Prognostic Value of Magnetic Resonance Imaging in Post-Resuscitation Encephalopathy
ABSTRACT Prediction of the prognosis of comatose survivors after cardiopulmonary arrest (CPA), so-called post-resuscitation encephalopathy (PRE), relies on neurological examination findings. Early laboratory indicators of poor prognosis (vegetative state/death) are not sensitive enough.
We analyzed the results of magnetic resonance (MR) imaging with fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI) in 22 consecutive patients with PRE. Clinical details such as arrest place and anoxia time along with neurological examination findings including items of Glasgow coma scale (GCS) and the Full Outline of UnResponsiveness (FOUR) score were determined. Receiver Operator Characteristics (ROC) curves were produced to determine prognostic yield of the parameters studied.
Prognosis was classified as 'poor' (Glasgow-Pittsburg Cerebral Performance -CPC-score 4 or 5) in 16 and 'better' (CPC score 1-3) in 6 patients. The lower limit of confidence interval (CI) of the area under the curve (AUC) of the ROC was higher than 0.5 for visual, motor and total scores of GCS and FOUR score. Presence of a lesion pattern of multilobar, or diffuse, cortical involvement, termed as "extensive cortical lesion pattern" in MR imaging was a very good predictor of poor prognosis with an AUC of ROC of 0,937. Sensitivity of GCS motor part score and MR was 87.5% (95% CI: 61.6%-92.6%). Motor part of the FOUR score has a slightly lower sensitivity (68.7% with 95% CI from 41.4% to 88.9%). Incorporating of MR to the motor scores (either GCS or FOUR score) improved sensitivity to 100 % (95% CI: 79.2%-100%). AUC of the ROC was 1.000 (95%CI: 0.844-1.000) for the combination of MR and GCS motor score.
This study provides the preliminary evidence that MRI, when used in conjunction with a neurological examination, may have potential in terms of predicting outcome in patients with PRE.
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ABSTRACT: This paper describes the hardware design and implementations of the forward path for the back propagation algorithm of an analog neural network. The design considers the voltage range for fractional and floating point processing in multimedia applications. The PSpice simulation using MOSIS device parameters are presented
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ABSTRACT: Background: To evaluate the post-resuscitation intensive care unit outcome of patients who initially survived out-of-hospital cardiac arrest (OHCA). Methods: We retrospectively analyzed patients who were admitted to the ICU after OHCA in a tertiary hospital between January, 2005 and December, 2009. We compared the patients' clinical data, the factors associated with ad-mission and the prognosis of patients in cardiac and non-cardiac groups. Results: Sixty-four patients were included in this study. Thirty-four patients were in the cardiac group and thirty patients were in the non-cardiac group. The mean age was 57.3 ± 15.1 years of age in the cardiac group and 61.9 ± 15.7 years of age in the non-cardiac group (p = 0.235). The collapse-to-start of the CPR interval was 5.9 ± 3.8 min in the cardiac group and 6.0 ± 3.2 min in the non-cardiac group (p = 0.851). The complaint of chest pain oc-curred in 12 patients (35.3%) in the cardiac group and 1 patient (3.3%) in the non-cardiac group (p = 0.011). The time duration for making a decision for admission was 285.2 ± 202.2 min in the cardiac group and 327.7 ± 264.1 min in the non-cardiac group (p = 0.471). The regional wall motion abnormality and ejection fraction decrease were significant in the cardiac group (p = 0.002, 0.030). Grade 5 CPC was present in 8 patients (23.5%) in the cardiac group and 14 patients (46.7%) in the non-cardiac group. Conclusions: The key symptom that could initially differentiate the two groups was chest pain. The time duration for making an admission decision was long in both groups. The CPC score of the cardiac group was lower than that for the non-cardiac group.01/2010; 25(4). DOI:10.4266/kjccm.2010.25.4.212
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ABSTRACT: Hypothermia improves survival and neurological recovery after cardiac arrest. Pro-inflammatory cytokines have been implicated in focal cerebral ischemia/reperfusion injury. It is unknown whether cardiac arrest also triggers the release of cerebral inflammatory molecules, and whether therapeutic hypothermia alters this inflammatory response. This study sought to examine whether hypothermia or the combination of hypothermia with anesthetic post-conditioning with sevoflurane affect cerebral inflammatory response after cardiopulmonary resuscitation. Thirty pigs (28 to 34 kg) were subjected to cardiac arrest following temporary coronary artery occlusion. After seven minutes of ventricular fibrillation and two minutes of basic life support, advanced cardiac life support was started according to the current American Heart Association guidelines. Return of spontaneous circulation was achieved in 21 animals who were randomized to either normothermia at 38 degrees C, hypothermia at 33 degrees C or hypothermia at 33 degrees C combined with sevoflurane (each group: n = 7) for 24 hours. The effects of hypothermia and the combination of hypothermia with sevoflurane on cerebral inflammatory response after cardiopulmonary resuscitation were studied using tissue samples from the cerebral cortex of pigs euthanized after 24 hours and employing quantitative RT-PCR and ELISA techniques. Global cerebral ischemia following resuscitation resulted in significant upregulation of cerebral tissue inflammatory cytokine mRNA expression (mean +/- SD; interleukin (IL)-1beta 8.7 +/- 4.0, IL-6 4.3 +/- 2.6, IL-10 2.5 +/- 1.6, tumor necrosis factor (TNF)alpha 2.8 +/- 1.8, intercellular adhesion molecule-1 (ICAM-1) 4.0 +/- 1.9-fold compared with sham control) and IL-1beta protein concentration (1.9 +/- 0.6-fold compared with sham control). Hypothermia was associated with a significant (P < 0.05 versus normothermia) reduction in cerebral inflammatory cytokine mRNA expression (IL-1beta 1.7 +/- 1.0, IL-6 2.2 +/- 1.1, IL-10 0.8 +/- 0.4, TNFalpha 1.1 +/- 0.6, ICAM-1 1.9 +/- 0.7-fold compared with sham control). These results were also confirmed for IL-1beta on protein level. Experimental settings employing hypothermia in combination with sevoflurane showed that the volatile anesthetic did not confer additional anti-inflammatory effects compared with hypothermia alone. Mild therapeutic hypothermia resulted in decreased expression of typical cerebral inflammatory mediators after cardiopulmonary resuscitation. This may confer, at least in part, neuroprotection following global cerebral ischemia and resuscitation.Critical care (London, England) 02/2010; 14(1):R21. DOI:10.1186/cc8879