Characteristics of Septic Shock
Septic shock is defined as a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities substantially increase mortality risk, characterized by hypotension requiring vasopressors to maintain mean arterial pressure ≥65 mmHg and serum lactate >2 mmol/L despite adequate fluid resuscitation. 1, 2
Definition and Diagnostic Criteria
- Septic shock is a life-threatening condition representing the most severe form of sepsis with significantly higher mortality rates (>40%) compared to sepsis alone 2, 3
- Requires the presence of both:
- Represents a state where underlying circulatory and cellular-metabolic abnormalities are profound enough to substantially increase mortality 1, 2
Hemodynamic Characteristics
- Hypotension (systolic BP <90 mmHg, MAP <70 mmHg, or decrease in systolic BP >40 mmHg from baseline) that persists despite adequate fluid resuscitation 1, 4, 5
- Requires vasopressor support (typically norepinephrine as first-line agent) to maintain adequate perfusion 1, 6
- May present with either:
Metabolic Abnormalities
- Elevated serum lactate (>2 mmol/L) indicating tissue hypoperfusion and cellular metabolic dysfunction 1, 2, 3
- Metabolic acidosis often present due to lactic acidosis and other metabolic derangements 1
- Hyperglycemia (plasma glucose >140 mg/dL) in the absence of diabetes 4
- Hyperlactatemia may persist despite restoration of blood pressure, indicating ongoing cellular dysfunction 1
Organ Dysfunction
- Acute alteration in mental status (confusion, lethargy, decreased consciousness) 1
- Oliguria (urine output <0.5 mL/kg/h for >2 hours) despite adequate fluid resuscitation 1, 4
- Respiratory dysfunction (tachypnea >20 breaths/min, PaO₂/FiO₂ <300) 1, 4
- Coagulation abnormalities (INR >1.5, aPTT >60s, thrombocytopenia <100,000/μL) 1, 4
- Liver dysfunction (hyperbilirubinemia >2 mg/dL) 1, 4
- Kidney dysfunction (creatinine increase ≥0.5 mg/dL) 1, 4
Inflammatory Response
- Dysregulated host response to infection with activation of inflammatory signaling pathways 1
- Recognition of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) triggering immune response 1
- May present with either:
- Leukocytosis (WBC >12,000/μL), leukopenia (WBC <4,000/μL), or >10% immature forms 1, 4
- Elevated inflammatory markers (C-reactive protein, procalcitonin) 4
Clinical Progression and Recognition
- Typically begins with signs of infection and systemic inflammatory response 1
- Progresses to organ dysfunction (sepsis) and then to refractory hypotension with metabolic abnormalities (septic shock) 1
- Early recognition is critical using bedside clinical criteria such as qSOFA (respiratory rate ≥22/min, altered mentation, systolic BP ≤100 mmHg) 4, 2
- Rapid deterioration can occur, requiring prompt intervention 1, 7
Management Considerations
- Requires immediate fluid resuscitation with crystalloids (at least 30 mL/kg) 1, 4
- Vasopressors (typically norepinephrine) should be initiated if hypotension persists after fluid challenge 1, 6
- Target MAP ≥65 mmHg as the initial goal during hemodynamic support 1
- Avoid fluid overload which may worsen tissue edema and increase intra-abdominal pressure 1
- Early identification of source of infection and prompt antimicrobial therapy are essential 4, 7
Pitfalls and Caveats
- Relying solely on blood pressure for diagnosis can delay recognition; tissue perfusion abnormalities may be present despite normal blood pressure 1
- Lactate elevation may result from causes other than tissue hypoperfusion (e.g., liver dysfunction, medications) 8, 3
- Fluid overload can worsen outcomes; careful monitoring during resuscitation is essential 1
- White blood cell count may not be reliable in neutropenic patients 4
- The term "severe sepsis" is now considered redundant under current definitions 1, 2