Die septische Enzephalopathie

 

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Zusammenfassung.

Bei Patienten mit systemischen Infektionen treten häufig zerebrale Funktionseinschränkungen auf. Dieses Krankheitsbild wird nach Ausschluß anderer Ursachen als septische Enzephalopathie bezeichnet. Leitsymptom einer septischen Enzephalopathie ist ein unspezifisches Psychosyndrom. Je nach Schwere des Krankheitsbildes treten quantitative Bewußtseinsstörungen (Somnolenz, Sopor, Koma) mit oder ohne Herdsymptomatik auf. Typisch ist eine Fluktuation des Befundes. Das Auftreten zerebraler Symptome bei Infektionen erhöht die Mortalität der Patienten. Erste Symptome der septischen Enzephalopathie treten früh und vor anderen Organmanifestationen im Verlauf einer Sepsis auf. Der sensibelste Parameter zur Diagnosestellung einer septischen Enzephalopathie ist das EEG. Es zeigt Allgemeinveränderungen, die mit dem steigenden Schweregrad der Erkrankung zunehmen.Als Auslöser der septischen Enzephalopathie wird ein multifaktorielles Geschehen angenommen. Bereits frühzeitig kommt es durch die Anwesenheit von Bakterien im Blut zur Ausschüttung von Zytokinen und anderen Mediatoren. Diese bewirken metabolische Störungen mit Veränderungen im zerebralen Aminosäure-, Glukose-, und Neurotransmitterstoffwechsel. Zusätzlich zerstören neurotoxisch wirkende Zytokine die Blut-Hirn-Schranke. Hierdurch werden histologisch nachweisbare Neuronenuntergänge getriggert. Weitere Folgen der Zytokinexposition sind perivaskuläre Ödeme und Einblutungen. Darüber hinaus tragen der Ausfall der metabolischen Steuerung der Gehirnperfusion und lokale zerebrale Ischämien zur Entstehung des Krankheitsbildes bei. Eine spezifische Therapie der septischen Enzephalopathie besteht derzeit nicht.

Impaired mental function, from clouding of consciousness to deep coma is often seen in patients with systemic inflammation. Diagnosis of this syndrome which is called „septic encephalopathy” is dependent on exclusion of other causes. The underlying mechanisms have only been defined in parts.The appearance of cerebral symptoms during an infection increases mortality. Primary symptoms of septic encephalopathy appear early, before other septic organmanifestations become apparent. The most sensible parameter for diagnosis of septic encephalopathy in comatose patients or under sedation is the EEG. It shows general alterations which increase parallelly to the severity of septic encephalopathy. Septic encephalopathy has to be considered a multifactorial event. In an early stage of the development of septic encephalopathy, bacteremia induces overproduction of cytokines and other mediators. This causes metabolic dysregulation with effects on the cerebral protein-, glucose and neurotransmitter metabolism. In addition, cytokines damage the blood-brain-barrier and exert direct cytotoxic effects. This results in histologic detectable neuronal damage. Further effects of the cytokine expression are perivascular edema and hemorrhage. The loss of metabolic regulation of the brain perfusion and local cerebral ischemia additionally contribute to the etiology of septic encephalopathy. A specific therapy is not yet known.

Literatur

• 1 Bolton CF, Young GB. Neurological complications in critical ill patients. In: Aminoff MJ Neurology and General Medicine. New York; Churchill Livingstone 1989: 713-729
  Google Scholar
• 2 Bolton CF, Young GB, Zochodne DW. The neurological complications of sepsis.  Ann Neurol. 1993;  33 94-100
  CrossrefPubMedGoogle Scholar
• 3 Bowton DL, Bertels NH, Prough DS, Stump DA. Cerebral blood flow is reduced in patients with sepsis syndrome (see comments).  Crit Care Med. 1989;  17 399-403
  PubMedGoogle Scholar
• 4 Bright R. Reports of medical cases selected with a view of illustrating the symptoms and cure of disease by a reference to morbid anatomy. London; Longman 1-88
• 5 Conroy B, Pollard V, Prough DS, Traber L, Traber D. Cerebral autoregulation during controlled hypotension in chronic septic sheep.  Anesthesiology. 1993;  81 -309
  PubMedGoogle Scholar
• 6 Eidelman LA, Putterman D, Putterman C, Sprung CL. The spectrum of septic encephalopathy. Definitions, etiologies, and mortalities.  J Amer Med Ass. 1996;  275 470-473
  PubMedGoogle Scholar
• 7 Ekstrom Jodal B, Haggendal E, Larsson LE. Cerebral blood flow and oxygen uptake in endotoxic shock. An experimental study in dogs.  Acta Anaesthesiol Scand. 1982;  26 163-170
  PubMedGoogle Scholar
• 8 Freund HR, Muggia Sullam M, Peiser J, Melamed E. Brain neurotransmitter profile is deranged during sepsis and septic encephalopathy in the rat.  J Surg Res. 1985;  38 267-271
  CrossrefPubMedGoogle Scholar
• 9 Freund HR, Muggia-Sullam M, LaFranca R, Holroyde J, Fischer JE. Regional brain amino acid and neurotransmitter derangements during abdominal sepsis and septic encephalopathy in the rat.  Arch Surg. 1986;  121 209-216
  PubMedGoogle Scholar
• 10 Freund HR, Ryan JA Jr, Fischer JE. Amino acid derangements in patients with sepsis: treatment with branched chain amino acid rich infusions.  Ann Surg. 1978;  188 423-430
  PubMedGoogle Scholar
• 11 Graham DI, Behan PO, More IAR. Brain damage complicating septic shock.  J Neurol Neurosurg Psych. 1979;  42 19-28
  PubMedGoogle Scholar
• 12 Gutierrez EG, Banks WA, Kastin AJ. Murine tumor necrosis factor alpha is transported from blood to brain in the mouse.  J Neuroimmunol. 1993;  47 169-176
  CrossrefPubMedGoogle Scholar
• 13 Hasselgren PO, Fischer JE. Septic encephalopathy. Etiology and management.  Intens Care Med. 1986;  12 13-16
  PubMedGoogle Scholar
• 14 Houtchens BA, Westenskow DR. Oxygen consumption in septic shock: collective review.  Circ Shock. 1984;  13 361-384
  PubMedGoogle Scholar
• 15 Jackson AC, Gilbert JJ, Young GB, Bolton CT. The encephalopathy of sepsis.  Can J Neurol Sci. 1985;  12 303-307
  PubMedGoogle Scholar
• 16 Jeppson B, Freund HR, Gimmon Z, James JH, Meyenfeldt MFv, Fischer JE. Blood-brain barrier derangement in sepsis: cause of septic encephalopathy?.  Amer J Surg. 1981;  141 136-142
  CrossrefPubMedGoogle Scholar
• 17 Kadoi Y, Saito S, Kunimoto F, Imai T, Fujita T. Impairment of the brain beta-adrenergic system during experimental endotoxemia.  J Surg Res. 1996;  61 496-502
  CrossrefPubMedGoogle Scholar
• 18 Krueger JM, Walter J, Dinarello CA, Wolff SM, Chedid L. Sleep-promoting effects of endogenous pyrogen (interleukin-1).  Amer J Physiol. 1984;  246 -999
  PubMedGoogle Scholar
• 19 Kubes P, Granger DN. Nitric oxide modulates microvascular permeability.  Amer J Physiol. 1992;  262 -615
  PubMedGoogle Scholar
• 20 Maekawa T, Fujii Y, Sadamitsu D, Yokota K, Soejima Y, Ishikawa T, Miyauchi Y, Takeshita H. Cerebral circulation and metabolism in patients with septic encephalopathy.  Amer J Emerg Med. 1991;  9 139-143
  PubMedGoogle Scholar
• 21 Matta BF, Stow PJ. Sepsis-induced vasoparalysis does not involve the cerebral vasculature: indirect evidence from autoregulation and carbon dioxide reactivity studies.  Brit J Anaesth. 1996;  76 790-794
  PubMedGoogle Scholar
• 22 Mizock BA, Sabelli HC, Dubin A, Javaid JI, Poulos A, Rackow EC. Septic encephalopathy. Evicende for altered phenylalanine metablism and comparison with hepatic encephalopathy.  Arch Intern Med. 1990;  150 443-449
  CrossrefPubMedGoogle Scholar
• 23 Moulin GCd, Paterson D, Hedley-Whyte J, Broitman SA. E. coli peritonitis and bacteremia cause increased blood-brain barrier permeability.  Elsevier Science Publishers B.V. 1985 340: 261-268
• 24 Müller N. Die Rolle des Zytokinnetzwerks im ZNS und psychische Störungen.  Nervenarzt. 1997;  68 11-20
  CrossrefPubMedGoogle Scholar
• 25 Neugebauer E, Dimmeler S, Troidl H. Mediatorensysteme und Sepsis.  Chirurg. 1995;  66 2-10
  PubMedGoogle Scholar
• 26 Osler W. The princicples of practice of medicine.  New York; D. Appelton 114-118
• 27 Palmer RM. The discovery of nitric oxide in the vessel wall. A unifying concept in the pathogenesis of sepsis.   Arch Surg. 1993;  128 396-401
  PubMedGoogle Scholar
• 28 Pan W, Banks WA, Kastin AJ. Permeability of the blood-brain and blood-spinal cord barriers to interferons.  N Neuroimmunol. 1997;  76 105-111
  PubMedGoogle Scholar
• 29 Pendlebury WW, Perl DP, Munoz DG. Multiple microabscesses in the central nervous system: a clinicopathology study.  J Neuropathol Exp Neurol. 1989;  48 290-300
  PubMedGoogle Scholar
• 30 Pine RW, Wertz MJ, Lennard ES, Dellinger EP, Carrico CJ, Minshew BH. Determinants of organ malfunction or death in patients with intra-abdominal sepsis. A discriminant analysis.  Arch Surg. 1983;  118 242-249
  PubMedGoogle Scholar
• 31 Sari A, Yamashita S, Ohosita S, Ogasahara H, Yamada K, Yonei A, Yokota K. Cerebrovascular reactivity to CO₂ in patients with hepatic or septic encephalopathy.  Resuscitation. 1990;  19 125-134
  CrossrefPubMedGoogle Scholar
• 32 Schwarz S, Schwab S, Fabian CW, Schellinger P, Orberk E, Hund E. Infection: impaired consciousness as the initial symptom. Clinical and pathophysiologic aspects of septic encephalopathy (see comments).  Nervenarzt. 1997;  68 292-297
  CrossrefPubMedGoogle Scholar
• 33 Soejima Y, Fujii Y, Ishikawa T, Takeshita H, Maekawa T. Local cerebral glucose utilization in septic rats.  Crit Care Med. 1990;  18 423-427
  PubMedGoogle Scholar
• 34 Sprung CL, Cerra FB, Freund HR, Schein RM, Konstantinides FN, Marcial EH, Pena M. Amino acid alterations and encephalopathy in the sepsis syndrome.  Crit Care Med. 1991;  19 753-757
  PubMedGoogle Scholar
• 35 Thompson BG, Pluta RM, Girton ME, Oldfield EH. Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates.  J Neurosurg. 1996;  84 71-78
  PubMedGoogle Scholar
• 36 Wijdicks EF, Stevens M. The role of hypotension in septic encephalopathy following surgical procedures.  Arch Neurol. 1992;  49 653-656
  PubMedGoogle Scholar
• 37 Young GB, Bolton CF, Archibald YM, Austin TW, Wells GA. The electroencephalogram in sepsis-associated encephalopathy.  J Clin Neurophysiol. 1992;  9 145-152
  CrossrefPubMedGoogle Scholar
• 38 Young GB, Bolton CF, Austin TW, Archibald YM, Gonder J, Wells GA. The encephalopathy associated with septic illness.  Clin Invest Med. 1990;  13 297-304
  PubMedGoogle Scholar
• 39 Young GB, Young GB, Bolton CF, Austin TW, Archibald YM, Gonder J, Wells GA. Neurologic complications of systemic criticall illness. The encephalopathy associated with septic illness.  Neurol Clin. 1995;  13 645-658
  PubMedGoogle Scholar

Dr. Ralph Bogdanski

Institut für Anästhesiologie | Technische Universität München

D-81675 München

Email: R.Bogdanski@lrz.tu-muenchen.de