Otani Go, Ohta Hiroshi
Veterinary Teaching Hospital, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Nara Animal Medical Center, Nara-shi, Nara, Japan.
JFMS Open Rep. 2024 Oct 17;10(2):20551169241282737. doi: 10.1177/20551169241282737. eCollection 2024 Jul-Dec.
Persistent and progressive weakness secondary to hypokalaemia, that is, hypokalaemic polymyopathy, is one of the most common clinical signs of primary hyperaldosteronism (PHA). Herein, we report a case of PHA with infraspinatus muscle necrosis. A 5-year-old castrated male domestic shorthair cat presented with a history of polyuria and polydipsia, decreased activity, staggering gait, difficulty in jumping and inward rotation of both forelimbs. Blood examination revealed hypokalaemia, increased serum creatinine kinase activity and high serum aldosterone concentration. Abdominal ultrasonography and CT revealed an enlarged right adrenal gland. Post-contrast thoracic CT showed peripheral contrast enhancement and a non-enhanced centre in the bilateral infraspinatus muscles. From the day of initial presentation, the cat was started on oral potassium replacement therapy. On day 17, the right adrenal gland was surgically resected and the left infraspinatus muscle was biopsied. Histopathological examination confirmed the presence of an adrenocortical adenoma in the right adrenal gland and necrosis of the muscle fibres in the left infraspinatus muscle. On day 29, all clinical signs had disappeared, and the serum potassium concentration, creatinine kinase activity and aldosterone concentration had normalised. On day 57, atrophy of the bilateral infraspinatus muscles was noted, but there was no evidence of any posture or gait abnormalities.
To the authors' knowledge, this is the first report of possible infraspinatus muscle necrosis in a cat with PHA. It is also possible that the infrinatus muscle necrosis with hypokalaemic polymyopathy secondary to PHA was caused by compartment syndrome in the cat described here.
低钾血症继发的持续性和进行性肌无力,即低钾性多肌病,是原发性醛固酮增多症(PHA)最常见的临床体征之一。在此,我们报告一例患有冈下肌坏死的PHA病例。一只5岁去势的雄性家养短毛猫出现多尿、多饮、活动减少、步态蹒跚、跳跃困难和双前肢内旋的病史。血液检查显示低钾血症、血清肌酸激酶活性升高和血清醛固酮浓度升高。腹部超声和CT显示右侧肾上腺增大。增强胸部CT显示双侧冈下肌外周强化和中心无强化。从初次就诊之日起,该猫开始口服补钾治疗。第17天,右侧肾上腺手术切除,左侧冈下肌活检。组织病理学检查证实右侧肾上腺存在肾上腺皮质腺瘤,左侧冈下肌肌纤维坏死。第29天,所有临床体征消失,血清钾浓度、肌酸激酶活性和醛固酮浓度恢复正常。第57天,注意到双侧冈下肌萎缩,但没有任何姿势或步态异常的证据。
据作者所知,这是首例关于PHA猫可能出现冈下肌坏死的报告。在此描述的猫中,PHA继发的低钾性多肌病伴冈下肌坏死也可能是由骨筋膜室综合征引起的。