Sepsis is a life-threatening condition that is characterized by an inflammatory response caused by an infection. Identifying and treating sepsis early is key to saving lives. Following are the sepsis definitions and treatment guidelines to help frame your approach to critically ill patients who have a suspected or confirmed diagnosis of sepsis.

An international pediatric sepsis consensus conference published a definition for pediatric systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, septic shock and organ dysfunction in 2005.¹

Definitions in Table 29-1.¹

Examples of organ dysfunction¹:

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  Cardiovascular: Despite 40 cc/kg intravenous fluid given over 1 hour, patient has either hypotension, need for vasoactive infusion to maintain blood pressure, or evidence of decreased perfusion (ex: capillary refill >5 seconds, arterial lactate greater than two times normal)

  
  
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  Respiratory: Need for invasive or noninvasive positive pressure support, PaO₂:FiO₂ <300, requirement of >50% FiO₂ to maintain saturations ≥92%, or PaCO₂ >65 torr

  
  
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  Renal: Serum creatinine more than two times upper limit of normal for age or twofold increase in baseline creatinine

  
  
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  Hepatic: Total bilirubin ≥4 mg/dL (except newborns), ALT two times upper limit of normal

  
  
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  Neurologic: Glasgow Coma Score ≤11 or acute change in mental status

  
  
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  Hematologic: Platelet count <80,000/mm³ or 50% drop in platelet count from highest value in previous 3 days (for chronic hematology/oncology patients) or INR >2

The host response to infection triggers both an inflammatory and compensatory anti-inflammatory response (CARS) mediated by the immune system. The balance between these two determines the extent of organ injury and patient recovery.

The innate immune response is nonspecific and triggered by the body’s recognition of antigen resulting in an effector response. Components of the innate immune system include physical barriers like skin and phagycytic cells, such as macrophages, that recognize pathogens.

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  Pattern-recognition receptors (PRRs) are molecules in the host that recognize pathogen-associated molecular patterns (PAMPs) on pathogens.²

  
  
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  Specific types of PRR called toll-like receptors (TLRs) recognize several types of PAMPs implicated in sepsis. For example:

  
  
  
  
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    TLR4 recognizes lipopolysaacharide present on gram-negative bacteria

    
    
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    TLR2 recognizes lipotechoic acid on gram-positive bacteria

  
  

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  Once PRR recognizes PAMP, activation of signal transduction pathways occurs, leading to downstream production of inflammatory cytokines (such as IL-1β and TNF-α) and other mediators such as nitric oxide.

The adaptive immune response involves a specific response to a pathogen and T- and B- cell proliferation with antibody response, as well as enhanced immunity (memory) upon re-exposure to that antigen.

For additional information see chapter 73.