Septic shock

Septic shock
Updated: 06/16/2022
© Jun Wang, MD, PhD

General features

  • A subset of sepsis with profound circulatory and cellular metabolism abnormalities with marked increased mortality
  • A type of distributive shock
  • Most common type of shock
  • Multiorgan failure due to dysregulated inflammatory response
  • Despite adequate fluid resuscitation
    • Persisting hypotension
    • Requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher
    • Serum lactate level greater than 2 mmol/L (18 mg/dL)
  • Increased risk of mortality than sepsis alone

Pathophysiology

  • Mediators
    • Microorganism factors

Bacterial components: Endotoxin, peptidoglycan, muramyl dipeptide, lipoteichoic acid, superantigens, etc

Bacterial products: Staphylococcal enterotoxin B, toxic shock syndrome toxin 1, Pseudomonas exotoxin A, M protein, etc

    • Proinflammatory mediators: TNF-alpha, Interleukin-1, granulocyte colony stimulating factor, platelet activating factor, etc
    • Complements
    • Immune cell activity regulators

Toll-like receptors

Nucleotide-oligomerization domain leucine-rich repeat protein

Caspase activation and recruitment domain helicases

  • Exaggerated systemic inflammatory type response
  • Tissue and cellular effects
    • Circulatory abnormalities
    • Immunosuppression
    • Tissue ischemia and hypoxia
    • Cytopathic injury: Direct cytotoxicity, apoptosis
  • Systemic dysfunctions
    • Coagulation: Capillary thrombosis and disseminated intravascular coagulation
    • Circulation: Pathologic vasodilation (arterial) and shunting
    • Metabolic: Insulin resistance and hyperglycemia, adrenal insufficiency (Waterhouse-Friderichsen syndrome), elevated lactate
    • Heart: Elevated cardiac output, reduced ejection fraction, reduced left ventricular stroke work index
    • Vessel: NO (Nitric Oxide) mediated dilation, impaired vasopressin secretion
    • Pulmonary: Acute lung injury, ARDS, due to vascular damage and increased permeability, alveolar edema, type II pneumocyte injury
    • Gastrointestinal: Bacterial overgrowth, ileus
    • Liver: Dysfunction
    • Kidney:  Acute kidney injury, impaired renal function due to tubular necrosis
    • Central nervous system: Encephalopathy, peripheral neuropathy

Clinical presentations

    • Fever at early phase
    • Tachypnea
    • Presentations associated with site of infection
    • Positive blood culture or clinical response to antibiotics
    • Hypotension
    • Tachycardia
    • Cool skin, decreased capillary refill, mottling, cyanosis
    • Other organ dysfunction: oliguria, acute kidney injury, altered mental status, etc

Key Laboratory findings

  • Hematology:
  • Chemistry
    • Hyperglycemia in the absence of diabetes
    • Hyperbilirubinemia
    • Hyperlactatemia
    • Elevated C-reactive protein
    • Elevated procalcitonin
  • Arterial hypoxia
  • Renal insufficiency: Oliguria, elevated creatinine
  • Adrenal insufficiency: Hyponatremia, hyperkalemia

Diagnosis

Management

    • ICU for hemodynamic monitoring
    • Supporting cardiac and respiratory functions
    • Supporting other organ systems
    • Correcting abnormal tissue perfusion
  • Treatment for infection: Antimicrobial therapy
  • Treatment of anemia and coagulopathy
  • Other support: metabolic, nutritional
  • Surgical removal of focal infections

Worse prognosis indicator

  • Overall worse prognosis
  • Delayed aggressive therapy
  • Decompensated metabolic acidosis
  • Multiorgan failure

 

 

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