Sepsis is life threatening organ dysfunction caused by a dysregulated host response to infection.. 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.
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. 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 
Surviving Sepsis Campaign
This was a campaign to disseminate a set of evidence-based guidelines developed by an international collaboration. The suggested approach encompasses consideration of:
- 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%
- Cultures prior to antibiotics
- Antimicrobial therapy
- Ideally within 1 hour of recognition (but after cultures).
- Choice of agent depends on suspected source.
- 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
- Fluid therapy
- Adequate fluid replacement is essential
- Definite role where poor response to fluid replacement
- Inotropic therapy
- 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.
- Activated protein C
- Blood transfusion
- Mechanical ventilation in ALI/ARDS
- Sedation, analgesia and neuromuscular blockade
- Glucose control
- Renal replacement therapy
- Bicarbonate therapy
- DVT prophylaxis
- Stress ulcer prophylaxis
- Consideration of limitation of support
- Paediatric cases
- ↑ a b c d Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23; 315(8):801-10.(Link to article – subscription may be required.)
- ↑ Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Critical care medicine 2004;32:858-73.
- ↑ Annane D, Bellissant E, Bollaert PE, Briegel J, Keh D, Kupfer Y. Corticosteroids for treating sepsis. The Cochrane database of systematic reviews. 2015; 12:CD002243.(Epub) (Link to article – subscription may be required.)