lecture section...septic encephalopathy

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Professor Yasser Metwally www.yassermetwally.com Septic encephalopathy

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Lecture section...Septic encephalopathy http://yassermetwally.com http://yassermetwally.net

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Page 1: Lecture section...Septic encephalopathy

Professor Yasser Metwallywww.yassermetwally.com

Septic encephalopathy

Page 2: Lecture section...Septic encephalopathy

IntroductionImpairment of cons., including coma, often

occurs in association with sepsis Occur in a range of 8–70% of septic patientsMay as an early sign of sepsis The term "septic encephalopathy" :

acute confusional episodes or other significant cognitive abnormalities that develop during sepsis

as an entity that cannot be explained by hepatic or renal dysfunction, hypotension, or hypoxia

Imply poor prognosis , higher mortality

Page 3: Lecture section...Septic encephalopathy

Etiology and Pathophysiology(1) Most likely multifactorial Underlying mechanisms only been defined in

parts Disseminated cerebral microabscesses

infecting organisms and/or their toxins do not directly cause encephalopathy

Systemic inflammation resulting from infection or other causes action of inflammatory mediators on the brain

, cytotoxic response of brain cells

Page 4: Lecture section...Septic encephalopathy

Etiology and Pathophysiology(2)Sepsis activate a variety of inflammatory

cascade , → SIRSInflammatory efffector cell

neutrophil , macrophage , plt , endothelial cell etc

Inflammatory mediators Cytokines , lipid products , complement etc

Free radicals

Page 5: Lecture section...Septic encephalopathy

Etiology and Pathophysiology (3)Free radicals

damage RBC and limit O2 delivery to brain Inflammatory mediators

impair mitochondrial function and O2 extraction by the brain

destroy BBB perimicrovessel edema disruption of astrocyte endfeet aromatic a.a enter brain parenchyma and disturb NT

Ultimately, extensive neuronal injury *

Page 6: Lecture section...Septic encephalopathy

Diagnosis (1)Evaluating depressed cons. in critically ill p`ts

(1) Receiving sedative and narcotic drugs (2) Head injury , intracranial event e.g.

cerebrovascular causes(3) Metabolic derangements :

Sugar , electrolytes (Na , Ca) , acid-base balance (acidemia , hypercapnia) , oxygenation (hypoxia , hypotention) , hepatic encephalopathy , uremic encephalopathy , septic encephalopathy , alcohol or drug

Page 7: Lecture section...Septic encephalopathy

Diagnosis (2)Evaluating coma in surgical patients

【 Failure to awaken after surgery 】 v.s. 【 Alteration of cons. that develops after an

asyrnptomatic interval 】Post-op hyponatremia

Free water administered under ADH↑ & renal f. ↓ Acute uremic encephalopathy

major heart surgery or major surgery complicated by sepsis or involves considerable GI repair

perioperative acute renal failure renal hypoperfusion and nephrotoxicity

Page 8: Lecture section...Septic encephalopathy

TreatmentCurrently, there is no treatment !!some patients with sepsis cons. remain

unresponsive after the associated life threatening conditions are controlled marked hypotension ↑ inotropic agent ischemic damage brain Ultimately, extensive neuronal injury in

pathophysiology of septic encephalopathy

Page 9: Lecture section...Septic encephalopathy

Prognosis

Page 10: Lecture section...Septic encephalopathy

JAMA. 1996 Feb 14;275(6):470-3(prospective study in 50 sepsis patients )

Severity of septic encephalopathy (graded by GCS ) correlated with mortality

Page 11: Lecture section...Septic encephalopathy

JAMA. 1996 Feb 14;275(6):470-3 (prospective study in 50 sepsis patients )

Bacteremia was more common in encephalopathic patients ( by altered mental status grading )

P`ts with bacteremia more commonly have an altered mental status, which is associated with a higher mortality

Page 12: Lecture section...Septic encephalopathy

PrognosisSeveral lab. values showed a linear

relationship with the severity of encephalopathy, including WBC, Po2, BUN/Cr, Bil, ALP, serum albumin and K. → one feature of more widespreading MOF

Disturbance of protein metabolism plasma and brain a.a were deranged aromatic a.a. levels correlated with APACHE

II scores and mortality

Page 13: Lecture section...Septic encephalopathy

Ongoing studyCSF protein content was mildly elevated

(60–85 mg/dL) EEG is a more sensitive detector of CNS

dysfunction than is the clinical examination and also is a powerful predictor of survival EEG provides a large amount of data that are often difficult to quantify