Pathophysiology

Sepsis occurs when the body’s immune response to an infection becomes dysregulated, causing widespread inflammation and cellular dysfunction. The inciting infection triggers immune activation and inflammatory mediator release (cytokines, chemokines, lipid mediators) which helps localize and eradicate the infection initially.

In sepsis, this response becomes amplified and systemic. The exaggerated immune response leads to endothelial damage, increased vascular permeability, impaired vasoregulation, and coagulopathy. Widespread inflammation, cellular injury, and microvascular thrombosis result in tissue hypoperfusion, cellular hypoxia, and multiorgan dysfunction.

Cardiovascular effects include myocardial depression, vascular dilation, and intravascular volume depletion. Respiratory effects include acute lung injury, impaired gas exchange, and altered ventilation perfusion matching.

Renal effects include acute tubular injury and reduced glomerular filtration.

Metabolic effects include impaired glucose regulation and mitochondrial dysfunction.

Central nervous system effects include altered mental status, encephalopathy, and seizures.

Disseminated intravascular coagulation can occur, depleting platelets and clotting factors.

Without intervention, cellular injury progresses, leading to shock, multiorgan failure, and potentially death.