Percutaneous transvenous coil embolization of portosystemic shunts

Article

See how this minimally invasive procedure helped a Labrador puppy.

A congenital portosystemic shunt (PSS) is a vascular anomaly connecting the portal venous system with the central venous system, allowing nutrient-rich blood to bypass the liver, avoid detoxification and enter the systemic circulatory system, leading to a variety of biochemical and clinical sequellae. See how a minimally invasive procedure helped this puppy.

Initial findings

  • Signalment: 5-month-old 22-kg intact male Labrador retriever

  • Presenting complaint: Hepatoencephalopathy due to suspected PSS

  • Pertinent history: Three-month history of intermittent ataxia, poor growth, exercise intolerance and reduced appetite; owners report some improvement with antibiotics

  • Medications: Ampicillin

  • Physical examination findings: Quiet, alert and responsive; heart rate = 70 beats/min; body condition score 3/9; no murmurs auscultated; no neurologic abnormalities; abdominal palpation unremarkable; rectal examination normal (no melena)

Diagnostic evaluation

  • Complete blood count: Moderately elevated white blood cell count with mature neutrophilia, with a nonregenerative microcytic anemia (mean corpuscular volume = 54, hematocrit = 31 percent)

  • Serum chemistry profile: Alanine transaminase = 154, aspartate transaminase = 87, blood urea nitrogen 3, albumin = 1.9, globulin = 2.2, cholesterol = 125

  • Bile acids: Pre-prandial = 119, post-prandial = 244

  • Protein concentration: 44

  • Urinalysis urine culture: Urine specific gravity = 1.016, ammonium biurate crystalluria; culture results pending

  • Abdominal ultrasonography: Declined in favor of future computed tomography (CT) angiography

Initial treatment decisions

After an intrahepatic PSS was diagnosed, a medical regimen was recommended to reduce the clinical signs associated with the hepatic dysfunction and gastrointestinal upset, including lactulose (dosed to produce soft but formed bowel movements), metronidazole (7.5 mg/kg b.i.d.), omeprazole (1 mg/kg b.i.d.) and a low-protein diet compatible with liver disease. The patient was discharged with instructions to return in about one month for CT angiography. The delay in further imaging was done to maximize the patient's medical regimen in order to reduce any potential risks associated with general anesthesia.

CT angiography and treatment options

The patient returned one month later with reports that it had dramatically improved on these medications. It had gained 4.5 kg and was having no further neurologic or ataxic episodes. A dual-phase CT angiogram was performed, which demonstrated a large, left divisional intrahepatic PSS. Portal perfusion to the liver was substantially diminished, and the liver was small. The kidneys were mildly enlarged with mild renal pelvic mineralization or nephrolithiasis.

Medical, surgical and interventional management was discussed with the owners. Understanding that medical management would likely be temporary and concerned about the risk associated with traditional open surgery, the owners opted for a minimally invasive approach using percutaneous transvenous coil embolization.

The procedure

The dog was anesthetized and positioned in dorsal recumbency. The entire procedure was performed through a 5-mm incision over the right jugular vein and under fluoroscopic guidance.

A 12-Fr vascular sheath was percutaneously placed into the right jugular vein. A combination of angiographic catheters and guide wires were used to select the left divisional PSS. A marker catheter and guidewire combination was then used to select the caudal vena cava. Angiograms were performed to determine the caudal vena cava diameter and location of the shunt entrance into the caudal vena cava (* in Figure 1A). Resting portal and caudal vena cava pressure measurements were obtained through the respective catheters.

Figures 1A-1F: Serial fluoroscopic images demonstrating transvenous coil embolization of a left divisional intrahepatic portosystemic shunt (PSS). In each image, the patient’s head is to the left of the image (CVC = caudal vena cava).

An appropriately sized self-expanding metallic stent (SEMS) was advanced into the caudal vena cava (Figure 1B) and deployed across the shunt entrance (Figure 1C). A catheter and guidewire combination was used to reaccess the shunt through the stent interstices (Figure 1D), and repeat pressure measurements were obtained. Thrombogenic coils were then consecutively passed and deployed through the catheter and into the shunt until portal pressure were raised appropriately (Figure 1E). Upon completion, the catheter was removed (Figure 1F), the sheath was replaced with a multilumen central line and the dog recovered.

Outcome

The patient was discharged from the hospital two days later with instructions to continue medical therapy for the next month. Discharge medications also included a two-week dose of amoxicillin-clavulanate (13.75 mg/kg b.i.d.) for the implanted devices. Follow-up phone calls each week confirmed the dog continued to do well. On examination the following month, repeat bloodwork demonstrated continued improvement.

Medical management was slowly discontinued (except for the omeprazole, which will be continued for life), a normal adult dog food was slowly introduced and the clinical signs have not returned. Routine screening bloodwork should be repeated every three to six months for the first year and then every six months thereafter, or sooner if needed. About 15 to 20 percent of dogs will require an additional coil procedure in the future if clinical signs return.1

Discussion

Patients with a congenital PSS often present as young animals with neurologic signs (hepatoencephalopathy) such as ataxia, wall-walking, star-gazing and even seizure activity. In addition, the dogs can present with urinary tract signs (ammonia biurate urolithiasis) or gastrointestinal signs (melena in intrahepatic PSS, pica, reduced appetite). Medical management is the mainstay of initial therapy, with the goal of minimizing the clinical signs through a reduction of circulating toxins achieved through a reduction in absorbed nitrogenous waste (low-protein diet, lactulose and antibiotics). In our experience, the addition of proton-pump inhibition has reduced complications associated with gastrointestinal hemorrhage in dogs with an intrahepatic PSS.

While medical therapy palliates clinical signs associated with PSS in dogs, it is typically temporary, and some evidence suggests medical therapy is inferior to attenuating the shunt.2,3 In addition, while surgical attenuation of extrahepatic PSS is typically safe, well-tolerated and successful in improving portal perfusion, surgery for intrahepatic shunts has been associated with perioperative complication rates as high as 77 percent, perioperative mortality rates up to 28 percent and overall mortality rates as high as 64 percent.4-8

Interventional radiology techniques have been demonstrated to provide a safe, reliable, rapid and effective minimally invasive alternative to open surgical treatment of canine intrahepatic PSS. In a recent abstract of 95 dogs with intrahepatic PSS treated by using interventional radiology techniques, major complications occurred in only 2 percent of cases, with good to excellent long-term outcome in about 75 percent of dogs and a median survival time of six years—longer than previously reported with any other treatment modality.1 These techniques have also been used in cats and are being explored for use in animals with an extrahepatic PSS as well.

A video of the procedure can be viewed at http://www.amcny.org/node/341#Liver_Shunts. The embolization procedure is fairly short (average 90 minutes), and the patients are typically discharged from the hospital two days later.

Dr. Berent is the director of Interventional Endoscopy Services in the Department of Diagnostic Imaging at The Animal Medical Center in New York City. Dr. Weisse is the director of Interventional Radiology Services in the Department of Diagnostic Imaging at The Animal Medical Center in New York City.

1. Weisse C, Berent A, Todd K, et al. Endovascular management of 100 dogs with intrahepatic portosystemic shunts: short- and long-term outcome, in Proceedings. Am Coll Vet Surg, 2011.

2. Watson PJ, Herrtage ME. Medical management of congenital portosystemic shunts in 27 dogs—a retrospective study. J Small Anim Pract 1998;39(2):62-68.

3. Greenhalgh SN, Dunning MD, McKinley TJ, et al. Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. J Am Vet Med Assoc 2010;236(11):1215-1220.

4. Komtebedde J, Koblik PD, Breznock EM, et al. Long-term clinical outcome after partial ligation of single extrahepatic anomalies in 20 dogs. Vet Surg 1995;24(5):379-383.

5. Hunt GB, Kummeling A, Tisdall PLC, et al. Outcomes of cellophane banding for congenital portosystemic shunts in 106 dogs and 5 cats. Vet Surg 2004;33(1):25-31.

6. White RN, Burton CA, McEvoy FJ. Surgical treatment of intrahepatic portosystemic shunts in 45 dogs. Vet Rec 1998;142(14):358-365.

7. Bostwick DR, Twedt DC. Intrahepatic and extrahepatic portal venous anomalies in dogs: 52 cases (1982-1992). J Am Vet Med Assoc 1995;206(8):1181-1185.

8. Smith KR, Bauer M, Monnet E. Portosystemic communications: follow-up of 32 cases. J Small Anim Pract 1995;36(10):435-440.

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