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Acute Renal FailureSystem inflammatory response syndrome and sepsis for surgery patients System inflammatory response syndrome (SIRS) - Sepsis — SIRS + septic site • 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: 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 • Gram (+) • Gram (-) • Aerobic • Anaerobic • Mycobacterial • Staphylococcus • Streptococcus • Mixt-sepsis Sepsis • Post-traumatic: – burn – wound • Lung • Angiogenic • Cardiogenic • Abdominal: – Biliary – Pancreatic – Intestinal – Peritoneal – Appendicular • Soft-tissue inglammation • Urological etc Sepsis • Toxemia • Septicemia • Septicopyemia Sepsis • Fulminant or the acutest • Acute • Chronic Sepsis Sepsis Severe sepsis – sepsis + organ dysfunction Septic shock – sepsis + hypotension (Multiple organ dysfunction) • 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 • 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 – Complement – Nitric Oxide – Lipid Mediators: Chemotaxis, Cell activation, Vascular Permeability Phospholipase A2 PAF Eicosanoids – Adhesion Molecules • Selectins • Leukocyte Antigens • Circulatory Manifestations – Vasodilation – Tachycardia – Increased Cardiac Output – Depressed Myocardial Function – Increased Delivery – Decreased Extraction – Downregulation of catecholamine receptors – Increased local vasodilating substances • Nitric oxide • Prostacyclin • Decreased Oxygen • Low pH • Increased anaerobic metabolism • Shunting
• 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
– GI • Ileus • Malabsorption • Overgrowth of bacteria, Translocation – Liver – Renal – CNS
• Organisms – Lower Respiratory Tract Infections (25%) – Urinary Tract Infections (25%) – Gastrointestinal Infections (25%) – Soft Tissue Infections (15%) – Reproductive Organs (5%)
• 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
• 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
• 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%)
• 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)
• 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 • 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 • 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 • 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)
• 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
Date: 2015-12-11; view: 1026
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