure of the relationship between pressure reactivity index (PRx) and CPP using a 4-h window, as previously described. The difference between an instantaneous CPP value and its corresponding CPPopt value was denoted every minute as ΔCPPopt. A negative ΔCPPopt that was associated with impaired PRx (>+0.15) was denoted as being below the lower limit of reactivity (LLR). Glasgow Outcome Scale (GOS) score was assessed at 6 months post-ictus. RESULTS: When ΔCPPopt was plotted against PRx and stratified by GOS groupings, data belonging to patients with a more unfavourable outcome had a U-shaped curve that shifted upwards. More time spent with a ΔCPPopt value below the LLR was positively associated with mortality (area under the receiver operating characteristic curve = 0.76 [0.68-0.84]). CONCLUSIONS: In a recent cohort of patients with severe TBI, the time spent with a CPP below the CPPopt-derived LLR is related to mortality. Despite aggressive CPP- and ICP-oriented therapies, TBI patients with a fatal outcome spend a significant amount of time with a CPP below their individualised CPPopt, indicating a possible therapeutic target.

Efficacy and safety of carbetocin given as an intravenous bolus compared with short infusion for Caesarean section - double-blind, double-dummy, randomized controlled non-inferiority trial.

BACKGROUND: Carbetocin is a synthetic oxytocin-analogue, which should be administered as bolus according to manufacturer's recommendations. A higher speed of oxytocin administration leads to increased cardiovascular side-effects. It is unclear whether carbetocin administration as short infusion has the same efficacy on uterine tone compared with bolus administration and whether haemodynamic parameters differ. METHODS: In this randomized, double-blind, non-inferiority trial, women undergoing planned or unplanned Caesarean section (CS) under regional anaesthesia received a bolus and a short infusion, only one of which contained carbetocin 100 mcg (double dummy). Obstetricians quantified uterine tone two, three, five and 10 min after cord-clamping by manual palpation using a linear analogue scale from 0 to 100. We evaluated whether the lower limit of the 95% CI of the difference in maximum uterine tone within the first five min after cord-clamping did not include the pre-specified non-inferiority limit of -10. RESULTS: Between December 2014 and November 2015, 69 patients were randomized to receive carbetocin as bolus and 71 to receive it as short infusion. Maximal uterine tone was 89 in the bolus and 88 in the short infusion group (mean difference -1.3, 95% CI -5.7 to 3.1). Bp, calculated blood loss, use of additional uterotonics, and side-effects were comparable. CONCLUSIONS: Administration of carbetocin as short infusion does not compromise uterine tone and has similar cardiovascular side-effects as a slow i.v. bolus. In accordance with current recommendations for oxytocin, carbetocin can safely be administered as short -infusion during planned or unplanned CS. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov NCT02221531 and www.kofam.ch SNCTP000001197.

Principles of intracranial pressure monitoring and treatment.

Intracranial pressure (ICP) is governed by volumes of intracranial blood, cerebrospinal fluid, and brain tissue. Expansion of any of these volumes will trigger compensatory changes in the other compartments, resulting in initially limited change in ICP. Due to the rigid skull, once compensatory mechanisms are exhausted, ICP rises very rapidly. Intracranial hypertension is associated with unfavorable outcome in brain-injured patients. This chapter discusses the pathophysiology of raised ICP, as well as typical waveforms, monitoring techniques, and clinical management. The dynamics of ICP are more important than the absolute value at any given time point, but mean ICP exceeding 20-25mmHg is usually treated aggressively. Algorithms based on data from patients with traumatic brain injury are applied also in other conditions. However, an understanding of the underlying pathophysiology allows adaptation of therapies to other pathologies. Typically, a three-staged approach is used, starting with restoration of systemic physiology, sedation, and analgesia. If these measures are insufficient, surgical options, such as drainage of cerebrospinal fluid or evacuation of mass lesions, are considered. In the absence of surgical options, stage 2 treatments are initiated, consisting of either mannitol or hypertonic saline. If these measures are insufficient, stage 3 therapies include hypothermia, metabolic suppression, or craniectomy.

Effect of n-3 fatty acids on markers of brain injury and incidence of sepsis-associated delirium in septic patients.

BACKGROUND: Data regarding immunomodulatory effects of parenteral n-3 fatty acids in sepsis are conflicting. In this study, the effect of administration of parenteral n-3 fatty acids on markers of brain injury, incidence of sepsis-associated delirium, and inflammatory mediators in septic patients was investigated. METHODS: Fifty patients with sepsis were randomized to receive either 2 ml/kg/day of a lipid emulsion containing highly refined fish oil (equivalent to n-3 fatty acids 0.12 mg/kg/day) during 7 days after admission to the intensive care unit or standard treatment. Markers of brain injury and inflammatory mediators were measured on days 1, 2, 3 and 7. Assessment for sepsis-associated delirium was performed daily. The primary outcome was the difference in S-100ß from baseline to peak level between both the intervention and the control group, compared by t-test. Changes of all markers over time were explored in both groups, fitting a generalized estimating equations model. RESULTS: Mean difference in change of S-100ß from baseline to peak level was 0.34 (95% CI: -0.18-0.85) between the intervention and control group, respectively (P = 0.19). We found no difference in plasma levels of S-100ß, neuron-specific enolase, interleukin (IL)-6, IL-8, IL-10, and C-reactive protein between groups over time. Incidence of sepsis-associated delirium was 75% in the intervention and 71% in the control groups (risk difference 4%, 95% CI -24-31%, P = 0.796). CONCLUSION: Administration of n-3 fatty acids did not affect markers of brain injury, incidence of sepsis-associated delirium, and inflammatory mediators in septic patients.

Effect of age on intraoperative cerebrovascular autoregulation and near-infrared spectroscopy-derived cerebral oxygenation.

BACKGROUND: Age is an important risk factor for perioperative cerebral complications such as stroke, postoperative cognitive dysfunction, and delirium. We explored the hypothesis that intraoperative cerebrovascular autoregulation is less efficient and brain tissue oxygenation lower in elderly patients, thus, increasing the vulnerability of elderly brains to systemic insults such as hypotension. METHODS: We monitored intraoperative cerebral perfusion in 50 patients aged 18-40 and 77 patients >65 yr at two Swiss university hospitals. Mean arterial pressure (MAP) was measured continuously using a plethysmographic method. An index of cerebrovascular autoregulation (Mx) was calculated based on changes in transcranial Doppler flow velocity due to changes in MAP. Cerebral oxygenation was assessed by the tissue oxygenation index (TOI) using near-infrared spectroscopy. End-tidal CO2, O2, and sevoflurane concentrations and peripheral oxygen saturation were recorded continuously. Standardized anaesthesia was administered in all patients (thiopental, sevoflurane, fentanyl, atracurium). RESULTS: Autoregulation was less efficient in patients aged >65 yr [by 0.10 (se 0.04; P=0.020)] in a multivariable linear regression analysis. This difference was not attributable to differences in MAP, end-tidal CO2, or higher doses of sevoflurane. TOI was not significantly associated with age, sevoflurane dose, or Mx but increased with increasing flow velocity [by 0.09 (se 0.04; P=0.028)] and increasing MAP [by 0.11 (se 0.05; P=0.043)]. CONCLUSIONS: Our results do not support the hypothesis that older patients' brains are more vulnerable to systemic insults. The difference of autoregulation between the two groups was small and most likely clinically insignificant.

Bupivacaine concentrations in lumbar cerebrospinal fluid in patients with failed spinal anaesthesia.

BACKGROUND: Spinal anaesthesia (SA) has high success rates. However, inadequate block after SA has been reported even in the absence of technical problems. Various mechanisms for failed SA (FSA) have been proposed, but reports of cerebrospinal fluid (CSF) concentrations of local anaesthetics (LA) after FSA are scarce. We report lumbar CSF concentrations of bupivacaine in 20 patients in whom adequate block after subarachnoid injection failed to develop. METHODS: All patients with inadequate block after subarachnoid injection of plain bupivacaine 0.5% and in whom a second subarachnoid injection of LA was to be performed as a rescue technique were eligible for entry into this study. A CSF sample was withdrawn immediately before injection of the second dose of LA. Patients in whom failure was obviously due to technical problems or inadequate dosage were excluded. Bupivacaine concentrations were assessed with high-performance liquid chromatography. RESULTS: During the study period of 15 months, 2600 spinal anaesthetics were performed. The failure rate was 2.7% (71 patients). In 20 patients (0.77%), CSF concentrations of bupivacaine were determined, which ranged from 3.36 to 1020 microg ml(-1). CONCLUSIONS: Inadequate CSF concentration of LA is a common reason for FSA. However, in 12 of our 20 patients, concentrations were above 73 microg ml(-1), a concentration that should lead to an adequate block. In these patients, maldistribution of bupivacaine could be responsible for FSA. In view of the absence of sufficient block, despite adequate lumbar CSF concentrations of bupivacaine, concerns about neurotoxicity with repeat injections may be warranted.

Bupivacaine concentrations in the lumbar cerebrospinal fluid of patients during spinal anaesthesia.

BACKGROUND: Data on bupivacaine concentrations in the cerebral spinal fluid (CSF) during spinal anaesthesia are scarce. The purpose of this study was to determine the concentration of bupivacaine in the lumbar CSF of patients with an adequate level of spinal anaesthesia after injection of plain bupivacaine 0.5%. METHODS: Sixty patients with an adequate level of spinal block after standardized administration of plain bupivacaine 20 mg in men and of 17.5 mg in women were studied. To measure the CSF bupivacaine concentration, we performed a second lumbar spinal puncture and obtained a CSF sample at a randomized time point 5-45 min after the bupivacaine injection. In addition, we calculated the half-life of bupivacaine in the CSF and tested the hypothesis that the level of spinal block is related to the lumbar CSF bupivacaine concentration. RESULTS: Men and women had CSF bupivacaine concentrations ranging from 95.4 to 773.0 microg ml(-1) (median 242.4 microg ml(-1)) and from 25.9 to 781.0 microg ml(-1) (median 187.6 microg ml(-1)), respectively. The large variability of bupivacaine concentrations obtained at similar times after subarachnoid administration made calculation of a meaningful half-life of bupivacaine in CSF impossible. There was no association between CSF bupivacaine concentration and spinal block level, and CSF bupivacaine concentrations for the same spinal block level differed between patients by six-fold. CONCLUSIONS: There is a large variability of CSF bupivacaine concentrations in patients with an adequate level of spinal anaesthesia.

Effects of catecholamines on cerebral blood vessels in patients with traumatic brain injury.

Data on the cerebrovascular effects of catecholamines after head injury are difficult both to interpret and to compare. Diverse parameters with regard to brain trauma animal models, methods of determining the effects on the cerebral blood flow and metabolism and choice of end-points have been used. Many studies investigate the cerebrovascular effects of catecholamines over a range of cerebral perfusion pressures above the range recommended by current guidelines. The relationship between patient outcome and the use of a specific substance to improve cerebral perfusion has not been investigated. Dopamine, norepinephrine and phenylephrine all seem to increase cerebral blood flow in various animal models and in patients. The data suggest that norepinephrine may be the most predictable. It is associated with an improved restoration of global and regional oxygenation when compared to dopamine. Dopamine has been associated with an increase in brain oedema. There is further evidence that dopamine has many disadvantages in critically ill patients due to its ability to suppress circulating concentrations of most anterior pituitary-dependent hormones. Both aspects would further discourage its use. Data on phenylephrine are scarce. It has been associated with increased intracranial pressure and a failure to improve cerebral oxygenation despite markedly improved cerebral perfusion pressure. For all other catecholamines and related substances there are insufficient data on the cerebrovascular effects after head injury. This suggests that norepinephrine may be the catecholamine that is the most suitable substance to maintain or restore adequate cerebral perfusion. The data, however, are insufficient to formulate a guideline.

Intracranial pressure in patients with sepsis.

INTRODUCTION: In sepsis the brain is frequently affected although there is no infection of the CNS (septic encephalopathy). One possible cause of septic encephalopathy is failure of the blood-brain barrier. Brain edema has been documented in animal models of sepsis. Aggressive fluid resuscitation in the early course of sepsis improves survival and is standard practice. We hypothesized that aggressive fluid administration will increase intracranial pressure (ICP) and may cause critical reductions in cerebral perfusion pressure (CPP). MATERIALS AND METHODS: Patients with sepsis were investigated daily on up to four consecutive days in the intensive care unit. Mean arterial blood pressure (MAP) and blood flow velocity in the middle cerebral artery were monitored for one hour each day. ICP was calculated non-invasively from MAP and flow velocity data. S-100beta was determined daily. FINDINGS: Fifty-two measurements were performed in 16 patients. ICP could be determined in 45 measurements in 15 patients. Seven patients had an ICP > 15 mmHg and 11 patients had a CPP < 60 mmHg on at least 1 day. We found no significant correlation between ICP and fluid administration, but low CPP was significantly correlated with elevated S-100beta (r = -0.47, p = 0.001). CONCLUSIONS: Further research is needed to determine the role of ICP/CPP monitoring in patients with sepsis.

The accuracy of non-invasive carbon dioxide monitoring: a clinical evaluation of two transcutaneous systems.

We determined the accuracy of two transcutaneous carbon dioxide monitoring systems (SenTec Digital Monitor with V-Sign Sensor and TOSCA 500 with TOSCA Sensor 92) for the measurement of single values and trends in the arterial partial pressure of carbon dioxide in 122 adult patients during major surgery and in 50 adult patients in the intensive care unit. One or several paired measurements were performed in each patient. The first measurement was used to determine the accuracy of a single value of transcutaneous carbon dioxide; the difference between the first and the last measurements was used to analyse the accuracy and to track trends. We defined a 95% limit of agreement of

Effects of simulated hypovolaemia on haemodynamics, left ventricular function, mesenteric blood flow and gastric Pco2.

BACKGROUND: Compensated clinically silent hypovolaemia may lead to low cardiac output, hypoperfusion and ischaemia. We investigated the cardiovascular effects of simulated hypovolaemia to determine whether it caused mesenteric ischaemia detectable by gastric tonometry. METHODS: Thirteen healthy volunteers, aged 21-36 years, were investigated. Lower body negative pressure (LBNP) was used to simulate normotensive hypovolaemia. Cardiovascular parameters were measured using echocardiography. Mesenteric blood flow was investigated using Doppler sonography of the superior mesenteric artery (SMA). Gastric Pco(2) (P(g)co(2)) was measured using gas tonometry. Data were collected at baseline, LBNP and during a recovery period. RESULTS: Normotensive hypovolaemia was induced successfully in 11 volunteers. There were no significant differences in mean arterial pressure between the three data points (91 +/- 6, 93 +/- 10 and 95 +/- 9 mmHg, respectively). With the induction of LBNP, the heart rate increased from 64 +/- 16 to 73 +/- 16 beats/min (P < 0.001), the cardiac index decreased from 2.7 +/- 1.0 to 1.8 +/- 0.6 l/min/m(2) (P= 0.002) and the systemic vascular resistance increased from 1535 +/- 445 to 2270 +/- 550 dyn s/cm(5) (P < 0.001). The SMA mean flow velocity decreased from 53 +/- 18 to 37 +/- 20 cm/s (69 +/- 20%) (P= 0.007), and increased to 56 +/- 34 cm/s (106 +/- 38%) (P= 0.001) during reperfusion. The SMA resistance increased from 92 +/- 30 to 174 +/- 110 mmHg/l/min (P= 0.004). These changes were reversible after termination of LBNP. By contrast, there were no significant differences in P(g)co(2) between the three data points. CONCLUSIONS: In these volunteers, the mesenteric vascular bed contributed importantly to the maintenance of arterial pressure during normotensive hypovolaemia. However, this compensated hypovolaemia did not compromise the mesenteric perfusion sufficiently to increase P(g)co(2) and to allow detection by tonometry.

Monitoring the injured brain: ICP and CBF.

Raised intracranial pressure (ICP) and low cerebral blood flow (CBF) are associated with ischaemia and poor outcome after brain injury. Therefore, many management protocols target these parameters. This overview summarizes the technical aspects of ICP and CBF monitoring, and their role in the clinical management of brain-injured patients. Furthermore, some applications of these methods in current research are highlighted. ICP is typically measured using probes that are inserted into one of the lateral ventricles or the brain parenchyma. Therapeutic measures used to control ICP have relevant side-effects and continuous monitoring is essential to guide such therapies. ICP is also required to calculate cerebral perfusion pressure which is one of the most important therapeutic targets in brain-injured patients. Several bedside CBF monitoring devices are available. However, most do not measure CBF but rather a parameter that is thought to be proportional to CBF. Frequently used methods include transcranial Doppler which measures blood flow velocity and may be helpful for the diagnosis and monitoring of cerebral vasospasm after subarachnoid haemorrhage or jugular bulb oximetry which gives information on adequacy of CBF in relation to the metabolic demand of the brain. However, there is no clear evidence that incorporating data from CBF monitors into our management strategies improves outcome in brain-injured patients.

Physiological thresholds for irreversible tissue damage in contusional regions following traumatic brain injury.

Cerebral ischaemia appears to be an important mechanism of secondary neuronal injury in traumatic brain injury (TBI) and is an important predictor of outcome. To date, the thresholds of cerebral blood flow (CBF) and cerebral oxygen utilization (CMRO(2)) for irreversible tissue damage used in TBI studies have been adopted from experimental and clinical ischaemic stroke studies. Identification of irreversibly damaged tissue in the acute phase following TBI could have considerable therapeutic and prognostic implications. However, it is questionable whether stroke thresholds are applicable to TBI. Therefore, the aim of this study was to determine physiological thresholds for the development of irreversible tissue damage in contusional and pericontusional regions in TBI, and to determine the ability of such thresholds to accurately differentiate irreversibly damaged tissue. This study involved 14 patients with structural abnormalities on late-stage MRI, all of whom had been studied with (15)O PET within 72 h of TBI. Lesion regions of interest (ROI) and non-lesion ROIs were constructed on late-stage MRIs and applied to co-registered PET maps of CBF, CMRO(2) and oxygen extraction fraction (OEF). From the entire population of voxels in non-lesion ROIs, we determined thresholds for the development of irreversible tissue damage as the lower limit of the 95% confidence interval for CBF, CMRO(2) and OEF. To test the ability of a physiological variable to differentiate lesion and non-lesion tissue, we constructed probability curves, demonstrating the ability of a physiological variable to predict lesion and non-lesion outcomes. The lower limits of the 95% confidence interval for CBF, CMRO(2) and OEF in non-lesion tissue were 15.0 ml/100 ml/min, 36.7 mumol/100 ml/min and 25.9% respectively. Voxels below these values were significantly more frequent in lesion tissue (all P < 0.005, Mann-Whitney U-test). However, a significant proportion of lesion voxels had values above these thresholds, so that definition of the full extent of irreversible tissue damage would not be possible based upon single physiological thresholds. We conclude that, in TBI, the threshold of CBF below which irreversible tissue damage consistently occurs differs from the classical CBF threshold for stroke (where similar methodology is used to define such thresholds). The CMRO(2) threshold is comparable to that reported in the stroke literature. At a voxel-based level, however (and in common with ischaemic stroke), the extent of irreversible tissue damage cannot be accurately predicted by early abnormalities of any single physiological variable.

Predicting the response of intracranial pressure to moderate hyperventilation.

BACKGROUND: Hyperventilation may cause brain ischaemia after traumatic brain injury. However, moderate reductions in PaCO(2) are still an option in the management of raised intracranial pressure (ICP) under some circumstances. Being able to predict the ICP-response to such an intervention would be advantageous. We investigated the ability of pre-hyperventilation ICP and cerebrospinal compensatory reserve to predict the reduction in ICP achievable with moderate hyperventilation in head injured patients. METHODS: Thirty head injured patients requiring sedation and mechanical ventilation were investigated. ICP was monitored via an intraparenchymal probe and intracranial cerebrospinal compensatory reserve was assessed using an index (R(ap)) based on the relationship between mean ICP and its pulse amplitude. Measurements were made at a constant level of PaCO(2) during a 20-minute baseline period. The patients were then subjected to an acute decrease in PaCO(2) of approximately 1 kPa and, after an equilibration period of 10 minutes, measurements were again made at a constant level of PaCO(2) for a further 20 minutes. A multiple linear regression model, incorporating baseline PaCO(2), ICP, and R(ap) was used to identify the relevant predictors of ICP reduction. FINDINGS: Baseline ICP and R(ap) were both significant predictors of ICP-reduction (p=0.02 and 0.001 respectively) with R(ap) being the more powerful parameter. CONCLUSIONS: A model based on cerebrospinal compensatory reserve and ICP can predict the achievable ICP-reduction and may potentially be used to optimise patient selection and intensity of hyperventilation.

Effects of moderate hyperventilation on cerebrovascular pressure-reactivity after head injury.

In volunteers, hyperventilation improves autoregulation. However, in head-injured patients, hyperventilation-induced deterioration and improvement of autoregulation have been reported. We have re-examined this question using an index of pressure reactivity. Thirty patients with severe or moderate head-injury were studied. Arterial blood pressure, cerebral perfusion pressure (CPP), and intracranial pressure (ICP) were recorded over 20 minute epochs separated by ten minutes of equilibration at baseline and during moderate (>3.5 kPa) hyperventilation. End-tidal CO2 was constant during each phase of data acquisition. Pressure reactivity was assessed using an index 'PRx' based on the response of ICP to spontaneous blood pressure changes. Hyperventilation decreased PaCO2 from 5.1 +/- 0.4 to 4.4 +/- 0.4 kPa (p < 0.0001). ICP decreased by 3.7 +/- 2.2 mmHg (p < 0.001). CPP increased by 5.9 +/- 8.2 mmHg (p < 0.001). Overall, PRx did not change significantly with hyperventilation. However, there was a significant negative correlation between baseline PRx and the change in PRx (r = -0.71, p < 0.0001). This suggests that patients with disturbed pressure-reactivity may improve, whereas patients with intact pressure reactivity remain largely unchanged. Our data suggest that the response of pressure reactivity to hyperventilation is heterogeneous. This could be due to hyperventilation-induced changes in cerebral metabolism, or the change in CPP.

Association between outcome, cerebral pressure reactivity and slow ICP waves following head injury.

OBJECTIVE: To investigate the relationships between slow vasogenic waves ('B waves') of intracranial pressure (ICP), pressure-reactivity and outcome after traumatic brain injury. MATERIAL AND METHOD: 193 head-injured patients (age 34 +/- 16.7 years; median GCS 6) were monitored from 1997 to 2002. ICP, arterial blood pressure (ABP) were continuously monitored. Pressure-reactivity index (PRx) and magnitude of ICP slow waves were evaluated using the bed-side computers. RESULTS: Distribution of PRx in different outcome groups indicated that pressure-reactivity was significantly worse in patients with fatal outcome. A magnitude of spontaneous slow waves of ICP was gradually decreasing in poorer outcome grades. Mortality indicated threshold rise from 20% to 70% when averaged PRx increased above 0.3 (p < 0.01). There was no threshold for mortality observed along distribution of magnitude of ICP slow waves. Mortality gradually increased when the magnitude of slow waves decreased (R = -0.26; p < 0.0001). CONCLUSION: Inadequate pressure-reactivity and low magnitude of slow vasogenic waves of ICP are associated with fatal outcome after head injury. Based on brain monitoring data, differentiation between favourable outcome and severe disability is more problematic than differentiation between survivors and non-survivors.