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EMRA Sepsis Card

EMRA Sepsis Card

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sepsis so sicu
sepsis so sicu

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Published by: sgod34 on Mar 10, 2014
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07/03/2015

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Sepsis Card

Authors: Stephen Boone, MD; Christian Coletti, MD; John Powell, MD

Severe sepsis affects approximately one million patients and claims more than 250,000 lives each year in the U.S. It is the second leading cause of death in non-cardiac ICU patients. Early and aggressive therapy influences outcomes. Utilizing the Surviving Sepsis Campaign Guidelines improves morbidity and can decrease mortality by 25%.

INFECTION
Defined as a pathologic process caused by the invasion of normally sterile tissue, fluid or body cavity by pathogenic microorganisms.

SEPSIS
Defined as a suspected or documented infection and two or more of the following variables: • Temperature: > 38.3°C (> 101°F) or < 36°C (< 96.8°F) • Heart Rate > 90 bpm • Respiratory Rate > 20 breaths/min • Acutely altered mental status • Hyperglycemia (glucose > 140 mg/dL OR 7.7 mmol/L) in the absence of diabetes • WBC > 12,000/mm3, < 4000/mm3, OR > 10% immature (band) forms • Plasma C-reactive protein more than two SD above the normal value • Plasma procalcitonin more than two SD above the normal value

SEVERE SEPSIS
Defined as sepsis-induced organ dysfunction or tissue hypoperfusion. Organ system dysfunction must be remote to the site of infection with the exception of pulmonary criteria. Cardiovascular • Hypotension (SBP < 90 mm Hg, MAP < 70 mm Hg OR an SBP decrease > 40 mm Hg) Pulmonary • Acute Respiratory Distress Syndrome: — PaO2/FiO2 < 250 in absence of PNA as source — PaO2/FiO2 < 200 with PNA as source Renal • Acute oliguria (UO < 0.5 mL/kg/hr for 2 hrs despite adequate fluid resuscitation) • Creatinine increase > 0.5 mg/dL from baseline Hemotologic • Coagulation dysfunction (INR > 1.5 OR PTT > 60 secs absent anticoagulant usage) • Thrombocytopenia (platelet count < 100,000/mm3) Hepatic/GI • Hyperbilirubinemia (total bilirubin > 2 mg/dL) Systemic • Hyperlactemia > 2 mmol/L (18.0 mg/dL) • Decreased capillary refill or skin mottling

SEPSIS-INDUCED TISSUE HYPOPERFUSION
Defined as (1) sepsis-induced persistent hypotension (SBP < 90 mmHg, a MAP < 70 or a SBP decrease > 40 mmHg from baseline) or (2) lactate ≥ 4.0 mg/dL or (3) oliguria. Septic shock is sepsis-induced tissue hypoperfusion not responding to 30 mL/kg crystalloid bolus.

A more conservative fluid strategy should be considered for patients with acute respiratory distress syndrome without evidence of tissue hypoperfusion. In some cases. A target MAP greater than 65 mm Hg may be required in patients with baseline hypertension showing persistent signs of inadequate perfusion despite meeting MAP goal. Administration as a continuous infusion may lower the incidence of hyperglycemia and hypernatremia. evidence for a non-invasive approach is available. should be the first alternative agent in septic shock that is poorly responsive to first-line therapy. Gradually taper steroid therapy when vasopressors are no longer needed. obtain two or more blood cultures.g. Consider your community and hospital microorganism susceptibility patterns.CONSIDERATION FOR A NON-INVASIVE APPROACH The literature supporting a bundled approach to sepsis management that includes CVC insertion is robust and must not be minimized. Additional fluid resuscitation should be guided by clinical assessment of need and tolerance. . substituted for or in addition to norepinephrine. Albumin may be used in the initial resuscitation of patients who require substantial amounts of crystalloids. e. Routine ACTH stimulation testing is not recommended. Steroids – Patients with persistent hypotension despite fluid resuscitation and vasopressor support should receive hydrocortisone 200 mg/day.03 units/min may be started as adjunct to norepinephrine at a non-titrated dose. At least one blood culture should be percutaneous. Addressing Goals of Care – Despite optimal medical therapy. Fluid Therapy – Initial fluid resuscitation should consist of rapid delivery of at least 30 mL/kg of crystalloid. Epinephrine. Norepinephrine infused via central access is the initial vasopressor of choice. severe sepsis is a devastating illness that often results in either death or survival with poor quality of life. It is essential that goals of care be addressed with patients and their families as early as is feasible. Antibiotics and Source Control – Broad spectrum intravenous anti-infective therapy should be started as soon as possible and within the first hour of recognition of severe sepsis. abscess drainage or tissue debridement. Potentially infected catheters should be removed promptly after other access is established. Before starting antibiotics. Initial empiric therapy should include one or more drugs that have activity against all likely pathogens (to include antifungals) that penetrate in adequate concentrations into the presumed source of sepsis. Physicians should establish realistic treatment goals and incorporate these goals of care into the treatment plan. Once vasopressors are initiated. Although further trials comparing the two approaches are in order. Rather than using CVP and ScVO2. Evaluate for a focus of infection and initiate source control. a non-invasive strategy should be considered in selected patients for whom placement of a central line is not feasible or incongruent with the patient’s goals of care. Vasopressin 0. proponents of this approach suggest use of dynamic IVC ultrasound to guide fluid administration along with lactate clearance of greater than 10% to guide further therapy. Dopamine should only be used in highly selected patients with bradycardia and low risk of tachyarrhythmia. Vasopressors – Start vasopressor therapy when fluid challenge fails to restore mean arterial pressure to ≥ 65 mmHg or prior to fluid resuscitation in the presence of very low MAP. provision of less aggressive treatments or withdrawal of life-sustaining measures may be in the patient’s best interest. Inotropic Therapy – Consider dobutamine in patients with ongoing evidence of hypoperfusion despite achieving adequate volume resuscitation and adequate mean arterial pressure. an arterial catheter should be placed as resources and time permit. Evidence is available that may support a practitioner’s decision to utilize such an approach in selected patients. Do not arbitrarily increase cardiac index to achieve an elevated level of oxygen delivery. however.

Blood Product Administration • Transfuse red blood cells when hemoglobin is < 7. et al. Lung Protective Strategy: Ventilation with Low Tidal Volumes • Avoid high tidal volume coupled with high plateau pressures by decreasing tidal volumes to 6 mL/kg (based on ideal body weight) with the goal of maintaining end-inspiratory plateau pressures < 30 cm H2O. Glucose Control – After the first six hours.32(8):1637-42.. Rivers EP. e.0-9. . CCM 2001(29)7 Martin GS et al. 29:352–360 Gaieski D. et al. or acute hemorrhage. 2004 Aug. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. • Raise head of bed 30-45 degrees (unless contraindicated) to prevent ventilator-acquired pneumonia. PCV or APRV for potentially injurious FiO2 or plateau pressure > 30 cm H2O.0 g/dL to a target of 7. • Consider alternative ventilation modes.46:S4. • Consider permissive hypercapnia (allowing PaCO2 to increase above its pre-morbid baseline) in patients with ARDS if needed to minimize plateau pressures and tidal volumes. Monitor blood glucose every 60 minutes until stabilized. Dellinger RP. Zeserson E. Consider higher platelet goal (50. Mortality benefit after implementation of early goal directed therapy protocol for the treatment of severe sepsis and septic shock.org References Bendjelid K. Arnold RC. Angus DC.0 g/dL. JAMA. Chase M. CCM 2013 (41)2 SSC: survingsepsis. 2009 Jul. (348)2 Dellinger RP. Ressler JA. NEJM 2003. the user must ultimately rely on current literature and the manufacturer’s product and package insert for additional information on the product’s recommended use. or may be used in combination with ScVO2 normalization. Trzeciak S. NEJM 2003 (348)16 Hotchkiss RS et al. Emergency Medicine Shock Research Network (EMShockNet) Investigators. Nguyen HB. • Set PEEP based on the severity of oxygenation deficit. Muzzin A. Parrillo JE. Jacobsen G. Jones AE.32(1):35-9. Goyal M. • Transfuse blood products to correct coagulopathy only in patients with active bleeding or planned invasive procedures. 2010 Feb. McCoy J.. Tomlanovich MC. then every 4 hours. In each individual case.000/mm3) for surgery or invasive procedures. Deep Vein Thrombosis and Stress Ulcer Prophylaxis – Administer prophylactic low molecular weight heparin or unfractionated heparin. Crit Care Med. Provide stress ulcer prophylaxis with either H2 receptor or proton pump inhibitors. Shapiro NI. Intensive Care Med 2003. Knoblich BP. Schorr C. • Transfuse platelets when count is <10. maintain blood glucose <180 mg/dL using continuous or intermittent insulin. Pope J. Shapiro NI. Use a mechanical compression device for patients with a contraindication to LMWH or UFH. Consider higher transfusion thresholds for patients with severe hypoxemia. 2005. Shock. Romand JA: Fluid responsiveness in mechanically ventilated patients: A review of indices used in intensive care.g. Ann Emerg Med. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Derived from the Levy MM et all CM 2003 (3)4 Osborn TM et al AEM 2005 (46)3 Dillenger RP et al. or if count is < 20... More recent analyses have provided evidence suggesting improved prophylaxis with proton pump inhibitors compared to H2 receptor blockers.000/mm3 with significant bleeding risk.000/mm3 regardless of bleeding. active ischemic coronary disease. Jones AE. The use of lactate clearance may be a feasible option for patients in whom ScVO2 is unavailable. CCM 2013 (41)2 ©2013 This card should be used only as a guideline. Emergency Medicine Shock Research Network (EMShockNet) Investigators.303(8) Multicenter study of early lactate clearance as a determinant of survival in patients with presumed sepsis. warnings and contraindications. Lactate Clearance – The inability to clear lactate during sepsis is associated with a higher mortality rate compared to patients who are able to clear their serum lactate early in resuscitation. et al.. Proning the patient is another option. Casner E.

MAP ≥ 65 mm Hg Scv02 ≥ 70% < 70% Oxygen Delivery If ScVO2 remains < 70%. oxygen delivery must be further optimized with pRBC transfusion and/or inotrope therapy: Transfuse two units pRBC’s for Hgb < 7g/dl or consider for Hgb < 10g/dl if ischemic heart disease or hypoxia. NEJM.SEPSIS BUNDLE GOALS FOR SEVERE SEPSIS/SEPTIC SHOCK: (PROTOCOL-DRIVEN SYSTEM RECOMMENDED) TO BE COMPLETED WITHIN 3 HOURS 1) Measure lactate level.* *Targets for quantitative resuscitation included in the guidelines are CVP of 8 mm Hg. ScvO2 of 70%. 29:352–360 Gaieski D. TO BE COMPLETED WITHIN 6 HOURS 5) Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) 65 mm Hg. Give Fluid: Give 500-1000 mL crystalloid boluses q30 minutes until CVP goal achieved. Norepinephrine: NE is the vasopressor of choice in the treatment of septic shock. Initiate inotrope therapy: Dobutamine 2-5 mcg/kg/min Goal Achieved Rivers E. 3) Administer broad spectrum antibiotics. Vasopressin: 0.345:1368-1377 . 4) Administer 30 mL/kg crystalloid for hypotension or lactate ≥ 4mmol/L. et al. et al.* – Measure central venous oxygen saturation (ScvO2). CVP CVP ≥ 8-12 mm Hg MAP < 65 mm Hg MAP Vassopressor If MAP <65.46:S4 Sepsis Pathway Lactate ≥ 4 mmol/L or persistent hypotension despite 30 mL/kg crystalloid or colloid equivalent Broad Spectrum Antibiotics < 8 mm Hg Central Line Placement for CVP/Scv02 Monitoring Fluid Bolus If CVP < 8 (< 12 if mechanically ventilated).* 7) Remeasure lactate if initial lactate was elevated. et al. initiate vasopressors. 6) In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate ≥ 4 mmol/L (36 mg/dL): – Measure central venous pressure (CVP). 2001. ICM 2003. Bendjelid K. 2) Obtain blood cultures prior to administration of antibiotics.03 units/min IV as adjunct to NE Epinephrine: Preferred 2nd line agent added to or substituted for NE Place arterial catheter as time and resources allow. then 150 mL/hr. and normalization of lactate. AEM 2005. Consider albumin boluses for patients requiring substantial amounts of crystalloid.

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