Vascular Surgery for Arteriovenous Malformations Workup
- Author: Allison Leigh Speer, MD; Chief Editor: Vincent Lopez Rowe, MD more...
Clinical diagnosis is confirmed by means of ultrasonography with color Doppler examination. Magnetic resonance imaging (MRI) is best for evaluating the extent of the AVM.
Bony AVMs may demonstrate osteolysis.[5, 13]
Ultrasonography with color Doppler of an AVM usually demonstrates low-resistance high-velocity arterial flow, above the baseline, with high diastolic flux, and pulsatile venous flow below the baseline. Vessels are tortuous. AV shunting is seen. Pulsed Doppler measures the arterial output on the affected side compared with the normal side (eg, carotid, humeral, femoral arteries). This noninvasive technique is an excellent and reliable way to follow the course of an AVM or to monitor response to treatment.
Computed tomography (CT) does not easily distinguish between hemangiomas and vascular malformations. CT with iodinated contrast identifies AVMs as a highly enhancing lesion and can demonstrate soft tissue involvement, as well as dilated feeding and draining vessels .
CT angiography (CTA; see the image below) provides three-dimensional (3D) reconstruction of the AVM. Cone-beam CTA (also referred to as rotational angiography) appears to be promising in the treatment of AVMs, both for facilitating preoperative surgical planning and for providing an intraoperative reference.[16, 17]
Magnetic resonance imaging
MRI of an AVM demonstrates a collection of vascular flow voids (black tubular structures) corresponding to fast-flow vessels, in all sequences (spin-echo T1- and T2-weighted sequences). (See the image below.) No contrast parenchymal enhancement (no tumor aspect) exists. If signal abnormalities are present, they may exist in relation to a fibrofatty matrix.[18, 19] Magnetic resonance angiography (MRA) also provides a 3D reconstruction of the AVM and its anomalous vascular network.
Angiography (see the image below) is not solely diagnostic but can be therapeutic with embolization. Angiography demonstrates variably dilated or tortuous feeding arteries, arterial venous shunting (occasionally with visualization of discrete fistulae), and dilated draining veins. Feeding arteries may be aneurysmal in older patients.
Proximal embolization of feeding vessels is contraindicated and should never be performed. After a period of improvement, a vascular recruitment phenomenon occurs with rapid recruitment of flow from nearby arteries, which allows new collaterals to supply the nidus. This allows the lesions to recur and progress. In addition, proximal arterial embolization denies access for subsequent embolization.[5, 1, 8]
Angiography typically precedes interventional therapy or surgical resection. Patients with AVMs that are unresectable may undergo palliative superselective arterial or retrograde venous embolization for control of pain, hemorrhage, or congestive heart failure. Typically, palliative embolization provides only transient improvement. Resectable AVMs may be surgically removed 24-72 hours after arterial embolization for temporary nidus occlusion. Embolization can be with coils or glue.
Sclerotherapy is another radiologic option that uses angiography and involves the injection of ethanol into the nidus. The risk of soft tissue and neurologic damage is high; therefore, this technique should be performed only by an experienced endovascular specialist in carefully selected patients. Although preoperative embolization or sclerotherapy may minimize intraoperative bleeding, these techniques do not reduce the limits of resection.
Vascular malformations are composed of vascular channels lined by flat “mature” epithelium and are not hypercellular, in contrast to hemangiomas. The endothelium is not proliferative. AVMs have predominately arterial and venous anomalous channels.
No laboratory tests reliably diagnose arteriovenous malformations (AVMs). Serum levels of vascular endothelial growth factor (VEGF) are significantly higher in proliferating hemangiomas than in involuting hemangiomas and vascular malformations. In addition, urinary high-molecular-weight (hMW) matrix metalloproteinases (MMPs) are elevated in vascular tumors and some vascular malformations; however, they can not distinguish between the two types of vascular lesions.
If a patient has spontaneous bleeding, perform a complete blood count (CBC), coagulation studies such as prothrombin time (PT) and partial thromboplastin time (PTT), a disseminated intravascular coagulation (DIC) panel, and a type and screen (T+S). This will allow a rapid diagnosis of anemia, coagulopathy, or DIC, if present, and will allow resuscitation with the appropriate intravenous fluids or blood products.
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|Vascular Tumors||Vascular Malformations|
|Complex-combined vascular malformations
|C=capillary, V=venous, L=lymphatic, A=arterial, M=malformation, F=fistula|
|I - Quiescence||Pink-bluish stain, warmth, and arteriovenous shunting are revealed by Doppler scanning. The arteriovenous malformation mimics a capillary malformation or involuting hemangioma.|
|II - Expansion||The description is the same as stage I, plus enlargement, pulsations, thrill, and bruit and tortuous/tense veins.|
|III - Destruction||The description is the same as stage II, plus dystrophic skin changes, ulceration, bleeding, persistent pain, or tissue necrosis. Bony lytic lesions may occur.|
|IV - Decompensation||The description is the same as stage III, plus congestive cardiac failure with increased cardiac output and left ventricle hypertrophy.|
|Absolute Indications||Relative Indications|
|Table modified from Lee et al.|