Lecture section...Septic encephalopathy

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

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Lecture section...Septic encephalopathy

  1. 1. Professor Yasser Metwally www.yassermetwally.com Septic encephalopathy
  2. 2. Introduction <ul><li>Impairment of cons., including coma, often occurs in association with sepsis </li></ul><ul><li>Occur in a range of 8–70% of septic patients </li></ul><ul><li>May as an early sign of sepsis </li></ul><ul><li>The term &quot; septic encephalopathy &quot; : </li></ul><ul><ul><li>acute confusional episodes or other significant cognitive abnormalities that develop during sepsis </li></ul></ul><ul><ul><li>as an entity that cannot be explained by hepatic or renal dysfunction, hypotension, or hypoxia </li></ul></ul><ul><li>Imply poor prognosis , higher mortality </li></ul>
  3. 3. Etiology and Pathophysiology(1) <ul><li>Most likely multifactorial </li></ul><ul><li>Underlying mechanisms only been defined in parts </li></ul><ul><li>Disseminated cerebral microabscesses </li></ul><ul><ul><li>infecting organisms and/or their toxins do not directly cause encephalopathy </li></ul></ul><ul><li>Systemic inflammation resulting from infection or other causes </li></ul><ul><ul><li>action of inflammatory mediators on the brain , cytotoxic response of brain cells </li></ul></ul>
  4. 4. Etiology and Pathophysiology(2) <ul><li>Sepsis activate a variety of inflammatory cascade , -> SIRS </li></ul><ul><li>Inflammatory efffector cell </li></ul><ul><ul><li>neutrophil , macrophage , plt , endothelial cell etc </li></ul></ul><ul><li>Inflammatory mediators </li></ul><ul><ul><li>Cytokines , lipid products , complement etc </li></ul></ul><ul><li>Free radicals </li></ul>
  5. 5. Etiology and Pathophysiology (3) <ul><li>Free radicals </li></ul><ul><ul><li>damage RBC and limit O2 delivery to brain </li></ul></ul><ul><li>Inflammatory mediators </li></ul><ul><ul><li>impair mitochondrial function and O2 extraction by the brain </li></ul></ul><ul><ul><li>destroy BBB </li></ul></ul><ul><ul><ul><li>perimicrovessel edema </li></ul></ul></ul><ul><ul><ul><li>disruption of astrocyte endfeet </li></ul></ul></ul><ul><ul><ul><li>aromatic a.a enter brain parenchyma and disturb NT </li></ul></ul></ul><ul><li>Ultimately, extensive neuronal injury * </li></ul>
  6. 6. Diagnosis (1) <ul><li>Evaluating depressed cons. in critically ill p`ts </li></ul><ul><ul><li>(1) Receiving sedative and narcotic drugs </li></ul></ul><ul><ul><li>(2) Head injury , intracranial event e.g. cerebrovascular causes </li></ul></ul><ul><ul><li>(3) Metabolic derangements : </li></ul></ul><ul><ul><ul><ul><li>Sugar , electrolytes (Na , Ca) , acid-base balance (acidemia , hypercapnia) , oxygenation (hypoxia , hypotention) , hepatic encephalopathy , uremic encephalopathy , septic encephalopathy , alcohol or drug </li></ul></ul></ul></ul>
  7. 7. Diagnosis (2) <ul><li>Evaluating coma in surgical patients </li></ul><ul><ul><li>【 Failure to awaken after surgery 】 v.s. 【 Alteration of cons. that develops after an asyrnptomatic interval 】 </li></ul></ul><ul><ul><li>Post-op hyponatremia </li></ul></ul><ul><ul><ul><li>Free water administered under ADH↑ & renal f. ↓ </li></ul></ul></ul><ul><ul><li>Acute uremic encephalopathy </li></ul></ul><ul><ul><ul><li>major heart surgery or major surgery complicated by sepsis or involves considerable GI repair </li></ul></ul></ul><ul><ul><ul><li>perioperative acute renal failure renal hypoperfusion and nephrotoxicity </li></ul></ul></ul>
  8. 8. Treatment <ul><li>Currently, there is no treatment !! </li></ul><ul><li>some patients with sepsis cons. remain unresponsive after the associated life threatening conditions are controlled </li></ul><ul><ul><li>marked hypotension ↑ inotropic agent </li></ul></ul><ul><ul><li>ischemic damage brain </li></ul></ul><ul><ul><li>Ultimately, extensive neuronal injury in pathophysiology of septic encephalopathy </li></ul></ul>
  9. 9. Prognosis
  10. 10. JAMA. 1996 Feb 14;275(6):470-3 (prospective study in 50 sepsis patients ) <ul><li>Severity of septic encephalopathy (graded by GCS ) correlated with mortality </li></ul>
  11. 11. JAMA. 1996 Feb 14;275(6):470-3 (prospective study in 50 sepsis patients ) <ul><li>Bacteremia was more common in encephalopathic patients ( by altered mental status grading ) </li></ul><ul><li>P`ts with bacteremia more commonly have an altered mental status , which is associated with a higher mortality </li></ul>
  12. 12. Prognosis <ul><li>Several 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 </li></ul><ul><li>Disturbance of protein metabolism </li></ul><ul><ul><li>plasma and brain a.a were deranged </li></ul></ul><ul><ul><li>aromatic a.a. levels correlated with APACHE II scores and mortality </li></ul></ul>
  13. 13. Ongoing study <ul><li>CSF protein content was mildly elevated (60–85 mg/dL) </li></ul><ul><li>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 </li></ul>

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