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Changes of cerebrospinal fluid pressure after thoracic endovascular aortic repair. | LitMetric

Changes of cerebrospinal fluid pressure after thoracic endovascular aortic repair.

Chin Med J (Engl)

Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, China.

Published: November 2013

AI Article Synopsis

Article Abstract

Background: Decreasing the intracranial pressure has been advocated as one of the major protective strategies to prevent spinal cord ischemia after endovascular aortic repair. However, the actual changes of cerebrospinal fluid (CSF) pressure and its relation with spinal cord ischemia have been poorly understood. We performed CSF pressure measurements and provisional CSF withdrawal after thoracic endovascular aortic repair, and compared the changes of CSF pressure in high risk patients and in patients with new onset paraplegia and paraparesis.

Methods: Four hundred and nineteen patients were evaluated for the risk of spinal cord ischemia after thoracic endovascular aortic repair. Patients with identified risk factors before the procedure constituted group H and received prophylactic sequential CSF pressure measurement and CSF withdrawal. Patients who actually developed spinal cord ischemia constituted group P and received rescue CSF pressure measurements and CSF withdrawal.

Results: Among the 419 patients evaluated, 17 were graded as high risk. Four patients actually developed spinal cord ischemia after endovascular repair. The incidence of spinal cord ischemia in this investigation was 0.9%. The patients who actually developed spinal cord ischemia had no identified risk factors and had elevated CSF pressure, ranging from 15.4 to 30.0 mmHg. Six of the 17 patients graded as high risk had elevated CSF pressure: >20 mmHg in two patients and >15 mmHg in four patients. Sequential CSF pressure measurements and provisional withdrawal successfully decrease CSF pressure and prevented symptomatic spinal cord ischemia in high-risk patients. However, these measurements could only successfully reverse the neurologic deficit in two of the patients who actually developed spinal cord ischemia.

Conclusions: Cerebrospinal fluid pressure was elevated in patients with spinal cord ischemia after thoracic endovascular aortic repair. Sequential measurements of CSF pressure and provisional withdrawal of CSF decreased CSF pressure effectively in high risk patients and provided effective prevention of spinal cord ischemia. Risk factor identification and prophylactic measurements play the key role in prevention of spinal cord ischemia after thoracic endovascular aortic repair.

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