Transforaminal Lumbar and Thoracic Interventions and Ischemic Spinal Cord Injury

2016 ◽  
Author(s):  
Scott E. Glaser ◽  
Rinoo Shah

Transforaminal epidural steroid injections have been shown to be associated with catastrophic neurologic complications secondary to spinal cord infarction. The reflexive, ad hoc response of practitioners to these injuries has been to recommend risk minimization strategies to prevent embolism of the injected particulate steroids and to use nonparticulate steroids. This focus on distal embolism as the sole or primary cause of catastrophic outcomes lacks conclusive supporting evidence and does not suffice to protect the patient from paraplegia as it fails to address the root cause of the complications. A root cause analysis of the procedure provides evidence that the injection technique itself—the “safe triangle”—creates a risk of arterial damage and sequelae leading to ischemia of the spinal cord. The evidence is strong that the only way to mitigate or eliminate the risk of paraplegia is to use a different technique to perform transforaminal injections: the Kambin triangle approach. This change in technique is the only definitive solution that addresses the root cause of these catastrophic sequelae associated with transforaminal epidural steroid injections. Key Words: Artery of Adamkiewicz, ischemic spinal cord injury, Kambin triangle, safe triangle, transforaminal epidural injection

2012 ◽  
Vol 6;15 (6;12) ◽  
pp. 515-523
Author(s):  
Kenneth D. Candido

Digital subtraction angiography (DSA) has been touted as a radiologic adjunct to interventional neuraxial procedures where it is imperative to identify vascular compromise during the injection. Transforaminal epidural steroid injections (TFESI) are commonly performed interventions for treating acute and chronic radicular spine pain. We present a case of instantaneous and irreversible paraplegia following lumbar TFESI wherein a local anesthetic test dose, as well as DSA, were used as adjuncts to fluoroscopy. An 80-year-old man with severe lumbar spinal stenosis and chronic L5 radiculopathic pain was evaluated at a university pain management center seeking symptomatic pain relief. Two prior lumbar interlaminar epidural steroid injections (LESI) provided only transient pain relief, and a decision was made to perform right-sided L5-S1 TFESI. A 5-inch, 22-gauge Quincke-type spinal needle with a curved tip was used. Foraminal placement of the needle tip was confirmed with anteroposterior, oblique, and lateral views on fluoroscopy. Aspiration did not reveal any blood or cerebrospinal fluid. Digital subtraction angiography was performed twice to confirm the absence of intravascular contrast medium spread. Subsequently, a 0.5mL of 1% lidocaine test dose was performed without any changes in neurological status. Two minutes later, a mixture of one mL of 1% lidocaine with 80 mg triamcinolone acetonide was injected. Immediately following the completion of the injection, the patient reported extreme bilateral lower extremity pain. He became diaphoretic, followed by marked weakness in his bilateral lower extremities and numbness up to his lower abdomen. The patient was transferred to the emergency department for evaluation. Magnetic resonance imaging (MRI) of the lumbar and thoracic spine was completed 5 hours postinjection. It showed a small high T2 signal focus in the thoracic spinal cord at the T7-T8 level. The patient was admitted to the critical care unit for neurological observation and treatment with intravenous methylprednisolone. Follow-up MRI revealed a hyper-intense T2 and short-tau inversion recovery signal in the central portion of the spinal cord beginning at the level of the T6 superior endplate and extending caudally to the T9-T10 level with accompanying development of mild spinal cord expansion. The patient was diagnosed with paraplegia from acute spinal cord infarction. At discharge to an acute inpatient rehabilitation program, the patient had persistent bilateral lower extremity paralysis, and incontinence of bowel and bladder functions. In the present patient, DSA performed twice and an anesthetic test dose did not prevent a catastrophic spinal cord infarction and resulting paraplegia. DSA use is clearly not foolproof and may not be sufficient to identify potentially life-or-limb threatening consequences of lumbar TFESI. We believe that this report should open further discussion regarding adding the possibility of these catastrophic events in the informed consent process for lumbar TFESIs, as it has for cervical TFESI. Utilizing blunt needles or larger bevel needles in place of sharp, cutting needles may minimize the chances of this event occurring. Considering eliminating use of particulate steroids for TFESI should be evaluated, although the use of nonparticulate agents remains controversial due to the perception that their respective duration of action is less than that of particulate steroids. Key words: Digital subtraction angiography, transforaminal epidural steroid injections, paraplegia, chronic low back pain.


2005 ◽  
Vol 103 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Manabu Kakinohana ◽  
Hideki Harada ◽  
Yasunori Mishima ◽  
Tatsuhiko Kano ◽  
Kazuhiro Sugahara

Background Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. Methods Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. Results Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. Conclusions Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.


2018 ◽  
Vol 28 (7) ◽  
pp. 2565-2566
Author(s):  
Daniela Popova ◽  
Mariela Filipova

Spinal stroke is a disease that is rare in neurological practice. Affects young people, mostly at the age of 30 years [2]. It may be ischemic or haemorrhagic. Etiological, ischemic spinal stroke is caused by atherosclerosis of the aorta and blood vessels of the spinal cord, muscle spasm, vasculitis, pregnancy, hemangioma or hernia [3, 4]. Hemorrhagic stroke is caused by dysplasia, tumors and blood diseases involving increased bleeding [1]. Spinal infarction most commonly develops in the basal spinal artery pool, which is responsible for the blood supply of the anterior 2/3 of the spinal cord tissue. Often, the disease starts with a sudden back pain with an enigmatic nature (in the area of the thoracic segment - Th 8), a gradually occurring weakness in the limbs and hypestesia, pelvic-tangle disorders [5]. The gait is very difficult to impossible.Purpose of the study: To test neurological tests in patients with spinal ischemic spinal cord injury. Assess their accessibility and reliability.


1993 ◽  
Vol 78 (4) ◽  
pp. 603-609 ◽  
Author(s):  
Philippe Pencalet ◽  
Freddy Ohanna ◽  
Philippe Poulat ◽  
Jean-Marc Kamenka ◽  
Alain Privat

✓ The purpose of this study was to evaluate treatment with the N-methyl-D-aspartate antagonist thienylphencyclidine (TCP) after spinal cord injury for its behavioral, electrophysiological, morphological, and immunohistochemical effects. Five minutes after a photochemical lesion was produced in rats at the T-8 level, the animals received TCP (1 mg/kg, intravenously) or TCP vehicle (saline). The animals were evaluated on Day 18 for neurological recovery by testing motor and sensory functions. The TCP-treated group showed less neurological impairment than the untreated group (p < 0.05 for inclined-plane stability and withdrawal reflex to extension). Somatosensory evoked potential testing was performed on Days 21 to 23 and the wave amplitude between the onset and P1 in the TCP-treated group was higher than in the untreated group (p < 0.05). Mean arterial blood pressure was not significantly modified after TCP injection. Morphometric studies of the lesion area in cross section revealed a significantly reduced spinal cord infarction in the TCP-treated group (p < 0.05). Immunohistochemical evaluation of the spinal cord in lumbar area showed an increased level of serotonin immunoreactivity in the dorsal horn of animals treated by TCP. These results demonstrate the efficacy of TCP in reducing secondary lesions after spinal cord injury in rats.


2006 ◽  
Vol 102 (6) ◽  
pp. 1722-1727 ◽  
Author(s):  
Shunsuke Tsuruta ◽  
Mishiya Matsumoto ◽  
Shiro Fukuda ◽  
Atsuo Yamashita ◽  
Ying Jun Cui ◽  
...  

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