Systemic Inflammatory Response Syndrome = SIRS

Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body, frequently a response of the immune system to infection.

The concept of SIRS was first conceived of and presented by Dr. William R. Nelson, of the Department of Surgery of the University of Toronto at the Nordic Micro Circulation meeting in 1983. The presentation followed a decade of research with colleagues including; Dr. J Vaage of the University of Oslo, Norway, Dr. D. Bigger, the Hospital for Sick Children, Toronto, Dr.D.Sepro of Boston University, and Dr. H Movat of the Department of Pathology at the University of Toronto. The laboratory experience was borne out in the clinical setting with Canada's first trauma unit for which Nelson was a co-founder. This allowed in the mid 1980's, the concepts of SIRS to be taught by Dr. Miles Johnson of the university of Toronto, Department of Pathology at the undergraduate dental school, as well as to residents in the Department of Surgery of the University of Toronto who rotated through the Regional Trauma Unit at Sunnybrook Medical Center. SIRS was more broadly adopted in 1991 at the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference with the goal of aiding in the early detection of sepsis.[1] In 2016 SIRS was completely eliminated from the definition of sepsis.[2] Many experts considered SIRS to be overly sensitive, as nearly all (>90%) of patients admitted to the ICU met the SIRS criteria.[3]

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.

Definition  

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.[5] SIRS is also closely related to sepsis, in which patients satisfy criteria for SIRS and have a suspected or proven infection.[4][6][7]

Adult SIRS Criteria[edit]

Manifestations of SIRS include, but are not limited to:

Body temperature less than 36 °C (96.8 °F) or greater than 38 °C (100.4 °F)

Heart rate greater than 90 beats per minute

Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial pressure of carbon dioxide less than 4.3 kPa (32 mmHg)

White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms). Band forms greater than 3% is called bandemia or a "left-shift."

Hyperglycemia (blood glucose >6.66 mmol/L [120 mg/dL]) in absence of diabetes mellitus

Altered mental state

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." [6][7][8][9] 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 

The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the pediatric population.[10]

In children, the SIRS criteria are modified in the following fashion:[11]

Heart rate is greater than 2 standard deviations above normal for age in the absence of stimuli such as pain and drug administration, or unexplained persistent elevation for greater than 30 minutes to 4 hours. In infants, also includes heart rate less than 10th percentile for age in the absence of vagal stimuli, beta-blockers, or congenital heart disease or unexplained persistent depression for greater than 30 minutes.

Body temperature obtained orally, rectally, from Foley catheter probe, or from central venous catheter probe less than 36 °C or greater than 38.5 °C. Temperature must be abnormal to qualify as SIRS in pediatric patients.

Respiratory rate greater than 2 standard deviations above normal for age or the requirement for mechanical ventilation not related to neuromuscular disease or the administration of anesthesia.

White blood cell count elevated or depressed for age not related to chemotherapy, or greater than 10% bands plus other immature forms.

Additional Information 

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.[4] The conference concluded that the manifestations of SIRS include, but are not limited to the first four described above under adult SIRS critera.

In septic patients, these clinical signs can also be seen in other proinflammatory conditions, such as trauma, burns, pancreatitis, etc. A follow-up conference therefore decided to define the patients with a documented or highly suspicious infection that results in a systemic inflammatory response as having sepsis.[12]

Note that SIRS criteria are non-specific,[12] 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.

Causes 

The causes of SIRS are broadly classified as infectious or noninfectious. Causes of SIRS include:

trauma

burns

pancreatitis

ischemia

hemorrhage

Other causes include:[4][6][7]

Complications of surgery

Adrenal insufficiency

Pulmonary embolism

Complicated aortic aneurysm

Cardiac tamponade

Anaphylaxis

Drug overdose

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).[13] Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving symptoms in clinical trials.[14][15] Other antioxidants such as vitamin E may be helpful as well.[16]

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 which patients may have sepsis. However, these rules lack specificity, i.e. 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.[17]

In cases caused by an implanted mesh, removal (explantation) of the polypropylene surgical mesh implant may be indicated.[18]

Complications 

SIRS is frequently complicated by failure of one or more organs or organ systems.[4][6][7] The complications of SIRS include:

Acute lung injury

Acute kidney injury

Shock

Multiple organ dysfunction syndrome

References 

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Jump up ^ Shankar-Hari, Manu, Gary S. Phillips, Mitchell L. Levy, Christopher W. Seymour, Vincent X. Liu, Clifford S. Deutschman, Derek C. Angus, Gordon D. Rubenfeld, and Mervyn Singer. "Developing a New Definition and Assessing New Clinical Criteria for Septic Shock." Jama 315.8 (2016): 775. Web.

Jump up ^ Lord, Janet M., Mark J. Midwinter, Yen-Fu Chen, Antonio Belli, Karim Brohi, Elizabeth J. Kovacs, Leo Koenderman, Paul Kubes, and Richard J. Lilford. "The Systemic Immune Response to Trauma: An Overview of Pathophysiology and Treatment." The Lancet 384.9952 (2014): 1455-465. Web.

^ Jump up to: a b c d e "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). Critical Care Medicine. 20 (6): 864–74. 1992. doi:10.1097/00003246-199206000-00025. PMID 1597042.

Jump up ^ Parson, Melissa, Cytokine Storm in the Pediatric Oncology Patient (section "Differential Diagnoses and Workup", Journal of Peddanana is a good idea and is not the same tric Oncology Nursing, 27(5) Aug/Sep 2010, 253–258.

^ Jump up to: a b c d 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.

^ Jump up to: a b c d Marino, Paul L. (1998). The ICU book. Baltimore: Williams & Wilkins. ISBN 0-683-05565-8.

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Jump up ^ 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.

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^ Jump up to: 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.

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Jump up ^ 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.

Jump up ^ 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.

Jump up ^ 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.

Jump up ^ 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.

Jump up ^ 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 1345243Freely accessible. PMID 6455099.