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Brain Damage Following Smoke Inhalation and Skin Burn
Author(s) -
Randolph Anita,
Ihara Koji,
Escobar Kenneth,
Fukuda Satoshi,
Salsbury John Randall,
Prough Donald,
Herndon David,
Enkhbaatar Perenlei
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1179.12
Subject(s) - smoke inhalation , medicine , smoke inhalation injury , inhalation , smoke , burn injury , total body surface area , anesthesia , luxol fast blue stain , brain damage , h&e stain , pathology , surgery , staining , chemistry , myelin , organic chemistry , central nervous system
RATIONALE In the U.S., there is an estimated 300,000 to 500,000 patients hospitalized annually due to burn related injuries. Mortality and morbidity of burn patient's increase significantly when combined with smoke inhalation injury. Previous studies have shown combined burn and smoke inhalation results in systemic changes including hypermetabolic response, microvascular hyperpermeability and multiorgan dysfunctions. With the advanced technology and treatment, mortality of burn victims is remarkably reduced. However, there is no follow up study, among the survivors, on possible effects of burn and smoke on brain dysfunction. In this study, we tested the hypothesis that burn and smoke inhalation injury is sufficient to induce brain dysfunction by activating astrocytes and causing neuronal injury. METHODS To test our hypothesis, we used our well‐characterized ovine model of skin flame burn (40% TBSA, 3rd degree) and smoke inhalation (48 breaths of cooled cotton smoke). After the injury we studied the animals 48 hours in a conscious state under mechanical ventilation, recording hemodynamics and ventilator variables as well as taking blood samples every 6 hours. Postmortem, brains were taken and placed into 10% formalin for 4–6 weeks. We compared 3 different groups: n=3 sham (no injury), n=3 smoke only, n=3 combined burn and smoke. Brain tissue slides were prepared from the hippocampus and basal ganglial area (ten slides for each sheep) and stained with Luxol Fast Blue (LFB) to assess myelinated axon damage and Hematoxylin & Eosin (H&E) to assess astrocyte activation and neuronal damage/death. RESULTS Average carboxyhemoglobin levels were 2.1%, 67.3%, 60.4% in sham, smoke only and burn/smoke groups, respectively. No noticeable brain tissue changes were observed in sham, whereas there were clear evidences of astrocyte activation and neuron death in the smoke only group. The number of activated astrocytes per field and damaged neurons were significantly increased in the smoke only and burn/smoke groups. The percentage of damaged neurons in the smoke only and burn/smoke groups were 41.0% and 59.9% respectively compared to sham of 19.2%. Observed basophilic neuronal necrosis in smoke only vs. sham was increased as well. These changes were augmented by skin burn. In addition, vascular congestion and hemorrhage were observed in both smoke only and combined burn/smoke groups. CONCLUSIONS Smoke inhalation causes brain damage characterized by astrocyte activation, neuronal and myelinated axon damage and hemorrhage. Presence of skin burn exacerbates smoke‐induced brain injury. Support or Funding Information Shriners Hospital for Children SHC84050; SHC85220