兽研简要概述
胆囊增大会导致腹痛和消化不适。这项小型研究描述了如何通过减压性抽吸增大的胆囊来改善犬持续性消化系统症状。共对14只犬进行了评估，这些犬因持续呕吐、腹泻和腹痛且对常规医疗护理无反应而就诊。所有犬均存在胆囊增大，并且均进行了抽吸以缓解其症状。所有犬均表现出症状改善。目前对胆囊增大如何影响犬以及如何解读胆囊体积知之甚少。我们提出了病理生理学假设，并就该主题的未来研究展开公开讨论。
1. 引言
诊断性胆囊穿刺术（CC）的技术和安全性此前已在兽医学中有所描述[1,2,3]。DCC已用于缓解胰腺外胆管梗阻（EHBDO）中的胆道梗阻压力[4]。胆囊体积评估也已有研究，正常犬的空腹和餐后正常范围已有报道。据报道，正常空腹体积约为1 mL/kg，餐后体积较空腹体积减少25–50%[5,6,7]。患有胆囊疾病的犬，特别是存在胆泥和胆囊黏液囊肿（GBM）的犬，据报道其射血分数降低[8]。一项单病例系列记录了犬食欲改变与胆囊运动性降低之间的关系[9]。关于胆囊体积与犬原发性消化系统症状管理之间的关系知之甚少。本病例系列描述了DCC作为伴有持续性原发性消化系统症状犬的症状管理组成部分的特征和结局。
2. 材料与方法
对一项回顾性病例系列研究进行了评估。鉴于缺乏操作先例，已获得畜主对这一非标准操作的知情同意，并在干预前充分讨论了风险和潜在获益。纳入标准为：超声检查存在GBD（通过椭球公式计算估计约≥1 mL/kg）且经常规医疗管理后仍存在各种但持续的原发性消化系统症状的犬。GBD这一表述特意同时涵盖空腹体积正常上限和病理性增大状态，而未具体指明其中任何一种。EGBV通过椭球法计算（0.52（L × W × H）），并与采集体积进行比较。胆囊穿刺术在全身麻醉下通过超声引导进行。所有胆汁样本均提交通过下一代测序进行感染性疾病检测。所有患者均在医院监测术后并发症，通过常规生命参数和消化功能评估进行。对任何出现发热、腹胀、腹痛或整体疾病持续存在的犬均计划进行积液评估。所有患者至少接受一次术后评估；计算空腹eGBV并与初始值进行比较。分析症状的缓解或持续情况。
3. 结果
群体特征显示，犬的年龄为6–72月龄，平均35月龄。体重范围为2.3至37 kg，平均8.1 kg。性别分布为7/14例FS、6/14例MN和1/14例M。品种分布显示3只腊肠犬、2只西施犬和2只约克夏犬，另有单只的其他多个品种。
临床表现特征显示，这些犬因持续1–3天的多种消化系统症状而住院，对常规分诊医疗支持无反应。在13/14的病例中，胆囊扩张被定义为约1 mL/kg或以上。单只患者的eGBV计算为0.95 mL/kg。该群体中eGBV平均值为2.2 mL/kg。表1。超声检查显示9/14存在浓缩胆汁。没有犬被特征性地诊断为GBM。所有犬均报告有原发性消化系统疾病的各种表现，包括厌食（12/14）、呕吐（11/14）、腹泻（10/14）、存在DI模式（7/14）和BV（12/14）。生化面板检测因分诊临床医生的偏好而在各病例间有所不同；报告的异常包括肝酶病；ALT（>125 IU/L，2/13）、ALP（>212 U/L，2/14）、GGT（>11 U/L，1/6）和tbili（>0.9 mg/dL，0/7）。注意到白细胞增多；tWBC（>16.76 K/µL，5/13）和中性粒细胞增多（>11.64 K/µL，7/13）。未报告低白蛋白血症（<2.3 g/dL）（0/14）（IDEXX Labs, Westbrook, ME, USA, https://www.idexx.com）。注意到D3不足（<100 ng/mL）（6/14），平均值为97.1 ng/dL（范围24.5–147.6 ng/mL）。注意到B12不足（<300 pg/mL，2/12）。叶酸报告为正常（4.3–21 ng/mL，10/12），叶酸升高（2/12）。注意到总镁不足（<2.2 mg/dL，12/14），平均值为1.7 mg/dL（范围1.3–2.3 mg/dL）（VDI Labs, Chatsworth, CA, USA, https://vdilab.com/）。测量的平均抽吸胆汁量为2.4 mL/kg（范围0.78–5.9 mL/kg）。DCC后残余eGBV似乎可忽略不计，大多数操作减少至可见的管腔塌陷（见图1）。作者承认，仍有未可靠定量的胆汁残留，会在每个病例中略微增加实际GBV。利用椭球体计算，残余体积被分类为<1 mL（7/13）、1–2 mL（5/13）和<5 mL（1/13）。所有样本均提交通过下一代测序进行感染检测（MiDog Animal Diagnostics, Tuston, CA, USA, https://www.midogtest.com/）。总共2/14病例产生阳性结果，但未报告显著病原体。胆汁细胞学未提交外部临床病理学审查。
在术后期间，没有患者需要在住院出院常规检查之外进行额外评估。没有患者记录到需要额外住院或与DCC相关的资源分配的不良事件。
术后数据包括至少一次随访检查，14/14病例均可获得。随访观察期为2至22个月，平均10.5个月。所有接受治疗的犬在24–48小时内主要症状消退，并在功能上从住院中出院。所有病例均开具了联合治疗。没有病例仅接受DCC干预，因此无法确定干预与康复之间的明确关联。常见的DCC前后治疗包括广谱抗生素（14/14）、maropitant（14/14）、促动力药（9/14）、硫糖铝（8/14）、质子泵抑制剂（12/14）、液体疗法（14/14）、根据实践标准给予胃肠外Dexamethasone 0.05–0.1 mg/kg一次（10/14）、口服prednisone/olone以短期抗炎剂量< 0.5 mg/kg/天（2/14）和熊去氧胆酸10–15 mg/kg/天（14/14）。作者再次强调，该系列中所有患者在介入性DCC之前，均已接受常规对症治疗，采用上述治疗的各种组合。所有患者均开具或继续采用常见但多样的清淡低脂、从家庭自制到处方消化饮食支持疗法。
随访时禁食eGBV平均值报告为1.04 mL/kg，7/14犬仍低于1 mL/kg。总共7/14病例测量为1 mL/kg或以上。12/14病例维持正常食欲，6/7病例DI模式消退。8/12有症状病例的BV已消退。值得注意的是，在厌食、DI和BV症状以任何报告程度持续存在的病例中，平均eGBV为1.3 mL/kg（范围0.3–2.2 mL/kg），而在症状消退的病例中，eGBV报告为0.8 mL/kg（范围0.5–2.1 mL/kg）。该系列中有两例因持续症状被转诊至手术；这些病例报告的eGBV值为1.8 mL/kg（DCC后10个月）和2.2 mL/kg（DCC后5个月）。单只犬保持无症状，eGBV为2.1 mL/kg（DCC后22个月）。随访时9/14持续存在超声检查浓缩胆汁。在该系列时间范围内未注意到进展为明显的GBM。
4. 讨论
在该群体中，出现症状持续并接受DCC前住院的时间范围为1至3天，病例间存在差异，但均使用了显著的多药联合治疗。由于畜主追求诊断性超声检查的意愿存在差异，住院时间无法作为疾病严重程度的指标加以考量。DCC后评估时间在2至22个月之间变化，差异显著。DCC后评估的平均时间为10个月。需要延长且统一的监测数据才能进行更明确的评估。由于样本量有限、分诊阶段缺乏统一的临床评估以及既有的多药干预，未采用标准化的疾病评分评估（CIBDAI（犬炎症性肠病活动指数）或CCECAI（犬慢性肠病临床活动指数））。对该群体进行进一步对照评估将受益于更具体的分类。
约1 mL/kg定义的GBD与多种消化系统症状（厌食、呕吐、腹泻、嗜睡）呈正相关。DI和BV的病史和/或慢性症状在该病例群体中常见，提示存在急性叠加于慢性的疾病因素。据报道，DI与犬非重力依赖性胆泥相关，并在胆囊切除术后改善[10]。该病例系列中未报告GBV，但已知患有胆泥的犬GBEF降低，提示存在运动障碍性病理[8]。胆汁性呕吐综合征（BVS）已被研究并推测涉及胃肠动力异常[11]。据作者所知，尚未在患有BV的犬中评估潜在的胆囊病动力学。本系列病例未进行射血分数检测，主要因其共同存在的功能性消化不稳定。射血分数检测有助于更好地理解类似病例的病理生理动力学。在本病例系列中，多种原发性胃肠道症状（厌食、呕吐和腹泻）伴随DI和BV模式，对联合持续常规医疗支持治疗（所有病例均在治疗中但症状持续）和DCC产生应答。作者提出，GBD可能仅仅是内脏疼痛的一个原因，当常规医疗支持失败时，DCC可能使其改善。本系列中若干病例显示明显的GBD > 2–5 mL/kg，不太可能为急性扩张所致，且无高胆红素血症或超声证据显示肝外胆管梗阻。考虑到餐后协调排胆的正常生理，食物摄入和胃扩张导致胆囊收缩素（CCK）释放，刺激胆囊收缩和肠道运动，与胃排空协调进行。进入小肠的初级胆汁酸最终在回肠被重吸收，经肠肝循环返回肝脏，进而抑制进一步的CCK释放并结束消化周期[12]。在本系列中，持续性胆汁性呕吐/反流是与GBD并存的常见症状特征（12/14）。作者提出，过量胆汁分泌进入空肠可预见性地促进进行性胆囊淤滞、GBD和运动障碍，其机制为CCK的 prolonged 抑制。反过来，GBD会促进不协调的胆汁持续排入小肠，尤其是在与呕吐相关的腹腔腔室压迫动力学下，可能形成循环性病理。通过DCC打破这一循环，若存在病理性CCK抑制间歇期，可能使其得以中断，并可能部分解释该群体中观察到的症状缓解。这可能是过于简化的病理生理学，但可能具有重要意义。所提出的病理生理动力学合理地适用于从突然扩张至正常最大值以及慢性病理伴进行性扩张至超正常容量两种情况。患有胆汁反流和BVS的犬的胆囊动力学（容量和收缩性）可能受益于进一步研究。在随访期间，本系列中少数病例出现复发或症状持续（4/14）。在研究群体中，DCC前禁食平均eGBV为2.2 mL/kg，DCC后禁食平均eGBV为1.0 mL/kg，提示整体容量动力学改善。两例因持续症状被转诊行胆囊切除术。这两例在DCC后5个月和10个月评估时，分别显示持续性GBD为2.2和1.8 mL/kg。所注意到的趋势提示持续性GBD可能与持续症状相关。无症状病例中测得的EGBV报告为平均0.8 mL/kg，而有症状病例中报告的eGBV平均为1.3 mL/kg。然而，一例报告偶发胆汁性呕吐，其eGBV为0.3 mL/kg，而另一例持续无症状，其eGBV为2.1 mL/kg，这提示容量并非唯一决定因素。
在该群体中，以总镁低于2.2 mg/dL定义的镁不足较为常见（12/14）。平均总镁为1.7 mg/dL（正常1.7–2.9 mg/dL，群体范围1.3–2.2 mg/dL）。离子镁是诊断犬临床低镁血症的标准，并且在住院动物中常被报告[13]。已证明总镁与离子镁水平相关，但在住院动物中相关性可能较弱[14]。镁的分布形式为离子型63%、复合型6%和蛋白结合型31%[15]。本系列中未报告有任何犬存在低白蛋白血症，因此低蛋白血症性假性结果的可能性较小。据报道，离子性低钙血症（IHC）是住院犬发生离子性低镁血症的危险因素，最常见于患有胃肠道疾病的犬[16]。该群体中未获得离子钙水平数据。我们没有关于胆囊疾病犬镁动态变化的数据。然而，据报道，人口服镁用于刺激胆囊收缩，胃肠外镁已用于刺激犬胆囊收缩，二者均通过刺激CCK释放的机制实现[17,18]。该群体中镁不足的高发生率可能是一种动态易感性或合并症，值得进一步研究。
这一小系列中的病例数不足以对症状的容量和持续性进行任何具有统计效力的相关性分析，可能受益于进一步研究。在本系列中，未确定所观察到的GBD的病因。所有病例均基于超声和正常胆红素水平排除了EHBDO。潜在的运动障碍性病理需要射血分数检测，但未进行该检测。非梗阻性、运动障碍性病理生理机制需要进一步研究，以阐明分类性刺激缺陷（神经激素性）或潜在平滑肌收缩力缺陷（如电解质不足）。
5. 结论
在该患者群体中，用于胆囊减压的DCC成功实施。观察到GBD表现为消化系统症状在常见对症治疗之外持续存在，尤其是日间食欲不振和胆汁性呕吐。对于症状持续并伴有GBD的病例，DCC可能有所帮助。在整个系列中，DCC似乎对随访时空腹eGBV具有减小作用。在这一小群体中进行的下一代测序未能确定原发性感染因素。对犬症状性胆囊病的客观评估可能受益于除浓缩性观察之外的特征，并包括容积动力学。需要进一步开展对照良好且周密的研究。
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Simple Summary
Gallbladder enlargement can result in abdominal pain and digestive distress. This small study describes how decompressive aspiration of the enlarged gallbladder may improve persistent digestive symptoms in dogs. In total, 14 dogs were evaluated for ongoing vomiting, diarrhea, and abdominal pain non-responsive to routine medical care. All dogs had gallbladder enlargement, and all had aspiration performed to mitigate their symptoms. All dogs showed symptomatic improvement. Little is known about how gallbladder enlargement affects dogs and how gallbladder volume should be interpreted. We propose pathophysiology and open discussion for future study of this subject.
1. Introduction
The technique and safety of diagnostic cholecystocentesis (CC) have been described previously in veterinary medicine [1,2,3]. DCC has been used to relieve biliary obstructive pressure in pancreatic extra-hepatic bile duct obstruction (EHBDO) [4]. Gallbladder volume assessment has also been studied with fasting and post-prandial normal ranges reported in normal dogs. Normal fasting volumes are reported to be around 1 mL/kg and post-prandial volumes reduced by 25–50% of the fasting volume [5,6,7]. Dogs with gallbladder disease, notably with biliary sludge presence and Gallbladder Mucocele (GBM), have been reported to have diminished ejection fraction [8]. A single case series documented altered appetite in relation to decreased gallbladder motility in dogs [9]. Little is known about the relationship between gallbladder volume and primary digestive symptom management in dogs. This case series describes the characteristics and outcomes of DCC as part of symptom management in dogs with ongoing primary digestive symptoms.
2. Materials and Methods
A retrospective case series study was evaluated. Given the lack of procedural precedent, informed owner consent was obtained for this non-standard procedure, and the risks and potential benefits were thoroughly discussed prior to intervention. Dogs were included with sonographic GBD (approximately 1 mL/kg or greater estimated by the ellipsoid calculation) and varied but persistent primary digestive symptoms following routine medical management. GBD is specifically phrased to include both the upper limit of normal fasting volume and a pathologic voluminous state without specifying either. EGBV was calculated by the ellipsoid method (0.52(L × W × H)) and compared to collected volumes. Cholecystocentesis was performed under general anesthesia by ultrasound guidance. All bile samples were submitted for infectious disease testing by next generation sequencing. All patients were monitored in hospital for post-procedure complications by routine vital parameters and digestive functional assessment. Effusion evaluation was planned for any dog with fever, abdominal distension, abdominal pain or overall disease persistence. All patients received at least one post-procedure evaluation; fasting eGBV was calculated and compared to initial values. The resolution or persistence of symptoms was analyzed.
3. Results
Population characteristics revealed the dogs were aged 6–72 months with a mean of 35 mo. Body weight ranged from 2.3 to 37 kg with a mean of 8.1 kg. Sex distribution was 7/14 FS, 6/14 MN, and 1/14 M. Breed distribution revealed three Daschunds, two Shi Tzu, and two Yorkies, with single various additional breeds.
Presentation clinical characteristics revealed the dogs were hospitalized for 1–3 days duration with varied digestive symptoms not responding to routine triage medical support. Gallbladder distension was defined as approximately 1 mL/kg or greater in 13/14 patients. A single patient’s eGBV was calculated at 0.95 mL/kg. eGBVmean in the population was 2.2 mL/kg. Table 1. Sonographic inspissation was present in 9/14. No dog was characterized with GBM. All dogs reported variations of primary digestive disease including anorexia (12/14), vomiting (11/14), diarrhea (10/14), the presence of DI patterns (7/14) and BV (12/14). Biochemical panel testing varied among cases based on triage clinician preference; reported abnormalities included hepatic enzymopathy; ALT (>125 IU/L, 2/13), ALP (>212 U/L, 2/14), GGT (>11 U/L, 1/6), and tbili (>0.9 mg/dL, 0/7). Leukocytosis was noted; tWBC (>16.76 K/µL, 5/13) and neutrophilia (>11.64 K/µL, 7/13). Hypoalbuminemia (<2.3 g/dL) was not reported (0/14) (IDEXX Labs, Westbrook, ME, USA, https://www.idexx.com). D3 insufficiency (<100 ng/mL) was noted (6/14) with a mean of 97.1 ng/dL (range 24.5–147.6 ng/mL). B12 insufficiency was noted (<300 pg/mL, 2/12). Folate was reported to be normal (4.3–21 ng/mL, 10/12) with folate elevations (2/12). Total magnesium insufficiency was noted (<2.2 mg/dL, 12/14), with a mean of 1.7 mg/dL (range 1.3–2.3 mg/dL) (VDI Labs, Chatsworth, CA, USA, https://vdilab.com/). The measured mean aspirated volume of bile was 2.4 mL/kg (range 0.78–5.9 mL/kg). Residual eGBV post-DCC appeared negligible with most procedures reduced to visible luminal collapse (see Figure 1). The author concedes that an unreliably quantified volume of bile remained that would increase the actual GBV marginally in each case. Utilizing the ellipsoid calculation, the residual volumes were categorized as <1 mL (7/13), 1–2 mL (5/13) and <5 mL (1/13). All samples were submitted for infection testing by next generation sequencing (MiDog Animal Diagnostics, Tuston, CA, USA, https://www.midogtest.com/). In total, 2/14 cases yielded positive results but with no significant pathogen reported. Bile cytology was not submitted for external clinical pathologic review.
During the post-procedure period, no patient required additional evaluation beyond routine examination through hospitalization discharge. No adverse event was recorded in any patient that required additional hospitalization or resource allocation associated with DCC.
Post-procedural data including at least one follow up examination was available for 14/14 cases. Follow up periods of observation ranged from 2 to 22 months with a mean of 10.5 months. All dogs treated showed resolution of their primary symptoms within 24–48 h and were discharged functionally from hospitalization. A combination of treatments was prescribed for all cases. No case received DCC intervention alone, making a definitive association between intervention and recovery impossible. Common pre- and post-DCC treatments including broad spectrum antibiotics (14/14), maropitant (14/14), prokinetics (9/14), sucralfate (8/14), proton pump inhibitors (12/14), fluid therapy (14/14), parenteral Dexamethasone per practice standard of 0.05–0.1 mg/kg once (10/14), oral prednisone/olone at short-term anti-inflammatory dosing < 0.5 mg/kg/day (2/14) and ursodiol at 10–15 mg/kg/day (14/14) were prescribed. The author re-iterates that all patients in the series had been treated with conventional symptomatic therapies employing various combinations of the aforementioned treatments, prior to interventional DCC. Common but varied bland and low-fat, home-cooked to prescription digestive dietary supportive therapies were prescribed or continued in all patients.
Fasted eGBV mean at follow up was reported to be 1.04 mL/kg with 7/14 dogs remaining under 1 mL/kg. In total, 7/14 cases measured 1 mL/kg or greater. Normal appetite was maintained in 12/14 cases with a resolution of DI patterns in 6/7 cases. BV had resolved in 8/12 symptomatic cases. Notably, of the cases in which anorexic, DI and BV symptoms persisted to any reported degree, the mean eGBV was 1.3 mL/kg (range 0.3–2.2 mL/kg) and in cases with a resolution of symptoms eGBV was reported to be 0.8 mL/kg (range 0.5–2.1 mL/kg). Two cases in the series were referred to surgery due to persisting symptoms; those cases reported eGBV values of 1.8 mL/kg (10 months post-DCC) and 2.2 mL/kg (5 months post-DCC). A single dog remained asymptomatic with an eGBV of 2.1 mL/kg (22 months post-DCC). Sonographic inspissation was persistent in 9/14 at follow up. Progression to overt GBM was not noted within the series time frame.
4. Discussion
In this population, pre-DCC hospitalization with symptom persistence ranged from 1 to 3 days with a case variable but significant polypharmacy prescribed. Duration of hospitalization could not be factored as an indicator of disease severity due to variations in owner motivation to pursue diagnostic ultrasound. Duration of post-DCC evaluation varied between 2 and 22 months, which is a significant variance. Mean post-DCC evaluation was 10 months. A prolonged and uniform duration of monitoring data would be needed for more definitive assessment. A standardized disease scoring assessment (CIBDAI (Canine Inflammatory Bowel Disease Activity Index) or CCECAI (Canine Chronic Enteropathy Clinical Activity Index)) was not pursued due to the sample size, lack of uniform clinical assessment during triage phase and pre-existing polypharmaceutical interventions. Further controlled evaluation of this population would benefit from more specific categorization.
GBD defined at approximately 1 mL/kg was positively correlated with variable digestive symptoms (anorexia, vomiting, diarrhea, lethargy). Historical and/or chronic symptoms of DI and BV were common in this case population, suggesting an acute on chronic disease element. DI has been reported to be associated with non-gravity-dependent biliary sludge in dogs and improves following cholecystectomy [10]. GBV was not reported in that case series but dogs with biliary sludge are known to have reduced GBEF implying a dyskinetic pathology [8]. Bilious vomiting syndrome (BVS) has been studied and surmised to involve abnormal gastrointestinal motility [11]. Potential cholecystopathic dynamics have not been evaluated in dogs with BV to this author’s knowledge. Cases in this series did not undergo ejection fraction testing, primarily due to their shared functional digestive instability. Ejection fractional testing would be helpful to better understand pathophysiologic dynamics in similar cases. In this case series, varied primary gastrointestinal symptoms (anorexia, vomiting and diarrhea) along with DI and BV patterns responded to combined continued routine medical supportive care (all were under treatment with persisting symptoms) and DCC. The author would propose that GBD may simply be a cause of visceral pain that may improve with DCC when routine medical support has failed. Several cases in this series showed marked GBD > 2–5 mL/kg, not likely to be of acute distension origin, without hyperbilirubinemia or sonographic evidence of extra-hepatic bile duct obstruction. Considering the normal post-prandial physiology of coordinated bile expulsion, food ingestion and gastric distension result in cholecystokinin (CCK) release which stimulates gallbladder contraction and intestinal motility coordinated with gastric emptying. Primary bile acids entering the small intestine are eventually reabsorbed in the ileum, returned to the liver via enterohepatic recirculation, and in turn inhibit further CCK release and end the digestive cycle [12]. In this series, persistent bilious vomiting/reflux was a common symptomatic characteristic in conjunction with GBD (12/14). The author proposes that excessive bile secretion into an empty intestine would predictably favor progressive cholecystostasis, GBD and dysmotility via prolonged CCK inhibition. In turn GBD would favor persistent uncoordinated bile expulsion into the small intestine, especially under the abdominal compartmental compressive dynamics associated with vomiting, likely creating a cyclic pathology. Breaking this cycle with DCC may allow for a pathologic CCK inhibitory intermission if present and may in part explain the symptom relief observed in this population. This is likely an overly simplistic pathophysiology but potentially important. The proposed pathophysiologic dynamics would reasonably apply to both an abrupt distension to normal maximum as well as a chronic pathology with progressive distension to supranormal volumes. Cholecystic dynamics (volume and contractility) in dogs with bile reflux and BVS may benefit from additional study. Through the follow up period, few cases in this series had relapsed or continued symptoms (4/14). In the population studied, fasted pre-DCC mean eGBV was 2.2 mL/kg with the fasted post-DCC mean eGBV of 1.0 mL/kg suggesting improved volume dynamics overall. Two cases were referred for a cholecystectomy due to ongoing symptoms. These two cases, assessed at 5 and 10 months post-DCC, showed persistent GBD at 2.2 and 1.8 mL/kg respectively. The trend noted suggested that persistent GBD may be associated with ongoing symptoms. The EGBV measured in the asymptomatic cases was reported as a mean of 0.8 mL/kg, while the eGBV in the symptomatic cases was reported at a mean of 1.3 mL/kg. However, a single case reported occasional bilious vomiting with an eGBV of 0.3 mL/kg while another case continued to have no symptoms with an eGBV of 2.1 mL/kg which would suggest volume is not the only determining factor.
In this population, magnesium insufficiency defined as total magnesium below 2.2 mg/dL was common (12/14). Mean total magnesium was 1.7 mg/d (normal 1.7–2.9 mg/dL, population range 1.3–2.2 mg/dL). Ionized magnesium is the standard for the diagnosis of clinical hypomagnesemia in dogs and is reported commonly in hospitalized animals [13]. Total magnesium has been shown to correlate with ionized magnesium levels but may be weaker in the hospitalized animal [14]. Fractionation of magnesium occurs as ionized 63%, complexed 6% and protein bound 31% forms [15]. No dog in this series was reported to have hypoalbuminemia, making a hypoproteinemic artifact less likely. Ionized hypocalcemia (IHC) was reported to be a risk factor for ionized hypomagnesemia in hospitalized dogs, most commonly in dogs with gastrointestinal illness [16]. Ionized calcium levels were not available in this population. We have no data on magnesium dynamics in dogs with gallbladder disease. However, it has been reported that oral magnesium administration is used to stimulate GB contraction in people and parenteral magnesium has been used to stimulate gallbladder contraction in dogs, both by CCK release stimulated mechanisms [17,18]. The high incidence of magnesium insufficiency in this population may be a dynamic predisposition or co-morbidity that could benefit from further study.
The case number in this small series is insufficient to have any statistical power of correlation relative to volume and persistence of symptoms and may benefit from further study. In this series, the cause of observed GBD was not identified. EHBDO was excluded in all cases based on ultrasound and normal bilirubin levels. An underlying dyskinetic pathology would require ejection fraction testing which was not performed. A non-obstructive, dyskinetic pathophysiology would require further investigation to clarify categorical stimulation deficits (neurohormonal) or potential smooth muscle contractility deficits (such as electrolyte insufficiencies).
5. Conclusions
In this patient population, DCC for GB decompression was performed successfully. GBD was observed with the persistence of digestive symptoms beyond common symptomatic therapies, particularly diurnal inappetence and bilious vomiting. DCC may help in cases with ongoing symptoms and concurrent GBD. DCC did appear to have a reductive effect on follow up fasted eGBV across the series. Next generation sequencing performed in this small population failed to identify a primary infectious element. Objective assessment of symptomatic cholecystopathy in dogs may benefit from characteristics beyond inspissative observations and include volumetric dynamics. Further controlled and thoughtful study is needed.