Aktuelle Neurologie 2016; 43(05): 298-308
DOI: 10.1055/s-0042-105276
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Zerebrale Hypoxie nach Reanimation

Cerebral Hypoxia after Cardiopulmonary Resuscitation
J. Schill
1   Klinik für Neurologie und Neurogeriatrie, Klinikum Darmstadt, Darmstadt
,
R. Kollmar
1   Klinik für Neurologie und Neurogeriatrie, Klinikum Darmstadt, Darmstadt
› Author Affiliations
Further Information

Publication History

Publication Date:
14 June 2016 (online)

Zusammenfassung

Die zerebrale Hypoxie ist eine häufige Ursache für die Morbidität und Mortalität von Patienten nach kardiopulmonaler Reanimation. In diesem Artikel werden pathophysiologische Zusammenhänge, die selektive neuronale Vulnerabilität und therapeutische Optionen der zerebralen Hypoxie beschrieben. Von besonderem Interesse ist die therapeutische Hypothermie (TH), die als erste neuroprotektive Methode einen positiven klinischen Effekt zeigte. Zudem spielen in der Therapie Blutdruckmanagment, Oxygenierung und Glukosestoffwechsel eine Rolle. Die Behandlung und Vermeidung epileptischer Anfälle wird erörtert, da anhaltende epileptische Anfälle weitere Schädigungen verursachen können und unverzüglich und effektiv behandelt werden müssen. Die Prognoseeinschätzung von Patienten mit zerebraler Hypoxie ist häufig schwierig. Wesentliche Parameter, die zur Einschätzung des Outcomes komatöser Patienten nach Reanimation dienen, werden diskutiert. Vor allem hinsichtlich ihrer Reliabilität und Rate an falsch-positiven Ergebnissen bei Patienten, die mit oder ohne therapeutische Hypothermie behandelt wurden, werden klinische Parameter (Pupillenreaktion, Cornealreflex usw.), Biomarker (NSE), elektrophysiologische Untersuchungen (SEP und EEG) und CT- und MR-basierte Parameter erörtert. Aufgrund der aufgeführten Daten sollte die Prognoseeinschätzung besonders nach therapeutischer Hypothermie vorsichtig und mit einem ausreichenden zeitlichen Abstand zum Ereignis erfolgen und sich nicht auf einzelne Parameter allein stützen.

Abstract

Cerebral hypoxia is a common cause of morbidity and mortality in post-cardiac arrest patients. In this article, the pathophysiology, selective neuronal vulnerability and therapeutic strategies of brain injury are described. Therapeutic hypothermia (TH) has been the first clinically proven neuroprotective method; blood pressure management, oxygenation and control of glycemia also play a therapeutic role. Seizure management and prevention are major treatment targets, since prolonged seizures may cause further cerebral injury and should therefore be treated promptly and effectively. Prognosis of comatose patients with post-cardiac arrest brain injury is crucial. Parameters widely used to determine the outcome in comatose patients after cardiac arrest are discussed. With the focus on the reliability and false-positive rate in patients treated with or without mild hypothermia, clinical parameters (pupillary reactivity, corneal reflex e. g.), biomarkers (NSE), electrophysiological parameters (SEP and EEG), and CT- and MRI-based parameters are elucidated. Based on data described, prognosis should be made with precaution especially after mild hypothermia and after appropriate lapse of time and not be based on any single parameter.

 
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