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Sepsis/Septic shock

Sepsis/Septic shock. Introduction. When bacteria is not effectively cleared by host defenses, a systemic inflammatory response is activated →sepsis. I ntroduction.

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Sepsis/Septic shock

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  1. Sepsis/Septic shock

  2. Introduction • When bacteria is not effectively cleared by host defenses, a systemic inflammatory response is activated →sepsis

  3. Introduction SIRS(systemic inflammatory response system)- cardinal signs are fever or hyothermia, leukocytosisor leukopenia, tachypnea,and tachycardia • If SIRS is accompanied by an infections it is termed SEPSIS Severe sepsis- when sepsis is associated with dysfunction of organs distant from the sight of infection Septic shock- when hypotension cannot be corrected by infusing fluids Harrisons 17th ed.

  4. Etiology • Sepsis may developed as a complication of localized community-aquired infections or may follow colonization and local mucous invasion by virulent pathogens • Children 3mos-3years of age are at risk for occult bactermia, which occasionally progresses to sepsis

  5. Pathogenesis • SIRS related to sepsis results from tissue damage following the host response to bacterial products • When bacterial cell wall components are released onto the bloodstream, cytokines are activated, and these in turn can lead to further physiologic derangements

  6. Pathogenesis Alone or in combination, bacterial products and proinflammatory cytokines trigger physiologic responses to inhibit microbial invaders: • Activation of the complement system • Activation of Hageman factor (factor XII), which then initiates the coagulation cascade • Aderenocorticotropic hormones and B-endorphin release • Stimulation of polymorphonuclearneutrophils • Stimulation of the kallikrein-kinin system

  7. Pahogenesis • TNF and other inflammatory mediators increase vascular permeability, producing diffuse capillary leakage, reduced vascular tone, and at microcirculatory level an imbalance between perfusion and increased tissue metabolic needs Shock- is a disruption in circulatory function leading to poor perfusion and inadequate delivery of oxygen and other nutrients to tissues

  8. Pathogensis • Shock is not diagnosed by a decrease in blood pressure because compensatory mechanisms work to maintain the BP(↑HR and peripheral vasoconstriction) • Hypotension→ compensatory mechanisms are failing→ cardiorespiratory arrest

  9. Pathogensis Early phase of sepsis: • ↓systemic vascular resistance • ↓preload → tachycardia, widened pulse pressure, ↑CO • Patients are usually warm and have rebounding pulses w/ brisk capillary refill

  10. Pathogenesis Late phases of septic shock: • Cool extremities • Poor peripheral pulses • ↓BP (myocardial dysfunction) • ↓CO • As tissue O2 consumption exceeds O2 delivery, the tissue hypoxia leads to lactic acidosis

  11. Clinical manifestations • Fever • Shaking chills • Hyperventilation • Tachycardia • Hypothermia • Cutaneous lesions • Changes in mental status (confusion, agitation, anxiety, excitation, lethargy, obtundation, or coma)

  12. Diagnosis • Microbial confirmation if an infectious agent: blood culture, gram stain • a CBC, platelet count, PT and aPTT, fibrinogne level and D-dimer, arterial blood gas, renal and hepatic profiles, and ionized calcium should me obtained

  13. Lab findings • Metabolic acidosis • Thrombocytopenia • Prolonged PT and aPTT • Elevated fibrin split products • Anemia • Decrease PaO2 and increasePaCO2 • Alteration in morphology and # of neutrophils Neutropeniasign of overwhelming sepsis

  14. Treatment • Broad-spectrum bactericidal synergistic antimicrobial agents should be given to a patient in septic shock For community acquired and nosocomial sepsis: 3rd generations cephalosporins (ceftriaxone, cefotaxime) For fungal infections: amphotericin B

  15. Prevention • Immunization with conjugate H. influenzae and S. pneumoniaevaccine is recommended for all infants

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