Educational resource · Not a medical device · Infectious diseases review in progress · Does not replace clinical judgement

Diagram — Sepsis and septic shock — SeptiMap

trace the path from infection to organ failure and state the Sepsis-3 definitions of sepsis and septic shock. Educational resource, not a medical device.

Diagrams: mechanisms and principles

17 sourced diagrams · for medical students and practice

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Clinical years · OSCE

Sepsis and septic shock

Objective: trace the path from infection to organ failure and state the Sepsis-3 definitions of sepsis and septic shock.

Step 6 / 6
Sepsis and septic shock1. Recognition — Pathogen molecular patterns (PAMPs: endotoxins, β-glucans…) bind innate immune receptors (TLR, NOD, RIG-I, C-type lectins). 2. Two responses from the start — Sepsis activates early pro- and anti-inflammatory responses; the initial phase is often followed by prolonged immunosuppression. 3. Endothelium — Loss of barrier function, vasodilation, leucocyte adhesion and a procoagulant state. 4. Coagulation and microcirculation — Activated coagulation forms microthrombi: local perfusion defects, tissue hypoxia, organ dysfunction. 5. Sepsis definition — Sepsis-3: life-threatening organ dysfunction caused by a dysregulated host response to infection; identified by a SOFA rise of at least 2 points. 6. Septic shock definition — Vasopressors needed for MAP ≥ 65 mmHg and lactate > 2 mmol/L despite adequate fluids. These are definitions, not a management protocol.Infection: PAMPs (endotoxins,fungal β-glucans…)Innate immune receptors:TLR, NOD, RIG-I, C-type lectinsPro-inflammatoryresponseAnti-inflammatoryresponseProlongedimmunosuppressionEndothelium: leak,vasodilation,procoagulantCoagulation → microthrombi →hypoperfusion, tissue hypoxiaSepsis: organ dysfunction(SOFA rise ≥ 2 points)Septic shock: vasopressors forMAP ≥ 65 mmHg and lactate > 2 mmol/Ldespite adequate fluids
  • Pathogen
  • Immunity
  • Toxin, damage
  • Clinical consequence

Key points

  • Sepsis: organ dysfunction from a dysregulated host response (SOFA rise of 2 or more).
  • Septic shock: vasopressors for MAP ≥ 65 mmHg and lactate > 2 mmol/L despite fluids.
  • Endothelium and coagulation link infection to organ failure.

Classic pitfall

Reducing sepsis to a “cytokine storm”: anti-inflammatory responses start early and immunosuppression may later dominate.

Related pathogen pages (6)

Sources

Educational content · Illustrative mechanisms · Not applicable to individual clinical decisions · MDR 2017/745

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