Septic shock

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Jason Le, B.S.[1]

Overview

• Septic shock is the most severe clinical phenotype of Sepsis, characterized by profound circulatory and cellular/metabolic abnormalities associated with a substantially increased risk of death.
• The Sepsis-3 operational definition is vasopressor requirement to maintain a mean arterial pressure (MAP) of 65 mm Hg or greater and serum lactate concentration greater than 2 mmol/L in the absence of hypovolemia. Septic shock is associated with in-hospital mortality rates greater than 40%.
• Septic shock is the most common form of distributive (vasodilatory) shock and must be distinguished from hypovolemic, cardiogenic, and obstructive shock; detailed differentiation is addressed in the Differentiating septic shock from other diseases microchapter.
• Clinical assessment should integrate hemodynamics, tissue perfusion, lactate concentration, response to initial fluid administration, and the likelihood and source of infection.

Natural History, Complications and Prognosis

• Septic shock requires simultaneous treatment of infection, circulatory failure, and tissue hypoperfusion rather than sequential management of individual abnormalities.
• Persistent vasopressor requirements should prompt reassessment of volume status, ongoing infection, source-control adequacy, cardiac function, and other causes of refractory shock.
• Complications and adverse outcomes are related to persistent circulatory dysfunction, tissue hypoperfusion, ongoing infection, and progressive multiorgan dysfunction.
• Prognosis is poor. Pooled in-hospital mortality is approximately 39% across definitions and rises to approximately 52% when Sepsis-3 criteria are applied; 30-day mortality is approximately 35% and 90-day mortality approximately 38%.

Diagnosis

Diagnostic Criteria

• Septic shock is a subset of Sepsis identified within the Sepsis-3 framework by a SOFA score increase of 2 or more points, with both of the following septic shock criteria after adequate volume resuscitation:

• Vasopressor requirement to maintain a MAP of 65 mm Hg or greater.
• Serum lactate concentration greater than 2 mmol/L in the absence of hypovolemia.

• The Sepsis-3 septic shock criteria are operational criteria for clinical and epidemiologic classification and should not delay treatment when septic shock is clinically suspected.

History and Symptoms

• Septic shock should be suspected in any patient with suspected or confirmed infection who develops hypotension requiring vasopressors and/or hyperlactatemia. Presentations are heterogeneous and may be subtle early.
• General features include fever or hypothermia and malaise; site-specific symptoms such as cough, dysuria, and erythema may point to the source; and organ-dysfunction symptoms include confusion, oliguria, and dyspnea.
• Altered mentation, hypotension, and tachypnea are particularly suggestive of sepsis in a patient with infection, although their absence does not exclude it, and signs may be masked by beta-blockers or antipyretics.

Physical Examination

• Physical examination should assess hemodynamics, tissue perfusion, and findings that may identify the source of infection.
• Findings may include hypotension, tachypnea, altered mentation, oliguria, and other manifestations of organ dysfunction.
• General signs may include fever or hypothermia and malaise; source-specific findings may include erythema or other localizing signs.
• Clinical findings may be attenuated or masked by beta-blockers or antipyretics.
• Capillary refill time may be used as a marker of tissue perfusion to guide ongoing fluid and vasopressor titration.

Laboratory Findings

• Serum lactate concentration is a key component of the Sepsis-3 operational definition of septic shock.
• Serum lactate concentration greater than 2 mmol/L, together with vasopressor requirement to maintain a MAP of 65 mm Hg or greater in the absence of hypovolemia after adequate volume resuscitation, fulfills the Sepsis-3 septic shock criteria.
• Characteristic laboratory abnormalities include leukocytosis or leukopenia, more than 10% immature granulocytes (bandemia), hyperglycemia, and elevated creatinine, in addition to elevated lactate.
• Serial lactate assessment and lactate clearance can help guide ongoing resuscitation and assessment of tissue perfusion.

Treatment

Medical Therapy

• The mainstay of therapy for septic shock is simultaneous treatment of infection, circulatory failure, and tissue hypoperfusion.
• Antimicrobial therapy: In possible septic shock, antimicrobial therapy should be initiated immediately. Antimicrobial therapy should subsequently be refined according to microbiologic results and clinical response.
• Antimicrobial de-escalation: Narrowing antimicrobial therapy once a microbiologic diagnosis and antimicrobial susceptibilities are available is recommended.
• Source control: An anatomic source of infection that is amenable to intervention should be identified and controlled promptly.
• Fluid resuscitation: Crystalloid solutions are the initial IV fluid of choice, with balanced crystalloids favored over 0.9% saline. SSC 2026 suggests administering at least 30 mL/kg IV crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock (conditional recommendation, low certainty), calculated on actual body weight (adjusted or ideal body weight if BMI >30 kg/m²), with frequent reassessment to avoid under- or over-resuscitation. This differs from the ESICM guideline, which suggests up to 30 mL/kg.
• Vasopressor therapy: Norepinephrine is first-line (strong recommendation over dopamine, epinephrine, and selepressin; conditional over vasopressin and angiotensin II). Vasopressin is suggested for escalating norepinephrine doses, with panel practice approximately 0.25–0.5 µg/kg/min, followed by epinephrine if MAP remains inadequate. In septic shock with concomitant cardiac dysfunction, either norepinephrine or epinephrine is suggested first-line.
• Timing of vasopressors: Vasopressors should be initiated promptly when hypotension persists or is severe; in unstable shock, vasopressor therapy may be started concurrently with initial fluid administration, including through a peripheral IV when necessary rather than delaying treatment for central venous access.
• Blood pressure target: An initial MAP target of approximately 65 mm Hg is recommended during vasopressor-supported resuscitation. A lower MAP target of 60–65 mm Hg may be acceptable in older patients with vasodilatory shock.
• Perfusion-guided resuscitation: Beyond MAP, serial assessment of tissue perfusion, including lactate clearance and capillary refill time, should inform ongoing fluid and vasopressor titration.
• Cardiac dysfunction and persistent hypoperfusion: In septic shock with concomitant cardiac dysfunction, norepinephrine or epinephrine may be used as first-line vasopressor therapy. For persistent hypoperfusion despite adequate intravascular volume and arterial pressure, dobutamine or epinephrine may be considered to provide inotropic support.
• Corticosteroids: SSC 2026 makes a conditional recommendation (low certainty) favoring IV hydrocortisone in septic shock, typically 200 mg/day (divided every 6 hours or by continuous infusion) for ongoing vasopressor requirement. A practical trigger used in the SSC 2021 guideline is norepinephrine or epinephrine ≥0.25 µg/kg/min for ≥4 hours. Corticosteroids reliably increase shock reversal, while the mortality effect is small and uncertain. Addition of fludrocortisone 50 µg daily may confer further benefit, but practice remains variable.
• Adjunctive catecholamine-sparing therapy: Adjunctive catecholamine-sparing and non-adrenergic vasoactive strategies remain an evolving area of evidence and should not replace established norepinephrine-based first-line management.

Surgery

• An anatomic source of infection that is amenable to procedural intervention should be identified and controlled promptly as part of septic shock management. Detailed source-control procedures are addressed in the Source control microchapter.

Prevention

• Primary prevention of septic shock is addressed through prevention and early treatment of the underlying infectious conditions.
• Once septic shock is recognized, prompt antimicrobial therapy, appropriate fluid and vasopressor resuscitation, source control, and ongoing perfusion assessment are intended to reduce progression of circulatory dysfunction and associated complications.