Sepsis and septic shock


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  • Sepsis and septic shock

    1. 1. Sepsis and Septic Shock Akram M Fayed, MD, ABIM Lecturer, Department of Critical Care Medicine Faculty of Medicine University of Alexandria Pharmacotherapy 2008. S. LENA KANG-BIRKEN AND JOSEPH T. DIPIRO
    2. 2. Prevalence and Incidence <ul><li>Sepsis represents a significant burden to the national health care </li></ul><ul><li>system </li></ul><ul><li>In 2000, sepsis affected approximately 660,000 people, an </li></ul><ul><li>increase of 8.7 % per year since 1979 </li></ul><ul><li>More than one-half of the patients were admitted to the ICU with a </li></ul><ul><li>mean length of stay of 15.7 days </li></ul>
    3. 3. Prevalence and Incidence <ul><li>The total number of deaths increased from 21.9 per 100,000 </li></ul><ul><li>population in 1979 to 43.9 per 100,000 populations in 2000 </li></ul><ul><li>With the annual cost of approximately $16.7 billion, there remains a </li></ul><ul><li>vital need for clinicians to comprehend the pathophysiology and to </li></ul><ul><li>appreciate the management options available for acutely ill patients </li></ul><ul><li>with sepsis or septic shock </li></ul>
    4. 4. Definition <ul><li>The criteria for the new terms provide specific physiologic variables </li></ul><ul><li>that can be used to categorize a patient as having: </li></ul><ul><li>Bacteremia, </li></ul><ul><li>Systemic inflammatory response syndrome (SIRS), </li></ul><ul><li>sepsis, </li></ul><ul><li>severe sepsis, </li></ul><ul><li>septic shock, or </li></ul><ul><li>multiple-organ dysfunction syndrome (MODS), </li></ul><ul><li>Suggesting an important continuum of progressive physiologic decline </li></ul>
    5. 5. Definition
    6. 6. Definition <ul><li>Introduction of the term SIRS reflects the knowledge that a </li></ul><ul><li>physiologically similar systemic inflammatory response can be seen </li></ul><ul><li>even in the absence of identifiable infection </li></ul><ul><li>Severe sepsis refers to patients with an acute organ dysfunction such </li></ul><ul><li>as acute renal failure or respiratory failure </li></ul><ul><li>These patients have a mortality rate of approximately 40% </li></ul>
    7. 7. Definition <ul><li>Septic shock refers to sepsis patients with arterial hypotension that </li></ul><ul><li>is refractory to adequate fluid resuscitation, thus requiring vasopressor </li></ul><ul><li>administration </li></ul><ul><li>These patients usually require intensive care and ultimately die in </li></ul><ul><li>50% to 80% of cases </li></ul><ul><li>It is important to note that progression from sepsis to MODS can </li></ul><ul><li>occur in the absence of an intervening period of septic shock </li></ul>
    8. 8. Definition
    9. 9. INFECTION SITES AND PATHOGENS <ul><li>The leading primary sites of microbiologically documented infections </li></ul><ul><li>that led to sepsis were: </li></ul><ul><li>The respiratory tract (21%–68%), </li></ul><ul><li>Intraabdominal space (14%–22%), and </li></ul><ul><li>Urinary tract (14%–18%) </li></ul><ul><li>Although almost any microorganism can be associated with sepsis </li></ul><ul><li>and septic shock, the most common etiologic pathogens are: </li></ul><ul><li>- Gram-positive bacteria (40% of patients), followed by </li></ul><ul><li>- Gram-negative bacteria (38%) and </li></ul><ul><li>- Fungi (17%) </li></ul><ul><li>Certain viruses and rickettsiae can produce a similar syndrome </li></ul>
    10. 10. GRAM-POSITIVE BACTERIAL SEPSIS <ul><li>Since 1987, gram-positive organisms are the predominant </li></ul><ul><li>Pathogens in sepsis and septic shock, accounting for approximately </li></ul><ul><li>40% to 50% of all cases </li></ul><ul><li>They are commonly caused by: </li></ul><ul><li>Staphylococcus aureus, </li></ul><ul><li>Streptococcus pneumoniae, </li></ul><ul><li>Coagulase-negative staphylococci,and </li></ul><ul><li>Enterococcus species . </li></ul><ul><li>Streptococcus pyogenes and viridans streptococci are less </li></ul><ul><li>commonly involved </li></ul>
    11. 11. GRAM-NEGATIVE BACTERIAL SEPSIS <ul><li>A greater proportion of patients with gram-negative bacteremia </li></ul><ul><li>develop clinical sepsis, and gram-negative bacteria are also more </li></ul><ul><li>likely to produce septic shock in comparison to gram-positive </li></ul><ul><li>organisms, 50% versus 25%, respectively </li></ul><ul><li>Gram-negative sepsis also results in a higher mortality rate </li></ul><ul><li>compared with sepsis from any other groups of organisms </li></ul><ul><li>The major factor associated with the outcome of gram-negative </li></ul><ul><li>sepsis appears to be the severity of any underlying condition </li></ul>
    12. 12. GRAM-NEGATIVE BACTERIAL SEPSIS <ul><li>Patients with rapidly fatal conditions, such as acute leukemia, </li></ul><ul><li>aplastic anemia, and >70% of the body’s surface burn injury, have a </li></ul><ul><li>significantly worse prognosis than do those patients with nonfatal </li></ul><ul><li>underlying conditions, such as diabetes mellitus or chronic renal </li></ul><ul><li>Insufficiency </li></ul><ul><li>Escherichia coli and Pseudomonas aeruginosa are the most </li></ul><ul><li>Commonly isolated gram-negative microorganisms in sepsis </li></ul>
    13. 13. GRAM-NEGATIVE BACTERIAL SEPSIS <ul><li>Other common gram-negative pathogens include: </li></ul><ul><li>- Klebsiella species, </li></ul><ul><li>- Serratia species, </li></ul><ul><li>- Enterobacter species, and </li></ul><ul><li>- Proteus species </li></ul><ul><li>P. aeruginosa, although not considered a predominant endogenous </li></ul><ul><li>flora, is found widely in the environment and is the most frequent cause </li></ul><ul><li>of sepsis fatality </li></ul>
    14. 14. ANAEROBIC AND MISCELLANEOUS BACTERIAL SEPSIS <ul><li>Anaerobes are usually considered low-risk organisms for the </li></ul><ul><li>development of sepsis </li></ul><ul><li>If present, anaerobes are often found together with other pathogenic </li></ul><ul><li>bacteria that are commonly found in sepsis </li></ul><ul><li>Epidemiology reports suggested that polymicrobial infections </li></ul><ul><li>accounted for 5% to 39% of sepsis </li></ul>
    15. 15. ANAEROBIC AND MISCELLANEOUS BACTERIAL SEPSIS <ul><li>Mortality rates associated with polymicrobial infections are similar </li></ul><ul><li>to sepsis caused by a single organism </li></ul><ul><li>Although some clinicians believe the particular combination of </li></ul><ul><li>organisms present in polymicrobial sepsis can provide clues to the </li></ul><ul><li>source of infection, no clear source for the infection can be identified </li></ul><ul><li>in up to 25% of cases </li></ul>
    16. 16. FUNGAL SEPSIS <ul><li>The rate of fungal infections increased more than 200% from </li></ul><ul><li>1979 to 2000 </li></ul><ul><li>Candida species are common causes of fungal sepsis </li></ul><ul><li>in hospitalized patients </li></ul><ul><li>Although Candida albicans remains the most dominant species, </li></ul><ul><li>non- albicans Candida species, particularly Candida glabrata, Candida </li></ul><ul><li>parapsilosis, Candida tropicalis , and Candida krusei , have gradually </li></ul><ul><li>emerged from 24% in the 1980s to 46% during 1997 to 2000 </li></ul>
    18. 18. PRO- AND ANTIINFLAMMATORY MEDIATORS The balance between pro- and antiinflammatory mediators (CARS, compensatory antiinflammatory response syndrome; IL, interleukin; IL-1RA, interleukin-1 receptor antagonist; SIRS, systemic inflammatory response syndrome; TNF-α , tumor necrosis factor-α.)
    19. 19. PRO- AND ANTIINFLAMMATORY MEDIATORS Cascades of sepsis
    22. 22. PROGNOSIS <ul><li>As the patient progresses from SIRS to sepsis to severe sepsis to </li></ul><ul><li>septic shock, mortality increases in a stepwise fashion </li></ul><ul><li>Mortality rates are higher for patients with advanced age, preexisting </li></ul><ul><li>disease including chronic obstructive pulmonary disease, neoplasm, </li></ul><ul><li>and human immunodeficiency virus (HIV) disease, ICU care, more organ </li></ul><ul><li>failure, positive blood cultures, and Pseudomonas species infection </li></ul><ul><li>Mortality increased with age from 10% in children to 38.4% in those </li></ul><ul><li>≥ 85 years </li></ul>
    23. 23. PROGNOSIS <ul><li>ICU admission was required in 51.1% of the patients with severe </li></ul><ul><li>sepsis and of those patients, mortality was reported in 34.1% </li></ul><ul><li>Mortality from severe sepsis and MODS is most closely related to the </li></ul><ul><li>number of dysfunctioning organs </li></ul><ul><li>As the number of failing organs increased from two to five, mortality </li></ul><ul><li>increased from 54% to 100% </li></ul><ul><li>Duration of organ dysfunction can also affect the overall mortality rate </li></ul>
    24. 24. PROGNOSIS
    25. 25. PROGNOSIS <ul><li>An elevated lactate concentration of >4 mmol/L in the presence </li></ul><ul><li>of the SIRS significantly increases intensive care unit admission </li></ul><ul><li>rates, and persistent elevations in lactate for more than 24 hours </li></ul><ul><li>are associated with a mortality rate as high as 89% </li></ul><ul><li>Inversely, patients with higher lactate clearance after 6 hours of </li></ul><ul><li>Emergency Department intervention have improved outcome compared </li></ul><ul><li>with those lower lactate clearance </li></ul><ul><li>There was an approximately 11% decrease likelihood of mortality for </li></ul><ul><li>each 10% increase in lactate clearance </li></ul>
    26. 26. TREATMENT
    27. 27. TREATMENT
    28. 28. EARLY GOAL-DIRECTED THERAPY <ul><li>Initial resuscitation of a patient in severe sepsis or sepsis-induced </li></ul><ul><li>tissue hypoperfusion should begin as soon as the syndrome is </li></ul><ul><li>recognized </li></ul><ul><li>A randomized, controlled trial evaluated the timing of the goal- </li></ul><ul><li>directed therapy involving adjustments of cardiac preload, afterload, </li></ul><ul><li>and contractility to balance oxygen delivery with demand </li></ul><ul><li>prior to admission to the ICU </li></ul>
    29. 29. EARLY GOAL-DIRECTED THERAPY <ul><li>The goals during the first 6 hours included: </li></ul><ul><li>Central venous pressure of 8 to 12 mm Hg, </li></ul><ul><li>Mean arterial pressure of ≥65 mm Hg, </li></ul><ul><li>Urine output of ≥0.5 mL/kg/h, and </li></ul><ul><li>A central venous or mixed venous oxygen saturation of ≥70% </li></ul><ul><li>During the first 6 hours of resuscitation, the early goal-directed therapy </li></ul><ul><li>group had a central venous catheter placed and received more fluid </li></ul><ul><li>than with traditional therapy (5 versus 3.5 L), dobutamine therapy to </li></ul><ul><li>a maximum of 20 mcg/kg/min, and red blood cell transfusions </li></ul>
    30. 30. EARLY GOAL-DIRECTED THERAPY <ul><li>The 28-day mortality rate was 30% in the early goal-directed therapy </li></ul><ul><li>group, in comparison to 46.5% in the traditional therapy group </li></ul><ul><li>consisting of fluid resuscitation, followed by vasopressor therapy if </li></ul><ul><li>required </li></ul><ul><li>Increased oxygen delivery from the red blood cell transfusions </li></ul><ul><li>to achieve a hematocrit of ≥30% in the early goal-directed therapy </li></ul><ul><li>group appeared to be the primary difference between the two groups </li></ul>
    31. 31. EARLY GOAL-DIRECTED THERAPY <ul><li>One institution evaluated the impact of 6-hour sepsis care bundle </li></ul><ul><li>and found the compliance rate to be 52% </li></ul><ul><li>The noncompliant group had a more than twofold increase in hospital </li></ul><ul><li>mortality in comparison to the compliant group (49% vs. 23%) </li></ul>
    32. 32. Thank You