Full Thickness Burns: Pathogenesis and clinical findings
Radiation
Sunlight, x-ray, nuclear
Emission/explosion can cause damage to keratinocytes (see Calgary Guide
Slide: Superficial Thickness Burns: Pathogenesis and Clinical Findings)
Author and Illustrator: Amanda Eslinger Tracey Rice Reviewers:
Sunawer Aujla Alexander Arnold Duncan Nickerson* Jori Hardin*
* MD at time of publication
Epidermis
Dermis
Sub-cutaneous tissue
Fire
Contact Scald Chemical Electrical
Transfer of heat energy causes direct injury to keratinocytes
Hypoxic injury (lack of oxygen) causes ischemia-related cell death leading to necrosis
Full thickness burn
Non-uniform damage to the epidermal, dermal & subcutaneous layers at varying widths & depths due to unpredictable injury pattern
Degraded
epidermal
& dermal layers cover granulated tissue
Ulceration covered by eschar: a thick, dried, black (necrotic) layer
Long-term risk of ulcers & infections
↑ Vascular permeability in subcutaneous layers
↑ Intravascular fluid leaves capillaries, ↓ uptake by lymph vessels
Edema
Compression of surrounding muscles, nerves & vessels
Ischemia and/or necrosis
↓ Immunologic
response due to impaired epidermal barrier function
↑ Microbial growth creating biofilm & secretion of chemicals that inhibit natural protective process
Irritated,
inflamed wound bed +/- exudate
↑ Risk of infection & septic shock
Destruction
of somatosensory structures
Hypoesthesia (↓ sensation to stimuli)
↑ Risk of
repeated injury due to ↓ response to noxious stimuli
Destruction of cutaneous capillary beds
↓ Healing due to ↓ dermal structures throughout wound
White or leathery appearance
Chronic wounds require surgical interventions
↑ Risk of contractures & skin barrier weakness
Legend:
Mechanism of Injury
Pathophysiology
Sign/Symptom
Complication
Published December 2, 2013, updated June 26, 2023 on www.thecalgaryguide.com