Sepsis & SHOCK

Serratia marcescens

Serratia marcescens

Today we discussed a case of a patient with history of CHF ( EF 30%) and gout (recent R ankle & knee arthrocentesis 1 month ago) who presented with right ankle  pain, found to have profound hypotension, tachycardia, tachypnea, AKI, anuria, and lactic acidosis to 8--along with peripheral edema, JVP to the mandible, and cool extremities. The patient was ultimately found to have septic shock from Serracia marcescens septic joint infection and bacteremia, thought to be from inoculation from previous arthrocentesis--and cardiogenic shock requiring inotropic support. Besides Serracia species being an uncommon cause of skin and soft tissue infections, some learning points:

1) New definitions for sepsis and septic shock: The Sepsis-3 Consensus was published in February 2016 in JAMA, defining sepsis as NOT SIRS + infectious source, but rather "life-threatening organ dysfunction due to dysregulated host response to infection." SIRS criteria are not specific (capturing people with non-infectious/non-life threatening situations). So, the SOFA (Sequential Organ Failure Assessment) score was validated in this large retrospective study to capture the sickest patients. Mortality can be estimated from the calculated full SOFA score.

A quick bedside assessment comes from the qSOFA score below (put your sepsis HAT on), a point for each and 2 or more with a source of infection is concerning for sepsis:

  • Hypotension: SBP <100
  • AMS
  • Tachypnea: RR> 20

2) Pressor choice is guided by the clinical picture, pairing the type of shock with the receptor activity of the agents:

This is case illustrates a time to consider a Swan-Ganz or pulmonary artery catheter to distinguish distributive from cardiogenic shock and also to monitor resuscitative efforts and inotrope use.

3) What is SvO2? The percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart. This is drawn from a central line and tells us if the cardiac output and oxygen delivery is high enough to meet the patient's needs. If SvO2 is low, compensation is first increasing cardiac output, then increasing tissue oxygen extraction, then anaerobic metabolism (increasing lactic acid production). 

Delivery of oxygen=

cardiac output (HR x stroke volume) x oxygen content (Hgb x SaO2)

Clinically, if a septic patient has an Sv02 <70%, using the equation above, this means the CO is too low (think inotropes or fluids to increase preload and SV), hemoglobin is too low (think blood transfusion), or SaO2 is too low (think pressors, supplemental oxygen).