Systemic inflammatory response syndrome

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Systemic inflammatory response syndrome
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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 both meet criteria for SIRS and have a known or highly suspected infection.

Classification

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]

Definition

Systemic inflammatory response syndrome[5]
Finding Value
Temperature <36 °C (96.8 °F) or >38 °C (100.4 °F)
Heart rate >90/min
Respiratory rate >20/min or PaCO2<32 mmHg (4.3 kPa)
WBC <4x109/L (<4000/mm3), >12x109/L (>12,000/mm3), or ≥10% bands

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 manifestations of SIRS include, but are not limited to:


SIRS can be diagnosed when two or more of these criteria are present.[3][4][6][7]

The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the pediatric population.[8]

Fever and leukocytosis are features of the acute-phase reaction, while tachycardia is often the initial sign of hemodynamic compromise. Tachypnea 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.

In children, the SIRS criteria are modified in the following fashion:[9]

Note that SIRS criteria are very non-specific,[10] 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.

As an alternative, when two or more of the systemic inflammatory response syndrome criteria are met without evidence of infection, patients may be diagnosed simply with "SIRS." Patients with SIRS and acute organ dysfunction may be termed "severe SIRS."

Causes

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]

Treatment

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).[1] 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]

Complications

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

References

  1. ^ Parsons, 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.{{cite journal}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  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.{{cite book}}: CS1 maint: multiple names: authors list (link)
  4. ^ a b c d e Marino, Paul L. (1998). The ICU book. Baltimore: Williams & Wilkins. ISBN 0-683-05565-8.
  5. ^ Bone RC, Balk RA, et al. (The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine) (June 1992). "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis". Chest. 101 (6): 1644–55. doi:10.1378/chest.101.6.1644. PMID 1303622.
  6. ^ Sharma S, Steven M. Septic Shock. eMedicine.com, URL: http://www.emedicine.com/MED/topic2101.htm Accessed on Nov 20, 2005.
  7. ^ Tsiotou AG, Sakorafas GH, Anagnostopoulos G, Bramis J (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Brahm Goldstein et al., International pediatric sepsis consensus, Pediatr Crit Care Med 2005 Vol. 6, No. 1
  9. ^ Goldstein B, Giroir B, Randolph A (2005). "International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics". Pediatr Crit Care Med. 6 (1): 2–8. doi:10.1097/01.PCC.0000149131.72248.E6. PMID 15636651.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Berger MM, Chioléro RL (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. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Rinaldi, S (2009 Sep). "Antioxidant therapy in critically septic patients". Current drug targets. 10 (9): 872–80. doi:10.2174/138945009789108774. PMID 19799541. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  13. ^ Bulger EM, Maier RV (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. {{cite journal}}: Unknown parameter |month= ignored (help)