兽研简要摘要
淋巴静脉交通是淋巴系统与静脉系统之间的异常连接，在兽医学中特征描述尚不充分。本研究描述了通过计算机断层扫描在三只老年猫中疑似淋巴静脉交通的影像学表现。在所有猫中，对比增强计算机断层扫描均识别出异常扩张和迂曲的血管，连接门静脉系统分支与乳糜池——一个主要的腹部淋巴结构。乳糜池和胸导管也扩张并显示对比增强。其他反复出现的发现包括门静脉狭窄、胸腔或腹腔内液体积聚以及皮下水肿。这些交通的相似解剖分布及相关异常提示，这些血管可能代表预先存在的连接，在门静脉或淋巴循环慢性改变的响应下增大并具有功能相关性，尽管不能完全排除先天性起源。识别这一影像学模式可能有助于兽医识别此前未被认识的淋巴静脉交通，并改善对接受对比增强计算机断层扫描的猫中复杂门静脉和淋巴异常的解读。
1. 引言
淋巴系统由淋巴管、淋巴干和淋巴导管组成。主要的淋巴引流途径围绕胸导管（TD）和右淋巴导管（RLD）组织[1]。胸导管代表身体大部分淋巴回流的主要途径，起自乳糜池（CC）的颅侧延续，终止于颈外静脉与颈内静脉的交汇处或颈静脉与左锁骨下静脉的交汇处[1]。这些终末淋巴静脉连接构成淋巴系统与静脉系统之间的主要生理性交通部位。在腹腔内，来自内脏的淋巴通过数条淋巴干到达乳糜池，包括肠干和腹腔干[1]。解剖学研究已证明这些淋巴途径的组织结构存在相当大的变异性，尤其是肠干，其属支可能在进入乳糜池之前围绕肠系膜前动脉形成广泛的互联淋巴网络（肠网）[2]。
在人类医学中，被归类为正常且常见的淋巴静脉交通（LVCs）包括胸导管终末、右淋巴导管终末和结内LVCs[3]。病理性LVCs也已在多种疾病状态中被描述，包括原发性和继发性淋巴水肿，以及累及淋巴结的原发性和转移性恶性肿瘤[3]。此外，淋巴静脉交通可通过手术建立，用于治疗继发性淋巴水肿和其他淋巴疾病[3]。
在兽医学方面，Threefoot（1968）[4]在包括犬在内的几种哺乳动物中证明了生理性LVCs的存在，涉及全身多个静脉区域；而Zajac（1972）[5]描述了乳糜池与后腔静脉之间的交通。此外，Griaznova（1962）[6]以及Kagan和Breznock（1979）[7]的实验研究表明，完全性胸导管阻塞导致阻塞部位近端LVCs的开放，支持其作为维持淋巴引流的代偿途径的作用。获得性LVCs也被认为在胸导管结扎术治疗乳糜胸的成功中发挥重要作用[8]。最近，在犬和猫中的实验研究已证明在胸导管与静脉系统之间建立直接LVCs作为淋巴疾病潜在治疗策略的技术可行性[9,10]。
然而，病理性LVCs在兽医学中特征描述仍然不足，现有文献主要限于解剖学观察和实验研究。因此，其临床意义、影像学特征以及与潜在疾病的可能关联在很大程度上仍然未知。据作者所知，这是首个使用对比增强计算机断层扫描描述猫中疑似自发性LVCs的病例系列，提供了关于其解剖分布、影像学特征及相关异常的新信息。
2. 材料与方法
在这项回顾性研究中，通过检索词“淋巴静脉分流”和“淋巴管静脉交通”从2024年至2025年的远程影像学提交资料中识别出疑似淋巴静脉交通病例。纳入标准为：可获得完整的胸腹部增强CT检查，并显示以下表现：（1）一条异常扩张且迂曲的血管结构，起源于门静脉系统属支或与其直接相连；（2）该结构与乳糜池和/或胸导管之间存在可追踪的解剖走行连接。CT检查需具备足够的诊断质量以评估所涉及的门静脉和淋巴结构。初步识别出4只疑似淋巴静脉交通的猫，其中3只符合纳入标准并入组研究，1只因仅有胸部CT检查而被排除，无法评估疑似交通的腹部起源及完整走行。数据库检索期间未发现累及其他解剖部位的疑似淋巴静脉交通。联系转诊兽医并提供所有可获得的临床信息，包括信号特征、临床病史、既往诊断检查及治疗、体格检查、血液分析、细胞学/组织病理学以及临床转归。
根据转诊机构不同，使用了不同的CT设备和扫描方案：病例1和病例2使用Aquilion Start 16排CT扫描仪（Canon Medical Systems，小田原，日本）成像。图像采集采用螺旋模式，层厚1.0 mm，螺距0.94，机架旋转时间0.75 s，管电压100 kVp，管电流90 mA。病例3使用SOMATOM 32排CT扫描仪（Siemens Healthineers，埃尔朗根，德国）检查，层厚2 mm，螺距1.2，机架旋转时间0.33 s，管电压100 kVp，管电流41 mA。
所有方案均在全身麻醉下取腹卧位进行。包括整个腹部的软组织和骨算法图像，以及静脉注射碘对比剂（Iohexol，Omnipaque®，GE Healthcare，奥斯陆，挪威）前后图像，剂量为600 mg/kg，分期方案未明确说明。
每项CT检查均由两名委员会认证的兽医放射科医师（V.C.C.和N.I.）、一名二年级诊断影像住院医师（L.L.F.）和一名诊断影像实习生（I.R.A.）使用图像分析工作站（Horos，版本3.3.6，Horos Project，安纳波利斯，马里兰州，美国）仔细审阅。审阅并记录以下特征：通过对比增强识别异常淋巴静脉连接及相关淋巴管；交通的起源、路径、引流及大小；腹膜或胸腔积液的存在；以及肿块、淋巴结受累或慢性炎症改变等结构性疾病。所有评估均由审阅者达成共识，审阅者在判读时已知晓患者的转归。
3. 结果
3.1. 信号特征、临床症状、体格检查及血液实验室检查结果
共纳入3只猫。信号特征和临床症状总结于表1。
病例1和病例3进行CT检查以评估胸腔积液和呼吸窘迫，病例1同时伴有腹腔积液。病例2进行CT检查作为神经系统症状及餐前餐后胆汁酸浓度升高诊断评估的一部分，上述表现提示肝胆功能障碍。
3.2. 计算机断层扫描表现
病例1中，增强CT显示一条异常扩张且迂曲的血管起自脾静脉，向颅背侧走行朝向乳糜池（图1）。该异常血管在约第二和第三腰椎（L2和L3）椎间盘间隙水平进入乳糜池右侧。乳糜池和胸导管扩张，静脉注射对比剂后呈明显均匀强化。向颅侧，胸导管经背侧纵隔延伸，分为多条相互连接的 branch，最终在左颈外静脉与左头臂静脉吻合水平汇入体静脉循环。交通处颅侧可见门静脉管径轻度减小。
观察到一不规则、明显对比增强的肿块，中心位于回盲区及颅肠系膜淋巴中心。该肿块伴有区域淋巴结肿大，包绕颅肠系膜血管和门静脉属支，但无明显的血管侵犯证据。还存在双侧胸腔积液伴继发性肺不张以及中度至重度腹腔积液。其他表现包括沿腹侧腹壁的皮下液体积聚、汇入左肾静脉的侧支血管化以及一个小低密度肝脏结节。
病例2（图2）显示一条由迂曲、扩张血管组成的血管网，起源于颅肠系膜静脉，向背内侧走行，经右肾及后腔静脉内侧，最终到达乳糜池。怀疑存在双重起源，并在约L2和L3水平分别插入乳糜池右侧壁，两者中一个稍靠颅侧。乳糜池和胸导管中度扩张，呈均匀对比增强，衰减程度与门静脉系统相当。胸导管在主动脉和奇静脉之间向颅侧延伸，在约第11胸椎（T11）水平分叉，较大分支在第9胸椎（T9）水平进一步分支。门静脉在吻合口颅侧管径轻度减小。
其他腹部表现包括少量腹膜积液、腹壁尾腹侧轻度皮下积液，以及轻度多灶性肝内和肝外胆管扩张。胰管亦呈轻度弥漫性扩张。方叶内可见一边界不清、对比增强不良的肝脏结节。
病例3中，一条异常交通支起源于中度扩张的脾静脉，沿迂曲的颅背侧走行方向通向乳糜池（图3）。主要插入点位于约L2和L3水平乳糜池右侧壁，另有插入点分别位于L3水平左侧壁和第四腰椎（L4）水平右侧壁。乳糜池和胸导管扩张并呈弥漫性对比增强。胸导管经背侧纵隔向颅侧走行，在汇入体静脉循环前分为多个分支。门静脉在吻合口颅侧管径中度减小。
其他表现包括左结肠静脉显著扩张和迂曲，邻近腹膜脂肪衰减不均匀增高。还可见双侧胸腔积液伴继发性肺不张，以及胸腔入口处皮下积液。另可见多灶性、边界清楚的低衰减肝脏结节，对比增强不良。
3.3. 辅助诊断、临床管理、细胞学/组织病理学表现及结局
病例1中，胸腔和腹腔积液的细胞学分析符合非脓性炎症过程，伴大量成熟淋巴细胞。胸腔积液的生化分析证实为乳糜性，甘油三酯浓度>375 mg/dL，而血清中为165 mg/dL。腹部肿块及区域淋巴结细胞学显示未分化肿瘤，细胞异型性显著，认为最符合肉瘤性病变。超声心动图显示心包壁层回声增强，但无心包积液或缩窄性疾病证据。进行性临床恶化伴反复胸腔和腹腔积液及疑似肿瘤性疾病，最终导致安乐死。
病例2中，应主人要求，CT检查后未再进行侵入性诊断操作，长期结局未知。
病例3中，胸腔积液细胞学分析符合乳糜性积液，SNAP Feline proBNP检测阴性。该猫随后被安乐死，未进行死后组织采样。
三只猫均未对疑似淋巴静脉交通支进行手术探查或治疗，所有病例均未获得交通支的组织病理学确认。
4. 讨论
本组病例首次提供了猫疑似累及门静脉系统和淋巴系统的淋巴静脉交通支的断层影像学特征，据作者所知，也是兽医学中对该现象的首个影像学描述。
三只猫共有的主要CT特征为从门静脉属支延伸至乳糜池的扩张迂曲血管，伴乳糜池和胸导管扩张及对比增强。尽管其门静脉起源和淋巴插入数目存在差异，交通支走行遵循相似的解剖路径。其他反复出现的表现包括吻合口颅侧门静脉管径减小，以及胸腔或腹膜积液和皮下水肿的不同组合。各病例中门静脉和淋巴异常的一致关联可能反映共同的潜在血流动力学紊乱，并可能提示在接受对比增强CT的猫中应怀疑异常淋巴静脉交通支。
这些猫中疑似淋巴静脉交通（LVCs）的性质和起源仍不确定，可考虑两种主要假说。首先，这些异常血管可能代表真正的淋巴静脉分流，允许对比增强的血液进入淋巴循环，因为病理性淋巴静脉分流已在人类患者的淋巴疾病中被描述[3,11]。或者，这些血管可能代表位于广泛肠道淋巴网络内预先存在且通常不明显的淋巴静脉连接，在获得性血流动力学紊乱的作用下被募集、扩张并具有功能意义[2]。这些交通的反复解剖位置也可能由腹部淋巴系统的正常组织所解释。Baum（2023）[2]描述了一个广泛的肠道淋巴网络，接收来自空肠、结肠、脾、肝和腰部区域的引流，然后进入乳糜池（CC），其淋巴管数量和排列存在相当大的变异性[2]。这种解剖组织与当前病例特别相关，因为交通一致涉及脾静脉或颅肠系膜静脉，并在相似的腰椎水平进入CC。先前的解剖学和实验兽医研究也证明了自发性LVCs以及胸导管阻塞后淋巴静脉通路的募集[4,5,6,7]。
已知门静脉压力升高会增加肝淋巴生成和胸导管（TD）淋巴流[12,13]，而淋巴压力升高或淋巴引流受损可能促进预先存在的淋巴静脉交通的募集和扩大[3,6,7,11,14]。本病例中CC和TD的一致扩张，连同可能影响门静脉或淋巴引流的并发异常，可能与预先存在的淋巴静脉通路的募集和扩大相符。在病例1中，浸润性回盲部和颅肠系膜肿块、区域淋巴结肿大以及肠系膜和门静脉属支的包绕可能同时损害了静脉和淋巴引流，而病例2和3分别显示肝胆和门静脉血管异常，无明显腹部肿块。在病例2中，餐前和餐后胆汁酸浓度升高进一步支持肝胆功能障碍，尽管其与CT所识别血管异常的关系无法确定。
反复出现的积液和皮下水肿同样可能反映淋巴血流动力学改变，而非交通的直接后果。淋巴生成增加和/或TD引流受损可能超过淋巴系统的运输能力，导致淋巴管扩张和静水压升高，最终促使乳糜漏入体腔[13,15,16]。在我们的病例中，三只猫均存在TD扩张和皮下水肿，而两只猫有符合乳糜胸的胸腔积液，两只猫有符合乳糜腹的腹腔积液。然而，淋巴高压以及这些发现与疑似LVCs之间的因果关系均无法证实。
三只猫均年龄较大且先前无公认的临床表现，这可能更符合在生命后期才具有功能相关性的交通。然而，先前的横断面影像不可用，不能排除先天性起源，特别是在病例2中，因为其构型更复杂且有多处插入。总体而言，影像学发现的组合提示预先存在的淋巴静脉通路可能因门静脉和/或淋巴血流动力学改变而被募集和扩张；然而，这应被视为一种提出的机制而非已证实的发病机制。
通过这些交通的血流方向与其解释特别相关。这些交通头侧门静脉管径的减小，连同静脉注射对比剂后异常血管的明显强化以及这些交通插入处头侧CC和TD的扩张，支持图像采集时存在门静脉至淋巴的流动。尽管无法获得直接压力测量，因此门静脉高压仍为疑似而非确认。门静脉压力升高可提供对比增强的门静脉血液通过这些交通进入淋巴系统所需的压力梯度。
因此，继发于门静脉高压的获得性门静脉侧支化是一个重要的鉴别考虑。然而，常规门静脉侧支应提供从门静脉循环进入体静脉系统的替代引流，而所有三只猫的异常血管均一致终止于CC内，并伴有TD扩张和对比增强。这种反复出现的淋巴受累支持将这些血管推定为淋巴静脉交通而非常规获得性门静脉侧支。
对比增强CT对于识别这些交通支至关重要，因为它能够同时评估门静脉属支、异常血管、胸导管和乳糜池。已有报道显示，在生理条件下，尤其在延迟采集期，猫科动物淋巴系统在常规静脉注射对比剂后会出现强化[17,18]。然而，门静脉属支与淋巴结构之间存在直接解剖连续性的额外发现，加之交通部位头侧的淋巴管明显强化和扩张，被认为提示病理性淋巴静脉交通而非正常淋巴强化。
基于对现有文献的全面回顾，本病例系列首次描述了使用对比增强CT在猫科患者中疑似自然发生的病理性淋巴静脉交通。虽然生理性和病理性淋巴静脉交通此前已在人类医学中有所描述，与淋巴疾病、门静脉高压、肿瘤和淋巴管阻塞相关[3,12]，但兽医文献仍局限于解剖学观察[4,5]、胸导管阻塞的实验模型[6,7]以及手术创建的淋巴静脉吻合术[9,10]。
本研究存在若干局限性，包括病例数量少、回顾性设计、缺乏完整的长期随访，以及缺乏对疑似淋巴静脉交通的手术或组织病理学确认。研究的回顾性性质还导致患者之间临床和诊断数据的可获得性不一致，以及各病例缺乏标准化的诊断和影像学方案。最重要的是，未测量门静脉压或淋巴压，也无法直接证明血流方向。此外，所有病例均未进行淋巴造影，包括病例1和病例3中已确认乳糜性胸腔积液的病例。由于这是一项基于提交远程放射学解读病例的回顾性多中心病例系列，诊断检查由转诊机构独立决定，临床调查时未进行淋巴造影研究。这是一个重要的局限性，因为淋巴造影评估本可提供关于中枢淋巴解剖和引流的额外信息，并允许进一步表征疑似交通支，包括对比剂通过和血流方向。尽管静脉和淋巴结构的同步强化支持两个系统之间的直接交通，但缺乏淋巴造影妨碍了对这些血管及其与中枢淋巴系统关系的明确表征。另一个局限性是并非所有研究均可获得确切的对比后采集期相，无法精确评估血管强化与淋巴强化之间的时间关系。
5. 结论
总之，本病例系列描述了三只猫疑似获得性病理性淋巴静脉交通的CT特征。本病例系列中描述的发现提示，涉及门静脉系统和淋巴系统的淋巴静脉交通可能代表猫适应性淋巴-静脉重塑的表现。基于其相似的解剖分布和已知的猫肠道淋巴网络组织方式，这些交通可能通过募集和扩张预先存在的淋巴静脉通路而产生，而非响应门静脉或淋巴血流动力学慢性紊乱的新生血管形成。
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Simple Summary
Lymphovenous communications are abnormal connections between the lymphatic and venous systems that are poorly characterized in veterinary medicine. This study describes the computed tomography findings of suspected lymphovenous communications in three older cats. In all cats, contrast-enhanced computed tomography identified abnormally dilated and tortuous vessels connecting branches of the portal venous system with the cisterna chyli, a major abdominal lymphatic structure. The cisterna chyli and thoracic duct were also dilated and showed contrast enhancement. Additional recurrent findings included narrowing of the portal vein, fluid accumulation within the thorax or abdomen, and subcutaneous edema. The similar anatomical distribution of the communications and the associated abnormalities suggest that these vessels may represent pre-existing connections that became enlarged and functionally relevant in response to chronic changes in portal or lymphatic circulation, although a congenital origin cannot be completely excluded. Recognition of this imaging pattern may help veterinarians identify previously unrecognized lymphovenous communications and improve the interpretation of complex portal and lymphatic abnormalities in cats undergoing contrast-enhanced computed tomography.
1. Introduction
The lymphatic system is formed by lymphatic vessels, trunks and ducts. The major lymphatic drainage pathways are organized around the thoracic duct (TD) and the right lymphatic duct (RLD) [1]. The TD represents the principal route for lymph return from most of the body, arising as the cranial continuation of the cisterna chyli (CC), terminating at the junction of the external and internal jugular veins or the junction between the jugular and left subclavian veins [1]. These terminal lymphovenous connections constitute the main physiological sites of communication between the lymphatic and venous systems. Within the abdomen, lymph from the viscera reaches the CC through several lymphatic trunks, including the intestinal and celiac trunks [1]. Anatomical studies have demonstrated considerable variability in the organization of these lymphatic pathways, particularly the intestinal trunk, whose tributaries may form an extensive interconnected lymphatic network (rete intestinale) surrounding the cranial mesenteric artery before entering the cisterna chyli [2].
In human medicine, the lymphovenous communications (LVCs) classified as normal and commonly seen are the thoracic duct termination, right lymphatic duct termination and intra-nodal LVCs [3]. Pathological LVCs have also been described in a variety of disease states, including primary and secondary lymphedema, as well as primary and metastatic malignancies involving the lymph nodes [3]. In addition, lymphovenous communications can be performed surgically for the management of secondary lymphedema and other lymphatic disorders [3].
Regarding veterinary medicine, Threefoot (1968) [4] demonstrated physiologic LVCs in several mammalian species, including dogs, involving multiple venous territories throughout the body, while Zajac (1972) [5] described communications between the cisterna chyli and the caudal vena cava. Furthermore, experimental studies by Griaznova (1962) [6] and by Kagan and Breznock (1979) [7] showed that complete thoracic duct obstruction resulted in the opening of LVCs proximal to the site of obstruction, supporting their role as compensatory pathways for maintaining lymphatic drainage. Acquired LVCs are also believed to play an important role in the success of the TD ligation procedures for the treatment of chylothorax [8]. More recently, experimental studies in dogs and cats have demonstrated the technical feasibility of creating direct LVCs between the thoracic duct and the venous system as a potential therapeutic strategy for lymphatic disorders [9,10].
However, pathological LVCs remain poorly characterized in veterinary medicine, with the available literature largely limited to anatomical observations and experimental studies. Consequently, their clinical significance, imaging characteristics, and potential association with underlying disease remain largely unknown. To the authors’ knowledge, this is the first case series describing suspected spontaneous LVCs in cats using contrast-enhanced computed tomography, providing novel information on their anatomical distribution, imaging features, and associated abnormalities.
2. Materials and Methods
In this retrospective study, cases of presumptive lymphovenous communications were identified from teleradiology submissions between 2024 and 2025 using the search terms “lymphovenous shunt” and “lymphaticovenous communication.” Cats were included if a complete contrast-enhanced CT examination of the thorax and abdomen was available and demonstrated the following: (1) an anomalously dilated and tortuous vascular structure arising from or showing direct continuity with a tributary of the portal venous system; (2) a traceable anatomical course connecting this structure with the CC and/or TD. CT studies were required to be of sufficient diagnostic quality to evaluate the portal venous and lymphatic structures involved. Four cats with suspected LVCs were initially identified. Three fulfilled the inclusion criteria and were included in the study, whereas one cat was excluded because only a thoracic CT examination was available, precluding assessment of the abdominal origin and complete course of the suspected communication. No suspected LVCs involving other anatomical locations were identified during the database search. Referring veterinarians were contacted and requested to provide all available clinical information, including signalment, clinical history, previous diagnostic investigations and treatment, physical examination, blood analysis, cytology/histopathology, and clinical outcome.
Different CT machines and protocols were used depending on the referring institution: Cases 1 and 2 were imaged using a Aquilion Start 16-detector-row CT scanner (Canon Medical Systems, Otawara, Japan). Image acquisition was performed in helical mode using a slice thickness of 1.0 mm, pitch of 0.94, gantry rotation time of 0.75 s, tube voltage of 100 kVp, and tube current of 90 mA. Case 3 was examined using a SOMATOM 32-detector-row CT scanner (Siemens Healthineers, Erlangen, Germany) with a slice thickness of 2 mm, pitch of 1.2, gantry rotation time of 0.33 s, tube voltage of 100 kVp, and tube current of 41 mA.
All protocols were performed in ventral recumbency under general anaesthesia. They included soft tissue and bone algorithm images of the entire abdomen, before and after intravenous iodinated contrast medium administration (Iohexol, Omnipaque®, GE Healthcare, Oslo, Norway), at 600 mg/kg with unspecified phase protocols.
Each CT study was carefully reviewed by two board-certified veterinary radiologists (V.C.C. and N.I.), one second-year diagnostic imaging resident (L.L.F.) and one diagnostic imaging intern (I.R.A.) using an image analysis workstation (Horos, version 3.3.6, Horos Project, Annapolis, MD, USA). The following characteristics were reviewed and recorded: the identification of an anomalous lymphovenous connection with associated lymphatic ducts via contrast enhancement; origin, path, drainage and size of the communication; the presence of peritoneal or pleural effusion; and structural conditions such as masses, lymph node affection or chronic inflammatory changes. All assessments were reached by consensus among the reviewers, who were aware of patient’s outcomes at the time of interpretation.
3. Results
3.1. Signalment, Clinical Signs, Physical Examination and Blood Laboratory Findings
A total of three cats were included. Signalment and clinical signs are summarized in Table 1.
CT examination was performed to investigate pleural effusion and respiratory distress in cases 1 and 3, with concurrent abdominal effusion in case 1. In case 2, CT was performed as part of the diagnostic investigation of the neurological signs and increased pre- and postprandial bile acid concentrations, which raised suspicion of hepatobiliary dysfunction.
3.2. Computed Tomography Findings
In case 1, contrast-enhanced CT revealed an abnormally dilated and tortuous vessel arising from the splenic vein and coursing craniodorsally toward the CC (Figure 1). The anomalous vessel entered the right lateral aspect of the CC at approximately the level of the intervertebral disc space between the second and third lumbar vertebrae (L2 and L3). The CC and TD were dilated and showed marked homogeneous enhancement following intravenous contrast administration. Cranially, the TD extended through the dorsal mediastinum, dividing into multiple interconnected branches before terminating within the systemic venous circulation at the level of the left external jugular vein, at its anastomosis with the left brachiocephalic vein. A mild reduction in portal vein calibre was identified cranial to the communication.
An irregular, strongly contrast-enhancing mass centered on the ileocecal region and cranial mesenteric lymphocenter was observed. The mass was associated with regional lymphadenopathy and encased the cranial mesenteric vessels and portal tributaries without evidence of overt vascular invasion. Bilateral pleural effusion with secondary pulmonary atelectasis and moderate to severe peritoneal effusion were also present. Additional findings included subcutaneous fluid accumulation along the ventral abdominal wall, collateral vascularization inserting in the left renal vein, and a small hypoattenuating hepatic nodule.
Case 2 (Figure 2) showed a network of tortuous, dilated vessels that originated from the cranial mesenteric vein and coursed dorsomedially, medial to the right kidney and caudal vena cava, before reaching the CC. A double origin was suspected, together with two separate insertions into the right lateral aspect of the CC at approximately the level of L2 and L3, one slightly cranial to the other. The CC and TD were moderately distended and demonstrated homogeneous contrast enhancement equal in attenuation to the portal venous system. The TD extended cranially between the aorta and azygos vein, bifurcating at approximately eleventh thoracic vertebrae (T11), with further division of the larger branch at the level of ninth thoracic vertebrae (T9). The portal vein was mildly reduced in calibre cranial to the communication.
Other abdominal findings consisted of minimal peritoneal effusion, mild subcutaneous fluid accumulation along the caudoventral abdominal wall, and mild multifocal intra- and extrahepatic biliary dilatation. The pancreatic duct was also mildly and diffusely dilated. A poorly defined, poor contrast-enhancing hepatic nodule was present within the quadrate hepatic lobe.
In case 3, an anomalous communication originated from a moderately dilated splenic vein and followed a tortuous craniodorsal course toward the CC (Figure 3). The main insertion was identified on the right lateral aspect of the CC around the level of L2 and L3, with additional insertions involving the left lateral aspect at the L3 and the right lateral aspect at fourth lumbar vertebra (L4). The CC and TD were distended and diffusely contrast-enhancing. The TD coursed cranially through the dorsal mediastinum and divided into multiple branches before draining into the systemic venous circulation. The portal vein was moderately decreased in calibre cranial to the communication.
Additional findings included marked dilatation and tortuosity of the left colic vein, with heterogeneous increased attenuation of the adjacent peritoneal fat. Bilateral pleural effusion with secondary pulmonary atelectasis and subcutaneous fluid accumulation at the thoracic inlet were also present. Multifocal, well-defined hypoattenuating hepatic nodules with poor contrast enhancement were also identified.
3.3. Ancillary Diagnosis, Clinical Management, Cytological/Histopathological Findings and Outcome
In case 1, cytological analysis of the pleural and abdominal effusions was consistent with a non-septic inflammatory process with abundant mature lymphocytes. Biochemical analysis of the pleural effusion confirmed its chylous nature, with a triglyceride concentration > 375 mg/dL compared with 165 mg/dL in serum. Cytology of the abdominal mass and regional lymph nodes revealed an undifferentiated neoplasm with marked cellular atypia, considered most consistent with a sarcomatous process. Echocardiography showed increased echogenicity of the parietal pericardium without pericardial effusion or evidence of constrictive disease. Progressive clinical deterioration associated with recurrent pleural and abdominal effusions and suspected neoplastic disease ultimately led to euthanasia.
In case 2, no further invasive diagnostic procedures were pursued following CT examination at the owners’ request, and the long-term outcome was unknown.
In case 3, cytological analysis of the pleural effusion was consistent with a chylous effusion, and a SNAP Feline proBNP test was negative. The cat was subsequently euthanized, and post-mortem tissue sampling was not performed.
No surgical exploration or treatment of the suspected lymphovenous communications was performed in any of the three cats, and histopathological confirmation of the communications was unavailable in all cases.
4. Discussion
The present cases provide the first tomographic characterization of suspected lymphovenous communications involving the portal venous and lymphatic systems in feline patients and represent, to the authors’ knowledge, the first radiological description of this phenomenon in veterinary medicine.
The main CT features shared by the three cats were dilated and tortuous vessels extending from portal venous tributaries to the CC, associated with dilatation and contrast enhancement of the CC and TD. Despite variation in their portal venous origin and number of lymphatic insertions, the communications followed a similar anatomical course. Additional recurrent findings included reduced portal vein caliber cranial to the communication and variable combinations of pleural or peritoneal effusion and subcutaneous edema. The consistent association of portal and lymphatic abnormalities across cases may reflect a common underlying hemodynamic disturbance and may raise suspicion for abnormal LVCs in cats undergoing contrast-enhanced CT.
The nature and origin of the suspected LVCs identified in these cats remain uncertain, and two main hypotheses may be considered. First, the anomalous vessels may represent true lymphovenous shunts permitting the passage of contrast-enhanced blood into the lymphatic circulation, as pathological lymphovenous shunting has been described in association with lymphatic disease in human patients [3,11]. Alternatively, these vessels may represent pre-existing and normally inconspicuous lymphovenous connections located within the extensive intestinal lymphatic network that become recruited, dilated, and functionally significant in response to acquired hemodynamic disturbances [2]. The recurrent anatomical location of these communications may also be explained by the normal organization of the abdominal lymphatic system. Baum (2023) [2] described an extensive intestinal lymphatic network receiving drainage from the jejunal, colic, splenic, hepatic, and lumbar territories before entering the CC, with considerable variability in the number and arrangement of its lymphatic channels [2]. This anatomical organization is particularly relevant to the present cases, as the communications consistently involved the splenic or cranial mesenteric veins and entered the CC at similar lumbar levels. Previous anatomical and experimental veterinary studies have also demonstrated spontaneous LVCs and recruitment of lymphovenous pathways following thoracic duct obstruction [4,5,6,7].
Increased portal pressure is known to increase hepatic lymph production and TD lymph flow [12,13], whereas increased lymphatic pressure or impaired lymphatic drainage may promote recruitment and enlargement of pre-existing lymphovenous communications [3,6,7,11,14]. The consistent dilatation of the CC and TD in the present cases, together with concurrent abnormalities potentially affecting portal or lymphatic drainage, may be compatible with the recruitment and enlargement of pre-existing lymphovenous pathways. In case 1, the infiltrative ileocecal and cranial mesenteric mass, regional lymphadenopathy, and encasement of mesenteric and portal tributaries could have impaired both venous and lymphatic drainage, whereas cases 2 and 3 showed hepatobiliary and portal vascular abnormalities, respectively, without an overt abdominal mass. In case 2, increased pre- and postprandial bile acid concentrations further supported hepatobiliary dysfunction, although their relationship with the vascular abnormalities identified on CT could not be established.
The recurrent effusions and subcutaneous edema may similarly reflect altered lymphatic hemodynamics rather than being a direct consequence of the communications. Increased lymph production and/or impaired TD drainage could exceed the transport capacity of the lymphatic system, resulting in lymphatic distension and increased hydrostatic pressure ultimately promoting leakage of chyle into body cavities [13,15,16]. In our cases, TD dilatation and subcutaneous edema was present in all three cats, while two had pleural effusion compatible with chylothorax and two had abdominal effusion compatible with chyloabdomen. However, neither lymphatic hypertension nor a causal relationship between these findings and the suspected LVCs could be demonstrated.
The advanced age of all three cats and the absence of previously recognized clinical manifestations may be more consistent with communications that became functionally relevant later in life. Nevertheless, previous cross-sectional imaging was unavailable, and a congenital origin cannot be excluded, particularly in case 2 because of its more complex configuration and multiple insertions. Overall, the combination of radiological findings raises the possibility that pre-existing lymphovenous pathways became recruited and dilated in response to altered portal and/or lymphatic hemodynamics; however, this should be regarded as a proposed mechanism rather than a demonstrated pathogenesis.
The direction of flow through these communications is particularly relevant to their interpretation. The reduction in calibre of the portal vein cranial to these communications, together with the marked enhancement of the anomalous vessels following intravenous contrast administration and the distension of the CC and TD cranial to the insertion of these communications, supports portal-to-lymphatic flow at the time of image acquisition. Although direct pressure measurements were not available, and portal hypertension therefore remains suspected rather than confirmed. Increased portal pressure could provide the pressure gradient required for contrast-enhanced portal blood to enter the lymphatic system through these communications.
Acquired portal venous collateralization secondary to portal hypertension was therefore an important differential consideration. However, conventional portal collaterals would be expected to provide alternative drainage from the portal circulation into the systemic venous system, whereas the anomalous vessels in all three cats consistently terminated within the CC and were associated with TD dilatation and contrast enhancement. This recurrent lymphatic involvement supports the presumptive interpretation of these vessels as lymphovenous communications rather than conventional acquired portal collaterals.
Contrast-enhanced CT was essential for recognizing the communications because it allowed simultaneous evaluation of the portal tributaries, anomalous vessels, CC, and TD. Enhancement of the feline lymphatic system following routine intravenous contrast administration has been reported under physiological conditions, particularly on delayed acquisitions [17,18]. However, the additional findings of direct anatomical continuity between portal tributaries and lymphatic structures, together with the avid lymphatic enhancement and dilatation cranial to the site of communication, were considered suggestive of pathological LVCs rather than normal lymphatic enhancement.
Based on a thorough review of the existing literature, this case series represents the first description of suspected natural occurring, pathological LVCs in feline patients using contrast-enhanced CT. While physiological and pathological LVCs have been previously described in human medicine in association with lymphatic disorders, portal hypertension, neoplasia, and lymphatic obstruction [3,12], the veterinary literature remains limited to anatomical observations [4,5], experimental models of TD obstruction [6,7], and surgically created lymphovenous anastomoses [9,10].
This study has several limitations, including the small number of cases, retrospective design, incomplete long-term follow-up, and the absence of surgical or histopathological confirmation of the suspected LVCs. The retrospective nature of the study also resulted in heterogeneous clinical and diagnostic data availability among patients and a lack of standardized diagnostic and imaging protocols across cases. Most importantly, neither portal nor lymphatic pressures were measured, and the direction of flow could not be directly demonstrated. Furthermore, lymphography was not performed in any of the cases, including cases 1 and 3, in which chylous pleural effusion was identified. As this was a retrospective multicentre case series based on cases submitted for teleradiology interpretation, diagnostic work-up was determined independently by the referring institutions, and lymphographic studies were not performed at the time of clinical investigation. This represents an important limitation, as lymphographic evaluation could have provided additional information regarding central lymphatic anatomy and drainage and allowed further characterization of the suspected communications, including contrast transit and flow direction. Although the concurrent enhancement of venous and lymphatic structures supported direct communication between both systems, the absence of lymphography precluded the definitive characterization of these vessels and their relationship with the central lymphatic system. An additional limitation is that the exact post-contrast acquisition phases were unavailable for all studies, preventing precise assessment of the temporal relationship between vascular and lymphatic enhancement.
5. Conclusions
In conclusion, this case series describes the CT features of suspected acquired, pathological LVCs in three cats. The findings described in this case series suggest that lymphovenous communications involving the portal venous system and lymphatic system may represent manifestations of adaptative lymphatic-venous remodelling in cats. Based on their similar anatomical distribution and the known organization of the feline intestinal lymphatic network, these communications may arise though recruitment and dilation of pre-existing lymphovenous pathways rather than de novo vascular formation in response to chronic disturbances in portal or lymphatic hemodynamics.