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Nama : Deded Yudha Pranatha NPM : 1106026091

Systemic Inflammatory Response Syndrome (SIRS) Definitions Systemic Inflammation Response Syndrome is systemic level of acute inflammation, that may or may not be due to infection, and is generally manifested as a combination of vital sign abnormalities including fever, hypothermia, tachycardia, and tachypnea1. SIRS can be caused by a variety of disease processes including pancreatitis, poly-trauma, malignancy, transfusion reaction, and infection. SIRS that caused by infection is termed as sepsis and is mediated with production of cascade of pro-inflammatory mediators products in response to microbiological products exposure. Patients have developed sepsis if they have met clinical criteria for SIRS with evidence of a local or systemic source of infection1. Criteria of SIRS : requires 2 of the following 4 features to be present :2 1. Temp > 38,3 degree or < 36 degree 2. Tachypnea (RR > 20 or MV > 10 L) 3. Tachycardia ( HR> 90 x/minute, in the abscense of intrinsic heart disease) 4. WBC > 12,000/mm or < 4,000/mm Criteria for severe SIRS : must meet criteria for SIRS, plus 1 of the following :2 1. Altered mental status 2. SBP < 90 mmHg or fall of > 40 mmHg from baseline 3. Impaired gas exchange (PaO2/FiO2 ratio < 200-250) 4. Metabolic acidosis (pH < 7.30 and lactate > 1.5 x upper limit of normal)

5. Oliguria ( < 0,5 mL/kg/hr) or renal failure 6. Hyperbilirubinemia 7. Coagulopathy (platelets < 80,000 100,000/mm, INR > 2.0, PTT > 1.5 x control, or elevated fibrin degradation products) Risk factors for SIRS :3 1. Extreme of age 2. Indwelling lines/catheters 3. Immunocompromised states 4. Malnutrition 5. Alcoholism 6. Malignancy 7. Diabetes 8. Cirrhosis 9. Male Sex 10. Genetic : predisposition Pathophysiology Although inflammation is essential to host response against infection, SIRS result from a dysregulation of the normal response, with massive, uncontrolled release of pro inflammatory mediators. Trigger maybe endotoxin, TSST-1, GBS toxin , early mediators like TNF and IL-1 and Late mediators are IL-1, IL-6, IL-8, TNF, proteases o2 radicals, and prostaglandins3. 1. Insult : hypoxic reperfusion damage, infection (endotoxin, other microbial toxins or microorganisms), primary mediators (histamin, anaphylatoxins/C3a,C5a/), complexes antigen-antibody, thrombin a plasmin.

2. Defensive Reactions : first detected signs of defense after insult are local and generalized hemodynamic changes (vasodilation, vasoconstriction). 3. Regulation of Hemodynamic Changes : systemic symphatic-adrenal activation (changes in organ blood distribution of minute volume), local microcirculatory changes mediators produced by endothelial cells and other inflammatory systems (NO,PGI2, x endothelin-1,thromboxan A2). 4. Endothelial cells reaction : result of endothelial stimulation process thrombogenic vascular intima with increased permeability. 5. Activation of other inflammation components ; if insult persist, activation of endothelial cells, platelets, neutrophils, plasmatic hemocoagulation system, and complement. 6. Tissue damage : the degree of revesibility of secondary MODS is influenced by necrotic tissue damage, changes of vessel wall caused by proinflammatory cytokines, during chronic process proliferation of less valuable cells (fibroblast), apoptosis (induced during SIRS).4 Treatment 1. Fluid Resuscitation 2. Vasopressors 3. Antibiotics 4. Eradication of infection 5. Ventilatory support, activated protein C, steroids, glycemic control, nutrition4

References

1. Burdette, Steven D, Systemic Inflammatory Response Syndrome, diunduh dari http://emedicine.medscape.com/article/168943-overview tanggal 7 Februari 2012 pukul 22.00. 2. Systemic Inflammatory Response Syndrome, diunduh dari http://en.wikipedia.org/wiki/Systemic_inflammatory_response_syndrome, tanggal 7 februari 2012, pukul 22.15. 3. Sepsis and Systemic Inflamatory Response Syndrome (Diunduh dari : https://docs.google.com/viewer?a=v&q=cache:DRa4hXzVPTcJ:patf.lf1.cuni.cz/stuma t_en/sirs_mods_en.pdf+systemic+inflammatory+response+syndrome+etiology&hl=id &gl=id&pid=bl&srcid=ADGEEShRssdUAOvxvzUqVArwVuNkj-ydIGS2PqUCo8rVOo_7b2uAXOybkgMiPWKsWx9rlsk9fXClG8oOuyzWYVewYf5YrRgYkn3XFMyl1Wn0DdbSm9iKwZolpr1zMqsZzL_R6wHnQY &sig=AHIEtbREK8fEzRYuy8oNXiT4OXLkQ42JSQ&pli=1 tanggal 7 Februari 2012 pukul 22.35) 4. Janota Jan, MD,Systemic Inflammatory Response Syndrome and MODS, https://docs.google.com/viewer?a=v&q=cache:jTpTlHZwMFEJ:medresidents.stanfor d.edu/TeachingMaterials/Shock%2520and%2520Sepsis/Sepsis%2520and%2520SIRS .ppt+systemic+inflammatory+response+syndrome&hl=id&gl=id&pid=bl&srcid=AD GEESjB3hwmZViXlAf3kD0BPbgS58UrX6tOLDjQB7O_fjnx5hGguxeL7Z5dvjMAK3KmqoN0E9GQrEbt1ofPxxc_DmR1JclcmEags7Jd7AAkHLvv4fdXlR9m8AvxliHqpPUkceSBYo&sig =AHIEtbSq-n95pq49GRkFobfPSLGytxkpAQ

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