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Noninvasive Monitoring of Brain Damage

  • Nariyuki Hayashi
  • Dalton W. Dietrich

Abstract

The monitoring of brain tissue temperature, intracranial pressure (ICP), SjO2, oxygen delivery, and cerebral perfusion pressure (CPP) is necessary in intensive care unit (ICU) brain hypothermia management as fundamentals of the technique [1,8]. However, these monitors require considerable skill, are invasive to critically ill patients, and are difficult to perform in the early part of the acute stage. In addition, information about the severity of the catecholamine surge, blood-brain barrier (BBB) dysfunction, cerebral blood flow (CBF) disturbances, microcirculatory disturbances, brain metabolism and release of neurotoxic amino acids are useful to ICU brain hypothermia management [1,8]. However, these monitors cannot always be used because of practical limitations that include small medical teams at night, no monitoring system for the microdialysis technique, no high-speed liquid chromatography, limited insurance cover for brain hypothermia management, and limited economic support of these advanced monitors [8]. In addition, we have no times to monitors by abruptly rapid fall to critical conditions.

Keywords

Cerebral Blood Flow Albumin Ratio Indirect Parameter Carotid Blood Flow Tympanic Membrane Temperature 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Hayashi N (1995) Cerebral hypothermia treatment. In: Hayashi N (ed) Cerebral hypothermia treatment. Sogo Igaku, Tokyo, pp 1–105Google Scholar
  2. 2.
    Hayashi N, (2000) Enhanced neuronal damage in severely brain injured patients by hypothalamus, pituitary, and adrenal axis neuro-hormonal changes. In: Hayashi N (ed) Brain hypothermia. Springer, Berlin Heidelberg New York Tokyo, pp 3–26CrossRefGoogle Scholar
  3. 3.
    Hayashi N (2000) The clinical issue and effectiveness of brain hypothermia treatment for severe brain injured patients. In: Hayashi N (ed) Brain hypothermia. Springer, Berlin Heidelberg New York Tokyo, pp 121–151CrossRefGoogle Scholar
  4. 4.
    Hayashi N, Utagawa A, Kinosita K, Izumi T (1999) Application of a novel technique for clinical evaluation of nitric oxide-induced free radical reactions in ICU patients. Cell Mol Neurobiol 19:3–17PubMedCrossRefGoogle Scholar
  5. 5.
    Kossmann T, Hans V, Lenzlinger PM, Csuka E, Stsahel PF, Trentz O, Morgani-Kossmann MC (1996) Analysis of immune mediator production following traumatic brain injury. In: Schlag G, Redel H, Traber D (eds) Shock, sepsis and organ failure. Springer, Berlin Heidelberg New York, pp 263–297Google Scholar
  6. 6.
    Pasko SA, Volosheniuk TG (1990) Disordered phosphorus metabolism and its correction in the acute period of severe craniocerebral trauma. Zh Vopr Neirokhir Im NN Burdenko 3:14–16Google Scholar
  7. 7.
    Shoemaker WC, Apple PL, Kram HB, Waxman K, Lee T (1988) Prospective trial of supernormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 94:1176–1186PubMedCrossRefGoogle Scholar
  8. 8.
    Swan HJC, Ganz W (1983) Hemodynamic measurements in clinical practice: a decade in review. J Am Coll Cardiol 1:103–113PubMedCrossRefGoogle Scholar

Copyright information

© Springer Japan 2004

Authors and Affiliations

  • Nariyuki Hayashi
    • 1
    • 2
  • Dalton W. Dietrich
    • 3
    • 4
  1. 1.Nihon University Emergency Medical CenterTokyoJapan
  2. 2.Department of Emergency and Critical Care MedicineNihon University School of MedicineTokyoJapan
  3. 3.Department of Neurological Surgery, Neurology and Cell Biology and AnatomyUniversity of Miami School of MedicineMiamiUSA
  4. 4.The Miami Project to Cure ParalysisMiamiUSA

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