Ann Thorac Surg 2003;76:1293-1295
© 2003 The Society of Thoracic Surgeons
Case report
Thrombolytic therapy for delayed, in-hospital stroke after cardiac surgery
Ikuo Fukuda, MD*a,
Tomohiro Imazuru, MDb,
Motoo Osaka, MDb,
Ko Watanabe, MDb,
Kotoo Meguro, MDc,
Mitsuyosi Wada, MDd
a Department of Surgery I, Hirosaki University School of Medicine, Hirosaki, Aomori, Japan
b Department of Cardiovascular Surgery, Tsukuba Medical Center Hospital, Japan
c Department of Neurosurgery, Tsukuba Medical Center Hospital, Japan
d Department of Radiology, Tsukuba Medical Center Hospital, Tsukuba, Ibaraki, Japan
Accepted for publication February 15, 2003.
* Address reprint requests to Dr Fukuda, Department of Surgery I, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori, 036-8562 Japan
e-mail: ikuofuku{at}cc.hirosaki-u.ac.jp
 |
Abstract
|
|---|
Five patients who had delayed stroke after cardiac surgery underwent intraarterial administration of a fibrinolytic agent for thromboembolism (n = 4) or thrombosis (n = 1) of the cerebral artery. Complete recanalization of the occluded artery was obtained in 3 patients and partial recanalization in 2. Additional angioplasty for basilar artery stenosis was performed in 1 patient. No patients exhibited rebleeding into the pericardial space or wound bleeding. All patients survived with moderate or full functional recovery. Immediate cerebral angiography and local thrombolysis may improve functional outcome and survival in patients with postcardiotomy cerebral thromboembolism.
|
Introduction
|
|---|
Postoperative stroke is a devastating complication after cardiac surgery. Although the incidence is low, treatment of postoperative cerebral thromboembolism is challenging. We evaluated the results of aggressive strategy with early diagnosis and local administration of fibrinolytic agent for stroke after cardiovascular surgery.
We performed intraarterial thrombolysis for 5 in-hospital patients with delayed stroke after cardiovascular surgery. Stroke occurred 2 to 8 days (average, 6.8 ± 2.8 days) after surgery. All of these patients were free from neurologic deficits in the immediate postoperative period. Intracranial hemorrhage and completed cerebral infarction were excluded by computed tomography of the brain. Then cerebral angiography was performed immediately in all patients. Immediate cerebral angiography revealed cerebral embolism in 4 patients and cerebral thrombosis in 1 with occlusion of the major intracranial arteries. The average interval between onset of symptoms and cerebral angiography was 3.0 ± 0.7 hours (range, 2 to 4 hours) (Table 1).
Local intraarterial administration of a thrombolytic agent through a catheter monitored by repeat angiography was carried out in all patients, and mechanical destruction of embolus was attempted in 1 patient. Recanalization of the occluded artery was obtained by intraarterial administration of urokinase in a total dose of 48 or 96 x 104 units. Complete recanalization of the occluded artery was achieved in 3 patients (60%) and partial recanalization in 2 (40%). Although a tiny hemorrhagic cerebral infarction, which had been detected by the computed tomography, occurred in 1 patient (patient 3), neurologic improvement was satisfactory. In patient 5, additional balloon angioplasty for residual stenosis of the basilar artery was performed 1 week after fibrinolytic therapy (Fig 1).
Although 1 patient underwent resternotomy and refixation because of sternal dehiscence, no patients exhibited rebleeding into the pericardial space or wound bleeding. Blood transfusion was necessary in patient 5.
View larger version (112K):
[in this window]
[in a new window]
|
Fig 1. Cerebral angiogram in patient 5 (A) before local thrombolysis and (B) after local thrombolysis.
|
|
Almost full functional recovery was attained in 3 patients (60%) with complete recanalization and moderate disability remained in 2 patients (40%).
|
Comment
|
|---|
Acute occlusion of major cerebral arteries caused by thromboembolism induces large cerebral infarction accompanied by consequential severe, fatal swelling of the brain [1, 2]. Immediate restoration of cerebral blood flow within a short period after cerebral infarction may improve morbidity and mortality [3]. Intraarterial administration of a fibrinolytic agent has been shown to extend the window of therapy to 6 hours from onset of stroke. In the PROACT study, partial recanalization was significantly greater in a local administration of a pro-urokinase group than a placebo group, whereas the incidence of intracranial hemorrhagic deterioration was the same [4]. Several large series of patients treated by local thrombolysis with urokinase or tissue plasminogen activator reported complete or partial recanalization in 74% of the patients, higher than that of the intravenous administration, with a lower incidence of symptomatic intracranial hemorrhage than that reported for the intravenous thrombolysis [5]. These results suggest potential benefits and acceptable safety of intraarterial thrombolysis.
Use of fibrinolytic agents may induce hemorrhagic infarction, accompanied by acute expansion of the lesion and surrounding edema, resulting in functional deterioration and death. Interval between onset and reperfusion is an important predictor for hemorrhagic infarction.Because the interval between the onset and angiography was short in our patients, neurologic improvement was marked because of early recanalization of the occluded cerebral artery. Although 1 patient showed a small hemorrhagic infarction on computed tomography, brain swelling was minimal and moderate functional recovery was obtained.
Another concern of using a fibrinolytic agent is the risk of rebleeding from the surgical wound. Moazami and colleagues [6] reported the effectiveness of intraarterial thrombolysis in 13 cardiac surgery patients with recanalization and neurologic improvement rates of 46% and 38%, respectively, and no patient exhibited surgical wound rebleeding. In local thrombolysis, the dose of the fibrinolytic agent could be reduced to the minimum amount required to recanalize the target arteries. Direct intervention to the occluded cerebral artery is also possible when immediate cerebral angiography can be performed, as in patient 4. In patient 5, delayed additional angioplasty was also efficacious.
In conclusion, local thrombolytic therapy for cerebral thromboembolism may reduce mortality and improve functional prognosis without serious complications in patients after cardiovascular operations.
|
References
|
|---|
- Hinchey J.A., Furlan A.J., Barnett H.J.M. Cardiogenic brain embolism: incidence, varieties, and treatment. In: Barnett H.J.M., Mohr J.P., Stein B.M., Yatsu F.M., eds. Stroke, 3rd ed. New York: Churchill Livingstone, 1998:1087-1119.
- Lodder J., Krijne-Kubat B., Broekman J. Cerebral hemorrhagic infarction at autopsy: cardiac embolic cause and the relationship to the cause of death. Stroke 1986;17:626-629.[Abstract/Free Full Text]
- Hacke W., Kaste M., Fieschi C., et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. JAMA 1995;274:1017-1025.[Abstract/Free Full Text]
- del Zoppo G.J., Higashida R.T., Furlan A.J., Pessin M.S., Rowley H.A., Gent M. PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. PROACT Investigators. Prolyse in acute cerebral thromboembolism. Stroke 1998;29:4-11.[Abstract/Free Full Text]
- Brott T.G., Hache W. Thrombolytic and defibrinogenating agents for ischemic and hemorrhagic stroke. In: Barnett H.J.M., Mohr J.P., Stein B.M., Yatsu F.M., eds. Stroke, 3rd ed. New York: Churchill Livingstone, 1998:1155-1176.
- Moazami N., Smedira N.G., McCarthy P.M., et al. Safety and efficacy of intraarterial thrombolysis for perioperative stroke after cardiac operation. Ann Thorac Surg 2001;72:1933-1939.[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
A. Aleu, P. Mellado, C. Lichy, M. Kohrmann, and P. D. Schellinger
Hemorrhagic Complications After Off-Label Thrombolysis for Ischemic Stroke
Stroke,
February 1, 2007;
38(2):
417 - 422.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
