Objectives: Pathophysiologic changes of frostbite have been postulated but rarely understood, especially the changes caused by chilly high altitude environment. Therefore, we investigated the pathophysiologic changes of high altitude frostbite (HAF) caused by cold and hypoxia.
Methods: Forty Sprague-Dawley rats were randomly divided into 5 equal groups, namely, control, superficial HAF (S-HAF), partial-thickness HAF (PT-HAF), full-thickness HAF (FT-HAF), and partial-thickness normal frostbite (PT-NF) groups. The S-HAF, PT-HAF, and FT-HAF groups were fed under hypobaric hypoxic conditions simulating an altitude of 5000 m. Then, the PT-NF, S-HAF, PT-HAF, and FT-HAF models were constructed by controlling the duration of the direct freezing by liquid nitrogen. Animal vital signs were measured after the operation, and histopathologic changes were observed after routine hematoxylin and eosin staining. In addition, the microcirculation of frostbite tissues was monitored and compared by contrast ultrasonography during wound healing.
Results: The S-HAF, PT-HAF, and FT-HAF groups showed significant differences in the microcirculatory and histopathologic changes in the various tissue layers (P < .05). In addition, combined cold and hypoxia caused more damage to frostbite tissue than pure cold. The circulation recovery of HAF models was significantly slower relative to NF models (P < .05).
Conclusions: A safe and reproducible HAF model was proposed. More important, pathophysiologic determination of HAF provided the foundation and potential for developing novel and effective frostbite therapies.
Keywords: contrast ultrasonography; high altitude environment; high altitude frostbite; microcirculation; pathophysiology.
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