Perry Kayla M, Enders Brittany D, Negrão Watanabe Tatiane Terumi
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.
Small Animal Emergency and Triage Services, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.
J Vet Emerg Crit Care (San Antonio). 2023 Mar;33(2):257-262. doi: 10.1111/vec.13280. Epub 2023 Feb 17.
To describe the clinical findings and case progression in a dog presenting with severe systemic inflammatory response, refractory shock, progressive metabolic acidosis, and respiratory failure that was ultimately diagnosed with hypertrophic osteodystrophy (HOD).
A 4-month-old male intact Mastiff presented with a 24-hour history of lethargy and generalized ostealgia. On examination, the dog was recumbent, febrile, and tachycardic with pain on palpation of the abdomen, right femur, and mandible. Appendicular joint radiographs showed changes consistent with osteochondrosis and ulnar-retained cartilaginous cores, with no overt evidence of HOD. Initial treatment included IV fluid therapy, multimodal analgesia, and broad-spectrum antimicrobials. Vasopressor therapy was initiated following hemodynamic decompensation. Synovial fluid cytological analysis and culture revealed nonseptic suppurative inflammation and no bacterial growth, respectively. Blood and urine cultures also yielded no growth. Viscoelastic testing was consistent with hypercoagulability. The dog initially had a metabolic acidosis with appropriate respiratory compensation that progressed to a mixed metabolic and respiratory acidosis despite aggressive therapies that included antimicrobials, vasopressors, positive inotropes, and corticosteroids. Humane euthanasia was elected approximately 32 hours after admission. Necropsy yielded a diagnosis of HOD.
This is the first report detailing the occurrence of refractory shock and hypercoagulability associated with HOD in a dog without evidence of another identified comorbidity. HOD should be considered in any young, large-breed dog with generalized ostealgia and signs of systemic illness, even in the absence of classic radiographic abnormalities. Further investigation of coagulation status in dogs with HOD and a secondary systemic inflammatory response is warranted.
描述一只出现严重全身炎症反应、难治性休克、进行性代谢性酸中毒和呼吸衰竭并最终被诊断为肥厚性骨营养不良（HOD）的犬的临床症状及病例进展。
一只4月龄未绝育的雄性獒犬出现了24小时的嗜睡和全身骨痛病史。检查时，该犬侧卧、发热且心动过速，触诊腹部、右股骨和下颌时有疼痛。四肢关节X线片显示与骨软骨病和尺骨保留软骨核一致的变化，无明显的HOD证据。初始治疗包括静脉输液治疗、多模式镇痛和广谱抗菌药物。血流动力学失代偿后开始使用血管活性药物治疗。滑液细胞学分析和培养分别显示非感染性化脓性炎症且无细菌生长。血培养和尿培养也均无生长。粘弹性测试结果与高凝状态一致。该犬最初为代谢性酸中毒且有适当的呼吸代偿，尽管采取了包括抗菌药物、血管活性药物、正性肌力药物和皮质类固醇在内的积极治疗措施，但仍进展为混合性代谢性和呼吸性酸中毒。入院约32小时后选择实施安乐死。尸检诊断为HOD。
这是第一份详细报道一只无其他明确合并症证据的犬中与HOD相关的难治性休克和高凝状态发生情况的报告。对于任何有全身骨痛和全身疾病体征的年轻大型犬，即使没有典型的影像学异常，也应考虑HOD。有必要进一步研究患有HOD和继发性全身炎症反应的犬的凝血状态。
