From Ganfyd

Jump to: navigation, search

Sepsis is life threatening organ dysfunction caused by a dysregulated host response to infection.[1]. It is a continuum of disease resulting from the systemic inflammatory response to an infection. It has several clinical features and is often characterised by certain physiological derangements, though no single feature is defining.



LogoKeyPointsBox.pngAdult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following clinical criteria (quickSOFA, qSOFA)[1]:
  1. Respiratory rate of 22/min or greater
  2. Altered mentation
  3. Systolic blood pressure of 100 mm Hg or less

Sepsis can be thought of as systemic inflammatory response syndrome in response to infection although this term (SIRS) should no longer be used as a research definition given that it is included in the new medical definition of sepsis[1]. Similarly the concept of "Severe Sepsis" is no longer in research. Many of these physiological derangements result not from the infectious agent itself, but from the body's response to it. The inflammatory response invoked by the presence of infection or inflammation is normally a physiological adaptive process designed to create conditions to allow the body deal with the sequelae of infection or inflammation. However, an inappropriately or excessively activated inflammatory response is damaging.


Viable bacteria present in the blood; may be transient.
Blood poisoning 
Layman equivalent of septicaemia.
Use of this term is no longer recommended. Taken to mean bacteraemia with sepsis.
Septic shock 
sepsis where vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L in the absence of hypovolemia [1]

Surviving Sepsis Campaign

This was a campaign to disseminate a set of evidence-based guidelines developed by an international collaboration.[2] The suggested approach encompasses consideration of:

  1. Initial resuscitation
    • Early goal-directed therapy, i.e. aim for CVP 8-12mmHg, MAP >65mmHg, urine output >0.5ml/kg/hour, central venous or mixed venous oxygen saturation >70%
  2. Diagnosis
    • Cultures prior to antibiotics
  3. Antimicrobial therapy
    • Ideally within 1 hour of recognition (but after cultures).
    • Choice of agent depends on suspected source.
  4. Source control
    • Identify source and, if treat promptly if amenable to definitive control (e.g. drainage of abscess).

The remainder of the guidelines considers evidence on

  1. Fluid therapy
    • Adequate fluid replacement is essential
  2. Vasopressors
    • Definite role where poor response to fluid replacement
  3. Inotropic therapy
  4. Steroid
    • While 2012 guidelines only recommend corticosteroids as an add-on therapy for people whose circulation has not been restored by adequate fluid replacement and vasopressors a 2015 Cochrane review found that with the addition of further studies treatment with low dose corticosteroids (< 400 mg hydrocortisone equivilent/day) given over three or more days reduces the death rate from blood poisoning by 13% (0-24% 95% CI), saving about 43 lives per 1000. Blood glucose and sodium levels tended to increase[3].
  5. Activated protein C
  6. Blood transfusion
  7. Mechanical ventilation in ALI/ARDS
  8. Sedation, analgesia and neuromuscular blockade
  9. Glucose control
  10. Renal replacement therapy
  11. Bicarbonate therapy
  12. DVT prophylaxis
  13. Stress ulcer prophylaxis
  14. Consideration of limitation of support
  15. Paediatric cases