Sepsis and Septic Shock

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection, and septic shock is its most severe form, defined by circulatory and metabolic abnormalities that substantially increase the risk of death. It is one of the central syndromes of critical and emergency nursing because it is common, rapidly progressive, and highly time-sensitive.

Definition

Under the Sepsis-3 consensus, sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, operationalised as an acute increase of at least two points in the Sequential Organ Failure Assessment (SOFA) score; septic shock is a subset in which persisting hypotension requires vasopressors to maintain mean arterial pressure and serum lactate remains elevated despite adequate fluid resuscitation (Singer, 2016).

Scope

This entry covers the consensus definition of sepsis and septic shock, the underlying pathophysiology of the dysregulated host response, the concepts used to recognise and grade severity (organ dysfunction and lactate/vasopressor criteria), and the epidemiologic burden of the syndrome. It is a conceptual reference and does not provide resuscitation protocols, fluid or antibiotic dosing, or individualized management instructions.

Core questions

• What separates sepsis from an uncomplicated infection?
• How is organ dysfunction operationalised in the Sepsis-3 definition?
• What distinguishes septic shock from sepsis without shock?
• Why is time to recognition considered central to sepsis outcomes?

Key concepts

• Dysregulated host response to infection
• Organ dysfunction and the SOFA score
• Septic shock (vasopressor requirement plus elevated lactate)
• Tissue hypoperfusion and hyperlactataemia
• Quick SOFA (qSOFA) as a bedside screening concept
• Source of infection and source control
• Capillary leak and distributive shock physiology

Mechanisms

Sepsis begins when the immune system mounts a response to infection that becomes dysregulated, producing both excessive inflammation and immune dysfunction. Pro-inflammatory and anti-inflammatory mediators, complement activation, and endothelial injury lead to widespread vasodilation, increased capillary permeability with fluid leak into tissues, microvascular thrombosis, and impaired cellular oxygen utilisation (Angus, 2013). The result is distributive shock with relative and absolute hypovolaemia, maldistribution of blood flow, and progressive organ dysfunction. In septic shock, hypotension and hyperlactataemia persist despite fluid resuscitation, reflecting both circulatory failure and a cellular metabolic derangement (Singer, 2016).

Clinical relevance

Sepsis is one of the most consequential syndromes a critical care or emergency nurse encounters, and understanding its definition and pathophysiology underpins recognition of the deteriorating patient. This entry explains how sepsis is defined and studied and how its severity is graded; it is a reference resource and is not a basis for individual diagnosis, antibiotic selection, fluid prescription, or other treatment decisions, which follow current institutional and clinical guidelines.

Epidemiology

Sepsis is a leading cause of death among critically ill patients and accounts for a large global burden of mortality and intensive care utilisation (Angus, 2013). Incidence estimates vary widely with case definition and ascertainment method, and reported mortality is higher for septic shock than for sepsis without shock. Large trials of early resuscitation strategies have refined the evidence base on how the syndrome is managed (Mouncey, 2015).

History

The terminology of sepsis has evolved through successive consensus conferences. Early definitions in the 1990s framed sepsis as infection plus the systemic inflammatory response syndrome (SIRS), with 'severe sepsis' and 'septic shock' as escalating tiers. The 2016 Sepsis-3 consensus redefined sepsis around organ dysfunction rather than inflammatory signs, discarded the term 'severe sepsis', and introduced the qSOFA screening concept (Singer, 2016). The Surviving Sepsis Campaign has periodically synthesised the management evidence into international guidelines (Evans, 2021).

Debates

Is qSOFA an adequate screening tool for sepsis?

The Sepsis-3 group proposed qSOFA as a simple bedside prompt, but its sensitivity for early identification has been questioned, and guidelines caution against using it as a single screening test in isolation.

How aggressive should early protocolised resuscitation be?

After early-goal-directed therapy was popularised, large randomised trials found that strict protocolised resuscitation did not improve survival over usual care, reshaping how early sepsis management is framed.

Seminal works

• singer-2016
• angus-2013
• evans-2021

Frequently asked questions

What is the difference between sepsis and septic shock?

Sepsis is life-threatening organ dysfunction from a dysregulated response to infection; septic shock is the more severe subset in which low blood pressure requires vasopressors and lactate stays elevated despite fluid resuscitation, carrying a higher risk of death.

Why was the term 'severe sepsis' removed?

The 2016 Sepsis-3 consensus redefined sepsis itself as infection plus organ dysfunction, making the separate category of 'severe sepsis' redundant.