Ann Thorac Surg 1998;66:1370-1371
© 1998 The Society of Thoracic Surgeons
Original articles: cardiovascular
Invited commentary
Joseph J. Amato, MDa
a Section of Pediatric Cardiovascular Surgery, Rush-Presbyterian-St. Luke’s Medical Center, 1653 W Congress Pkwy, Chicago, IL 60612-3833, USA
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Invited commentary
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Doctor Backer and his associates have presented in this article the concept that repair of coarctation of the aorta with resection and extended end-to-end anastamosis is their procedure of choice for infants with this lesion. The basis for this conclusion in their series of 55 patients with this repair is supported by a low mortality rate of 1.8% and low recoarctation rate of 3.6%. Although in the majority of these children the repair was performed through a standard left posterolateral thoracotomy, 38% of these were operated on through a median sternotomy. Their patients were categorized into three groups, which consisted of (1) isolated coarctation in 26 patients, (2) coarctation with a ventricular septal defect in 20 patients, and (3) coarctation with associated intracardiac lesions in 9 patients. Both early and later deaths occurred only in the groups with coarctation and ventricular septal defect or coarctation with associated anomalies. There were no deaths in the isolated coarctation group. My comments on this article will focus on three specific issues, which are as follows: - I take issue with Dr Backer and his colleagues with the method of the extended end-to-end anastamosis repair. They state that "adequate (but not excessive) mobilization of the descending thoracic aorta is obtained by dividing intercostal collaterals ... In most cases we have found it useful to ligate and divide three sets of collaterals ... to provide adequate mobility of the descending thoracic aorta." They also state that "in some cases as many as five sets of collaterals were divided." The ligation and division of these collaterals is disturbing to me. An extensive review of the literature written on the techniques for repair of coarctation of the aorta states that caution must be taken to gently mobilize and preserve the intercostal arteries. Doctor Kirklin, in his textbook, states that one should avoid damage to the intercostal arteries. Doctor Castañeda, in his textbook, states that in the dissection of the distal aorta, control of these vessels should be done gently, whether by metallic clips or by tourniquets, which are to be removed upon completion of repair. Other surgeons state that on occasion the sacrifice of one or two intercostal collaterals may be necessary; however, every effort should be made to perform adequate anastamosis with division or clamping of as few intercostal collaterals as possible. Having said the above, nowhere in the literature did I find any correlation between paralysis and the number of intercostal vessels that were sacrificed. Most articles refer to the classic report presented by Dr Lyman Brewer in 1972, in which he documents that neither the length of aortic cross-clamp time nor the number of intercostals that were sacrificed made any difference in the cases of paralysis that occurred. This classic report was compiled from responses to letters that were sent to leading thoracic surgeons in the United States. Through a study of 12,000 cases, there was a reported incidence of 0.41% of paralysis resulting from repair of coarctation of the aorta. Doctor Brewer’s study determined that 91% of those patients without spinal cord injury had four or more intercostal collaterals divided or clamped during the procedure. Doctor Backer restates these facts in the chapter on coarctation in the sixth edition of Glenn’s Thoracic and Cardiovascular Surgery. He also states that paraplegia is a possible complication of coarctation repair. The condition of paraplegia remains a very serious and feared complication. It carries with it life-long implications not only for the child, but also for the parents. Therefore, if neither length of cross-clamp time nor number of intercostal arteries divided can prove to be statistically significant, we are to then look for some other cause of paraplegia. There is no doubt that it is multifactorial and still remains unclear. Contrary to Dr Brewer’s findings in 1972, excessive cross-clamp time has been listed as a potential cause of paraplegia. During the period of cross-clamping, the blood supply to the lower extremities is partially provided by the collaterals. Normally there are 11 pairs of intercostal arteries. If cross-clamping occurs at T-3 or T-4, there are seven or eight intercostal arteries to supply the lower body. Ligating and dividing three to five sets of intercostal arteries would greatly diminish the flow of blood to the lower extremities, which could potentially cause paraplegia. I suggest that the factors that are necessary to consider to avoid paraplegia include the following: (1) the duration of spinal cord ischemia, (2) the duration of intercostal artery ischemia, (3) interoperative proximal hypotension, (4) postoperative hypotension, (5) hyperthermia during the operation, (6) careful technique to avoid anastamosis with tension, and (7) avoidance of acidosis in the operative and postoperative period.
- A second issue is the statement of "our procedure of choice for infants with coarctation of the aorta." I would maintain that the surgeon must not be intellectually inflexible. We have stated that the anatomicopathologic condition or morphology in each patient should dictate the method of repair. Of the numerous repairs in the surgeon’s armamentarium, the preferred choices have been simple end-to-end anastamosis, subclavian aortoplasty, and finally the end-to-end anastamosis with extended modifications. All of these methods have advantages and disadvantages, which have been described a number of times. The final determination of success is measured by low mortality, low morbidity, and the rate of recoarctation. If one were to weigh on the scale of importance the complexities of the end-to-end resection with extended repair, one may choose to accept a less extensive procedure. We know that recoarctation can develop after the use of any and all surgical techniques. We are now in an era in which recoarctation can be addressed by interventional pediatric cardiologists and that balloon angioplasty in recoarctation is not only accepted, but very successful. Therefore, I would urge the readers to become flexible in the technical factors of the operation and consider the procedure of choice to be that which would be the simplest procedure tolerated by the infant or child and familiar to the surgeon performing the procedure.
- The third issue is that of classification of coarctation. In the beginning of this article, Backer and associates divided their patients into three specific groups. In 1991 my colleagues and I presented a classification of coarctation of the aorta [1] that divided it into three types: (1) coarctation alone, (2) coarctation with ventricular septal defect, and (3) coarctation with other major defects. We further divided these groups into three anatomic types: (1) discrete coarctation, (2) coarctation including the isthmus, and (3) coarctation with hypoplasia of the arch. In doing so we can separate out not only the morbidity of each type and the rate of recoarctation but also early and late mortality of each subgroup. The choice of anatomic repair would appear to be easier if one considers the above variable associated factors in the spectrum of coarctations.
I congratulate Dr Backer and his colleagues on an excellent study with excellent results, but also have felt compelled to address the division and ligation of more than one or two intercostal blood vessels, which should be performed only if and when necessary.
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References
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- Amato J.J., Galdicri R.J., Cotroneo J.V. Role of extended aortoplasty related to the definition of coarctation of the aorta. Ann Thorac Surg 1991;52:615-620.[Abstract/Free Full Text]
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Invited commentary
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