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
- Diffuse endothelial activation and damage
- Vasodilation
- Increased vascular permeability
- Capillary thrombosis
- Disseminated intravascular coagulation
- 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
- Presentations of sepsis
- Fever at early phase
- Tachypnea
- Presentations associated with site of infection
- Positive blood culture or clinical response to antibiotics
- Presentations of shock
- Hypotension
- Tachycardia
- Cool skin, decreased capillary refill, mottling, cyanosis
- Other organ dysfunction: oliguria, acute kidney injury, altered mental status, etc
Key Laboratory findings
- Hematology:
- Leukocytosis or leukopenia
- Normal WBC count with >10% immature forms
- Thrombocytopenia
- Coagulopathy
- 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
- Evidence of shock
- Evidence of sepsis: Sequential Organ Failure Assessment (SOFA) ≥2
Management
- Managements for shock
- 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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