sepsis septic shock n.
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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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introduction
Introduction
  • When bacteria is not effectively cleared by host defenses, a systemic inflammatory response is activated →sepsis
slide3

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.

e tiology
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
p athogenesis
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
pathogenesis
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
pahogenesis
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

pathogensis
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
pathogensis1
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
pathogenesis1
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
clinical manifestations
Clinical manifestations
  • Fever
  • Shaking chills
  • Hyperventilation
  • Tachycardia
  • Hypothermia
  • Cutaneous lesions
  • Changes in mental status (confusion, agitation, anxiety, excitation, lethargy, obtundation, or coma)
diagnosis
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
lab findings
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

treatment
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

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