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SEPTIC SHOCK By Marian D. Williams RN BN CEN CFRN CCRN SEPTIC SHOCK Most common cause of death in noncardiac ICU’s in the US Most cases are nosocomial Increased incidence due to advanced invasive technology Elderly are at greatest risk Mortality:40%-85% SEPTIC SHOCK 10th leading cause of death in the United States 139% increase from 1979 - 1987 SEPTIC SHOCK DEFINITIONS – Bacteremia Presence of BACTERIA in the blood Body’s defense systems effectively destroy bacteria – Septicemia Presence of MICROBES in the blood associated with systemic infection SEPTIC SHOCK Sepsis – Systemic inflammatory response to infection. Severe Sepsis/SIRS – Sepsis associated with evidence of one or more acute organ dysfunctions SEPTIC SHOCK RISK FACTORS Patient related – – – – – < 1 year of age > 65 years of age Debilitated Malnourished Chronic health problems SEPTIC SHOCK RISK FACTORS Treatment Related – – – – Invasive lines and procedures Surgical procedures Treatment for burns or traumatic wounds Immuno-suppression SEPTIC SHOCK CAUSATIVE MICROORGANISMS Gram Negative – – Most cases E. COLI – – – – – – Most likely Klebsiella pneumoniae Enterobacter aerogenes Serratia marcescens Gram Positive Less common Staphylococcus aureus Viruses Fungi Rickettsiae Protozoans SEPTIC SHOCK CAUSATIVE MICROORGANISMS Gram Negative – Responsible for the majority of the cases ENTRY SITES FOR SEPTIC SHOCK Most common - GU Tract GI Tract Respiratory Tract Skin SEPTIC SHOCK PATHOGENESIS Proinflammatory and procoagulation responses dominate and lead to uncontrolled inflammation and advanced coagulopathy SEPTIC SHOCK PATHOGENESIS Three known problems 1. Excess Coagulation 2. Exaggerated or malignant inflammation 3. Impaired fibrinolysis SEPTIC SHOCK PATHOGENESIS Balance of coagulation and fibrinolysis shifts toward increased coagulation via the extrinsic pathway SEPTIC SHOCK PATHOGENESIS In mice, microthrombi developed in the hepatic circulation within 5 minutes of injection of endotoxin SEPTIC SHOCK PATHOGENESIS Endotoxin is within the Gram Negative bacteria wall Released into the blood during bacterial cell lysis PATHOGENESIS OF SEPTIC SHOCK Macrophages – – Phagocytic cells found in the lung interstitium and alveoli, liver, sinuses etc. Activated by endotoxin to release cytokines Cytokines – Tumor necrosis factor – – Major endogenous toxin * Interleukin-1 Interleukin-2 PATHOGENESIS OF SEPTIC SHOCK Endotoxins activates GRANULOCYTES – – Releases toxic mediators e.g. platelet activating factor, Oxygen derived free radicals Proteolytic enzymes Endotoxins activate arachidonic acid cascade – Results in prostaglandin, leukotrienes, thromboxane A etc effecting smooth muscle PATHOGENESIS OF SEPTIC SHOCK Thromboxane A2 and B2 – Pulmonary vasoconstriction – Mediate bronchoonstriction – Potent platelet aggregator Prostaglandin E and Prostacyclin – – Potent vasodilator May be responsible for hypotension PATHOGENESIS OF SEPTIC SHOCK Complement System Activated – – Produce microemboli Endothelial cell destruction Histamine – – – Potent Vasodilator Released by mast cells Increases Capillary permeability (Fluid moves from vascular bed) PATHOGENESIS OF SEPTIC SHOCK Myocardial Depressant factor (MDF) – Released from pancreas – Decreases contractility of the heart – Coagulation system is activated Kinin System activated – Bradykinin is released – Vasodilation – Increased capillary permeability PATHOGENESIS OF SEPTIC SHOCK MYOCARDIAL DEPRESSANT FACTOR – MAY ENHANCE DEVELOPMENT OF MICRO EMBOLI HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK Profound Vasodilation – Systemic vascular resistance is decreased – Blood Pressure falls – Veins dilate – Intravascular pooling in the venous capacitance system HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK Mal-distribution of blood flow – Some tissues under-perfused and some tissues are over-perfused – Excessive flow rates to areas of low metabolic demand limits O2 extraction – Therefore, difference in arterial and venous O2 content HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK Decreased ejection fraction – Definition: Percent of diastolic volume that is ejected during systole HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK Decreased Ejection Fraction – Depressed myocardial contractility despite increased cardiac output – Right ventricular dysfunction is common – usually as a result of pulmonary hypertension and myocardial depression HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK Increased capillary permeability – Fluid movement out of the vascular beds and into the interstitial space – Generalized soft tissue edema results – Edema can interfere with tissue oxygenation and organ function HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK Microembolization – – Results in sluggish blood flow Decreased oxygen utilization therefore increased risk of D. I. C. HYPERDYNAMIC PHASE CLINICAL MANIFESTATIONS BP Falls – – Decreased SVR Decreased venous return Decreased sympathetic tone – Diastolic pressure falls HYPERDYNAMIC PHASE CLINICAL MANIFESTATIONS Increased sympathetic tone – – Widened pulse pressure Heart rate increases in attempt to increase CO to compensate for decreased blood pressure HYPERDYNAMIC PHASE CLINICAL MANIFESTATIONS Impaired gas exchange – Pulmonary blood congestion – Pulmonary blood flow decreases Respiratory rate and depth increase – Early respiratory alkalosis Crackles may be audible – Interstitial pulmonary edema HYPERDYNAMIC PHASE CLINICAL MANIFESTATIONS Impaired Gas Exchange Pulmonary vascular resistance increases Pulmonary congestion results HYPERDYNAMIC PHASECLINICAL MANIFESTATIONS Febrile Possible associated chills Skin pink and warm – Peripheral vasodilation LOC may be altered – Cerebral ischemia HEMODYNAMIC MANIFESTATIONSHYPERDYNAMIC PHASE Decreased SVR – – Cardiac output high Cardiac Index high Decreased venous return – Pulmonary artery pressures below normal – PCWP below normal HEMODYNAMIC MANIFESTATIONSHYPERDYNAMIC PHASE Maldistribution of blood flow Oxygen consumption is decreased SVO2 levels are above normal HYPODYNAMIC PHASECLINICAL MANIFESTATIONS Decreased cardiac output – Rapid, shallow respirations – Crackles and wheezes Pulmonary congestion – Decreased Urinary output Renal – hypoperfusion Lethargic HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS SNS Stimulation – Peripheral vasoconstriction Narrowing pulse pressure Cool, clammy skin Increased afterload Decreased contractility PROFOUND HYPOTENSION HEMODYNAMIC MANIFESTATIONSHYPODYNAMIC PHASE SVR increased CO decreased CI decreased SEVERE MYOCARDIAL DEPRESSION PA and PAWP pressures increased Metabolic and respiratory acidosis with hypoxemia CLINICAL MANAGEMENT Fluid Administration 1. – To restore adequate ventricular preload Maintain PAWP: 12 MM HG Colloids vs. crystalloids – 2. Colloids my cause movement of fluid into interstitial space because of the capillary permeability If ineffective, may need Dopamine and Dobutamine CLINICAL MANAGEMENT 3. Mechanical Ventilation – Greater risk for acute lung injury and ARDS – Low tidal volume of 6 ml/kg – Maintain plateau pressures at 30 cm H2O or less • Reduction of mortality of 9% CLINICAL MANAGEMENT 4. Glycemic Control Blood sugar 80-100 mg/dl Mortality reduced by 3.4% Blood glucose levels of 110-150 mg/dl associated with a worse outcome were CLINICAL MANAGEMENT 5. Prevention of Infection – Prevent ventilator associated pneumonia (VAP) Maintain head of bed elevated at 30 degrees – Increase 23% infection in supine position – Oral Care – mouth is colonized within 24 hours – Deep oral suctioning above the ET cuff CLINICAL MANAGEMENT 6. Xigris (Drotrecognifa-activated) aka Drotrecogin alfa (activated) – Approved by US Food and Drug in 2001 – Recombinant form of human activated protein C PROWESS Trial CLINICAL MANAGEMENT Xigris Guidelines – Known or suspected infection – 2 or more signs of SIRS – At least 1 failing organ – High risk for death CLINICAL MANAGEMENT Xigris Contraindications – Active internal bleeding – Recent hemorrhagic stroke (3 mos) – Head traum (recent) – Epidural catheter – Intracranial mass CLINICAL MANAGEMENT Xigris Cost - $6800/96 hour infusion Dosage: 24 mcg/kg/hour Dedicated IV line 80% of the drug’s effects cleared within 30 minutes Activity is reduced substantially in 15 minutes CLINICAL MANAGEMENT 7.Antibiotic therapy – Instituted after the cultures are obtained – Third generation cephalosporins plus an aminoglycoside CLINICAL MANAGEMENT Possible anti-endotoxin drugs – In research phase – Have been shown to decrease mortality significantly in patients with septic shock and gram negative bacteremia COMPLICATIONS OF SHOCK ARDS ACUTE RENAL FAILURE ACUTE RENAL FAILURE MULTIPLE ORGAN DYSFUNCTION SYNDROME DIC SEVERE SEPSIS/SIRS Sepsis with acute organ dysfunction 750,000 cases /year 28%-50% mortality – Definition: SIRS Systemic Inflammatory Response Syndrome – 2 or more of: Body Temperature > 38 degrees C or < 36 degrees F Heart Rate >90/min RR - >20/min; or PaCO2 <32 mm Hg WBC - > 12,000 or > 10% bands SEVERE SEPSIS/SIRS Associated with organ dysfunction, hypoperfusion or hypotension – May include but are not limited to: Lactic acidosis Oliguria Acute alteration in mental status SEPSIS (SIRS)-INDUCED HYPOTENSION Systolic BP of < 90 mm Hg or a reduction of > 40 mm Hg from baseline in the absence of other causes for hypotension SEPTIC SHOCK / SIRS SHOCK Subset of severe sepsis and defined as sepsis (SIRS)-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include but not limited to: SEPTIC SHOCK / SIRS SHOCK – Lactic acidosis – Oliguria – Acute alteration in mental status MODS Multiple Organ Dysfunction Syndrome – Presence of altered organ dysfunction in an acutely ill patient such that homeostasis cannot be maintained without intervention MODS Factors in the development – Result of Bacterial factors Inflammatory mediators Endothelial injury Disturbed hemostasis Microcirculatory failure MODS Factors – Patients Advancing age Pre-existing illness – Primary Cellular Injury Underlying disease processes Toxic effects of certain mediators MODS Factors – Microaggregates Platelets, neutrophils, RBC’s and fibrin impair microcirculatory blood flow and produce tissue ischemia MODS Factors – Endothelial Cell Injury Proinflammatory cytokines Alters vasomotor tone Capillary leakagepulmonary edema MODS Factors – Metabolic Derangement Mitochondrial dysfunction – Oxidants are produced during endotoxin induced shock MODS Factors – Humoral Mediators TNF- and IL-1 – Attract leukocytes to site of infection – Excess levels cause general response MODS Factors – Therapy –induced dysfunction Mechanical ventilation at higher volumes Blood transfusions Hyperglycemia – Activates tissue factor pathway for coagulation • Enhanced thrombin formation • Acute thrombosis MODS MODS MODS MODS MODS SIRS Systemic Inflammatory Response Syndrome SIRS Systemic Inflammatory Response Syndrome SIRS Systemic Inflammatory Response Syndrome SIRS Systemic Inflammatory Response Syndrome SIRS Systemic Inflammatory Response Syndrome SEVERE SEPSIS SEVERE SEPSIS SEVERE SEPSIS SEVERE SEPSIS SEVERE SEPSIS SEVERE SEPSIS IN SUMMARY...... SEPTIC SHOCK IS A MASSIVE INFECTION CAUSING VASODILATION AND INADEQUATE TISSUE PERFUSION THERAPY IS AIMED AT IMPROVING DISTRIBUTION OF BLOOD FLOW AND TREATING INFECTION THANK YOU