Necrotizing Fasciitis: Pathogenesis and Clinical Findings
Authors: Alyssa Federico, Amanda Eslinger, Matthew Harding, Mehul Gupta Reviewers: Heena Singh, Yan Yu*, Donald Graham*, Duncan Nickerson* * MD at time of publication
Diabetes
Loss of protective sensation in lower extremities
Peripheral vascular disease
Poor arterial perfusion causes necrosis of tissue
Immune compromised host
Increased susceptibility to infection
Bacteria introduced to tissue
Pharyngitis
Blood carries bacteria from throat to other tissue (hematogenous spread)
Laceration
Recent surgery
Injection
Burn
Blunt force trauma
Childbirth
Lower extremity wounds
Bacteria enters tissue through open wound
Infection of muscle fascia Local immune response
Production of exotoxins by bacteria
Disruptions of protective skin barrier
Bacteria introduced into tissue during injury
Necrotizing Fasciitis
Type I infection: mixed aerobic and anaerobic bacteria Type II infection: group A streptococcus
Type III infection: marine organisms, clostridial infections Type IV infection: fungal organisms
Poor blood supply of muscle fascia allows for progressive spread of infection
Systemic immune response
Pyrogens produced by immune system
Pyrogens travel through
the bloodstream to the hypothalamus and alters the body’s thermal setpoint
Transmission of bacteria from infected tissue to blood
Sepsis
Streptolysin (exotoxin) causes blood clot formation
Blood clots in vessels
Tissue ischemia in epidermis, dermis, subcutaneous fat, muscle fascia, and/or muscle
Stimulation of programmed cell death
Tissue destruction
Pain more severe than clinical findings
↓ blood flow fails to meet tissue’s needs
Tissue death
Build up of gas in subcutaneous
tissue from bacteria metabolism
Crepitus
↑ serum creatinine
kinase from protein breakdown
↑ blood flow to infected tissue
Warmth Erythema
Immune cells release vasoactive cytokines into the blood
Capillary vasodilation
Fluid and proteins shift from cells and capillaries to interstitial space
Blood
vessel dilation
↓ perfusion of vital organs
Organ failure
Hypotension
↑ heart rate to perfuse vital organs
Tachycardia
Bacteria releases toxins which are taken up into the bloodstream
Immune cells produce inflammatory cytokines
Circulating toxins activate T cells, over- activating the systemic immune response
Toxic Shock syndrome
Infection ↑ white blood cell production in bone marrow
↑ white blood cells
Destructionof peripheral nerve endings
Insensitivity to pain
Tissue hypoxia à anaerobic metabolism
Poor perfusion of lungs impairs gas exchange
Tachypnea
Cytokines affect dopamine production in the basal ganglia
Acute malaise
Production of non-specific acute phase reactants
↑ C reactive protein and erythrocyte sedimentation rate
Fluid-filled blisters
Edema
Fever Compartment syndrome (see relevant Calgary Guide slide)
Amputation ↑ serum
lactate
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
First published Nov 20, 2013, updated Dec 19, 2021 on www.thecalgaryguide.com