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Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
Sepsis and septic shock
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Sepsis and septic shock

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

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