Discussion

Although the optimal management of arteriovenous malformations remains controversial, a multidisciplinary treatment strategy is currently recommended. Therapeutic options depend on the location, size, flow characteristics, and extent of the lesion and include clinical observation, sclerotherapy, embolisation, ablative and coagulative techniques, and surgical resection. ^{Reference Mattheis and Wanke3} While surgical excision may be curative for small, well-circumscribed arteriovenous malformations, complete resection is often not feasible in large or diffuse lesions. Moreover, incomplete excision is associated with high recurrence rates and may even stimulate aggressive lesion progression. Owing to these limitations and the potential morbidity of surgery, minimally invasive endovascular approaches have gained increasing acceptance. Various embolic materials, including sclerosants, absolute ethanol, liquid embolic agents, particulate embolic materials, and coils, have been used in the treatment of arteriovenous malformations. ^{Reference Griauzde, Wilseck and Chaudhary4–Reference Funaki, Mori and Onozawa8}

Although recurrence may occur following nonsurgical treatment, the risk of major complications is generally low. ^{Reference Mattheis and Wanke3} Treatment success and recurrence rates vary according to the embolic agent used and the vascular architecture of the lesion. Le Fourn et al. ^{Reference Le Fourn, Herbreteau and Papagiannaki9} performed 66 embolisation procedures for 32 arteriovenous malformations in 31 patients. Embolic agents included n-butyl cyanoacrylate, ethylene-vinyl alcohol copolymer, lauromacrogol, particulate embolic materials (collagen sponge and microspheres), and absolute ethanol. Cyanoacrylate glues were mixed with iodised oil in varying proportions to modify polymerisation and improve radiopacity. Among the eight patients with head and neck arteriovenous malformations, clinical improvement was achieved in five, one remained unchanged, and two experienced disease progression despite embolisation. Vascular coils have also been used as embolic devices in the endovascular management of arteriovenous malformations. These metallic devices produce mechanical vascular occlusion and are easily visualised under fluoroscopy. Coil embolisation may be particularly effective in arteriovenous malformations with a dominant feeding artery, a well-defined arteriovenous shunt, or a dominant draining vein. In cervical arteriovenous malformations, however, coils are most commonly used in combination with liquid embolic agents to reduce blood flow, prevent distal migration of liquid embolic materials, and improve control of venous outflow. ^{Reference Dawkins, Motiwala and Peterson7,Reference Funaki, Mori and Onozawa8} The angioarchitecture defined by the Yakes classification also influenced our treatment strategy. Type IIIb lesions are characterised by multiple arteriolar feeders converging into a dilated venous sac with multiple draining veins. Although liquid embolic agents are commonly recommended for Yakes type IIIb lesions, the presence of a limited number of dominant feeding arteries in our patient allowed complete exclusion of the shunt using detachable coils alone.

Funaki et al. ^{Reference Funaki, Mori and Onozawa8} reported a 10-year-old boy with a giant cervical arteriovenous malformation complicated by high-output cardiac failure who was successfully treated using detachable coils in combination with n-butyl cyanoacrylate, iodised oil, and ethanol, resulting in substantial clinical and echocardiographic improvement. In contrast, our patient had no evidence of high-output cardiac failure and was successfully treated using detachable coils alone. Gomes et al. ^{Reference Gomes10} described two adult patients with arteriovenous malformations who underwent coil embolisation in combination with other embolic agents. Following coil migration into the pulmonary circulation in one patient who underwent venous embolisation, the author recommended selecting coils slightly larger than the target vessel diameter to reduce the risk of migration.

In the present case, detachable coils alone were selected because angiography demonstrated a limited number of dominant feeding arteries that could be selectively catheterised and completely occluded. The cervical location of the lesion further supported avoidance of liquid embolic agents because of the potential risk of non-target embolisation and cranial nerve ischaemia. Furthermore, detachable coils allowed controlled deployment with repositioning before release and stable anchoring within the target vessels. Coil diameters were intentionally selected slightly larger than the target vessel diameter to minimise the risk of migration, consistent with previous recommendations. To our knowledge, reports describing successful treatment of paediatric cervical arteriovenous malformations using detachable coils as the sole embolic agent remain extremely limited.