Post on 24-Feb-2016
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Sepsis/Septic shock
Introduction
• When bacteria is not effectively cleared by host defenses, a systemic inflammatory response is activated →sepsis
SIRS(systemic inflammatory response system)- cardinal signs are fever or hyothermia, leukocytosis or 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
Introduction
Harrisons 17th ed.
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
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
Alone or in combination, bacterial products and proinflammatory cytokines trigger physiologic responses to inhibit microbial invaders:
1. Activation of the complement system2. Activation of Hageman factor (factor XII), which then
initiates the coagulation cascade3. Aderenocorticotropic hormones and B-endorphin
release4. Stimulation of polymorphonuclear neutrophils5. Stimulation of the kallikrein-kinin system
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
• 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
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
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
• Fever• Shaking chills• Hyperventilation• Tachycardia• Hypothermia• Cutaneous lesions• Changes in mental status (confusion, agitation,
anxiety, excitation, lethargy, obtundation, or coma)
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
• Metabolic acidosis• Thrombocytopenia • Prolonged PT and aPTT• Elevated fibrin split products• Anemia• Decrease PaO2 and increasePaCO2• Alteration in morphology and # of neutrophilsNeutropenia sign of overwhelming sepsis
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
• Immunization with conjugate H. influenzae and S. pneumoniae vaccine is recommended for all infants