Postoperative Bladder Atony in a Bitch following Surgical Resection of Urethral Leiomyosarcoma

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Background: Micturition requires coordinated activity between detrusor contraction and urethral relaxation mediated by parasympathetic and somatic pathways. Disruption of these neural or myogenic connections can result in bladder atony.Itis an important postoperative complication in dogs, particularly following lower urinary tract surgery. This condition can lead to urinary retention and long-term voiding dysfunction. This case report highlights the diagnostic challenges and therapeutic considerations of postoperative bladder atony following surgical resection of a urethral leiomyosarcoma, emphasizing the importance of early recognition and integrated management for optimal recovery. Case: An 11-year-old spayed bitch mongrel underwent surgical resection and end-to-end anastomosis for a urethral mass which was histopathologically confirmed as a low-grade urethral leiomyosarcoma. On postoperative day 5, urinary retention with marked bladder distension was observed following removal of the indwelling urethral catheter. Neurological examination revealed no abnormalities, and diagnostic imaging and urinalysis excluded mechanical obstruction and urinary tract infection. The bladder was flaccid and easily expressible without voluntary voiding effort, findings consistent with bladder atony. Medical therapy including bethanechol, terazosin and metoclopramide was initiated in combinationwith manual bladder expression which was performed several times daily to prevent overdistension. Gradual improvement was noted, and spontaneous urination resumed on postoperative day 18 and persisted for 2 weeks without recurrence of retention. The patient remained clinically stable and was discharged on postoperative day 44. Pharmacologic therapy was continued and manual bladder expression performed by the owner at home. Several weeks after discharge, the patient developed lethargy and hematuria following manual expression. The dog’s condition deteriorated rapidly and died. Necropsy was not performed at the owner’s request. Discussion: Postoperative bladder atony is a clinically significant complication following lower urinary tract surgery. The condition is primarily attributed to transient detrusor ischemia, neural traction or excessive bladder distension during or after surgery, which may collectively impair muscle excitability and contractility. Multifactorial influences such as ischemic, neurogenic, and pharmacologic factors may contribute to bladder atony, highlighting the need for early recognition and appropriate intervention. Functional recovery depends on the severity and duration of injury, as chronic atony may lead to irreversible degeneration of smooth muscle fibers and autonomic innervation. In this case, pharmacologic and mechanical interventionssupported functional improvement of bladder contractility and partial restoration of urination.Treatment includes parasympathomimetic, α-blocking and prokinetic agents to enhance detrusor contraction and reduce outlet resistance.Manual bladder expression or intermittent catheterization is also performed to prevent overdistension. These supportive therapeutic measures can contribute to preventing long-term detrusor damage and facilitating functional recovery. This case highlights that postoperative bladder atony can develop after successful urethral surgery, emphasizing the importance of early recognition, careful postoperative monitoring, and supportive management to preserve bladder function. Delayed intervention or improper bladder handling may exacerbate detrusor injury and lead to irreversible dysfunction or rupture. Awareness of this potential complication and timely pharmacologic and mechanical support are critical to improving outcomes in similar canine cases. Keywords: bladder atony, dog, postoperative complication, urethral neoplasm, urinary retention.

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