CASE REPORT

Veterinary Surgery28:489-495, 1999

Caudal Vena Cava Obstruction and Ascites in a Cat Treated byBalloon Dilation and Endovascular Stent Placement

DAVID HOLT, BVSc, Diplomate ACVS, H. MARK SAUNDERS, VMD, Diplomate ACVR,LILLIAN ARONSON, VMD, Diplomate ACVS, HEATHER PEIKES,VMD,

MICHEAL GOLDSCHMIDT, BVSc, Diplomate ACVP, and ZIV J. HASKAL, MD, FSCVIR

Objective—To present details of an unusual case of caudal vena caval obstruction and itsmanagement in a cat.Study Design—Clinical case report.Study Population—A 15 month old male castrated domestic shorthaired cat.Results—The diagnostic evaluation included the use of digital subtraction angiography andultrasonography to locate the caudal vena caval obstruction. Treatment initially involved punctureand balloon dilation of the obstructed area of the cava. After reobstruction, the stenotic area wasredilated and stented. The cat was euthanatized 4 weeks later because of vomiting, anorexia, andabnormal behavior, presumed to be associated with liver disease.Conclusion and Clinical Relevance—Interventional radiography provided a minimally invasiveway to manage this unusual vascular anomaly.©Copyright 1999 by The American College of Veterinary Surgeons

A 15 MONTH OLD male neutered domestic short-haired cat was taken to the referring veterinarian

for evaluation of abdominal distension which haddeveloped over the past 2 months. The cat was keptindoors and there was no history of trauma. The catwas eating normally, and was alert and active. Theonly abnormalities found on physical examinationwere severe abdominal distension and lumbar musclewasting. The cat weighed 5.5 kg, which was 1.3 kgmore than when it was examined 3 months previously.

No hematologic or biochemical abnormalities weredetected. Preprandial and 2-hour post-prandial serumbile acid concentrations were normal. Serology forfeline leukemia virus (FeLV), feline immunodefi-ciency virus (FIV), and feline infectious peritonitis(FIP) were negative. No abnormalities were seen onthoracic radiographs. Abdominal ultrasonographyshowed a large amount of peritoneal effusion. Theliver lobes were rounded and contained numerous 0.2

to 0.3 cm hyperechoic nodules. The omentum wasclumped. Peritoneal fluid obtained during ultrasonog-raphy was interpreted as a modified transudate. Thefluid was pale yellow with a specific gravity (SG) of1.022 and a total protein (TP) of 4.0 g/dL. The fluidred blood cell count (RBC) was 921 cells/mL and thenucleated cell count was 65 cells/ml. Smears from acentrifuged peritoneal fluid sample contained 46%nondegenerate neutrophils, 39% macrophages, and15% small mature lymphoctes. No infectious agents orneoplastic cells were seen. A coagulation screen andplatelet count were normal. Serology for heartwormwas negative.

An exploratory laparotomy was performed. A largevolume of peritoneal fluid was removed via suction.All organs appeared grossly normal, except the liver,which seemed small and irregular with a thickenedcapsule. Liver biopsy samples were submitted. His-topathologic sections of the liver revealed dilated

From the Department of Clinical Studies (DH, HMS, LA, HP) and Pathobiology (MG), University of Pennsylvania School of VeterinaryMedicine, Philadelphia, PA; and the Department of Radiology (ZJH), University of Pennsylvania School of Medicine, Philadelphia, PA.

Address reprint requests to David Holt, BVSc, Department of Clinical Studies, University of Pennsylvania School of VeterinaryMedicine, 3850 Spruce Street, Philadelphia, PA 19104-6010.

©Copyright 1999 by The American College of Veterinary Surgeons0161-3499/99/2806-0011$3.00/0

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hepatic lymphatics. Increased numbers of arterioleswere seen in the portal tried areas. The thickened livercapsule seen at surgery could not be visualized micro-scopically. The cat recovered from surgery unevent-fully and 24 days later was referred to the VeterinaryHospital, University of Pennsylvania for further eval-uation.

At referral examination, the cat had moderate ab-dominal distension and lumbar muscle wasting. Thecat weighed 4.75 kg. A complete blood count showeda mild normocytic, normochromic anemia, with apacked cell volume (PCV) of 26%. Mild elevations ofthe serum alanine aminotransferase (ALT; 330 U/L,normal, 20 to 107 U/L) and serum aspartate amino-transferase (AST; 85 U/L, normal, 1 to 37 U/L)concentrations were the only biochemical abnormali-ties. A fasting serum ammonia concentration (NH3)was within normal limits (13mmol/L, normal 11 to 35mmol/L). Abdominal ultrasonography (ATL Ultra-mark 9 HDI; Advanced Technology Laboratories,Bothell, WA) showed an echogenic peritoneal effu-sion and a small liver with rounded boarders andhyperechoic perivascular foci. The portal vein wasdilated (0.5 cm diameter) caudal to the liver, but itappeared to enter the liver normally at the portahepatis. The intrahepatic portion of the caudal venacava (CVC) appeared dilated and an abnormal plexusof vessels was visualized within either the quadrate orright medial liver lobes. Examination of the vascularplexus with spectral and color flow Doppler revealedmultidirectional, undulating venous-type flow veloci-ties, which were believed to be caused by the changesin intrathoracic pressure associated with respiration.

A caudal vena cavagram was performed with a19-gauge, 8-inch intravenous catheter placed in theCVC through the left medial femoral vein to a levelapproximately 2 cm caudal to the left renal vein. One7 mL bolus of 66% meglumine diatrizoate/10% so-dium diatrizoate was used to evaluate venous bloodflow. Contrast filled the CVC cranially only to thelevel of the renal veins. Contrast was also seen inmany collateral veins that communicated with thevertebral venous sinuses and the azygous vein (Fig 1).Abdominal ultrasonography was repeated after con-trast venography. Spectral and color Doppler showedabnormal CVC flow similar to that seen in the caudalvena cavagram. Normal flow in the cranial directionwas seen in the CVC from the external iliac veins tothe level of the vertebral venous collateral vessels.Starting between the renal and hepatic veins, reverse

CVC flow was seen with blood flowing caudally to thevertebral venous collateral vessels. Within the hepaticportion of the CVC, normal cranial blood flow wasseen in the CVC. At the site where blood flow changeddirection from caudal to cranial, an echogenic struc-ture was seen within the CVC. The vascular plexuspreviously seen within either the caudate or rightmedial liver lobes was visualized but the nature of thislesion could not be further defined.

Angiography was performed 10 days after the initialcontrast study to rule out an arteriovenous fistulawithin the liver. The cat weighed 5.6 kg at this timeand was anesthetized with propofol (2 mg/kg intrave-nously [IV]), midazolam hydrochloride (0.4mg/kg IV)and glycopyrrolate (0.005mg/kg IV). Anesthesia wasmaintained with isoflurane and oxygen deliveredthrough a cuffed endotracheal tube. Abdominocentesiswas performed and 570 mL of a hemorrhagic fluid wascollected. The PCV of the fluid was 4%, the TP was2.2 g/dL, and the SG was 1.014. The peripheral PCVwas 19 and the TP was 5.1. A CBC showed anoromocytic, hypochromic anemia. A coagulationscreen and platelet count were subsequently per-formed; results were normal. The cat was blood typedand 40 mL of matched, fresh whole feline blood wasadministered over the next 2 hours. A nonselectiveangiogram was performed by injecting a 10 mL bolusof 76% meglumine diatrizoate into a 19-gauge catheterplaced in the right jugular vein. There was no radio-graphic evidence of a hepatic arteriovenous fistula.The CVC opacified normally caudal to the liver, butcould not be visualized clearly within the liver. Con-trast was again seen to enter multiple collateral vesselscommunicating with the vertebral venous sinuses andthe azygous vein. The CVC was dilated at the level of

Fig 1. Venogram after injection of contrast material into thecaudal vena cava. Radioopaque contrast medium fills the venacava only to the level of the kidneys. Contrast material shuntsinto the vertebral venous sinuses and the azygous vein.

490 CAUDAL VENA CAVA OBSTRUCTION IN A CAT

the diaphragm. This appeared to be the area where theabnormal plexus of vessels previously visualized byultrasound in either the caudate or right medial liverlobes entered the CVC.

The next day, the cat was anesthetized with asimilar anesthetic protocol and an exploratory laparot-omy was performed in an attempt to locate both theobstruction in the CVC and the source of hemorrhage.At laparotomy, individual liver lobes were not discern-able. The liver appeared as a single entity, coveredwith a thick grey capsule. There were old blood clotson the capsule, but the source(s) of the hemorrhagewas not apparent. The spleen was folded onto itselfand the two “halves” of the spleen were adheredtogether. The entire omentum was bunched; both thespleen and the omentum appeared to be covered by agrey membrane similar to the tissue covering the liver.The mesenteric lymph nodes were enlarged. Therewere no gross portocaval shunting vessels visible. TheCVC was dissected cranially to the level of the liver,and then from the cranial aspect of the liver to thediaphragm. Numerous small abnormal vessels wereseen entering or leaving the CVC and running dor-sally. The intrahepatic portion of the CVC could notbe easily dissected because of the thick capsule cov-ering the liver. Biopsies of the liver, omentum, andlymph nodes were obtained. The liver parenchymashowed no evidence of congestion, fibrosis, or bileduct proliferation. There was some proliferation ofsmall arterioles present in the portal areas. On theserosal surfaces of the liver and omentum, thick bandsof an amorphous, eosinophilic material were presentwith interspersed spindle cells and occasional lym-phoid cells. The spindle cells had elongated nuclei thatappeared more cigar shaped than fusiform, suggestingthat they were smooth muscle cells rather than fibro-blasts. Special stains with trichrome stains showed thatthe cells were smooth muscle cells that were produc-ing a fine, fibrillar collagenous matrix (Fig 2). Thelymph node biopsies showed reactive hyperplasia.

After consultation with a human radiologist(Haskal), it was decided that selective CVC catheter-ization would better delineate the level of the obstruc-tion. One week after the laparotomy, the cat wasanesthetized and 20mg/kg of cefazolin was adminis-tered intravenously. The CVC was catheterized via theleft femoral vein with a 5F Berenstein catheter (CookInc, Bloomington, IN). A digital subtraction cavagramusing a 5cc bolus of iohexol (240 mg I/mL) showed ashort caval obstruction at the cranial portion of the

intrahepatic CVC (Fig 3). It was possible to canulateone of the hepatic veins from the CVC, indicating thatthe obstruction was cranial to at least this hepaticvein’s caval opening. The caval obstruction was punc-tured and traversed using a 50-cm 21-gauge needle(Cook Inc, Bloomington, IN) introduced coaxially intothe CVC through the Berenstein catheter. A guide wirewas threaded through the needle, the needle removedand a 5 F, 7 mmdiameter by 2 cm long angioplastyballoon catheter (Medi-Tech/Boston Scientific, Water-town, MA) was used to dilate the site of the cavalobstruction (Fig 4). Repeated venography showed noresidual stenosis with brisk caval flow into the rightatrium. The catheter was removed from the femoralvein, and the vein wall closed with a simple continu-ous suture of 7-0 prolene. The cat recovered fromanesthesia uneventfully and was discharged the nextday.

The cat re-presented 10 days later without resolu-tion of the ascites. Spectral and color Doppler ultra-sonography showed caudal blood flow in the CVCfrom the intrahepatic portion to the region of thecollateral vessels. The cat was anesthetized and 20mg/kg of cefazolin was administered intravenously.Repeat venography, performed through a similar rightfemoral vein approach, demonstrated recurrent steno-sis of the previously dilated caval segment (Fig 5).One hundred units of heparin/kg was administeredslowly IV. The narrowed area of the CVC was thendilated and stented using a 2-cm long, 8-mm diameterWallstent (Schnieder USA, Minneapolis, MN) (Figs 6and 7). The stent is a self-expanding, braided helicalmesh made from a biomedical grade alloy of cobalt,

Fig 2. Biopsy of the liver stained with trichrome (300 3magnification). Note the proliferation of smooth muscle cellson the liver’s surface.

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chromium, nickel, molybdenum, and iron. The stent isheld on its delivery catheter by an outer constrictingmembrane, and is deployed by retracting this mem-brane, which allows the stent to self-expand. Afterplacement, the stent was balloon dilated to expand and“seat” it in place in the CVC. The catheter wasremoved from the femoral vein and the vein wallclosed with a simple continuous suture of 7-0 prolene.Fluid was not removed from the peritoneal cavity. Thecat recovered from anesthesia uneventfully and wasdischarged the next day. The owner was instructed togive the cat 20 mg aspirin every 3 days for 2 weeks toprevent thrombus formation at the site of the stent.

The cat presented to the referring veterinarian 10days after the stenting procedure for abnormal behav-ior. On physical examination, the cat was hypothermic(98.7°F), with moderate generalized muscle wastingand ascites. Cranial nerve examination was not re-markable, but the cat appeared to be demented. Ab-dominocentesis was performed and 400 mL of fluidwas obtained from the peritoneal cavity. The cat wasmildly anemic (PCV, 26%) and had abnormal liverfunction (fasting serum bile acid concentration: 80mmol/L, normal, 0 to 5mmol/L, and fasting serum

Fig 3. Digital subtraction angiogram of the caudal vena cavaafter injection of 5cc Iohexol. The intrahepatic portion of thecava is obstructed.

Fig 4. Digital subtraction angiogram showing dilation of thenarrowed area of the caudal vena cava using a 5F, 7 mmdiameter by 2 cm long angioplasty balloon catheter (Medi-Tech/Boston Scientific, Watertown, MA).

Fig 5. Digital subtraction angiogram showing restenosis ofthe caudal vena cava 10 days after balloon dilation. A guidewire is in has been passed easily across the stenotic area of thecaudal vena cava, but contrast flows into the azygous vein.

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ammonia concentration: 353mmol/L, normal, 11 to 35mmol/L). The serum ALT, AST, and lactate dehydro-genase enzyme concentrations were elevated (232U/L, normal, 10 to 100 U/L; 112 U/L, normal 10 to100 U/L; and 754 U/L, normal 20 to 500 U/L,respectively). The cat was treated with intravenousfluids (2 mL/kg/hr IV), cimetidine (5 mg/kg IV every8 hrs), cefoxitin (20 mg/kg IV every 6 hrs), andlactulose (1 mL/kg by enemas every 8 hrs). The catimproved clinically and was discharged 7 days later.

The cat was seen by the referring veterinarian twiceover the next week as an outpatient, initially forvomiting and subsequently for anorexia. The cat wasrehospitalized by the referring veterinarian one weekafter the second outpatient examination for bilateralmucopurrulent nasal discharge, decreased appetite,and vomiting. At this time the ascites had clinicallyresolved. The cat was treated with intravenous fluids,cimetidine and cefoxitin. The fasting serum bile acidconcentration was 75mmol/L. An abdominal ultra-sound revealed a small amount of peritoneal fluid. TheCVC stent was in place and the CVC was patent. Theliver appeared small with irregular margins. No nor-mal intrahepatic portal vasculature could be visual-ized. The cat’s condition failed to improve over the

next 5 days and the owner requested euthanasia. Postmortem examination was not permitted.

DISCUSSION

The abdominal effusion in this cat was most likelycaused by obstruction of the intrahepatic portion of theCVC. During angiography, at least one of the hepaticveins could be canulated from the CVC, indicatingthat the obstruction was cranial to some or all of theopenings of the hepatic veins into the CVC. The cat’scondition was similar to Budd-Chiari syndrome (BCS)in human beings, in which postsinusoidal obstructionof hepatic venous blood flow causes hepatomegaly,proteinaceous abdominal effusion, and abdominalpain.1 However this cat did not have either the gross

Fig 7. (A) Lateral and (B) ventrodorsal radiographs showingthe 2 cm long, 8 mm diameter Wallstent (Schnieder USA,Minneapolis, MN) deployed in the caudal vena cava.

Fig 6. Digital subtraction angiogram showing flow of positivecontrast through the stented area of the caudal vena cava.

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hepatomegaly or the histologic centrilobular hepaticcongestion and sinusoidal dilation characteristic of thepostsinusoidal obstruction of hepatic venous bloodflow seen in human beings with BCS.1,2 The reasonfor the lack of characteristic histologic findings in thiscat is unknown. Presumably in this cat the obstructionof the CVC was caudal to the openings of some of thehepatic veins, that then had unimpeded drainage intothe CVC.

Obstruction of the posthepatic CVC causing BCSwas described in a kitten.3 Exploration of the CVC inthis kitten revealed a “thin, fibrous, web-like mem-brane” at the site of the obstruction. Microscopicexamination of a biopsy sample of the membraneshowed collagen extending from the wall of the CVCand forming the membrane. Fibrous webs obstructingthe inferior vena cava are a common cause of BCS inthe Japanese, Indian, and South African human popu-lations.2,4,5 In human beings, the webs were formerlybelieved to be a congenital anomaly,6 and a similaretiology was proposed for the web found in the kitten.3

A more recent human study provided compellinghistologic evidence that the obstructing membraneswere not congenital, but were “explainable on thebasis of organization of various sized thrombi thatoccurred within the inferior vena cava in the past”.7

We do not know the cause of the CVC obstruction inthe cat in our report. There was no history of trauma,and two coagulation screens showed no evidence ofhypercoagulability.

The kitten in the previous report had a web occlud-ing the CVC at the level of the diaphragm. The kittenwas treated by partially resecting the web via venot-omy, and widening the CVC by suturing a Dacronpatch graft into the venotomy site.3 The exposure ofthe CVC was achieved using a right eighth intercostalthoracotomy.3 In the cat described in our report, theintrahepatic location of the CVC obstruction madedirect surgical access impossible. Balloon dilation(“angioplasty”) was considered the only viable treat-ment option for this cat. Human beings with a focalstenosis of a hepatic vein or inferior vena cava areconsidered ideal candidates for percutaneous translu-minal angioplasty1 which was first described in 1974.8

Angioplasty with stent insertion was first described asa treatment for BCS in 1991.9 Appropriate catheters,guide wires, and expertise are required to perform theprocedure. Potential complications of stent placementinclude stent migration10 and neointimal hyperpla-sia.11 In the cat described here, vascular access was

easily obtained via a routine approach to the proximalportion of the femoral vein. The only difficultiesencountered were: (1) correctly orienting the needlecaudal to cranial in the vena cava to puncture only themembrane and not the wall of the CVC, and (2)inserting the large diameter catheter containing theWallstent into the femoral vein.

Both ultrasonography and angiography are usefultools for diagnosing CVC obstruction in human be-ings.1 Angiography is the classical imaging modalityused to diagnose BCS in human beings.1 The digitalsubtraction vena cavagrams performed in this catallowed precise location of the CVC obstruction. TheCVC obstruction was not suspected on the initialultrasound examinations; more thorough examinationusing spectral and color Doppler ultrasonographyshowed retrograde flow in the intrahepatic portion ofthe CVC and allowed visualization of the obstruction.The unusual plexus of vessels seen in the area of theright medial or quadrate liver lobes was likely a groupof collateral vessels formed secondary to the cavalobstruction. After the initial angioplasty and subse-quent stenting, ultrasound provided a non-invasivemeans of assessing caval blood flow.

Recurrence of obstruction after balloon angioplastyoccurs in humans with reported frequencies of be-tween 2.4% and 50%.12,13Humans with membranousobstructions of the inferior vena cava treated withangioplasty and stenting had a lower incidence ofrecurrent stenosis (12%) than those treated with an-gioplasty alone (48%).12 A stent was not placed in thecat after initial successful dilation of the stenotic areaof the cava because of concern that it might promoteboth thrombosis and perhaps endothelialization at thehepatic veins’ openings into the CVC. The stent wasstill in position and the CVC was patent on ultrasoundthree weeks after placement. Animal studies haveshown that stents in the venous system are incorpo-rated into the vein wall and covered by endotheliumwithin 4 weeks of implantation.14 However, the re-sponse of the CVC to the stent in this cat is unknownsince a postmortem examination was not permitted.

Despite the angioplasty and stent placement, theascites failed to resolve in the cat in this report, andabdominocentesis was performed by the referringveterinarian 10 days after the stenting procedure.Subsequently the ascites did not reform clinically buta “small” amount of ascites was visualized by ultra-sound one month after stenting. After stent placement,one would expect that the pre-existing increase in

494 CAUDAL VENA CAVA OBSTRUCTION IN A CAT

hydrostatic pressure in the CVC would disappear, andfluid in the peritoneal cavity should be reabsorbed andsubsequently excreted through the kidneys. However,we suspect that the thick layer of smooth muscle andcollagenous matrix covering the liver, spleen, andomentum interfered with fluid reabsorption by pre-venting the free flow of fluid across the peritonealmembrane into the adjacent lymphatics and venules.In addition, there was obvious evidence of liverdysfunction when the cat was re-evaluated by thereferring veterinarian. It is possible that the stentcaused hepatic venous obstruction, although this com-plication has not been reported in humans.9-11,13It ismore likely that progressive liver disease and portalhypertension developed as a response to chronic post-sinusoidal hepatic venous obstruction.

The cause of the proliferation of smooth muscle cellson the visceral peritoneum of the liver, spleen, andomentum is not known. However, it is possible that thecause is related to the chronic effusion caused by theCVC obstruction. At celiotomy, the changes were grosslyreminiscent of descriptions of sclerosing encapsulatingperitonitis (SEP), but the histologic appearance of the biopsysamples taken was quite different from those describedfor this condition.15-17 In this case there was only smoothmuscle proliferation, whereas in the cases of SEP there wasmesothelial proliferation on the surface of the affectedorgans with neovascularization and fibroplasia, typicallyseen with immature granulation tissue.

Although unsuccessful in this case, interventionalradiographic techniques, including balloon angioplastyand stent placement provided a unique, minimally inva-sive way to manage this unusual vascular anomaly.

REFERENCES

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