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35 Aortic Trauma inChildren
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effort futility in severely injured children under the age of
16years. A total of 1169 children survived, and 123 (9.5%)
died. Those who died were usually younger, had head injuries, and severe Injury Severity Scores. When two laboratory values of pH less than or equal to 6.95, base excess less
than 22, platelet counts less than or equal to 30,000, hemoglobin less than or equal to 5.0g/dL, rapid thromboelastography less than or equal to 30mm, and/or the presence of
traumatic brain injury were present, the potential salvage of
the child was extremely guarded. Specic injury location,
exclusive of the brain, is not listed, but reference to lack of
response to resuscitative efforts after 15minutes (pupils,
pulse, and EKG) suggested a potential fatal outcome as
noted in our patient #1 [19].
A registry has been developed for evaluating the effect
of resuscitative balloon aortic occlusion or open thoracotomy aortic control in profound hemorrhage situations. This
registry attempts to dene the value of descending thoracic
aortic occlusion in individuals without penetrating thoracic
injury but hemorrhagic shock. Five percent of the 285
patients survived to discharge with a slight favor to the balloon ER occlusive technique. The study involved patients
older than 18years of age and thus would not apply to our
patients #1 and #2 due to age and thoracic penetration.
Patients #4 through #6 could possibly be considered for this
technique, but the aorta was successfully handled without
utilizing this study protocol. One does wonder however if
all trauma- oriented ERs should also have a complete ER
OR located within the ER for care of these emergency
patients [20].
Summary
Aortic trauma in the age group from 0 to 21years is uncommon to rare except in the individual ages of 18–21years. In
this latter group, automobile and motorcycle injuries cause
a number of cardiac, aortic, and other bodily injuries. Many
of these patients may be treated conservatively until the
most opportune treatment time. The individual may then be
treated with either transfemoral endografting or open thoracic aortic surgery. Aortic trauma under the age of 10 is
very uncommon but may be lethal. With future development of newer diagnostic techniques, such as 3D imaging
and reconstruction, a better anatomic knowledge may be
assistive in the therapeutic approach to the patient and his/
her aortic injury.
Acknowledgments We wish to acknowledge and thank the entire medical care and hospital staff for all their efforts and assistance in the provision of care and their support provided to the patients, families and we
physicians.
References
1. Lowe LH, Bulas DI, Eichelberger MD, Martin GR.Traumatic aortic
injuries in children: radiologic evaluation. AJR Am J Roentgenol.
1998;170:39–42.
2. Karmy-Jones R, Hoffer E, Meissner M, Bloch RD.Management
of traumatic rupture of the thoracic aorta in pediatric patients. Ann
Thorac Surg. 2003;75(5):1513–7.
3. Takach TJ, Anstadt MP, Moore HV.Pediatric aortic Disruption. Tex
Heart Inst J. 2005;32:16–20.
4. Heckman SR, Trooskin SZ, Burd RS.Risk factors for blunt thoracic
aortic injury in children. J Pediatr Surg. 2005;40(1):98–102.
5. Feliciano DV. Vascular trauma revisited. (Scudder oration on
trauma). Am Coll Surg. 2018;226(1):1–12.
6. Hormuth D, Cefali D, Rouse T, Cutshaw J, Turner W Jr, Rodman G
Jr. Traumatic disruption of the thoracic aorta in children. Arch Surg.
1999;134:759–63.
7. Trachiotis GD, Sell JE, Pearson GD, Martin GR, Midgley
FM.Traumatic thoracic aortic rupture in the pediatric patient. Ann
Thorac Surg. 1996;62(3):724–31.
8. Tiao GM, Grifth PM, Szmuszkovicz JR, Mahour GH.Cardiac and
great vessel injuries in children after blunt trauma: an institutional
review. J Pediatr Surg. 2000;35(11):1656–60.
9. Tashiro J, Hannay WM, Naves C, Allen CJ, Perez EA, Rey J, Sola
JE. Mechanism and mortality of pediatric aortic injuries. J Surg
Res. 2015;198(2):456–61.
10. Sadaghianloo N, Jean-Baptiste E, Breaud J, Declemy S, Kurzenne
JY, Hassen-Khodja R.Blunt abdominal aortic trauma in pediatric
patients. Injury. 2014;45:183–91.
11. Choit RL, Tredwell SJ, Leblanc JG, Reilly CW, Mulpuri
K. Abdominal aortic injuries associated with chance fractures in
pediatric patients. J Pediatr Surg. 2006;41(6):1184–90.
12. Heck JM, Bittles MA.Traumatic abdominal aortic dissection in a
16 month-old child. Pediatr Radiol. 2009;39(7):750–3.
13. Anderson SA, Day M, Chen MK, Huber T, Lottenberg LL, Kays
DW, Beierle EA.Traumatic aortic injuries in the pediatric population. J Pediatr Surg. 2008;43(6):1077–81.
14. Saad NE, Pegoli W, Aleris G, Waldman DL, Davies
MG.Endovascular repair of a traumatic aortic transection in a pediatric patient. J Vasc Interv Radiol. 2007;18:443–6.
15. Goldstein BH, Hirsch R, Zussman ME, Vincent JA, Torres AJ, Coulson
J, Ringel RE, Beekman RH III.Percutaneous ballooon- expandable
covered stent implantation for treatment of traumatic aortic injury in
children and adolescents. Am J Cardiol. 2012;110:1541–5.
16. Milas ZL, Milner R, Chaikoff E, Wulkan M, Ricketts R.Endograft
stenting in the adolescent population for traumatic aortic injuries. J
Pediatr Surg. 2006;41(5):e27–30.
17. Keyhani K, Estrera AL, Sa HJ, Azizzadeh A. Endovascular
repair of traumatic aortic injury in a pediatric patient. J Vasc Surg.
2009;50(3):652–4.
18. Dieter RA Jr, Asselmeier GH, Hamouda F, Kuzycz GB, McCray
RM.Traumatic disruption of the thoracic aorta: a community hospital experience. Mil Med. 1963;148:502–6.
19. Kalkwarf KJ, Jensen SD, Allukian M, Harting MT, Cox CS, Fox
EE, Wade CE, Colton BA.Can we identify futility in kids? an evaluation of admission parameters predicting 100% mortality in 1,292
severely injured children. J Am Coll Surg. 2018;226(4):662–8.
20. Brenner M, Inaba K, Aiol A, DuBose J, Fabian T, Bee T, Holocomb
JB, Moore L, Skarupa D, Scalea TM. Resuscitative endovascular balloon occlusion of the aorta and resuscitative thoracotomy
in select patients with hemorrhagic shock: early results from the
American association for the surgery of trauma’s aortic occlusion in
resuscitation for trauma and acute care surgery registry. J Am Coll
Surg. 2018;226(5):730–40.

Aortic Valve Repair
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ChawkiElzein, DavidRoberson, andMichelN.Ilbawi
36
Introduction
Surgical management of aortic valve presents a difcult
dilemma. On the one hand, early surgery protects the myocardium from volume and pressure overload and decreases
the chance of brosis and remodeling. On the other hand,
early valve replacement is suboptimal because of the lack of
an ideal valve substitute that does not need anticoagulation
or frequent replacement. Autologous pulmonary valve has
emerged recently as an attractive aortic valve substitute that
fullls these criteria, but concerns persist over the long-term
fate of the pulmonary valve in the aortic position.
The dichotomy created by the absence of the ideal valve
substitute and the deleterious effects of long-standing ventricular volume and/or pressure overload associated with
aortic valve disease has renewed interest in aortic valvuloplasty. Although several techniques, such as annular reduction, commissural resuspension, and cusp extension, were
used in the past, aortic valvuloplasty remained an evolving
approach rather than a denitive treatment, due in part to
incomplete understanding of the functional anatomy and
geometry of the aortic valve. Recently, success in atrioven-
C. Elzein
The Heart Institute for Children, Advocate Children’s Hospital,
Oak Lawn, IL, USA
Cardiothoracic Surgery, University of Illinois at Chicago,
Oak Lawn, IL, USA
D. Roberson
Pediatric Cardiology, Advocate Children’s Heart Institute,
Advocate Children’s Hospital, Oak Lawn, IL, USA
M. N. Ilbawi (
Pediatric Cardiac Surgery, The Heart Institute for Children,
Advocate Children’s Hospital, Oak Lawn, IL, USA
Pediatric Cardiac Surgery, University of Illinois,
Oak Lawn, IL, USA
Pediatric Cardiac Surgery, Rush University, Chicago, IL, USA
Surgery, University of Illinois, Oak Lawn, IL, USA
*)
tricular valve repair, progress in myocardial protection,
renements in three-dimensional imaging of the aortic valve,
and detailed analysis of valve anatomy and function have led
to improved results of aortic valve reconstruction [1, 2].
Anatomy andFunction oftheAortic Valve
The three leaets of the aortic valve are attached to the aortoventricular junction. The collagenous condensation at the
point of attachment of each leaet has been termed the annulus brosis. There is, however, no true “ring” of the annular
tissue supporting the leaets in a straight circular plane. The
hemodynamic stresses on the leaets, therefore, are counteracted at several structural levels. The margin of coaptation of
a competent valve is more than a nite point of contact. It
extends along the whole margin of the leaet in length and
several millimeters in depth. Beneath the apices formed by
leaet attachment, the so-called commissures, there are subcommissural or interleaet triangles. The wide base of these
triangles follows the ventricular contraction pattern and
allows optimal retraction of leaets during systole. The sinotubular bar marks the junction with the ascending aorta. It is
thicker than the adjacent sinuses. It is circular with areas of
increased collagen. It acts as a suspension post that supports
the peripheral attachments (the commissures) of the valve
leaets. The parabolic shape of the leaets resembles a suspension bridge. Their attachments to the sinotubular bar are
several millimeters above the level of coaptation. As these
support poles stretch outward by as much as 16–44% during
early systole, the leaet edges (the cables) become straighter,
aiding in the opening of the valve.
The aortic root is also a complex hemodynamic system.
Its component parts change in size and shape during the cardiac cycle. Its distal portion is exposed to the aortic pressure.
It expands to allow leaet retraction. Its base is exposed to
ventricular dynamics. It contracts during the peak of systole
to decrease the distance the leaets have to close and to
reduce the stress forces applied to leaets in early diastole.
© Springer Nature Switzerland AG 2019
R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_36
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Moreover, the leaet-sinus assembly behaves as an
independent unit to store the diastolic pressure within. It
allows the aortic valve to remain competent. The instantaneous changes in the aortic valve orice have been shown to
precede movement of the blood in the ventricle. The transformation of the aortic orice from a closed position to a
triangle and then to a circle without causing exion deformity of the cusp tissue is related to aortic root distensibility
and the mechanism of leaet suspension.
Pathology andFunction oftheAbnormal
Aortic Valve
Aortic Valve Stenosis
The Congenital Bicuspid Aortic Valve
In type I, there is no median raphe at the junction of two
cusps. As a result, there are two rather symmetric aortic
sinuses and leaet base attachment. The valve orice is central. The commissural triangle is rather well developed. The
leaets are suspended at the sinotubular bar and have adequate depth. In type II, which is more prevalent, a median
raphe is present. The cusps are asymmetric, and the fused
leaet is longer and shallower and takes up more of the circumference of the valve. In contrast to the normal tricuspid
valve, the leaet edges are excessive and sagging. As a result,
there is increased folding and crossing and a compensatory
extension of the area of leaet approximation from their
edges (doming). The opening of the valve is eccentric due to
discrepancy in leaet sizes. The orice also has an elliptical
rather than a circular opening. The resultant distortion in
blood ow pattern exaggerates turbulence and predisposes to
degenerative changes. Frequently, there is commissural
fusion that limits the leaet movement and exaggerates the
eccentricity of valve opening and the decrease in its effective
orice diameter. The narrowed opening, often combined
with annular hypoplasia, impairs the ability of the leaets to
escape systolic or diastolic pressure load, further exaggerating the stress on the valve. The subcommissural triangle is
severely attenuated. It limits leaet movement in early systole and the change in orice conguration necessary for
appropriate leaet coaptation at the end of systole. The leaflet edges are suspended below the sinotubular bar. This,
combined with redundant leaet edges, results in shallow
sinuses, decreases coaptation area, and exaggerates leaetdeforming dynamic forces [3].
The Rheumatic Aortic Valve
The continued inammatory process causes progressive
scarring and thickening of the leaets and fusion of the commissures. The valve becomes progressively stenotic.
Aortic Valve Regurgitation
There are three types of regurgitant aortic valves. Type I is
dilatation of the aortic annulus, the ventricular aortic junction, or sinotubular bar. Type II is leaet prolapse. Type III is
leaet restriction and scarring. It is the most common pathology of the congenital regurgitant valve.
Regurgitation inPatients withCongenital
Valvar Stenosis
The continued trauma to the leaet edges produced by hemodynamic stress and abnormal ow patterns results in progressive scarring, thickening, deformity, and retraction of the
leaet edges and subsequent lack of coaptation (type III).
Aortic Regurgitation Secondary toSubaortic
Fibromuscular Stenosis
The abnormal blood ow pattern produced by the subaortic
stenosis results in progressive deformity of the leaet.
Tethering of the leaets by the subvalvar brous tissue, causing obstruction, exaggerates the regurgitation (type III).
Regurgitation inMarfan Syndrome
The pathology is progressive dilation of the aortic root wall
due to fragmentation of its elastic support. The dilated sinotubular bar and valve sinuses stretch apart the commissural
suspension and leaet edges. The increase in hemodynamic
stress due to changes in the leaet suspension mechanism
combined with an enlarged aortoventricular junction leads to
poor leaet coaptation and central regurgitation (type I).
Postballoon Regurgitation
This condition is usually caused by leaet(s) tear close to the
fused commissure. The leaet becomes ail and eccentric
regurgitation results (types II and III).
Aortic Regurgitation Secondary
toRheumatic Disease
There is cusp retraction secondary to inammation and
scarring. The hemodynamic sequelae result in progressive
annular dilation and worsening of the regurgitation (types II
and III).
Timing ofSurgical Intervention
To achieve optimal short- and long-term results, surgical
intervention should be timed appropriately. The decision
relies on achieving the goals of valve surgery, which include
relief of symptoms, restoration of exercise capacity, improved
quality of life, and, most importantly, protection of the myocardium from chronic pressure and/or volume overload.
Most of the reported guidelines for the timing of valve
surgery are based on studies that use mortality rates as a

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follow- up endpoint but fail to analyze myocardial performance and reserve several years postoperatively. They utilize
as their database several single-center observational studies
and very few prospective, randomized trials.
The introduction of and renement in valvuloplasty techniques has prompted critical evaluation of these older guidelines for timing of surgical intervention on the diseased aortic
valve. The availability of a surgical alternative that avoids
valve replacement or anticoagulation has liberalized the
older rigid criteria [4]. Although large-scale, long-term data
on repaired valves are not available, there is unquestionable
evidence that valvuloplasty extends the functional longevity
of the native aortic valve and may safely delay the need for
replacement, thus justifying earlier surgical intervention.
Waiting for symptoms to appear or for ejection fraction to
decrease prolongs the duration of ventricular pressure and
volume overload and may lead to irreversible ventricular
dysfunction [5].
Techniques ofSurgical Valvuloplasty
Several principles have evolved that helped in improving
short- and long-term outcomes of valve repair. These include
the following:
1. Detailed pre- and intraoperative analysis of pathology.
This is best achieved by two- and three-dimensional
echocardiography. Pliability of each cusp is estimated
by the apparent change in its area from systole to diastole. Adequacy of cusp tissue for coaptation is estimated
by measuring the curvilinear height of the leaet. In
addition, 3D echocardiography helps in measuring leaflet free edge, the depth of the sinus, and areas of tissue
deciency or prolapse.
2. More than one technique needs to be performed to
achieve both competence and relief of obstruction. The
different steps in the procedure should be tailored to
address the specic pathology types.
3. Reconstructive steps should be preceded by relief of
obstruction as completely as possible. All areas of leaet
fusion or stenotic lesions should be relieved rst even if
that reduces leaet support. Subsequent reconstructive
steps of such leaets should aim at restoring the normal
morphology, function, and support.
4. Isolated repair of only one leaet or cusp without
addressing the pathology of the whole aortic root is
inadequate and leads to early failure.
5. Fresh autologous tissues such as pericardium or fascia
lata cannot withstand dynamic stress when used for
repair and tend to retract and scar with time; therefore,
glutaraldehyde xation is necessary.
6. “Overcorrection” in cases of aortic valve incompetence
might be needed, but excessive correction may lead to
crowding and distortion of the repaired valve if the root
is normal or smaller than normal in diameter.
7. Centralizing blood ow through the valve decreases turbulence and extends the longevity of the repair; therefore, tricuspidization of the valve is advantageous when
possible.
8. It is essential to incorporate in the procedure the necessary steps that address the interaction between aortic
root dynamics and valve mechanics, namely, maintaining annular and commissural exibility and movement
in order to avoid accelerated stress-induced valve degeneration. Mobilization of the subcommissural triangle
and avoiding subtotal excision of the leaets close to the
aorto-ventricular zone are important to avoid the disruption of the delicate and complex relationship between
the root and leaet.
9. Continued root dilatation whether at the aorto- ventricular
or sinotubular bar junction induces recurrent aortic
insufciency and renders the repair ineffective. The
integrity of these junctions should be restored whenever
they are dilated.
10. The abnormal ascending aorta should be replaced at the
time of valvuloplasty especially in patients who demonstrate associated morphologic, histologic, or molecular
abnormalities of the aortic wall.
11. Realization that there is a dynamic interplay between the
valve and the aortic root that is essential for valve function has refocused attention on the importance of repairing all the root components, namely, the annulus, the
sinus, the cusps, and the sinotubular junction.
All valvuloplasties are performed through an oblique aortotomy above the sinotubular bar. Antegrade and retrograde
blood cardioplegia is used. Placement of commissural
sutures aids exposure. Axial traction (perpendicular to the
annulus plane) applied to the commissural sutures allows
assessment of the valve leaets and annulus. In addition, a
centrally placed suture helps in evaluating the structure, the
deciency, and the redundancy of the different cusps by traction on the suture and pushing the leaets gently toward the
ventricle.
Approach totheAorto-Ventricular Junction
In regurgitant valves, there is a variable degree of annular
dilatation that is accelerated in patients with bicuspid valves
or distorted septo-aortic angle. Signicant dilatation (Z≥+
2) impacts negatively on long-term outcome if not addressed
at the time of valvuloplasty.

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C. Elzein et al.
Various internal or external annuloplasty techniques have
been described. In the internal approach, a double row of
sutures are placed in the subannular area or at midcommissural level to avoid injury to the conduction system
(Fig.36.1). The sutures are tied around a dilator, the diameter of which is determined by the use of a nomogram or
approximated to 12–14mm/m2. It is benecial to have the
annuloplasty sutures slightly on the tight side, as some of
these sutures might cut through the tissue or erode into the
membranous septum in a small percentage of cases. Braided
suture material has the advantage of allowing tissue ingrowth but could cause more trauma and uneven reduction of
the annulus when compared with monolament material.
External annuloplasty requires extensive mobilization of the
aortic root and involves placement of a circumferential suture
or complete/incomplete ring. It has better long-term outcome
than internal xation [6–9] (Fig.36.2).
Surgical Approach totheAortic Sinuses
Management of the dilated sinus consists of sinus wall plication at mid-distance between the involved two commissures.
In occasional cases, when the valve opening is not at the center, asymmetric plication may centralize blood ow through
the valve. Severe dilatation of the sinuses may necessitate
reduction of the sinus wall by resection of a triangular piece
[10] (Fig. 36.3). Restrictive sinus wall, on the other hand,
limits cusp movement, attenuates the Eddie currents, and
leads to dysplasia of the leaet. Management consists of
sinus enlargement with a triangular patch (Fig. 36.1). The
degree of enlargement or reduction of a sinus diameter is
determined by the use of published nomograms that outline
the appropriate sinus diameter for age and weight (Fig.36.4).
Surgical Approach totheValve Cusps
(Leaets)
Prolapse is managed by central plication of the leaet
(Fig. 36.5). Triangular resection of the involved area is
needed in cases with severe redundancy or calcication. An
alternative approach is enforcement of the prolapsing margin
with a running suture (Fig.36.6) [11, 12]. Additional sinus
wall plication is helpful if there is an associated signicant
dilatation of the sinotubular bar.
Reconstruction of the defective leaet is the cornerstone
of any valvuloplasty. It involves thorough debridement and
extensive but safe thinning of the effected leaet of all nodularities or calcication. An appropriately shaped patch that
matches the irregular edge is then sutured to the leaet
defective- free margin. More patch length than leaet length
is sutured at the center of the cusp to give it the normal bulging “cusp” conguration (Fig.36.7). The reconstructed leaflet is suspended to the aortic wall at the level of the sinotubular
junction (Fig.36.8). Patch dimensions are crucial for optimal
immediate and long-term results. Excessive height and width
results in stenosis due to crowding or may cause coronary
ostial obstruction. On the other hand, a short and narrow
patch results in residual regurgitation. The actual length and
depth of the patch is inferred from the intercommissural
distance based on correlation equation or, less reliability,
b
Fig. 36.1 Internal subvalvar annuloplasty with two rows of suture. (a) Transaortic view. (b) Longitudinal view showing the annuloplasty sutured
in the subvalvar area

ab
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Fig. 36.2 Techniques of annuloplasty. Following complete mobilization, an external suture or ring is placed at the base of the root. (a) External
placement of annuloplasty sutures. (b) Completed annuloplasty ring at the base of the aortic root
Fig. 36.3 Reduction technique for dilated sinus of Valsalva. (From
ElZein etal. [21]. Reprinted with permission from Elsevier)
Fig. 36.4 Augmentation technique for restrictive sinus of Valsalva.
(From ElZein etal. [21]. Reprinted with permission from Elsevier)

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Fig. 36.5 Leaet plication using pledgeted sutures. (From ElZein
etal. [21]. Reprinted with permission from Elsevier)
C. Elzein et al.
Fig. 36.7 Patch augmentation of the defective leaets. The patch
width normalizes the leaet depth. Note the irregular edge of the patch.
(From ElZein etal. [21]. Reprinted with permission from Elsevier)
Fig. 36.6 Suture plication of redundant leaets. The sutures are exteri-
orized at the commissures and tied. (From ElZein etal. [21]. Reprinted
with permission from Elsevier)
Fig. 36.8 The reconstructed leaet is suspended at the ST junction.
(From ElZein etal. [21]. Reprinted with permission from Elsevier)
from nomograms, or an approximate estimate of cusp height
of 10mm/m2 [13, 14]. The width of the patch is determined
by subtracting the normal leaet depth from the actual depth
of the defective leaet. Leaet augmentation should achieve
central coaptation of 3–5mm in height [15, 16].
There is no ideal patch material. Several commercially
available patches have been used. Most of these, however,
develop brosis and calcication, limiting the functional life
of the valvuloplasty. Autologous pericardial patient debrided
thoroughly from all fat and adventitial tissue, treated with
glutaraldehyde 0.625% for 2minutes and rinsed thoroughly
has proven to be the best option.

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Surgical Approach totheSinotubular
Junction
Management of dilated sinotubular junction is plication at
the intercommissural point. It is tightened until the junctionto- annulus diameter ratio is 1.3:1 or the normal diameter predicted from nomograms is achieved. Another approach is to
reduce the diameter of the ascending aorta at the dilated
junction by resecting a triangular piece of the aortic wall.
Anastomosis to reestablish aortic continuity is reinforced
with a circular pericardial strip (Fig.36.9) [17].
Tricuspidization
Tricuspidization of the bicuspid aortic valve is indicated in
cases where the valve opening is eccentric. It centralizes
blood ow, thus minimizing turbulence and hemodynamic
trauma to the reconstructed valve, and consequently prolongs
the functional life of the repaired valve [18]. However, it may
increase the complexity of the repair and weakens the reconstruction because of increased length of suture line and use of
an excessive patch material. Technical aspects consist of
incising the rudimentary commissure and patch augmentation
of the resultant three defective leaets (Fig.36.10). Analternative approach to tricuspidization is changing the commis-
455
Fig. 36.10 Tricuspidization technique. (From ElZein et al. [21].
Reprinted with permission from Elsevier)
sural orientation by plicating the dilated sinus and annulus at
midpoint of the larger leaet. This maneuver centralizes the
valve opening to a certain extent but is not as effective as tricuspidization in restoring the valve structure to normal.
Ozaki Technique
Fig. 36.9 The reduction technique of the ST junction. Note the ratio of
the ST junction diameter to annulus diameter. (From ElZein etal. [21].
Reprinted with permission from Elsevier)
Described by Ozaki et al. in 2006, this technique involves
independent replacement of the three cusps by three separate
autologous pericardial patches. The size of the cusp is determined from a template that incorporates the intercommissural distance as the reference point. Long-term fate of
subtotal replacement of the leaet with patch material has
not been determined especially in pediatric patients [19].
Results
The techniques of aortic valvuloplasty are in evolution.
Several series have reported results using one or more of the
techniques mentioned here. None of these results, however,
reects the present knowledge of the surgical anatomy or the
outcome of valve repair when these technical steps are used
in combination.
A review of our total experience with these different
approaches revealed a signicant drop in pressure gradient
across the valve, a decrease in aortic regurgitation as judged
by grade and by ratio of the regurgitant jet to aortic annulus
diameter, and a decrease in indexed left ventricular enddiastolic volumes [20].
Long-term postoperative follow-up revealed a progressive
increase in pressure gradient in 42% of patients, associated

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with stiffening or calcication of the patch used for leaet
augmentation. When restenosis was analyzed, it was apparent
that patients who had valvar stenosis and annular hypoplasia
had the highest incidence of restenosis. This increased incidence might have been due to the crowding of the hypoplastic
aortic root when aggressive overcorrection is used. Recurrence
of regurgitation was not a problem in follow- up, and most
patients maintain competent valves. Therefore, a selective
approach to aortic valve disease should be adopted. Patients
with primary valvar stenosis and associated annular hypoplasia should undergo Ross with Konno Procedure or valve
replacement. On the other hand, patients with primary regurgitation or annular dilatation are best managed early by using
the described valvuloplasty techniques.
Conclusions
Aortic valvuloplasty as currently used has very low operative mortality. It provides an excellent alternative to valve
replacement. It maintains the patient’s own valve and does
not preclude other alternatives when deemed necessary. It
is probably superior to the Ross procedure in patients who
are very young or have signicant annular dilation due to
regurgitation or other causes. Its use in patients with aortic
annular hypoplasia should be limited to avoid recurrent stenosis. The use of patch material not xed with glutaraldehyde might provide a decrease in the incidence of
restenosis.
References
1. Karamichalis J, Aguib H, Anastasopulos A, et al. Design, dynamism and valve repair. J Thorac Cardiovasc Surg. 2017;153:396–8.
2. Roman M, Devereux R, Kramer-Fox R, et al. Two-dimensional
echocardiographic aortic root dimensions in normal children and
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Aortic Pseudoaneurysms
https://t.me/med1917
LeonieK.Stabenow
37
Introduction
Aortic pseudoaneurysms are blood-lled cavities formed
between the two outer layers of the vessel, the muscularis
propria and adventitia. The dilated segment of the aorta of
the pseudoaneurysm is lined only by the adventitia which
distinguishes pseudoaneurysms from true aneurysms in
which all three layers of the vessel wall are involved.
Pseudoaneurysms can occur after injury to the vessel, and
most cases arise due to prior aortic or cardiac surgery. Other
causes leading to impairment in the integrity of the vessel
wall can be blunt trauma, percutaneous surgical procedures, autoimmune diseases, inammation, and mycotic
pseudoaneurysms secondary to tuberculosis [1].
Complications of pseudoaneurysms are unpredictable, and
they have the potential to create life-threatening conditions.
Therefore, early diagnosis and treatment is essential to
maximize survival. Even though endovascular techniques
to repair aortic pseudoaneurysms are emerging, open surgery plays an important role and still counts as the standard
treatment [2, 3]. Endovascular repair methods are limited to
high-risk surgical patients, but these methods including
stent grafts, coil embolization [4], thrombin injections [5],
septal occluder devices [6], and vascular plugs become
more and more popular.
Epidemiology
The occurrence of aortic pseudoaneurysms is rare, but they
are often serious complications mostly caused iatrogenically.
Throughout the literature, the incidence rates of pseudoaneurysms are highly variable. Concerning ascending aortic
L. K. Stabenow (*)
Institute of Molecular Cell Biology, University Hospital Jena,
Friedrich-Schiller-University Jena, Jena, Germany
pseudoaneurysms, the occurrence has been reported to be as
low as 0.5% [1]. Nevertheless, in a surveillance imaging
series after cardiac or aortic surgery, the incidence rates
reported were up to 13% [1, 7]. For thoracic aortic pseudoaneurysms, the incidence rates are also less than 0.5% [8].
Other rare complications are anastomotic and paraanastomotic pseudoaneurysms after abdominal aortic reconstruction. Here, the incidence rate has been reported to be
5% 8years after cardiac surgery and 27% after 15years [4].
Regarding anastomotic pseudoaneurysms after ascending or
aortic arch replacement, rates range from 2% to 38% [9].
Pathophysiology
The most common cause of aortic pseudoaneurysms is injury
to the vessel wall due to prior aortic or cardiac surgery. For
instance, ascending aortic pseudoaneurysms are nearly always
associated with a history of aortic surgery and cannulation of
the ascending aorta [1]. Other causes leading to impairment in
the integrity of the vessel wall can be blunt trauma, percutaneous surgical procedures, autoimmune diseases, inammation,
and mycotic pseudoaneurysms secondary to tuberculosis
(Table37.1) [1]. Mycotic pseudoaneurysms arise from bacterial infection of the vessel wall. This term was rst used in
1885 by William Osler who used the description mycotic
aneurysm to describe the mushroom shape [10]. Furthermore,
also spontaneous formations of aortic pseudoaneurysms have
been reported, where none of these factors were found to be
the cause. Aortic pseudoaneurysms communicate with the
aorta through a hole in the vessel wall. Depending on the size
of the dilatation, spontaneous clot formation and complete
thrombosis can occur, leading to spontaneous resolution, but
this has rarely been reported. However, most frequently, the
enlargement exceeds a critical size, and progressive expansion
can then cause rupture or compression of surrounding structures which can lead to severe complications.
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