Severe spinal cord ischemia subsequent to fibrocartilaginous embolism

2007 ◽  
Vol 263 (1-2) ◽  
pp. 211-213 ◽  
Author(s):  
Jan Thöne ◽  
Andreas Hohaus ◽  
Andreas Bickel ◽  
Frank Erbguth
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Fibrocartilaginous Embolism

scholarly journals Successful management of spinal cord ischemia in a pediatric patient with fibrocartilaginous embolism: illustrative case

2021 ◽  
Vol 2 (11) ◽  
Author(s):  
Augustinas Fedaravičius ◽  
Yael Feinstein ◽  
Isaac Lazar ◽  
Micky Gidon ◽  
Ilan Shelef ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Aortic Surgery ◽  
Spinal Cord Ischemia ◽  
Blood Perfusion ◽  
Hemodynamic Instability ◽  
Illustrative Case ◽  
Diagnostic Challenge ◽  
Neurological Improvement ◽  
Fibrocartilaginous Embolism ◽  
Pulse Steroids

BACKGROUND Fibrocartilaginous embolism (FCE) is a rare cause of ischemic myelopathy that occurs when the material of the nucleus pulposus migrates into vessels supplying the spinal cord. The authors presented a case of pediatric FCE that was successfully managed by adapting evidence-based recommendations used for spinal cord neuroprotection in aortic surgery. OBSERVATIONS A 7-year-old boy presented to the emergency department with acute quadriplegia and hemodynamic instability that quickly progressed to cardiac arrest. After stabilization, the patient regained consciousness but remained in a locked-in state with no spontaneous breathing. The patient presented a diagnostic challenge. Traumatic, inflammatory, infectious, and ischemic etiologies were considered. Eventually, the clinical and radiological findings led to the presumed diagnosis of FCE. Treatment with continuous cerebrospinal fluid drainage (CSFD), pulse steroids, and mean arterial pressure augmentation was applied, with subsequent considerable and consistent neurological improvement. LESSONS The authors proposed consideration of the adaptation of spinal cord neuroprotection principles used routinely in aortic surgery for the management of traumatic spinal cord ischemia (FCE-related in particular), namely, permissive arterial hypertension and CSFD. This is hypothesized to allow for the maintenance of sufficient spinal cord perfusion until adequate physiological blood perfusion is reestablished (remodeling of the collateral arterial network and/or clearing/absorption of the emboli).

Effects of HBO with reduction of iNOS and HIF -1α in motor neurons after transient spinal cord ischemia in rabbits

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S452-S452
Author(s):  
Noritaka Murakami ◽  
Masahiro Sakurai ◽  
Takashi Horinouchi ◽  
Jun Ito ◽  
Shin Kurosawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Spinal Cord Ischemia

Collateral circulation prevents spinal cord ischemia after thoracic aortic endovascular repair

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
B Zipfel ◽  
S Buz ◽  
R Hammerschmidt ◽  
V Düsterhöft ◽  
R Hetzer
Keyword(s):  
Spinal Cord ◽  
Endovascular Repair ◽  
Collateral Circulation ◽  
Spinal Cord Ischemia

Spinal cord ischemia after thoracic stent-grafting: Causes apart from intercostal artery coverage

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
B Zipfel ◽  
S Buz ◽  
D Hullmeine ◽  
V Düsterhöft ◽  
R Hammerschmidt ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Intercostal Artery ◽  
Stent Grafting

Thoracoabdominalis aortakirekesztés során fellépő elektrofiziológiai változások a gerincvelőben

2020 ◽  
Vol 73 (4) ◽  
pp. 160-166
Author(s):  
Csaba Dzsinich ◽  
Péter Gloviczki ◽  
Gabriella Nagy ◽  
Klaudia Vivien Nagy
Keyword(s):  
Spinal Cord ◽  
Motor Evoked Potentials ◽  
Spinal Cord Ischemia ◽  
Experimental Studies ◽  
Neuron Specific Enolase ◽  
Neurological Complications ◽  
Neurologic Outcome ◽  
Published Data ◽  
Aortic Clamping ◽  
Sensory Evoked

Összefoglaló. A thoracoabdominalis aortakirekesztés okozta gerincvelő ischemia súlyos neurológiai következményeit számos klinikai és kísérleti tanulmány bizonyítja. E nehezen kiszámítható, súlyos szövődmény megelőzésének érdekében régi törekvés megfelelő intra- és posztoperatív monitorizálás kifejlesztése, ami előre jelzi a gerincvelő-funkció romlását, illetve a kialakuló celluláris károsodást. A legelterjedtebb, a klinikai gyakorlatban széles körben alkalmazott megoldás a gerincvelői kiváltott motoros potenciál (MEP) folyamatos ellenőrzése. Ritkábban alkalmazott – bár ígéretes – eljárás a biokémiai változások nyomon követése, ami a sejtszintű károsodás markereit használja fel az ischemia okozta változások felismerésére. Korábbi dolgozatunkban kutyákon végzett kísérleteink azon eredményeit ismertettük, amelyekben a 60 perces thoracoabdominalis aortakirekesztés okozta neurológiai változások és a perfúzió adatainak összefüggéseit tárgyaltuk. Jelen tanulmányunkban a gerincvelői motoros (MEP) és szenzoros (SEP) kiváltott potenciálok változásait vizsgáljuk a neurológiai végállapot vonatkozásában. Megállapítottuk, hogy SEP változásai a neurológiai károsodás mértékével értékelhető összefüggést nem mutatnak. A MEP-amplitúdó és -latencia értékei biztonsággal jelzik a fenyegető gerincvelő ischemiát. A neurológiai deficit mélységét (Tarlov 2,1,0) a MEP-értékek változásai numerikusan nem értékelhetően követik. Summary. Severe neurological complications of the thoracoabdominal aortic clamping were published in numerous clinical and experimental studies. These hardly predictable, devastating consequences demanded to develop a monitoring system which might detect impending level of spinal cord ischemia in time – in order to introduce or enhance protective procedures and prevent permanent neurological deficit. The most widely used monitoring in clinical practice is the continuous surveillance of the motor evoked potentials (MEP) during and after thoracoabdominal aortic clamping. Much less used, but promising opportunity is to control the metabolic changes and cellular integrity utilizing specific markers like liquor lactate and neuron specific enolase (NSE) etc. In our earlier study we published data of our canine experiment related to coherencies between neurological outcome and specific perfusion of the spinal cord during and after one hour thoracoabdominal aortic clamping. In the present paper we investigate the behavior of motor evoked (MEP) and sensory evoked (SEP) potentials related to neurological changes. We conclude the behavior of SEP values hardly correlate with the neurologic outcome, meanwhile decrease of MEP amplitude provides reliable signal for developing spinal cord ischemia. We could not confirm a numeric correlation of these data and the level of the final neurologic outcome.

Hypogastric Artery Stenting for Chronic Intermittent Spinal Cord Ischemia After Thoracic Endovascular Aortic Repair

2020 ◽  
Vol 27 (5) ◽  
pp. 801-804
Author(s):  
Catharina Gronert ◽  
Nikolaos Tsilimparis ◽  
Giuseppe Panuccio ◽  
Ahmed Eleshra ◽  
Fiona Rohlffs ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Ischemia ◽  
Thoracic Endovascular Aortic Repair ◽  
Neurological Symptoms ◽  
Endovascular Aortic Repair ◽  
Hypogastric Artery ◽  
Lower Extremity Weakness ◽  
Aortic Repair ◽  
The Right

Purpose: To report a case of chronic intermittent spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR) and its successful treatment using hypogastric artery stenting. Case Report: A 79-year-old patient presented in May 2013 with a thoracic aortic aneurysm (TAA) and a contained rupture. He urgently underwent TEVAR that covered 274 mm of descending thoracic aorta without immediate postoperative signs of acute SCI. At 3-month follow-up, he reported repeating incidents of sudden lower extremity weakness leading to a fall with a humerus fracture. A neurological consultation revealed the tentative diagnosis of intermittent SCI caused by TEVAR and initially recommended a conservative approach. During the following year there was no clinical improvement of the symptoms. Computed tomography angiography showed a high-grade stenosis of the right hypogastric artery, which was stented in November 2014 to improve the collateral network of spinal cord perfusion. Following treatment, the patient had no further neurological symptoms; at 32 months after the reintervention, the imaging follow-up documented a patent stent and continued exclusion of the TAA. Conclusion: Intermittent neurological symptoms after TEVAR should be suspected as chronic intermittent SCI. The improvement of collateral networks of the spinal cord by revascularization of the hypogastric artery is a viable treatment option.

scholarly journals Acute-onset paraplegia as an unexpected complication under general anesthesia in supine position during abdominal endovascular aneurysm repair: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Atsushi Morio ◽  
Hirotsugu Miyoshi ◽  
Noboru Saeki ◽  
Yukari Toyota ◽  
Yasuo M. Tsutsumi
Keyword(s):  
Spinal Cord ◽  
General Anesthesia ◽  
Supine Position ◽  
Spinal Cord Ischemia ◽  
Endovascular Aneurysm Repair ◽  
Acute Onset ◽  
Lower Limbs ◽  
Canal Stenosis ◽  
Cord Injury ◽  
Aneurysm Repair

Abstract Background Acute onset paraplegia after endovascular aneurysm repair (EVAR) is a rare but well-known complication. We here show a 79-year-old woman with paraplegia caused by static and dynamic spinal cord insult not by ischemia after EVAR. Case presentation The patient underwent EVAR for abdominal aortic aneurism under general anesthesia in the supine position. She had a medical history of lumbar canal stenosis. After the surgery, we recognized severe paraplegia and sensory disorder of lower limbs. Although the possibility of spinal cord ischemia was considered at that time, postoperative magnetic resonance imaging (MRI) revealed burst fracture of vertebra and compressed spinal cord. Conclusions Patients with spinal canal stenosis can cause extrinsic spinal cord injury even with weak external forces. Thus, even after EVAR, it is important to consider extrinsic factors as the cause of paraplegia.

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