Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3711_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
32 Мб
Скачать
35 Aortic Trauma inChildren
https://t.me/med1917
447
effort futility in severely injured children under the age of 16years. 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 5.0g/dL, rapid thromboelastog­raphy less than or equal to 30mm, and/or the presence of traumatic brain injury were present, the potential salvage of the child was extremely guarded. Specic injury location, exclusive of the brain, is not listed, but reference to lack of response to resuscitative efforts after 15minutes (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 dene 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 18years 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 21years is uncom­mon to rare except in the individual ages of 18–21years. 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, Grifth 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, Aleris 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
https://t.me/med1917
ChawkiElzein, DavidRoberson, andMichelN.Ilbawi
36
Introduction
Surgical management of aortic valve presents a difcult 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 fullls 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 denitive 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, renements 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 andFunction oftheAortic Valve
The three leaets of the aortic valve are attached to the aor­toventricular junction. The collagenous condensation at the point of attachment of each leaet has been termed the annu­lus brosis. There is, however, no true “ring” of the annular tissue supporting the leaets in a straight circular plane. The hemodynamic stresses on the leaets, 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 leaet in length and several millimeters in depth. Beneath the apices formed by leaet attachment, the so-called commissures, there are sub­commissural or interleaet triangles. The wide base of these triangles follows the ventricular contraction pattern and allows optimal retraction of leaets 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 leaets. The parabolic shape of the leaets 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 leaet 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 leaet retraction. Its base is exposed to ventricular dynamics. It contracts during the peak of systole to decrease the distance the leaets have to close and to reduce the stress forces applied to leaets 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
449
450
https://t.me/med1917
C. Elzein et al.
Moreover, the leaet-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 orice have been shown to precede movement of the blood in the ventricle. The trans­formation of the aortic orice 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 leaet suspension.
Pathology andFunction oftheAbnormal 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 leaet base attachment. The valve orice is cen­tral. The commissural triangle is rather well developed. The leaets 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 leaet is longer and shallower and takes up more of the cir­cumference of the valve. In contrast to the normal tricuspid valve, the leaet edges are excessive and sagging. As a result, there is increased folding and crossing and a compensatory extension of the area of leaet approximation from their edges (doming). The opening of the valve is eccentric due to discrepancy in leaet sizes. The orice 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 leaet movement and exaggerates the eccentricity of valve opening and the decrease in its effective orice diameter. The narrowed opening, often combined with annular hypoplasia, impairs the ability of the leaets to escape systolic or diastolic pressure load, further exaggerat­ing the stress on the valve. The subcommissural triangle is severely attenuated. It limits leaet movement in early sys­tole and the change in orice conguration necessary for appropriate leaet coaptation at the end of systole. The leaf­let edges are suspended below the sinotubular bar. This, combined with redundant leaet edges, results in shallow sinuses, decreases coaptation area, and exaggerates leaet­deforming dynamic forces [3].
The Rheumatic Aortic Valve
The continued inammatory process causes progressive scarring and thickening of the leaets 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 leaet prolapse. Type III is leaet restriction and scarring. It is the most common pathol­ogy of the congenital regurgitant valve.
Regurgitation inPatients withCongenital Valvar Stenosis
The continued trauma to the leaet edges produced by hemo­dynamic stress and abnormal ow patterns results in pro­gressive scarring, thickening, deformity, and retraction of the leaet edges and subsequent lack of coaptation (type III).
Aortic Regurgitation Secondary toSubaortic Fibromuscular Stenosis
The abnormal blood ow pattern produced by the subaortic stenosis results in progressive deformity of the leaet. Tethering of the leaets by the subvalvar brous tissue, caus­ing obstruction, exaggerates the regurgitation (type III).
Regurgitation inMarfan 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 leaet edges. The increase in hemodynamic stress due to changes in the leaet suspension mechanism combined with an enlarged aortoventricular junction leads to poor leaet coaptation and central regurgitation (type I).
Postballoon Regurgitation
This condition is usually caused by leaet(s) tear close to the fused commissure. The leaet becomes ail and eccentric regurgitation results (types II and III).
Aortic Regurgitation Secondary toRheumatic Disease
There is cusp retraction secondary to inammation and scarring. The hemodynamic sequelae result in progressive annular dilation and worsening of the regurgitation (types II and III).
Timing ofSurgical 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
36 Aortic Valve Repair
https://t.me/med1917
451
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 renement 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 ofSurgical 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 leaet. In addition, 3D echocardiography helps in measuring leaf­let free edge, the depth of the sinus, and areas of tissue deciency 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 specic pathology types.
3. Reconstructive steps should be preceded by relief of
obstruction as completely as possible. All areas of leaet fusion or stenotic lesions should be relieved rst even if that reduces leaet support. Subsequent reconstructive steps of such leaets should aim at restoring the normal morphology, function, and support.
4. Isolated repair of only one leaet 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 leaets close to the aorto-ventricular zone are important to avoid the disrup­tion of the delicate and complex relationship between the root and leaet.
9. Continued root dilatation whether at the aorto- ventricular or sinotubular bar junction induces recurrent aortic insufciency 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 leaets and annulus. In addition, a centrally placed suture helps in evaluating the structure, the deciency, and the redundancy of the different cusps by trac­tion on the suture and pushing the leaets gently toward the ventricle.
Approach totheAorto-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. Signicant dilatation (Z+
2) impacts negatively on long-term outcome if not addressed at the time of valvuloplasty.
452
a
https://t.me/med1917
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 12–14mm/m2. It is benecial 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 monolament 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 [69] (Fig.36.2).
Surgical Approach totheAortic 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 leaet. 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 totheValve Cusps (Leaets)
Prolapse is managed by central plication of the leaet (Fig. 36.5). Triangular resection of the involved area is needed in cases with severe redundancy or calcication. 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 signicant dilatation of the sinotubular bar.
Reconstruction of the defective leaet is the cornerstone of any valvuloplasty. It involves thorough debridement and extensive but safe thinning of the effected leaet of all nodu­larities or calcication. An appropriately shaped patch that matches the irregular edge is then sutured to the leaet defective- free margin. More patch length than leaet length is sutured at the center of the cusp to give it the normal bulg­ing “cusp” conguration (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
36 Aortic Valve Repair
https://t.me/med1917
453
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 etal. [21]. Reprinted with permission from Elsevier)
Fig. 36.4 Augmentation technique for restrictive sinus of Valsalva.
(From ElZein etal. [21]. Reprinted with permission from Elsevier)
454
https://t.me/med1917
Fig. 36.5 Leaet plication using pledgeted sutures. (From ElZein
etal. [21]. Reprinted with permission from Elsevier)
C. Elzein et al.
Fig. 36.7 Patch augmentation of the defective leaets. The patch
width normalizes the leaet depth. Note the irregular edge of the patch. (From ElZein etal. [21]. Reprinted with permission from Elsevier)
Fig. 36.6 Suture plication of redundant leaets. The sutures are exteri-
orized at the commissures and tied. (From ElZein etal. [21]. Reprinted with permission from Elsevier)
Fig. 36.8 The reconstructed leaet is suspended at the ST junction.
(From ElZein etal. [21]. Reprinted with permission from Elsevier)
from nomograms, or an approximate estimate of cusp height of 10mm/m2 [13, 14]. The width of the patch is determined by subtracting the normal leaet depth from the actual depth of the defective leaet. Leaet augmentation should achieve central coaptation of 3–5mm in height [15, 16].
There is no ideal patch material. Several commercially available patches have been used. Most of these, however, develop brosis and calcication, limiting the functional life of the valvuloplasty. Autologous pericardial patient debrided thoroughly from all fat and adventitial tissue, treated with glutaraldehyde 0.625% for 2minutes and rinsed thoroughly has proven to be the best option.
36 Aortic Valve Repair
https://t.me/med1917
Surgical Approach totheSinotubular 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 leaets (Fig.36.10). Analter­native 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 leaet. 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 etal. [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 leaet 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, reects 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 signicant 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
456
C. Elzein et al.
https://t.me/med1917
with stiffening or calcication of the patch used for leaet 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 signicant 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 adults. Am J Cardiol. 1989;64:507–12.
3. DeCampli W. Ascending aortopathy with bicuspid aortic valve: more, but not enough, evidence for the hemodynamic theory. J Thorac Cardiovasc Surg. 2017;153:6–7.
4. Sharma V, Suri R, Dearani J, etal. Expanding relevance of aortic valve repair– is earlier operation indicated? J Thorac Cardiovasc Surg. 2014;147:100–8.
5. Suri R, Schaff H.Aortic valve repair: dening the patient popu­lation and timing of intervention. J Thorac Cardiovasc Surg. 2014;148:2477–8.
6. deKerchove L, Jashari R, Boodhwani M, etal. Surgical anatomy of the aortic root: implication for valve-sparing reimplanta­tion and aortic valve annuloplasty. J Thorac Cardiovasc Surg. 2015;149:425–33.
7. David T. Additional anatomic information on the aortic root. J Thorac Cardiovasc Surg. 2015;149:408–10.
8. Khelil N, Sleilaty G, Palladino M, et al. Surgical anatomy of the aortic annulus: landmarks for external annuloplasty in aortic valve repair. Ann Thorac Surg. 2015;99:1220–7.
9. Schneider U, Hofmann C, Aicher D, etal. Suture annuloplasty sig­nicantly improves the durability of bicuspid aortic valve repair. Ann Thorac Surg. 2017;103:504–10.
10. Schneider U, Schmied W, Aicher D, et al. Sinus plication to improve valve conguration in bicuspid aortic valve repair– early results. Ann Thorac Surg. 2017;103:580–6.
11. El Khoury G, Vanoverschelde JL, Glineur DM, etal. Repair of aor­tic valve prolapse: experience with 44 patients. Eur J Cardiothorac Surg. 2004;26:628–33.
12. Gleason T.To pleat or not to pleat…it that the question? J Thorac Cardiovasc Surg. 2017;153:239–40.
13. Schafers HJ, Schmied W, Marom G, etal. Cusp height in aortic valves. J Thorac Cardiovasc Surg. 2013;146:269–74.
14. Subramanian S, Tikhomirov V, Bharati S, et al. Relationship of normal aortic valve cusp dimensions: a tool to optimize cusp reconstruction valvuloplasty. Semin Thorac Cardiovasc Surg. 2016;28:521–7.
15. Rankin JS, Badhwar V.Design of replacement Leaets for the aortic valve. Semin Thorac Cardiovasc Surg. 2016;28:528–30 (editorial).
16. Maselli D, Weltert L, Scaffa R, et al. Differences in aortic cusp coaptation between the reimplantation and the remodeling tech­niques of aortic valve-sparing surgery: An invitro porcine model study. J Thorac Cardiovasc Surg. 2014;147:615–8.
17. Yousse P, Gomez A, He T, etal. Patient specic computational uid dynamics – assessment of aortic hemodynamics in a spec­trum of aortic valve pathologies. J Thorac Cardiovasc Surg. 2017;153:8–20.
18. Aicher D, Kunihara T, Abou Issa O, etal. Valve conguration deter­mines long-term results after repair of the bicuspid aortic valve. Circulation. 2011;123:178–85.
19. Ozarki S, Kawase I, Yamashita H, etal. A total of 404 cases of aortic valve reconstruction with glutaraldehyde-treated autologous pericardium. J Thorac Cardiovasc Surg. 2014;147:301–6.
20. Polimenakous AC, Sathanadan S, et al. Aortic Cusp Extension Valvuloplasty with or without tricuspidization in children and ado­lescents: long term results and freedom from aortic valve replace­ment. J Thorac Cardiovasc Surg. 2010;139:933–41.
21. ElZein C, Roberson D, Hammad N, Ilbawi M.Aortic valvuloplasty or rootplasty for aortic regurgitation. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2018;21:33–40.
Aortic Pseudoaneurysms
https://t.me/med1917
LeonieK.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, inammation, 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% 8years after cardiac surgery and 27% after 15years [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, inammation, and mycotic pseudoaneurysms secondary to tuberculosis (Table37.1) [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.
© 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_37
457