General pathology · Hemodynamic disorders
How septic shock develops !
- Mechanism
In septic shock the defence against infection runs out of control: mediators widen the vessels, make them leaky and switch on clotting.
Updated 2026-11-01
What it is
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is sepsis with hypotension that needs vasopressors and a high lactate despite adequate fluid replacement. Microbial components activate innate immune receptors, which release cytokines in excess. The result is vasodilation, capillary leak, disseminated clotting, myocardial depression and metabolic disturbance, often followed by immunosuppression.
Step by step
- Microbes or their products (lipopolysaccharide, peptidoglycan) activate receptors on macrophages, neutrophils and endothelium.
- TNF, IL-1 and IL-6 are released; complement generates C3a and C5a.
- Activated endothelium makes nitric oxide: arterioles dilate and pressure falls.
- Junctions between endothelial cells loosen: capillary leak, edema and less circulating volume.
- Tissue factor rises and natural anticoagulants fall: microthrombi and DIC.
- The myocardium is depressed, insulin resistance appears and oxygen extraction fails.
- Hypoperfusion and direct injury lead to multiorgan failure: lung, kidney, liver, brain.
- A later phase of immunosuppression favours new infections.
Clinical notes
- Superantigens of Staphylococcus aureus and Streptococcus pyogenes activate T cells en masse: toxic shock syndrome.
- Meningococcemia can move from fever to shock with purpura and DIC within hours.
- In hospitals in Medellín, researchers have studied how the site of infection affects the mortality of sepsis in the emergency department.
In the lab
- Lactate that is high and does not fall with fluids: a marker of severity.
- Blood cultures before antibiotics when possible; platelets and clotting tests to detect DIC.
Test yourself
Think of the answer, then tap the question to see it.
Which mediator mainly explains the vasodilation of septic shock?
Nitric oxide made by the endothelium and other cells activated by cytokines.
Which component of gram-negative bacteria triggers the septic response?
Lipopolysaccharide (endotoxin), recognised by Toll-like receptor 4.
How does a superantigen cause shock?
It links MHC class II molecules with T-cell receptors outside the normal site and activates a large fraction of T cells, which release cytokines en masse.
Why does sepsis favour DIC?
Because it raises tissue factor and lowers thrombomodulin, protein C and antithrombin, leaving coagulation without a brake.
Related
- Shock: types, stages and the organs it damages
- Disseminated intravascular coagulation: how consumption causes both clots and bleeding
- Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsis
- Mediators of inflammation: the table to know
Related conditions
- Sepsis and septic shock
- Toxic shock syndrome
- Meningococcal disease (meningococcemia)
- Disseminated intravascular coagulation
- Acute respiratory distress syndrome (ARDS)
- Acute kidney injury
- Community-acquired pneumonia
- Bacterial meningitis
Elsewhere in DurgiPedia
- Cytokines: the table to know
- Innate immunity (overview, barriers)
- Complement: three pathways, MAC, regulators
- Acute-phase response and fever (CRP, ESR, procalcitonin)
- Nitric oxide (NO)
Microorganisms
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Septic shock: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Shock: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Association between site of infection and in-hospital mortality in patients with sepsis admitted to emergency departments of tertiary hospitals in Medellin, Colombia (Revista Brasileira de terapia intensiva, 2019).
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Representative model, for educational purposes only.