These lesions are broadly classified as capillary, venous, or lymphatic malformations .

The sclerosant is usually reconstituted with a contrast agent, either water soluble, lipophilic (such as ethiodol), or negative contrast (air or carbon dioxide) to allow fluoroscopic and ultrasound monitoring of the injection [12] (Fig. 5.2b, e, f). Vigilantly watching for any extravasations during injection is mandatory, to prevent tissue or nerve damage. Applying direct pressure over venous drainage pathways during injection, using a tourniquet, or using double needle technique, which provides a low-pressure exit valve, can stop drainage to critical outflow veins. Escape of sclerosant into the venous drainage could potentially result in ophthalmic, cavernous, or intracranial venous thrombosis in head and neck lesions .

We most commonly use 3 % sodium tetradecyl sulfate (STS), a detergent, as the sclerosant Foaming the solution prior to injection has been reported to increase efficacy, perhaps by maximizing the surface area contact between the agent and the lesional endothelium. Ethanol, the most potent sclerosant, and one we make regular but judicious use of as well, unfortunately, has the highest rate of reported serious complications such as skin necrosis, nerve damage, central nervous system depression, acute pulmonary hypertension, thromboembolism, disseminated intravascular coagulation (DIC), hyperthermia, cardiac arrhythmias, and cardiovascular collapse and death [13]. However, STS and related detergents can cause serious adverse effects as well. Platinum coils or liquid embolics may serve as adjuncts to sclerotherapy in larger lesions, primarily to close prominent or recurrent venous channels. These agents are particularly effective in achieving preoperative short-term occlusion [12]. Bleomycin, an antibiotic with cytotoxic properties, can be of particular use in patients with intra-orbital and airway lesions, because of significantly less posttreatment edema than is seen with other agents [14]. Presclerotherapy steroids are imperative in orbital and airway malformations, for reducing postprocedural edema, which could result in increased intraocular pressure or airway compression. Sclerosants cause immediate local hemolysis and subsequent hemoglobinuria, though lesions in the head and neck are rarely large enough for the hemolysis to cause systemic problems. Generous hydration (doubling of the maintenance intravenous fluid for 4 h post procedure), monitoring of urinary output, and urinary alkalization with sodium bicarbonate intravenous fluid is recommended [12] .

Localized VMs have the best responses to sclerotherapy. Diffuse malformations are less likely to have a complete response, and the treatment should, therefore, be targeted at the most symptomatic portions. For all but the smallest lesions, sclerotherapy is often repeated. Among the LMs, the macroystic variety typically responds well to sclerotherapy, whereas microcystic lesions are technically difficult to treat and show a poor response (Fig. 5.2c). Sclerosants reported for use in treating macrocystic LMs include ethanol, doxycycline, bleomycin, Ethibloc, and OK-432. Our first-line agent is most commonly doxycycline at a concentration of 10 mg/ml. For large cysts, a pigtail catheter aspiration of the contents and volume measurement is made, followed by injection and drainage of the cyst with the sclerosant. The sclerosant is allowed to dwell in the cyst for 2–3 h and then drained out. The procedure is repeated sequentially on days 2 and 3, through the indwelling catheters. It is important to disrupt the internal septations to increase the contact of the sclerosants within different compartments. Cyst involution can be assessed approximately 6 weeks after the procedure. For microcystic LM, sclerotherapy using bleomycin or OK-432 is often used. Other techniques using in-column electrocoagulation, carbon dioxide laser excision and radiofrequency ablation (RFA) have also been described [14–16]. The overall complication rate for sclerotherapy to treat VMs is 12 % [13]. Peripheral neuropathy is seen in approximately 1 %, but can be avoided if care is taken not to cause extravasation during injection; when it occurs, neuropathy is usually transient. Skin blistering and, in rare occurences, skin necrosis with permanent scarring can occur, particularly when the lesion has a more superficial component. For lesions involving the tongue, buccal surfaces, soft palate, or airway, marked postprocedural edema can cause transient dysphagia and breathing difficulties. Many such patients have a tracheostomy placed before commencing the procedure. Other lesser adverse effects include muscle atrophy and contracture if the sclerosant infiltrates the tissues [12] .

JNA is a benign vascular tumor composed of a rich vascular network within a fibrous stroma [17]. It most commonly arises in the posterolateral nasopharynx of prepubertal and adolescent males (Fig. 5.3a). JNA can behave aggressively and tend to bleed frequently. They can expand commonly beyond the nasopharynx into the cranium, nose, and paranasal sinuses [17, 18]. Profuse intraoperative bleeding leading to incomplete resection and tumor recurrence can occur, and preoperatively transarterial tumor embolization can greatly facilitate resection. JNAs are primarily fed from distal internal maxillary artery branches (Fig. 5.3b), and may recruit arterial supply from any nearby ipsilateral or contralateral vessel, requiring bilateral internal and external carotid arteriography for elucidation. Anastomosis between branches of the external and internal carotid artery and vascular spasm has to be considered when planning superselective embolization. Silastic spheres, Gelfoam, dura mater, and polyvinyl alcohol (PVA) particles (Fig. 5.3c) have been used to embolize the tumor bed and the feeding vessels [19], with PVA particles often preferred, as they are efficient and cost effective. Nontarget embolization of particles to the ophthalmic artery, the internal carotid, or vertebral arteries via anastomosis or reflux of particles injected in the external carotid artery may cause retinal or brain ischemic deficits, and thus preembolization and intraprocedural angiography must be scrupulously studied .

Paragangliomas, also called glomus tumors, are highly vascularized tumors of neural crest origin that are derived from chemoreceptor organs in the walls of blood vessels or specific nerves in the head and neck area. They can develop in the middle ear (glomus tympanicum), the jugular foramen of the skull base (glomus jugulare), or other head and neck areas (glomus caroticum, glomus vagale). They are usually benign but locally destructive [20–23]. Preoperative embolization for devascularization greatly reduces the perioperative blood loss by a factor of 2–3, with reduction of need of transfusion in the postoperative period to less than 50 % [24]. However, extreme caution is warranted during embolization of these lesions. In particular, during embolization of carotid body tumors, particles can escape into the internal carotid artery and result in stroke, especially if particles < 150 μm in size are used. As in the case of JNA, vigilant angiographic search for anastomosis between the intra- and extracranial circulation is imperative. Collaterals between the vertebral artery and the C1, C2, and C3 musculoskeletal branches are common. Lower cranial nerves, such as the facial nerve or hypoglossal nerve can undergo ischemia if the vaso nervorum is inadvertently embolized. When embolizing glomus tumors, preprocedural administration of an alfa-blocking agent is often necessary to reduce catecholaminergic activity. Not infrequently, complete arterial devascularization of the tumor bed is not achieved, and several groups have recently described direct puncture and the slow injection of acrylic glue to allow for permeation of the vascular tumor bed while avoiding its passage to the venous side or its reflux into normal arterial territory [25] .