Topic 19 — Sepsis and Septic Shock

Connect the major mechanisms, clinical features and outcomes for rapid revision.

1. THE TOPIC IN ONE CONNECTED FLOW

Sepsis develops when infection triggers a dysregulated host response that spreads beyond local defence and begins to injure the patient’s own tissues. The key connection is infection → inflammatory and endothelial dysfunction → abnormal coagulation and circulation → tissue hypoperfusion → organ dysfunction, with septic shock representing the severe circulatory and metabolic end of this process.

Infection

Gram-negative, gram-positive or fungal organisms

→

Innate Immune Recognition

PAMPs and DAMPs activate pattern-recognition receptors

→

Inflammatory Activation

TNF, IL-1 and other mediators activate endothelium

→

Vascular + Coagulation Dysfunction

Vasodilation, capillary leakage and microthrombi

→

Tissue Hypoperfusion

Reduced and uneven capillary oxygen delivery

→

Organ Dysfunction

Brain, kidneys, lungs and other organs become impaired

→

Septic Shock

Profound circulatory, cellular and metabolic failure

2. KEY CLINICAL CONNECTIONS

Hypotension + Tissue Edema

Endothelial activation
→
vasodilation + increased permeability
→
reduced effective circulating volume
→
hypotension and poor tissue perfusion.

Oliguria + Confusion

Microcirculatory failure
→
reduced renal and cerebral perfusion
→
reduced urine output and altered mental status
→
organ dysfunction.

Microthrombi + Bleeding

Inflammation activates coagulation
→
fibrin deposition in small vessels
→
factor and platelet consumption
→
DIC with thrombosis and bleeding.

3. AIM HIGH-YIELD INTEGRATION REVIEW

⭐ Infection + organ dysfunction
→
think sepsis; bacteremia itself is not the defining feature.

Gram-negative, gram-positive and fungal organisms
→
all can trigger the dysregulated host response.

⭐ PAMPs/DAMPs + pattern-recognition receptors
→
cytokine release and widespread innate immune activation.

TNF and IL-1 + endothelial activation
→
systemic vascular and inflammatory effects.

⭐ Vasodilation + capillary leakage
→
falling vascular resistance and reduced effective circulating volume.

Coagulation activation + microthrombi
→
impaired microcirculation and possible DIC.

Microcirculatory failure + cellular metabolic disturbance
→
progressive tissue hypoxia and organ dysfunction.

⭐ Septic shock
→
not simply low blood pressure; it reflects profound circulatory, cellular and metabolic dysfunction.

AIM Exam Trap:
Sepsis is not synonymous with bacteremia. The key concept is infection-associated dysregulated host response producing organ dysfunction.