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blunt splenic injuries: effects on the intrasplenic blood pressure. Eur
Radiol. 2004;14(9):1718–1719.
94. Bessoud B, Duchosal MA, Siegrist CA, et al. Proximal splenic artery
embolization for blunt splenic injury: clinical, immunologic, and
ultrasound-Doppler follow-up. J Trauma. 2007; 62(6):1481–1486.
95. Madoff DC, Denys A, Wallace MJ, et al. Splenic arterial interventions:
anatomy, indications, technical considerations, and potential
complications. Radiographics. 2005;25(suppl 1):S191–S211.
96. Kessaris DN, Bellman GC, Pardalidis NP, et al. Management of
hemorrhage after percutaneous renal surgery. J Urol. 1995; 153(3, pt
1):604–608.
97. Phadke RV, Sawlani V, Rastogi H, et al. Iatrogenic renal vascular
injuries and their radiological management. Clin Radiol.
1997;52(2):119–123.
98. Breyer BN, McAninch JW, Elliott SP, et al. Minimally invasive
endovascular techniques to treat acute renal hemorrhage. J Urol.
2008;179(6):2248–2252; discussion 2253.
99. Mays ET, Wheeler CS. Demonstration of collateral arterial flow after
interruption of hepatic arteries in man. N Engl J Med. 1974;
290(18):993–996.
artery embolization in patients with delayed postoperative hemorrhage
following hepatobiliary pancreatic surgery. Acta Radiol.
2011;52(4):393–400.
aneurysms and false aneurysms with endovascular treatment in 12
patients. Cardiovasc Intervent Radiol. 2003; 26(3):256–260.
artery embolization: a review of an 11-year experience. Am J Surg. 2013;
205(3):250–254; discussion 254.
splenic embolization after blunt splenic trauma. Am J Surg.
2005;189(3):335–339.
multicenter review. J Trauma. 2004;56(3):542–547.
compression repair of pseudoaneurysms: further experience from a
single institution. AJR Am J Roentgenol. 1999; 173(6):1567–1573.
of femoral artery pseudoaneurysm: management with intraarterial
thrombolysis. J Vasc Interv Radiol. 2001; 12(5):633–636.
aneurysms using percutaneous injection of fibrin adhesive. Br J Radiol.
1998;71(852):1255–1259.
percutaneous treatment of iatrogenic pseudoaneurysms. Cardiovasc
Intervent Radiol. 2002;25(2):115–118.
percutaneous transhepatic embolization of a bleeding hepatic artery
branch aneurysm. Acta Radiol. 2006; 47(5):461–464.
P
Section E Peripheral Embolization
27
Peripheral Vascular Malformations
Jose Luiz Orlando • Francisco Ramos • Bruno C. Odisio
eripheral vascular malformations arise as a result of a focal vascular
differentiation embryologic failure leading to an abnormal
development of the vascular system. They are responsible for
important functional and aesthetic changes that often impact on the
individual’s daily routine. Diagnosis and treatment of this condition is still
considered challenging in view of the various presentations and complexity
levels of lesions.
CLASSIFICATION AND DESCRIPTION
Mulliken and Glowacki
1,2
described in 1982 a useful classification system,
which gained acceptance by the scientific community based on the histologic
findings, the flow characteristics, and the clinical aspects of the vascular
anomalies. According to this classification, vascular anomalies fall into two
major categories: hemangiomas and vascular malformations.
1,2
Hemangiomas are not included in the scope of the this chapter and therefore
will not be discussed.
Vascular malformations arise from dysplastic vascular channels. These
channels, generally presented at birth, will grow in proportion to the
development of the individual and will never suffer involution.
1,3
Although
congenital, in approximately 10% of patients, the lesions cannot be identified
at birth, appearing later triggered by hormonal stimuli during adolescence and
gestation or exacerbating their symptoms after infection, thrombosis, or local
trauma.4 The vascular malformations were initially classified according to the
prevalence of the vascular channels in five different forms: venous,
lymphatic, capillary, arterial, or combined. In 1993, Jackson et al.,5 based on
the classification system by Mulliken and Glowacki,
1,2
reclassified vascular
malformations considering its hemodynamic characteristics, dividing them
into low- and high-flow lesions. The low-flow lesions are classified as
venous malformation, lymphatic capillaries, or venolymphatic forms
(capillary venous and the lymphatic–venous capillary lesions); the high-flow
lesions are divided in arteriovenous malformations (AVMs) and
arteriovenous fistulas.6 In 1996, this classification system was adopted and
expanded by the International Society for the Study of Vascular Anomalies
and is currently widely used.
7
PATHOPHYSIOLOGY
The most accepted theory for the origin of vascular malformations is that they
are caused by a total or partial agenesis of the capillary bed of a given
territory. This agenesis would be associated with primitive persistent
arteriovenous communications that constitute the AVM nidus.8 The AVMs
are basically characterized by presenting abnormal communications between
the arterial and venous system, without the interposition of the capillary
network. These shunts are, in most cases, multiple and configured as a
conglomerate of vessels known as vascular nidus.9 The advent of digital
subtraction selective angiography along with the development of
microcatheterization techniques allowed the angioarchitecture of these
lesions to be identified with greater precision. The angioarchitecture is
divided into three distinct segments: nourishing artery(ies), a nidus, and the
draining vein(s).
10
The nourishing arteries can be classified as direct or indirect branches
and can present as single or multiple branches. The direct branches directly
supply the region of the vascular nidus and, in general, have a large diameter.
The indirect branches supply the nidus and the surrounding tissues and may
have blood flow opposite to its natural direction through anastomoses with
neighboring arteries, where other arterial segments participate in the nutrition
of the tissue. In this case, the preexisting arterioarterial anastomosis increases
their caliber and promotes the passage of blood flow in a reversed direction.
This compensatory phenomenon, characterized by the recruitment of
collateral vessels to reconstruct the arterial supply distal to the AVM, is
usually present in high-flow AVMs.
11
The vascular nidus represents the core of the AVM and is interposed
between the distal segment of the feeding artery(ies) and the proximal
segment of the draining vein(s).12 These arteriovenous communications are
called shunts and are responsible for the secondary angiopathy induced by the
increased blood flow. The nidus is a complex vascular structure and can be
presented in three distinct patterns (Fig. 27.1):
• Plexiform: composed of a tangle of arteriolar and venular structures with a
coiled and wrapped aspect. In this pattern, the supplying arteries ends in a
cluster of multiple vessels with arteriovenous communications in which
one or multiple channels emerge as the venous drainage.
• Fistulas: characterized by the presence of communication between artery
and vein called arteriovenous fistulas. In this case, one or multiple arteries
of anomalous path starting from a truncal artery empties into the venous
system directly or in a venous lake located, for example, in the
compartment muscle or subcutaneous tissue.
• Mixed pattern: a combination of both patterns mentioned earlier, with a
predominance of one over the other. The nidus may also be constituted by
one or more compartments.
The AVM draining veins corresponds mostly to the topography of the
lesion and can be classified as deep or shallow. Drainage can occur from
multiple compartments to a single main draining vein or smaller caliber
accessory veins. Additionally, a single drainage vein from the AVM may
branch into other veins, which can be confused with multiple draining veins
(Fig. 27.2).
CLINICAL EVALUATION
Vascular malformations can occur anywhere in the body and can have either
a localized or extensive distribution pattern. Commonly, its diagnosis is the
result of a clinical history and detailed physical examination. The clinical
presentation of peripheral AVMs is diverse and can range from asymptomatic
to disabling pain cases. The presence of pain may be related to the presence
of mass effect, varicose veins, thrombophlebitis, bone erosion, and mixedorigin ulcers caused by venous hypertension due to ischemia caused by
preferential blood flow to the vascular malformation in detriment of the
normal tissues.
1,13
The lesions on the extremities are characterized by the presence of
pulsatile tumor of firm consistency and slightly compressible, with thrill or
murmur that result from turbulent blood flow.14 Other characteristic findings
of these injuries are a wide arterial pulse and the presence of a prominent
proximal venous drainage, generally elongated and tortuous. Additionally,
changes may occur secondary to the ischemia and the venous hypertension
such as edema, skin pigmentation, stasis eczema, ulcers, and gangrene
13,15
(Fig. 27.3). The hypertrophy of the involved extremity is a frequent finding
and may be evident only in late childhood.
16,17
Pelvic AVMs are
characterized by an increased soft tissue mass and can cause severe pain,
pelvic congestion, sexual dysfunction, and hemorrhage.
18–20
In the presence
of a large number of high-flow fistulae, congestive heart failure can occur in
varying degrees as a result of cardiac overload.
21
IMAGING EVALUATION
The use of different imaging modalities is an essential tool for differentiating
between the different types of vascular malformations and between these and
soft tissue tumors, assessing the exact extension of the lesions, and
correlating the findings with other anatomical structures involved. The most
common imaging modalities used in the diagnosis of vascular abnormalities
are the ultrasonography (US), magnetic resonance imaging (MRI), computed
tomography (CT), and angiography.
US is considered the imaging modality of choice for the initial
evaluation of patients with soft tissue lesions of possible vascular origin.
22,23
The US Doppler allows characterizing the morphologic and hemodynamic
aspects of the vascular malformations. The color mapping allows
distinguishing the afferent arteries constituted of elongated and tortuous
vessels, the nidus that is characterized by a conglomerate of vessels in the
core of the lesion, and the draining veins. The hemodynamic changes in high-
flow vascular malformations are characterized by the presence of a biphasic
pattern with high systolic and diastolic velocities, indicating low resistance
due to the presence of shunts. The nidus is recognized by the presence of
high-velocity turbulent flow with a mosaic of colors. The venous segment of
the malformation presents with a high-flow monophasic pattern that might be
associated with some pulsatile pattern (Fig. 27.4
). The MRI allows for
assessment of the extent of the injury and its relationship to adjacent
anatomical structures. It is also useful in differentiating between lesions of
high and low flow.
3
,24
AVMs are characterized as areas of absence of signal
(flow-void) on T1 and T2 weighted sequences corresponding to the nurturing
arteries and the nidus
15,25
(Fig. 27.5). MRI can also help in the differential
diagnosis of tumors. Noteworthy are the proliferative hemangiomas that,
despite showing hyperintense signal on T2 sequences and intermediate signal
on T1 and areas of flow voids, has a well-defined and lobulated
contours.
3,23,26
Other tumors such as sarcomas, neuroblastomas,
hemangiopericytomas, fibrosarcomas, and rhabdomyosarcomas exhibit
features of tissue invasion that can be associated with perilesional
edema.
23,27–29
CT provides limited information regarding the extent of the
lesion, generally underestimating its size and its flow characteristics when
compared to MRI. The use of ionizing radiation is also another disadvantage
associated with this method. CT can be useful in the differential diagnosis
with soft tissue tumors to evaluate its mass effect and provide more detailed
evaluation of changes in the adjacent structures such as bone erosions,
periosteal reaction, pathologic fractures, and presence of phleboliths. The
phlebolith lesions are characteristic of venous malformations.30 The use of
angiography involves the selective catheterization of all pedicles involved for
a complete study of the extension of the lesion and its flow characteristics.
The angiographic findings of AVMs include feeding artery(ies) with
increased caliber and tortuous path, a conglomerate of arteries and veins
(nidus), and an early venous filling segment characterized by elongated and
large-caliber veins
12,31
(Fig. 27.6). An alternative access by direct puncture of
the nidus transcutaneously allows for evaluation of extension and flow
characteristics
31,32
(Fig. 27.7).