Portosystemic shunts (PSSs) are anomalous vascular communications between the portal venous and systemic circulations that result in a clinical syndrome with various neurological, biochemical, and hematological consequences. Single, extrahepatic PSSs are amenable to relatively uncomplicated surgical attenuation with a reported success rate of 90-95%. Alternatively, single intrahepatic PSSs are consistently more challenging to treat surgically. Numerous techniques have been described for intrahepatic PSS attenuation, ranging from careful liver dissection around the shunting vessel to more technically demanding and complicated procedures involving temporary vascular hepatic inflow occlusion for intravascular repair. A review of some of the major veterinary reports on canine intrahepatic PSSs reveals mortality rates following surgical treatment as high as 60% and post-operative complications rates of 77%. Interestingly, the majority of mortalities occurred peri-operatively. The goal of treating intrahepatic PSSs with interventional radiology is to reduce the unacceptably high, peri-operative morbidity and mortality rates associated with traditional open surgical techniques and hopefully improve the outcome for these cases. Intrahepatic portosystemic shunt PTCE has been reported to have reduced peri-operative morbidity rates with similar long-term success as that reported for many open surgical procedures.
Percutaneous transvenous coil embolization of right divisional intrahepatic portosystemic shunt. (A) DSA of portal vein (PV), shunt (PSS), and caudal vena cava (CVC) through transjugular catheter. (B) Simultaneous DSA of CVC and PV through two separate transjugular catheters demonstrating location of shunt entrance into CVC. (C) Radiograph following caval stent deployment across shunt orifice. (D) DSA of PSS via catheter passed through stent interstices demonstrating appropriate stent position across shunt entrance. (E) DSA of PSS following placement of multiple thrombogenic coils (white arrows) within PSS. (F) Final radiograph of caval stent and coils prior to catheter removal.
Chemoembolization involves super-selective, intra-arterial chemotherapy delivery in conjunction with subsequent or simultaneous particle embolization. The rationale for chemoembolization for primary and metastatic tumors of the liver is based on anatomic studies that demonstrated that most hepatic tumors depend upon hepatic arterial blood supply (up to 95%) for growth in contrast to the normal liver parenchyma that receives the majority of its blood supply via the portal vein (only 20% from the hepatic artery). Hepatic artery embolization causes more ischemia to the liver tumor while the remaining normal hepatic parenchyma obtains sufficient oxygenation from the portal venous blood supply to remain viable. Furthermore, pharmacological studies indicate that intra-arterial delivery of chemotherapy results in a 10- to 50-fold increase in intra-tumoral drug concentrations when compared to systemic intravenous chemotherapy administration in certain locations.
Particle embolization may cause tumor necrosis but also has a synergistic effect with the intra-arterial delivery of chemotherapy because the ischemia it induces in tumor cells inhibits the excretion of chemotherapy resulting in a higher concentration of drug accumulation within the cell. This effect maximizes cell death while minimizing systemic toxicity. This procedure is most commonly used in the treatment of diffuse hepatocellular carcinoma or metastatic liver disease in humans.
In addition, when used within the liver, the chemotherapy is mixed with a carrier agent, Ethiodol (Savage Laboratories, Melville, NY). This iodized oily substance supplies radiographic contrast to the chemotherapy as well as acting as a tumor localizer and embolic agent. Hepatic tumors lack Kupfer cells which are important for metabolizing oily substances (lipid) in normal hepatic parenchyma. Therefore, the Ethiodol and accompanying chemotherapy are concentrated within the liver tumor rather than the surrounding healthy hepatic parenchyma. Chemoembolization is currently being evaluated in veterinary patients with non-resectable or metastatic liver tumors as well as other locations throughout the body of both dogs and cats.
Complete hepatic chemoembolization in animals with diffuse or metastatic liver disease. (A) DSA of hepatic artery (HA) in a dog before chemoembolization. Note hepatic artery branches to liver parenchyma and patent gastroduodenal artery (GDA). (B) Same patient post-chemoembolization DSA demonstrating patent GDA but lack of perfusion to the hepatic artery branches following the procedure. (C) Axial CT angiogram of a cat with a large hepatic neuroendocrine tumor (black arrows) and metastatic lesion in adjacent lobe (black arrowheads). (D) Non-contrast enhanced, axial CT scan post-chemoembolization of the majority of the liver demonstrating increased uptake of chemotherapy mixture within primary (large *) and metastatic (small *) tumor as compared to normal liver parenchyma, even when performed non-selectively.
Vascular Obstructions: Palliative Venous Stenting for Malignant Obstructions
Peri-vascular tumors can occasionally invade a vessel lumen resulting in vascular occlusion and peripheral edema (e.g. vena cava obstruction), ascites (e.g. portal hypertension due to hepatic vein obstruction), or both. Examples include vascular sarcomas and adrenal tumors. Self-expanding metallic stents can be placed under fluoroscopic guidance across malignant obstructions to relieve vascular occlusions and reduce venous congestion resulting in profound clinical improvement.
Palliative stenting for malignant venous obstruction leading to hepatic congestion, portal hypertension, severe ascites, and hind limb edema. (Pre-Stenting) Percutanous transjugular catheterization of left hepatic vein (HV) and caudal vena cava (CVC). Simultaneous DSA of HV and CVC demonstrate large filling defect (Tumor) at junction of left HV and CVC resulting in severe distension of HV and CVC caudal to the tumor. (Post-Stenting) Simultaneous DSA through both catheters immediately following self-expanding metallic stent (Stents) placement within the left HV and CVC demonstrating recanalization and decompression of both veins.
Extrahepatic biliary obstructions present a great dilemma as they induce life-threatening metabolic derangements, causing excessive illness, and potential death. Surgical treatment is often indicated, but the outcome with biliary re-routing surgery holds such a high risk, with the mortality rate ranging from 25-70% in dogs and over 75% in cats. If the metabolic derangements can be relieved by a fast and effective decompressive procedure than future surgical interventions for a more definitive fixation may be safer for the patient.
Endoscopic retrograde cholangiopancreatotgraphy (ERCP) and biliary stent placement
Endoscopic retrograde cholangiopancreatography (ERCP) is an IE technique used for the diagnosis, and potential treatment, of biliary tract disease, pancreatitis, or pancreatic obstructive lesions in humans. To date biliary stents have been successfully placed in a small handful of normal purpose-bred dogs, and clinical investigation is underway. Using an endoscope a stent is passed into the biliary tract, eliminating the need for excessive surgical manipulation. This can be left in place until the obstructive lesion resolves (ie pancreatitis), or a permanent metallic stent can be used in the case of neoplasia. This bypasses the need for re-routing biliary surgery for biliary obstruction.
Kugel found us or we found Kugel only a few years ago - not sure how the story starts. But, since we first got Kugel she was very sick. The fabulous Dr. Kim Alexander helped us determine it was gastric lymphoma.
Thanks to Dr. Chick Weisse, Katie will turn 3 this October. Katie was diagnosed with a liver shunt at 3 months old. Dr. Weisse put her on medications till she was old enough to have the surgery correct her problem.
Read the 2013 UPDATE! Two years ago Sandy, my 10 year old Beagle began drinking excess amounts of water. Concerned, but not thinking it was life threatening, I brought her to my local vet. The doctor ran some blood tests. Then he told me it could be a sign of cancer.