Description
Acute Neuropathological Alterations after Smoke Inhalation Injury, with and without Third-degree Skin Burn
Anita Randolph, Koji Ihara, Satoshi Fukuda, Perenlei Enkhbaatar, Maria- Adelaide Micci
Department of Anesthesiology, University of Teas Medical Branch, Galveston, TX
Introduction: Some evidence exists in the literature describing neurological complications following smoke inhalation injury. In one case report, smoke inhalation alone was associated with a progressive decrease in metabolic activity and diffuse neurodegeneration in the brain. The goal of this work was to describe acute neuropathological alterations in the brain following smoke inhalation and burn injury. Specifically, we tested the hypothesis that smoke inhalation alone can lead to blood-brain barrier dysfunction.
Methods: Female Merino sheep were subjected to skin burn (40% TBSA, 3rd degree) and smoke inhalation injury (48 breaths of cooled cotton smoke). Hemodynamic measurements were collected every 6 hours for 48 hours. The frontal cortex, basal ganglia, amygdala, hippocampus, cerebellum, and pituitary gland were stained with Hematoxylin & Eosin, Luxol fast blue, Periodic acid-Schiff (PAS), and Martius, Scarlet and Blue (MSB) to assess blood vessel damage and hemorrhage. Three groups were compared: sham (n=8), smoke only (n=7), burn and smoke (n=7).
Results: Extensive neuropathological changes were observed throughout the brain. There was a significant increase in the number of dilated congested blood vessels between both injured groups as compared to sham. Positive PAS staining confirmed damage to the basement membrane of congested and dilated vessels. There was also severe rupturing of blood vessels and microvascular hemorrhaging following smoke inhalation ± third-degree skin burn. Bleeding was confirmed by positive MSB staining. No significant changes in hemodynamics (cardiac output, heart rate, mean arterial pressure, temperature) and PaO2 were observed.
Conclusion: For the first time, we demonstrated that acute smoke inhalation third-degree skin burn result in diffuse BBB dysfunction throughout the brain that is not secondary to hypoxia and changes in hemodynamics. These findings provide key insight into neuropathological alterations after third-degree burn injury and points to the smoke component as a major contributing factor to progressive neurological deficits observed after acute exposure.
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