Sepsis 6b3j6d
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Sepsis Dr M. Kothalawela Infection -2 2009/10 batch
Objective • Understanding sepsis –pathogenesis and role of cytokines in genesis of sepsis • Detection of sepsis –Sepsis markers • Sepsis treatment –Early aggressive AB therapy • Outcome of sepsis and Prevention • Guiding therapy using markers • New trends –POCT and NAT •14/05/2013 Summary
How deadly is sepsis, comparison with acute MI, Lung, Colon and Breast Cancer Mortality in US
14/05/2013
In Sri Lanka • Burden of disease; masked due to given undue attention to NCDs ?
14/05/2013
Understanding Sepsis • Sepsis is not a specific disease • But, a continuum of events triggered by the body’s inflammatory immune responses to a – bacterial, – viral, – fungal, or – parasitic infection. 14/05/2013
14/05/2013
Why People die of sepsis INSULT INFLAMMATORY PROCES Renal Cardiac
TISSUE INJURY
Hepatic ORGAN DAMAGE
ORGAN DISFUNCTION
Heam Pulmonary GI
DEATH 14/05/2013
ORGAN FAILURE
Cerebral
Pathogenesis • Sepsis is a manifestation of release of , cytokines in a sequential manner - “cytokine cascade”.
• Cascade initiation with the production of TNF-a and IL- 1ß (proximal cytokines) • TNF-a and IL- 1ß –Responsible for most of the patho-physiologic process in sepsis 14/05/2013
TNF-a and IL- 1ß • TNF-a and IL- 1ß - mediate directly or indirectly the hemodynamic and inflammatory changes characteristic of sepsis
• TNF and IL-1 initiate a pro-inflammatory cascade, → production of pro-inflammatory cytokines.... – – – – 14/05/2013
IL-6, interferon (IFN)-g, IL-12, and And various chemokines
• These cytokines are necessary for normal function of the immune systems • But, un-cordinated response of pro-inflammatory cytokines leads to sepsis cascade leading to – – – – 14/05/2013
Endothelial damage, immune cell activation, tissue hypoxia, hemodynamic instability etc
14/05/2013
14/05/2013
The two phases of sepsis—an early pro-inflammatory phase follows onto a later antiinflammatory phase.
Webster N R , Galley H F Br. J. Anaesth. 2009;103:70-81 © The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of 14/05/2013 the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected]
Detection of Sepsis • First noticeable change occur in molecular level – Production of cytokines • Then cellular changes take place (Slightly later than molecular changes) • Noticeable increase of bio-markers
• Clinical Signs of sepsis – occur late (Symptoms of SIRS secondary to confirmed infective cause) 14/05/2013
Sepsis Clock
14/05/2013
Sepsis Treatment • Sepsis → is a medical emergency. • Sepsis need to be → treated quickly and efficiently as possible and as soon as it has been identified. • Clinical Features- Late • Bio Markers- Early 14/05/2013
Sepsis Treatment • Antibiotics broad-spectrum • Intravenous – Ensure rapid action and rapid distribution to the target • Risk of death from sepsis increases by 7.6% with every hour that es before treatment begins 14/05/2013
Risk of death ↑ by 7.6% with every hour es before commencing of appropriate therapy
14/05/2013
Appropriate Antimicrobial Treatment • Two-fold increase in mortality with inappropriate antimicrobial therapy • Statistically significant increase in mortality with each hour from the onset of septic shock.
• During First encounter → initiate empiric antibiotics • Choice of antibiotics - guided by the knowledge of most common sites of infection and the most common infecting organisms –
Most common site Lungs, Abdomen, GUT, Soft Tissue, Unknown – Common pathogens Gram Positives more than Gram Negatives Most common Gram Positives –Staph and Pneumococcus Most Common Gram Negatives- Escherichia coli, Klebsiella spp., Pseudomonas spp., and Enterobacter spp. Fungi approximately 6%
• Samples for blood cultures should be taken from a per-cutaneous site and from any intravascular catheters. 14/05/2013
Over the years –Gram Positives have overtaken Gram Negatives
14/05/2013
Site of Infection
Microorganisms
Therapeutic Choices
Streptococcus pneumoniae, Community-acquired Haemophilus influenzae, Third-generation cephalosporin with macrolide pneumonia Legionella pneumophila, or respiratory quinolone Mycoplasma pneumoniae S. pneumoniae, H. Early hospitalinfluenzae, L. pneumophila, Ceftriaxone, respiratory quinolone or ampicillinacquired pneumonia M. pneumonia; sulbactam, or ertapenem (<5 days) nonresistant gram-negative rods Pseudomonas aeruginosa, Klebsiella spp., Late hospitalAcinetobacter spp., acquired pneumonia methicillin-resistant Staphylococcus aureus
Antipseudomonal cephalosporin or carbapenem, or antipseudomonal beta-lactam or beta-lactamase inhibitor, plus linezolid or vancomycin
Intra-abdominal infections
Third-generation cephalosporin with Enteric gram-negative rods metronidazole, or beta-lactam or betaand anaerobes lactamase inhibitor, or carbapenem or moxifloxacin
Urinary tract infections
Gram-negative rods; Enterococcus spp.
14/05/2013
Extended-spectrum beta-lactam or aztreonam, with or without an aminoglycoside; ampicillin or vancomycin if Enterococcus is present
Source Control of Infection • Adequate source control of infection is as important as appropriate antimicrobial therapy in severe sepsis. • Source control includes – removal of infected foreign bodies, • • • • • • •
urinary catheters, intravascular catheters, peritoneal dialysis cannulas, prosthetic ts, vascular grafts, and mechanical valves. JJ shunts etc
• Incision and drainage of abscesses • cutaneous abscesses, • open or per-cutaneous drainage of intra-abdominal abscesses
•
For necrotizing fasciitis, Rapid and early surgical intervention 14/05/2013
Objective of source control • Reduction bacterial/fungal density at sight – included removal of biofilms • Facilitate antibiotic entry to the areas and early recovery
• Prevent overwhelming cytokine activity
14/05/2013
Other Modalities • • • •
Fluid Resuscitation Optimizing Tissue Oxygenation Vasopressor Treatment Xigiris etc
14/05/2013
Outcomes • Although the incidence of severe sepsis is increasing, mortality rates continue to decrease. • A recent study in a sepsis cohort, age was found to be an independent risk factor for death by sepsis • mortality rates > 65y → 27.7% < 65 → 17.7% • An increasing number of older survivors of sepsis require skilled nursing facilities 14/05/2013
Prevention • Efforts to decrease the incidence of this infection of pneumonia – Vaccinate susceptible individuals against • influenza, • H. influenzae, • and S. pneumoniae.
• Additionally, asplenic patients should receive vaccination against N. meningitidis • The incidence of intravascular catheter-related blood stream infections – can be reduced by Intra venous catheter bundle and exist site chlorhexidine applications • Cases of VAP can be ↓ by maintaining ventilator patients semirecumbent at a 45-degree to prevent aspiration
14/05/2013
Objective • Understanding sepsis –pathogenesis and role of cytokines in genesis of sepsis • Detection of sepsis –Sepsis markers • Sepsis treatment –Early aggressive AB therapy • Outcome of sepsis and Prevention • Guiding therapy using markers • New trends –POCT and NAT •14/05/2013 Summary
How deadly is sepsis, comparison with acute MI, Lung, Colon and Breast Cancer Mortality in US
14/05/2013
In Sri Lanka • Burden of disease; masked due to given undue attention to NCDs ?
14/05/2013
Understanding Sepsis • Sepsis is not a specific disease • But, a continuum of events triggered by the body’s inflammatory immune responses to a – bacterial, – viral, – fungal, or – parasitic infection. 14/05/2013
14/05/2013
Why People die of sepsis INSULT INFLAMMATORY PROCES Renal Cardiac
TISSUE INJURY
Hepatic ORGAN DAMAGE
ORGAN DISFUNCTION
Heam Pulmonary GI
DEATH 14/05/2013
ORGAN FAILURE
Cerebral
Pathogenesis • Sepsis is a manifestation of release of , cytokines in a sequential manner - “cytokine cascade”.
• Cascade initiation with the production of TNF-a and IL- 1ß (proximal cytokines) • TNF-a and IL- 1ß –Responsible for most of the patho-physiologic process in sepsis 14/05/2013
TNF-a and IL- 1ß • TNF-a and IL- 1ß - mediate directly or indirectly the hemodynamic and inflammatory changes characteristic of sepsis
• TNF and IL-1 initiate a pro-inflammatory cascade, → production of pro-inflammatory cytokines.... – – – – 14/05/2013
IL-6, interferon (IFN)-g, IL-12, and And various chemokines
• These cytokines are necessary for normal function of the immune systems • But, un-cordinated response of pro-inflammatory cytokines leads to sepsis cascade leading to – – – – 14/05/2013
Endothelial damage, immune cell activation, tissue hypoxia, hemodynamic instability etc
14/05/2013
14/05/2013
The two phases of sepsis—an early pro-inflammatory phase follows onto a later antiinflammatory phase.
Webster N R , Galley H F Br. J. Anaesth. 2009;103:70-81 © The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of 14/05/2013 the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected]
Detection of Sepsis • First noticeable change occur in molecular level – Production of cytokines • Then cellular changes take place (Slightly later than molecular changes) • Noticeable increase of bio-markers
• Clinical Signs of sepsis – occur late (Symptoms of SIRS secondary to confirmed infective cause) 14/05/2013
Sepsis Clock
14/05/2013
Sepsis Treatment • Sepsis → is a medical emergency. • Sepsis need to be → treated quickly and efficiently as possible and as soon as it has been identified. • Clinical Features- Late • Bio Markers- Early 14/05/2013
Sepsis Treatment • Antibiotics broad-spectrum • Intravenous – Ensure rapid action and rapid distribution to the target • Risk of death from sepsis increases by 7.6% with every hour that es before treatment begins 14/05/2013
Risk of death ↑ by 7.6% with every hour es before commencing of appropriate therapy
14/05/2013
Appropriate Antimicrobial Treatment • Two-fold increase in mortality with inappropriate antimicrobial therapy • Statistically significant increase in mortality with each hour from the onset of septic shock.
• During First encounter → initiate empiric antibiotics • Choice of antibiotics - guided by the knowledge of most common sites of infection and the most common infecting organisms –
Most common site Lungs, Abdomen, GUT, Soft Tissue, Unknown – Common pathogens Gram Positives more than Gram Negatives Most common Gram Positives –Staph and Pneumococcus Most Common Gram Negatives- Escherichia coli, Klebsiella spp., Pseudomonas spp., and Enterobacter spp. Fungi approximately 6%
• Samples for blood cultures should be taken from a per-cutaneous site and from any intravascular catheters. 14/05/2013
Over the years –Gram Positives have overtaken Gram Negatives
14/05/2013
Site of Infection
Microorganisms
Therapeutic Choices
Streptococcus pneumoniae, Community-acquired Haemophilus influenzae, Third-generation cephalosporin with macrolide pneumonia Legionella pneumophila, or respiratory quinolone Mycoplasma pneumoniae S. pneumoniae, H. Early hospitalinfluenzae, L. pneumophila, Ceftriaxone, respiratory quinolone or ampicillinacquired pneumonia M. pneumonia; sulbactam, or ertapenem (<5 days) nonresistant gram-negative rods Pseudomonas aeruginosa, Klebsiella spp., Late hospitalAcinetobacter spp., acquired pneumonia methicillin-resistant Staphylococcus aureus
Antipseudomonal cephalosporin or carbapenem, or antipseudomonal beta-lactam or beta-lactamase inhibitor, plus linezolid or vancomycin
Intra-abdominal infections
Third-generation cephalosporin with Enteric gram-negative rods metronidazole, or beta-lactam or betaand anaerobes lactamase inhibitor, or carbapenem or moxifloxacin
Urinary tract infections
Gram-negative rods; Enterococcus spp.
14/05/2013
Extended-spectrum beta-lactam or aztreonam, with or without an aminoglycoside; ampicillin or vancomycin if Enterococcus is present
Source Control of Infection • Adequate source control of infection is as important as appropriate antimicrobial therapy in severe sepsis. • Source control includes – removal of infected foreign bodies, • • • • • • •
urinary catheters, intravascular catheters, peritoneal dialysis cannulas, prosthetic ts, vascular grafts, and mechanical valves. JJ shunts etc
• Incision and drainage of abscesses • cutaneous abscesses, • open or per-cutaneous drainage of intra-abdominal abscesses
•
For necrotizing fasciitis, Rapid and early surgical intervention 14/05/2013
Objective of source control • Reduction bacterial/fungal density at sight – included removal of biofilms • Facilitate antibiotic entry to the areas and early recovery
• Prevent overwhelming cytokine activity
14/05/2013
Other Modalities • • • •
Fluid Resuscitation Optimizing Tissue Oxygenation Vasopressor Treatment Xigiris etc
14/05/2013
Outcomes • Although the incidence of severe sepsis is increasing, mortality rates continue to decrease. • A recent study in a sepsis cohort, age was found to be an independent risk factor for death by sepsis • mortality rates > 65y → 27.7% < 65 → 17.7% • An increasing number of older survivors of sepsis require skilled nursing facilities 14/05/2013
Prevention • Efforts to decrease the incidence of this infection of pneumonia – Vaccinate susceptible individuals against • influenza, • H. influenzae, • and S. pneumoniae.
• Additionally, asplenic patients should receive vaccination against N. meningitidis • The incidence of intravascular catheter-related blood stream infections – can be reduced by Intra venous catheter bundle and exist site chlorhexidine applications • Cases of VAP can be ↓ by maintaining ventilator patients semirecumbent at a 45-degree to prevent aspiration
14/05/2013
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