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System inflammatory response syndrome and sepsis for surgery patients Surgery department №2 DSMA System inflammatory response syndrome (SIRS) Sepsis — SIRS + septic site SIRS • Continuum of clinical pathophysiology and severity • Process rather than an event • Mild dysfunction to frank organ failure • Changes in the function of every organ system mediated by the host immune system. SIRS • Systemic Inflammatory Response Syndrome Criteria (ACCP/SCCM Consensus) – Temperature >38°C or <36° – Heart rate >90 bpm – Respiratory Rate>20 or PaCO2<32mmHg – WBC>12,000/μl or <4,000/μl Sepsis • Sepsis: 2 or more– Tachycardia >90bpm – Rectal temp>38°C or <36°C – Tachypnea(>20bpm) • With 1 or more – Alteration in mental status – Hypoxemia (PaO2<72mmHG at FiO20.21) – Elevated plasma lactate – Oligouria Sepsis classification by ethiology • • • • • • • • Gram (+) Gram (-) Aerobic Anaerobic Mycobacterial Staphylococcus Streptococcus Mixt-sepsis Sepsis classification by primary focus • Post-traumatic: – burn – wound • • • • Lung Angiogenic Cardiogenic Abdominal: – – – – – Biliary Pancreatic Intestinal Peritoneal Appendicular • Soft-tissue inglammation • Urological etc Sepsis classification by development with a time (stages) • Toxemia • Septicemia • Septicopyemia Sepsis classification by clinical course • Fulminant or the acutest • Acute • Chronic Sepsis classification by clinical severity Sepsis Severe sepsis – sepsis + organ dysfunction Septic shock – sepsis + hypotension (Multiple organ dysfunction) Sepsis • Severe Sepsis – – – – – Tachycardia >90bpm Rectal temp>38°C or <36°C Tachypnea(>20bpm) or PaCO2<32mmHg Hypotension despite fluid resuscitation Presence of perfusion abnormalities: lactic acidosis, oligouria, alteration in mental status Sepsis • Mediators of Sepsis – – – – Lipospolysaccharide (gram-negative bacteria) Lipoteichoic acid (gram-positive bacteria Peptidoglycan Cytokines • IL-1 – mediates systemic effects of infection • IL-6 – effects liver function • TNF-α- potentiates the activation of neutrophils and macrophages • IL-8 – regulates neutrophil function, mediates lung injury in sepsis Sepsis • Mediators of Sepsis – Complement – Nitric Oxide – Lipid Mediators: Chemotaxis, Cell activation, Vascular Permeability Phospholipase A2 PAF Eicosanoids Sepsis • Mediators of Sepsis – Adhesion Molecules • Selectins • Leukocyte Antigens Sepsis • Circulatory Manifestations – – – – – – Vasodilation Tachycardia Increased Cardiac Output Depressed Myocardial Function Increased Delivery Decreased Extraction Sepsis • Circulatory Manifestations – Downregulation of catecholamine receptors – Increased local vasodilating substances • • • • • • Nitric oxide Prostacyclin Decreased Oxygen Low pH Increased anaerobic metabolism Shunting Sepsis • Pulmonary Dysfunction – – – – – – – Endothelial Injury Interstitial Edema Alveolar Edema Neutrophil entrapment Injury Type I pneumocyte Hyperplasia Type II pneumocyte Continued Neutrophil, monocyte, leukocyte and platelet aggregation Sepsis • Other Organ Dysfunction – GI • Ileus • Malabsorption • Overgrowth of bacteria, Translocation – Liver – Renal – CNS Sepsis • Organisms – – – – – Lower Respiratory Tract Infections (25%) Urinary Tract Infections (25%) Gastrointestinal Infections (25%) Soft Tissue Infections (15%) Reproductive Organs (5%) Sepsis • Risk Factors – – – – – – – – Extremes of Age (<10 and >70 years) Pre-existing Organ Dysfunction Immunosuppression Major Surgery, Trauma, Burns Indwelling Devices Prolonged Hospitalization Malnutrition Prior Antibiotic Treatment Sepsis • Principles for Management of Sepsis – – – – Early Recognition Early and Adequate Antibiotic Therapy Source Control Early Hemodynamic Resuscitation and continued support – Drotrecogin Alpha (Apache II>25) – Tight Glycemic Control – Ventilatory Support Sepsis • Drotrecogin-alpha/Recombinant Human Activated Protein C – Reduced levels of anti-inflammatory mediators – Activated Protein C • Inhibits thrombosis • Decreases inflammation • Promotes fibrinolysis – Side Effect: Bleeding – PROWESS study group • Lower mortality rate (24.7 vs. 30.8%) Sepsis • Steroids??? – Older trials used high doses – Recent trials suggest low dose, with taper and tight glycemic control may improve outcome – Vasopressor-dependent shock – Cosyntropin Stim Test-Relative Adrenal Insufficiency (<9mcg/dL) Sepsis • Experimental Therapies – Dopexamine- beta 2 adrenergic and dopaminergic effects, NO alpha adrenergic activity – Vasopressin- reduces inducible NO synthase, upregulates endogenous catecholamine receptors – Phosphodiesterase Inhibitors-ionotropic agents with vasodilating actions – Nitric Oxide Inhibitors- N-monomethyl-l-arginine ARDS • Frequent Complication in Sepsis(40%) • Adult Respiratory Distress Syndrome – Oxygenation abnormality: PaO2/FiO2 ratio less than 200 – Bilateral opacities on CXR – PAOP <18mm Hg or no evidence of L atrial hypertension ARDS • Frequent Complication in Sepsis(40%) • Adult Respiratory Distress Syndrome – Oxygenation abnormality: PaO2/FiO2 ratio less than 200 – Bilateral opacities on CXR – PAOP <18mm Hg or no evidence of L atrial hypertension – Frequency of ARDS in sepsis 18-38% – 16% patients die w/irreversible respiratory failure ARDS • Pathophysiology – Injury to Alveolocapillary unit – Exudative Phase • Endothelial injury, immune cell infiltration, pneumocyte and endothelial injury and necrosis – Proliferative Phase • Organization of exudate, myofibroblast proliferation • Conversion of exudate to fibrous tissue – Fibrotic Phase • Remodeling of fibrosis, microcystic honeycomb formation and traction bronchiectasis ARDS • Management – Lung-Protective Strategy-Reduction of Barotrauma – TV 5ml/kg – Longer inspiratory time – Peak Inspiratory Pressure<35-40cmH2O – Permissive Hypercapnea – PEEP Acute Renal Failure • Increases Mortality in ICU 30% • Physiology – Glomerular Filtration dependent on perfusion pressure (MAP 60-80mmHg) – Less than 60mmHG • Decreased flow • Arterial dilation in pre-glomerular arterioles (prostaglandins) • Constriction of post-glomerular arterioles (angiotensin II) Acute Renal Failure • As Renal Perfusion Falls – Increased reabsorption in proximal tubules • 90% water is reabsorbed (normal is 60%) – Decreased fluid to the distal tubules • Loss of potassium elimination – Tubular cells dependent on aerobic respiration • Ascending loop is most sensitive to ischemia Acute Renal Failure • Dose all drugs appropriately • Correction of Metabolic Acidosis – Isotonic Bicarbonate – Cannot Correct Ongoing Hypoperfusion • Renal Replacement Therapy – Absolute indication • Acidosis • Hyperkalemia • Uremia (relative) Sepsis • Principles for Management of Sepsis – – – – Early Recognition Early and Adequate Antibiotic Therapy Source Control Early Hemodynamic Resuscitation and continued support – Drotrecogin Alpha (Apache II>25) – Tight Glycemic Control – Ventilatory Support