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Year : 2008  |  Volume : 41  |  Issue : 2  |  Page : 183-189

Management strategy for facial arteriovenous malformations

Department of Plastic Surgery, Armed Forces Medical College and Command Hospital (SC) Pune-40, India

Correspondence Address:
P S Bhandari
Senior Advisor Reconstructive Surgery, Command Hospital (SC), Pune- 411 040
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-0358.44943

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 » Abstract 

Arteriovenous malformations (AVMs) are uncommon errors of vascular morphogenesis; haemodynamically, they are high-flow lesions. Approximately 50% of AVMs are located in the craniofacial region. Subtotal excision or proximal ligation of the feeding vessel frequently results in rapid progression of the AVMs. Hence, the correct treatment consists of highly selective embolisation (super-selective) followed by complete resection 24-48 hours later. We treated 20 patients with facial arteriovenous malformation by using this method. Most of the lesions (80%) were located within the cheek and lip. There were no procedure related complications and cosmetic results were excellent.

Keywords: Arteriovenous malformation, super-selective embolisation, resection

How to cite this article:
Bhandari P S, Sadhotra L P, Bhargava P, Bath A S, Mukherjee M K, Maurya S. Management strategy for facial arteriovenous malformations. Indian J Plast Surg 2008;41:183-9

How to cite this URL:
Bhandari P S, Sadhotra L P, Bhargava P, Bath A S, Mukherjee M K, Maurya S. Management strategy for facial arteriovenous malformations. Indian J Plast Surg [serial online] 2008 [cited 2019 Jul 21];41:183-9. Available from:

 » Introduction Top

Arteriovenous malformations (AVMs) are the result of errors of vascular development between the 4 th and 6 th weeks of gestation. [1] Failure to prune unwanted primitive communications between the arterial and venous systems may result in a malformation. Most of these lesions are obvious at birth while some are obvious during adolescence or adulthood. It is believed that enlargement is the result of changes in pressure and flow, ectasia, shunting and collateral proliferation, rather than cellular proliferation. AVMs have a tendency to grow with the child and after the individual has attained full growth, AVMs remain stable throughout life. Some enlargement may occur in response to trauma or hormonal disturbances during puberty or pregnancy. [2]

Treatment of AVMs can be difficult, as frequently, following an apparently successful extirpation, there is regrowth of the tumour to a size larger than its original size, often with supply by surgically inaccessible vessels. [3] Furthermore, the high flow rates and hyper vascularity of these lesions can lead to life-threatening complications, such as haemorrhage and/or cardiovascular instability. With the advent of super-selective angiography and new embolic agents, embolisation has become an integral part of treatment. The pre-operative embolisation diminishes blood loss and facilitates complete surgical extirpation. We report here our experience with super-selective embolisation, followed by surgical resection in 20 cases of facial AVMs .

 » Material and Methods Top

Twenty consecutive patients with AVMs in the facial region were treated at the Army Hospital (R and R), Delhi Cantonment, in the period between December 2001 and October 2005. There were eight males and 12 females (male: female ratio of 1:1.5). Patients' age at presentation ranged from four to 56 years. Eighteen patients (90%) had a vascular malformation at birth or during infancy. In 16 (80%) patients, the majority of malformations occurred in the middle area of the face (cheek, nose, and upper lip). Two malformations (10%) occurred on the upper face (forehead) and two others (10%) on the lower face (lower lip) [Table 1]. The interval between the onset and presentation varied from a few days to 17 years, men tending to present later than women. Sixteen patients presented in clinical stage II and the remaining four in stage III of Schobinger's classification [Table 2]. The most common presenting features were facial disfigurement from the swelling, skin discoloration, and nasal bleeding. The case listed as serial No. 1 [Table 1], [Figure 1A] presented with proptosis and severe epistaxis and required blood transfusion. All patients were evaluated preoperatively and detailed history was taken with regards to the onset and progression of the AVMs. The size and the site of the lesion was documented and associated symptoms and findings in the form of pain, ulceration, or bleeding were also noted. All AVMs were confirmed by colour Doppler and Magnetic Resonance Imaging (MRI) angiography [Figure 1B],[Figure 2B]. Computed tomography was done to exclude skeletal involvement in one patient who had a large orbital malformation. All AVMs were submitted to embolisation by the interventional radiologists. The embolic agents used were polyvinyl alcohol in 14 cases, absorbable gelatine sponge particles in four cases, and n-butyl cyanoacrylate (NBCA) in two cases. A super-selective embolisation was performed with the introduction of micro catheters into the distal feeding arteries as close to the nidus as possible. In the majority of cases, 90-100% devascularisation could be achieved and the lesions were resected 24-48 hours after the embolisation, except in one female patient (Case No: 19; [Table 1]) who had an AVM in her lower lip and was treated with NBCA and excision done 1 week later. In this patient due to extreme tortuosity of the feeder it became impossible for the interventional radiologist to negotiate a micro catheter. Since the lesion was superficial it could be embolised with direct percutaneous injection of NBCA under fluoroscopic control. Surgical resection was facilitated by the subcutaneous infiltration of adrenaline in normal saline (1: 2, 00,000). During resection, branches of the facial nerve were preserved [Figure 1D]. Four patients required resection of a portion of the involved skin along with resection of the malformation. Tissue deficits were covered with a split skin graft (on the forehead) and the rotation of a skin flap (on the cheek).

 » Results Top

Twenty consecutive patients with high-flow AVMs on the facial region were treated by super-selective embolisation, followed by surgical resection 24-48 h later except in one case where surgery was deferred by 7 days. Postembolisation arteriograms showed that 14 lesions were completely devascularised and five were effectively devascularised (> 90%). In one malformation (Case No: 3; [Table 1]), although only 70% devascularisation was achieved, the lesion was successfully resected with no significant blood loss. There were no embolisation-related complications with polyvinyl alcohol or gel foam particles. Two lip lesions treated with NBCA developed severe local reaction with edema and necrosis of tissues that healed well after debridement [Figure 2E] and [Figure 2F]. In 18 out of 20 lesions, a complete resection was possible. In the patient with a combined orbital and facial malformation, a small portion of the lesion extended deep to the neck of mandible. After maximum possible surgical excision of this lesion, Sclerosant (Polidocanol) was injected into the inaccessible portion of the malformation.

Transient neuropraxia of the VII th nerve occurred in one patient (Case No. 3) but improved in a week's time. Postoperative results were pleasing with improvement in both cosmesis and function. No recurrences were observed in the follow-up period which ranged from five months to three and half years (average period 15.2 months).

 » Discussion Top

AVMs are the result of a failure of regression of the arteriovenous channels in the primitive retiform plexus. [1] They are composed of a central nidus with anomalous congenital shunts between the arterial and venous systems. These abnormal vascular channels may not canalize or conduct blood flow for many years. An enlargement is the result of dilatation of the adjacent arteries and veins (collateralisation and recruitment) [4] rather than endothelial proliferation. Clinically, AVMs present with pain, hyperaemia, thrill, trophic changes, ulceration, and bleeding. Puberty and pregnancy affect the onset and progression of these lesions.

AVMs can be diagnosed with Pulsed Doppler which documents the arterial output and can be used to follow the progression of an AVM. With MRI best demonstrating the extent of malformation, angiography is unnecessary until intervention is contemplated.

AVMs present a therapeutic challenge because of their haemodynamic characteristics and their modality of growth. Surgical resection is often associated with extensive blood loss and an incomplete resection frequently leads to re-growth of the tumour to sizes that are often larger than its original size. [3] Proximal ligation of the parent vessel should be avoided as it is ineffective and may aggravate the problem making future endovascular therapy difficult or impossible.

In an effort to circumvent these problems, preoperative embolisation of the feeding arteries has been shown to reduce the hypervascularity and therefore, to aid surgical resection of these lesions. Recent developments in the design of micro catheters and distal navigation techniques have facilitated the catheterization of feeding arteries close to the nidus. The first therapeutic vascular embolisation using muscular tissue was described in 1930 by Brooks. [5] In 1972, Longacre et al. [6] reported good results with intravascular embolisation of a facial haemangioma using silicone balls impregnated with barium or tantalum. At present, the embolic materials generally employed are absorbable gelatine foam, polyvinyl alcohol (PVA), absolute alcohol, and NBCA. Gel foam is a temporary vessel occluder and will be resorbed in 1-2 weeks. [3] Polyvinyl alcohol is a permanent material and one of the most commonly used embolising agents. NBCA and alcohol are liquid embolising agents. NBCA has been used in the direct puncture technique in scalp arteriovenous malformations. Direct puncture with NBCA is an effective and safe technique for preoperative devascularisation of craniofacial AVMs. [7],[8],[9] Direct puncture embolisation of the venous pouch of an AVM has the advantages of reducing the risk of ischemia (i.e, skin necrosis and compromise of the central retinal artery) and being technically simple when compared to transarterial embolisation. [9] This embolising agent i.e. NBCA should be used with extreme care as being a liquid, it may progress more distally within the vasa nervosa leading to cranial nerve deficits. [10],[11]

Complications from embolisation are infrequently seen; however, necrosis of adjacent tissues may occur. Hence, patients must be adequately treated with broad-spectrum antibiotics. The most serious complication is the backflow of the embolus into the internal carotid or vertebral arteries as a result of circulatory sluggishness. A distal placement of the micro catheter close to the nidus will avoid this complication.

Highly selective embolisation as a single treatment modality is rarely successful with high-flow lesions because of the later development of new vascular pathways. [12],[13] However, it leads to a significant reduction in the blood flow within the vascular tumour which decreases operative blood loss and permits complete resection of the tumour. [14],[15] Experience has shown that the 24 to 48 h period following embolisation is the ideal time for surgical intervention. The aim is complete resection, unlike staged resection that is applicable to slow-flow vascular malformations to minimize the chances of recurrence. The pattern of bleeding from the wound edges is the best way to determine whether or not the resection is adequate. A more than normal bleeding indicates presence of residual malformed tissue. Combined embolisation and resection is most successful for well-localized stage I or stage II AVMs. [16]

To conclude, super-selective embolisation followed by a complete surgical resection is the correct treatment for arteriovenous malformations on the facial region. Surgical resection of the vascular tumour should be performed with a skin-sparing incision to avoid disfigurement. Excision should be followed by primary closure whenever possible. Superficial tissue losses can be covered with a split thickness skin graft. Local tissue flaps (skin rotation flap for cheek) and Estlander's flap for the upper lip will give better cosmetic results. There may be a need for free tissue transfer in the reconstruction of more complex defects. After this combined modality of embolisation, followed by resection, the patient must be followed up for years by clinical examination, ultrasonography, and/or MRI.[Figure 1C],[Figure 1E],[Figure 2A],[Figure 2C],[Figure 2D]

 » References Top

1.Kohout MP, Hansen M, Prebaz JJ, Mulliken JB. Arterio venous malformation of the head and neck: natural history and management. Plast Reconstr Surg 1998;102:643-54.  Back to cited text no. 1    
2.Jackson IT, Carreno R, Potparic Z, Hussain K. Haemangiomas, vascular malformations and lympho-venous malformations: Classification and methods of treatment. Plast Reconstr Surg 1993;91:1216-30.  Back to cited text no. 2    
3.Leikensohn JR, Epstein LI, Vasconez LO. Super-selective embolization and surgery of non-involuting haemangiomas and A-V malformations. Plast Reconstr Surg 1981;68:143-52.   Back to cited text no. 3  [PUBMED]  
4.Holman E. The physiology of an arterio-venous fistula. Am J Surg 1955;89:1101.   Back to cited text no. 4  [PUBMED]  
5.Brooks B. The treatment of traumatic arterio-venous fistula. South Med J 1930;23:106.   Back to cited text no. 5    
6.Longacre JJ. Benton C, Unterthiner RA. Treatment of facial haemangioma by intravascular embolization with silicone spheres. Plast Reconstr Surg 1972;50:618-21.  Back to cited text no. 6    
7.Barnwell SL, Halbach VV, Dowd CF, Higashida RT, Hieshima GB. Endovascular treatment of scalp arteriovenous fistulas associated with a large varix. Radiology 1989;173:533-9.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Mathis JM, DeNardo AJ, Jensen ME, Lin KY, Dion JE. Arteriovenous fistula of the scalp after hair transplantation treated by endovascular embolization. Ann Plast Surg 1994;33:633-7.  Back to cited text no. 8  [PUBMED]  
9.Han MH, Seong SO, Kim HD, Chang KH, Yeon KM, Han MC. Craniofacial arteriovenous malformation: Preoperative embolization with direct puncture and injection of n-butyl cyanoacrylate. Radiology 1999;211:661-6.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.10 Kesavadas C, Joseph S, Gupta AK, Nair R, Rao VRK, Mandalam R, et al. Craniofacial vascular malformation: Preoperative embolization. Indian J Plast Surg 2000;33:58-64.  Back to cited text no. 10    
11.Han MH, Seong SO, Kim HD, Chang KH, Yeon KM, Han MC. Craniofacial arteriovenous malformation: Preoperative embolization with direct puncture and injection of n-butyl cyanoacrylate. Radiology 1999;211:661-6.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Seccia A, Salgarello M, Farallo E, Falappa PG. Combined radiological and surgical treatment of arteriovenous malformations of the head and neck. Ann Plast Surg 1999;43:359-66.  Back to cited text no. 12  [PUBMED]  
13.Lane F, Donnaldy, Denise M. Vascular malformations and hemangiomas: A practical approach via multidisciplinary clinic. Centennial dissertation. Am J Roentgenol 2000;174:577-608.  Back to cited text no. 13    
14.Enjolras O, Mulliken JB. The current management of vascular birthmarks. Pediatr Dermatol 1993;10:311-3.  Back to cited text no. 14  [PUBMED]  
15.Herbreteau D, Enjolras O, Gelbert F. The current management of cervico-cephalic venous malformations. Pediatr Surg Int 1996;11:304-7.  Back to cited text no. 15    
16.Marler JJ, Mulliken JB. Current management of haemangioma and vascular malformations. Clin Plast Surg 2005;32:99-116.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]


  [Figure 1A], [Figure 1B], [Figure 1C], [Figure 1D], [Figure 1E], [Figure 2A], [Figure 2B], [Figure 2C], [Figure 2D], [Figure 2E], [Figure 2F]

  [Table 1], [Table 2]

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