Publications by authors named "Cornelia W E Hoedemaekers"

28 Publications

  • Page 1 of 1

Near-Infrared Spectroscopy-Derived Dynamic Cerebral Autoregulation in Experimental Human Endotoxemia-An Exploratory Study.

Front Neurol 2021 10;12:695705. Epub 2021 Sep 10.

Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Cerebral perfusion may be altered in sepsis patients. However, there are conflicting findings on cerebral autoregulation (CA) in healthy participants undergoing the experimental endotoxemia protocol, a proxy for systemic inflammation in sepsis. In the current study, a newly developed near-infrared spectroscopy (NIRS)-based CA index is investigated in an endotoxemia study population, together with an index of focal cerebral oxygenation. Continuous-wave NIRS data were obtained from 11 healthy participants receiving a continuous infusion of bacterial endotoxin for 3 h (ClinicalTrials.gov NCT02922673) under extensive physiological monitoring. Oxygenated-deoxygenated hemoglobin phase differences in the (very)low frequency (VLF/LF) bands and the Tissue Saturation Index (TSI) were calculated at baseline, during systemic inflammation, and at the end of the experiment 7 h after the initiation of endotoxin administration. The median (inter-quartile range) LF phase difference was 16.2° (3.0-52.6°) at baseline and decreased to 3.9° (2.0-8.8°) at systemic inflammation ( = 0.03). The LF phase difference increased from systemic inflammation to 27.6° (12.7-67.5°) at the end of the experiment ( = 0.005). No significant changes in VLF phase difference were observed. The TSI (mean ± SD) increased from 63.7 ± 3.4% at baseline to 66.5 ± 2.8% during systemic inflammation ( = 0.03) and remained higher at the end of the experiment (67.1 ± 4.2%, = 0.04). Further analysis did not reveal a major influence of changes in several covariates such as blood pressure, heart rate, PaCO, and temperature, although some degree of interaction could not be excluded. A reversible decrease in NIRS-derived cerebral autoregulation phase difference was seen after endotoxin infusion, with a small, sustained increase in TSI. These findings suggest that endotoxin administration in healthy participants reversibly impairs CA, accompanied by sustained microvascular vasodilation.
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http://dx.doi.org/10.3389/fneur.2021.695705DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461327PMC
September 2021

Targeting Autoregulation-Guided Cerebral Perfusion Pressure after Traumatic Brain Injury (COGiTATE): A Feasibility Randomized Controlled Clinical Trial.

J Neurotrauma 2021 10 16;38(20):2790-2800. Epub 2021 Aug 16.

Department of Intensive Care Medicine, University Maastricht (KEMTA), Maastricht University Medical Center+, Maastricht, The Netherlands.

Managing traumatic brain injury (TBI) patients with a cerebral perfusion pressure (CPP) near to the cerebral autoregulation (CA)-guided "optimal" CPP (CPPopt) value is associated with improved outcome and might be useful to individualize care, but has never been prospectively evaluated. This study evaluated the feasibility and safety of CA-guided CPP management in TBI patients requiring intracranial pressure monitoring and therapy (TBIicp patients). The CPPopt Guided Therapy: Assessment of Target Effectiveness (COGiTATE) parallel two-arm feasibility trial took place in four tertiary centers. TBIicp patients were randomized to either the Brain Trauma Foundation (BTF) guideline CPP target range (control group) or to the individualized CA-guided CPP targets (intervention group). CPP targets were guided by six times daily software-based alerts for up to 5 days. The primary feasibility end-point was the percentage of time with CPP concordant (±5 mm Hg) with the set CPP targets. The main secondary safety end-point was an increase in therapeutic intensity level (TIL) between the control and intervention group. Twenty-eight patients were randomized to the control and 32 patients to the intervention group. CPP in the intervention group was in the target range for 46.5% (interquartile range, 41.2-58) of the monitored time, significantly higher than the feasibility target specified in the published protocol (36%;  < 0.001). There were no significant differences between groups for TIL or for other safety end-points. Conclusively, targeting an individual and dynamic CA-guided CPP is feasible and safe in TBIicp patients. This encourages a prospective trial powered for clinical outcomes.
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http://dx.doi.org/10.1089/neu.2021.0197DOI Listing
October 2021

Neurofilament to predict post-anoxic neurological outcome: are we ready for the prime time?

Intensive Care Med 2021 01 9;47(1):77-79. Epub 2020 Nov 9.

Department of Intensive Care, Radboud University Nijmegen Hospital, Nijmegen, The Netherlands.

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http://dx.doi.org/10.1007/s00134-020-06309-7DOI Listing
January 2021

Adult Advanced Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations.

Resuscitation 2020 Nov 21;156:A80-A119. Epub 2020 Oct 21.

This 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations for advanced life support includes updates on multiple advanced life support topics addressed with 3 different types of reviews. Topics were prioritized on the basis of both recent interest within the resuscitation community and the amount of new evidence available since any previous review. Systematic reviews addressed higher-priority topics, and included double-sequential defibrillation, intravenous versus intraosseous route for drug administration during cardiac arrest, point-of-care echocardiography for intra-arrest prognostication, cardiac arrest caused by pulmonary embolism, postresuscitation oxygenation and ventilation, prophylactic antibiotics after resuscitation, postresuscitation seizure prophylaxis and treatment, and neuroprognostication. New or updated treatment recommendations on these topics are presented. Scoping reviews were conducted for anticipatory charging and monitoring of physiological parameters during cardiopulmonary resuscitation. Topics for which systematic reviews and new Consensuses on Science With Treatment Recommendations were completed since 2015 are also summarized here. All remaining topics reviewed were addressed with evidence updates to identify any new evidence and to help determine which topics should be the highest priority for systematic reviews in the next 1 to 2 years.
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http://dx.doi.org/10.1016/j.resuscitation.2020.09.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576326PMC
November 2020

Adult Advanced Life Support: International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.

Resuscitation 2020 Sep 21. Epub 2020 Sep 21.

This 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations for advanced life support includes updates on multiple advanced life support topics addressed with 3 different types of reviews. Topics were prioritized on the basis of both recent interest within the resuscitation community and the amount of new evidence available since any previous review. Systematic reviews addressed higher-priority topics, and included double-sequential defibrillation, intravenous versus intraosseous route for drug administration during cardiac arrest, point-of-care echocardiography for intra-arrest prognostication, cardiac arrest caused by pulmonary embolism, postresuscitation oxygenation and ventilation, prophylactic antibiotics after resuscitation, postresuscitation seizure prophylaxis and treatment, and neuroprognostication. New or updated treatment recommendations on these topics are presented. Scoping reviews were conducted for anticipatory charging and monitoring of physiological parameters during cardiopulmonary resuscitation. Topics for which systematic reviews and new Consensuses on Science With Treatment Recommendations were completed since 2015 are also summarized here. All remaining topics reviewed were addressed with evidence updates to identify any new evidence and to help determine which topics should be the highest priority for systematic reviews in the next 1 to 2 years.
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http://dx.doi.org/10.1016/j.resuscitation.2020.09.012DOI Listing
September 2020

MRI in neuroprognostication after cardiac arrest: It's time for the next step.

Resuscitation 2020 12 20;157:264-265. Epub 2020 Oct 20.

Radboud University Medical Centre, Department of Neurology, Centre of Expertise for Parkinson & Movement Disorders, Nijmegen, The Netherlands; Donders Institute for Brain, Cognition, and Behavior, Centre for Cognitive Neuroimaging, Radboud University Nijmegen, Nijmegen, The Netherlands.

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http://dx.doi.org/10.1016/j.resuscitation.2020.10.011DOI Listing
December 2020

Adult Advanced Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.

Circulation 2020 10 21;142(16_suppl_1):S92-S139. Epub 2020 Oct 21.

This for advanced life support includes updates on multiple advanced life support topics addressed with 3 different types of reviews. Topics were prioritized on the basis of both recent interest within the resuscitation community and the amount of new evidence available since any previous review. Systematic reviews addressed higher-priority topics, and included double-sequential defibrillation, intravenous versus intraosseous route for drug administration during cardiac arrest, point-of-care echocardiography for intra-arrest prognostication, cardiac arrest caused by pulmonary embolism, postresuscitation oxygenation and ventilation, prophylactic antibiotics after resuscitation, postresuscitation seizure prophylaxis and treatment, and neuroprognostication. New or updated treatment recommendations on these topics are presented. Scoping reviews were conducted for anticipatory charging and monitoring of physiological parameters during cardiopulmonary resuscitation. Topics for which systematic reviews and new Consensuses on Science With Treatment Recommendations were completed since 2015 are also summarized here. All remaining topics reviewed were addressed with evidence updates to identify any new evidence and to help determine which topics should be the highest priority for systematic reviews in the next 1 to 2 years.
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http://dx.doi.org/10.1161/CIR.0000000000000893DOI Listing
October 2020

Prediction of poor neurological outcome in comatose survivors of cardiac arrest: a systematic review.

Intensive Care Med 2020 10 11;46(10):1803-1851. Epub 2020 Sep 11.

Department of Clinical Sciences Lund, Neurology, Lund University, Skane University Hospital, Lund, Sweden.

Purpose: To assess the ability of clinical examination, blood biomarkers, electrophysiology, or neuroimaging assessed within 7 days from return of spontaneous circulation (ROSC) to predict poor neurological outcome, defined as death, vegetative state, or severe disability (CPC 3-5) at hospital discharge/1 month or later, in comatose adult survivors from cardiac arrest (CA).

Methods: PubMed, EMBASE, Web of Science, and the Cochrane Database of Systematic Reviews (January 2013-April 2020) were searched. Sensitivity and false-positive rate (FPR) for each predictor were calculated. Due to heterogeneities in recording times, predictor thresholds, and definition of some predictors, meta-analysis was not performed.

Results: Ninety-four studies (30,200 patients) were included. Bilaterally absent pupillary or corneal reflexes after day 4 from ROSC, high blood values of neuron-specific enolase from 24 h after ROSC, absent N20 waves of short-latency somatosensory-evoked potentials (SSEPs) or unequivocal seizures on electroencephalogram (EEG) from the day of ROSC, EEG background suppression or burst-suppression from 24 h after ROSC, diffuse cerebral oedema on brain CT from 2 h after ROSC, or reduced diffusion on brain MRI at 2-5 days after ROSC had 0% FPR for poor outcome in most studies. Risk of bias assessed using the QUIPS tool was high for all predictors.

Conclusion: In comatose resuscitated patients, clinical, biochemical, neurophysiological, and radiological tests have a potential to predict poor neurological outcome with no false-positive predictions within the first week after CA. Guidelines should consider the methodological concerns and limited sensitivity for individual modalities. (PROSPERO CRD42019141169).
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http://dx.doi.org/10.1007/s00134-020-06198-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7527362PMC
October 2020

EEG reactivity testing for prediction of good outcome in patients after cardiac arrest.

Neurology 2020 08 10;95(6):e653-e661. Epub 2020 Jul 10.

From the Departments of Neurology/Clinical Neurophysiology (M.M.A., A.-F.v.R.) and Intensive Care (J. Horn, M.J.S.), Amsterdam Neuroscience, and Laboratory for Experimental Intensive Care and Anesthesiology (J. Horn, M.J.S.), Amsterdam UMC, University of Amsterdam; Department of Neurology (J. Hofmeijer, H.M.K.), Rijnstate Hospital, Arnhem; Clinical Neurophysiology (J. Hofmeijer, M.J.A.M.v.P.), MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede; Department of Intensive Care (C.W.E.H., C.R.v.K.) and Department of Intensive Care Medicine and Neurology, Donders Institute for Brain, Cognition, and Behaviour (H.M.K.), Radboud University Medical Center, Nijmegen; Department of Clinical Neurophysiology (M.J.A.M.v.P.), Medisch Spectrum Twente, Enschede, the Netherlands; Nuffield Department of Medicine (M.J.S.), University of Oxford, UK; and Mahidol-Oxford Tropical Medicine Research Unit (MORU) (M.J.S.), Mahidol University, Bangkok, Thailand.

Objective: To determine the additional value of EEG reactivity (EEG-R) testing to EEG background pattern for prediction of good outcome in adult patients after cardiac arrest (CA).

Methods: In this post hoc analysis of a prospective cohort study, EEG-R was tested twice a day, using a strict protocol. Good outcome was defined as a Cerebral Performance Category score of 1-2 within 6 months. The additional value of EEG-R per EEG background pattern was evaluated using the diagnostic odds ratio (DOR). Prognostic value (sensitivity and specificity) of EEG-R was investigated in relation to time after CA, sedative medication, different stimuli, and repeated testing.

Results: Between 12 and 24 hours after CA, data of 108 patients were available. Patients with a continuous (n = 64) or discontinuous (n = 19) normal voltage background pattern with reactivity were 3 and 8 times more likely to have a good outcome than without reactivity (continuous: DOR, 3.4; 95% confidence interval [CI], 0.97-12.0; = 0.06; discontinuous: DOR, 8.0; 95% CI, 1.0-63.97; = 0.0499). EEG-R was not observed in other background patterns within 24 hours after CA. In 119 patients with a normal voltage EEG background pattern, continuous or discontinuous, any time after CA, prognostic value was highest in sedated patients (sensitivity 81.3%, specificity 59.5%), irrespective of time after CA. EEG-R induced by handclapping and sternal rubbing, especially when combined, had highest prognostic value. Repeated EEG-R testing increased prognostic value.

Conclusion: EEG-R has additional value for prediction of good outcome in patients with discontinuous normal voltage EEG background pattern and possibly with continuous normal voltage. The best stimuli were clapping and sternal rubbing.
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http://dx.doi.org/10.1212/WNL.0000000000009991DOI Listing
August 2020

Electroencephalographic reactivity as predictor of neurological outcome in postanoxic coma: A multicenter prospective cohort study.

Ann Neurol 2019 07 8;86(1):17-27. Epub 2019 Jun 8.

Amsterdam University Medical Centers, University of Amsterdam, Department of Intensive Care, Amsterdam Neuroscience, Amsterdam, the Netherlands.

Objective: Outcome prediction in patients after cardiac arrest (CA) is challenging. Electroencephalographic reactivity (EEG-R) might be a reliable predictor. We aimed to determine the prognostic value of EEG-R using a standardized assessment.

Methods: In a prospective cohort study, a strictly defined EEG-R assessment protocol was executed twice per day in adult patients after CA. EEG-R was classified as present or absent by 3 EEG readers, blinded to patient characteristics. Uncertain reactivity was classified as present. Primary outcome was best Cerebral Performance Category score (CPC) in 6 months after CA, dichotomized as good (CPC = 1-2) or poor (CPC = 3-5). EEG-R was considered reliable for predicting poor outcome if specificity was ≥95%. For good outcome prediction, a specificity of ≥80% was used. Added value of EEG-R was the increase in specificity when combined with EEG background, neurological examination, and somatosensory evoked potentials (SSEPs).

Results: Of 160 patients enrolled, 149 were available for analyses. Absence of EEG-R for poor outcome prediction had a specificity of 82% and a sensitivity of 73%. For good outcome prediction, specificity was 73% and sensitivity 82%. Specificity for poor outcome prediction increased from 98% to 99% when EEG-R was added to a multimodal model. For good outcome prediction, specificity increased from 70% to 89%.

Interpretation: EEG-R testing in itself is not sufficiently reliable for outcome prediction in patients after CA. For poor outcome prediction, it has no substantial added value to EEG background, neurological examination, and SSEPs. For prediction of good outcome, EEG-R seems to have added value. ANN NEUROL 2019.
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http://dx.doi.org/10.1002/ana.25507DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6618107PMC
July 2019

Quantification of Macrocirculation and Microcirculation in Brain Using Ultrasound Perfusion Imaging.

Acta Neurochir Suppl 2018 ;126:115-120

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Objective: The aim of this study was to investigate the feasibility of simultaneous visualization of the cerebral macrocirculation and microcirculation, using ultrasound perfusion imaging (UPI). In addition, we studied the sensitivity of this technique for detecting changes in cerebral blood flow (CBF).

Materials And Methods: We performed an observational study in ten healthy volunteers. Ultrasound contrast was used for UPI measurements during normoventilation and hyperventilation. For the data analysis of the UPI measurements, an in-house algorithm was used to visualize the DICOM files, calculate parameter images and select regions of interest (ROIs). Next, time intensity curves (TIC) were extracted and perfusion parameters calculated.

Results: Both volume- and velocity-related perfusion parameters were significantly different between the macrocirculation and the parenchymal areas. Hyperventilation-induced decreases in CBF were detectable by UPI in both the macrocirculation and microcirculation, most consistently by the volume-related parameters. The method was safe, with no adverse effects in our population.

Conclusions: Bedside quantification of CBF seems feasible and the technique has a favourable safety profile. Adjustment of current method is required to improve its diagnostic accuracy. Validation studies using a 'gold standard' are needed to determine the added value of UPI in neurocritical care monitoring.
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http://dx.doi.org/10.1007/978-3-319-65798-1_25DOI Listing
July 2018

Repeatability of Bolus Kinetics Ultrasound Perfusion Imaging for the Quantification of Cerebral Blood Flow.

Ultrasound Med Biol 2017 12 28;43(12):2758-2764. Epub 2017 Sep 28.

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. Electronic address:

Ultrasound perfusion imaging (UPI) can be used for the quantification of cerebral perfusion. In a neuro-intensive care setting, repeated measurements are required to evaluate changes in cerebral perfusion and monitor therapy. The aim of this study was to determine the repeatability of UPI in quantification of cerebral perfusion. UPI measurement of cerebral perfusion was performed three times in healthy patients. The coefficients of variation of the three bolus injections were calculated for both time- and volume-derived perfusion parameters in the macro- and microcirculation. The UPI time-dependent parameters had overall the lowest CVs in both the macro- and microcirculation. The volume-related parameters had poorer repeatability, especially in the microcirculation. Both intra-observer variability and inter-observer variability were low. Although UPI is a promising tool for the bedside measurement of cerebral perfusion, improvement of the technique is required before implementation in routine clinical practice.
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http://dx.doi.org/10.1016/j.ultrasmedbio.2017.08.1880DOI Listing
December 2017

Potential of Contrast-Enhanced Ultrasound as a Bedside Monitoring Technique in Cerebral Perfusion: a Systematic Review.

Ultrasound Med Biol 2017 12 28;43(12):2751-2757. Epub 2017 Sep 28.

Department of Intensive Care, Radboud University Medical Centre, Nijmegen, The Netherlands. Electronic address:

Contrast-enhanced ultrasound (CEUS) has been suggested as a new method to measure cerebral perfusion in patients with acute brain injury. In this systematic review, the tolerability, repeatability, reproducibility and accuracy of different CEUS techniques for the quantification of cerebral perfusion were assessed. We selected studies published between January 1994 and March 2017 using CEUS to measure cerebral perfusion. We included 43 studies (bolus kinetics n = 31, refill kinetics n = 6, depletion kinetics n = 6) with a total of 861 patients. Tolerability was reported in 28 studies describing 12 patients with mild and transient side effects. Repeatability was assessed in 3 studies, reproducibility in 2 studies and accuracy in 19 studies. Repeatability was high for experienced sonographers and significantly lower for less experienced sonographers. Reproducibility of CEUS was not clear. The sensitivity and specificity of CEUS for the detection of cerebral ischemia ranged from 75% to 96% and from 60% to 100%. Limited data on repeatability, reproducibility and accuracy may suggest that this technique could be feasible for use in acute brain injury patients.
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http://dx.doi.org/10.1016/j.ultrasmedbio.2017.08.935DOI Listing
December 2017

Middle cerebral artery flow, the critical closing pressure, and the optimal mean arterial pressure in comatose cardiac arrest survivors-An observational study.

Resuscitation 2017 01 10;110:85-89. Epub 2016 Nov 10.

Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.

Aim: This study estimated the critical closing pressure (CrCP) of the cerebrovascular circulation during the post-cardiac arrest syndrome and determined if CrCP differs between survivors and non-survivors. We also compared patients after cardiac arrest to normal controls.

Methods: A prospective observational study was performed at the ICU of a tertiary university hospital in Nijmegen, the Netherlands. We studied 11 comatose patients successfully resuscitated from a cardiac arrest and treated with mild therapeutic hypothermia and 10 normal control subjects. Mean flow velocity (MFV) in the middle cerebral artery was measured by transcranial Doppler at several time points after admission to the ICU. CrCP was determined by a cerebrovascular impedance model.

Results: MFV was similar in survivors and non-survivors upon admission to the ICU, but increased stronger in non-survivors compared to survivors throughout the observation period (P<0.001). MFV was significantly lower in survivors immediately after cardiac arrest compared to normal controls (P<0.001), with a gradual restoration toward normal values. CrCP decreased significantly from 61.4[51.0-77.1]mmHg to 41.7[39.9-51.0]mmHg in the first 48h, after which it remained stable (P<0.001). CrCP was significantly higher in survivors compared to non-survivors (P=0.002). CrCP immediately after cardiac arrest was significantly higher compared to the control group (P=0.02).

Conclusions: CrCP is high after cardiac arrest with high cerebrovascular resistance and low MFV. This suggests that cerebral perfusion pressure should be maintained at a sufficient high level to avoid secondary brain injury. Failure to normalize the cerebrovascular profile may be a parameter of poor outcome.
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http://dx.doi.org/10.1016/j.resuscitation.2016.10.022DOI Listing
January 2017

Seventy-two hours of mild hypothermia after cardiac arrest is associated with a lowered inflammatory response during rewarming in a prospective observational study.

Crit Care 2014 Oct 11;18(5):546. Epub 2014 Oct 11.

Department of Intensive Care, Radboud University Nijmegen Medical Centre, PO Box 9101, Nijmegen, 6500 HB, The Netherlands.

Introduction: Whole-body ischemia and reperfusion trigger a systemic inflammatory response. In this study, we analyzed the effect of temperature on the inflammatory response in patients treated with prolonged mild hypothermia after cardiac arrest.

Methods: Ten comatose patients with return of spontaneous circulation after pulseless electrical activity/asystole or prolonged ventricular fibrillation were treated with mild therapeutic hypothermia for 72 hours after admission to a tertiary care university hospital. At admission and at 12, 24, 36, 48, 72, 96 and 114 hours, the patients' temperature was measured and blood samples were taken from the arterial catheter. Proinflammatory interleukin 6 (IL-6) and anti-inflammatory (IL-10) cytokines and chemokines (IL-8 and monocyte chemotactic protein 1), intercellular adhesion molecule 1 and complement activation products (C1r-C1s-C1inhibitor, C4bc, C3bPBb, C3bc and terminal complement complex) were measured. Changes over time were analyzed with the repeated measures test for nonparametric data. Dunn's multiple comparisons test was used for comparison of individual time points.

Results: The median temperature at the start of the study was 34.3°C (33.4°C to 35.2°C) and was maintained between 32°C and 34°C for 72 hours. All patients were passively rewarmed after 72 hours, from (median (IQR)) 33.7°C (33.1°C to 33.9°C) at 72 hours to 38.0°C (37.5°C to 38.1°C) at 114 hours (P <0.001). In general, the cytokines and chemokines remained stable during hypothermia and decreased during rewarming, whereas complement activation was suppressed during the whole hypothermia period and increased modestly during rewarming.

Conclusions: Prolonged hypothermia may blunt the inflammatory response after rewarming in patients after cardiac arrest. Complement activation was low during the whole hypothermia period, indicating that complement activation is also highly temperature-sensitive in vivo. Because inflammation is a strong mediator of secondary brain injury, a blunted proinflammatory response after rewarming may be beneficial.
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http://dx.doi.org/10.1186/s13054-014-0546-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209077PMC
October 2014

Effects of viscosity on cerebral blood flow after cardiac arrest.

Crit Care Med 2014 Mar;42(3):632-7

1Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. 2Department of Cardiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. 3Department of Clinical Epidemiology, Biostatistics and Health Technology Assessment, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. 4Department of Obstetrics and Gynecology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Objectives: To determine blood viscosity in adult comatose patients treated with mild therapeutic hypothermia after cardiac arrest and to assess the relation between blood viscosity, cerebral blood flow, and cerebral oxygen extraction.

Design: Observational study.

Setting: Tertiary care university hospital.

Patients: Ten comatose patients with return of spontaneous circulation after out-of-hospital cardiac arrest.

Intervention: Treatment with mild therapeutic hypothermia for 24 hours followed by passive rewarming to normothermia.

Measurements And Main Results: Median viscosity at shear rate 50/s was 5.27 mPa · s (4.29-5.91 mPa · s) at admission; it remained relatively stable during the first 12 hours and decreased significantly to 3.00 mPa · s (2.72-3.58 mPa · s) at 72 hours (p < 0.001). Median mean flow velocity in the middle cerebral artery was low (27.0 cm/s [23.8-30.5 cm/s]) at admission and significantly increased to 63.0 cm/s (51.0-80.0 cm/s) at 72 hours. Median jugular bulb saturation at the start of the study was 61.5% (55.5-75.3%) and significantly increased to 73.0% (69.0-81.0%) at 72 hours. Median hematocrit was 0.41 L/L (0.36-0.44 L/L) at admission and subsequently decreased significantly to 0.32 L/L (0.27-0.35 L/L) at 72 hours. Median C-reactive protein concentration was low at admission (2.5 mg/L [2.5-6.5 mg/L]) and increased to 101 mg/L (65-113.3 mg/L) in the following hours. Median fibrinogen concentration was increased at admission 2,795 mg/L (2,503-3,565 mg/L) and subsequently further increased to 6,195 mg/L (5,843-7,368 mg/L) at 72 hours. There was a significant negative association between blood viscosity and the mean flow velocity in the middle cerebral artery (p = 0.0008).

Conclusions: Changes in blood viscosity in vivo are associated with changes in flow velocity in the middle cerebral artery. High viscosity early after cardiac arrest may reduce cerebral blood flow and may contribute to secondary brain injury. Further studies are needed to determine the optimal viscosity during the different stages of the postcardiac arrest syndrome.
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http://dx.doi.org/10.1097/CCM.0000000000000027DOI Listing
March 2014

On-line blood viscosity monitoring in vivo with a central venous catheter, using electrical impedance technique.

Biosens Bioelectron 2013 Mar 4;41:595-601. Epub 2012 Oct 4.

Department of Cardiology, Radboud University Nijmegen Medical Centre, P.O Box 9101, 6500 HB Nijmegen, The Netherlands.

Blood viscosity is an important determinant of microvascular hemodynamics and also reflects systemic inflammation. Viscosity of blood strongly depends on the shear rate and can be characterized by a two parameter power-law model. Other major determinants of blood viscosity are hematocrit, level of inflammatory proteins and temperature. In-vitro studies have shown that these major parameters are related to the electrical impedance of blood. A special central venous catheter was developed to measure electrical impedance of blood in-vivo in the right atrium. Considering that blood viscosity plays an important role in cerebral blood flow, we investigated the feasibility to monitor blood viscosity by electrical bioimpedance in 10 patients during the first 3 days after successful resuscitation from a cardiac arrest. The blood viscosity-shear rate relationship was obtained from arterial blood samples analyzed using a standard viscosity meter. Non-linear regression analysis resulted in the following equation to estimate in-vivo blood viscosity (Viscosity(imp)) from plasma resistance (R(p)), intracellular resistance (R(i)) and blood temperature (T) as obtained from right atrium impedance measurements: Viscosity(imp)=(-15.574+15.576R(p)T)SR ((-.138RpT-.290Ri)). This model explains 89.2% (R(2)=.892) of the blood viscosity-shear rate relationship. The explained variance was similar for the non-linear regression model estimating blood viscosity from its major determinants hematocrit and the level of fibrinogen and C-reactive protein (R(2)=.884). Bland-Altman analysis showed a bias between the in-vitro viscosity measurement and the in-vivo impedance model of .04 mPa s at a shear rate of 5.5s(-1) with limits of agreement between -1.69 mPa s and 1.78 mPa s. In conclusion, this study demonstrates the proof of principle to monitor blood viscosity continuously in the human right atrium by a dedicated central venous catheter equipped with an impedance measuring device. No safety problems occurred and there was good agreement with in-vitro measurements of blood viscosity.
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http://dx.doi.org/10.1016/j.bios.2012.09.033DOI Listing
March 2013

Brain resuscitation in the drowning victim.

Neurocrit Care 2012 Dec;17(3):441-67

The Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Suite 7C23, Philadelphia, PA 19104, USA.

Drowning is a leading cause of accidental death. Survivors may sustain severe neurologic morbidity. There is negligible research specific to brain injury in drowning making current clinical management non-specific to this disorder. This review represents an evidence-based consensus effort to provide recommendations for management and investigation of the drowning victim. Epidemiology, brain-oriented prehospital and intensive care, therapeutic hypothermia, neuroimaging/monitoring, biomarkers, and neuroresuscitative pharmacology are addressed. When cardiac arrest is present, chest compressions with rescue breathing are recommended due to the asphyxial insult. In the comatose patient with restoration of spontaneous circulation, hypoxemia and hyperoxemia should be avoided, hyperthermia treated, and induced hypothermia (32-34 °C) considered. Arterial hypotension/hypertension should be recognized and treated. Prevent hypoglycemia and treat hyperglycemia. Treat clinical seizures and consider treating non-convulsive status epilepticus. Serial neurologic examinations should be provided. Brain imaging and serial biomarker measurement may aid prognostication. Continuous electroencephalography and N20 somatosensory evoked potential monitoring may be considered. Serial biomarker measurement (e.g., neuron specific enolase) may aid prognostication. There is insufficient evidence to recommend use of any specific brain-oriented neuroresuscitative pharmacologic therapy other than that required to restore and maintain normal physiology. Following initial stabilization, victims should be transferred to centers with expertise in age-specific post-resuscitation neurocritical care. Care should be documented, reviewed, and quality improvement assessment performed. Preclinical research should focus on models of asphyxial cardiac arrest. Clinical research should focus on improved cardiopulmonary resuscitation, re-oxygenation/reperfusion strategies, therapeutic hypothermia, neuroprotection, neurorehabilitation, and consideration of drowning in advances made in treatment of other central nervous system disorders.
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http://dx.doi.org/10.1007/s12028-012-9747-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677166PMC
December 2012

Risk factors for hypoglycaemia in neurocritical care patients.

Intensive Care Med 2012 Dec 21;38(12):1999-2006. Epub 2012 Aug 21.

Department of Intensive Care Medicine, University Medical Center, Utrecht, The Netherlands.

Purpose: To identify risk factors for hypoglycaemia in neurocritical care patients receiving intensive insulin therapy (IIT).

Methods: We performed a nested case-control study. All first episodes of hypoglycaemia (glucose <80 mg/dL, <4.4 mmol/L) in neurocritical care patients between 1 March 2006 and 31 December 2007 were identified. Patients were treated according to the local IIT protocol, with target blood glucose levels between 4.5 and 6.0 mmol/L (81.0-108.0 mg/dL). The first hypoglycaemic event of every patient (index moment) was used to match to a control patient. Possible risk factors preceding the index moment were scored using hospital records and analysed with conditional logistic regression.

Results: Of 786 neurocritical care patients, 449 developed hypoglycaemia (57.1 %). Independent risk factors for hypoglycaemia were lowering nutrition 6 h before the index moment without insulin dose reduction (odds ratio (OR) 5.25, 95 % confidence interval (95 % CI) 1.32-20.88), mechanical ventilation (OR 2.59, 95 % CI 1.56-4.29), lowering the dosage of norepinephrine 3 h before the index moment (OR 2.44, 95 % CI 1.07-5.55), a hyperglycaemic event (>10 mmol/L, >180.0 mg/dL) in the 24 h preceding the index moment (OR 2.40, 95 % CI 1.26-4.58), gastric residual in the 6 h preceding the index moment without insulin dose reduction (OR 1.76, 95 % CI 1.05-2.96) and dosage of insulin at the index moment (OR 0.83, 95 % CI 0.76-0.90).

Conclusion: Hypoglycaemia occurs in a considerable proportion of neurocritical care patients. We recommend the identification of these risk factors in these patients to avoid the occurrence of hypoglycaemia.
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http://dx.doi.org/10.1007/s00134-012-2681-2DOI Listing
December 2012

Effects of prolonged mild hypothermia on cerebral blood flow after cardiac arrest.

Crit Care Med 2012 Aug;40(8):2362-7

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Objective: The aim of the present study was to assess the cerebral blood flow and cerebral oxygen extraction in adult patients after pulseless electrical activity/asystole or resistant ventricular fibrillation who were treated with mild therapeutic hypothermia for 72 hrs.

Design: Observational study.

Setting: Tertiary care university hospital.

Patients: Ten comatose patients with return of spontaneous circulation after pulseless electrical activity/asystole or prolonged ventricular fibrillation.

Intervention: Treatment with mild therapeutic hypothermia for 72 hrs.

Measurements And Main Results: Mean flow velocity in the middle cerebral artery was measured by transcranial Doppler at 12, 24, 36, 48, 60, 72, 84, 96, and 108 hrs after admission. Jugular bulb oxygenation was measured at the same intervals. Mean flow velocity in the middle cerebral artery was low (26.5 (18.7-48.0) cm/sec) at admission and significantly increased to 63.9 (45.6-65.6) cm/sec at 72 hrs (p=.002). Upon rewarming, the mean flow velocity in the middle cerebral artery remained relatively constant with a mean flow velocity in the middle cerebral artery of 71.5 (56.0-78.5) at 108 hrs (p=.381). Jugular bulb oxygenation at the start of the study was 57.0 (51.0-61.3)% and gradually increased to 81.0 (78.5-88.0)% at 72 hrs (p=.003). Upon rewarming, the jugular bulb oxygenation remained constant with a jugular bulb oxygenation of 84.0 (77.3-86.3)% at 108 hrs (p=.919). There were no differences in mean flow velocity in the middle cerebral artery, pulsatility index, and jugular bulb oxygenation between survivors and nonsurvivors.

Conclusions: Temperature by itself is probably not a major determinant in regulation of cerebral blood flow after cardiac arrest. The relatively low mean flow velocity in the middle cerebral artery in combination with normal jugular bulb oxygenation values suggests a reduction in cerebral metabolic activity that may contribute to the neuroprotective effect of (prolonged) mild therapeutic hypothermia in the delayed hypoperfusion phase.
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http://dx.doi.org/10.1097/CCM.0b013e318255d983DOI Listing
August 2012

Factors influencing intracranial pressure monitoring guideline compliance and outcome after severe traumatic brain injury.

Crit Care Med 2012 Jun;40(6):1914-22

Department of Neurology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

Objective: To determine adherence to Brain Trauma Foundation guidelines for intracranial pressure monitoring after severe traumatic brain injury, to investigate if characteristics of patients treated according to guidelines (ICP+) differ from those who were not (ICP-), and whether guideline compliance is related to 6-month outcome.

Design: Observational multicenter study.

Patients: Consecutive severe traumatic brain injury patients (≥16 yrs, n = 265) meeting criteria for intracranial pressure monitoring.

Measurements And Main Results: Data on demographics, injury severity, computed tomography findings, and patient management were registered. The Glasgow Outcome Scale Extended was dichotomized into death (Glasgow Outcome Scale Extended = 1) and unfavorable outcome (Glasgow Outcome Scale Extended 1-4). Guideline compliance was 46%. Differences between the monitored and nonmonitored patients included a younger age (median 44 vs. 53 yrs), more abnormal pupillary reactions (52% vs. 32%), and more intracranial pathology (subarachnoid hemorrhage 62% vs. 44%; intraparenchymal lesions 65% vs. 46%) in the ICP+ group. Patients with a total intracranial lesion volume of ~150 mL and a midline shift of ~12 mm were most likely to receive an intracranial pressure monitor and probabilities decreased with smaller and larger lesions and shifts. Furthermore, compliance was low in patients with no (Traumatic Coma Databank score I -10%) visible intracranial pathology. Differences in case-mix resulted in higher a priori probabilities of dying (median 0.51 vs. 0.35, p < .001) and unfavorable outcome (median 0.79 vs. 0.63, p < .001) in the ICP+ group. After correction for baseline and clinical characteristics with a propensity score, intracranial pressure monitoring guideline compliance was not associated with mortality (odds ratio 0.93, 95% confidence interval 0.47-1.85, p = .83) nor with unfavorable outcome (odds ratio 1.81, 95% confidence interval 0.88-3.73, p = .11).

Conclusions: Guideline noncompliance was most prominent in patients with minor or very large computed tomography abnormalities. Intracranial pressure monitoring was not associated with 6-month outcome, but multiple baseline differences between monitored and nonmonitored patients underline the complex nature of examining the effect of intracranial pressure monitoring in observational studies.
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http://dx.doi.org/10.1097/CCM.0b013e3182474bdeDOI Listing
June 2012

Rewarming after hypothermia after cardiac arrest shifts the inflammatory balance.

Crit Care Med 2012 Apr;40(4):1136-42

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands.

Objectives: The aim of this study was to simultaneously analyze the key components of the cerebral and systemic inflammatory response over time in cardiac arrest patients during mild therapeutic hypothermia and rewarming.

Design And Setting: Clinical observational study in a tertiary care university hospital.

Patients: Ten comatose patients after out-of-hospital cardiac arrest.

Interventions: All patients were cooled to 32-34°C for 24 hrs. After 24 hrs patients were passively rewarmed to normothermia.

Measurements And Main Results: On admission and at 3, 6, 12, 24, and 48 hrs blood samples were taken from the arterial and jugular bulb catheter. Proinflammatory and anti-inflammatory cytokines and chemokines (interleukin-1ra, interleukin-1β, interleukin-6, interleukin-8, interleukin-10, interleukin-18, monocyte chemotactic protein-1, high-mobility group box-1 and tumor necrosis factor-α), complement activation products (C4d, Bb, C3a, and terminal complement complex), and the adhesion molecule soluble intercellular adhesion molecule were measured. Mean temperatures at the start of the study and at 12 and 24 hrs were 33.7 ± 0.9°C, 32.7 ± 0.92°C, and 34.5 ± 1.5°C, respectively. Passive rewarming resulted in a temperature of 37.8 ± 0.5°C at 48 hrs. The proinflammatory cytokine interleukin-6 increased from 12 to 24 hrs and returned to baseline levels after 48 hrs. In contrast, the chemokines interleukin-8 and monocyte chemotactic protein-1 stayed relatively high from the start and during the hypothermia period, decreasing to baseline levels after 48 hrs. The anti-inflammatory cytokines interleukin-10 and interleukin-1ra did not significantly change during mild therapeutic hypothermia and rewarming, although low values of interleukin-10 were observed after rewarming. A significant increase after rewarming was demonstrated on high-mobility group box-1 concentrations in the jugular bulb, whereas soluble intercellular adhesion molecule increased significantly during hypothermia and remained at this level after rewarming. Complement activation was increased on admission and decreased after induction of hypothermia, followed by a secondary increase during rewarming. No significant differences between any of the biomarkers were found between samples from the arterial and jugular bulb catheter.

Conclusions: Complement activation occurs during rewarming from mild therapeutic hypothermia after cardiac arrest. Interleukin-6 increased already from 12 to 24 hrs, concomitantly with a significant increase in the temperature seen during this period of mild therapeutic hypothermia. The optimal rate of rewarming is unknown. Additional clinical studies are needed to determine the optimal rewarming rate and strategy.
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http://dx.doi.org/10.1097/CCM.0b013e3182377050DOI Listing
April 2012

Intensive insulin therapy increases the risk of hypoglycemia in neurocritical care patients.

J Neurosurg Anesthesiol 2011 Jul;23(3):206-14

Department of Intensive Care Medicine, Rudolf Magnus Institute of Neuroscience, University Medical Center, Utrecht, The Netherlands.

Background: Intensive insulin therapy protocols are widely used in intensive care medicine. A disadvantage of these protocols may be the occurrence of hypoglycemic episodes. Neurocritical care patients are particularly vulnerable to the effects of hypoglycemia. We aimed to study the risk of hypoglycemia in neurocritical care patients in relation to intensive insulin therapy.

Methods: To determine the effects of 2 different intensive insulin therapy protocols on glucose levels and hypoglycemia incidence, we collected data before and after implementation of the protocols in 2 university hospitals. The risk of hypoglycemia (blood glucose level below 3.0 mmol/L) was studied retrospectively with logistic regression analyses.

Results: In hospital A, data were obtained on 152 patients before implementation of the protocol and on 649 patients after implementation of the protocol. In hospital B, data were obtained on 111 patients before implementation of the protocol and on 118 patients thereafter. Implementation of intensive insulin therapy protocols increased the time spent in the desired blood glucose range of 4.6 to 6.0 mmol/L in both hospitals, but increased the risk of hypoglycemia: the absolute risk of hypoglycemia during intensive care unit admission increased in hospital A from 14.5% to 20.3% (adjusted odds ratio=1.3; 95% confidence interval: 0.8-2.3) and in hospital B from 3.6% to 29.7% (adjusted odds ratio=28.6; 95% confidence interval: 5.9-138.9).

Conclusions: Implementation of intensive insulin therapy protocols in neurocritical care patients not only seems to increase the time spent in the desired blood glucose range, but also seems to increase the risk of hypoglycemia. The risk of hypoglycemia strongly depends on characteristics of the intensive insulin therapy protocol.
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http://dx.doi.org/10.1097/ANA.0b013e31821aa6f2DOI Listing
July 2011

Predictors of poor neurologic outcome in patients after cardiac arrest treated with hypothermia: a retrospective study.

Resuscitation 2011 Jun 17;82(6):696-701. Epub 2011 Mar 17.

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Introduction: Outcome studies in patients with anoxic-ischemic encephalopathy focus on the early and reliable prediction of an outcome no better than a vegetative state or severe disability. We determined the effect of mild therapeutic hypothermia on the validity of the currently used clinical practice parameters.

Methods: We conducted a retrospective cohort study of adult comatose patients after cardiac arrest treated with hypothermia. All data were collected from medical charts and laboratory files and analyzed from the day of admission to the intensive care unit until day 7, discharge from the intensive care unit or death using the Utstein definitions for the registration of the data.

Results: We analyzed the data of 103 patients. The combination of an M1 or M2 on the Glasgow Coma Scale or absent pupillary reactions or absent corneal reflexes on day 3 was present in 80.6% of patients with an unfavourable and 11.1% of patients with a favourable outcome. The combination of M1 or M2 and absent pupillary reactions to light and absent corneal reflexes on day 3 was present in 14.9% of patients with an unfavourable and none of the patients with a favourable outcome. None of the patients with a favourable outcome had a bilaterally absent somatosensory evoked potential of the median nerve. The value of electroencephalogram patterns in predicting outcome was low, except for reactivity to noxious stimuli.

Conclusions: No single clinical or electrophysiological parameter has sufficient accuracy to determine prognosis and decision making in patients after cardiac arrest, treated with hypothermia.
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http://dx.doi.org/10.1016/j.resuscitation.2011.02.020DOI Listing
June 2011

Hypothermia does not increase the risk of infection: a case control study.

Crit Care 2011 3;15(1):R48. Epub 2011 Feb 3.

Department of Intensive Care, Radboud University Nijmegen Medical Centre PO Box 9101, 6500 HB Nijmegen, The Netherlands.

Introduction: Hypothermia may improve outcome in patients after traumatic brain injury, especially when hypothermia is maintained for more than 48 hours. In the acute phase, patients with severe brain injury are more vulnerable to infections. Prolonged hypothermic treatment may further enhance the risk of infection. Selective decontamination of the digestive tract (SDD) reduces the risk of respiratory tract infections. The aim of this study was to investigate the incidence of infections in patients treated with hypothermia and normothermia while receiving SDD.

Methods: In this retrospective case control study 35 patients treated with prolonged hypothermia (cases) were identified and 169 patients with severe brain injury were included (controls). Propensity score matching was performed to correct for differences in baseline characteristics and clinical parameters. Primary outcome was the incidence of infection. The secondary endpoints were the micro-organisms found in the surveillance cultures and infection. In addition, a number of clinical characteristics were assessed.

Results: The demographic and clinical data indicated that the cases and controls were well matched. The overall risk of infection during ICU stay was 20% in the hypothermia groups versus 34.4% in the normothermia group (P = 0.388). Pneumonia was diagnosed in 11.4% of patients in both groups (P = 1.000). The incidence of meningitis, wound infection, bacteremia, and urinary tract infection was low and comparable between the groups. SDD surveillance cultures indicated a higher colonization with gram-negative bacteria in the rectal samples of the hypothermia patients.

Conclusions: Hypothermia does not increase the risk of infection in patients treated with SDD.
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http://dx.doi.org/10.1186/cc10012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221978PMC
December 2011

Preserved metabolic coupling and cerebrovascular reactivity during mild hypothermia after cardiac arrest.

Crit Care Med 2010 Jul;38(7):1542-7

Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Objective: Although mild hypothermia improves outcome in patients after out-of-hospital cardiac arrest, the cardiodepressive effects of hypothermia may lead to secondary brain damage. This study was performed to assess the cerebral blood flow, cerebral oxygen extraction, and cerebrovascular reactivity to changes in partial pressure of carbon dioxide in the arterial blood in comatose patients after out-of-hospital cardiac arrest treated with mild hypothermia.

Design: Observational study.

Setting: Tertiary care university hospital.

Patients: Ten comatose patients after out-of-hospital cardiac arrest.

Interventions: All patients were cooled to 32-34 degrees C for 24 hrs. Cerebrovascular reactivity to changes in carbon dioxide in the arterial blood was measured after increasing or decreasing the minute ventilation by 20%.

Measurements And Main Results: Mean flow velocity in the middle cerebral artery and pulsatility index were measured by transcranial Doppler at 0, 3, 6, 9, 12, 18, 24, and 48 hrs after admission. Jugular bulb oxygenation was measured at the same intervals. Cerebrovascular reactivity to changes in carbon dioxide in the arterial blood was studied on admission to the intensive care unit and at 6, 12, 18, and 24 hrs by measurement of mean flow velocity in the middle cerebral artery and jugular bulb oxygenation. Mean flow velocity in the middle cerebral artery was low (30.3+/-9.5 cm/sec) on admission and remained relatively stable for the first 24 hrs. After rewarming, it increased to 67.5+/-33.0 cm/sec at 48 hrs after admission from 30.3+/-9.5 at admission (p=.009). Jugular bulb oxygenation at the start of the study was 66.2+/-8.5% and gradually increased to 82.9+/-4.9% at 48 hrs (p<.001). Regression analysis showed a significant correlation between changes in carbon dioxide in the arterial blood, mean flow velocity in the middle cerebral artery (p<.001) and jugular bulb oxygenation (p<.001). The mean percentage change in mean flow velocity in the middle cerebral artery was 3.6+/-2.9% per 1-mm Hg change of carbon dioxide in the arterial blood.

Conclusions: The mean flow velocity in the middle cerebral artery, as a parameter of cerebral blood flow, was low during mild hypothermia, whereas cerebral oxygen extraction remained normal, suggesting decreased cerebral metabolic activity. We demonstrated that CO2 reactivity is preserved during hypothermia in these patients.
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http://dx.doi.org/10.1097/CCM.0b013e3181e2cc1eDOI Listing
July 2010

Accuracy of bedside glucose measurement from three glucometers in critically ill patients.

Crit Care Med 2008 Nov;36(11):3062-6

Departments of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Objective: Implementation of strict glucose control in most intensive care units has resulted in increased use of point-of-care glucose devices in the intensive care unit. The aim of this study was to determine the reliability of point-of-care testing glucose meters among critically ill patients under intensive insulin treatment.

Design: Prospective observational study.

Patients: Intensive care unit and non-intensive care unit patients in a tertiary care teaching hospital.

Measurements: A glucose oxidase method was used to validate the point-of-care testing devices. Three different point-of-care testing devices, Accu-Chek Sensor (Roche Diagnostics), Precision (Abbott Diagnostics), and HemoCue were tested. Glucose measurements were performed in duplicate by an experienced technician under standardized conditions in the hospital's laboratory, using arterial (intensive care unit patients) and arterial or venous (non-intensive care unit patients) heparinized whole blood samples.

Main Results: A strong correlation was found between the glucose oxidase method and the Accu-Chek device (r = .9596, p < 0.001). Mean absolute difference between the glucose oxidase and Accu-Chek was -0.32 mmol/L (95% confidence interval -0.84 to 1.48 mmol/L). Using the International Organization for Standardization (ISO) criteria, 27 of 197 samples (13.7%) were inaccurate. In all samples that failed to meet the ISO criteria, glucose values measured by the Accu-Chek device were higher compared with the glucose oxidase method. In another set of experiments among intensive care unit patients, strong positive correlations were also found between the other point-of-care testing devices and the glucose oxidase method. However, paired samples from Accu-Chek, HemoCue, and Precision failed the ISO criteria in 9 of 82 (11.0%), 4 of 82 (4.9%), and 11 of 82 (13.4%) of cases, respectively. In non-intensive care unit patients paired samples from Accu-Chek, HemoCue, and Precision failed the ISO criteria in 3 of 120 (2.5%), 11 of 120 (9.2%), and 16 of 120 (13.3%) cases, respectively.

Conclusions: Under standardized conditions, glucose results from three point-of-care testing devices were inaccurate in both intensive care unit and non-intensive care unit patients. Among intensive care unit patients, inaccurate glucose readings were most frequently falsely elevated, resulting in misinterpretation of high glucose values with subsequent inappropriate insulin administration or masking of true hypoglycemia.
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http://dx.doi.org/10.1097/CCM.0b013e318186ffe6DOI Listing
November 2008
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