Sepsis-associated encephalopathy

被引:540
作者
Gofton, Teneille E. [1 ]
Young, G. Bryan [1 ]
机构
[1] Univ Western Ontario, Dept Clin Neurol Sci & Med, London Hlth Sci Ctr, Univ Hosp, London, ON N6A 5A5, Canada
关键词
INTENSIVE-CARE-UNIT; NEURON-SPECIFIC ENOLASE; QUALITY-OF-LIFE; CONFUSION ASSESSMENT METHOD; TERM COGNITIVE IMPAIRMENT; CRITICALLY-ILL PATIENTS; SEPTIC ENCEPHALOPATHY; MITOCHONDRIAL DYSFUNCTION; BRAIN-INJURY; ROUTINE USE;
D O I
10.1038/nrneurol.2012.183
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body without overt CNS infection. SAE is frequently encountered in critically ill patients in intensive care units, and in up to 70% of patients with severe systemic infection. The severity of SAE can range from mild delirium to deep coma. Seizures and myoclonus are infrequent and cranial nerves are almost always spared, but most severe cases have an associated critical illness neuromyopathy. Development of SAE probably involves a number of mechanisms that are not mutually exclusive and vary from patient to patient. Substantial neurological and psychological morbidities often occur in survivors. Mortality is almost always due to multiorgan failure rather than neurological complications, and is almost 70% in patients with severe SAE. Further research into the pathophysiology, management and prevention of SAE is needed. This Review discusses the epidemiology and clinical presentation of SAE. Recent evidence for SAE pathophysiology is outlined and a diagnostic approach to patients with this syndrome is presented. Lastly, prognosis and management of SAE is discussed. Gofton, T. E. & Young, G. B. Nat. Rev. Neurol. 8, 557-566 (2012); published online 18 September 2012; doi:10.1038/nrneurol.2012.183
引用
收藏
页码:557 / 566
页数:10
相关论文
共 83 条
  • [1] Oxidative variables, in the rat brain after sepsis induced by cecal ligation and perforation
    Barichello, T
    Fortunato, JJ
    Vitali, AM
    Feier, G
    Reinke, A
    Moreira, JCF
    Quevedo, J
    Dal-Pizzol, F
    [J]. CRITICAL CARE MEDICINE, 2006, 34 (03) : 886 - 889
  • [2] Long-term cognitive impairment in sepsis survivors
    Barichello, T
    Martins, MR
    Reinke, A
    Feier, G
    Ritter, C
    Quevedo, J
    Dal-Pizzol, F
    [J]. CRITICAL CARE MEDICINE, 2005, 33 (07) : 1671 - 1671
  • [3] Serum neuron-specific enolase, S100B, and myelin basic protein concentrations after inflicted and noninflicted traumatic brain injury in children
    Berger, RP
    Adelson, PD
    Pierce, MC
    Dulani, T
    Cassidy, LD
    Kochanek, PM
    [J]. JOURNAL OF NEUROSURGERY, 2005, 103 (01) : 61 - 68
  • [4] NEUROLOGIC COMPLICATIONS OF CRITICAL MEDICAL ILLNESSES
    BLECK, TP
    SMITH, MC
    PIERRELOUIS, SJC
    JARES, JJ
    MURRAY, J
    HANSEN, CA
    [J]. CRITICAL CARE MEDICINE, 1993, 21 (01) : 98 - 103
  • [5] Drug effects on EEG
    Blume, Warren T.
    [J]. JOURNAL OF CLINICAL NEUROPHYSIOLOGY, 2006, 23 (04) : 306 - 311
  • [6] THE NEUROLOGICAL COMPLICATIONS OF SEPSIS
    BOLTON, CF
    YOUNG, GB
    ZOCHODNE, DW
    [J]. ANNALS OF NEUROLOGY, 1993, 33 (01) : 94 - 100
  • [7] DEFINITIONS FOR SEPSIS AND ORGAN FAILURE
    BONE, RC
    SPRUNG, CL
    SIBBALD, WJ
    [J]. CRITICAL CARE MEDICINE, 1992, 20 (06) : 724 - 726
  • [8] Mitochondrial dysfunction in a long-term rodent model of sepsis and organ failure
    Brealey, D
    Karyampudi, S
    Jacques, TS
    Novelli, M
    Stidwill, R
    Taylor, V
    Smolenski, RT
    Singer, M
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2004, 286 (03) : R491 - R497
  • [9] Plasmapheresis in severe sepsis and septic shock: a prospective, randomised, controlled trial
    Busund, R
    Koukline, V
    Utrobin, U
    Nedashkovsky, E
    [J]. INTENSIVE CARE MEDICINE, 2002, 28 (10) : 1434 - 1439
  • [10] Inflammatory response in microvascular endothelium in sepsis: Role of oxidants
    Cepinskas, Gediminas
    Wilson, John X.
    [J]. JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION, 2008, 42 (03) : 175 - 184