Case of the month from the Desai Sethi Urology Institute, Florida, USA: bladder outlet obstruction-induced urinothorax after percutaneous nephrolithotomy

IF 4.4 2区 医学 Q1 UROLOGY & NEPHROLOGY BJU International Pub Date : 2024-05-08 DOI:10.1111/bju.16393
Ryan Chen, Joao G. Porto, Ruben Blachman-Braun, Diana M. Lopategui, Robert Marcovich, Hemendra N. Shah
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While the literature reports cases of urinothorax due to isolated obstructive uropathies (e.g., prostatic adenocarcinoma) [<span>2, 3</span>] or iatrogenic causes [<span>4-7</span>], our case report introduces what we believe to be the first documented instance of urinothorax precipitated by urine retention secondary to an enlarged prostate in the postoperative period after percutaneous nephrolithotomy (PCNL) with subcostal access.</p><p>A 51-year-old male with a history of hypertension and recurrent nephrolithiasis was found to have elevated PSA of 9.16 ng/mL and a left upper ureteric stone on renal ultrasonography that was carried out as a part of his annual physical examination by his primary care provider. He was asymptomatic from the stone but had LUTS with an IPSS of 13. He had a history of nephrolithiasis over the previous two decades and had undergone five ureteroscopies and one PCNL. He also had a family history of nephrolithiasis and prostate cancer. He was started on tamsulosin for LUTS by his primary care provider. His serum creatinine was 71.62 and CT confirmed the presence of a 1.3 × 3.0 × 1.5-cm stone in the left upper ureter (1630 Hounsfield units) with severe proximal hydroureteronephrosis (Fig. 1A). Multiparametric MRI of the prostate indicated a prostate size of 101.3 g, with no lesions suspicious for prostate cancer (Fig. 1C,D). His uroflowmetry was obstructed with a peak urinary flow rate (Q<sub>max</sub>) of 7.4 mL/s and a postvoid residual urine volume (PVR) of 21 mL.</p><p>Considering the large stone burden, the patient elected to proceed with left PCNL, and after shared decision making, he decided to monitor his PSA. However, before his surgery was scheduled, he developed a fever, and a left ureteric stent was placed at an outside facility to treat pyelonephritis (Fig. 1B). We subsequently performed a left tubeless PCNL with fluoroscopy-guided subcostal renal access in the prone position. During cystoscopy, we encountered a trilobar enlarged prostate with a median lobe, making access to the ureteric orifice challenging. The percutaneous tract was dilated with metal telescoping Alken dilators up to 24-Fr. Subsequently, a 24-Fr Amplatz sheath was introduced into the left kidney and the stone was fragmented with a Swiss Lithoclast™ Trilogy lithotripter (Boston Scientific, Marlborough, MA, USA; Fig. 2A). After confirming complete endoscopic and fluoroscopic stone removal, a 6-Fr 26-cm ureteric stent was deployed in an antegrade manner, and no nephrostomy tube was placed. The procedure was completed with no intra-operative complications. On postoperative day 1, the patient's serum creatinine level was 0.87 mg/dL, CT confirmed stone-free status, and he was discharged home after a successful voiding trial (Fig. 2B). Stone composition was 70% brushite, 20% calcium oxalate monohydrate, and 7% calcium phosphate hydroxyl form.</p><p>Ten days after discharge the patient returned to the emergency department complaining of abdominal pain that worsened with inspiration, worsening LUTS, and constipation that developed over the preceding 3–4 days. On evaluation, he had leucocytosis (white blood cells of 15.9 × 10<sup>3</sup>/μL) and acute kidney injury (creatinine of 3.34 mg/dL). A new CT scan demonstrated severe left hydroureteronephrosis with a 3-cm perinephric fluid collection that opacified with contrast, consistent with urine leak from a lower pole renal access with marked bladder distention and appropriately positioned left ureteric stent (Fig. 3). There was a moderate left pleural effusion of approximately 100 mL and basilar linear atelectasis, which was also observed on a chest X-ray (Figs. 3C and 4A). The patient was started on ceftriaxone, chest spirometry and physiotherapy, and was recommended to undergo Foley catheter placement. Initially, he refused the placement of a catheter, until the second day of admission, at which time he acquiesced, prompted by a rise in serum creatinine to 4.36 mg/dL and a chest X-ray that showed worsening of the left pleural effusion (Fig. 4B). He was also scheduled for thoracentesis, following a pulmonology consultation. Remarkably, after the Foley catheter was placed, there was a significant overnight decrease in his serum creatinine to 0.95 mg/dL. A subsequent chest X-ray indicated considerable reduction in the pleural effusion (Fig. 4C), leading to cancellation of the planned thoracentesis. As a result, the patient was managed conservatively, maintaining the Foley catheter for continuous drainage, and engaging in chest spirometry exercises.</p><p>On the 4th day after emergency admission the patient's serum creatinine level had further declined to 0.80 mg/dL, and a chest X-ray showed continued improvement (Fig. 4D). Consequently, he was discharged with an indwelling Foley catheter in place. At a 2-week follow-up, both his serum creatinine levels and chest X-ray had normalized, and a renal ultrasonography confirmed resolution of the perinephric fluid collection as well as a reduction in hydronephrosis, with the ureteric stent still in place (Fig. 5). Five weeks after surgery, the patient had his stent removed. However, his urinary flow remained obstructed, evidenced by a voided volume of 207 mL, a Q<sub>max</sub> of 8.7 mL/s, and a PVR of 95 mL. Despite this, he chose to persist with medical management, continuing treatment with tamsulosin.</p><p>The patient in the present report had both obstructive uropathy due to urinary retention secondary to an enlarged prostate, and iatrogenic renal trauma resulting from PCNL. Others have similarly reported urinothorax following iatrogenic trauma from PCNL, ureteroscopy, and partial nephrectomy [<span>4-9</span>]. Urinothorax has also been found to arise in the setting of obstructive prostatic adenocarcinoma and renal calculi [<span>7, 9, 10</span>]. However, each of these reported cases had a clear aetiology, and management was thus straightforward: addressing the root cause resolved the urinothorax.</p><p>The pathogenesis of urinothorax is primarily explained by two theories: one theory suggests that urine crosses a diaphragmatic defect to reach the pleural space, while the other proposes that urine from the retroperitoneal area enters the peritoneal cavity, eventually reaching the pleural cavity via lymphatic channels [<span>6, 9</span>]. We propose that our patient developed postoperative urine retention due to his large prostate, which led to secondary left vesico-ureteric reflux aggravated by an indwelling ureteric stent, thereby causing urine leakage from the site of his PCNL. 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However, it is important to highlight that resolution of symptoms was delayed due to the patient's repeated refusal of catheter placement in the first 2 days after emergency admission, which worsened his pleural effusion and serum creatinine level. Therefore, early consideration for placement of a urethral catheter is recommended, potentially even prior to thoracentesis, especially in cases where urinothorax is suspected. Additionally, it is widely recognized that patients with symptomatic enlarged prostate and concurrent nephrolithiasis can benefit from simultaneous surgical treatment, addressing both the enlarged prostate and the stones [<span>11</span>]. Such an approach can prevent complications such as those detailed in this report.</p><p>Delayed urinothorax is a rare complication that may arise secondary to PCNL or prostate enlargement. We present a unique case of urinothorax in a patient with both an obstructive uropathy due to urinary retention resulting from an enlarged prostate and iatrogenic renal trauma resulting from PCNL. 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引用次数: 0

Abstract

Urinothorax, a rare cause of pleural effusion characterised by the presence of urine in the pleural space, typically occurs iatrogenically after urological procedures or spontaneously due to obstructive uropathies. Its diagnosis centres on high clinical suspicion and the biochemical analysis of pleural fluid, with treatment focusing on alleviating urinary obstruction or treating traumatic injuries [1-3]. While the literature reports cases of urinothorax due to isolated obstructive uropathies (e.g., prostatic adenocarcinoma) [2, 3] or iatrogenic causes [4-7], our case report introduces what we believe to be the first documented instance of urinothorax precipitated by urine retention secondary to an enlarged prostate in the postoperative period after percutaneous nephrolithotomy (PCNL) with subcostal access.

A 51-year-old male with a history of hypertension and recurrent nephrolithiasis was found to have elevated PSA of 9.16 ng/mL and a left upper ureteric stone on renal ultrasonography that was carried out as a part of his annual physical examination by his primary care provider. He was asymptomatic from the stone but had LUTS with an IPSS of 13. He had a history of nephrolithiasis over the previous two decades and had undergone five ureteroscopies and one PCNL. He also had a family history of nephrolithiasis and prostate cancer. He was started on tamsulosin for LUTS by his primary care provider. His serum creatinine was 71.62 and CT confirmed the presence of a 1.3 × 3.0 × 1.5-cm stone in the left upper ureter (1630 Hounsfield units) with severe proximal hydroureteronephrosis (Fig. 1A). Multiparametric MRI of the prostate indicated a prostate size of 101.3 g, with no lesions suspicious for prostate cancer (Fig. 1C,D). His uroflowmetry was obstructed with a peak urinary flow rate (Qmax) of 7.4 mL/s and a postvoid residual urine volume (PVR) of 21 mL.

Considering the large stone burden, the patient elected to proceed with left PCNL, and after shared decision making, he decided to monitor his PSA. However, before his surgery was scheduled, he developed a fever, and a left ureteric stent was placed at an outside facility to treat pyelonephritis (Fig. 1B). We subsequently performed a left tubeless PCNL with fluoroscopy-guided subcostal renal access in the prone position. During cystoscopy, we encountered a trilobar enlarged prostate with a median lobe, making access to the ureteric orifice challenging. The percutaneous tract was dilated with metal telescoping Alken dilators up to 24-Fr. Subsequently, a 24-Fr Amplatz sheath was introduced into the left kidney and the stone was fragmented with a Swiss Lithoclast™ Trilogy lithotripter (Boston Scientific, Marlborough, MA, USA; Fig. 2A). After confirming complete endoscopic and fluoroscopic stone removal, a 6-Fr 26-cm ureteric stent was deployed in an antegrade manner, and no nephrostomy tube was placed. The procedure was completed with no intra-operative complications. On postoperative day 1, the patient's serum creatinine level was 0.87 mg/dL, CT confirmed stone-free status, and he was discharged home after a successful voiding trial (Fig. 2B). Stone composition was 70% brushite, 20% calcium oxalate monohydrate, and 7% calcium phosphate hydroxyl form.

Ten days after discharge the patient returned to the emergency department complaining of abdominal pain that worsened with inspiration, worsening LUTS, and constipation that developed over the preceding 3–4 days. On evaluation, he had leucocytosis (white blood cells of 15.9 × 103/μL) and acute kidney injury (creatinine of 3.34 mg/dL). A new CT scan demonstrated severe left hydroureteronephrosis with a 3-cm perinephric fluid collection that opacified with contrast, consistent with urine leak from a lower pole renal access with marked bladder distention and appropriately positioned left ureteric stent (Fig. 3). There was a moderate left pleural effusion of approximately 100 mL and basilar linear atelectasis, which was also observed on a chest X-ray (Figs. 3C and 4A). The patient was started on ceftriaxone, chest spirometry and physiotherapy, and was recommended to undergo Foley catheter placement. Initially, he refused the placement of a catheter, until the second day of admission, at which time he acquiesced, prompted by a rise in serum creatinine to 4.36 mg/dL and a chest X-ray that showed worsening of the left pleural effusion (Fig. 4B). He was also scheduled for thoracentesis, following a pulmonology consultation. Remarkably, after the Foley catheter was placed, there was a significant overnight decrease in his serum creatinine to 0.95 mg/dL. A subsequent chest X-ray indicated considerable reduction in the pleural effusion (Fig. 4C), leading to cancellation of the planned thoracentesis. As a result, the patient was managed conservatively, maintaining the Foley catheter for continuous drainage, and engaging in chest spirometry exercises.

On the 4th day after emergency admission the patient's serum creatinine level had further declined to 0.80 mg/dL, and a chest X-ray showed continued improvement (Fig. 4D). Consequently, he was discharged with an indwelling Foley catheter in place. At a 2-week follow-up, both his serum creatinine levels and chest X-ray had normalized, and a renal ultrasonography confirmed resolution of the perinephric fluid collection as well as a reduction in hydronephrosis, with the ureteric stent still in place (Fig. 5). Five weeks after surgery, the patient had his stent removed. However, his urinary flow remained obstructed, evidenced by a voided volume of 207 mL, a Qmax of 8.7 mL/s, and a PVR of 95 mL. Despite this, he chose to persist with medical management, continuing treatment with tamsulosin.

The patient in the present report had both obstructive uropathy due to urinary retention secondary to an enlarged prostate, and iatrogenic renal trauma resulting from PCNL. Others have similarly reported urinothorax following iatrogenic trauma from PCNL, ureteroscopy, and partial nephrectomy [4-9]. Urinothorax has also been found to arise in the setting of obstructive prostatic adenocarcinoma and renal calculi [7, 9, 10]. However, each of these reported cases had a clear aetiology, and management was thus straightforward: addressing the root cause resolved the urinothorax.

The pathogenesis of urinothorax is primarily explained by two theories: one theory suggests that urine crosses a diaphragmatic defect to reach the pleural space, while the other proposes that urine from the retroperitoneal area enters the peritoneal cavity, eventually reaching the pleural cavity via lymphatic channels [6, 9]. We propose that our patient developed postoperative urine retention due to his large prostate, which led to secondary left vesico-ureteric reflux aggravated by an indwelling ureteric stent, thereby causing urine leakage from the site of his PCNL. Such leakage caused a pseudo-acute kidney injury with a significant increase in creatinine levels but also facilitated the migration of urine into the pleural cavity, presenting as a pleural effusion.

Management of urinothorax typically necessitates prompt diagnosis through pleural fluid analysis via thoracentesis, immediately followed by intervention for diversion, drainage, or alleviation of the obstruction [2]. The pleural fluid characteristic of urinothorax is transudative, with a defining feature being its creatinine concentration, which exceeds that of serum levels. Generally, the effusion is unilateral and occurs on the same side as the underlying uropathy. Many others have reported placing a pleural drainage tube to aid in the resolution of the pleural effusion [5, 6]. In our patient's case, the unilateral pleural effusion was swiftly resolved following insertion of a Foley catheter (Fig. 4). However, it is important to highlight that resolution of symptoms was delayed due to the patient's repeated refusal of catheter placement in the first 2 days after emergency admission, which worsened his pleural effusion and serum creatinine level. Therefore, early consideration for placement of a urethral catheter is recommended, potentially even prior to thoracentesis, especially in cases where urinothorax is suspected. Additionally, it is widely recognized that patients with symptomatic enlarged prostate and concurrent nephrolithiasis can benefit from simultaneous surgical treatment, addressing both the enlarged prostate and the stones [11]. Such an approach can prevent complications such as those detailed in this report.

Delayed urinothorax is a rare complication that may arise secondary to PCNL or prostate enlargement. We present a unique case of urinothorax in a patient with both an obstructive uropathy due to urinary retention resulting from an enlarged prostate and iatrogenic renal trauma resulting from PCNL. Initial conservative treatment that relieved the obstruction was sufficient and should be considered even before thoracocentesis in patients with urinothorax and multiple possible aetiologies.

The authors have no conflicts of interest to declare.

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来自美国佛罗里达州德赛-塞西泌尿外科研究所的本月病例:经皮肾结石切开术后膀胱出口梗阻引发的尿气胸。
尿胸是一种罕见的胸膜积液的病因,其特征是胸膜腔内有尿液,通常发生在泌尿外科手术后或由于梗阻性尿病而自发发生。其诊断以临床高度怀疑和胸水生化分析为中心,治疗重点是减轻尿路梗阻或治疗外伤性损伤[1-3]。虽然文献报道了由于孤立的梗阻性尿路病变(如前列腺腺癌)[2,3]或医源性原因[4-7]而导致尿胸的病例,但我们的病例报告介绍了我们认为是第一例有文献记载的经皮肾镜取石术(PCNL)术后伴有前列腺肥大的尿潴留的尿胸病例。一名51岁男性,有高血压和复发性肾结石病史,在其初级保健医生的年度体检中,通过肾脏超声检查发现PSA升高9.16 ng/mL,左侧输尿管上部结石。他无结石症状,但有LUTS, IPSS为13。他在过去的二十年中有肾结石病史,并接受了五次输尿管镜检查和一次PCNL。他也有肾结石和前列腺癌的家族史。他的初级保健提供者开始使用坦索罗辛治疗LUTS。他的血清肌酐为71.62,CT证实在左输尿管上部(1630 Hounsfield单位)存在一个1.3 × 3.0 × 1.5 cm的结石,并伴有严重的近端输尿管积水(图1A)。前列腺多参数MRI显示前列腺大小为101.3 g,未见可疑前列腺癌病变(图1C,D)。尿流测量受阻,峰值尿流率(Qmax)为7.4 mL/s,空后残留尿量(PVR)为21 mL。考虑到结石负担较大,患者选择进行左侧PCNL,在共同决策后,他决定监测PSA。然而,在他的手术安排之前,他出现发烧,并在外部设施放置左侧输尿管支架治疗肾盂肾炎(图1B)。随后,我们在俯卧位进行了左侧无管PCNL,透视引导下肋下肾通道。在膀胱镜检查时,我们遇到了一个三叶状的前列腺肥大伴正中叶,使得进入输尿管口变得困难。经皮道用金属伸缩式Alken扩张器扩张至24fr。随后,将24 fr Amplatz鞘引入左肾,并用瑞士Lithoclast™Trilogy碎石机(Boston Scientific, Marlborough, MA, USA;图2 a)。经内镜和透视确认结石完全清除后,顺行放置6-Fr 26 cm输尿管支架,未放置肾造口管。手术完成,无术中并发症。术后第1天,患者血清肌酐水平为0.87 mg/dL, CT证实无结石,排尿试验成功后出院(图2B)。石料成分为70%的刷石,20%的一水草酸钙和7%的磷酸钙羟基形式。出院后10天,患者返回急诊科,主诉腹痛,吸气加重,LUTS恶化,便秘发生在前3-4天。经检查,患者白细胞增多(白细胞15.9 × 103/μL),急性肾损伤(肌酐3.34 mg/dL)。新的CT扫描显示严重的左侧输尿管积水伴3厘米的肾周积液,造影剂使其不透明,与肾下极通道的尿漏相一致,伴有明显的膀胱膨胀和适当位置的左侧输尿管支架(图3)。胸部x线片上也观察到约100 mL的中度左侧胸腔积液和基底线状不张(图3C和4A)。患者开始使用头孢曲松,胸部肺活量测定和物理治疗,并建议行Foley导管置入。最初,患者拒绝置管,直到入院第二天,由于血清肌酐升高至4.36 mg/dL,胸部x线片显示左侧胸腔积液恶化,患者默认了置管(图4B)。在肺科会诊后,他也被安排进行胸腔穿刺。值得注意的是,在Foley导管放置后,他的血清肌酐在夜间显著下降至0.95 mg/dL。随后的胸部x光片显示胸腔积液明显减少(图4C),导致计划的胸腔穿刺取消。因此,对患者进行保守治疗,维持Foley导管持续引流,并进行胸肺活量测定练习。 急诊入院后第4天,患者血清肌酐水平进一步下降至0.80 mg/dL,胸片显示持续改善(图4D)。因此,他在留置Foley导尿管的情况下出院。随访2周后,患者血清肌酐水平和胸片均恢复正常,肾超声检查证实肾周积液消失,肾积水减少,输尿管支架仍在原位(图5)。术后5周,患者将支架取出。然而,他的尿流仍然受阻,空气量为207 mL, Qmax为8.7 mL/s, PVR为95 mL。尽管如此,他还是选择坚持医疗管理,继续用坦索罗辛治疗。本报告中的患者有两种梗阻性尿病,一种是继发于前列腺肥大的尿潴留,另一种是由PCNL引起的医源性肾损伤。其他人也有类似的报道,PCNL、输尿管镜检查和部分肾切除术后的医源性创伤导致尿胸[4-9]。尿胸也被发现出现在梗阻性前列腺癌和肾结石中[7,9,10]。然而,这些报告的病例都有一个明确的病因,因此管理很简单:解决根本原因解决了尿胸。尿胸的发病机制主要有两种解释:一种理论认为尿液穿过膈缺损到达胸膜间隙,另一种理论认为尿液从腹膜后区进入腹膜腔,最终通过淋巴通道到达胸膜腔[6,9]。我们认为患者术后尿潴留是由于前列腺肥大,留置输尿管支架加重了继发性左膀胱输尿管反流,导致PCNL部位尿漏。这种渗漏引起假性急性肾损伤,肌酐水平显著升高,但也促进尿液向胸腔内迁移,表现为胸腔积液。尿胸的治疗通常需要通过胸腔穿刺进行胸腔积液分析,及时诊断,随后立即采取转移、引流或缓解梗阻的干预措施。尿胸的胸水特征是变性的,其决定性特征是肌酐浓度高于血清水平。一般情况下,积液是单侧的,发生在同一侧的泌尿系统疾病。许多其他报道放置胸腔引流管以帮助解决胸腔积液[5,6]。在我们的病例中,单侧胸腔积液在插入Foley导管后迅速得到解决(图4)。然而,需要强调的是,由于患者在急诊入院后的前2天多次拒绝放置导管,导致胸腔积液和血清肌酐水平恶化,症状的解决被推迟。因此,建议尽早考虑放置导尿管,甚至可能在胸腔穿刺之前,特别是在怀疑有尿胸的情况下。此外,人们普遍认为,伴有症状性前列腺肥大和并发肾结石的患者可以同时接受手术治疗,同时解决前列腺肥大和肾结石问题。这种方法可以防止本报告中详述的各种并发症。延迟性尿胸是一种罕见的并发症,可能继发于PCNL或前列腺肿大。我们报告一个独特的尿胸病例,患者同时患有前列腺肥大引起的尿潴留和PCNL引起的医源性肾创伤的梗阻性尿病。对于有尿胸和多种可能病因的患者,最初的保守治疗缓解梗阻是足够的,在进行胸穿刺术之前就应该考虑。作者无利益冲突需要申报。
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来源期刊
BJU International
BJU International 医学-泌尿学与肾脏学
CiteScore
9.10
自引率
4.40%
发文量
262
审稿时长
1 months
期刊介绍: BJUI is one of the most highly respected medical journals in the world, with a truly international range of published papers and appeal. Every issue gives invaluable practical information in the form of original articles, reviews, comments, surgical education articles, and translational science articles in the field of urology. BJUI employs topical sections, and is in full colour, making it easier to browse or search for something specific.
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Response to comment by Semwal et al. Comment on 'Prostate zonal impact of 5α-reductase inhibitors on multiparametric MRI characteristics and detection of prostate cancer'. Area deprivation and cancer-specific mortality in non-muscle-invasive bladder cancer: a statewide analysis. Correction to “Long‐term multicentre analysis of robot‐assisted radical cystectomy for non‐muscle‐invasive bladder cancer” Response to ‘Letters to the Editor’ comments on the paper ‘Impact of positive surgical margins on biochemical recurrence and metastases after radical prostatectomy’
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