| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2006;81:1348-1351
© 2006 The Society of Thoracic Surgeons
Cattedra di Cardiochirurgia, Università degli Studi di Milano, Policlinico MultiMedica, Milan, Italy
Accepted for publication September 30, 2005.
* Address correspondence to Dr Pocar, Via Pompeo Litta 2, Milan, 20122 Italy (Email: mpocar{at}milanocuore.org; mpocar{at}tiscali.it).
 |
Abstract |
|---|
 Top Abstract IntroductionPatients and MethodsResultsCommentReferences |
|---|
METHODS: Five comatose (median Glasgow coma score, 5.5), hemodynamically stable (systolic blood pressure 
100 mm Hg) patients with preserved pupillary reactivity and coma duration of less than 12 hours underwent emergency surgical repair. The ascending aorta was always replaced using profound hypothermic circulatory arrest.
RESULTS: There were no operative deaths. No hemorrhagic brain infarction developed postoperatively. Ischemic strokes were documented by radiology in 3 patients, and were always right-sided. Four patients returned to normal life with no neurologic sequelae, whereas 1 patient showed partially recovered left hemiparesis and mild cognitive impairment.
CONCLUSIONS: Coma may not represent an absolute contraindication for resuscitative surgery in hemodynamically stable patients with acute type A aortic dissection. A larger experience is necessary to draw more definitive conclusions.
|
Introduction |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
|---|
We describe and discuss our initial experience with emergency operation in selected patients with acute type A aortic dissection complicated by coma.
|
Patients and Methods |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
|---|
100 mm Hg), preserved pupillary reactivity, time interval within coma onset of less than 12 hours, and exclusion of intracranial hemorrhage or massive cerebral ischemia with severe edema and brainstem compression (see as follows). Four patients were referred from other hospitals. Coma was the presenting sign of aortic dissection in 3 patients, whereas 2 became unconscious approximately 1 hour after acute chest pain. All patients had acute type A dissection with the proximal intimal tear located in the ascending aorta and a distal abdominal or more peripheral extension. No patient had severe acidosis (pH < 7.3), electrolyte imbalance or other metabolic impairment suggestive for unrecognized hypotension with brainstem malfunction. Analgesic or sedative medications were also ruled out in this respect. Two patients experienced generalized seizures. Patients' characteristics and outcomes are summarized in Table 1.
|
-stat acid-base management) was used for the construction of an open distal anastomosis on the proximal arch. Selective antegrade cerebral perfusion at a 10 mL · Kg–1
· min–1 flow rate was used in 4 instances. Platelets were transfused after discontinuation of extracorporeal circulation and heparin reversal, whereas tranexamic acid was routinely used as an anti-fibrinolytic agent (15 mg · Kg–1 bolus prior to heparinization and 2.5 mg · Kg–1
· hr–1 infusion for 6 hours after protamine administration). Informed consent was obtained from the patients at the time follow-up data were collected.
|
Results |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
|---|
|
|
Comment |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
|---|
In our brief experience, all patients survived at operation and 80% recovered completely. This most probably represents a very optimistic result because operative mortality in larger cohorts of unselected patients range between 20% and 30% in tertiary referral centers [2, 3, 6]. In this respect, hemodynamic stability correlates well with a reduced probability of death and younger age affects the likelihood of a more favorable neurologic recovery. Furthermore, hemodynamic instability aggravates critical cerebral ischemia and is more commonly associated with alterations of pupillary reactivity. Conversely, severe brain damage with brainstem dysfunction generally causes hypotension. These aspects reflect our selection criteria.
During the same period, 29 emergency operations for acute type A dissection were performed, whereas 3 patients with dissection and coma were refused for surgery (2 from our institutional emergency department and 1 from a different hospital), in relation to a compromised pupillary reactivity or to a deteriorating hemodynamic status with prolonged hypotension and shock, or to both. However this number could be underestimated, because very critical patients may not be referred to a cardiovascular surgical team in time, especially if they are initially admitted to emergency units of hospitals without a local cardiovascular surgery unit. Our criteria for operability did not consider age per se, but admittedly most patients were younger than 60 years of age. Also, we prospectively adopted the policy to operate on selected comatose patients with acute type A aortic dissection on an emergency basis after observing a positive outcome in the first patient (July 2000). The latter was considered for resuscitative surgery in view of his relatively young age, and thus of a higher potential for recovery. Although we would hesitate to operate on patients older than 75 years of age, the other anecdotal report in the literature describes a successful repair, which also included partial arch reconstruction with innominate artery reimplantation in a 79-year-old man [5].
Intracranial hemorrhage or other pre-existing cerebral diseases were preoperatively ruled out with computed tomography. Furthermore, signs of severe brain edema or increased intracranial pressure with brainstem compression reflect the magnitude and often the duration of global brain ischemia, and in our opinion contraindicate early surgery (as previously mentioned). As a result, patients in this series who were operated on within 12 hours from the onset of coma had substantially normal preoperative brain scans. In this context, the distinction between global versus focal ischemia in an acute setting is difficult, and the severity of the ischemic insult represents an important issue because an established infarct can be worsened by reperfusion. However, neurologic risks should be balanced with the risk of aortic rupture. We excluded patients with coma duration greater than 12 hours who are likely to have a lower potential for neurologic recovery, and possibly a lower probability of impending aortic rupture. Interestingly the Glasgow coma score, which was originally developed to stratify the probability of functional recovery after head trauma, seems of little value in this context. In fact all patients would have been classified with severe brain injury (ie, with a Glasgow coma score 
8), but they showed a dramatic improvement when compared with the predicted probability of recovery in neurogically similar trauma patients. More specifically, only 1 patient had permanent signs of global brain hypoperfusion and cognitive dysfunction postoperatively.
A focal stroke could be radiologically documented in 3 of 5 cases, and lesions never involved the left cerebral hemisphere. Strokes thus seem related to a somewhat more severe involvement of the innominate artery in the malperfusion process with respect to the contralateral vessels. Pupillary reactivity served as a major criterion to define the presence of preserved brainstem function. Doppler flow evaluation of the supraaortic trunks could further help to identify the degree of malperfusion in different territories, but would require additional time, and this was not performed preoperatively. It is thus impossible to determine the impairment of arterial flow in the vertebro-basilar system specifically. Speculatively, however, the origins of the left carotid and subclavian arteries from the aortic arch were also compressed by the false lumen, because unilateral involvement of the innominate artery alone is insufficient to produce brainstem hypoperfusion and coma in the absence of systemic hypotension or circulatory collapse, or other cause of coma on an extravascular basis. An intraoperative embolic (iatrogenic) mechanism cannot be excluded to explain the right-sided ischemic lesions. However, this seems unlikely because transient or permanent left-sided motor impairment was observed in all cases. Although residual and partially thrombosed residual false channels were often visible (Fig 1C), postoperative Doppler ultrasound showed normal perfusion flow patterns in the supraaortic trunks after surgical repair, possibly because the intimal tear was always located in the ascending aorta and completely resected. In view of the desperately critical state of these patients, it is difficult to suggest a more aggressive aortic operation with respect to a potential short-term benefit, (ie, in relation to the postoperative neurologic outcome). However, it can be inferred that a more extensive resection may be justified if the intimal tear involves the aortic arch.
In comatose patients, the risk of perioperative intracranial bleeding may be increased with high-dose heparinization (3 mg/Kg initial intravenous bolus, activated clotting time 480 secs). Prolonged cardiopulmonary bypass also determines an inflammatory response and platelet dysfunction, especially at lower temperatures. We observed no hemorrhagic infarction or severe brain edema postoperatively, but the prevalence can be higher with longer intervals before surgical repair or in older patients [5]. Furthemore, the administration of antifibrinolytic agents is important to reduce bleeding complications, and we routinely administer tranexamic acid to cardiovascular surgical patients for this purpose. In this respect, although benefits are somewhat more controversial in cases of hypothermic circulatory arrest, aprotinin has been shown to reduce perioperative cerebrovascular accidents after cardiac operations, possibly in relation to specific anti-inflammatory mechanisms, and could represent a first-choice drug in spite of higher costs [7, 8]. However, we have no experience applied to aortic dissection with cerebral ischemia, because in recent years aprotinin has been commercially unavailable in Italy in relation to the concerns of bovine spongiform encephalopathy. Finally, routine platelet availability after discontinuation of extracorporeal circulation could represent an additional pitfall.
Anecdotal reports describe neurologically successful resuscitation with extracorporeal perfusion and rewarming in patients with body temperatures as low as 13.7°C due to accidental hypothermia [9]. The role of current cerebral protective strategies in this context, especially selective arterial perfusion techniques, is difficult to define in a small series. However, the worst outcome was observed when hypothermic circulatory arrest was used without adjuncts. This could be related to an additional ischemia-reperfusion injury after the initial ischemic insult. We always applied deep hypothermic regimens, but higher core temperatures may provide adequate protection when associated with selective cerebral perfusion. This strategy could reduce the duration and overall impact of cardiopulmonary bypass in neurologically compromised patients.
In conclusion, initial experience suggests that coma may not represent an absolute contraindication for resuscitative surgery with contemporary techniques in hemodynamically stable patients with acute type A aortic dissection, provided that operation is performed expeditiously after the onset of brain malperfusion. Further experience and a better understanding of dissection-related brain malperfusion pathophysiology are needed to extrapolate initial observations in these critically ill patients.
|
References |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. Ando, K. Imanaka, H. Yamabi, and H. Sato Successful emergency surgery for coexistent acute aortic syndrome and acute carotid artery obstruction. J. Thorac. Cardiovasc. Surg., September 1, 2009; 138(3): 771 - 773. [Full Text] [PDF]
|
|
|
|
|
|
R. Zegdi, B. Amahzoune, P. Achouh, C. Latremouille, A. Deloche, and J.-N. Fabiani Periaortic glue application may prevent fatal aortic rupture in nonoperable patients with acute type A aortic dissection. J. Thorac. Cardiovasc. Surg., November 1, 2007; 134(5): 1349 - 1350. [Full Text] [PDF]
|
|
|
|
|
|
M. Pocar, D. Passolunghi, A. Moneta, and F. Donatelli Immediate surgery in aortic dissection with cerebral malperfusion J. Thorac. Cardiovasc. Surg., June 1, 2007; 133(6): 1684 - 1685. [Full Text] [PDF]
|
|
|
|
|
|
A. L. Estrera and H. J. Safi Reply to the Editor J. Thorac. Cardiovasc. Surg., June 1, 2007; 133(6): 1685 - 1685. [Full Text] [PDF]
|
|
|
|
|
|
A. L. Estrera, Z. Garami, C. C. Miller, E. E. Porat, P. E. Achouh, J. Dhareshwar, R. Meada, A. Azizzadeh, and H. J. Safi Acute type A aortic dissection complicated by stroke: Can immediate repair be performed safely? J. Thorac. Cardiovasc. Surg., December 1, 2006; 132(6): 1404 - 1408. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. N. Girardi Invited commentary Ann. Thorac. Surg., April 1, 2006; 81(4): 1351 - 1352. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |
