Systemic inflammatory response syndrome

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Systemic inflammatory response syndrome
Classification and external resources
Specialty Infectious disease
ICD-10 R65
ICD-9-CM 995.90

Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body, frequently a response of the immune system to infection, but not necessarily so. It is related to sepsis, a condition in which individuals meet criteria for SIRS and have a known infection.

It is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components.


SIRS is a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines.[1] SIRS is also closely related to sepsis, in which patients satisfy criteria for SIRS and have a suspected or proven infection.[2][3][4]

Adult SIRS Criteria[edit]

Manifestations of SIRS include, but are not limited to:

When two or more of these criteria are met with or without evidence of infection, patients may be diagnosed with "SIRS." Patients with SIRS and acute organ dysfunction may be termed "severe SIRS." [3][4][5][6] Note: Fever and an increased white blood cell count are features of the acute-phase reaction, while an increased heart rate is often the initial sign of hemodynamic compromise. An increased rate of breathing may be related to the increased metabolic stress due to infection and inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic cellular metabolism.

Pediatric SIRS Criteria[edit]

The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the pediatric population.[7]

In children, the SIRS criteria are modified in the following fashion:[8]

Additional Information[edit]

SIRS was first described by Dr. William R. Nelson, of the University of Toronto, in a presentation to the Nordic Micro Circulation meeting in Geilo, Norway in February 1983. There was intent to encourage a definition which dealt with the multiple (rather than a single) etiologies associated with organ dysfunction and failure following a hypotensive shock episode. The active pathways leading to such pathophysiology may include fibrin deposition, platelet aggregation, coagulopathies and leukocyte liposomal release. The implication of such a definition suggests that recognition of the activation of one such pathway is often indicative of that additional pathophysiologic processes are also active and that these pathways are synergistically destructive. The clinical condition may lead to renal failure, respiratory distress syndrome, central nervous system dysfunction and possible gastrointestinal bleeding.

Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference.[2] The conference concluded that the In septic patients, these clinical signs can also be seen in other proinflammatory conditions, such as trauma, burns, pancreatitis, etc. The Sepsis Definition Conference therefore decided to define the patients with a documented or highly suspicious infection that results in a systemic inflammatory response as having sepsis. For example, in the ICU, sepsis patients might present with organ dysfunction (severe sepsis) or septic shock (with or without multiple organ dysfunction syndrome).[9]

Note that SIRS criteria are non-specific,[9] and must be interpreted carefully within the clinical context. These criteria exist primarily for the purpose of more objectively classifying critically ill patients so that future clinical studies may be more rigorous and more easily reproducible.


The causes of SIRS are broadly classified as infectious or noninfectious. As above, when SIRS is due to an infection, it is considered sepsis. Noninfectious causes of SIRS include trauma, burns, pancreatitis, ischemia, and hemorrhage.[2][3][4]

Other causes include:[2][3][4]


Generally, the treatment for SIRS is directed towards the underlying problem or inciting cause (i.e. adequate fluid replacement for hypovolemia, IVF/NPO for pancreatitis, epinephrine/steroids/diphenhydramine for anaphylaxis).[10] Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving symptoms in clinical trials.[11][12] Other antioxidants such as vitamin E may be helpful as well.[13]

Septic treatment protocol and diagnostic tools have been created due to the potentially severe outcome septic shock. For example, the SIRS criteria were created as mentioned above to be extremely sensitive in suggesting what patients may have sepsis. However, these rules lack in specificity - not a true diagnosis of the condition, but rather a suggestion to take necessary precautions. The SIRS criteria are guidelines set in place to ensure septic patients receive care as early as possible.[14]

In cases caused by an implanted mesh, removal (explantation) of the polypropylene surgical mesh implant may be indicated.[15]


SIRS is frequently complicated by failure of one or more organs or organ systems.[2][3][4] The complications of SIRS include:


  1. ^ Parson, Melissa, Cytokine Storm in the Pediatric Oncology Patient (section "Differential Diagnoses and Workup", Journal of Pediatric Oncology Nursing, 27(5) Aug/Sep 2010, 253–258.
  2. ^ a b c d e &Na; (1992). "American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis" (PDF). Crit. Care Med. 20 (6): 864–74. doi:10.1097/00003246-199206000-00025. PMID 1597042. 
  3. ^ a b c d e Rippe, James M.; Irwin, Richard S.; Cerra, Frank B (1999). Irwin and Rippe's intensive care medicine. Philadelphia: Lippincott-Raven. ISBN 0-7817-1425-7. 
  4. ^ a b c d e Marino, Paul L. (1998). The ICU book. Baltimore: Williams & Wilkins. ISBN 0-683-05565-8. 
  5. ^ Sharma S, Steven M. Septic Shock., URL: Accessed on Nov 20, 2005.
  6. ^ Tsiotou AG, Sakorafas GH, Anagnostopoulos G, Bramis J (March 2005). "Septic shock; current pathogenetic concepts from a clinical perspective". Medical Science Monitor : International Medical Journal of Experimental and Clinical Research 11 (3): RA76–85. PMID 15735579. 
  7. ^ Brahm Goldstein et al., International pediatric sepsis consensus, Pediatric Critical Care Medicine 2005 Vol. 6, No. 1
  8. ^ Goldstein B, Giroir B, Randolph A (2005). "International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics". Pediatric Critical Care Medicine 6 (1): 2–8. doi:10.1097/01.PCC.0000149131.72248.E6. PMID 15636651. 
  9. ^ a b Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G (Apr 2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit Care Med 31 (4): 1250–1256. doi:10.1097/01.CCM.0000050454.01978.3B. PMID 12682500. 
  10. ^ "Systemic Inflammatory Response Syndrome Treatment & Management". Mescape. 
  11. ^ Berger MM, Chioléro RL (September 2007). "Antioxidant supplementation in sepsis and systemic inflammatory response syndrome". Critical Care Medicine 35 (9 Suppl): S584–90. doi:10.1097/01.CCM.0000279189.81529.C4. PMID 17713413. 
  12. ^ Rinaldi, S; Landucci, F; De Gaudio, AR (September 2009). "Antioxidant therapy in critically septic patients". Current drug targets 10 (9): 872–80. doi:10.2174/138945009789108774. PMID 19799541. 
  13. ^ Bulger EM, Maier RV (February 2003). "An argument for Vitamin E supplementation in the management of systemic inflammatory response syndrome". Shock 19 (2): 99–103. doi:10.1097/00024382-200302000-00001. PMID 12578114. 
  14. ^ Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, Schein RM, Sibbald WJ. (1992). "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine.". Chest 101 (6): 1644–55. doi:10.1378/chest.101.6.1644. PMID 1303622. 
  15. ^ Voyles, CR; Richardson, JD; Bland, KI; Tobin, GR; Flint, LM; Polk Jr, HC (1981). "Emergency abdominal wall reconstruction with polypropylene mesh: short-term benefits versus long-term complications". Annals of Surgery 194 (2): 219–223. doi:10.1097/00000658-198108000-00017. PMC 1345243. PMID 6455099. 

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