Risk of spinal cord dysfunction in patientsundergoing thoracoabdominal aortic replacement

Hollier, Larry H.; Money, Samuel R.; Naslund, Thomas C.; Procter, Charles D.; Buhrman, William C.; Marino, Robert J.; Harmon, Donald E.; Kazmier, Francis J.

doi:10.1016/s0002-9610(05)81072-4

Cited by 211 publications

(6 citation statements)

References 14 publications

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“…Mention must be made of incidence of SCI that occurs as a complication arising from surgery for thoracic or abdominal aortic aneurysms during the procedure to repair the damaged aorta (Hollier et al, 1992 ). Prolonged aortic cross-clamping or ligation of intercostal or lumber arteries proceeds to spinal cord ischemia.…”

Section: Introductionmentioning

confidence: 99%

Inflammogenesis of Secondary Spinal Cord Injury

Anwar

Shehabi

Eid

2016

Front. Cell. Neurosci.

355

258

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Spinal cord injury (SCI) and spinal infarction lead to neurological complications and eventually to paraplegia or quadriplegia. These extremely debilitating conditions are major contributors to morbidity. Our understanding of SCI has certainly increased during the last decade, but remains far from clear. SCI consists of two defined phases: the initial impact causes primary injury, which is followed by a prolonged secondary injury consisting of evolving sub-phases that may last for years. The underlying pathophysiological mechanisms driving this condition are complex. Derangement of the vasculature is a notable feature of the pathology of SCI. In particular, an important component of SCI is the ischemia-reperfusion injury (IRI) that leads to endothelial dysfunction and changes in vascular permeability. Indeed, together with endothelial cell damage and failure in homeostasis, ischemia reperfusion injury triggers full-blown inflammatory cascades arising from activation of residential innate immune cells (microglia and astrocytes) and infiltrating leukocytes (neutrophils and macrophages). These inflammatory cells release neurotoxins (proinflammatory cytokines and chemokines, free radicals, excitotoxic amino acids, nitric oxide (NO)), all of which partake in axonal and neuronal deficit. Therefore, our review considers the recent advances in SCI mechanisms, whereby it becomes clear that SCI is a heterogeneous condition. Hence, this leads towards evidence of a restorative approach based on monotherapy with multiple targets or combinatorial treatment. Moreover, from evaluation of the existing literature, it appears that there is an urgent requirement for multi-centered, randomized trials for a large patient population. These clinical studies would offer an opportunity in stratifying SCI patients at high risk and selecting appropriate, optimal therapeutic regimens for personalized medicine.

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Section: Introductionmentioning

confidence: 99%

Inflammogenesis of Secondary Spinal Cord Injury

Anwar

Shehabi

Eid

2016

Front. Cell. Neurosci.

355

258

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“…Some patients experience acute spinal cord dysfunction after thoracic aortic occlusion which is usually believed to be spinal cord ischemia from hypoperfusion during cross-clamping. Some patients undergoing thoracoabdominal aneurysm repairs, however, develop delayed-onset paraplegia 1-5 days later [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

et al. 2010

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Postoperative neurologic deficit due to spinal cord ischemia-reperfusion (I/R) injury is the most devastating complication following thoracoabdominal aortic aneurysm repairs. The protective potential for 17β-Estradiol has not been yet studied in such injury. In this study, ischemia induction for 18 min in male New Zealand White rabbits resulted in the highest percentage (80%) of biphasic paraplegic outcome assessed by Tarlov's score. Acute Estradiol pretreatment (1 mg/kg, i.p., 30 min before I/R induction) altered this outcome and significantly prevented the worsening pattern of neurologic deficits over 48 h of observation. Histopathologic and oxidative stress evaluations of lumbar spinal cords taken in delayed permanent paraplegic phase (48 h after ischemia induction), further confirmed protective efficacy of Estradiol in such context. In western blot analysis, the expression of cleaved caspase-3 and heat shock protein 70 declined in Estradiol pretreated group compared to ischemic control group. TUNEL assay also showed the efficacy of Estradiol to abate motor neuron apoptosis. Interestingly, Estradiol respectively increased and decreased the expression of Cyclooxygenase (COX)-1 and COX-2, to a significant extent. Estradiol, exerting its protection through affecting one or a combination of involved biochemical factors can constitute a potential candidate to protect against thoracoabdominal aortic aneurysm repairs induced spinal cord I/R injury.

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“…In the largest reported series (605 patients), the incidence of paraplegia ranged from 11% -25% depending on patient age, surgical technique, aortic cross clamp duration, and aneurysm length and location (1). Cerebral spinal fluid (CSF) drainage (2), shunts (3)(4)(5), pharmacological intervention (6,7), and hypothermia (8)(9)(10) are various adjuncts that have increased spinal cord protection and the prevention of paraplegia.…”

Section: Introductionmentioning

confidence: 99%

Descending Aortic Aneurysm Repair Utilizing Moderate Hypothermia (30°C) in Conjunction with Left Heart Bypass

Clark,

Frank,

Williams

et al. 1994

J Extra Corpor Technol

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Thoracic and thoracoabdominal aortic aneurysm repair are frequently associated with ischemic paraplegia, renal failure and death. In order to decrease the incidence of ischemic events and allow for a longer aortic cross clamp time, we combined our previous technique of segmental sequential repair, left heart bypass and cerebral spinal fluid drainage in conjunction with moderate hypothermia (30°C). Twenty-seven adult patients underwent elective thoracic (n=6) or thoracoabdominal (n=21) aortic aneurysm repair from January 1992 to September 1993 utilizing this hypothermic technique. A heat exchanger was integrated in the centrifugal left heart bypass circuit to achieve moderate hypothermia (30°C) and regain normothermia (37°C) prior to partial bypass termination. Cannulation for left heart bypass was aortafemoral artery (n=10) or left atrium-femoral artery (n=17). The surgical technique of segmental sequential repair helps to minimize visceral, kidney and spinal cord ischemia. Among these 27 patients, one developed delayed paraplegia on postoperative day #3 and three suffered postoperative death. The average aortic cross clamp time was 76 ± 7 minutes. Previous studies have demonstrated a significant increase of ischemic morbidity (11-25%) when cross clamp times exceeded 30 minutes. We conclude that the combination of left heart bypass, moderate hypothermia and cerebral spinal fluid drainage allow for a longer duration of aortic cross clamp time and a relatively low incidence of ischemic complications.

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Risk of spinal cord dysfunction in patientsundergoing thoracoabdominal aortic replacement

Cited by 211 publications

References 14 publications

Inflammogenesis of Secondary Spinal Cord Injury

Inflammogenesis of Secondary Spinal Cord Injury

Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

Descending Aortic Aneurysm Repair Utilizing Moderate Hypothermia (30°C) in Conjunction with Left Heart Bypass

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