Sandbox Sepsis medical therapy: Difference between revisions

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1. A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible. {{GRADE1|C}}
1. A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible. {{GRADE1|C}}
2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred. {{GRADE2|B}}
2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred. {{GRADE2|B}}
3. When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess).
3. When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess).
4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established.
4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established.
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Revision as of 20:03, 3 March 2015


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The "Surviving Sepsis Campaign" was an international effort organized by physicians that developed and promoted widespread adoption of practice improvement programs grounded in evidence-based guidelines. The goal was to improve diagnosis and treatment of sepsis. Included among the guidelines were sepsis screening for high-risk patients; taking bacterial cultures soon after the patient arrived at the hospital; starting patients on broad-spectrum intravenous antibiotic therapy before the results of the cultures are obtained; identifying the source of infection and taking steps to control it (e.g., abscess drainage); administering intravenous fluids to correct a loss or decrease in blood volume; and maintaining glycemic (blood sugar) control. These and similar guidelines have been tested by a number of hospitals and have shown potential for decreasing hospital mortality due to sepsis.[1][2]

Medical Therapy

The delay in administering therapy after sepsis has been recognized, is the main problem in the adequate management of septic patients. For every hour delay in the administration of appropriate antibiotic therapy there is an associated 7% rise in mortality. A large international collaboration was established to educate people about sepsis and to improve patient outcomes with sepsis, entitled the "Surviving Sepsis Campaign".

Early Goal Directed Therapy (EGDT)

Early Goal Directed Therapy (EGDT), developed at Henry Ford Hospital by E. Rivers, MD, is a systematic approach to resuscitation that has been validated in the treatment of severe sepsis and septic shock.[3] It is meant to be started in the Emergency Department. The theory is that one should use a step-wise approach, having the patient meet physiologic goals, to optimize cardiac preload, afterload, and contractility, thus optimizing oxygen delivery to the tissues.

Although initial studies reported benefit from EGDT,[4][3][5] the more recent ProCESS[6] and ARISE[7] trials failed to demonstrate any benefit. However, the outcomes in the control groups of these trials were much more favorable than in the earlier trials. The extent of protocol-based care in the 'usual care' of the control groups is not known.

In Early Goal Directed Therapy:

  • Fluids are administered until the central venous pressure (CVP), as measured by a central venous catheter, reaches 8-12 cm of water (or 10-15 cm of water in mechanically ventilated patients).
  • If the mean arterial pressure is less than 65 mmHg or greater than 90 mmHg, vasopressors or vasodilators are given as needed to reach the goal.
  • The central venous saturation (ScvO2), i.e. the oxygen saturation of venous blood as it returns to the heart as measured at the superior vena cava, is optimized. If the ScvO2 is less than 70%, blood is given to reach a hemoglobin of 10 g/dl and then inotropes are added until the ScvO2 is optimized. Elective intubation may be performed to reduce oxygen demand if the ScvO2 remains low despite optimization of hemodynamics.
  • Urine output is also monitored, with a goal of 0.5 mL/kg/h. In the original trial, mortality was cut from 46.5% in the control group to 30.5% in the intervention group. The Surviving Sepsis Campaign guidelines recommends EGDT for the initial resuscitation of the septic patient with a level B strength of evidence.

GENESIS Project

The protocol per the GENESIS Project is:[5]

  • Measure serum lactate
  • Obtain blood cultures and administer broad-spectrum antibiotic within 3 hours of emergency department admission
  • If hypotensive or serum lactate 4 mmol/L:
    • Administer 20 mL/kg of crystalloid
    • If needed, add vasopressors to keep mean arterial pressure >65 mm Hg
    • If needed, aim for central venous pressure 8 mm Hg
    • If needed, aim for central venous oxygen saturation 70%

Standard treatment of infants with suspected sepsis consists of supportive care, maintaining fluid status with intravenous fluids, and the combination of a beta-lactam antibiotic (such as ampicillin) with an aminoglycoside such as gentamicin.

Transfusion

In septic shock, leukoreduced erythrocyte transfusion is associated with similar clinical outcomes (90 day mortality and ischemic events) among patients who are administered erythrocyte transfusion at a hemoglobin threshold of 7 g/dL compared to those who receive it at a higher threshold of 9 g/dL.[8]

Contraindicated Medications

Sepsis is considered an absolute contraindication to the use of the following medications:

2012 Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock (DO NOT EDIT)[9]

Initial Resuscitation and Infection Issues

Initial Resuscitation

1. Protocolized, quantitative resuscitation of patients with sepsis-induced tissue hypoperfusion (hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmol/L). Goals during the first 6 hrs of resuscitation:

  • Central venous pressure 8–12 mm Hg
  • Mean arterial pressure (MAP) ≥ 65 mm Hg
  • Urine output ≥ 0.5 mL/kg/hr
  • Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively. (Grade 1C)

2. In patients with elevated lactate levels targeting resuscitation to normalize lactate. (Grade 2C)

Screening for Sepsis and Performance Improvement

1. Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy. (Grade 1C)

2. Hospital–based performance improvement efforts in severe sepsis.

Diagnosis

1. Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s). (Grade 1C) At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted. (Grade 1C)

2. Use of the 1,3 beta-D-glucan assay (Grade 2B), mannan and anti-mannan antibody assays (Grade 2C), if available and invasive candidiasis is in differential diagnosis of cause of infection.

3. Imaging studies performed promptly to confirm a potential source of infection.

Antimicrobial Therapy

1. Administration of effective intravenous antimicrobials within the first hour of recognition of septic shock (Grade 1B) and severe sepsis without septic shock (Grade 1C) as the goal of therapy.

2a. Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis. (Grade 1B)

2b. Antimicrobial regimen should be reassessed daily for potential deescalation. (Grade 1B)

3. Use of low procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection. (Grade 2C)

4a. Combination empirical therapy for neutropenic patients with severe sepsis (Grade 2B) and for patients with difficult-to-treat, multidrug- resistant bacterial pathogens such as Acinetobacter and Pseudomonas spp. (Grade 2B) For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia. (Grade 2B) A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections. (Grade 2B)

4b. Empiric combination therapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known. (Grade 2B)


5. Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia. (Grade 2C) 6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin. (Grade 2C) 7. Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause.

Source Control

1. A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible. (Grade 1C)

2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred. (Grade 2B)

3. When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess).

4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established.

Infection Prevention

1a. Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of ventilator-associated pneumonia; This infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective. (Grade 2B)

1b. Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of ventilator-associated pneumonia in ICU patients with severe sepsis. (Grade 2B)

References

  1. "Products - Data Briefs - Number 62 - June 2011". Retrieved 2012-09-17.
  2. Wiedermann CJ, Adamson IY, Pert CB, Bowden DH (1988). "Enhanced secretion of immunoreactive bombesin by alveolar macrophages exposed to silica". Journal of Leukocyte Biology. 43 (2): 99–103. PMID 2826633. Retrieved 2012-09-17. Unknown parameter |month= ignored (help)
  3. 3.0 3.1 Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B; et al. (2001). "Early goal-directed therapy in the treatment of severe sepsis and septic shock". N Engl J Med. 345 (19): 1368–77. PMID 11794169. Review in: ACP J Club. 2002 May-Jun;136(3):90
  4. Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA; et al. (2010). "Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial". JAMA. 303 (8): 739–46. doi:10.1001/jama.2010.158. PMID 20179283.
  5. 5.0 5.1 Cannon CM, Holthaus CV, Zubrow MT, Posa P, Gunaga S, Kella V; et al. (2012). "The GENESIS Project (GENeralized Early Sepsis Intervention Strategies): A Multicenter Quality Improvement Collaborative". J Intensive Care Med. doi:10.1177/0885066612453025. PMID 22902347.
  6. ProCESS Investigators. Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA; et al. (2014). "A randomized trial of protocol-based care for early septic shock". N Engl J Med. 370 (18): 1683–93. doi:10.1056/NEJMoa1401602. PMC 4101700. PMID 24635773. Review in: Ann Intern Med. 2014 Jun 17;160(12):JC9
  7. The ARISE Investigators and the ANZICS Clinical Trials Group (2014). "Goal-Directed Resuscitation for Patients with Early Septic Shock". N Engl J Med. doi:10.1056/NEJMoa1404380. PMID 25272316.
  8. Holst LB, Haase N, Wetterslev J, Wernerman J, Guttormsen AB, Karlsson S; et al. (2014). "Lower versus higher hemoglobin threshold for transfusion in septic shock". N Engl J Med. 371 (15): 1381–91. doi:10.1056/NEJMoa1406617. PMID 25270275.
  9. Dellinger, R. Phillip; Levy, Mitchell M.; Rhodes, Andrew; Annane, Djillali; Gerlach, Herwig; Opal, Steven M.; Sevransky, Jonathan E.; Sprung, Charles L.; Douglas, Ivor S.; Jaeschke, Roman; Osborn, Tiffany M.; Nunnally, Mark E.; Townsend, Sean R.; Reinhart, Konrad; Kleinpell, Ruth M.; Angus, Derek C.; Deutschman, Clifford S.; Machado, Flavia R.; Rubenfeld, Gordon D.; Webb, Steven A.; Beale, Richard J.; Vincent, Jean-Louis; Moreno, Rui; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup (2013-02). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. ISSN 1530-0293. PMID 23353941. Check date values in: |date= (help)