SEPSIS – Flashcard

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Epidemiology-Severe Sepsis:
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-Leading cause of death in non-coronary intensive care units -Septicemia rated as the 10th leading cause of death in the United States by the CDC -Mortality rate approaches 50% -Incidence in United States has risen each year since 1979 -Trend expected to continue because of increased elderly and immunocompromised patients
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Recognition
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-Extremely important to recognize the connection between infection, sepsis, and secondary organ failure -Signs and symptoms can be subtle -Pt often die in the ICU but sepsis usually begins in the home or on the Med-surg unit
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Inflammation vs. Infection: Inflammation
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-Complex reaction to death or injury of cells or tissues -Defense mechanism initiated to control and/or eliminate the offending agent and prepare an environment conducive to healing and repair -Initiated by any type of injury -Microbial -Mechanical -Thermal
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Infection
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-Follows the invasion of cells and/or tissues by living organisms -Bacteria -Viruses -Fungi
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Progression
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-Systemic Inflammatory Response Syndrome (SIRS) -Sepsis -Severe Sepsis -Septic Shock -Multiple Organ Dysfunction Syndrome (MODS)
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Systemic Inflammatory Response Syndrome (SIRS)
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-SIRS is a widespread inflammatory response to a variety of severe clinical injuries -Clinically indicated by the presence of 2 or more of the following: -Temperature >38 C (100.4 F) or 90 -Respiratory rate > 20/min or PaCO2 12,000 or 10% immature (bands) forms
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Sepsis
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_In sepsis, the clinical signs of SIRS are present together with definitive evidence of infection
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Severe Sepsis
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-Sepsis is considered severe when it is associated with organ dysfunction, hypotension, or hypoperfusion.
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The manifestations of hypoperfusion include, but are not limited to:
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-Lactic acidosis -Oliguria -Acute alteration in mental status
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Septic Shock
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-Septic shock is sepsis with hypotension despite adequate fluid replacement combined with perfusion abnormalities that may include but are not limited to: -Lactic acidosis -Oliguria -Acute alteration in mental status
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Septic Shock (cont.)
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-Patients who require vasopressor or inotropic support despite adequate fluid replacement are in septic shock
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Multiple Organ Dysfunction Syndrome (MODS)
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MODS: Refers to the presence of altered organ function in an acutely ill patient that homeostasis cannot be maintained without intervention
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Multiple Organ Dysfunction Syndrome (MODS)
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-Hypotension: a systolic BP of < 90mm Hg or a reduction of 40 mm Hg from baseline in absence of other causes for hypotension
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Multiple Organ Dysfunction Syndrome (MODS)-Risk Factors
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-Extremes of age ( 65 years) -Malnutrition -Hypothermia -Use of central venous catheters -Endotrachial intubation/mechanical ventilation -Aspiration
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Multiple Organ Dysfunction Syndrome (MODS)-Risk Factors-Chronic illness
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-Diabetes -Renal failure -Hepatic failure
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Multiple Organ Dysfunction Syndrome (MODS)-Immunodeficiency
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-Aids -Alcoholism -Use of chemotherapeutic agents
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Multiple Organ Dysfunction Syndrome (MODS)-Risk Factors
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-Use of surgery or invasive procedures
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Multiple Organ Dysfunction Syndrome (MODS)-Lab Assessment
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-Microbiology -Cultures: urine, blood, sputum, any wounds
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Multiple Organ Dysfunction Syndrome (MODS)-Lab Assessment
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-CBC- -WBC-"left shift" -Platelet ct
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Multiple Organ Dysfunction Syndrome (MODS)-Lab Assessment
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-Lactate level
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Multiple Organ Dysfunction Syndrome (MODS)-Lab Assessment
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-Coagulation profile -PT -PTT
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Multiple Organ Dysfunction Syndrome (MODS)-Lab Assessment
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-D-Dimer -Activated protein C -Specific cytokines
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Multiple Organ Dysfunction Syndrome (MODS)-Pathophysiology
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-Sepsis results from a variety of responses to an infectious process, including: -Activation of inflammation -Activation of coagulation -Impairment of fibrinolysis
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Multiple Organ Dysfunction Syndrome (MODS)-Pathophysiology (Normal)
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-Antigen (invader) of any type (bacteria, virus, parasite) enters the blood stream -Immune system recognizes the invader -Circulating monocytes release a series of mediators called cytokines -Cytokines isolate the invaders by clotting -Cytokines kill the invader by attracting neutrophils and other components of the immune system -When the invader is destroyed, the mediators signal to each other so that no more are released and the body returns to normal
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Multiple Organ Dysfunction Syndrome (MODS)-Pathophysiology
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-In sepsis, the immune system overreacts to the invader
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Multiple Organ Dysfunction Syndrome (MODS)-Pathophysiology
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-Reasons are not fully understood: -Large numbers of invaders -Presence of super invaders -Invaders' resistance to neutrophils -Invaders' resistance to antibiotics
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Multiple Organ Dysfunction Syndrome (MODS)-Pathophysiology
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-In sepsis, the immune system initiates clotting in many places -The body starts attacking normal tissue -Excessive clotting and cellular dysfunction interfere with blood flow and diminish cellular oxygenation -Cells start to shut down (cell stunning) and die -Then organs start to fail -The patient dies if process not stopped in time
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Multiple Organ Dysfunction Syndrome (MODS)-Patho-Role of Endothelium
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-Single layer of cells lining the blood vessels
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Multiple Organ Dysfunction Syndrome (MODS)-Patho-Role of Endothelium
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-Normally resists clot formation because : -Endothelial protein C receptors -Local generation and secretion of antithrombotic substances -Also secretes vasodilating substances including nitric oxide
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Multiple Organ Dysfunction Syndrome (MODS)-Patho-Role of Endothelium
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-When endothelium injured: -Produces substances that encourage localized clotting -Clots form in the microvasculature further damaging the endothelium
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Multiple Organ Dysfunction Syndrome (MODS)-Patho-Role of Endothelium
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-If endothelial damage is extensive: -Fluids can move into the interstitial spaces triggering edema and compounding hypovolemia -Increased secretion of nitric oxide impairs vasoregulation leading to abnormal endothelium dependent vascular relaxation -As sepsis progresses- causes severe vasodilation, refractory hypotension and impaired microcirculation- leading to MODS and death
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Multiple Organ Dysfunction Syndrome (MODS)-Signs and Symptoms
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-Alteration in WBC count -Increased number of bands -Alteration in temperature -Chills -Decreased skin perfusion -Decreased urine output -Decreased number of platelets
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Multiple Organ Dysfunction Syndrome (MODS)-Signs and Symptoms (cont)
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-Hypo- or hyperglycemia -Petechiae or purpura -Poor capillary refill -Skin mottling -Tachypnea -Tachycardia -Unexplained change in mental status
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Markers of Organ Dysfunction-Cardiovascular
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-Tachycardia -Dysrhythmias -Hypotension -Elevated central venous and pulmonary artery pressures -Decreased systemic vascular resistance -Need for vasopressor support
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Markers of Organ Dysfunction-Respiratory
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-Tachypea -Dyspnea -Hypoxemia -Need for mechanical ventilation
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Markers of Organ Dysfunction-Metabolic
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-Acidosis -Elevated lactate
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Markers of Organ Dysfunction-Neurologic
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-Confusion -Disorientation -Psychosis
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Markers of Organ Dysfunction-Renal
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-Oliguria (urine output < 0.5ml/kg/hr is an indicator of renal dysfunction) -Anuria -Elevated creatinine
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Markers of Organ Dysfunction-Endocrine
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-Adrenal insufficiency -Hyper- or hypoglycemia
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Markers of Organ Dysfunction-Hepatic
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-Jaundice -Elevated liver enzymes -Decreased albumin -Coagulopathy
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Markers of Organ Dysfunction-Hematologic
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-Thrombocytopenia -Coagulopathy (septic emboli)(DIC) -Decreased protein C levels -Increased D-dimer levels -Septic emboli
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Disseminated Intravascular Coagulation (DIC)
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-Essentially an imbalance between the processes of coagulation and anticoagulation
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Disseminated Intravascular Coagulation (DIC)
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-May be directly or indirectly initiated by conditions that trigger one of 4 mechanisms: -Factor XII formation: sepsis, anoxia, burns -Activation of factor II and X: proteolytic enzymes in snake venom -Activation of factor VII: massive trauma -Tissue thromboplastin release: amniotic fluid release entering maternal circulation
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DIC- Pathophysiology
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-Primary disease initiates the clotting process -Response is generalized and occurs throughout the vascular system -Creates a state of hypercoagulability -Fibrinolytic processes are then stimulated -Clotting factors become depleted and fibrinolysis continues -State of hypocoagulability develops
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DIC- Pathophysiology
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-Most common sequela of DIC is hemorrhage -This is caused by: -Decreased platelets -Depletion of clotting factors II, V, VIII, and fibrinogen in the clotting process -Production of FDPs through fibrinolysis -FDPs act as anticoagulants and increase the hemorrhagic tendency
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DIC- Clinical Manifestations
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-Signs/Symptoms: Bleeding -Mucous membranes and tissues -Petechiae and ecchymosis -Oral, GI, GU, & rectal bleeding -Bleeding after injections and venipunctures -Hypoxia, tachypnea, hemoptysis, hypotension, acidosis, and fever may also be present
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DIC- Diagnosis
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-Bleeding time-prolonged -Platelet count- decreased -Prothrombin time (PT)-prolonged (elevated) -Partial thromboplastin time (PTT)- prolonged (elevated) -Fibrinogen level- decreased -Fibrinogen/fibrin degradation products (FDPs)- increased -D-Dimer- increased (positive) -Factor assay- decreased levels of factor I, II, V, VIII, X, & XIII
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DIC- Treatment
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-Treatment of primary disease -Then goal is to control bleeding and restore normal levels of clotting factors -Blood products -Fresh frozen plasma (FFP) -Platelets -Cryoprecipitate -Fresh whole blood
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DIC- Treatment
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-Heparin -Inhibits underlying thrombotic process -Also promotes rather than decreases bleeding -Use is controversial
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Sepsis "Bundles"
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-Bundling system to encourage change in practice -Checklist for instituting guidelines in a user friendly manner -For sepsis, recommendations are divided into 6 hr and 24 hr with and without shock -Hospitals are using these for making their protocols
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Sepsis "Bundles"
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-Surviving Sepsis Campaign- -Institute for Healthcare Improvement-100,00 Lives Campaign -Society of Critical Care Medicine, American College of Chest Physicians -http://www.survivingsepsis.org
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Procedures/Treatments for Sepsis
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-Volume replacement -Antibiotics -Steroid therapy -Intensive insulin therapy -Protective lung ventilation
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Procedures/Treatments for Sepsis-Volume Replacement
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-Fluid resuscitation -Venous dilation causes relative hypovolemia and hypotension -Endothelial damage also allows fluids to escape into the extravascular space, creating edema and contributing to hypotension
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Procedures/Treatments for Sepsis-Volume Replacement
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-Fluid Type -Crystalloids - Normal saline -Colloids -Blood replacement- for hematocrit < 30, hemoglobin < 8
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Procedures/Treatments for Sepsis
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-Vasopressors -If fluid resuscitation doesn't stabilize the patients' BP, administer an IV vasopressor -Norepinephrine (Levophed) is preferred -Others: Dopamine, phenylephrine, epinephrine, vasopressin -May also need an inotrope (dobutamine) as an adjunct myocardium is depressed
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Procedures/Treatments for Sepsis
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-Antimicrobial Therapy -Eliminating the source of infection -AND -Initiating early, adequate antimicrobial therapy (after obtaining appropriate cultures) is critical
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Procedures/Treatments for Sepsis
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-Tight Glycemic Control -Hyperglycemia and insulin resistance commonly develop in sepsis -Hyperglycemia -Has a procoagulant effect -Can interfere with the normal immune response -Impaired neutrophil function -Increased risk of infection -Impaired wound healing
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Procedures/Treatments for Sepsis
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-Tight Glycemic Control -Keeping the blood glucose levels below 180mg/dl and preferably 80-110mg/dl by giving insulin (either sliding scale or insulin drip) has been shown to reduce morbidity and mortality
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Procedures/Treatments for Sepsis
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-Corticosteroid Replacement -Low dose therapy can be helpful in patients with relative adrenal insufficiency -Hypotensive (need for vasopressors) -Low serum cortisol levels -High dose therapy is not effective -200mg to 300mg of hydrocortisone daily for 7 days as replacement therapy
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Procedures/Treatments for Sepsis
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-Protective Lung Ventilation -For patients requiring mechanical ventilation -Avoid high plateau pressures (greater than 30cm H2O) in patients with acute lung injury or acute respiratory distress syndrome (ARDS) to prevent barotrauma -Use low tidal volumes (6ml/kg of ideal body weight) -Elevate HOB 30-45 degrees to reduce incidence of pneumonia and aspiration
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Procedures/Treatments for Sepsis
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-Prevention of Sepsis -Use good handwashing techniques -Follow universal precautions -Enforce infection control measures -Institute measures to prevent nosocomial infections: -Oral care, proper positioning -Turning and skin care -Care of invasive catheters -Wound care
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Nursing Care of Patients with Sepsis
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-Identify patients at risk -Assign high priority to cultures/pan-cultures (ie. Sputum, blood, urine, wound) for febrile episodes -Provide astute clinical assessments -Detection of Sepsis -Be aware of patients at risk for sepsis -Be Vigilant!
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Nursing Care of Patients with Sepsis
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-Detection of Sepsis -Be aware of patients at risk for sepsis -Be Vigilant!
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Nursing Care of Patients with Sepsis
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-Physical assessment and monitoring -General: -Fever/hypothermia -Tachycardia -Tachypnea -Hypotension
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Nursing Care of Patients with Sepsis
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-Hemodynamic status -Monitor HR/rhythm, and observe for ectopy -Monitor hemodynamic parameters for evidence of elevated cardiac output and low systemic vascular resistance
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Nursing Care of Patients with Sepsis
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-Ventilatory status -Monitor respiratory rate -Monitor lung sounds -Monitor oxygenation status via pulse oximetry, measurements of arterial blood gases, or mixed venous oxygen saturation
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Nursing Care of Patients with Sepsis
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-Renal status -Monitor hourly urine output -Note sudden /gradual decreases in urine output (< 0.5ml/kg/hr) -Monitor laboratory indicators of renal function: levels of creatinine, BUN, fractional excretion of sodium
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Nursing Care of Patients with Sepsis
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-Hematologic status -Monitor for bruising, bleeding -Monitor indicators of coagulation: platelet count, prothrombin time, activated partial thromboplastin time -Dialysis
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Nursing Care of Patients with Sepsis
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-Nutritional/metabolic status -Provide nutritional support -Recognize the role of intact gut barrier in preventing translocation of gram negative bacteria -Maintain nitrogen balance in hypermetabolic state Provide normalization of hyperglycemia
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Nursing Care of Patients with Sepsis
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-Hepatic/gastrointestinal status -Monitor for signs of GI dysfunction: nausea, vomiting, abdominal distention, changes in bowel sounds, high enteral feeding residuals (>200ml) -Monitor for signs of hepatic dysfunction: hyperbilirubinemia, elevated levels of liver enzymes
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Nursing Care of Patients with Sepsis
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-Neurological status -Monitor for changes in mental status: -Restlessness -Confusion -Changes in score on Glascow Coma scale
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Nursing Care of Patients with Sepsis
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-Other physical parameters: -Monitor for changes in skin color or temperature
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Nursing Care of Patients with Sepsis
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-Comprehensive treatment of sepsis: -Provide circulatory support with fluids, inotropes, and vasopressors -Provide oxygenation and ventilation as needed -Administer antibiotics -Monitor patients' response to treatment
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Nursing Care of Patients with Sepsis
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-Comfort and care of patients and their families: -Promote patients' comfort and provide pain relief and sedation -Provide turning, repositioning, and skin care -Teach patients and their families about sepsis and its treatment -Address needs of patients' family members
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Nursing Care of Patients with Sepsis
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-Conclusion -Sepsis with acute organ dysfunction is a common and often fatal disorder -Very important for nurses to recognize patients at risk and signs/symptoms Sepsis -Prevention is the key
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