{"title":"[Monitoring of intracranial pressure].","authors":"F Artru","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The use of intraparenchymatous ICP sensor is becoming increasingly popular at the expense of the traditional intraventricular catheter method, in spite of the impossibility, with the former technic, to correct a possible zero drift. The decision to initiate or discontinue ICP monitoring is essentially based upon whether suggestive aspects of raised ICP are or not present on CT-scan. The degree of basal cisterns effacement is particularly informative. The same data from successive CT-scans are used to check the validity of the monitoring. Predefining critical levels of ICP and cerebral perfusion pressure (CPP) allows to establish practical guide-lines for treatment. Cerebral ischemia is considered very likely when ICP rises above 30 mmHg. Regarding CPP, the therapeutical goal is to avoid its reduction under the critical level of 60-80 mmHg. As these thresholds vary with the patients age and the type of lesion, a parallel evaluation of cerebral ischemia by other methods is mandatory. Transcranial doppler allows an easy detection of critical reduction of arterial flow. However, in case of flow hypervelocity, interpretation needs measurement of absolute cerebral blood flow values. Cerebral venous oxygen saturation monitoring, at the level of the jugular golf, shows desaturation episodes indicative of cerebral ischemia. Blood sampling for determination of arterial and jugular venous lactate concentrations allows calculation of the lactate oxygen index, a practical correlate of the degree of cerebral ischemia. ICP measurement alone is of limited value to understand the cerebral hemodynamical and metabolical situation in severe brain injury. Preceding the rise of ICP, there exists a compensation phase during which a progressive decrease of intracranial compliance is the important event. Even more earlier, posttraumatic cellular metabolic dysfunctions are to-day objectives for a neurochemical monitoring. Therefore a special technical and human environment has became mandatory to take a real benefit from ICP monitoring.</p>","PeriodicalId":77055,"journal":{"name":"Cahiers d'anesthesiologie","volume":"44 1","pages":"87-90"},"PeriodicalIF":0.0000,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cahiers d'anesthesiologie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The use of intraparenchymatous ICP sensor is becoming increasingly popular at the expense of the traditional intraventricular catheter method, in spite of the impossibility, with the former technic, to correct a possible zero drift. The decision to initiate or discontinue ICP monitoring is essentially based upon whether suggestive aspects of raised ICP are or not present on CT-scan. The degree of basal cisterns effacement is particularly informative. The same data from successive CT-scans are used to check the validity of the monitoring. Predefining critical levels of ICP and cerebral perfusion pressure (CPP) allows to establish practical guide-lines for treatment. Cerebral ischemia is considered very likely when ICP rises above 30 mmHg. Regarding CPP, the therapeutical goal is to avoid its reduction under the critical level of 60-80 mmHg. As these thresholds vary with the patients age and the type of lesion, a parallel evaluation of cerebral ischemia by other methods is mandatory. Transcranial doppler allows an easy detection of critical reduction of arterial flow. However, in case of flow hypervelocity, interpretation needs measurement of absolute cerebral blood flow values. Cerebral venous oxygen saturation monitoring, at the level of the jugular golf, shows desaturation episodes indicative of cerebral ischemia. Blood sampling for determination of arterial and jugular venous lactate concentrations allows calculation of the lactate oxygen index, a practical correlate of the degree of cerebral ischemia. ICP measurement alone is of limited value to understand the cerebral hemodynamical and metabolical situation in severe brain injury. Preceding the rise of ICP, there exists a compensation phase during which a progressive decrease of intracranial compliance is the important event. Even more earlier, posttraumatic cellular metabolic dysfunctions are to-day objectives for a neurochemical monitoring. Therefore a special technical and human environment has became mandatory to take a real benefit from ICP monitoring.