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VII. Aortic Injury
87.9 Ô 9.5%, respectively. The actuarial freedom from reintervention on the descending thoracic aorta was 100
and 90.9Ô 8.7% at 1 and 3 years, respectively. The actuarial freedom from treatment failure (a conservative,
all-encompassing performance indicator including endoleak, device mechanical fault, reintervention, late aortic-related death, or sudden, unexplained late death) at
1 and 3 years was 97.7 Ô 2.3 and 74.6 Ô 11.9, respectively.
The mean diameter of the pseudoaneurysm was
44 Ô 18 mm before treatment and decreased significantly
(p<0.001) to 40 Ô 18 mm after treatment.
35.5 Results from the Literature
These results from the literature are summarized in Tables 35.1 and 35.2.
Table 35.1. Surgical results from the literature
Finkelmeyer
et al. [3]
Patients (N) 413 50 20 19
Operative
mortality (%)
Respiratory
complications (%)
Paraplegia (%) 1.4 ± ± ±
Paraparesia (%) 1.4 ± 15 ±
Stroke (%) 1.1 ± ± ±
Renal failure (%) 1.4 2 ± ±
Recurrent
paralysis (%)
McCollum
et al. [4]
4.6 4 0 0
0.7 2 ± 26
6.7 4 ± 10
Soyer
et al. [5]
Roques
et al.
[6]
35.6 Discussion
Elective surgery of posttraumatic pseudoaneurysms has
proven efficient. Direct suturing with cardiopulmonary
bypass is possible in nearly half of cases. It carries a
low mortality, and a low renal and respiratory morbidity. The rate of paraplegia is close to zero in the best series. So, in these cases, the only advantage of endovascular techniques is the mini-invasivity. Stent-graft treatment has proven its feasibility. As the adjacent aortic
wall is normal, nondegenerative, late endoleaks are
more unlikely than in cases of degenerative aneurysms
[7]. The limits are known. Long proximal necks and
long one-piece stent-grafts are required to achieve good
preliminary results. This will probably make more frequent prior surgical bypass of the left supra-aortic vessels (Fig. 35.3) in order (1) to get a longer proximal
neck and (2) to maintain the patency of the left subclavian artery, essential for spinal cord blood perfusion as
has been shown by surgery studies, because long stentgrafts will increase the risk of paraplegia if the left subclavian artery has to be intentionally occluded [10].
Table 35.2. Endovascular results from the literature
Demers
et al. [7]
Patients (N)15108 47
Operative mortality 1 0 0 0
Respiratory
complications
Paraplegia ± ± ± 0
Paraparesia ± ± ± 1
Stroke ± ± ± ±
Renal failure ± ± ± ±
Recurrent paralysis ± ± ± ±
Vascular access
complication
±11±
±11 2
Kato
et al. [8]
Rousseau
et al. [9]
French
multicenter
study
Fig. 35.3. Computed tomography (CT) angiography, 3D recon-
struction, volume rendering. Control of a stent-graft 4 years
after endovascular treatment of a chronic posttraumatic pseudoaneurysm. The left supra-aortic vessels have been bypassed
(arrow), in order to get a longer proximal neck
J.-P. Verhoye et al. Chapter 35 Classification and Decision Algorithm of Posttraumatic Chronic Lesions of the Isthmus and the Descending Thoracic Aorta
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son of surgical and stent-graft repair. J Thorac Cardiovasc
35.7 Conclusion
The management of acute and chronic lesions of the
isthmus and the descending aorta has markedly evolved
with advances of imaging and intensive care.
Endovascular techniques, limiting the morbidity of
the treatment at the acute, delayed acute and controlled
chronic phases in unstable and trauma patients, do not
preclude delayed surgical options, currently the gold
standard for definitive lesion exclusion.
The endovascular techniques also seem a good option in incidental lesions, with favourable anatomy, in
elderly patients.
It must be kept in mind that currently to deploy is
not to cure, and that life-long imaging follow-up is necessary.
Acknowledgements. Frdric Thony (University Hospi-
tal, Grenoble), Herv Rousseau (University Hospital,
Toulouse), Pascal Leprince (University Hospital, Paris
Salpetrire), Philippe Douek (University Hospital, Lyon)
and Louis Boyer (University Hospital, Clermont-Ferrand) are thanked for their contribution to the French
multicenter retrospective study of endovascular treatment of chronic posttraumatic aortic false aneurysms.
References
1. Rousseau H, Dambrin C, Marcheix B, Richeux L, Mazerolles M, Cron C, Watkinson A, Mugniot A, Soula P, Chabbert V, Canevet G, Roux D, Massabuau P, Meites G, Tran
Van T, Otal P. Acute traumatic aortic rupture: a compari-
Surg 2005; 129:1050±1055.
2. Bortone AS, Schena S, D'Agostino D, Dialetto G, Paradiso
V, Mannatrizio G, Fiore T, Cotrufo M, de Luca Tupputi
Schinosa L. Immediate vs delayed endovascular treatment
of post-traumatic aortic pseudoaneurysms and type B dissections: retrospective analysis and premises to the upcoming European trial. Circulation 2002; 106:I234±240.
3. Finkelmeier BA, Mentzer RM Jr, Kaiser DL, Tegtmeyer CJ,
Nolan SP. Chronic traumatic thoracic aneurysm. Influence
of operative treatment on natural history: an analysis of
reported cases, 1950±1980. J Thorac Cardiovasc Surg
1982; 84:257±266.
4. McCollum CH, Graham JM, Noon GP, De Bakey MC.
Chronic traumatic aneurysms of the thoracic aorta: an
analysis of 50 patients. J Trauma 1979; 19:248±252.
5. Soyer R, Brunet A, Piwnica A, Blondeau P, Carpentier A,
Donzeau-Gouge P, Bical O, Dubost C. Traumatic rupture
of the thoracic aorta with reference to 34 operated cases. J
Cardiovasc Surg (Torino) 1981; 22:103±108.
6. Roques X, Remes J, Laborde MN, Guibaud JP, Rosato F,
MacBride T, Baudet E. Surgery of chronic traumatic aneurysm of the aortic isthmus: benefit of direct suture. Eur
J Cardiothorac Sur. 2003; 23:46±49.
7. Demers P, Miller C, Scott Mitchell R, Kee ST, Lynn Chagonjian RN, Dake MD. Chronic traumatic aneurysms of
the descending thoracic aorta: mid-term results of endovascular repair using first and second-generation stentgrafts. Eur J Cardiothorac Surg 2004; 25:394±400.
8. Kato N, Dake MD, Miller DC, Semba CP, Mitchell RS, Razavi MK, Kee ST. Traumatic thoracic aortic aneurysm:
treatment with endovascular stent-grafts. Radiology 1997;
205:657±662.
9. Rousseau H, Soula P, Perreault P, Bui B, Janne d'Othee B,
Massabuau P, Meites G, Concina P, Mazerolles M, Joffre F,
Otal P. Delayed treatment of traumatic rupture of the
thoracic aorta with endoluminal covered stent. Circulation
1999; 99:498±504.
10. Rehders TC, Petzsch M, Ince H, Kische S, Korber T,
Koschyk DH, Chatterjee T, Weber F, Nienaber CA. Intentional occlusion of the left subclavian artery during stentgraft implantation in the thoracic aorta: risk and relevance. J Endovasc Ther 2004; 11:659±666.
349
Neonatal and Early Childhood
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Thoracic Aorta Abnormalities and
Their Current Surgical Treatment
Francois G. Lacour-Gayet, John H. Artrip
Chapter
36
Contents
36.1 Introduction .......................
36.2 Aortic Coarctation .................... 353
36.2.1 Anatomy ...................... 353
36.2.2 Occurrence .................... 353
36.2.3 Clinical Presentation and Diagnosis ...... 354
36.2.4 Surgical Treatment ................ 355
36.2.5 Surgical Results .................. 357
36.2.6 Interventional Approach to Coarctation . . . 357
36.3 Interrupted Aortic Arch ................. 357
36.3.1 Anatomy ...................... 357
36.3.2 Occurrence .................... 358
36.3.3 Clinical Presentation and Diagnosis ...... 358
36.3.4 Surgical Treatment ................ 358
36.3.5 Surgical Results .................. 359
36.4 Vascular Rings ...................... 359
36.4.1 Anatomy and Embryology ........... 359
36.4.2 Occurrence .................... 360
36.4.3 Clinical Presentation and Diagnosis ...... 361
36.4.4 Surgical Treatment ................ 361
36.4.5 Surgical Results .................. 361
36.5 Conclusion ........................ 361
353
36.1 Introduction
Thoracic aortic abnormalities encountered with neonates and young children are primarily confined to the
aortic arch and isthmus. The International Congenital
Heart Surgery Nomenclature defines the aortic arch as
the segment of aorta between the braciocephalic artery
and the left subclavian artery and the aortic isthmus as
the segment of aorta between the left subclavian artery
and the ductus arteriosus [3]. Malformations in this region include aortic coarctation, interrupted aortic arch
(IAA) and vascular ring malformations.
36.2 Aortic Coarctation
36.2.1 Anatomy
Coarctation encompasses a variety of obstructive lesions of the aorta. Bonnet [6] was the first to recognize
distinct anatomical subsets of coarctation and classify
them into an adult and an infantile type. The adult type
depicts a discrete obstructive lesion just distal to the
left subclavian artery, whereas the infantile type depicts
a diffuse narrowing of the aortic isthmus (Fig. 36.1).
Terms such as ªpreductalº and ªpostductalº are employed to describe the lesion in relation to the ductus
arteriosus. Although these terms are widely used clinically, they are anatomically incorrect. Coarctation is almost always juxtaductal and positioned between the
isthmus and the descending aorta [24]. When the ductus is patent, the coarctation can be shown to be a curtain of ductal tissue encircling the aortic isthmus; this
becomes less obvious as the ductus closes [5]. The segment of aorta proximal to the coarctation usually tapers
gradually, but this is distinct from tubular hypoplasia,
where there is uniform narrowing of an entire aortic
segment. Tubular hypoplasia of the aortic arch is rarely
seen with isolated coarctation; however, it is commonly
present when the coarctation exists with complex intracardiac abnormalities (transposition of the great arteries with ventricular septal defect, hypoplastic left
heart syndrome, etc.) [15]. Arch hypoplasia usually involves the distal arch but it can involve the proximal
arch, creating a hypoplasia of the total transverse arch.
36.2.2 Occurrence
Coarctation occurs in 20±60 per 100,000 live births and
represents 5±8% of all congenital cardiovascular lesions
[11, 13]. It is an isolated lesion 82% of the time and is
approximately twice as common in male [14]. The reported frequency of important associated cardiac malformations depends on the patient population studied.
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VIII. Congenital Diseases of the Thoracic Aorta
Fig. 36.1. To p: Illustration and angiogram of an ªadultº-type
coarctation with a typical ªshelflikeº lesion distal to the left
subclavian artery. The large arterial vessels present on the angiogram supply collateral circulation to the descending aorta.
Ventricular septal defects occur in 11% of cases when
coarctation occurs in infancy or childhood; however,
this rises to 36% when coarctation occurs in the neonate [17]. Bicuspid aortic valve occurs in 27±46% of
cases with coarctation. Coarctation accompanies other
cardiovascular lesions and is present in 7% of major
congenital cardiac malformations [14]: single ventricle
anatomy, 7%; transposition of the great arteries, 6%; atrioventricular septal defects, 4%; and double-outlet
right ventricle, 2±3% [17].
36.2.3 Clinical Presentation and Diagnosis
The neonate with coarctation may have severe heart
failure with acidosis, tachypnea and a profound diaphoresis with feeding. Depending on the patency of the
Bottom: Illustration and angiogram of an ªinfantileº-type coarctation with tubular hypoplasia of the aortic arch and the isthmus.
The angiogram demonstrates early washout of contrast material
in the descending aorta from a patent ductus arteriosus
ductus arteriosus and the severity of the coarctation,
differential cyanosis may be present. Severe obstruction
at the isthmus and ductus arteriosus requires intravenous infusion of prostaglandin E
in the neonate. This
1
relaxes the ductal tissue, lowering the resistance of flow
through the aorta, improving ventricular function.
Echocardiography allows the diagnosis of coarctation
and associated cardiac malformations. Rarely is cardiac
catheterization or MRI needed to confirm the diagnosis.
Older infants and children uncommonly have asso-
ciated cardiac lesions. Systemic hypertension with a differential noted on upper and lower extremity blood
pressures is the usual presentation. A differential of
more than 20 mmHg should warrant further investigation. Echocardiography is performed to rule out associated cardiac lesions, and computed tomography (CT)
scan of the chest or MRI is performed to precisely define the anatomy and extent of arterial collaterals.
F. G. Lacour-Gayet, J.H. Artrip Chapter 36 Neonatal and Early Childhood Thoracic Aorta Abnormalities and Their Current Surgical Treatment
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355
36.2.4 Surgical Treatment
Several techniques for repair of coarctation are advocated by various authors. The choice of the particular
technique depends on the anatomy confronted by the
surgeon and the experience of the surgeon with each
procedure. Tubular hypoplasia of the transverse arch is
an important anatomic feature dictating surgical method. A simple formula used to assess the adequacy of
the arch in the neonate is the weight of the child in
kilograms plus 1 should approximate the diameter of
the arch in millimeters. It has been suggested that hypoplasia of the arch will enlarge with time, especially if
associated intracardiac lesions are fixed at the time of
coarctation repair. Although this may be uncommonly
true, it is prudent to repair the arch hypoplasia. The
techniques the surgeon should be familiar with are the
standard end-to-end anastomosis [8], the subclavian
flap angioplasty [26], the extended end-to-end anastomosis [27] and the end-to-side anastomosis [25].
Standard end-to-end coarctation repair remains the
procedure of choice in infants less than 3 months of age
and in young children. A left posterolateral thoracotomy
utilizing the fourth interspace is performed (Fig. 36.2).
If associated cardiac lesions are being repaired at the
same time, a sternotomy is preferred. The lung is retracted anteriorly and inferiorly with stay sutures placed
on the pleural reflection. The vagus and recurrent laryngeal nerve are identified and preserved. The aorta is
dissected from the left carotid artery to the second set
of intercostal arteries. The aorta should be freely mobilized to prevent tension on the anastomosis; often this
requires sacrificing one to two sets of intercostal arteries. This can be done without consequence in the
neonate and infant. Systemic heparinization (1 mg/kg)
has been advocated by some surgeons; however, this is
not necessary in neonates and infants. The ligamentum
or ductus arteriosus is ligated. Aortic clamps are placed
proximally at the base of the origin of the left subclavian artery and distally below the coarctation. The
coarctation is excised and a polypropylene 6-0 or 7-0
suture is used for standard running anastomosis. The
distal aortic clamp is first released and the anastomosis
is deaired and examined for hemostasis. The proximal
aortic clamp is then released, which may precipitate
considerable hypotension and acidosis. Administration
of sodium bicarbonate and replacement of the proximal
aortic clamp may be needed until acidosis is corrected
and the ventricle has been properly volume loaded.
Subclavian flap angioplasty is rarely used today in
neonates because it does not address the arch hypoplasia. The sacrifice of the left subclavian artery can be associated in rare cases with severe left arm ischemia and
is not recommended for infants older than 3 months of
age. Surgical incision and aortic mobilization are similar to the standard end-to-end repair (Fig. 36.3). The
left subclavian artery is further mobilized to the point
of origin of the vertebral artery and ligated. The ductus
arteriosus is ligated and aortic clamps are placed proximally on the arch at the base of the left common carotid artery and distally beyond the coarctation. The left
Fig. 36.2. Standard end-to-
end coarctation repair
Fig. 36.3. Subclavian flap an-
gioplasty. The left subclavian
artery is divided and an incision is made posteriorly on
the aorta extending inferiorly
across the coarctation. The
subclavian artery is folded
downwards over the coarctation and sewn
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VIII. Congenital Diseases of the Thoracic Aorta
Fig. 36.4. Extended end-to-end repair. The aortic
isthmus is hypoplastic. An incision is made on
the undersurface of the aortic arch to the level
of the left common carotid artery. The descending aorta is sewn to the concavity of the aortic
arch
Fig. 36.5. End-to-side repair.
The hypoplastic isthmus is
ligated and divided. An incision is made on the undersurface of the aortic arch
encroaching upon the ascending aorta. The descending aorta is sewn to the concavity of the aortic arch
Fig. 36.6. Subclavian augmentation procedure. An incision is
made on the lateral wall of the left common carotid artery and
continued across the arch onto the medial wall of the left subclavian artery. The left common carotid and subclavian ar-
subclavian artery is divided distally and a longitudinal
incision is made in the descending aorta and carried
across the coarctation and into the transected left subclavian artery. The subclavian flap is then folded down
into the aortic incision and sewn with a running 7-0
polypropylene suture.
The procedure of choice in neonatal coarctation is
resection and extended end-to-end anastomosis [15,
28]. This technique addresses coarctation and the associated hypoplasia of the transverse arch (Fig. 36.4). An
extended mobilization of the transverse arch, left subclavian artery, left carotid artery and descending aorta
teries are sewn together creating an effective large aortic orifice. This can be done with the ductus arteriosus patent to preserve blood flow to the lower extremities. An extended end-toend or end-to-side anastomosis is then performed
requiring sacrificing one or two intercostal arteries is
required. An aortic clamp is placed proximally across
the aortic arch at the base of the innominate artery
while occluding the left common carotid and left subclavian arteries. The clamp should not obstruct flow
through the innominate artery, which is monitored by
arterial pressure measurement in the right arm. The
ductus arteriosus is ligated and a distal aortic clamp is
placed beyond the coarctation. The coarctation is completely excised and an incision is made on the undersurface of the aortic arch crossing under the left common carotid artery. Failing to bring the incision proxi-
F. G. Lacour-Gayet, J.H. Artrip Chapter 36 Neonatal and Early Childhood Thoracic Aorta Abnormalities and Their Current Surgical Treatment
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357
mal will result in obstructed flow across the aortic arch.
A running 7-0 polypropylene suture is used to complete
the anastomosis. A longitudinal incision placed posteriorly on the descending aorta may be needed to enlarge
the anastomosis and receive the segment of arch containing the left subclavian artery.
Occasionally, there is a long segment of hypoplastic
arch that despite the use of an extended end-to-end
technique will result in obstructed flow across the proximal aortic arch. An end-to-side technique that brings
the distal aorta underneath the proximal arch is well
adapted to this severe form of arch hypoplasia. Depending on the degree of proximal arch hypoplasia, this
approach may require sternotomy and cardiopulmonary
bypass. An aortic clamp is placed across the proximal
aortic arch occluding the left common carotid and left
subclavian arteries (Fig. 36.5). The ductus arteriosus
and aortic isthmus are ligated and the coarctation is
completely excised. An incision is made on the undersurface of the transverse arch coursing proximal into
the ascending aorta. A running 7-0 polypropylene suture is used to perform an end-to-side anastomosis. A
subclavian augmentation procedure of the distal arch
may be required to further enlarge the transverse arch
(Fig. 36.6) [2]. An incision is made in the lateral wall of
the left common carotid artery and the medial wall of
the left subclavian artery. A 7-0 polypropylene suture is
used to bring these vessels together, creating an effective larger aortic arch. This can be performed prior to
an extended end-to-end or end-to-side anastomosis
with clamps placed proximally on the transverse arch
and distally on the aortic isthmus above the ductus arteriosus to preserve flow to the lower extremities.
isting gradients warrant cardiac catheterization. Percutaneous balloon angioplasty can be performed safely
6 weeks following surgical repair and can easily dilate
most recoarctations. Occasionally, surgery is required
for recoarctation and the techniques already described,
especially the addition of a subclavian augmentation
procedure, may be needed for repair. Rarely is an interposition graft necessary for aortic repair and it is not
recommended in infancy or childhood.
36.2.6 Interventional Approach to Coarctation
Percutaneous balloon angioplasty is associated with
lower hospital charges, shorter lengths of stay and fewer
complications than surgical repair, and is suggested by
some authors to be used for primary coarctation, as
well as recoarctation [22]. However, angioplasty does
not remove ductal tissue, but rather creates intimal disruption, analogous to a ªcontrolled dissectionº [10]. Review of recent literature concludes that during the first
2 months of life mortality is higher for balloon angioplasty (8 versus 2±4% for surgery), reintervention rates
are higher (28 versus 7% for surgery) and late aneurysm formation or dissection occurs up to 8% of the
time following angioplasty [16]. Surgical repair of
coarctation remains the best option for neonates and
young infants.
36.3 Interrupted Aortic Arch
36.3.1 Anatomy
36.2.5 Surgical Results
The incidence of recoarctation defined as a peak gradient of more than 20 mmHg is estimated to be approximately 10% in neonates [15]. Nevertheless, new or ex-
Interruption of the aortic arch is seen in neonates with
survival depending on the patency of the ductus arteriosus. Rare cases of aortic atresia of the distal arch and the
isthmus have been encountered in childhood where the
ductus is closed and distal aortic perfusion is via a large
Fig. 36.7. Classification of in-
terrupted aortic arch (IAA).
Type A, there is interruption
between the left subclavian
artery and the ductus arteriosus. Type B, there is interruption between the left subclavian and left common carotid arteries. Type C, there is
interruption between the brachiocephalic and left common carotid arteries
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VIII. Congenital Diseases of the Thoracic Aorta
collateral network. The classification of arch interruption
put forth by Celoria and Patton [7] has been almost uniformly accepted and defines three anatomic types based
on the location of the interruption (Fig. 36.7). Type B is
the commonest, representing 55% of the cases, followed
by type A (40%) and type C (5%) [23]. An aberrant origin of the right subclavian artery from the distal aortic
arch may accompany type B interruptions.
36.3.2 Occurrence
Interruption of the aortic arch is a rare lesion occurring
in 0.3 per 100,000 live births and representing 1.3% of
all congenital cardiovascular lesions [23]. Type B interruptions are commonly associated with chromosome
22q11.2 deletion in the context of DiGeorge syndrome
[9]. A conoventricular ventricular septal defect is usually present with a posterior malalignment of the outlet
septum. Severe subaortic obstruction from the malaligned septum may require modification in surgical
approach (Fig. 36.8). As with other aortic arch abnormalities, bicuspid aortic valve occurs frequently with
IAA. Major other congenital heart malformations accompanying IAA include the following: truncus arteriosus, 10%; aortopulmonary window; 4%; transposition
of the great arteries, 3% [12]. IAA may be part of a
complex set of lesions constituting hypoplastic left
heart syndrome.
Fig. 36.8. Echocardiogram of a patient with IAA. The conal sep-
tum (CS) is malaligned posteriorly creating a ventricular septal
defect and obstruction of the left ventricular outflow tract
(LVO T ). AA ascending aorta, RV right ventricle, LV left ventricle,
LA left atrium
36.3.3 Clinical Presentation and Diagnosis
The neonate with IAA is critically ill. As the ductus arteriosus closes, severe heart failure develops secondary
to the volume overload from the ventricular septal defect and the increased afterload of the arch obstruction.
Intravenous administration of prostaglandin E
is start-
1
ed immediately to maintain the ductal patency. With a
patent ductus arteriosus, anticipated differential cyanosis may not be present owing to a large intracardiac
shunt minimizing the O
saturation difference between
2
the right and left ventricular chambers. Echocardiography establishes the diagnosis of IAA and provides the
necessary information on the ventricular septal defect
and the severity of left ventricular outflow tract obstruction. Cardiac catheterization is rarely needed to
confirm the diagnosis.
36.3.4 Surgical Treatment
Currently IAA is repaired in the neonate utilizing a
one-stage approach that addresses both the arch anomaly and the associated intracardiac lesion. The two-stage
approach is reserved for treatment of the neonate with
a subarachnoid hemorrhage, contraindicating systemic
heparinization and cardiopulmonary bypass [20]. The
staged correction consists of an arch repair and pulmonary artery banding in the neonatal period followed by
ventricular septal defect closure and debanding at 2±
3 months of age. With a one-stage approach, a median
sternotomy is performed and the arch vessels, branch
pulmonary arteries, ductus arteriosus and the proximal
portion of the descending aorta are fully mobilized.
The classic approach utilizes deep hypothermia (18±
208C) with circulatory arrest. More recently, the arch is
repaired without circulatory arrest using selective antegrade cerebral perfusion and hypothermia (20±228C)
(Fig. 36.9). A single aortic cannulation technique can be
used if uniform cooling is achieved between the upper
and lower extremities. If the lower extremities fail to
cool, a second cannula is placed in the main pulmonary
artery with the branch pulmonary arteries snared. Cardioplegia is administered antegrade through the aorta
cannula with the head vessels snared. The aorta cannula
is then moved into the innominate artery, and the flow
is reduced to 30±50 ml/kg. The pulmonary cannula is
removed and the ductus is ligated and divided. All ductal tissue should be removed. A longitudinal incision is
made on the left side of the ascending aorta and an
end-side aortic anastomosis is performed with a 7-0
polypropylene suture. The descending aorta often cannot reach the ascending aorta despite adequate mobilization. Dividing the left subclavian artery will provide
further length to the descending aorta. If an aberrant
F. G. Lacour-Gayet, J.H. Artrip Chapter 36 Neonatal and Early Childhood Thoracic Aorta Abnormalities and Their Current Surgical Treatment
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359
Fig. 36.9. Repair of type B IAA. Left: Two arterial cannulas are
placed, one in the ascending aorta and one in the pulmonary
artery. The branch pulmonary arteries are snared. Upper right:
The arterial cannula is placed into the brachiocephalic artery
right subclavian artery is present, this is divided to
fully mobilize the descending aorta. The use of interposition grafts should be avoided. In cases of severe tension on the anastomosis, a homograft patch of pulmonary autograft is placed on the anterior aspect of the
anastomosis [19]. Closure of the ventricular septal defect is performed and depending on the length of conal
septum, a right atrial or right ventricular approach is
preferred.
36.3.5 Surgical Results
Current data from the Congenital Heart Surgeons Society suggest that 14% of patients undergoing direct
arch anastomosis will require reintervention within
3 years [12]. Avoidance of the use of interposition grafts
and balloon angioplasty of recurrent obstruction has
virtually eliminated the need for surgical reintervention.
and the other arterial cannula is removed. The ductus arteriosus and left subclavian arteries are ligated and divided. Lower
right: An end-to-side anastomosis is performed
36.4 Vascular Rings
36.4.1 Anatomy and Embryology
Vascular rings are congenital malformations of the aortic
arch where vascular structures completely encircle and
compress the trachea and esophagus. In the embryonic
arch system, six primitive aortic arches arise from the
primitive aortic sac. These arches terminate between a
ventral and dorsal aorta. Although six pairs of aortic arches eventually develop, they are not present at the same
time. When the sixth set of arches develops, the first two
sets have already regressed. The formation of vascular
rings depends on the preservation or absence of specific
segments of the rudimentary arch complex.
Normally, the right fourth arch involutes at 36±
38 days of gestation, leaving the left fourth arch to form
the normal adult arch system. If the right fourth aortic
arches persist, a double arch system is formed. The ascending aorta gives rise to two arches that pass on both
sides of the trachea and esophagus and join the descending aorta forming a complete ring (Fig. 36.10). Of
infants presenting with a double aortic arch, 75% have
a dominant right arch, 20% have a dominant left arch,
and 5% have equal-sized arches. With a right dominant
pattern, the left arch is frequently severely narrowed or
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VIII. Congenital Diseases of the Thoracic Aorta
Fig. 36.10. Double aortic arch. Left: Cartoon il-
lustrating a double aortic arch. Right: Magnetic
resonance angiogram nicely illustrating the vascular ring that forms from the double aortic
arch. LCCA left common carotid artery, RCCA
right common carotid artery, LSA left subclavian artery, RSA right subclavian artery
Fig. 36.11. Three types of right aortic arches.
Note that a vascular ring is not created if the ligamentum arteriosus connects to an anterior
left subclavian artery (right). LCCA left common carotid artery, RCCA right common carotid artery, LSA left subclavian artery, RSA right
subclavian artery
atretic in the segment distal to the origin of the left
subclavian artery. This is represented by a fibrous cord
joining the descending aorta, often at the site of a diverticulum ± Kommerell's diverticulum. With a left
dominant pattern, the right arch is rarely atretic.
If the left arch involutes, a right aortic arch is
formed. The aortic arch is to the right of the trachea
and passes behind the esophagus to join the descending
aorta. Depending on the site of involution of the left
arch and the branching pattern of the head and upper
extremity arteries, different configurations are possible
(Fig. 36.11). The commonest variant of right aortic arch
has the left subclavian artery arising from the descending aorta (retroesophageal left subclavian) with the ligamentum arteriosus connecting the pulmonary artery to
the descending aorta, completing a vascular ring. If the
left subclavian artery originates anterior to the esophagus from a left-sided brachiocephalic vessel (mirror-image branching) a vascular ring is created if the ligamentum connects the pulmonary artery to the descending
aorta. No vascular ring is present if the ligamentum
connects the pulmonary artery to the left subclavian artery. The latter configuration is common with tetralogy
of Fallot and truncus arteriosus.
Other variations of aortic arch configuration and
branching pattern of the head and upper extremity ar-
teries exist. Largely, these other malformations do not
form a complete ring around the trachea and esophagus. These partial or incomplete vascular rings are
rarely of clinical significance. An aberrant origin of the
right subclavian artery from the descending aorta occurs in 0.5% of the general population [1]. Because this
artery passes behind the esophagus, it has been implicated as a rare cause of dysphagia ± the so called dysphagia lusoria. An abnormal leftward and posterior
coursing of the brachiocephalic artery may be drawn
taut against the anterior surface of the trachea, causing
respiratory compromise. The ªinnominate artery compression syndromeº is uncommon.
36.4.2 Occurrence
Vascular ring malformations usually account for 1±2%
of all congenital cardiovascular lesions [14]. Because of
the variability of arch pattern and the severity of symptoms at presentation, it is difficult to know the incidence of each arch malformation. The frequencies of
double aortic arch and right aortic arch are approximately equal for all patients presenting with complete
vascular rings; however, infants presenting with clini-
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