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Sepsis markers. Dr. Natalie Leung 6 th January 2012 ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong. Introduction. Sepsis can occur suddenly and deteriorate rapidly Timely diagnosis of sepsis is the key of success. However…… can sometimes be challenging.

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Sepsis markers


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    1. Sepsis markers Dr. Natalie Leung 6th January 2012 ICU, Pamela Youde Nethersole Eastern Hospital, Hong Kong

    2. Introduction • Sepsis can occur suddenly and deteriorate rapidly • Timely diagnosis of sepsis is the key of success

    3. However…… can sometimes be challenging

    4. How to improve the outcome of sepsis? • Early diagnosis and treatment • Surviving Sepsis Campaign • reduction in mortality rate of severe sepsis.

    5. Septic shock: Mortality risk and time Early diagnosis is a key to reduce mortality Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shockCrit Care Med 2006;34:1589-96

    6. Sepsis markers • Diagnostic • Useful for identifying or ruling out sepsis • Identifying patients who may benefit from specific therapies • Assessing the response to therapy • Prognostic

    7. Ideal sepsis markers • High sensitivity (increase pathologically in the presence of disease) • High specificity (does not increase in the absence of disease) • Related to the disease burden and extent • Changes in accordance with the clinical evolution • Anticipates clinical changes before it happens

    8. Ideal sepsis markers • Adds independent information about the risk or prognosis • Reproducible • Easy and cheap

    9. What do we have now? • WCC • Lactate • Tissue perfusion variables • Biomarkers • C-reactive protein (CRP) • Procalcitonin (PCT) • Cytokines • New markers

    10. What do we have now? • A review of sepsis biomarkers • 178 different biomarkers • Most of them had been tested clinically • Primiarily as prognostic markers • Relatively few have been used for diagnosis Sepsis biomarkers: a review. Critical Care. 2010; 14(1): R15

    11. What do we have now? • Large numbers of markers • Cytokines • Receptors biomarkers • Coagulation biomarkers • Biomarkers related to vascular endothelial damage • Markers related to organ dysfunction • Acute phase protein biomarkers • others Sepsis biomarkers: a review Crit Care. 2010; 14(1): R15

    12. Sepsis biomarkers: a review Crit Care. 2010; 14(1): R15

    13. Sepsis biomarkers: a review Crit Care. 2010; 14(1): R15

    14. Sepsis markers • Lactate • C-reactive protein (CRP) • Procalcitonin (PCT) • Newer sepsis markers

    15. Sepsis markers • Lactate • C-reactive protein (CRP) • Procalcitonin (PCT) • Newer sepsis markers

    16. Lactate production Critical illness leading to increased tissue oxygen extraction Oxygen delivery Oxygen consumption Oxygen debt Global tissue hypoxia Anaerobic metabolism Lactate production

    17. Lactate • Raised in severe sepsis and septic shock • Hypoperfusion (secondary to anaerobic metabolism) • Cellular metabolic failure • Decrease clearance by the liver

    18. Numerous studies have established that lactate is a good marker of global hypoxia in circulatory shock

    19. Use of lactate as a sepsis marker • Diagnosis • Prognostic and predict mortality

    20. Diagnosis • Limited role in diagnostic • Surviving Sepsis Campaign guidelines 2008 • “begin resuscitation immediately in patients with hypotension/ elevated serum lactate >=4mmol/l”

    21. Prognostic and predict mortality • It can be used as … • Monitoring response of septic patients to resuscitation • Stratification and prognosis • Serial lactate level monitoring is recommended • High lactate clearance: • less required vasopressors therapy, greater improvements in APACHE II scores and decreased mortality rates

    22. Lactate clearance • In patients with septic shock • Survivors vs non-survivors • Initial lactate level did not differ much • Survivors had a significant decrease in lactate levels and less “lactate clearance time” Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill septic patients. Crit Care Med. 2003;31(3):705-710.

    23. Lactate clearance • 111ED and ICU patients with severe sepsis and septic shock • Lactate clearance • The percentage lactate decrease over the initial 6 hr ED evaluation and treatment period Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill septic patients. Crit Care Med. 2003;31(3):705-710.

    24. Lactate clearance • All patients were followed for 72 hrs and received a protocol-driver EGDT • Results • The higher the lactate clearance, the lower the mortality Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill septic patients. Crit Care Med. 2003;31(3):705-710.

    25. Single-center cohort study • 830 patients • Test the association between initial serum lactate level and mortality in patients presenting to AED with severe sepsis is independent of organ dysfunction and shock

    26. Sepsis markers • Lactate • C-reactive protein (CRP) • Procalcitonin (PCT) • Newer sepsis markers

    27. CRP • Acute phase protein • Synthesized in liver • IL-6 (and IL-1 and TNFα) stimulate synthesis • Binds bacterial polysaccharide/ chromatin • Activates the classical complement pathway • Increase the immune inflammatory response • Esp. in bacteria infection (vs viral)

    28. CRP • Level of CRP begins within 4-6hrs after stimulus • Doubles every 8hrs • Peaks at 36-50 hrs • Half-life 19hrs

    29. CRP • A sensitive marker of inflammation and tissue damage • Other conditions result in raised in CRP • Rheumatological disease • SLE • Systemic sclerosis • Dermatomyositis • Sjogren’s disease • Inflammatory bowel disease • Haematological disease • E.g. leukaemia • Graft-versus-host disease

    30. CRP

    31. CRP as a marker of sepsis resolution CRP of non-survivors was significantly higher since D3 onward

    32. Sepsis markers • Lactate • C-reactive protein (CRP) • Procalcitonin (PCT) • Newer sepsis markers

    33. Procalcitonin • A peptide precursor of calcitonin • Produced by • parafollicular cells of the thyroid • neuroendocrine cells of the lung and the intestine (extrathyroidal) • It raises in a response to a proinflammatory stimulus • Esp of bacterial origin (mainly from the cells of lung and the intestine)

    34. PCT- characteristics • Fast response (2-4hrs) • Peak values 8-24hr

    35. PCT- characteristics • Short half-life (~24hrs) independent of renal function • Easy to measure in serum and plasma (stable in vivo and in vitro) • Plasma concentration ~ <0.05-1000ng/ml

    36. In systemic inflammation or in infection • Persists as long as inflammatory process continues • Mechanical trauma • Increase within 2-4hrs • Peak in 1st or 2nd day then diminish

    37. Procalcitonin (PCT) • Reference values (except newborn) • Significantly lower in leukopenic patients

    38. Use of PCT • Sepsis diagnosis • Antibiotic guidance • Patient prognosis

    39. Sepsis diagnosis • Prospective single centre, non-interventional study • Patients > 38C Bruno Riou et al. Critical Care 2007; 11:R60

    40. Antibiotic therapy • Multicentre, prospective, parallel-group, open-label trial • 1:1 ratio of procalcitonin (n=311) and control group (n=319)

    41. Antibiotics were started/ stopped based on a predefined cut-off ranges of PCT value • Primary end point • 28 and 60 days mortality • No. of days without antibiotics

    42. Primary endpoint: all-cause mortality at 60 days