What is the definition of sepsis and septic shock in clinical practice?

Definition of Sepsis and Septic Shock

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, operationalized by an acute increase in the Sequential Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with in-hospital mortality greater than 10%. 1, 2, 3

Sepsis Definition (Sepsis-3 Criteria)

The current definition framework, established in 2016 and endorsed by the Society of Critical Care Medicine and European Society of Intensive Care Medicine, fundamentally shifted away from inflammation-focused criteria to emphasize organ dysfunction 1, 3:

• Organ dysfunction is the defining feature, represented by an increase in SOFA score of ≥2 points from baseline 2, 3
• The previous concepts of SIRS (Systemic Inflammatory Response Syndrome) and "severe sepsis" are no longer used in clinical practice 2, 4
• This definition replaced the outdated 1991 and 2001 consensus definitions that relied heavily on inflammatory markers (temperature, heart rate, respiratory rate, white blood cell count) which proved to have inadequate specificity and sensitivity 3, 4

Quick SOFA (qSOFA) for Rapid Bedside Screening

For patients outside the ICU with suspected infection, qSOFA provides rapid risk stratification 2, 3:

• Respiratory rate ≥22 breaths/min
• Altered mental status (Glasgow Coma Scale score ≤13)
• Systolic blood pressure ≤100 mmHg

Presence of at least 2 of these 3 criteria suggests higher risk of poor outcomes and should prompt consideration of sepsis 2, 3. However, qSOFA is a screening tool, not a diagnostic criterion—the formal diagnosis still requires SOFA score assessment 3.

Septic Shock Definition

Septic shock is a subset of sepsis with particularly profound circulatory, cellular, and metabolic abnormalities, clinically identified by the requirement for vasopressor therapy to maintain mean arterial pressure ≥65 mmHg AND serum lactate level >2 mmol/L (>18 mg/dL) in the absence of hypovolemia. 2, 5, 6, 3

Key Diagnostic Criteria

Both criteria must be present simultaneously after adequate fluid resuscitation 5, 6, 3:

1. Vasopressor requirement to maintain MAP ≥65 mmHg
2. Lactate >2 mmol/L (>18 mg/dL) despite adequate volume resuscitation

This combination is associated with hospital mortality rates greater than 40%, substantially higher than sepsis without shock 5, 3.

Pathophysiological Mechanisms

Septic shock involves multiple interconnected abnormalities 5, 6:

• Profound vasodilation and increased vascular permeability leading to distributive shock 5, 6
• Microcirculatory dysfunction causing tissue hypoperfusion despite adequate macrocirculatory parameters 5, 6
• Altered cellular metabolism resulting in lactate accumulation even with adequate oxygen delivery 5, 6

Clinical Implications for Practice

Early Recognition is Critical

Early identification and appropriate management in the initial hours after sepsis develops improves outcomes and reduces mortality 1, 2, 7:

• Sepsis represents a medical emergency similar to acute myocardial infarction or stroke 1
• The pathophysiology involves dysregulated inflammatory response leading to multi-organ failure 2, 7
• Patient factors including age, comorbidities, and immune status significantly affect disease course 2

Common Pitfalls to Avoid

When identifying septic shock, clinicians frequently make these errors 6:

• Failing to measure lactate levels, which are essential for diagnosis according to current definitions 6
• Delaying vasopressor initiation while continuing excessive fluid administration 5, 6
• Not recognizing perfusion abnormalities despite normal blood pressure in patients already receiving vasopressors 5, 6
• Confusing septic shock with other forms of distributive shock (anaphylactic, neurogenic), leading to inappropriate management 6

Special Population Considerations

Certain patient populations require heightened clinical suspicion 2:

• Elderly patients may present with attenuated inflammatory responses and fewer clinical signs despite severe infection 2, 5
• Immunocompromised patients (HIV-positive, transplant recipients, chemotherapy patients) have increased susceptibility due to pre-existing immune system activation and exhaustion 2, 5
• The inflammatory response depends on both the causative pathogen (>90% bacterial, with Gram-negative and Gram-positive organisms equally frequent) and host genetic characteristics 2

Evolution from Previous Definitions

Understanding the historical context clarifies why current definitions are superior 3, 4:

• The 1991 definition focused excessively on inflammation and the misleading model that sepsis follows a continuum through "severe sepsis" to shock 3
• SIRS criteria (used 1991-2016) had poor specificity—many non-infectious conditions trigger SIRS, and many septic patients lack SIRS criteria 3, 4
• The 2016 Sepsis-3 definitions improved specificity and eliminated the redundant term "severe sepsis" 3, 4