What are the major changes in the definition of “sepsis” under the 3rd International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)?

Under Sepsis-3 [1], sepsis is defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection (suspected or confirmed)”. Systemic inflammatory response syndrome (SIRS) is no longer defined as part of the sepsis spectrum, and its criteria have been replaced by the Sequential Organ Failure Assessment (SOFA) with a change in score ≥2 (Table) having >10% in-hospital mortality. Septic shock is defined as hypotension requiring vasopressors to maintain a MAP ≥65 mm Hg and a lactate >2 mmol/L (18 mg/dL) despite adequate volume (>40% in-hospital mortality).

A bedside clinical tool “quickSOFA” (qSOFA), not meant to substitute for SOFA, is also proposed to identify patients primarily outside of the ICU who may be at high risk of adverse outcomes, based on the following criteria: systolic blood pressure ≤100 mmHg, respiratory rate ≥22/min, and altered mental status. A qSOFA score ≥2 is associated with poorer outcomes [1,2].

So what do these new guidelines mean for clinicians? Under the new terminology, “sepsis” now refers only to what was previously considered severe sepsis with or without shock, and those who may need more aggressive therapy, closer monitoring and possible transfer to an ICU [1,2]. As the guidelines stress, however, failure to meet qSOFA or SOFA criteria should by no means lead to a deferral or delay in evaluation or treatment of infection deemed necessary by clinicians, and SIRS criteria may still be useful in identification of infection [1]. It remains to be seen whether limiting the definition of sepsis to only patients with associated organ dysfunction will translate into an overall earlier diagnosis and improved prognosis for this condition. Stay tuned!

 

Table. Sequential (sepsis-related) organ failure assessment (SOFA) score (adapted from ref.1)____________________________________________________________________________________________________

                                                                                             Points

Parameter                                0                      1                      2                      3                      4

____________________________________________________________________________________________________

Pa02/Fi02                           ≥400                 <400                <300                 <200*          <100*

Platelets (no./mL)           >150,000         <150,000         <100,000         <50,000       <20,000

Bilirubin (mg/dL)            <1.2                  1.2-1.9              2.0-5.9             6.0-11.9       >12.0

MAP (mm Hg) or VP      MAP≥70         MAP<70          DPA≤5           DPA 5.1-15        DPA>15

Glascow Coma Scale       15                    13-14            10-12                    6-9                 3-6

Creatinine (mg/dL)        <1.2                 1.2-1.9           2.0-3.4                  3.5-4.9        >5.0

OR U.O.  (mL/dL)                                                                                              <500                <200

____________________________________________________________________________________________________

MAP= mean arterial pressure, VP=vasopressor (includes agents other than dopamine), DPA=dopamine (in mcg/kg/min for ≥1 hour);U.O.= urine output

*With respiratory support

References:

  1. Singer MS, Deutschman CS, Seymour CW, et al; The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315[8]:801-810. https://jamanetwork.com/journals/jama/fullarticle/2492881  
  2. Jacob JA. New Sepsis Diagnostic Guidelines Shift Focus to Organ Dysfunction. JAMA. 2016;213[8]:739-740. https://www.ncbi.nlm.nih.gov/pubmed/26903319

 

Contributed by Erik Kelly MD, Mass General Hospital, Boston, MA

What are the major changes in the definition of “sepsis” under the 3rd International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)?

Can syncope be related to pulmonary embolism (PE) in the absence of hemodynamic instability or right ventricular failure?

Although we often think of syncope caused by PE in the setting of right ventricular failure and shock, less serious PE can also cause syncope by triggering a vaso-vagal reflex as supported by several case reports (1). Further supporting the potential role of neurogenic cause of syncope in at least some cases of PE is a study demonstrating that patients with syncope as a presenting symptom of PE did not show a more serious clinical picture (e.g. shock) than those without syncope (1). In another study of the clinical presentation of acute PE, EKG signs of acute right ventricle overload was found in only 25% of patients with syncope (2).  So we shouldn’t rule out PE as cause of syncope just because signs of hemodynamic compromise are absent.

1.  Castelli R, Tarsia P, Tantardini G et al. Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope. Vascular Medicine 2003;8:257-261.

2. Miniati M, Cenci, Monti S, et al. Clinical presentation of acute pulmonary embolism: survey of 800 cases. PloS One 2012;7:e30891.

Can syncope be related to pulmonary embolism (PE) in the absence of hemodynamic instability or right ventricular failure?