Objective: To investigate the morphological and pathological changes of the larynx after severe laryngeal burn in dogs and their relationship with laryngostenosis. Methods: Eighteen healthy, male beagle dogs were assigned into control group, immediately after injury group, and 2, 4, 6, and 8 weeks after injury groups according to the random number table, with 3 dogs in each group. Dogs of injury group inhaled saturated steam through mouth for 5 seconds to reproduce severe laryngeal burn. Tracheotomy and intubation were performed immediately after injury, and 400 000 U/d penicillin was intravenously infused for 1 week. The feeding, activity, and vocalization of dogs in each group after injury were observed until they were sacrificed. Immediately after injury and 2, 4, 6, and 8 weeks after injury, the laryngeal morphology of the dogs in corresponding time point groups were observed by endoscope. After the observation, the dogs in each injury group were sacrificed, and the laryngeal tissue was taken. The epiglottis, glottis, and cricoid cartilage were collected to make full-thickness tissue slice, respectively, and their pathological changes were observed with hematoxylin and eosin staining. The dogs of control group were not specially treated, and their life activities, laryngeal morphological and pathological changes were observed. Results: (1) The dogs of control group had normal feeding, activities, and vocalization. All the dogs in injury group survived until they were sacrificed, and their feeding, activities, and vocalization were obviously reduced after injury compared with those of control group. The dogs of 2, 4, 6 and 8 weeks after injury groups ate and moved normally 2 weeks after injury but vocalized abnormally in frequency and volume compared with those of control group, which lasted until they were sacrificed. (2) The dog's laryngeal mucosa in control group was complete and pink, without obvious exudation. The laryngeal mucosa of the dog in immediately after injury group was pale and edematous, with obvious exudation, local ulceration, necrosis, and exfoliation, and dilated microvessels on the surface. The laryngeal mucosa of the dogs in 2 weeks after injury group was pale, edematous, and oozed less than that of immediately after injury group, and the glottis was blocked by an obviously extruding mass. The paleness and edema of laryngeal mucosa were significantly reduced in the dogs of 4 weeks after injury group compared with those of 2 weeks after injury group, without dilated microvessel, and the glottic extruding mass was obviously smaller than that of 2 weeks after injury group. The sizes of glottic mass were similar between the dogs of 6 and 8 weeks after injury groups, which were obviously smaller than that in 4 weeks after injury group. (3) In the dogs of control group, the epithelial cells of epiglottis, glottis, and cricoid cartilage were normal in morphology, the proper glands were visible in the intrinsic layer, and the muscle fibers and the chondrocytes were normal in morphology. In the dogs of immediately after injury group, large sheets of epiglottis epidermis exfoliated, the epithelial cells were swollen and necrotic, the intrinsic glands were atrophic and necrotic, and the chondrocytes were degenerated and necrotic. The epidermis of the glottis partially exfoliated, the epithelial cells were swollen and necrotic, the intrinsic glands were atrophic and necrotic, the muscle fibers were partially atrophic and fractured, and the vacuolar chondrocytes were visible. The cricoid cartilage epidermis was ablated, the epithelial cells were swollen, the intrinsic layer and submucosal layer were slightly edematous, and the morphological structure of glands, chondrocytes, and muscle fibers were normal. In the dogs of 2 weeks after injury group, the epiglottis epidermis was completely restored, a small amount of glands in the intrinsic layer were repaired, and obsolete necrotic chondrocytes and new chondrocytes could be seen. A large number of fibroblasts, new capillaries, and inflammatory cells infiltration were observed in the epidermis of glottis, and intrinsic layer glands were repaired. The cricoid cartilage epidermis was repaired intactly, and there was no edema in the intrinsic layer. In the dogs of 4 weeks after injury group, the epiglottis intrinsic layer glands were further repaired compared with those of 2 weeks after injury group, and new chondrocytes were seen in the submucosa of the glottis. The condition of cricoid cartilage was consistent with that of control group. The dog's epiglottis, glottis, and cricoid cartilage were similar between the 6 and 8 weeks after injury groups, and no significant change was observed compared with those of 4 weeks after injury group. Conclusions: The morphological changes of larynx after severe laryngeal burn in dogs include mucosa detachment and necrosis, and mass blocking glottis. Pathological changes include epidermis shedding and necrosis, gland atrophy and necrosis, vascular congestion and embolism, chondrocytes degeneration, necrosis and proliferation, even local granulation tissue formation and cartilaginous metaplasia. These results may be the cause of laryngostenosis after laryngeal burn.
目的： 探讨犬重度喉烧伤后的喉形态和病理改变及其与喉狭窄的关系。 方法： 将18只健康雄性比格犬按随机数字表法分为对照组、伤后即刻组及伤后2、4、6、8周组，每组3只。拟致伤组犬予以经口吸入饱和水蒸气5 s造成重度喉烧伤，伤后即刻予以气管切开置管并静脉输注青霉素40万U/d，持续1周。观察各组犬致伤后进食、活动及发声情况至处死前。伤后即刻及伤后2、4、6、8周采用内镜观察对应各时间点组犬喉部形态；观察结束后处死各组犬并取喉部组织，针对会厌、声门、环状软骨分别制作全层组织切片，行苏木素-伊红染色，观察各部分组织病理改变。对照组犬不予特殊处理，同前行生命活动、喉形态及病理学观察。 结果： (1)对照组犬进食、活动、发声正常。致伤组犬均存活至处死前，伤后进食、活动、发声较对照组明显减少；伤后2～8周组犬进食、活动于伤后2周恢复，发声频率及音量低于对照组并持续至处死前。(2)对照组犬喉黏膜外观完整、呈粉色，无明显渗出。伤后即刻组犬喉黏膜表面苍白、水肿，渗出明显，局部可见溃烂、坏死、脱落，表面可见扩张微小血管。伤后2周组犬喉黏膜苍白、水肿、渗出较伤后即刻组减轻，声门处见明显突出肿物阻塞声门。伤后4周组犬喉黏膜苍白、水肿较伤后2周组明显好转，未见扩张微小血管，声门突出肿物较伤后2周组明显缩小。伤后6、8周组犬声门肿物大小相近，较伤后4周组明显缩小。(3)对照组犬会厌、声门、环状软骨上皮细胞形态正常，固有层可见正常腺体，肌纤维形态正常，软骨细胞形态正常。伤后即刻组犬会厌上皮大片脱落，上皮细胞肿胀、坏死，固有层腺体萎缩、坏死，软骨细胞变性坏死；声门上皮部分脱落，上皮细胞肿胀、坏死，固有层腺体萎缩、坏死，肌纤维部分萎缩、断裂，可见空泡状软骨细胞；环状软骨上皮局灶脱落，上皮细胞肿胀，固有层及黏膜下层轻度水肿，腺体、软骨细胞和肌纤维形态结构正常。伤后2周组犬会厌上皮层完全修复，固有层少量腺体修复，可见陈旧坏死软骨细胞及新生软骨细胞；声门处上皮层可见大量成纤维细胞、新生毛细血管、炎性细胞浸润，固有层腺体修复；环状软骨上皮修复完整，固有层未见水肿。伤后4周组犬会厌固有层腺体较伤后2周组进一步修复；声门黏膜下层可见新生软骨细胞；环状软骨情况与对照组一致。伤后6、8周组犬会厌、声门、环状软骨情况相近，较伤后4周组无明显变化。 结论： 犬重度喉烧伤后喉黏膜形态学上可发生黏膜脱落、坏死，形成肿物阻塞声门；病理学上可出现上皮脱落、坏死，腺体萎缩、坏死，血管充血、栓塞，软骨细胞变性坏死、增殖，甚至局部出现肉芽组织、软骨化生等。这些结果可能是喉烧伤后喉狭窄的原因。.
Keywords: Burns, inhalation; Laryngeal burn; Laryngostenosis; Morphology; Pathology.