Early prediction of neurologic prognosis after post-anoxic coma

Pifferi, S.; Codazzi, Daniela; Savioli, M.; Langer, Martin

doi:10.1007/s001340050609

Cited by 4 publications

(4 citation statements)

References 3 publications

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“…However, there were 6 studies that included severe neurological disability (ie, CPC 3) as a good outcome; 4 of which included fewer than 65 patients. [15][16][17][18][19][20] We included only studies from which combined outcome data for severe neurological disability, vegetative state, and death (ie, CPC 3-5) could be extracted. We did this because most primary studies presented outcome data in this fashion and because we could not combine studies that had differing definitions of good vs poor outcomes.…”

Section: Deathmentioning

confidence: 99%

See 1 more Smart Citation

Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

Booth¹,

Boone²,

Tomlinson³

et al. 2004

JAMA

458

210

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Section: Deathmentioning

confidence: 99%

“…to 5 as poor outcomes,[15][16][17][18][19][20] studies in which patients were not comatose,[47][48][49][50][51][52] studies that included only patients in persistent vegetative state,53,54 studies that included other forms of medical ASSESSING OUTCOME FOR COMATOSE SURVIVORS OF CARDIAC ARREST ©2004 American Medical Association. All rights reserved.…”

mentioning

confidence: 99%

Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

Booth¹,

Boone²,

Tomlinson³

et al. 2004

JAMA

458

210

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“…Moreover, residual neurological damage, especially in patients with anoxic coma, who will regain consciousness, is not fully predictable. Some predictive factors for neurological recovery in anoxic coma patients after CPA are neurological findings (Pifferi et al, 1998;Jorgensen et al, 1999), cerebral perfusion pressure (Gueugniaud et al, 1991), somatosensory evoked potential selectroencephalography findings (Zandbergen et al, 2000), neuroproteins (Pfeifer et al, 2005), and cerebral blood flow (CBF) (Roine et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Acute Cerebral Blood Flow Variations after Human Cardiac Arrest Assessed by Stable Xenon Enhanced Computed Tomography

Inoue

Shiozaki²,

Irisawa³

et al. 2007

CNR

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In this study, changes in cerebral blood flow (CBF) during acute phase after cardiopulmonary arrest (CPA) were examined in patients using stable Xenon enhanced computed tomography (Xe-CT). All patients (8) were stabilized hemodynamically within 4 hours after admission, and Xe-CT was performed immediately after restoration of spontaneous circulation (ROSC) at 8, 24, 48, 96 and 168 hours after ROSC. The progress of patients was monitored in other hospitals and clinics after discharge. Neurological outcomes were evaluated using the Glasgow outcome scale (GOS) 6 months after admission, and scores were compared against changes in CBF. Patients were grouped by prognosis. Four patients belonged to Group A (good recovery) and Group B (2 severely disabled, 2 in persistent vegetative state). The pattern of change in CBF after ROSC was found to be significantly different between Groups A and B (p <0.05). The CBF ratio relative to normal controls was higher in Group B than Group A within 48 hours after ROSC. However, at 48, 96, and 168 hours after ROSC, the opposite was observed: The CBF ratio was significantly higher in Group A than Group B (p<0.05). Based on these results, we concluded that CBF in the patients who survived after CPA changed remarkable especially within the first week. Furthermore, patients with abnormally low CBF that returns to supernormal within the first 48 hours following CPA can be expected to recover well neurologically.

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“…Mit einer seriellen differenzierten neurologischen Untersuchung am ersten und dritten Tag [69,91,93]…”

Section: Zusammenfassende Bewertungunclassified

Hypoxisch-ischämische Enzephalopathie

Müllges¹,

Stoll²

2002

Akt Neurol

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EinleitungDie globale Mangelversorgung des Gehirns mit Sauerstoff führt zu einer diffusen Enzephalopathie. In leichten Fällen kommt es zu einer reversiblen zerebralen Dysfunktion mit Bewusstlosigkeit, in schweren Fällen entstehen abhängig von Ausprägung und Dauer der Minderversorgung anhaltende funktionelle Stö-rungen, die auf eine strukturelle Hirnschädigung zurückzufüh-ren sind. Im klinischen Alltag liegt ursächlich meist eine Kombination aus Hypoxämie und Ischämie vor (Tab. 1) z. B. im Rahmen einer kardiopulmonalen Reanimation, weswegen hier der Begriff hypoxisch-ischämische (HIE) und nicht der auch geläufige einer (post-)anoxischen Enzephalopathie verwendet wird.In der vorliegenden Übersicht werden zunächst pathophysiologische Konzepte der globalen hypoxämischen Hirnschädigung anhand tierexperimenteller Untersuchungsergebnisse und histopathologischer Autopsiebefunde beim Menschen dargestellt. Der zweite Teil widmet sich der klinischen Manifestation und dem Stellenwert zusatzdiagnostischer Verfahren. Dabei wird in Perakutphase und Postakutphase unterteilt, um den typischen Fragestellungen gerecht zu werden. Zunächst muss die Diagnose gesichert werden, dann muss eine Prognose gestellt werden. Abschlieûend werden anhand tierexperimenteller Befunde Strategien zur Neuroprotektion bei globaler Hirnischämie/-hypoxie aufgezeigt und im klinischen Kontext diskutiert. Aufgrund der Vielzahl insbesondere von tierexperimentellen Befunden erhebt die Übersicht keinen Anspruch auf Vollständigkeit. ZusammenfassungDiese Übersicht beschreibt die Pathophysiologie und Nosologie der hypoxisch-ischämischen Hirnschädigung. Nach einer kurzen Einführung in die Mechanismen des hypoxischen neuronalen Zelltods werden die verschiedenen Möglichkeiten zur Einschät-zung der Prognose insbesondere nach Reanimationen unter klinischen und zusatzdiagnostischen Gesichtspunkten für die Perakutphase und an den folgenden Tagen erörtert. Am sichersten ist eine Prognose zu stellen anhand serieller klinischer-neurologischer Untersuchung und somatosensibel evozierten Potenzialen. Zwei unabhängige Studien zeigten aktuell den therapeutischen Nutzen einer Behandlung mit moderater Hypothermie nach Reanimation. AbstractThis article reviews the pathophysiology and clinical course of anoxic brain damage. A short introduction into the mechanisms of hypoxic neuronal death is given. Clinical, brain imaging, biochemical, and electrophysiological parameters of the hyperacute period as well as during the following days are discussed especially with respect to outcome prediction after cardiopulmonary resuscitation. Most useful parameters are derived from serial clinical neurologic examination and from somatosensory evoked potentials. Recently, two clinical studies showed benefit from treatment with moderate hypothermia after cardiopulmonary resuscitation. Übersicht 431Heruntergeladen von: University of Pennsylvania Libraries. Urheberrechtlich geschützt.

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Early prediction of neurologic prognosis after post-anoxic coma

Cited by 4 publications

References 3 publications

Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

Acute Cerebral Blood Flow Variations after Human Cardiac Arrest Assessed by Stable Xenon Enhanced Computed Tomography

Hypoxisch-ischämische Enzephalopathie

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