Trans-Arterial Embolization for Hemorrhage or Vascular Malformations
Veterinary patients occasionally suffer from hypovolemic shock secondary to severe hemorrhage from a number of different causes including neoplasia, coagulopathy, GI ulceration, and trauma. In the majority of cases, standard medical and surgical procedures can be used to stabilize these often severely debilitated animals. Occasionally, standard therapies fail and alternatives are necessary.
For example, severe epistaxis can typically be managed conservatively. However, once intractable, few options remain. Carotid ligation can be performed and although this may temporize bleeding, once collateral blood supply develops bleeding may resume and no further treatment options exist. This is an especially important consideration when the underlying cause of epistaxis persists because the patient remains at risk for bleeding. An alternative to carotid ligation that permits repeated treatments if necessary is super-selective arterial embolization of the affected vascular bed. Trans-arterial embolization (TAE) entails selective, catheter-directed delivery of particulate material in order to induce thrombosis, control hemorrhage, occlude vascular malformations, or reduce tumor growth.
Under fluoroscopic guidance, a catheter placed into the femoral artery is used to super-selectively catheterize the maxillary artery. Polyvinyl alcohol particles are then injected through the catheter to “embolize” the nasal blood supply. This causes a mechanical obstruction to blood flow, induces thrombosis and decreases the pressure head on the capillary bed that drives hemorrhage.1 This technique has been successfully performed in veterinary patients with intractable epistaxis secondary to severe rhinitis, neoplasia, inherited thrombocytopathia, and vasculitis. In addition, because the carotid artery remains patent, the procedure can be repeated in the future if necessary. Similar trans-arterial embolization (TAE) techniques are used in humans to treat severe, life-threatening hemorrhage secondary to trauma, infection, neoplasia, and other causes throughout the body.
Symptomatic vascular communications between an artery and vein are uncommon in veterinary medicine but can be acquired through trauma or neoplasia (arteriovenous fistulas or AVFs), or can occur congenitally such as those reported within the liver (arteriovenous malformations or AVMs, or multiple AVFs). These vascular anomalies can result in varying degrees of clinical signs depending upon their high- or low-flow nature and anatomical location. Those seen peripherally typically result in palpable, pulsatile vascular dilations that can cause severe hemorrhage if traumatized. Within the liver, congenital hepatic AVMs (HAVMs) result in severe portal hypertension, multiple acquired portosystemic shunts, and often profound ascites. Surgical resection of these anomalies can be very complicated due to their profoundly vascular nature and if incompletely resected can recur. Peri-operative mortality rates associated with HAVM resection have been reported to be approximately 30%.2 Interventional techniques permit percutaneous arterial embolization of these vascular anomalies with cyanoacrylate glue that can result in complete occlusion obviating the need for invasive and potentially life-threatening surgery (FIGURE 1)
Figure 1. Digital subtraction arteriograms of hepatic arterio-venous malformation (HAVM) pre- and post-glue embolization. (A) 4 Fr angled catheter (white arrows) in distended common hepatic artery (CHA) demonstrating small, patent gastroduodenal artery (GDA) and large vascular plexus of the HAVM (*). (B) Post-glue embolization DSA demonstrating reflux into celiac artery with improved filling of left gastric (LGA) and splenic arteries (SA) with now identifiable additional arterial feeder (black arrows) to the AVM. (C) DSA of feeding vessel through microcatheter demonstrating patent HAVM (*). (D) Final celiac DSA demonstrating embolized HAVM (*).