兽研简要概述
表皮样囊肿是猫中不常见的良性囊性病变，其发生于软腭的报道极为罕见。本病例中，通过计算机断层扫描在一只17岁猫中发现了软腭肿物，手术切除后经组织病理学确认为表皮样囊肿。术后短期内未再观察到流涎和吞咽困难，尽管这种时间关联不能确立因果关系。该猫随后出现严重的胃肠道功能障碍、电解质紊乱和反复癫痫发作，并于术后27天死亡。囊肿的起源尚不确定，发育性和获得性机制均有可能。本病例突出了老年猫软腭表皮样囊肿的临床和诊断特征。
1. 引言
口腔肿物约占猫所有肿物的3%-12%，其中>89%为恶性[1,2,3]。相比之下，口腔囊肿不常见，组织学特征为衬覆上皮的液体或半液体填充腔隙[4,5]。在各种类型的口腔囊肿中，牙源性囊肿在猫中相对有较多文献记载。这些囊肿起源于与牙齿发育相关的牙源性上皮残余，约占猫口腔肿物或口腔组织标本的0.19%-2%[6,7,8,9]。
非牙源性囊肿与牙源性囊肿的区别在于其发育起源与牙齿形成组织无关。猫中此类病变的报道极为有限。仅在年轻猫中描述了个别病例，包括一例鼻咽部皮样囊肿[10]和一例年轻猫中含分泌性蛋白样物质的鼻咽部囊肿[11]。
皮样囊肿的特征为含角蛋白样、皮脂样内容物或存在皮肤衍生物[12]。在人类中，发生于口底和其他口内部位的皮样囊肿根据Meyer分类进行组织学分类[13]，该分类根据囊肿组织成分区分三种类型。表皮样囊肿衬覆复层鳞状上皮，含角蛋白样物质，但缺乏皮肤附属器结构。真性皮样囊肿含有皮肤附属器，如汗腺、皮脂腺和毛囊。畸胎样囊肿起源于全能细胞，含有源自全部三个胚胎胚层的组织，包括肌肉、骨骼、软骨和各种上皮组织[5,14]。在兽医学中，已描述了发生于不同解剖部位的皮样囊肿，并根据上皮衬里和囊肿内容的性质进行了分类[15,16]。然而，这些囊肿发生于口腔内的报道极为有限[10,17,18,19]，且兽医学中尚未建立针对口腔表皮样囊肿、真性皮样囊肿和畸胎样囊肿的广泛接受的分类系统。
手术切除通常被认为是表皮样囊肿的首选治疗方法[5,10,11,13,17,18,19]。本报告描述了一只老年猫软腭起源的表皮样囊肿，包括其诊断影像学、组织病理学发现和外科处理。
2. 病例描述
一只17岁、体重2.82 kg的已绝育雌性家养短毛猫表现为轻度流涎和吞咽困难。该猫有多颗牙齿拔除史。就诊前17个月，因牙结石相关的牙龈炎拔除了牙齿308、309、408和409。当时存在的牙齿为304、308、309、404、408、409、103和203。除牙结石影响牙齿周围的牙龈炎外，未发现提示广泛性口炎的口腔病变。拔牙后，剩余牙齿为304、404、103和203。该猫有2年甲状腺功能亢进病史，使用卡比马唑控制；有7年慢性便秘病史，使用高纤维处方粮和偶尔灌肠管理。就诊前3个月出现癫痫发作，正在使用左乙拉西坦控制。进行了全面的诊断评估以评估该猫的整体健康状况。收缩压为160 mmHg，胸部听诊未见异常。血液学、血清生化和血气分析显示NT-proBNP（155.7 pmol/L，参考区间0-100 pmol/L）和fPLI（3.8 μg/L，参考区间0-3.5 μg/L）轻度升高，以及高钠血症（160 mmol/L，参考区间145-151 mmol/L）。总甲状腺素（T4）浓度在参考范围内。血液检查中未发现其他临床相关异常。
胸部X线片未见异常，而腹部X线片显示降结肠和直肠粪便性扩张。腹部超声检查发现脾脏和肝脏病变，脾脏病变细胞学检查提示肥大细胞增生，遂同期进行脾切除术和肝脏活检。
为进行肿瘤分期并评估癫痫发作的潜在颅内病因，对患猫进行了头部、胸部和腹部计算机断层扫描（CT）检查。CT检查前，患猫预先使用布托啡诺（0.2 mg/kg，静脉注射）进行麻醉前给药。使用丙泊酚（6 mg/kg，静脉注射，至效应）诱导麻醉，并以异氟烷-氧气维持麻醉。未见转移或颅内病变证据。然而，CT偶然发现一个边界清晰、息肉样肿块（8.5 × 9.9 × 10.0 mm），起源于右侧软腭远端并延伸至口咽腔，导致邻近鼻咽部狭窄（图1）。邻近骨性结构未见骨质侵犯或骨质溶解征象，使牙源性来源的可能性较小。静脉注射碘海醇（2.5 mL/kg）后，肿块仅表现为轻微对比增强，平扫图像平均衰减值为96.09 ± 3.46 HU，增强后图像为102.11 ± 4.27 HU。相对较高的平扫衰减值和轻微的对比增强使单纯液性囊肿或增强性实性肿瘤的可能性较小。然而，仅凭CT表现无法排除炎症性病变（包括脓肿和肉芽肿）以及其他肿瘤。
在全身麻醉下，软腭肿块手术切除与脾切除术和肝活检同时进行。麻醉前患猫临床状态稳定，给予静脉输液治疗以预防脱水并纠正电解质异常。患猫预先使用布托啡诺（0.2 mg/kg，静脉注射）进行麻醉前给药，围手术期给予头孢唑林（30 mg/kg，静脉注射）和左乙拉西坦（20 mg/kg，静脉注射）。使用丙泊酚（6 mg/kg，静脉注射）诱导麻醉，并以吸入异氟烷维持麻醉。口腔彻底检查未发现其他口腔或牙齿异常。口腔检查时肿块不易直接看到；然而，指触诊发现右侧口咽区有一质硬、轻度突出的病变。使用无创镊夹持病变并轻柔地向头侧牵拉，显示活动度良好且视野清晰。在肿块尾侧放置纱布填塞物以将其向头侧推移并改善手术暴露。肿块表面覆盖黏膜，呈光滑的圆顶状（图2A）。使用15号手术刀片作黏膜切口，随后使用蚊式止血钳、虹膜剪和棉签钝性分离肿块与周围组织（图2B）。黏膜与下方肿块紧密粘连，肿块内含黄褐色奶油样物质（图2C）。肉眼完整切除肿块后，手术部位出血极少，未予缝合，以待二期愈合。
鉴于肿块内容物的肉眼外观，感染性或炎症性病变被纳入鉴别诊断。为探究潜在感染性病因，进行了猫不明原因发热RealPCR检测组合（IDEXX Laboratories, Inc., Westbrook, ME, USA）以及猫呼吸道病原体Plus检测组合和细菌培养（GreenVet Laboratory, Yongin, Republic of Korea）。两个检测组合均包含可能与口腔相关的感染性病原体（补充表S1）。所有PCR检测和细菌培养均为阴性结果。因此，该病变的感染性病因被认为不太可能。
组织病理学检查（IDEXX Laboratories, Inc., Westbrook, ME, USA）证实脾脏多灶性非典型肥大细胞增生和肝脏肝细胞结节性增生。软腭肿块被鉴定为囊肿，内衬角化复层鳞状上皮，厚度相对均匀，为2至5层细胞（图3）。角化完全为正角化，透明角质颗粒不明显。衬里上皮广泛被致密、成熟、反应性、密集的纤维血管结缔组织包绕。囊腔内充满颗粒状嗜酸性物质、含针状胆固醇裂隙的角化碎片以及混合性核碎片。病变组织延伸至送检标本边缘；因此，组织学上无法确认完全切除。这些发现与良性表皮样囊肿一致。
术后，该猫接受头孢唑林（30 mg/kg，每12小时一次，静脉注射）、法莫替丁（2 mg/kg，每12小时一次，静脉注射）和布托啡诺（0.2 mg/kg，每6小时一次，静脉注射）治疗三天。由于软腭手术部位采用二期愈合方式且暴露于口腔环境，基于患者的个体风险因素（包括高龄、并发全身性疾病及并发腹部手术），选择了短期术后头孢唑林给药。这是针对该患者的个体化临床决策，而非口腔手术的常规术后抗菌预防。布托啡诺用于术后镇痛三天。由于患者高龄、长期便秘、癫痫发作性疾病及既存肾脏异常，其他镇痛选择受到限制。芬太尼因患者的胃肠道病史被认为较不理想，而NSAIDs因患者年龄和肾脏异常而避免使用。此后未再给予额外镇痛药。术后不再观察到流涎和吞咽困难，自主进食恢复；然而，这一改善仅记录到约24小时，因为次日出现了符合胃肠动力减弱的明显胃扩张和反复癫痫发作。尽管一般状况和食欲有所改善，胃肠动力障碍持续存在，并伴有代谢性碱中毒、高钠血症和氮质血症。支持治疗包括昂丹司琼（0.1 mg/kg，每8小时一次，静脉注射）、马罗匹坦（1 mg/kg，每24小时一次，静脉注射）、甲氧氯普胺恒速输注（CRI，0.08 mg/kg/h，静脉注射）、肠外营养以及液体和电解质纠正。该猫好转并于术后第7天出院。出院三天后，该猫因反复呕吐、胃肠动力减弱和粪便潴留再次入院，灌肠和甲氧氯普胺CRI后短暂改善。术后第23天再次出现严重胃肠扩张，需经鼻食管管饲。在最后一次住院期间，放置了中心静脉导管以促进长期强化支持治疗，包括肠外营养支持和静脉液体及电解质治疗。两天后，出现严重胃肠动力减弱和反复癫痫发作，随后出现严重呕吐、肌肉震颤、代谢性碱中毒和明显高钠血症。尽管给予支持治疗，该猫于术后第27天死亡。
3. 讨论
表皮样囊肿在猫中已有报道，见于多个解剖部位，包括肠道[20]、肺[21]和颅内腔[22,23,24]。在口腔中，仅有一例年轻猫的软腭囊肿被报道，其大体和组织病理学特征与本案相似[11]。在人类中，口腔表皮样囊肿为发育性或获得性起源[5,13]。发育性囊肿源于胚胎融合过程中外胚层组织的陷入，而获得性囊肿可能源于创伤性或医源性上皮植入深部组织[5,13]。兽医学中已提出类似机制。先前报道的一例年轻猫软腭囊肿被怀疑为先天性，发生于腭板从上颌突向内侧生长融合形成腭的过程中[11]。相反，获得性病变可能继发于老年犬的炎症或创伤[17]。
此前，鼻咽部表皮样囊肿延伸至鼓泡[17]，类似于报道的犬猫伴有口咽受累的耳部胆脂瘤病例[25,26,27]。胆脂瘤在某些方面与表皮样囊肿具有相似的组织病理学特征。与原发性口腔表皮样囊肿相比，累及口咽部的胆脂瘤起源于鼓泡内，随着疾病进展随后延伸至口咽部或颅内腔[28]。因此，中耳受累是区分这些病变与原发性口腔表皮样囊肿的重要特征。在本病例中，囊肿主要局限于软腭，CT上无异常证据或与中耳结构的连续性。本病例提供了老年猫软腭表皮样囊肿的额外临床、诊断影像、手术和组织病理学信息。
鉴别诊断中考虑了几种囊性或囊样病变。唾液腺黏液囊肿的可能性较小，因为本病变为离散的、衬覆上皮的囊肿，内含角化物质，而非与唾液腺组织相关或唾液外渗所致的充满黏液的腔隙。由于有拔牙史，也考虑过牙源性角化囊性病变。然而，CT上未见邻近骨质受累，组织病理学上缺乏特征性的腔面角化不全和基底细胞栅栏状排列，使该诊断可能性较小[9]。也考虑过漏斗部角化性囊性病变；但缺乏附件结构以及位于软腭内的解剖位置不支持毛囊性或皮肤附件来源。囊性或角化性鳞状细胞癌曾作为肿瘤性鉴别诊断予以考虑，但组织病理学检查缺乏细胞异型性、浸润性上皮生长和恶性角化，不支持该诊断[1,2,3]。
虽然获得性起源被认为是可能的解释，但囊肿的起源无法确定。不能排除一直无临床症状直至老年才发现的发育性囊肿。在人类，上皮细胞创伤性植入深部组织已被提出作为获得性表皮样囊肿发生的机制[29]。在体内大鼠模型中，自体皮肤皮下植入导致植入上皮增殖并形成衬覆上皮的囊腔，内含角蛋白、毛发及其他碎屑，类似表皮样囊肿或皮样囊肿[30]。
虽然本病例没有已知的直接创伤史，但与既往黏膜损伤相关的获得性起源被认为是一种可能的解释。该猫在发现囊肿前17个月曾在全身麻醉气管插管下接受过口腔后部拔牙。尽管该猫有拔牙史并持续食用干粮，但没有记录证据将这些因素与黏膜损伤或囊肿形成联系起来[29]。因此，这些暴露因素均不能视为因果关系的证据，所提出的获得性机制仍属推测。
既往报道的猫鼻咽囊肿与呼吸道症状和明显的鼻咽阻塞相关[10,11]。由于解剖位置，也考虑过鼻咽息肉。猫鼻咽息肉是良性炎性纤维血管增生，通常起源于中耳或听管，表面覆盖上皮。组织学上，它们由伴有炎性细胞的纤维血管结缔组织构成，而非衬覆复层鳞状上皮的离散含角蛋白囊肿[31]。在本病例中，病变为边界清楚、含角蛋白、衬覆复层鳞状上皮的囊肿，起源于软腭远端，而CT显示无中耳或鼓泡受累证据，使鼻咽息肉不太可能。该猫也没有明显的呼吸道症状，这可能与囊肿体积小且主要局限于口咽部、导致鼻咽阻塞轻微有关。此外，该病变是在头颅CT上偶然发现的，可能在其增大到足以引起临床相关鼻咽阻塞之前。
术前存在轻度流涎和吞咽困难，被认为可能与软腭病变有关。切除后，在临床稳定期间未观察到这两种体征。也考虑了其他可能的解释。在全身麻醉下全面检查口腔或CT上均未发现其他可轻易解释这些症状的口腔或牙齿异常。胰腺异常和fPLI升高在术前已被确定为慢性表现，术后实验室或影像学发现无实质性变化，使急性胰腺炎相关恶心成为可能性较小的解释。术前不存在氮质血症，因此不太可能解释初始体征。甲状腺功能亢进以及卡比马唑和左乙拉西坦的潜在不良反应也被认为可能性较小，因为术后继续使用相同药物，在临床稳定期间流涎或吞咽困难未复发。相比之下，术前和随后伴呕吐的胃肠道功能障碍发作期间均记录到高钠血症，因此不能排除其作为促成因素。虽然术后改善的解读因同期脾切除术及围手术期镇痛和胃保护治疗而混杂，但切除与流涎和吞咽困难缓解之间的时间关联提示软腭病变可能促成了这些体征。尽管病变体积小且阻塞程度相对较轻，但可能引起了局部不适或干扰吞咽。
无论解剖位置如何，表皮样囊肿均建议行手术切除[10,11,17,20,21,22,23,24,29,32,33,34,35]。在兽医患者中，手术切除后复发不常见；然而，已有报道一例犬硬膜外表皮样囊肿在次全切除后28个月囊肿重新生长并出现临床症状复发[34]。同样，在人类中复发不常见，且与不完全切除相关[36,37]。在本病例中，无法确认组织学上的完全切除；然而，切除后肉眼未见明显残留病变，因此未进行进一步手术干预。术后随访时间短，无法评估后续复发。最近一项关于小脑脑桥角表皮样囊肿的长期随访研究发现，切除范围与复发之间无关联[38]。因此，作者主张如果完全切除存在显著的术后并发症风险，应优先考虑手术安全性而非积极尝试完全切除[38]。
有趣的是，人类中已有表皮样囊肿恶变为癌的报道，尽管极为罕见[39,40,41,42,43,44,45,46,47]。这种风险在未手术治疗或切除不完全的病变中更高。由于人类的复发和恶变通常需要数年时间才能发生，由于长期随访的可得性有限，这些结局在兽医医学中可能被低估。
在本病例中，初次癫痫发作大约出现在就诊前三个月，当时猫临床状态稳定，未发现明显的电解质异常。据主人所述，发作常由响亮声音诱发，听觉反射性癫痫发作被认为是一种可能的癫痫表型。然而，在术后病程中，具有临床意义的电解质紊乱（包括高钠血症）复发，并伴有胃肠动力低下和呕吐。鉴于猫长期便秘且就诊时粪便膨胀，慢性脱水也可能促成了既存的高钠血症。尽管这些异常被反复纠正，但在死亡前不久癫痫发作日益频繁，可能因电解质紊乱而加重。因此，既存的高钠血症和可能的慢性脱水可能促成了术前临床症状，也可能加重了终末期临床病程；然而，其具体贡献无法从现有临床数据中确定。脾脏肥大细胞增生已在初次手术中切除，此后无临床复发证据。尽管如此，不能排除隐匿性内脏肥大细胞肿瘤作为病情恶化的潜在因素。根据临床病程，病情恶化似乎与并发腹部手术后的胃肠功能障碍关系更密切，而非软腭手术本身。然而，由于主人在多次住院后拒绝尸检，这一归因仍属推测，无法确定死亡原因。其他并发症，包括隐匿性感染，也不能完全排除。
4. 结论
我们描述了一例老年猫的软腭表皮样囊肿，包括详细的临床、诊断影像、手术和组织病理学发现。病变主要局限于软腭的口咽部，无中耳或骨质受累的证据。术后短期内不再观察到流涎和吞咽困难；然而，这种时间关联并不能建立因果关系，且由于随后发生的致死性胃肠和全身并发症，无法评估长期结局。囊肿的起源仍不确定，应考虑发育性和获得性两种机制。
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Simple Summary
Epidermoid cysts are uncommon benign cystic lesions in cats, and their occurrence in the soft palate is rarely reported. In this case, a soft palate mass was identified by computed tomography in a 17-year-old cat and confirmed histopathologically as an epidermoid cyst after surgical excision. Hypersalivation and dysphagia were no longer observed during the short postoperative period, although this temporal association does not establish causation. The cat subsequently developed severe gastrointestinal dysfunction, electrolyte disturbances, and recurrent seizures and died 27 days after surgery. The origin of the cyst remains uncertain, with both developmental and acquired mechanisms possible. This case highlights the clinical and diagnostic features of a soft palate epidermoid cyst in a geriatric cat.
1. Introduction
Oral masses account for approximately 3–12% of all masses in cats, and >89% are malignant [1,2,3]. In contrast, oral cysts are uncommon and histologically characterized by fluid- or semi-fluid-filled cavities lined by epithelium [4,5]. Among the various types of oral cysts, odontogenic cysts are relatively well-documented in cats. These cysts arise from remnants of odontogenic epithelium associated with tooth development and account for approximately 0.19–2% of feline oral masses or oral tissue specimens [6,7,8,9].
Non-odontogenic cysts are distinguished from odontogenic cysts by their developmental origin, which is unrelated to tooth-forming tissues. Reports of such lesions in cats are extremely limited. Only a few cases have been described in young cats, including a nasopharyngeal dermoid cyst [10] and a nasopharyngeal cyst containing secretory proteinaceous material in a young cat [11].
Dermoid cysts are characterized by keratinous, sebum-like content or the presence of skin derivatives [12]. In humans, dermoid cysts arising on the floor of the mouth and other intraoral sites are histologically classified according to the Meyer classification [13], which distinguishes three types based on cyst tissue components. Epidermoid cysts are lined with stratified squamous epithelium and contain keratinaceous material but lack skin adnexal structures. True dermoid cysts contain skin appendages, such as sweat glands, sebaceous glands, and hair follicles. Teratoid cysts arise from totipotent cells and contain tissues derived from all three embryonic germ layers, including muscles, bones, cartilage, and various epithelial tissues [5,14]. In veterinary medicine, dermoid cysts arising at various anatomical sites have been described and classified according to the nature of the epithelial lining and cyst contents [15,16]. However, reports of these cysts arising within the oral cavity are extremely limited [10,17,18,19], and no widely accepted classification system specific to oral epidermoid, true dermoid, and teratoid cysts has been established in veterinary medicine.
Surgical excision is generally considered the treatment of choice for epidermoid cysts [5,10,11,13,17,18,19]. This report describes an epidermoid cyst arising from the soft palate of a geriatric cat, including its diagnostic imaging, histopathological findings, and surgical management.
2. Case Description
A 17-year-old, 2.82 kg, neutered female domestic shorthair cat presented with mild hypersalivation and dysphagia. The cat had a history of multiple dental extractions. Seventeen months before presentation, teeth 308, 309, 408, and 409 were extracted because of gingivitis associated with dental calculus. At that time, teeth 304, 308, 309, 404, 408, 409, 103, and 203 were present. No oral lesions suggestive of generalized stomatitis were identified other than gingivitis surrounding the teeth affected by dental calculus. After these extractions, teeth 304, 404, 103, and 203 remained. The cat had a 2-year history of hyperthyroidism managed with carbimazole and a 7-year history of chronic constipation managed with a high-fiber prescription diet and occasional enemas. Seizure episodes had developed 3 months before presentation and were being managed with levetiracetam. Comprehensive diagnostic evaluation was performed to assess the overall health status of the cat. Systolic blood pressure was 160 mmHg, and thoracic auscultation revealed no abnormalities. Hematologic, serum biochemical, and blood gas analyses revealed mild elevations in NT-proBNP (155.7 pmol/L, RI 0–100 pmol/L) and fPLI (3.8 μg/L, RI 0–3.5 μg/L), as well as hypernatremia (160 mmol/L, RI 145–151 mmol/L). Total thyroxine (T4) concentration was within the reference range. No other clinically relevant abnormalities were identified in blood tests.
Thoracic radiographs were unremarkable, whereas abdominal radiographs revealed fecal distension of the descending colon and rectum. Abdominal ultrasonography identified splenic and hepatic lesions, and cytology of the splenic lesion was suggestive of mast cell proliferation, prompting concurrent splenectomy and liver biopsy.
Head, thoracic, and abdominal computed tomography (CT) were performed for tumor staging and to evaluate the potential intracranial causes of the seizures. For the CT examination, the cat was premedicated with butorphanol (0.2 mg/kg, IV). Anesthesia was induced with propofol (6 mg/kg, IV, to effect) and maintained with isoflurane in oxygen. There was no evidence of metastases or intracranial lesions. However, CT incidentally revealed a well-circumscribed, polypoid mass (8.5 × 9.9 × 10.0 mm) arising from the right distal soft palate and extending into the oropharyngeal lumen, causing adjacent nasopharyngeal narrowing (Figure 1). No signs of bony invasion or osteolysis were observed in the adjacent osseous structures, making an odontogenic origin less likely. Following intravenous administration of iohexol (2.5 mL/kg), the mass exhibited minimal contrast enhancement, with mean attenuation values of 96.09 ± 3.46 HU on pre-contrast images and 102.11 ± 4.27 HU on post-contrast images. The relatively high pre-contrast attenuation and minimal contrast enhancement made a simple fluid-filled cyst or an enhancing solid neoplasm less likely. Nevertheless, inflammatory processes, including abscess and granuloma, as well as other neoplasia, could not be excluded based on the CT findings alone.
Surgical excision of the soft palate mass was performed concurrently with splenectomy and liver biopsy under general anesthesia. Prior to anesthesia, the cat was clinically stable, and intravenous fluid therapy was administered to prevent dehydration and correct electrolyte abnormalities. The cat was premedicated with butorphanol (0.2 mg/kg, IV), while cefazolin (30 mg/kg, IV) and levetiracetam (20 mg/kg, IV) were administered perioperatively. Anesthesia was induced with propofol (6 mg/kg, IV) and maintained with inhaled isoflurane. Thorough examination of the oral cavity revealed no other oral or dental abnormalities. The mass was not readily visible on oral examination; however, digital palpation revealed a firm, mildly protruding lesion in the right oropharyngeal region. The lesion was grasped using atraumatic forceps and gently retracted rostrally, demonstrating good mobility and allowing clear visualization. Gauze packing was placed caudal to the mass to displace it rostrally and improve surgical exposure. The mass was covered with mucosa and had a smooth, dome-shaped surface (Figure 2A). A mucosal incision was made using a No. 15 scalpel blade, followed by blunt dissection of the mass from the surrounding tissue using a mosquito hemostat, iris scissors, and cotton-tipped applicators (Figure 2B). The mucosa was closely adhered to the underlying mass, which contained a yellow-brown creamy material (Figure 2C). Following grossly complete removal of the mass, the surgical site showed minimal hemorrhage and was left unsutured for second-intention healing.
Given the gross appearance of the mass contents, an infectious or inflammatory lesion was considered a differential diagnosis. To investigate a potential infectious etiology, the Feline Fever of Unknown Origin RealPCR Panel (IDEXX Laboratories, Inc., Westbrook, ME, USA) and the Feline Respiratory Pathogens Plus Panel and bacterial culture (GreenVet Laboratory, Yongin, Republic of Korea) were performed. The two panels included infectious agents potentially associated with the oral cavity (Supplementary Table S1). All PCR assays and the bacterial culture yielded negative results. Therefore, an infectious etiology of the lesion was considered unlikely.
Histopathological examination (IDEXX Laboratories, Inc., Westbrook, ME, USA) confirmed multifocal atypical mast cell proliferation in the spleen and hepatocellular nodular hyperplasia in the liver. The soft palate mass was identified as a cyst lined with keratinizing stratified squamous epithelium of relatively uniform thickness, ranging from 2 to 5 cell layers (Figure 3). Keratinization was exclusively orthokeratotic and keratohyalin granules were not prominent. The lining epithelium was extensively bordered by compact, mature, reactive, and dense fibrovascular connective tissue. The lumen of the cyst was filled with granular eosinophilic material, keratinaceous debris with entrapped acicular cholesterol clefts, and mixed nuclear debris. Lesional tissue extended to the edges of the submitted specimen; histologically complete excision could therefore not be confirmed. These findings were consistent with those of a benign epidermoid cyst.
Postoperatively, the cat received cefazolin (30 mg/kg, q12h, IV), famotidine (2 mg/kg, q12h, IV), and butorphanol (0.2 mg/kg, q6h, IV) for three days. Because the soft-palate surgical site was left to heal by second intention and was exposed to the oral environment, short-term postoperative cefazolin administration was selected based on the patient’s individual risk factors, including advanced age, concurrent systemic disease, and concurrent abdominal surgery. This was a patient-specific clinical decision rather than routine postoperative antimicrobial prophylaxis for oral surgery. Butorphanol was administered for postoperative analgesia for three days. Additional analgesic options were limited by the patient’s advanced age, longstanding constipation, seizure disorder, and pre-existing renal abnormalities. Fentanyl was considered less desirable because of the patient’s gastrointestinal history, whereas NSAIDs were avoided because of the patient’s age and renal abnormalities. No additional analgesic was administered thereafter. Hypersalivation and dysphagia were no longer observed after surgery and voluntary food intake resumed; however, this improvement was documented over a period of only approximately 24 h, as marked gastric distension consistent with gastrointestinal hypomotility and recurrent seizures developed on the following day. Despite improvement in general condition and appetite, gastrointestinal dysmotility persisted and was associated with metabolic alkalosis, hypernatremia, and azotemia. Supportive treatment included ondansetron (0.1 mg/kg, q8h, IV), maropitant (1 mg/kg, q24h, IV), a continuous rate infusion (CRI) of metoclopramide (0.08 mg/kg/h, IV), parenteral nutrition, and fluid and electrolyte correction. The cat improved and was discharged on postoperative day 7. Three days after discharge, the cat was rehospitalized for recurrent vomiting, gastrointestinal hypomotility, and fecal retention, with transient improvement following enemas and metoclopramide CRI. Severe gastrointestinal distension recurred on postoperative day 23, necessitating nasoesophageal tube feeding. During the final hospitalization, a central venous catheter was placed to facilitate prolonged intensive supportive treatment, including parenteral nutritional support and intravenous fluid and electrolyte therapy. Two days later, profound gastrointestinal hypomotility and recurrent seizures developed, followed by severe vomiting, muscle tremors, metabolic alkalosis, and marked hypernatremia. Despite supportive treatment, the cat died on postoperative day 27.
3. Discussion
Epidermoid cysts have been reported in cats at various anatomical sites, including the intestine [20], lung [21], and intracranial cavity [22,23,24]. In the oral cavity, only one soft palate cyst with gross and histopathological features similar to those of this case has been reported in a young cat [11]. In humans, oral epidermoid cysts are developmental or acquired in origin [5,13]. Developmental cysts result from the entrapment of ectodermal tissue during embryonic fusion, whereas acquired cysts may arise from traumatic or iatrogenic implantation of the epithelium into deeper tissues [5,13]. Similar mechanisms have been proposed in veterinary medicine. A previously reported soft palate cyst in a young cat was suspected to be congenital, arising during the fusion of the palatine plates as they grew medially from the maxillary processes to form the palate [11]. Conversely, acquired lesions may develop secondary to inflammation or trauma in an older dog [17].
Previously, the nasopharyngeal epidermoid cyst extended into the tympanic bulla [17], resembling reported cases of aural cholesteatoma with oropharyngeal involvement in dogs and cats [25,26,27]. Cholesteatomas share similar histopathological features with epidermoid cysts in some respects. Compared with primary oral epidermoid cysts, cholesteatomas involving the oropharynx originate within the tympanic bulla, with subsequent extension into the oropharynx or intracranial cavity as the disease progresses [28]. Thus, the involvement of the middle ear is an important feature that distinguishes these lesions from primary oral epidermoid cysts. In this case, the cyst was predominantly confined to the soft palate with no evidence of abnormalities or continuity with the middle ear structures on CT. The present case provides additional clinical, diagnostic imaging, surgical, and histopathological information on a soft-palate epidermoid cyst in a geriatric cat.
Several cystic or cyst-like lesions were considered in the differential diagnosis. A salivary mucocele was considered less likely because the present lesion was a discrete, epithelial-lined cyst containing keratinaceous material, rather than a mucus-filled cavity associated with salivary tissue or extravasated saliva. An odontogenic keratocystic lesion was also considered because of the history of dental extraction. However, the absence of adjacent osseous involvement on CT and the lack of characteristic luminal parakeratinization and basal cell palisading on histopathology made this diagnosis less likely [9]. Infundibular keratinizing cystic lesions were also considered; however, the absence of adnexal structures and the anatomic location within the soft palate were not supportive of a follicular or cutaneous adnexal origin. Cystic or keratinizing squamous cell carcinoma was considered as a neoplastic differential diagnosis, but the absence of cellular atypia, invasive epithelial growth, and malignant keratinization on histopathological examination did not support this diagnosis [1,2,3].
Although an acquired origin was considered as a possible explanation, the origin of the cyst could not be determined. A developmental cyst that remained clinically silent until old age cannot be excluded. In humans, traumatic implantation of epithelial cells into deeper tissues has been proposed as a mechanism for the development of acquired epidermoid cysts [29]. In an in vivo rat model, subcutaneous implantation of autogenous skin resulted in the proliferation of the implanted epithelium and formation of epithelium-lined cystic cavities containing keratin, hair, and other debris, resembling epidermoid or dermoid cysts [30].
Although there was no known history of direct trauma in this case, an acquired origin associated with previous mucosal injury was considered as one possible explanation. The cat had undergone caudal mouth extraction under general anesthesia with endotracheal intubation 17 months before the cyst was identified. Although the cat had a history of dental extractions and continued consumption of dry food, there was no documented evidence linking these factors to mucosal injury or cyst formation [29]. Therefore, none of these exposures can be considered evidence of a causal relationship, and the proposed acquired mechanism remains speculative.
Previously reported nasopharyngeal cysts in cats were associated with respiratory signs and marked nasopharyngeal obstruction [10,11]. Nasopharyngeal polyps were also considered because of the anatomical location. Feline nasopharyngeal polyps are benign inflammatory fibrovascular proliferations, typically arising from the middle ear or auditory tube and covered by epithelium. Histologically, they consist of fibrovascular connective tissue with inflammatory cells rather than a discrete keratin-filled cyst lined by stratified squamous epithelium [31]. In the present case, the lesion was a well-circumscribed, keratin-filled cyst lined by stratified squamous epithelium and arising from the distal soft palate, while CT showed no evidence of middle-ear or tympanic bulla involvement, making a nasopharyngeal polyp unlikely. The cat also showed no apparent respiratory signs, which may have been related to the small size of the cyst and its predominant confinement to the oropharynx, resulting in minimal nasopharyngeal obstruction. Furthermore, the lesion was detected incidentally on cranial CT, potentially before it had sufficiently enlarged to cause clinically relevant nasopharyngeal obstruction.
Mild hypersalivation and dysphagia were present before surgery and were considered possibly related to the soft palate lesion. Following excision, neither sign was observed during periods of clinical stability. Other potential explanations were also considered. No other oral or dental abnormalities that could readily account for them were identified on thorough examination of the oral cavity under general anesthesia or on CT. Pancreatic abnormalities and increased fPLI had been identified as chronic findings before surgery, without substantial changes in laboratory or imaging findings postoperatively, making acute pancreatitis-associated nausea a less likely explanation. Azotemia was not present preoperatively and therefore was unlikely to account for the initial signs. Hyperthyroidism and potential adverse effects of carbimazole and levetiracetam were also considered less likely because the same medications were continued after surgery without recurrence of hypersalivation or dysphagia during clinically stable periods. In contrast, hypernatremia was documented both preoperatively and during subsequent episodes of gastrointestinal dysfunction accompanied by vomiting and therefore could not be excluded as a contributing factor. Although interpretation of the postoperative improvement was confounded by concurrent splenectomy and perioperative analgesic and gastroprotective treatment, the temporal association between excision and resolution of hypersalivation and dysphagia suggests that the soft palate lesion may have contributed to these signs. Despite its small size and relatively mild degree of obstruction, the lesion may have caused local discomfort or interfered with swallowing.
Surgical excision is recommended for epidermoid cysts regardless of their anatomical location [10,11,17,20,21,22,23,24,29,32,33,34,35]. Recurrence following surgical excision is uncommon in veterinary patients; however, recurrence has been reported in a dog with an extradural spinal epidermoid cyst, in which the cyst regrew with recurrence of clinical signs 28 months after subtotal excision [34]. Similarly, recurrence is uncommon in humans and associated with incomplete excision [36,37]. In the present case, histologically complete excision could not be confirmed; however, no residual lesion was evident macroscopically after excision, and therefore no further surgical intervention was performed. The short postoperative follow-up precluded assessment of subsequent recurrence. A recent long-term follow-up study of cerebellopontine angle epidermoid cysts found no association between the extent of resection and recurrence [38]. Therefore, the authors advocated prioritizing surgical safety over aggressive attempts at complete removal if complete excision carries a substantial risk of postoperative complications [38].
Interestingly, malignant transformation of epidermoid cysts into carcinoma has been reported in humans, although it is exceedingly rare [39,40,41,42,43,44,45,46,47]. This risk is higher in surgically untreated or incompletely excised lesions. Because recurrence and malignant transformation in humans typically take several years to develop, these outcomes may be underrecognized in veterinary medicine owing to the limited availability of long-term follow-up.
In this case, the initial seizure episodes had developed approximately three months before presentation, when the cat was clinically stable and no major electrolyte abnormalities had been identified. According to the owner, the episodes were frequently triggered by loud sounds, and audiogenic reflex seizures were considered a possible seizure phenotype. During the postoperative course, however, clinically significant electrolyte disturbances, including hypernatremia, recurred in association with gastrointestinal hypomotility and vomiting. Given the cat’s longstanding constipation and fecal distension at presentation, chronic dehydration may also have contributed to the pre-existing hypernatremia. Although these abnormalities were repeatedly corrected, increasingly frequent seizures occurred shortly before death and may have been exacerbated by the electrolyte disturbances. Thus, pre-existing hypernatremia and possible chronic dehydration may have contributed to the preoperative clinical signs and may also have exacerbated the terminal clinical course; however, their specific contribution cannot be determined from the available clinical data. The splenic mast cell proliferation had been surgically removed during the initial procedure, with no clinical evidence of recurrence thereafter. Nevertheless, occult visceral mast cell neoplasia could not be excluded as a potential contributor to the deterioration. Based on the clinical course, the deterioration appeared to be more closely associated with gastrointestinal dysfunction following the concurrent abdominal surgery than with the soft-palate procedure itself. However, because the owner declined postmortem examination after several hospitalizations, this attribution remains speculative, and the cause of death could not be established. Other complications, including occult infection, also cannot be completely excluded.
4. Conclusions
We describe a soft-palate epidermoid cyst in a geriatric cat, with detailed clinical, diagnostic imaging, surgical, and histopathological findings. The lesion was predominantly confined to the oropharyngeal aspect of the soft palate and showed no evidence of middle-ear or bony involvement. Hypersalivation and dysphagia were no longer observed during the short postoperative period; however, this temporal association does not establish a causal relationship, and long-term outcome could not be assessed because of subsequent fatal gastrointestinal and systemic complications. The origin of the cyst remains uncertain, and both developmental and acquired mechanisms should be considered.