Case Report: Deep vein thrombosis and pulmonary embolism secondary to urinary retention in a neurogenic bladder

Kamran Zahoor , Mateja Jovanovic , Lekha Yadukumar , Atif Naseem , Hassan Chattha
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Abstract

Our patient is a 36-year-old man with a past medical history significant for the SCN-95 mutation associated with Brugada syndrome, two provoked episodes of DVT, and Hinman syndrome, also known as non-neurogenic neurogenic bladder, which is a voiding dysfunction of the urinary bladder of neuropsychological origin. Despite negative hypercoagulability workups in the past, the patient had experienced two provoked episodes of DVT, thirteen and nine years ago, respectively, leading to previous anticoagulant therapy with warfarin and Eliquis. However, he discontinued anticoagulation on the advice of his hematologist four years ago and currently manages his Hinman syndrome with intermittent straight catheterization, which poses challenges to adherence. The patient presented to the emergency department with right lower extremity pain, initially yielding a negative DVT workup. Subsequent presentation with exertional dyspnea led to the discovery of an acute non-occlusive thrombus in the right saphenofemoral junction and a chronic occlusive thrombus in the right femoral vein, with pulmonary emboli noted on imaging. Given his history of urinary retention secondary to Hinman syndrome, non-compliance by the patient to self-catheterize five times a day, and absence of any recent provoking factor, the thromboembolic events were attributed to right iliac vein obstruction caused by an enormously distended bladder compressing the anatomical structures in the vicinity and leading to DVT and pulmonary embolism. Hospitalization ensued, with the initiation of urethral catheterization and anticoagulant therapy, resulting in clinical improvement and the subsequent decision for lifelong anticoagulation. This case underscores the importance of recognizing rare etiologies of DVT/PE, particularly in patients with underlying urinary dysfunction, and highlights the need for timely intervention to prevent potentially fatal complications.
病例报告:神经源性膀胱尿潴留继发深静脉血栓和肺栓塞
我们的患者是一名 36 岁的男性,既往病史显示其 SCN-95 基因突变与 Brugada 综合征有关、两次深静脉血栓诱发发作以及 Hinman 综合征(又称非神经源性神经源性膀胱,是一种由神经心理因素引起的膀胱排尿功能障碍)。尽管过去的高凝状态检查结果呈阴性,但患者分别在十三年前和九年前经历过两次深静脉血栓的诱发发作,因此之前曾使用华法林和Eliquis进行抗凝治疗。然而,四年前他在血液科医生的建议下停止了抗凝治疗,目前通过间歇性直导管插入术来治疗欣曼综合征,这给坚持治疗带来了挑战。患者因右下肢疼痛到急诊科就诊,最初的深静脉血栓检查结果为阴性。随后,患者因劳累性呼吸困难就诊,结果发现右隐股交界处有急性非闭塞性血栓,右股静脉有慢性闭塞性血栓,影像学检查还发现了肺栓塞。考虑到患者曾因欣曼综合征(Hinman Syndrome)而出现尿潴留,且未坚持每天自行导尿五次,近期也没有任何诱发因素,因此将血栓栓塞事件归因于右髂静脉阻塞,原因是膀胱过度膨胀压迫了附近的解剖结构,导致深静脉血栓形成和肺栓塞。患者随后住院,接受了尿道导管插入术和抗凝治疗,临床症状有所改善,随后决定终身抗凝。该病例强调了识别深静脉血栓/肺栓塞罕见病因的重要性,尤其是在有潜在排尿功能障碍的患者中,并强调了及时干预以预防潜在致命并发症的必要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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