Comparison of a new brain tissue oxygenation probe with the established standard.

INTRODUCTION: Continuous bedside brain tissue oxygenation (p(br)O(2)) monitoring using the Licox system is an established method for detecting secondary ischemia in comatose patients with acute brain injury. The purpose of the current study was to compare the newly introduced Raumedic p(br)O(2) probe with the established standard. METHODS: Eighteen patients with acute traumatic brain injury or aneurysmal subarachnoid hemorrhage had p(br)O(2) probes of both types implanted side by side in the same vascular territory at risk of ischemia. Data were analyzed by the Bland-Altman method as well as random effect regression models to correct for multiple measurements per individual. RESULTS: Both types of probes were able to display spontaneous fluctuations of p(br)O(2) as well as reactions to therapy. Mean measurement difference between the Licox and Raumedic probes was -2.3 mmHg, with corresponding 95% limits of agreement of -32.3 to 27.5 mmHg. Regarding an ischemia threshold of 15 mmHg, both probes were in agreement in 78% and showed disparate results in 22%. CONCLUSIONS: Our data suggest that the p(br)O(2) measurements of the two systems cannot be interchanged. Although we were unable to determine which system delivers more valid data, we do think that more rigorous testing is necessary before implementing the new probe in clinical routine.

Drift of the Bowman Hemedex® cerebral blood flow monitor between calibration cycles.

INTRODUCTION: Since its introduction into clinical practice, the Bowman Hemedex® regional cerebral blood flow (CBF) monitor has provided a valuable tool for the bedside assessment of CBF in neurointensive care. The purpose of our study was to estimate the accuracy of CBF measurements between automatically performed self-calibration cycles at regular intervals. METHODS: We analyzed data from 75 CBF probes, predominantly implanted into patients after severe subarachnoid hemorrhage. Automatic recalibration of the regional CBF device was performed every 30 min. CBF data were averaged once per minute and the measurement cycles pooled. Statistical analysis was performed with generalized additive modeling and bootstrapping methods. RESULTS: Mean regional CBF was 24 mL/100 g/min after calibration and showed a mean drift of 2.3 mL/100 g/min per measurement cycle (p < 0.001). In every patient, the drift over the measurement cycle followed an exponential trend, with large heterogeneity between patients (-3.67 to 12.0 mL/100 g/min). A highly significant difference in drift was found for the internal software versions of the monitoring devices (p < 0.001). CONCLUSIONS: Data from the Bowman Hemedex® regional CBF monitor shows an upward measurement drift of clinically relevant magnitude. As the drift follows a stable exponential function over time, recalculation of drift-corrected data is possible after termination of the measurement.

Continuous selective intraarterial infusion of nimodipine for therapy of refractory cerebral vasospasm.

BACKGROUND: For endovascular treatment of vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), an intraarterial treatment course with the calcium channel antagonist nimodipine infused for 30 min is proposed. As some patients still show ongoing vasospasm thereafter, we report on our experience with an extended time period of selective intraarterial nimodipine administration. METHODS: In nine patients with aSAH and refractory cerebral vasospasm, we left the catheter in place within the internal carotid artery after angiography. On the neurosurgical ICU, a continuous infusion of intraarterial nimodipine was commenced, combined with intraarterial heparin anticoagulation. Therapy was controlled with extended neuromonitoring techniques. RESULTS: Three patients died from refractory vasospasm and a fourth suffered lethal sepsis. Three patients survived in a good clinical condition, two of them without apparent neurologic deficit. The efficacy of intraarterial nimodipine was best verified with regional CBF monitoring. TCD failed to detect vasospasm in two patients and missed improvement in four. Brain tissue oxygenation increased in all patients, but was not indicative of vasospasm in one. CT perfusion reflected the treatment course adequately in the qualitative scans. CONCLUSION: Selective continuous intraarterial nimodipine treatment for refractory cerebral vasospasm after aSAH seems feasible and may add to the endovascular therapeutic options. Appropriate monitoring technology is essential for further investigation of this novel technique.

Qualitative aspects of cranial CT perfusion scanning in a mixed neurosurgical patient collective.

BACKGROUND: In patients with ischemic stroke, computer tomography (CT) perfusion imaging provides rapid information on the penumbra adjacent to the infarct core. For neurosurgical patients with acute brain injury, the value of CT perfusion is undecided up to now. We present our experience in a series of 78 examinations in 35 patients with acute intracranial pathology. METHODS: CT perfusion was performed with a Siemens Emotion Duo CT scanner using a single slice at the level of the upper basal ganglia. Color maps of time to peak (TTP), cerebral blood flow (CBF) and cerebral blood volume (CBV) were analyzed according to qualitative criteria. Quantitative evaluation with self-defined regions of interest was not performed due to repeatability problems and inconsistent data. FINDINGS: TTP showed an interhemispheric difference in 45% and regional prolongation in 16% of the scans. Global TTP was prolonged in 60%, while global CBF was reduced in 43%. Two patients showed hyperemia. A CBF/CBV mismatch, indicating non-infarcted penumbra at risk, was seen in 67%. Six patients with aneurysmal SAH showed reduced CBF, and consecutive angiography confirmed vasospasm in every case. CONCLUSIONS: CT perfusion scanning gives valuable information at a low risk and with negligible additional time after a routine cranial CT. In our opinion, this modality may have considerable impact on the clinical management of severely brain injured patients in future.

The safety of the open lung approach in neurosurgical patients.

A recent randomized controlled trial in patients with ARDS showed the beneficial effect of mechanical ventilation according to the so called Open Lung Approach, consisting of low tidal volumes and elevated PEEP settings after performing recruiting maneuvers. However, neurosurgical patients were excluded from this and other ARDS trials due to concerns of intracranial deterioration. In this report, we present the clinical data of eleven patients with known intracranial pathology and concomitant ARDS which was treated according to the Open Lung concept. The mean oxygenation index (paO2/FiO2) increased from 132 +/- 88 to 325 +/- 64 measured 24 hours after initiation of Open Lung ventilation (p < 0.001). Mean PEEP level after the first recruiting maneuver was 14.9 +/- 3.2 mmHg. Comparison of mean and peak ICP values over 24 hours of time before and after the first recruitment maneuver revealed a non-significant decline in ICP despite a moderate increase in mean paCO2. Although two patients needed additional ICP treatment, no patient had to be withdrawn from Open Lung ventilation. In our series, Open Lung ventilation in neurosurgical patients with ARDS was a safe method to improve oxygenation. Careful ICP monitoring provided, there is no reason to withhold this modern ARDS treatment in the neurosurgical intensive care unit.

Management of severe traumatic brain injury by decompressive craniectomy.

OBJECTIVE: The beneficial effect of decompressive craniectomy in the treatment of head trauma patients is controversial. The aim of our study was to assess the value of unilateral decompressive craniectomy in patients with severe traumatic brain injury. METHODS: We retrospectively investigated 49 patients who underwent decompressive craniectomy. Intracranial pressure, cerebral perfusion pressure, therapy intensity level, and cranial computed tomographic scan features (midline shift, visibility of ventricles, gyral pattern, and mesencephalic cisterns) were evaluated before and after craniectomy. The gain of intracranial space was calculated from cranial computed tomographic scans. Patient outcome was graded using the Glasgow Outcome Scale. RESULTS: Thirty-one patients (63.3%) underwent rapid surgical decompression within 4.5 +/- 3.8 hours after trauma; in 18 patients (36.7%), delayed surgical decompression was performed 56.2 +/- 57.0 hours after injury. Patients younger than 50 years or patients who underwent rapid surgical decompression had a significantly better outcome than older patients or patients who underwent delayed surgical decompression. Craniectomy significantly decreased midline shift and improved visibility of the mesencephalic cisterns. The state of the mesencephalic cisterns correlated with the distance of the lower border of the craniectomy to the temporal cranial base. Alterations in intracranial pressure, cerebral perfusion pressure, and therapy intensity level were not significant. The overall mortality of the patients corresponded to the reports of the Traumatic Coma Data Bank (1991). CONCLUSION: Although there was a significant decrease in midline shift after craniectomy, this did not translate into decompressive craniectomy demonstrating a beneficial effect on patient outcome.

Leukocyte-endothelium-interaction in pial vessels following global, cerebral ischaemia.

BACKGROUND: Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. METHODS: Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. FINDINGS: Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p < 0.001) and a smaller increase of the venular diameters (p < 0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. INTERPRETATION: In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia.

Endothelin-1 in subarachnoid hemorrhage: An acute-phase reactant produced by cerebrospinal fluid leukocytes.

BACKGROUND AND PURPOSE: The most potent vasoconstrictor known, endothelin-1, is currently considered to mediate cerebral vasospasm in subarachnoid hemorrhage (SAH), which can cause delayed cerebral ischemia. In our study, we performed clinical and in vitro experiments to investigate the origin and the mechanisms of the secretion of endothelin-1 in SAH. METHODS: Endothelin-1 and markers of inflammatory host response (interleukin [IL]-1ss, IL-6, and tumor necrosis factor-alpha) were comparatively quantified in the cerebrospinal fluid (CSF) of SAH patients and control subjects, and concentrations were related to clinical characteristics. Furthermore, mononuclear leukocytes isolated from the CSF of SAH patients and control subjects were analyzed regarding their mRNA expression of endothelin-1 and inflammatory cytokines. Finally, complementary in vitro experiments were performed to investigate whether coincubation of blood and CSF can trigger leukocytic mRNA expression and release of these factors. RESULTS: Activated mononuclear leukocytes in the CSF of SAH patients synthesize and release endothelin-1 in parallel with known acute-phase reactants (IL-1ss, IL-6, and tumor necrosis factor-alpha). Complementary in vitro experiments not only further confirmed this leukocytic origin of endothelin-1 but also showed that aging and subsequent hemolysis of blood is sufficient to induce such endothelin-1 production. CONCLUSIONS: The demonstration that endothelin-1 is produced by activated CSF mononuclear leukocytes suggests that subarachnoid inflammation may represent a therapeutic target to prevent vasospasm and delayed cerebral ischemia after SAH.

Factors leading to hydrocephalus after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: The predisposing factors for the development of posthemorrhagic hydrocephalus, requiring shunt implantation, after subarachnoid hemorrhage (SAH) are still not exactly known. Therefore we analyzed the patients with SAH, who were treated in our department with respect to the development of chronical cerebro-spinal fluid (CSF) imbalance, trying to define predictive parameters for this entity. METHODS: All patients presenting with SAH were analyzed retrospectively between September 1992 and July 1998. Special consideration was given to the initial CT scan (cistern index, Fisher grade, bicaudate index) and the requirement for an external ventricular drainage. Other possible predictive factors as age, Hunt & Hess grade, electrolyte disturbances and operative techniques were also evaluated. RESULTS: During the investigation period, 283 patients presenting with aneurysmal SAH underwent surgery. Fifty-two patients (18.4%) required a shunting procedure due to chronic posthemorrhagic hydrocephalus. The mean time interval between the initial bleeding and shunting was 28 days. All of these patients required a significantly longer external CSF drainage (p < 0.001) with a much higher amount of daily drained CSF (p < 0.001). The evaluation of the initial CT scan revealed no correlation between the amount of blood and later shunt dependency. However, there was a significant correlation with the bicaudate index (p < 0.01). CONCLUSION: Chronic hydrocephalus after aneurysmal SAH is an important complication. The recovery-time of shunt dependent patients is definitely prolonged compared to non-shunted patients. Predictive factors of shunt dependency seem to be length and amount of the external CSF drainage, as well as a high bicaudate index.

Hypertonic saline solution for control of elevated intracranial pressure in patients with exhausted response to mannitol and barbiturates.

Critically elevated intracranial pressure (ICP) represents the most important cause of morbidity and mortality in patients suffering from severe traumatic brain injury (TBI) and is a serious complication after subarachnoid hemorrhage (SAH). Thus new strategies for the control of ICP are required. Based on the evidence available hypertonic saline solution (HSS) may be a promising approach. It was therefore the aim of the present study to evaluate in a prospective manner the effects of HSS on ICP and cerebral perfusion pressure (CPP) in patients with therapy-resistant elevation of ICP. A total of 48 bolus infusions of HSS (7.5%, 2 ml kg-1 b.w.; infusion rate 20 ml min-1) were given intravenously (range 1-15 per patient) to 10 patients (age 41 +/- 6 years) with TBI and SAH. Only patients with ICP > 25 mmHg not responding to standard ICP-management protocol and plasma sodium (Na+) concentration < 150 mmol l-1 were included in the study. Within the first hour after HSS application, ICP decreased from 33 +/- 9 mmHg to 19 +/- 6 mmHg (p < 0.05) and further to 18 +/- 5 mmHg at the time of maximum effect (98 +/- 11 min post bolus). Decrease of ICP was accompanied by a rise of CPP from 68 +/- 11 mmHg to 79 +/- 11 mmHg (p < 0.05) after 1 h and further to 81 +/- 11 mmHg at the time of maximum effect. Plasma Na+ concentration was 141 +/- 6 mmol l-1 before and 143 +/- 5 mmol l-1 1 h after HSS bolus. Corresponding values for plasma osmolality were 302 +/- 11 and 308 +/- 12 mOsm l-1. When the ICP lowering effect was transient, subsequent HSS bolus was necessary 163 +/- 54 min after previous dosing. The present results indicate that repeated bolus application of HSS (7.5% NaCl, 2 ml kg-1 b.w.) is an effective measure to decrease ICP which is otherwise refractory to standard therapeutic approaches. Whether or not the therapy scheme is also suited as primary measure for the control of ICP remains to be established.

Penetrating craniocerebral injuries in a civilian population in mid-Europe.

Our current neurosurgical understanding of civilian penetrating craniocerebral injuries is based on US metropolitan series. It is unknown whether all principles applied to these patients are relevant in the Mid-European setting with its distinct epidemiology. The objective of this study was to characterize our patients with penetrating craniocerebral injuries, to analyze their outcome, and to identify relevant prognostic factors. Thirty-two patients with penetrating craniocerebral injuries were entered into the study. Patient evaluation comprised neurological, laboratory and radiographic analyses. Motivating factors were suicide (75%), assault (13%), and accident (9%). Initial GCS score, coagulopathy on admission, and radiographic extent of injury could be identified as outcome predictors (P < 0.001). An aggressive therapeutic approach to patients with GCS 3-7 reduced mortality when compared to a conservative management (67 vs. 91%). Due to major differences in epidemiology and outcome of our penetrating craniocerebral injury patients when compared to major US metropolitan series, current therapeutic strategies applied to this patient population in mid-Europe should be reconsidered. The results of our study justify an aggressive neurosurgical approach even in those patients that are thought to have a deleterious prognosis. Predictive variables identified in this study and a novel CT-grading algorithm may help in decision making.

Influence of platelet-activating factor on cerebral microcirculation in rats: part 1. Systemic application.

BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) has been demonstrated to have a mediator function in shock, with some of its deleterious effects being attributed to its influence on microcirculation. Systemic PAF concentrations as found in shock could also compromise the cerebral microcirculation. Our purpose in the present study was to examine the influence of systemically applied PAF on microvascular perfusion and leukocyte-endothelium interactions in cerebral microvessels. METHODS: A closed cranial window technique was used for intravital fluorescence microscopy of the brain surface. PAF was infused in concentrations of 10(-12), 10(-9), and 10(-6) mol/L into the carotid artery (5 mL/h for 20 min) of Sprague-Dawley rats (n=30). The selective PAF receptor antagonist WEB 2170BS (2 mg/kg body weight) was used to inhibit specific PAF effects. RESULTS: The number of leukocytes (cells/100 microm. min) rolling along or adhering at the venular endothelium increased following infusion of PAF 10(-6) mol/L from 7.7+/-2.5 to 24.4+/-8.9 (P<0.05) and from 1.9+/-0.5 to 6.9+/-2.2 (P<0.05), respectively, within 2 hours. Mean arterial pressure decreased from 92+/-22 mm Hg to 49+/-17 mm Hg (P<0.05). The lower concentrations of PAF were less effective to decrease mean arterial pressure but also induced leukocyte-endothelium interactions. The intravenous administration of WEB 2170BS 15 min before the infusion of PAF 10(-6) mol/L prevented both systemic hypotension and activation of leukocyte-endothelium interactions. CONCLUSIONS: Increased systemic blood levels of PAF as found during shock can not only cause systemic arterial hypotension but also induce leukocyte-endothelium interactions in cerebral venules. The activation of leukocytes was found to be independent of PAF-induced arterial hypotension. The specificity of these results is confirmed by the findings that WEB 2170BS could inhibit the PAF-induced systemic hypotension as well as the activation of leukocytes.

Influence of platelet-activating factor on cerebral microcirculation in rats: part 2. Local application.

BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) is involved in the development of secondary brain damage after ischemic and traumatic brain injury. On the basis of data from studies in peripheral organs, we hypothesized that PAF-mediated effects after cerebral injury could be secondary to alterations in cerebral microcirculation. METHODS: Changes in cerebral microcirculation focusing on leukocyte-endothelium interactions were quantified with the use of a closed cranial window model in Sprague-Dawley rats (n=33) by means of intravital fluorescence microscopy. The brain surface was superfused with PAF in concentrations from 10(-3) (n=3) to 10(-12) mol/L (n=6) for 20 minutes (5 mL/h). RESULTS: PAF 10(-4) mol/L (n=4) increased the number of rolling and adherent leukocytes in venules from 9.7+/-0.4 to 19.7+/-2.3 cells/100 mm. min (P=NS versus control) and from 2.2+/-0.5 to 4.3+/-0.7 cells/100 mm. min (P<0.05 versus control), respectively. Lower concentrations did not elicit leukocyte-endothelium interactions. Vessel diameters remained unchanged except for a transient increase of arteriolar diameters during superfusion with PAF 10(-4) and 10(-6) mol/L (n=6). Although only a limited area of the brain surface was exposed to PAF, the mediator induced a significant dose-dependent transitory arterial hypotension and caused irreversible circulatory shock at the high concentration (PAF 10(-3) mol/L). Arterial hypotension after administration of PAF 10(-3) mol/L could be attenuated by the intravenous pretreatment with the PAF antagonist WEB 2170BS. CONCLUSIONS: PAF, when locally released after brain injury, can penetrate the blood-brain barrier and induce systemic effects, including arterial hypotension. Its role as a mediator in the development of secondary brain damage seems, at least in the initial phase, not to be associated with disturbances of cerebral microcirculation or activation of leukocytes.

The Camino intracranial pressure device in clinical practice: reliability, handling characteristics and complications.

Intracranial pressure monitoring has a key role in the management of patients developing increased intracranial pressure (ICP). We adopted the Camino fiberoptic system for intracranial pressure measurement in 1993 in our neurosurgical department. The aim of this study was to investigate reliability, handling characteristics and complication rate of the Camino intracranial pressure device. In an eighteen month period, we prospectively investigated 118 patients with intracranial pathology undergoing Camino fiberoptic intraparenchymal or intraventricular ICP monitoring. The assessment of reliability of ICP monitoring according to patients clinical condition, to cranial computed tomography (CCT) findings and ICP waveform was carried out. Position of the probe and intracranial bleeding complications related to probe insertion were confirmed by CCT. Technical complications, as well as infections due to the device, were documented. In vivo recalibration was performed in 22 patients. At the end of the measuring period the drift of the probe was evaluated and the accuracy of the fiberoptic device was measured by performing a two point calibration. Recordings of intracranial pressure were carried out with 136 Camino devices (104 parenchymal, 32 ventricular) in 118 patients with an average measuring time of 94.1 +/- 79.1 hrs. One hundred and fifteen Camino intracranial pressure devices (85.2%) demonstrated reliability according to the predetermined clinical parameters. The actual mean drift after removal of the devices was 3.4 mmHg +/- 3.2 with an actual daily drift of 3.2 +/- 17.2 mmHg. Recorded complications included infection (0.7%), intraparenchymal haematoma (5.1%), and a high complication rate (23.5%) with regard to technical aspects. The Camino intracranial pressure system offers reliable ICP measurements in an acceptable percentage of devices, and the advantage of in vivo recalibration. The high incidence of technical complications identifies a need for improvement in the fiberoptic cable and the fixation system.

Rapid active internal core cooling for induction of moderate hypothermia in head injury by use of an extracorporeal heat exchanger.

OBJECTIVE: Moderate hypothermia (32 degrees C) may limit postischemic neuronal damage and is increasingly used clinically in head injury and stroke. For the use of hypothermia as a neuroprotective agent in the prevention of ischemic damage, it is necessary to induce it as soon as possible after the insult and to keep it at the lowest safe level. Active core cooling using an extracorporeal heat exchanger may circumvent the rather slow induction speed and temperature drifts experienced with surface cooling techniques. METHODS: In eight patients with severe head injuries (Glasgow Coma Scale score, 4-5), a venovenous extracorporeal circulation was established via a percutaneously introduced double-lumen cannula in the femoral vein. A heat exchanger was connected via a pressure-controlled roller pump. In addition to standard parameters, brain white matter temperature was continuously recorded as the target temperature. Cooling was initiated as early as possible with an extracorporeal temperature of 30 degrees C and maintained at a 32 degrees C brain temperature for 48 hours, and then gradual rewarming for 24 hours. RESULTS: Cooling was able to be initiated within 6 hours and 48 minutes +/- 3 hours and 47 minutes (mean +/- standard deviation) after trauma. A brain temperature of 32 degrees C was reached within 1 hour and 53 minutes +/- 1 hour and 21 minutes after induction of cooling with a cooling speed of 3.5 degrees C per hour. Brain temperature was able to be controlled within 0.1 degrees C intervals, which was especially helpful in gradual rewarming. No cardiac abnormalities or statistically significant changes in coagulation parameters occurred. Mean platelet count decreased to 89,614+/-42,090 on Day 3 after treatment. No clinical bleeding complications or problems resulting from extracorporeal circulation occurred. Moderate hypothermia was a helpful tool for managing increased intracranial pressure; however, five patients of this series died either of their intracranial abnormalities (n = 4) or of a delayed septic shock after pneumonia (n = 1) at various points in time during therapy. The three survivors experienced either an excellent or a good recovery. CONCLUSION: The results of this investigation suggest that the use of an extracorporeal heat exchanger to achieve active core cooling is suitable for fast and accurately controllable induction, maintenance, and reversal of moderate hypothermia in emergency situations with reliable control of temperature. In this small series of highly selected patients with severe head injuries, we did not note a beneficial effect of hypothermic therapy on outcome.

Assessment of the CAMINO intracranial pressure device in clinical practice.

The purpose of this study was to investigate reliability, handling characteristics and complication rate of the CAMINO-ICP-monitor-system in clinical routine. In a case controlled study 82 patients with intracranial pathology necessitating ICP-monitoring received either a ventricular or a parenchymal CAMINO-device. Clinical assessment of curve shape and apparent reliability of the measurement was documented. Probe position and presence of hematoma was evaluated in all patients with a CT after probe insertion. Handling complications, i.e. dislocation were recorded. At the end of the measuring period the drift of the probe was checked ex vivo and a two point calibration was performed using a water column. During one year 82 patients received 95 probes (parench, 73. ventric. 22). The average measuring period was 91.3 +/- 70.6 hrs. Catheter position was verified by CCT for 67 (70.5%) probes. 92.5% of the devices were placed correctly. Clinically 88.4% of the measurements were assessed plausible, in 8.2% the displayed ICP-values were judged to be too high, in 2.1% too low. Probe drift after explanation was -0.21 mmHg/24 hrs. The mean value of the recalibrated probes in the water column corresponding to 15.8 mmHg was 14.7 +/- 1.9 mmHg. There was no correlation between neither drift nor function in the water column and the duration of the measurement. Technical complications exclusively related to the construction of the CAMINO-system like kinking of the cable, dislocation (probe pulled out) or dislocated fixation screw were too high (25.3%).

Experimental antileukocyte interventions in cerebral ischemia.

White blood cells (WBCs) play vital roles in host defense. Recently, increasing interest has been directed toward the question of whether WBCs, particularly polymorphonuclear leukocytes, could also act as mediators of secondary brain damage in the setting of focal and global cerebral ischemia with and without reperfusion. Considerable insight into the importance of WBC-mediated tissue injury has been gained from studies employing antileukocyte interventions in experimental cerebral ischemia. The purpose of this article is to survey the different approaches taken to interfere with WBC inflammatory function. Emphasis is laid on a discussion of the efficacy of these interventions, their effects and side effects on cerebral and systemic parameters, and the power of evidence they provide for identification of WBCs as important factors in cerebral ischemia. The role of WBCs has been investigated in a great variety of global and focal cerebral ischemia models with and without reperfusion, leading to sometimes contradictory results. In the light of currently available data, it seems likely that WBCs contribute to secondary brain damage in the scenario of experimental transient focal cerebral ischemia, if the insult is not too severe.

[Continuous fiberoptic monitoring of oxygen saturation in cerebral veins in severe craniocerebral trauma--experiences and results]. / Kontinuierliche fiberoptische Uberwachung der hirnvenösen Sauerstoffsättigung bei schwerem Schädel-Hirn-Trauma--Erfahrungen und Ergebnisse.

AIM: Monitoring of jugular-venous O2-saturation (SjO2) enables the assessment of cerebral oxygen supply and the rapid detection of cerebral desaturation in patients with severe head injury. Furthermore, it may help to optimize circulation, ventilation, and intracranial hypertension therapy in these patients. This study was performed to evaluate the reliability of SjO2-monitoring as well as to measure cerebral O2-extraction and the frequency of episodes of cerebral desaturation after traumatic brain injury. METHODS: In 16 patients with severe head injury (GCS 3-8), SjO2 (fibreoptic system), arterial blood pressure, and intracranial pressure were continuously recorded after admission of the patients to the intensive care unit. Fluctuations of SjO2 (> 10% within 30 min), which were not included by therapeutic measures, were classified by off-line analysis as irregular-isolated or irregular-combined, if accompanied by similar fluctuations of ICP and arterial blood pressure. Recordings which were unreliable due to technical reasons, mainly because of wall adherence of the tip of the fibreoptic catheter, were evaluated separately. Episodes of cerebral desaturations (SjO2 < 50%) were assessed with regard to their frequency, duration (5-10/> 10 min) and underlying mechanisms. Cerebral O2-extraction was calculated as the difference between arterial and cerebrovenous O2-saturation and averaged for each day after trauma. RESULTS: Mean time of measurement for each patient was 194 hrs, a total of 3106 hrs were recorded. The correlation coefficient between in-vivo and in-vitro measured SjO2 was r = 0.62 (n = 367, p < 0.001). Reliable and artifact-free measurements of SjO2 were obtained only during 58.3% of all hours. Irregular-isolated fluctuations of the SjO2 occurred in 22.2% of the hours, and technical problems in 14.5%. Erroneous readings due to irregular-combined fluctuations of the jugular-venous O2-saturation were detected in 5.0% of the time periods. A total number of 66 episodes of cerebral desaturation (SjO2 < 50%) were found in all 16 patients, 41 of them had a duration of more than 10 minutes. Cerebral hypoxia was attributed to low cerebral perfusion pressure in 35% and hypocapnia in 17%. Global cerebral O2-extraction was significantly elevated at the day of injury compared to days 1-5 after trauma (37.4% vs. 28.9%-31.9%, p < 0.05). CONCLUSIONS: Monitoring of SjO2 in severe head injury provides an estimate of cerebral oxygen supply and may improve the assessment of therapeutic measures in these patients. The high incidence of erroneous readings of the SjO2 is a major drawback of this method. Initially after trauma, a high extraction of oxygen was found, followed by a marked decrease in the subsequent days, presumably reflecting an early, decreased cerebral blood flow and a hyperaemic flow pattern thereafter. Continuous measurements of SjO2 may contribute to advanced, organ-specific cerebral monitoring in severe craniocerebral trauma. The reliability of data, however, should be considerably improved for common clinical use.

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury.

Severe head injury is frequently associated with focal or global disturbances of cerebral blood flow and metabolism. Routine monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these patients does not provide information about critically reduced local or global cerebral blood flow. Measurements of cerebral lactate difference, Lactate-Oxygen-Index (LOI) and cerebral oxygen extraction were evaluated for advanced monitoring by comparing these parameters with ICP, cranial computed tomography (CCT) findings, and outcome in a group of severely head-injured patients. In 21 patients with severe brain trauma (GCS < or = 8), arterial as well as jugular venous lactate levels and oxygen saturation were measured in vitro every 6 h after admission of patients to the intensive care unit (ICU) throughout the acute course of treatment. Arterial blood pressure, blood gases, and ICP were assessed by standard monitoring measurements. CCT was performed initially after admission of the patients to the hospital, during the acute period in the ICU, if indicated, and 10 to 14 days after trauma. Outcome was classified according to the Glasgow outcome scale (GOS) at six months after injury. Data were averaged in each patient for every day after trauma and over the entire monitoring period. Resulting values were tested for correlation by regression analysis. Additionally, the data of the group of patients with normal to minimally elevated mean ICP (ICP < 20 mmHg, n = 12) were compared to those of the patients with increased mean ICP (ICP > 20 mmHg, n = 9). The cerebral lactate difference in all patients on the day of trauma was significantly increased as compared to the later period (0.20 vs. 0.11-0.07 mmol/l, p < 0.05), but was not different with high or normal to minimally elevated ICP. In patients with intracranial hypertension, the cerebral lactate difference remained significantly increased from the first to the fifth day after injury, whereas it normalized in this period in the group with normal to minimally elevated ICP. Averaged over the acute course, patients with increased ICP had significantly higher mean lactate differences (0.18 +/- 0.16 vs. 0.067 +/- 0.025 mmol/l, p = 0.001) and higher mean LOIs (0.072 +/- 0.071 vs. 0.028 +/- 0.013, p = 0.011). There was a significant correlation of increased mean cerebral lactate difference to poor outcome (r = 0.46, p = 0.035). Cerebral oxygen extraction in all patients tended to increase on the day of trauma (36.7% vs. 29.2% to 31.5% during the subsequent course), but this difference was not significant. The initial degree of brain swelling, classified by CCT according to Marshall et al. (1991), showed no correlation with cerebral lactate differences, ICP, O2-extraction, or outcome. Neither was there a correlation of cerebral oxygen extraction to ICP nor to outcome. In conclusion, the severity of brain trauma and outcome of patients was reflected by increased cerebral lactate production. Unchanged values of global cerebral oxygen extraction suggest that the regulatory mechanisms of brain oxygen supply were not impaired by trauma. Measurements of cerebral lactate differences and brain oxygen extraction may contribute to advanced monitoring in severe head injury.

Correlation of jugular venous oxygen saturation to spontaneous fluctuations of cerebral perfusion pressure in patients with severe head injury.

Continuous measurements of mean arterial pressure (MAP), ICP, and jugular venous oxygen saturation (SjO2) were performed in 11 patients with severe head injury (GCS 3-7) to assess the dependence of SjO2 from the cerebral perfusion pressure (CPP), trying to establish an indirect measure of cerebrovascular autoregulation. Changes in CPP resulting from spontaneous fluctuations in MAP or ICP induced highly significant alterations in SjO2 in the range of 0.14-0.56% SjO2 mmHg-1 CPP in all patients and all periods after trauma. The analysis of the distribution of the SjO2:CPP-ratios showed the highest frequency of values in the range of 0.0-0.25% SjO2 mmHg-1 CPP in 9 of the 11 patients. Within the first 2 days after trauma, a more pronounced dependency of SjO2 from changes in CPP was found, but this was not statistically significant. No predictable relationship of the SjO2:CPP-ratio to the level of ICP could be demonstrated in the patients. Because changes in SjO2 induced by alterations in CPP were found in all patients and throughout the acute phase of severe head injury, these changes more probably reflect physiological alterations in CBF with varying perfusion pressure rather than impaired autoregulation after head trauma. Although assessment of cerebral autoregulation by estimation of the SjO2:CPP-ratio offers new possibilities for monitoring of these patients, the high frequency of erroneous readings or irregular fluctuations of the SjO2-signal from the fibreoptic catheter limits the usefulness of the SjO2-dependency from CPP for practical use in the intensive care unit.