SYSTEMATIC INFLAMMATORY RESPONSE SYNDROME SIRS AND MULTIPLE ORGAN DYSFUNCTION SYNDROME MODS ETIOLOGY AND PATHOPHYSIOLOGY Systemic inflammatory response syndrome o Systemic inflammatory response to a variety of insults Infection sepsis ischemia infarction and injury o Triggers Abscess formation intraabdominal extremities Ischemic or necrotic tissue pancreatitis vascular disease myocardial infarction Mechanical tissue trauma burns crush injuries surgical procedures Microbial invasion bacteria viruses fungi parasites Global perfusion deficits post CPR shock states Endotoxin release gram negative and positive bacteria Regional perfusion deficits distal perfusion deficits Multiple Organ Dysfunction Syndrome o Failure of two or more organ systems in an acutely ill person Homeostasis cannot be maintained without intervention ORGAN AND METABOLIC DYSFUNCTION Uncontrolled inflammatory response activation of inflammatory cells and release of mediators direct damage to the endothelium hypermetabloism Vasodilation decrease SVR and hypotension Increases vascular permeability mediators and protein leak out of the endothelium into the interstitial space White blood cells digest foreign debris coagulation cascade is activated Hypotension perfusion microemboli and redistributed shunted blood flow compromised o Inflammatory mediators directly affect pulmonary vasculature endothelial damage capillary permeability alveolar edema o Surfactant alveolar collapse shunting worsening ventilation perfusion o Myocardial depression and massive vasodilation increase tissue demands Vasodilation SVR and BP baroreceptor reflex release inotropic contractility and chronotrophic rate attempt to enhance CO to compensate for hypotension o Fluid and albumin shift third spacing venous return preload warm tachycardia high CO and low SVR capillary refill skin mottling CVP PAWP and dysrhythmias Neurologic dysfunction o Acute mental status change early sign o Confusion agitation combative disoriented lethargic or comatose organ perfusion Respiratory system fails first mismatch Cardiovascular changes Due to hypoxemia inflammatory mediators or impaired perfusion Acute kidney injury o Decreased kidney perfusion activates SNS and renin angiotensin system vasoconstriction and aldosterone mediated water and sodium reabsorption o Antibiotics tend to be nephrotoxic GI tract o motility abdomen distention and paralytic ileus o High risk of ischemia from shunting mucosal barrier break down bacteria from GI into circulation sepsis contributes to the development of SIRS MODS Metabolic changes o Hypermetabolic response triggered o Glycogen converts to glucose glycogen depletion amino acids convert to glucose depleted protein stores catabolic state muscle is lost o Leads to liver dysfunction Begins before clinical evidence is present Protein synthesis impairment Albumin administration does not normalize oncotic pressure at this point o DIC loss of clotting factors platelets and fibrinogen simultaneous microvascular Coagulation failure slotting and bleeding Electrolyte imbalance o Common result of hormonal changes metabolic chcnages and fluid shifts o Antidiuretic hormone and aldosterone water and sodium retention o Hypokalemia Aldosterone urinary potassium loss Catecholamines potassium shift into the cell Associated with dysrhythmias and muscle weakness o Impaired tissue perfusion hypoxia and anaerobic metabolism increased lactate metabolic acidosis o Hypokalemia hypomagnesaemia and hypophosphatemia also occur CLINICAL MANIFESTIONS Respiratory o Development of ARDS Severe dyspnea PaO2 FIO2 ratio 200 Bilateral fluffy infiltrated on chest x ray PAWP 18 Ventilation perfusion mismatch Pulmonary HTN minute ventilation and RR compliance Refractory hypoxemia o Management Prevention Optimize oxygen delivery minimize oxygen consumption Mechanical ventilation Positive end expiratory pressure Lung protective models Permissive hypercapnia Positioning continuously lateral rotation therapy prone positioning Cardiovascular o Myocardial depression o Massive vasodilation o SVR BP o MAP o HR Stroke volume o CO o Systolic diastolic dysfunction o Biventricular failure o Management Volume management Central venous or PA catheters for hemodynamic monitoring Preload via volume replacement Maintain MAP 65 Arterial pressure monitoring Vasopressors Monitor SvO2 ScvO2 balance O2 supply and demand Continuous ECG monitoring Circulatory assist devices IABP or VADs Venous thromboembolism prophylaxis Lovenox or sequential compression Central Nervous System o Acute change in neurologic status o Fever o Hepatic encephalopathy o Seizures o Confusion disorientation o Failure to wean prolong rehabilitation o Management Evaluate for hepatic metabolic encephalopathy Optimize cerebral blood flow cerebral oxygen requirements Prevent secondary tissue ischemia Calcium channel blockers cerebral vasospasm Renal o Prerenal renal hypoperfusion BUN creatinine ratio 20 1 urine Na 20 Loop diuretics Lasix May need to increase dose due to glomerular filtration rate urine specific gravity 1 020 urine osmolality o Intrarenal acute tubular necrosis BUN creatinine ratio 10 1 15 1 Urine Na 20 Urine osmolality Urine specific gravity 1 010 o Management Diuretics Dopamine intropin Enhances renal blood flow Improved renal perfusion Increases urine output May work synergistically with diuretics Continuous renal replacement therapy Gastrointestinal o Mucosal ischemia Intramucosal pH Potential translocation of gut bacteria Potential abdominal compartment syndrome o Hypoperfusion peristalsis paralytic ileus o Mucosal ulceration o GI bleeding o Management Stress ulcer prophylaxis Hepatic o Bilirubin 2 o liver enzymes ALT AST GGT o Serum NH3 o Serum albumin prealbumin transferrin o Jaundice o Hepatic encephalopathy o Management Maiantin adequate tissue perfusion Provide nutritional support enteral feedings Careful use of drugs metabolized by liver Antacids Maaloc H2 receptor blockers Pepcid Sucralfate Carafate Monitor abdominal distention intraabdominal pressures Dietary consultation Enteral feedings Stimulate mucosal activity Provide essential nutrients and optimal calories Hematologic o bleeding times PT PTT o PLT count thrombocytopenia o Fibrin split products o D Dimer test o Management Endocrine o Hyperglycemia hypoglycemia o Management Observe for bleeding from obvious and or occult sites Replace factors being lost PLT Minimize traumatic interventions IM injections multiple venipunctures