Vol.2, No.8, 906-912 (2010)
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Percutaneous coil embolisation of congenital hepatic
arteriovenous malformations in two patients with
congenital heart disease and review of the literature
Al-Ata Jameel¹,², Arfi Muhammed Amin¹*, Hussain Arif¹, Kouatli A. Amjad¹
¹King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia; *Corresponding Author: ped_cardiologist@doctor.com
²King Abdul Aziz University Hospital, Jeddah, Saudi Arabia
Received 30 March 2010; revised 26 April 2010; accepted 27 April 2010.
Congenital hepatic arterio-venous malformations
(AVM) are rare vascular anomalies and have
rarely been reported in the presence of congeni-
tal heart disease. The reported cases are mostly
hemangiomas fed either by the hepatic artery
itself or by one of its branches. We present two
unique hepatic AVM cases in the presence of
congenital heart defects in which the AVM was not
fed by the hepatic arterial system. Transcatheter
coil embolisation was successfully carried out in
both of them by using non-detachable Gianturco
coils. Complete occlusion was achieved without
any sequel.
Keywords: Arterio-venous Malformation;
Trans-Catheter Embolisation; Congenital Heart
Hepatic vascular malformations comprise about 10% of
all cases of abnormal vascular connections within the
hepatic parenchyma [1]. These are further classified into
fast-flow (AVMs, arterio-portal fistulas), slow-flow
(porto-systemic shunts, venous lymphatic malformations)
and combined forms [2]. Hepatic AVMs should be dif-
ferentiated from the benign hepatic vascular tumors
(HVT) when an AVM can occur within the tumor mass
itself. Unfortunately, the terms hemangioma and arte-
rio-venous malformation (AVM) have been confused or
used interchangeably in the literature [3]. Histologically,
HVT are derived from mesenchymal tissue elements and
are classified as hemangioendothelioma (HE) or cav-
ernous hemangioma (HC) [4,5]. More recently, these
tumors are classified into infantile hemangioendo-
thelioma (IHE) and arteriovenous malformations (AVM)
[6,7]. Hemangioendothelioma progresses in the first year
of life and then regresses spontaneously. On the other
hand hepatic AVMs (in the absence of HVT) result from
abnormalities in the formation of blood vessels that
shunt blood through direct arterio-venous connections
without abnormal neoplastic tissue between the anoma-
lous vessels. So AVMs are neither tumors with growth
potential, nor capable of regression [1,6] but have a
higher and not well documented mortality rate [8]. On
the contrary the HVT has an age related tendency of
malignancy [5].
Hepatic AVMs are diagnosed either incidentally on
abdominal sonography for other reasons or may result in
congestive heart failure (CHF) due to significant in-
tra-hepatic shortcircuiting of blood. Ultrasonography
(US) and magnetic resonance imaging (MRI) are useful
diagnostic tools [9,10] but selected angiography is an
optimum diagnostic modality. Hepatic AVMs have been
reported in association with hemangiomas, and heredi-
tary hemorrhagic telangiectasia but rarely been reported
in association with congenital heart defects. We encoun-
tered two such cases which are briefly described.
2. CASE 1
This young infant presented to our services at two
months of age (weight = 5 kg) with complaints of bluish
discoloration of lips and nails since early life. Pertinent
physical examination features included significant oxy-
gen desaturation to 58% on room air, normal SI, single
SII and systolic ejection murmur III/VI at the left upper
sternal border. He was finally diagnosed as a case of
complex congenital heart disease in the form of double
inlet left ventricle, hypoplastic right ventricle, transposed
great arteries, large ventricular septal defect, and severe
sub-pulmonary/pulmonary stenosis. Palliative balloon
atrial septostomy was carried out for adequate inter-atrial
mixing, which improved the oxygen saturation to 80%
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on room air. He was then discharged in a stable condi-
At the age of two years (weight = 12.5 kg) he under-
went diagnostic cardiac catheterization for hemody-
namic assessment and delineation of pulmonary artery
anatomy as a pre-Glen assessment. Descending aorto-
grapgy, done to rule out aorto-pulmonary collaterals,
revealed incidentally a significant hepatic AVM. The
Figure 1. Abdominal aortogram in straight antero-posterior
and lateral projections, showing feeder artery arising from
abdominal aorta and supplying the arterio-venous malforma-
tion. Abd = abdominal.
Figure 2. Abdominal aortogram in straight antero-posterior
and lateral projections, showing the malformation draining
through a vein (draining vein) to the hepatic portion of inferior
vena cava (IVC).
Figure 3. Selective angiogram in the arterio-venous malforma-
tion (AVM) in straight antero-posterior and lateral projections
after coil embolisation, showing almost complete occlusion.
feeder artery was seen arising from the abdominal aorta
(Figure 1) and the malformation was seen draining into
the hepatic portion of inferior vena cava (Figure 2). The
AVM was occluded by deploying multiple (four coils of
5 mm and one coil of 3 mm diameter) non-detachable
Gianturco coils (Mreye embolisation coils; Cook: Wil-
liam cook, Europe) retrogradely through a 4-French
end-hole catheter. No complications were encountered
and post occlusion angiography confirmed near com-
plete occlusion (Figure 3). At the same time he under-
went lateral tunnel fenestrated Fontan procedure. Lately
he was seen in the out-patient clinic at the age of 3 years
(weight = 15.5 kg). He was doing fine without signifi-
cant complaints and his oxygen saturation ranged be-
tween 88-90% on room air.
3. CASE 2
This was the product of 35 week gestation, born (weight
= 2.1 kg) to a 35 year old mother with good Apgar score
at one and five minutes. Her physical features were con-
sistent with Down syndrome (confirmed by chromosome
analysis). At day one of age she developed congestive
heart failure and was electively intubated because of
significant respiratory distress. Physical examination
revealed apparent distress with retractions, heart rate of
200/min, respiratory rate of 78/min, and liver palpable 4
cm down the right costal margin. Chest roentgenogram
showed cardiomegally and increased vascular markings.
Echocardiography confirmed her having juxta-ductal
coarctation of the aorta (gradient = 20 mmHg). Inciden-
tally, an abnormal flow reversal was also seen at the
transverse arch level in the absence of aortic insuffi-
ciency. The reason for this flow reversal could not be
ascertained. She was taken to the catheterization labora-
tory in view of looking for the reason of this abnormal
flow reversal in the aortic arch and possible balloon an-
gioplasty of coarctation. Pull back of catheter from as-
cending to the descending aorta revealed a pressure drop
of only 14 mmHg from ascending to descending aorta.
Aortic angiogram revealed a large aneurysmal and a bit
tortuous vascular channel (maximum diameter of 3 mm)
arising from the right internal mammary artery, supply-
ing the right lobe of the liver (Figure 4) and draining to
the hepatic portion of IVC (Figure 5). Small Patent
ductus arteriosus (PDA) was also seen. This vascular
malformation was successfully occluded by deploying
multiple (4 coils of 3 mm and one coil of 2.5 mm di-
ameter) non-detachable Gianturco coils (Mreye emboli-
sation coils; Cook: William cook, Europe) retrogradely
through an end-hole catheter. Repeat angiography con-
firmed complete occlusion of the AVM (Figure 6). Sub-
sequently the patient was successfully extubated and
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discharged in a stable condition.
She was followed regularly in the out-patient clinic
without much complaint till the age of 16 months, when
she started having shortness of breath on feeding and on
regular activities. Physical examination revealed absent
femoral pulses and a non-invasive blood pressure dif-
ference of 45 mmHg between the upper and the lower
limbs. Echocardiography confirmed the development of
significant coarctation with a gradient of 40 mmHg
Figure 4. Aortic angiogram in LAO 15/Cr 20 and lateral pro-
jections showing dilated and tortuous internal mammary artery,
feeding the arterio-venous malformation (AVM) to the right
lobe of the liver.
Figure 5. Selective angiogram in the internal mammary artery
in straight antero-posterior and lateral projections showing the
malformation draining through the hepatic portion of the infe-
rior vena cava (IVC). A portion of the right atrium (RA) is also
across it. Successful balloon angioplasty of the coarcta-
tion was carried out at that time. The PDA had already
been occluded spontaneously.
Lately she was seen in the out-patient clinic at the
age of 34 months (weight = 17 kg). She was doing
fine without any complaints and there was no signifi-
cant blood pressure difference between the upper and
the lower limbs.
Hepatic AVM can be of three types: a direct communica-
tion between a systemic artery and a hepatic vein (he-
patic AV fistula); a communication between the hepatic
artery and the portal venous system (hepatoportal fistula);
multiple arterio-venous miocrofistulae as part of the he-
reditary hemorrhagic talengiectasia or hemangioma.
There have been many reports in the literature discussing
all aspects ranging from diagnosis to treatment options
for hepatic AVMs, but most of the reports have included
hemangiomas and other proliferative disorders under this
condition. Ours are true AVMs, (hepatic AV fistula) in
the sense that there is a solitary feeder artery supplying
the AVM and then draining through a venous channel to
the hepatic portion of inferior vena cava without signifi-
cant capillary phase, resulting in high cardiac output
state. Also an association of hepatic AVM with cyanotic
congenital heart disease has never been reported before.
Keeping in view the importance of the condition and its
new association with the congenital heart disease, some
aspects are discussed below with a brief review of the
literature (Table 1).
Beside hepatic artery, the liver can be supplied by a
number of extra-hepatic arterial sources including, right
or left inferior mesenteric arteries, intercostal arteries,
superior mesenteric artery, celiac axis, left gastric artery
and the adrenal arteries. The extra-hepatic arterial supply
has been demonstrated in about 96% of patients studied
by balloon occlusion of the main hepatic artery [11].
These extra-hepatic arteries remain dormant under nor-
mal conditions. However, one or more of these can be-
come enlarged in patients with hepatic vascular malfor-
mations or tumors. This was true in our first case as the
course of the abnormal feeding artery to the AVM repre-
sented most probably one of the minor twigs arsing from
the abdominal aorta. But in our second case the feeding
artery represented a dilated and tortuous right internal
mammary artery arising from the innominate artery. This
was an unusual finding as the left or the right internal
mammary arteries do not normally contribute to the ex-
tra-hepatic arterial supply. To our knowledge internal
Figure 6. Selective angiogram in the internal mammary artery
in straight antero-posterior and lateral projections after the coil
embolisation of the malformation, showing complete occlusion.
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mammary artery feeding a hepatic AVM has not been
reported so far. Moreover, though the innominate artery
is derived from the neural crest, we did not encounter
any other neural crest anomaly in our case. Finally an
association of neural crest anomaly with Down syn-
drome is not documented and needs further elaboration.
Table 1. Review of the literature.
Study Pts AVM type Presentation Association Treatment
Nielsen et al. [12] 3 Cerebral = 1 CHF NA NA NA
Placental = 1 CHF NA NA NA
Pulmonary = 1 CHF NA NA NA
Israel et al. [13] 1 Retro-peritoneal CHF NA Emb with Evalon avascular mass
Favilli et al. [14] 4 Cerebral = 1 CHF NA None Died
Hepatic = 2 CHF NA Medical Improved
Pulmonary = 1 CHF NA embolisation Died months later
Subramanyam et al.
[15] 1 Hepatic CHF None coil embolisation Resolution
Chavan et al. [16] 15 Hepatic vascular Abdominal = 5 HHT Emb with PVA Cholangitis = 1
CHF = 11 HHT Cholecystitis = 3
Portal HTN = 4HHT One death
Cirrhosis = 1 HHT
Costa et al. [17] 1 Hepatic CHF NA Coil embolisation Resolution
Mejides et al. [18] 1 Hepatic Vascular Fetal CHF NA Hydrocortisone in
UV Resolution
Knudson et al. [19] 156 Cerebral = 86 CHF (67%) Medical and
surgical Mortality = 67%
Hepatic = 61 CHF (48%) Medical and
surgical Mortality = 55%
Abd. Mass =
Pulmonary = 14 CHF (67%) Medical and
surgical Mortality = 43%
Cyanosis (43%)
Chavan et al. [20] 5 Hepatic vascular CHF, Portal HTNHHT Embolisation
Cholangitis = 1
Abdominal angina
Hazebroek et al. [21] 2 Hepatic CHF,Abd.Distensi
on Hemangioma Surgical ligation Resolution
Portal HTN
Valerie et al. [22] 1 hepatic Portal HTN Small PDA, VSDCoil embolisation Resolution
Whiting et al. [23] 2 Hepatic Abdominal painHHT Embolisation with
PVA Both died later
Chen et al. [24] 1 hepatic Abdominal painIntrahepatic
Biloma Surgical ligation Progression of
Alexander et al. [25] 1 hepatic Persistant Pul.
HTN NA Coil embolisation Resolution
Hisamatsu et al. [26] 1 Hepatic Epistaxis, dyspneaOsler-Weber-
Rendu Coil embolisation Cholangitis
Prokurat et al. [27] 17 Hepatic vascular CHF in most
cases Hemangiomas Surgical lobec-
tomy Resolution
Akita et al. [28] 1 Abdominal wall CHF Aneurysmal PDASurgical ligation Liver dysfunction
Abreviations. Abd = abdominal, CHF = congestive heart failure, Emb = embolisation, HHT = hereditary hemorrhagic telangiectasia, HTN = hyper-
tension, NA = not available, PDA = patent ductus arteriosus, Pul = pulmonary, PVA = pollyvinyl alcohol, UV = umbilical vein, VSD = ventricular
septal defect.
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A cerebral, pulmonary or retro-peritoneal arterio-venous
malformation should be suspected in newborns if a bruit
or soft a continuous murmur is heard over the skull,
chest or the abdomen respectively. Also, an AVM should
be included in the differential diagnosis in a newborn or
an infant who had unexplained CHF in the setting of
normal echocardiogram. Retrospectively thinking, we
believe that an AVM should be suspected in a patient
who has relatively high systemic saturation for a single
ventricle physiology, as in our first case. A keen review
of the literature has also confirmed CHF as one of the
main presenting feature in majority of the studies
[12-20]. Other uncommon modes of presentation are
portal hypertension [16,20,21], abdominal pain, mass,
ischemia or distension [16,19-24], primary pulmonary
hypertension [25] and bleeding episodes [26]. One of
our cases presented in CHF and the other was diagnosed
incidentally during diagnostic cardiac catheterization.
Echocardiographic evaluation with colour flow mapping
and pressure doppler helps further in diagnosing an
AVM. Finding of an abnormal flow reversal in the aorta
raises the possibility of AVM. Advanced radiological
techniques including un-enhanced Computed Tomogra-
phy (CT) and Magnetic Resonance Imaging (MRI) are
the useful tools in confidently distinguishing an AVM
from other abnormal vascular connection including he-
mangiomas. Angiography during cardiac catheterization
helps not only in exact delineating the feeder and drain-
ing vessels but also can help in trans-catheter occlusion,
if indicated.
Antenatal diagnosis of a hepatic AVM has already been
reported [18]. Postnataly a hepatic AVM can present
during neo-natal period [12,14,15,17,20,25,27,28] or
during infancy [6,12,13,19]. It can also present during
childhood [21] especially in the setting of hereditary
hemorrhagic talengiectasia [29,30] or even during adult
life [20,23,24,26]. One of our patients presented during
neonatal period (case #2) in respiratory distress due to
high output CHF and in the other patient the hepatic
AVM was incidentally discovered during cardiac cathe-
terisation. This is in accordance with the study by Pro-
kurat and colleagues [27], who have shown that patients
presenting during neonatal period are almost always
symptomatic as compared to those who present during
Hepatic AVMs have been described in association with
hereditary hemorrhagic talengiectasias [16,20,23] or
intra-hepatic tumors [22,24]. In an adult patient [26] an
association of hepatic AVM and Osler-Weber-Rendu
Disease has also been described. To the best of our
knowledge there has been only one report [21] describ-
ing the association of hepatic AVM with a congenital
heart disease: a patent ductus arteriosus (PDA) and mul-
tiple ventricular septal defects (VSD). Though there is
another report describing the presence of a PDA aneu-
rysm in a patient who had abdominal AVM, ours is the
first report describing an association of hepatic AVM and
cyanotic congenital heart disease. This association is, not
only of clinical significance but also has therapeutic im-
plications, as CHD is the major cause of CHF during
neonatal period and early infancy and one should keep in
mind an AVM as an additional cause of high output CHF
in refractory cases who do not respond to usual antifail-
ure therapy or do not show improvement after trans-
catheter or surgical intervention for the primary cardiac
Therapeutic options for symptomatic AVMs include
transcatheter embolisation or surgical ligation of hepatic
artery or surgical hepatic lobectomy or liver transplanta-
tion in the advanced cases. Embolotherapy with Polyvi-
nyl Alcohol has been described by Chavan et al., and
whiting and colleagues [16,20,23], while Ivalon particles
were used for the same purposes by Israel et al. [13].
While many devices including non-detachable Gianturco
coils, detachable coils, Aga vascular plugs, and AGA
PDA occluders are now available for embolisation of
vascular malformations and fistulas, and can be used for
this purpose depending upon the location and the size of
the malformations. Transcatheter coil embolisation has
been described by many studies also [15,21,25,26]. We
opted for Gianturco coils, because of these being avail-
able to us in multiple sizes, our expertise to use these
because of frequent use and successful results in the lit-
erature [21,25,26]. Surgical ligation of hepatic artery has
also been described by some [22,24]. We used tran-
scatheter approach through femoral artery for coil em-
bolisation of AVM, though trans-umbilical approach has
also been described by Costa and colleagues [17]. All of
the studies have described acceptable results with the
occlusion of AVM and resolution of the symptoms.
Cholangitis in one and cholecystitis in another three pa-
tients has been described by Chavan et al. [16] out of 15
patients (one patient died due to the procedure), while
sepsis has been described in 2 patients after the same
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procedure by Whiting et al. [23]. Both of the patients
died 4 and 15 months after the procedure. Intrahepatic
cholangitis has been described after coil embolisation of
the hepatic artery in one patient by Hisamatsu and col-
leagues [26]. The patient ultimately died a year later due
to hepatic dysfunction. Ischemic cholangitis has also
been reported after the same procedure in one out of 5
patients by Chavan and colleagues [20] while one of
their patients died 7 months after the procedure due to
sepsis. Apart from theses two reports none has reported
any complications. Surgical ligation has generally been
described as risk free, and only one report has described
progression of the disease even after the procedure [24].
We did not encounter any immediate or early follow-up
complications, so far.
Hepatic AVMs are rare conditions in children and a high
index of suspicion is required to diagnose these espe-
cially in those cases who present with either unexplained
or refractory high output CHF or in those who had rela-
tively higher systemic saturation in the setting of com-
plex congenital heart disease with single ventricle physi-
ology. Many treatment options are available with ac-
ceptable results. Transcatheter coil embolisation is safe
and effective for this purpose. Care should be exercised
to avoid ischemic changes after either transcatheter em-
bolisation or surgical ligation of the hepatic artery. The
importance of these reports is not only the fact that such
an association has not been reported before and expands
our clinical differential, but also these give us clues to a
deeper insight in the mechanism of cardiovascular de-
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