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Sepsis car
| Question | Answer |
|---|---|
| Sepsis | - Signs and symptoms of an infection |
| Severe Sepsis = | SSI plus organ dysfunction due to hypoperfusion |
| MODS= Multi-organ dysfunction syndrome; | = SSI plus organ dyfuntion due to hyperfusion that does not respond to therapies that does not respond (fluid, antibodies and vasopressor infusions) |
| What are the risk factors for developing sepsis? | - Primary bloodstream infections - Pneumonia - Surgical wound infection - Urinary Tract Infection |
| Sepsis Circulation (Microcirculation- is key target organ | - Plugging of capillaries by blood cells - Tissue edema of protein rich fluid - Decrease in functioning capillaries causes an inability to extract oxygen |
| Sepsis Circulation – | - Reduced arterial vascular tone - Diminished venous return - Release of myocardial depressant substances LEADS TO PROFOUND HYPOTENSION |
| Sepsis Pulmonary | -Interstitial and alveolar edema - Trapping of neutrophils causes further capillary injury (result: ARDS) |
| Pulmonary | -Changes in airway diameter due to edema, accumulation of endotoxins and blood cells - Intrapulmonary shunting LEADS TO INCREASED WORK OF BREATHING, FATIGUE AND HYPOVENTILATION NONCARDIOGENIC PULMONARY EDEMA |
| Sepsis Gastrointestinal | -May propagate injury of sepsis by overgrowth of bacteria that may be aspirated into the lungs. -Normal barrier of gut may be altered bacteria and endotoxins to enter circulation. -Ileus blockage of intential sysyem non |
| +Septic Liver | -Alteration Reticulum Endothelium System allow spillage of bacteria into systemic circulation |
| Renal Sepsis | -Acute tubular necrosis secondary to hypotension, direct renal vasoconstriction, release of cytokines and activation of neutrophils |
| Sepsis Progression of Organ Dysfunction | -Autocatoblism – loss of lean body mass, severe weight loss, energy depletion and increased CO and oxygen demand. - Alterations in carbohydrate,fat, and protein metabolism. M.O.D.S. Multi-Organ Dysfunction Syndrome |
| -Clinical Manifestation Starting | -Tachypnea, restlessness, apprehension, moderate accessory muscle use, fine crackles. - PaO2 low despite increases in supplemental oxygen. - PaCo2 low -pH high - Chest X-Ray may be normal |
| Clinical Manifestation at Progression | - Pulmonary edema continues - More crackles, increased WOB, further agitation, Dyspnea, hemoptysis -Patchy infiltrates-“white out “ on Chest X-Ray -Worsening hypoxemia -Decrease PaO2 Increase PaCO2 decrease pH |
| Clinical Course- Summary | Period of circulatory instability and physiologic shock-Perpetuation of inflammation and organ hypoperfusion -Usually lungs first major organ affected -After insult and resuscitation, client develop a persistent hypermetabolism -Lasts 14-21days |
| Goal of Therapies- Collaborative Measures Team Effort | 1.Resusciation using measures to correct hypoxia, hypotension and impaired tissue oxygenation 2.Indentify and treat the source of infection w/ Antiobiotic, surgery or both 3.Main adequate organ system function guided by cardiovascular monitoring |
| Goal: Normalization of VS, improve capillary refill, improve mental status | RESTORATION OF INTRAVASCULAR VOLUME •Isotonic crystalloids- NS 0.9% or LR *500ml boluses; oMay need 4-6 liters oFrequent assessment |
| RESTORATION OF INTRAVASCULAR VOLUME • Colloids | oAlbumin 5% expands plasma volume to greater degree than isotonic and reduces the tendency for pulmonary and cerebral edema o-250-500ml over 20-30 minutes oPrecaution protein overload tends to exacerbate renal insufficiency |
| Vasopressor Therapy - Used when fluid resuscitation fails to restore hemodynamic stability - Goal: Increases blood pressure; Preserves perfusion to vital organs (MAP. | - Examples:nonepinephrine (Levophed), phenylephrine (neosynephrine), Dopamine, Epinephrine -Central Line Access is a MUST!!! |
| Improve Oxygenation Goal: Decrease oxygen demand Improve VENTILATION & ALLEVIATE HYPOXEMIA | -Turn at least q2hrs-prone ,side to side, semiererect, or sitting position. -Monitor ABG’s -Monitor pulse oximetry |
| Improve Oxygenation Goal: Decrease oxygen demand | -Promote secretion clearance oAdequate systemic hydration oHumidified oxygen oFrequent mouth care oSuctioning as needed oChest physiotherapy |
| Improve Oxygenation Goal: Minimize oxygen consumption | -Prevent oxygen desaturation oHyperoxygenation before suctioning oProvide adequate rest and recovery time between procedures oLimit activity oAdminister sedation to control anxiety oControl fever oMonitor pulse oximetry |
| Suctioning - Minimize hypoxemia | o 3 hyperoxygenated breaths before suctioning (100%) -Limit each pass to <10 seconds Limit of 3 passes or less- just enough to clear the airway oNO ROUTINE USE OF SALINE |
| CONTOL OF INFECTION Goal: Prevent further spread , promote healing, normal temperature | BROAD SPECTRUM ANTIBIOTICS oSelection is empirical and base on most likely organism, host defenses oAdministered IV to achieve adequate serum concentrations |
| Control Infection (Promote healing and enhance function of immune system) | -Hand washing aseptic dressing changes, monitor invasive catheters -Antibiotics must be given on time to promote adequate tissure penetration and serum levels tob bactericidal -Be alert for self infection through colonization of respiratory tract with GI |
| Control Infection (Temperature control) | -Antipyretics -Cooling blanket -Room control |
| Nutritional / Metabolic Support - Goal: Improve overall nutritional status, enhance the immune system, and preserve organ function and structure. | o Enteral feeding if gut is working o 25-30kcal/kg/day oMaintain TPN if necessary |
| What Can YOU do for the patient? | Early recognition !!! 1. Oxygen 2. Fluid Rescscitation (20mlkg Bolus, followed by 150-200ml/hr until urine output >.5ml/kg/hr OR MAP >/65 3. Cultures (respiratory, urine and blood) 4. Antibiotic and Antifungal (Multiple, be prepared to give one antib |
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