A 16-week-old 1.5-kg (3.3-lb) sexually intact male Ragdoll kitten with ascites was referred to the Oregon State University Veterinary Teaching Hospital for diagnostic workup of abdominal distension. The abdominal distension was initially noted at 7 weeks of age. The cat had no other clinical signs and was active and eating normally according to the owner. Results of a PCR assay for feline coronavirus run on a sample of peritoneal fluid were negative. Results of fecal flotation were also negative. Additionally, the cat was negative for both circulating FIV antibody and FeLV antigen.
Prior to the referral evaluation, hematologic and serum biochemical testing revealed no abnormalities. Repeated abdominocentesis yielded a yellow, hazy fluid with a total protein content of 3.4 g/dL and 1,412 nucleated cells/μL with no evidence of infectious agents, consistent with a modified transudate. Abdominal ultrasonography performed by a board-certified veterinary internist revealed a markedly distended CVC and hepatic vessels. A board-certified veterinary cardiologist performed echocardiography, which revealed no structural heart disease, and thoracic radiography, which revealed a normal cardiac silhouette with no pulmonary disease. The cat subsequently underwent a CT evaluation.
At the initial teaching hospital evaluation, physical examination abnormalities included severe abdominal distension and panting. Under anesthesia, abdominal CT angiography was performed with a 64-detector CT scannera before and after IV injection of iodinated contrast medium (2 mL of iopamidolb/kg [0.91 mL/lb]). Following contrast medium administration, CT images were acquired in arterial, portal, and venous vascular phases with the following conditions: voxel size, 0.5 mm; rotation speed, 0.5 seconds; matrix, 512 × 512; current, 250 mA; and voltage peak, 120 kV. The volume data were reconstructed in bone and soft tissue algorithms and in isovolumetric transverse, sagittal, and dorsal planes at a slice thickness of 1 mm. The images revealed that the liver was markedly enlarged with rounded and lobular margins and extended caudally to the level of vertebral body L3. At the cranial margin of the liver, the CVC focally tapered in diameter from 5 to 6 mm to 2 mm. At this focal tapering, there was a persistent curvilinear void in the contrast medium within the CVC, most clearly seen in the portal and venous phases (Figures 1 and 2). Multiple abnormal, tortuous, markedly dilated hepatic veins (up to 9 mm in diameter) were evident. These hepatic veins communicated with the CVC at multiple abnormal locations throughout the cranial to caudal extent of the liver. The communication points were all located caudal to the focal CVC narrowing. The portal vein appeared normal. There was a marked amount of non–contrast-enhancing fluid within the peritoneal cavity. Six days after the cat underwent abdominal CT angiography, selective vena caval angiography was performed under general anesthesia by advancing a 60-cm, 4F balloon wedge pressure catheterc into the CVC via the jugular vein under fluoroscopic guidance. Approximately 2 cm caudal to the diaphragm, advancement of the catheter met resistance. A 2-mL contrast medium bolus (1:1 ratio of iohexold and saline [0.9% NaCl] solution with heparin) was hand injected through the catheter, with the balloon inflated to assist retrograde flow. As a result, stenosis of the CVC approximately 5 cm caudal to the diaphragm (Figure 3) was confirmed. Pressure measurements were obtained at and cranial to the level of the stenosis, indicating a pressure difference of approximately 14 mm Hg. Despite several attempts, the catheter could not be maneuvered across the stenotic region into the caudal region of the CVC. The right jugular vein was ligated following the procedure, and the subcutaneous and cutaneous tissue layers were closed routinely.
On the basis of the pressure gradient at the CVC narrowing, it was determined that the cat might benefit from vascular stenting of the affected CVC region. Preoperative blood typing was performed by use of a commercial kit.e A week after selective vena caval angiography, the cat was anesthetized and the abdominal cavity was accessed via median celiotomy to locate the CVC. An 18-gauge IV catheter was placed caudal to the left and right renal veins to insert a 0.035-mm-diameter hydrophilic guidewiref into the CVC. When trying to advance the guidewire through the CVC narrowing, slight resistance located approximately 2.5 cm cranial to the right phrenicoabdominal vein was felt. With a mild increase in the amount of cranially directed force, the guidewire was advanced beyond the stenotic area. The catheter was removed, and a 6F introducerf was placed over the guidewire into the vena cava. The guidewire was removed, and a 6F 8 × 24-mm biliary stentf was advanced into the stenotic area under fluoroscopic guidance. A single dose of heparin (35 U/kg [15.9 U/lb], IV) was administered preceding the deployment of the vascular stent. The stent was expanded with saline solution under maintained fluoroscopic guidance to a pressure of 6 atm, as measured with a handheld pressure gauge. Electrocardiographic monitoring of the cat detected a transient decrease in heart rate from 200 to 180 beats/min accompanied by the appearance of 4 ventricular premature complexes during deployment of the intravascular stent, which resolved without intervention once the balloon of the expanding stent was deflated. The venotomy site was closed with 6–0 polydioxanone sutureg in a simple continuous pattern following removal of the introducer. The cat had moderate to severe hypotension (mean arterial pressure, 30 to 60 mm Hg) throughout the procedure, which necessitated treatment with constant rate infusions of dopamine (5 to 10 μg/kg/min [2.3 to 4.5 μg/lb/min], IV) and dobutamine (1 μg/kg/min [0.45 μg/lb/min], IV), hetastarch (6%; 2 mL/kg [0.9 mL/lb], IV, over a period of 10 minutes), and vasopressin (0.013 U/kg [0.006 U/lb], IV, once). The liver was diffusely nodular in appearance, and 4-mm punch biopsy specimens were obtained from right and left lateral liver lobes. The remainder of the intra-abdominal organs were grossly normal. The abdomen was lavaged and the incision routinely closed.
Stent placement in the abdominal CVC caudal to the diaphragm was confirmed with 2-view postoperative abdominal radiography. The stent extended from the caudal thoracic portion of the CVC to the cranial to mid aspect of the liver (ie, from the caudal aspect of the T11 vertebra to the midbody of the T13 vertebra). The cat recovered from anesthesia uneventfully and was hospitalized for 3 nights following the procedure.
Histologic examination of the liver biopsy specimens revealed focal areas of sinusoidal congestion with attenuation of hepatic cords. The amount of loose connective tissue within the liver capsule was greater than that considered normal and was accompanied by moderate vascular ectasia. Compared with findings typical of a healthy cat's liver, there was a moderate increase in portal collagen content with scattered, generally moderate dissection into the surrounding lobules, consistent with moderate fibrosis.
Recheck examinations at 3.5 and 7.5 months after surgery revealed that the cat was growing rapidly and its activity level was considered normal. The owner had no concerns regarding the cat's well-being except for intermittent soft feces. The cat was mildly overconditioned with a body condition score of 7 of 9, and mild distension of the abdomen was noted during both recheck examinations. A CBC and serum biochemical profile performed at each recheck examination revealed no remarkable findings. Serum alanine aminotransferase activity remained mildly high at the 3.5- and 7.5-month recheck examinations (180 and 73 U/L, respectively; reference range, 5 to 65 U/L). No peritoneal fluid was detected during recheck abdominal ultrasonography at 3.5 months after surgery.
At 7.5 months after stent placement, the cat was anesthetized and underwent abdominal CT angiography with settings similar to those used initially, except the current (300 mA) and contrast medium dose (1 mL of iopamidol/kg) were increased to account for the increased weight of the cat. Similar to initial findings, the liver remained enlarged and extended caudally to the L3 vertebra; however, the margins were less rounded and no longer lobular. The CVC stent was in a position similar to that detected radiographically after surgery and continued to bridge the location of the previous stenosis. The diameter of the CVC was 8 mm cranial to the stent, 9 mm at the level of the stent, and 4 mm caudal to the stent. The hepatic veins remained tortuous but were no longer dilated, with a maximal diameter of 5 mm. The multiple abnormal locations of entry of the hepatic veins into the intrahepatic CVC persisted. The peritoneal fluid accumulation detected at the initial evaluation had resolved. At this latter recheck examination, the portal vein at the porta hepatis was focally tortuous, which had not been detected previously. The cat recovered from the anesthetic episode uneventfully. At the time of the last telephone inquiry 13 months after stent placement, the owner reported that the cat remained free of clinical signs and continued to have a good appetite, normal energy level, and weight gain.
Caudal vena cava
Toshiba Aquilion, Toshiba American Medical Systems, Tustin, Calif.
Iopamidol (300 mg of iodine/mL), Bracco Diagnostics Inc, Princeton, NJ.
AI-07121, Arrow International Inc, Reading, Pa.
Omnipaque, GE Healthcare, Waukesha, Wis.
Alvedia Quick Test A+B, Alvedia, Limonest, France.
Infinity Medical Inc, Menlo Park, Calif.
Ethicon Inc, Somerville, NJ.
1. Horton JD, San Miguel FL, Ortiz JA. Budd-Chiari syndrome: illustrated review of current management [Erratum published in Liver Int 2008; 28:898]. Liver Int 2008; 28: 455–466.
2. Macintire DK, Henderson RH, Banfield C, et al. Budd-Chiari syndrome in a kitten, caused by membranous obstruction of the caudal vena cava. J Am Anim Hosp Assoc 1995; 31: 484–491.
3. Okuda K, Kage M, Shrestha SM. Proposal of a new nomenclature for Budd-Chiari syndrome: hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion. Hepatology 1998; 28: 1191–1198.
5. Cohn LA, Spaulding KA, Cullen JM, et al. Intrahepatic postsinusoidal venous obstruction in a dog. J Vet Intern Med 1991; 5: 317–321.
6. Kolata RJ, Cornelius LM, Bjorling DE, et al. Correction of an obstructive lesion of the caudal vena cava in a dog using a temporary intraluminal shunt. Vet Surg 1982; 11: 100–104.
8. Cornelius L, Mahaffey M. Kinking of the intrathoracic caudal vena cava in five dogs. J Small Anim Pract 1985; 26: 67–80.
9. Rosa C, Schoeman JP, Dvir E. Budd-chiari–like syndrome associated with a pheochromocytoma invading the right atrium in a dog. Isr J Vet Med 2012; 67: 180–185.
10. Schoeman JP, Stidworthy MF. Budd-Chiari–like syndrome associated with an adrenal phaeochromocytoma in a dog. J Small Anim Pract 2001; 42: 191–194.
11. Cave TA, Martineau H, Dickie A, et al. Idiopathic hepatic veno-occlusive disease causing Budd-Chiari–like syndrome in a cat. J Small Anim Pract 2002; 43: 411–415.
12. Holt D, Saunders HM, Aronson L, et al. Caudal vena cava obstruction and ascites in a cat treated by balloon dilation and endovascular stent placement. Vet Surg 1999; 28: 489–495.
13. Schrope DP. Hepatic vein stenosis (Budd-Chiari syndrome) as a cause of ascites in a cat. J Vet Cardiol 2010; 12: 197–202.
14. Haskal ZJ, Dumbleton SA, Holt D. Percutaneous treatment of caval obstruction and Budd-Chiari syndrome in a cat. J Vasc Interv Radiol 1999; 10: 487–489.
15. Darwish Murad S, Plessier A, Hernandez-Guerra M, et al. Etiology, management, and outcome of the Budd-Chiari syndrome. Ann Intern Med 2009; 151: 167–175.
16. Virmani V, Khandelwal N, Kang M, et al. MDCT venography in the evaluation of inferior vena cava in Budd-Chiari syndrome. Indian J Gastroenterol 2009; 28: 17–23.
18. Fisher NC, McCafferty I, Dolapci M, et al. Managing Budd-Chiari syndrome: a retrospective review of percutaneous hepatic vein angioplasty and surgical shunting. Gut 1999; 44: 568–574.
19. Dyet JF, Watts WG, Ettles DF, et al. Mechanical properties of metallic stents: how do these properties influence the choice of stent for specific lesions? Cardiovasc Intervent Radiol 2000; 23: 47–54.
20. Rossi P, Salvatori FM, Fanelli F, et al. Polytetrafluoroethylene-covered nitinol stent-graft for transjugular intrahepatic portosystemic shunt creation: 3-year experience. Radiology 2004; 231: 820–830.
21. Patil P, Deshmukh H, Popat B, et al. Spectrum of imaging in Budd Chiari syndrome. J Med Imaging Radiat Oncol 2012; 56: 75–83.
22. Orloff MJ, Daily PO, Orloff SL, et al. A 27-year experience with surgical treatment of Budd-Chiari syndrome. Ann Surg 2000; 232: 340–352.