Sepsis Ensefalopatisi
Özet
Sepsis ilişkili ensefalopati, enfeksiyonun tetiklediği sistemik enflamatuvar yanıt sonucu ortaya çıkan ve septik hastaların büyük bir kısmını etkileyen ciddi bir akut beyin işlev bozukluğudur. Nöroinflamasyon, iskemik olaylar, kan-beyin bariyerinin bozulması ve mitokondriyal disfonksiyon gibi karmaşık mekanizmalarla gelişen bu durum, konfüzyon, deliryum ve koma gibi çeşitli nörolojik tablolara yol açar. Belirli bir klinik bulgusu olmayan ve dışlama tanısı ile konulan bu sendrom, mortalite ve morbidite üzerinde belirleyici bir rol oynamaktadır. Semptomların erken tanınması ve hızlı tedavi yaklaşımı, hastaların klinik sonuçlarını iyileştirmek ve uzun dönem komplikasyonları azaltmak açısından hayati öneme sahiptir.
Sepsis-associated encephalopathy is a severe acute brain dysfunction resulting from an infection-triggered systemic inflammatory response, affecting a significant majority of septic patients. Characterized by complex mechanisms such as neuroinflammation, ischemic events, blood-brain barrier disruption, and mitochondrial dysfunction, it manifests as clinical conditions ranging from confusion and delirium to coma. As a diagnosis of exclusion with no specific clinical markers, it plays a decisive role in mortality and morbidity. Early recognition of symptoms and rapid treatment approaches are vital for improving clinical outcomes and reducing long-term complications in affected patients.
Referanslar
Duman M, Şevketoğlu E, Arslanköylü EA,’’et al’’.J Pediatr Emerg Intensive Care Med 2020:7:1:45-58
Judith A. Guzman-Cottrill,Louise Elaine Vaz. The Systemic Inflammatory Response Syndrome (SIRS), Sepsis, and Septic Shock. In: Long SS, Prober GC, Fisher M Eds. Principles and Practice of Pediatric Infectious Disease. ed. 5th, Philadelphia; Elsevier; 2018: 98-102.
Needham DM, Davidson J, Cohen H,’’ et al’’. Improving long-term outcomes after discharge from intensive care unit: report from a stakeholders’ conference. Crit Care Med. 2012;40(2):502–9.
Robba C, Crippa IA, Taccone FS. Septic encephalopathy. Curr Neurol Neurosci Rep. 2018;18:82.
Gofton TE, Bryan YG. Sepsis-associated encephalopathy. Nat Rev Neurol. 2012;8:557–66.
Barbosa-Silva MC, Lima MN, Battaglini D,’’ et al’’. Infectious disease-associated encephalopathies. Crit Care. 2021;25(1):236.
Singer M, Deutschman CS, Seymour CW, ’’ et al’’. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10.
Kuperberg SJ, Wadgaonkar R. Sepsis-Associated Encephalopathy: The Blood-Brain Barrier and the Sphingolipid Rheostat. Front Immunol. 2017 ;8:597.
Satta MA, Jacobs RA, Kaltsas GA, Grossman AB. Endotoxin induces interleukin-1β and nitric oxide synthase mRNA in rat hypothalamus and pituitary. Neuroendocrinology. 1998;67(2):109–16.
Korcok J, Wu F, Tyml K, Hammond RR, Wilson JX. Sepsis inhibits reduction of dehydroascorbic acid and accumulation of ascorbate in astroglial cultures: intracellular ascorbate depletion increases nitric oxide synthase induction and glutamate uptake inhibition. J Neurochem. 2002 Apr;81(1):185-93.
Heneka MT, Löschmann PA, Gleichmann M, ‘’et all’’.Induction of nitric oxide synthase and nitric oxide-mediated apoptosis in neuronal PC12 cells after stimulation with tumor necrosis factor-alpha/lipopolysaccharide. J Neurochem. 1998:71(1):88-94.
Semmler A, Hermann S, Mormann F, ‘’et al’’ .Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolism. J Neuroinflammation. 2008;5:38.
Bozza FA, Garteiser P, Oliveira MF, ‘’ET AL’’.Sepsis-associated encephalopathy: a magnetic resonance imaging and spectroscopy study. J Cereb Blood Flow Metab. 2010;30(2):440-8.
Orhun G, Tüzün E, Bilgiç B,’’et al’’. Brain Volume Changes in Patients with Acute Brain Dysfunction Due to Sepsis. Neurocrit Care. 2020;32(2):459-468.
Stubbs DJ, Yamamoto AK, Menon DK. Imaging in sepsis-associated encephalopathy--insights and opportunities. Nat Rev Neurol. 2013;9(10):551-61.
Heming N, Mazeraud A, Verdonk F, Bozza FA, Chrétien F, Sharshar T. Neuroanatomy of sepsis-associated encephalopathy. Crit Care. 2017;21(1):65.
Wilson JX, Young GB. Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts. Can J Neurol Sci. 2003;(2):98-105.
Consales G, De Gaudio AR. Sepsis associated encephalopathy. Minerva Anestesiol. 2005;71(1-2):39-52.
Bone RC, Balk RA, Cerra FB, ‘’et al’’.Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101(6):1644-55.
Zhang LN, Wang XT, Ai YH, Guo QL, Huang L, Liu ZY, Yao B. Epidemiological features and risk factors of sepsis-associated encephalopathy in intensive care unit patients: 2008-2011. Chin Med J (Engl). 2012;125(5):828-31.
Huang L, Peng S, Li R, Xie D, Huang D. Fulminant encephalopathy in a child with hyperferritinemic sepsis: a case report. BMC Neurol. 2020;20(1):73.
Als LC, Nadel S, Cooper M, Pierce CM, Sahakian BJ, Garralda ME. Neuropsychologic function three to six months following admission to the PICU with meningoencephalitis, sepsis, and other disorders: a prospective study of school-aged children. Crit Care Med. 2013;41(4):1094-103.
Hsu AA, Fenton K, Weinstein S, Carpenter J, Dalton H, Bell MJ. Neurological injury markers in children with septic shock. Pediatr Crit Care Med. 2008;9(3):245-51.
