JTCS Speed Up Your Browser
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Ruggero De Paulis
Alessandro Ricci
Luigi Chiariello
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by De Paulis, R.
Right arrow Articles by Chiariello, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by De Paulis, R.
Right arrow Articles by Chiariello, L.

J Thorac Cardiovasc Surg 1994;108:788-789
© 1994 Mosby, Inc.


LETTERS TO THE EDITOR

Type A aortic dissection: Management of brain malperfusion through retrograde cerebral perfusion

Ruggero De Paulis, MD, Dionisio F. Colella, MD, Carlo Bassano, MD, Alessandro Ricci, MD, Luigi Chiariello, MD

Departments of Cardiac Surgery and Anesthesiology
Tor Vergata University of Rome
Rome, Italy

To the Editor:

Antegrade organ malperfusion, and particularly cerebral malperfusion, is a life-threatening complication of acute aortic dissection that is due to an impaired flow in either the true or the false lumen. However, cerebral malperfusion can also occur at the time of surgical repair. This may be a consequence of the reversed flow from the femoral artery on initiation of cardiopulmonary bypass if no entry site is present in the ascending aorta; it may also appear when the intimal tear in the proximal ascending aorta is excluded at the moment the crossclamp is applied or when the surgical repair is completed. In the first two instances the problem is managed either by repositioning the arterial cannula into the true aortic lumen or fenestrating the membrane within the proximal arch Go 1 or, whenever possible, by pharmacologically maintaining an adequate pressure as systemic hypothermia is induced. Go 2 In the last case the problem is solved by reestablishing an antegrade perfusion via the ascending aortic graft. Go 3 Herein we present a case of cerebral malperfusion that was successfully managed by selective retrograde cerebral perfusion through the right internal jugular vein.

A 56-year-old woman was admitted with unreceding chest pain. Echocardiography and magnetic resonance imaging studies showed a type A aortic dissection with the two lumina extending from the proximal ascending aorta through to the abdominal aorta, as well as severe aortic valve insufficiency. All peripheral pulses were present. The patient underwent urgent surgical treatment. The left femoral artery did not have evidence of dissection and was cannulated for cardiopulmonary bypass. The right atrium was cannulated for venous return. Cardiopulmonary bypass was started and, on occurrence of ventricular fibrillation, the aorta was crossclamped. A few seconds after crossclamping of the aorta, at a core temperature of 32° C, sudden bilateral mydriasis developed, suggesting impaired cerebral perfusion. At the same time, the mean right radial artery pressure dropped suddenly. A self-inflating balloon cannula was inserted high into the internal jugular vein via the right atrium. The cannula was then connected with an arterial line to the heart-lung machine. A retrograde cerebral perfusion with oxygenated blood flowing in a retrograde direction through the jugular vein and thus to the brain was begun. The retrograde cerebral blood flow was maintained at 200 to 250 ml/min with a mean pressure of 25 mm Hg while the patient was cooled, the aortotomy performed, the aortic valve resuspended, and the proximal aortic anastomosis completed (45 minutes). Then, during deep hypothermic circulatory arrest, the aortic clamp was released and the distal aorta closely inspected. A single intimal tear was present 2 cm above the coronary ostia; no intimal tears were present in the aortic arch. Good back blood flow from the left common carotid artery and the innominate artery was evident. During the period of deep hypothermic (18° C) circulatory arrest (36 minutes), the arch anastomosis was performed. Blood samples simultaneously drawn from a side port of the cerebral perfusion cannula (arterial inflow) and from the back bleeding from the left carotid and innominate arteries (venous outflow) at the beginning of circulatory arrest were sent for arterial blood gases measurements. The results showed an oxygen extraction of 3.3 ml/dl throughout the brain. The postoperative course was uneventful and the patient awoke 6 hours after the operation. The way in which she awoke and behaved was within normal limits.

Encouraged by reported data, Go 4 we have recently been using retrograde cerebral perfusion during hypothermic circulatory arrest, and we are impressed by our good results. Therefore, faced with the sudden appearance of cerebral malperfusion, we thought that any neurologic sequelae could be prevented by a selective retrograde perfusion of the brain through the superior vena cava. The presence of cerebral malperfusion was suspected only on the basis of clinical findings; we do not have any direct anatomic evidence, as elegantly demonstrated by Neustein and associates. Go 2 Nevertheless, we think that the sudden occurrence of bilateral mydriasis associated with a fall in the right radial pressure at the time of aortic crossclamping is strongly suggestive of an impaired cerebral perfusion. Furthermore, monitoring of right radial versus femoral artery pressure is the most commonly used, although indirect, method to unveil a deficit of brain perfusion. A delay in correcting this anatomic condition diagnosed simply on the basis of this indirect method has been reported to lead to cerebral deficit or death. Go 1

We cannot state, on the basis of this clinical case, that the good surgical outcome is ascribed only to the use of retrograde cerebral perfusion before and during the period of circulatory arrest. Nonetheless, we can consider that our patient underwent 45 minutes of a somewhat impaired cerebral perfusion when the body temperature was well above the degree recommended for safe cerebral protection, followed by 36 minutes of total circulatory arrest at a temperature of 18° C. Given the patient's good outcome, it is possible that a cerebral perfusion sufficient for the brain's metabolic needs was always assured throughout the surgical procedure. Doubts remain regarding the retrograde cerebral blood path during the period preceding circulatory arrest. The cerebral venous outflow cannot be drained from the left carotid and innominate arteries, as during the period of circulatory arrest when the aortic arch is wide open. Then, given the fact that jugular venous pressure was always constant at values of 20 mm Hg during the retrograde perfusion, we can assume that the only cerebral drainage path was through the left jugular venous system. This latter aspect will need to be resolved if the reproducibility of the method is to be assessed.

If the findings herein reported can be confirmed in the future, retrograde cerebral perfusion could be considered another technical therapeutic option when cerebral malperfusion, occurring during aortic surgery, needs to be promptly corrected. This experience may help to provide some insights to the understanding of the efficacy and safety of retrograde cerebral perfusion during circulatory arrest.

References

  1. Borst HG, Laas J, Heinemann M. Type A aortic dissection: diagnosis and management of malperfusion phenomena. Semin Thorac Cardiovasc Surg 1991;3:238-41.[Medline]
  2. Neustein SM, Lansman SL, Quintana CS, Suriani R, Ergin A, Griepp RB. Transesophageal Doppler echocardiographic monitoring for malperfusion during aortic dissection repair. Ann Thorac Surg 1993;56:358-61.[Medline]
  3. Parr GVS, Manley NJ, Williams DR, et al. Obstruction of the true lumen during retrograde perfusion of type I aortic dissection: a simplified solution. Ann Thorac Surg 1980;30:495-8.[Abstract]
  4. Safi HJ, Brien HW, Winter JN, et al. Brain protection via cerebral retrograde perfusion during aortic arch aneurysm repair. Ann Thorac Surg 1993;56:270-6.[Abstract]



This article has been cited by other articles:


Home page
Ann. Thorac. Surg.Home page
H. Tanaka, K. Okada, T. Yamashita, Y. Morimoto, Y. Kawanishi, and Y. Okita
Surgical Results of Acute Aortic Dissection Complicated With Cerebral Malperfusion
Ann. Thorac. Surg., July 1, 2005; 80(1): 72 - 76.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Ruggero De Paulis
Alessandro Ricci
Luigi Chiariello
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by De Paulis, R.
Right arrow Articles by Chiariello, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by De Paulis, R.
Right arrow Articles by Chiariello, L.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS