Résumé
We report a rare case of paraplegia after emergency total arch replacement for type A acute aortic dissection. A 52-year-old man was referred to our hospital for acute aortic dissection. Contrast-enhanced computed tomography showed a type A aortic dissection extending from the aortic root into the right iliac arteries. The true lumen of the descending and abdominal aorta was collapsed and blood flow to the right lower limb had decreased. Large entry and re-entry tears were revealed in the ascending and distal arch aorta, respectively. His preoperative consciousness was clear, hemodynamics were stable, and there was no evidence of paraplegia or paraparesis. Extracorporeal circulation was established by femoral artery and right atrium cannulation. Total arch replacement was performed under moderate hypothermic circulatory arrest (lowest bladder temperature : 21.9°C). The postoperative course was uneventful and he was extubated 6 h postoperatively. Postoperative hemodynamic parameters were stable, the mean blood pressure was maintained at around 70 mmHg, and limb movements were confirmed at that time. Although there was no abnormality of lower limb movement until the following morning, paraplegia occurred about 17 h after surgery. While maintaining a mean blood pressure of over 90 mmHg, urgent cerebrospinal drainage was immediately performed and combined with steroid treatment and a continuous infusion of naloxone. The neurological defect was resolved immediately after cerebrospinal drainage, and neurological function steadily improved through rehabilitation. He was discharged 20 days after surgery with no neurological defects. Late paraplegia after total replacement for type A acute aortic dissection is a rare complication. From our experience, it is suggested that early diagnosis and treatment are important for improving paraplegia.
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Objective To explore the mechanism of neuropmtective effects of puerarin for the treatment of acute spinal ischenia-reperfusion injury in a rat model.Methods Acute spinal ischemia-reperfusion injury was induced via aortic occlusion in 28 male Sprague-Dawley rats.The animals were randomly divided into four groups,as follows:group negative contrast (NC sham operation),group positive control group (IR+ S ischemia/reperfusion + saline),group puerarin (IR+P ischemia/reperfusion + puerarin),group mscovitine (IR+R ischemia/reperfusion + roscovitine).The motor function,spinal infarction volume,apoptosis indices,and CDK5 and P25 activities were examined.Results Spinal ischemia-reperfusion caused the injury of the spines and was associated with motor deficit,elevation of CDK5 and P25 activities,and increase in the spinal apoptosis and spinal infarction volume.Puerarin improved motor function and decreased apoptosis,spinal infarction volume,and CDK5 and P25 activities.Conclusion The findings of the present study indicated that puerarin treatment-mediated reduction of spinal injury was associated with the inhibition of CDK5 and P25,and that the inhibition was one among the neuroprotective mechanisms of puerarin against acute ischemia/reperfusioninduced spinal injury in rats.
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Aims: Dexmedetomidine, anα2adrenergicagonist, provides neuroprotection in various cerebral ischemia models and against anesthesia-related neurotoxicity. Dexmedetomidine also improves paraplegia induced by intrathecal morphine after short-term spinal ischemia. In this preliminary study, we investigated whether dexmedetomidine provides spinal protection against transient spinal ischemia in rats. Methodology: Adult male Sprague-Dawley rats were randomly divided into the following 3 groups: 1) intravenous infusion of 0.9% NaCl at a rate of 0.5 mL/h (control), 2) dexmedetomidine 1 μg/kg/h, and 3) intravenous infusion of 0.9% NaCl without spinal ischemia (sham). The rats received saline solution or dexmedetomidine 30 min before spinal cord ischemia and for 24 h. Spinal cord ischemia was induced by intra-aortic balloon occlusion combined with proximal arterial hypotension for 10 min. Ischemic injury was assessed by the neurological deficit score and by the number of viable motor nerve cells in the anterior spinal cord at 24 h of reperfusion. Results: The neurological deficit score was significantly lower in the dexmedetomidine group compared to the control group (p< 0.05). The number of viable motor nerve cells in the dexmedetomidine group was significantly greater than was that in the control group (p< 0.05), but was lower than was that in the sham group.Conclusion: Our findings suggest that continuous administration of dexmedetomidine ameliorates short-term neurological and histological outcomes induced by transient spinal cord ischemia and reperfusion in rats; thus, dexmedetomidine appears to protect the spinal as well as the brain.
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We report a rare case of type A acute aortic dissection with paraplegia which was cured immediately after an emergency operation. A 79-year-old woman was transferred to our institution with sudden back pain and paraplegia. Computed tomographic scans revealed a cardiac tamponade with an acute type A aortic dissection. She went into shock soon after arrival, and about 4 hours from onset we performed an emergency replacement of the ascending aorta. Three hours after the operation, her neurological deficit gradually resolved and could walk by postoperative day 3. This case suggests that early restoration of the blood flow to the spinal cord is mandatory to relieve paraplegia caused by type A aortic dissection.
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BACKGROUND: Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. Excitatory amino acids have been known to cause neurologic injury after neuronal ischemia. The purpose of this study was to elucidate the effects of intrathecal ketamine or NBQX on neurologic outcome and NMDA receptor gene expression in transient spinal ischemia. METHODS: Sprague-Dawley rats were anesthetized with enflurane, divided by 4 groups: Control (C group), Intrathecal ketamine 0.1 mg (K-1 group), Intrathecal ketamine 0.2 mg (K-2 group), and intrathecal NBQX 1 nM (N group). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. After spinal ischemia, neurologic scores were assessed after 1, 2, 3 hours. After 3 hours rats were euthenized and spinal cords were removed for the assay of NMDAR and mGlu1 mRNA. RESULTS: The neurol ogic scores of K-2 and N groups were significantly lower than C group and K-1 group. There were no significant difference between K-1 group and C group. The NMDAR and mGlu1 gene expression was increase in C and K-1 group compared to sham operation. In K-2 and N groups, the gene expressions were significantly lesser than C group. CONCLUSIONS: The NMDAR and mGlu1 gene expressions were increased in transient spinal ischemia. Intrathecal ketamine and NBQX were effective in preventing neurologic injury after transient spinal ischemia. The NMDA antagonistic action of ketamine might involve to prevent neurologic injury.