Sepsis — Viva

Q1: Definition and classification (2 min)

"Define sepsis and septic shock."

• Sepsis (Singer 2016): life-threatening organ dysfunction caused by a dysregulated host response to infection. Operationally an increase in SOFA of 2 points or more (in-hospital mortality greater than 10%). SIRS and “severe sepsis” retired.^[1]
• Septic shock: vasopressor requirement to maintain MAP of 65 mm Hg or greater AND lactate greater than 2 mmol/L in the absence of hypovolaemia — hospital mortality greater than 40%.^[1]
• qSOFA: at least 2 of RR ≥22/min, altered mentation, SBP ≤100 mm Hg. SSC 2021 recommends against qSOFA as a single screening tool vs SIRS/NEWS/MEWS.^[1][2]

Q2: Pathophysiology (2 min)

Qualitative teaching: dysregulated host response (vasoplegia, capillary leak, cytopathic hypoxia). Do not quote unsourced cytokine percentages. Anchor the definitions to Singer, not a memorised mediator list.^[1]

Q3: Recognition (2 min)

Suspect infection plus new organ dysfunction. qSOFA is a prompt, not the sole screen. Lactate >2 mmol/L is the Sepsis-3 shock metabolic criterion with vasopressors — not an SSC 2021 “4 mmol/L fluid trigger.”^[1][2]

Q4: Early resuscitation (3 min)

• Shock / high-likelihood sepsis: antimicrobials immediately, ideally within 1 h of recognition.^[2]
• Possible sepsis without shock: rapid assessment within 3 h of presentation; if concern persists, antimicrobials within 3 h of first recognition (weak).^[2]
• ≥30 mL/kg IV crystalloid within 3 h for sepsis-induced hypoperfusion or septic shock (weak). Balanced crystalloid preferred; no starches. CLOVERS 90-day death 14.0% vs 14.9% (restrictive vs liberal; not significantly different).^[2][7]
• Norepinephrine first-line. Add vasopressin 0.03 units/min rather than escalating norepinephrine (often from 0.25–0.5 μg/kg/min).^[2]
• SEPSISPAM: MAP 80–85 vs 65–70 — no mortality difference (28-day 36.6 vs 34.0%); more new AF at the higher target; chronic-hypertension subgroup needed less RRT at the higher target.^[4]
• Hydrocortisone 200 mg/day (50 mg q6h or infusion) for ongoing vasopressor-dependent shock. APROCCHSS 90-day mortality 43.0% vs 49.1% (RR 0.88).^[2][5]
• Kumar: after hypotension, each hour of antimicrobial delay over 6 h — average 7.6% decrease in survival. Do not say “4% mortality per hour.”^[3]

Q5: What is not supported

• IV vitamin C: LOVIT composite death or persistent organ dysfunction 44.5% vs 38.5% (vitamin C vs placebo).^[6]
• Paediatric boluses without ICU: FEAST 48-hour mortality higher with boluses (albumin 10.6%, saline 10.5%, control 7.3%).^[8]
• Named mg antibiotic cocktails unless quoted from a fetched formulary — use source-directed broad-spectrum IV therapy.

Examiner notes

Fail a candidate who teaches lactate ≥4 as the SSC 2021 fluid trigger, qSOFA as the only screen, Kumar as 4% mortality/hour, or SEPSISPAM as “higher MAP harms chronic hypertensives.”

References8ShowHide

1. [1]Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903338
2. [2]Evans L, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021 Intensive Care Med, 2021.PMID 34599691
3. [3]Kumar A, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock Crit Care Med, 2006.PMID 16625125
4. [4]Asfar P, et al. High versus low blood-pressure target in patients with septic shock N Engl J Med, 2014.PMID 24635770
5. [5]Annane D, et al. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock N Engl J Med, 2018.PMID 29490185
6. [6]Lamontagne F, et al. Intravenous Vitamin C in Adults with Sepsis in the Intensive Care Unit N Engl J Med, 2022.PMID 35704292
7. [7]Shapiro NI, et al. Early Restrictive or Liberal Fluid Management for Sepsis-Induced Hypotension N Engl J Med, 2023.PMID 36688507
8. [8]Maitland K, et al. Mortality after fluid bolus in African children with severe infection N Engl J Med, 2011.PMID 21615299