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Can Direct Spinal Cord Injury Occur Without Paresthesia?

A Report of Delayed Spinal Cord Injury After Epidural

Placement in an Awake PatientBan C. H. Tsui, MD, MSc, FRCP(C)*, and Kevin Armstrong, MD, FRCP(C)*Department of Anesthesiology and Pain Medicine University of Alberta, Edmonton, Alberta, Canada, and Departmentof Anesthesia, University of Western Ontario, London, Ontario, Canada.

We discuss the etiology of a delayed spinal cord injuryafter epidural anesthesia without paresthesia. The de-scription of such a case in an awake, adult patient whounderwent a Whipple resection is provided. An epi-

dural was performed at approximately the T8-9 in-terspace with the patient in the sitting position after1 mg of midazolam was administered. On the first at-tempt, a dural puncture occurred. The patient did notreport any paresthesia or pain. The needle was with-drawn and a second attempt was made one interspacelower.At this level,the epidural catheter was advancedinto the epidural space uneventfully. Postoperatively,

the patient suffered decreased motor function in theright leg. Magnetic resonance imaging revealed highsignal intensity within the spinal cord, indicating cordedema compatible with directneedle trauma. An extra-

dural fluid collection consistent with a hematoma wasalso noted. Although it may be impossible to confirm ifthe spinal cord injury was a result of direct needletrauma, hematoma, or a combination of needle traumaand hematoma, these events clearly raise the importantquestion of whether an awake patient will always re-port paresthesia secondary to spinal cord trauma.

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eports of spinal cord injury occurring while perform-ing epidural anesthesia in unconscious patients havegenerated debate over the safety of performing epi-

dural anesthesia in awake versus unconscious patients (17). The main argument against the performance of centralneural blockade in anesthetized or heavily sedated patientsis that unconscious subjects are unable to report paresthe-sia. However, is the converse true? Will the conscious pa-tient always report a paresthesia in response to spinal cordor nerve root trauma?

Case ReportAn 81-yr-old male (69 kg) was scheduled to have a Whippleresection for pancreatic cancer. With the exception of pro-nounced thoracic kyphosis, the patients physical and neu-rological examinations were unremarkable.

An initial epidural needle was placed at the T8-9 in-terspace with the patient awake and in the sitting positionafter 1 mg of midazolam was administered. A right para-

median epidural was performed using a 17-gauge Tuohyneedle with a loss of resistance (LOR) to air. On the firstattempt, dural puncture occurred as free-flowing cerebro-spinal fluid (CSF) was seen in the syringe. No air wasinjected. A second single pass attempt was successfullymade one interspace lower and a soft-tipped epidural cath-eter was threaded easily into the epidural space. The anes-thesiologist recorded that there was no pain or discomfortduring the procedure. No blood or CSF was returnedthrough the catheter.

Three mL of 2% lidocaine was injected through the cath-eter and general anesthesia was then induced. Intraopera-tively, 2 5-mL boluses of 0.125% bupivacaine plus 5 g/mLof fentanyl were given and a 12 mL/h infusion of the same

solution was administered throughout the procedure. Twoepisodes of hypotension occurred: 80/50 mm Hg at 75 minand 75/45 mm Hg at 150 min postinduction. Both episodesresponded readily to ephedrine (5 and 10 mg respectively)and were 510 min in duration. Estimated blood loss was900 mL, which was replaced with 2000 mL of Ringerslactate solution and 1000 mL of Pentaspan. Surgery lastedapproximately 4 h with no obvious surgical complications.The patient was tracheally extubated in the operating roomand was admitted to the intensive care unit in stable condi-tion for postoperative monitoring.

Postoperatively, a formal neurological examination wasnot performed until postoperative day (POD) 4 because of adecreased level of consciousness. On POD 1 the patient was

Accepted for publication February 15, 2005.Supported, in part, by Education and Research Fund, Department

of Anesthesiology and Pain Medicine, University of Alberta, Edm-onton, Canada and Department of Anesthesia, University of West-ern Ontario, London, Ontario, Canada. Ban C.H. Tsui is a recipientof Clinical Investigatorship Award, Alberta Heritage Foundation forMedical Research, Alberta, Canada.

Address correspondence and reprint requests to Ban C.H. Tsui,MSC, MD, FRCP(C), Department of Anesthesiology and Pain Med-icine, 8120 Clinical Sciences Building, Edmonton, Alberta, CanadaT6G 2G3. Address e-mail to btsui@ualberta.ca.

DOI: 10.1213/01.ANE.0000175764.16650.85

2005 by the International Anesthesia Research Society1212 Anesth Analg 2005;101:12124 0003-2999/05

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significantly obtunded but he moved all four limbs sponta-neously and purposefully. A drug error was then noted: 5g/mL of epidural fentanyl and 0.125% bupivacaine was

being infused instead of 2 g/mL. This error was correctedby changing the epidural solution. On POD 2, the patientwas drowsy and the epidural infusion was reduced from12 mL/h to 9 mL/h. On POD 3, the patient was more alertbut appeared to have more difficulty when mobilizing forany activity. The epidural infusion rate was then furtherreduced to 6mL/h. On POD 4, 2.5 h after the infusion wasstopped, a neurological examination revealed little or nomovement (0/5) and no sensation to pinprick in the rightleg. Motor function and sensation were overall intact (4/5)but with decreased reflexes in his left leg. The epiduralcatheter was immediately removed intact.

Severe winter weather made travel unsafe. As a result theemergent neurological consultation and urgent magneticresonance imaging (MRI) did not take place as requested.On POD 5, neurological consultation confirmed that therewas a deficit in the right leg with 1/5 motor function anddecreased temperature, vibration, and position sensation.Spinal cord edema, a high T2 signal intensity on MRI, com-patible with direct trauma was noted from the mid T9 to themid T10 vertebral body (Figs. 1 and 2). Moreover, a posteriorextradural fluid collection from the T8-9 disk level extendinginferior to the T11 vertebral body consistent with a hema-toma was present. Its maximal anterior posterior dimensionwas 7 mm. There were compression fractures at T8 and T11.The neurosurgical team was consulted and subsequentlyperformed an emergency laminectomy and evacuation ofthe hematoma 7 h after the MRI results. Under direct surgi-cal examination, the hematoma did not appear to cause

significant compression.

Postlaminectomy, motor and sensory function was stillprofoundly depressed. This partially resolved over time.After 8 wk the patient was dependent on a wheelchair forambulation although he was able to bear weight on his rightleg and perform self-transfer from his wheelchair to bed.Sensation had returned to normal. At 12 wk, he could am-bulate with a walker but with impaired proprioception.

DiscussionThis report describes the case of delayed spinal cord

injury from epidural anesthesia without reported par-esthesia in an awake patient. Although it may beimpossible to confirm the etiology of the spinal cordinjury in this case, these events raise the importantquestion of whether an awake patient will always beable to report paresthesia secondary to spinal cordtrauma.

Spinal cord damage can result from needle or cath-eter trauma, local anesthetic toxicity, epidural hema-toma, ischemia from an arterial injury, or severe hy-potension. Although present, an epidural hematomawas unlikely to produce the patients neurologicaldeficit, as MRI did not suggest significant compres-sion of the spinal cord, a fact confirmed at laminec-tomy. As the clinical sign of spinal cord ischemia isnormally bilateral paresis of the legs, the fact that thispatient had a unilateral deficit of the right side is notconsistent with spinal cord ischemia from a vascularinsult (8,9). Spinal cord edema confined to the rightside suggests a small likelihood of injury to the Arteryof Adamkiewicz, as it is predominantly left sided (10).In addition, there was clear MRI evidence of edemamainly localized on the right side of the spinal cord(Fig. 2). Although the initial epidural infusion of12 mL/h with bupivacaine 0.125% plus 5 g/mL fen-

tanyl was larger than usual, it is highly unlikely that

Figure 1. Sagittal view of magnetic resonance imaging (MRI). Whitearrows indicate a high T2 signal intensity within the spinal cordextending from the mid T9 to mid T10 vertebral bodies. Blackarrows indicate high signal intensity extradurally.

Figure 2. Magnetic resonance image of the spinal cord. Blackarrows indicate the spinal cord and E indicates the edema

localized on the right side of the spinal cord.

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drug toxicity would account for this unilateral rightside spinal cord edema. However, the large opioiddose certainly could have contributed to the patientssedation in the postoperative period. This rapid infu-sion rate would make intrathecal catheter placement

very unlikely, as there was no sign of a total spinal.The fact that a soft catheter was used further reducesthe likelihood of direct catheter trauma. In contrast,the dura was clearly punctured around the level ofspinal cord edema on the first attempt of epiduralneedle placement. This certainly raises the possibilitythat the lesion on MRI resulted from an unrecognizedspinal cord puncture during the epidural needleplacement while using a right-sided paramedian ap-proach. Given that the epidural was performed withthe patient awake and in a standard fashion, the ques-tions are raised whether paresthesia is a reliable signof spinal cord encroachment and whether LOR alone

is sufficient to avoid adverse sequelae.Paresthesia associated with spinal cord injury can

occur at the time of needle placement but it also hasbeen reported to develop only at the time of injectionor secondary to irritation, edema, or hematoma(11,12). In addition, pain is more common in extra-axial lesions affecting the nerve roots or blood vesselsthat are innervated by sensory neurons mediatingpain (13). In contrast, because there are no pain recep-tors within the spinal cord itself (or the brain), intra-axial lesions may be painless (13). This allows percu-taneous cervical cordotomy to be performed in awakepatients (14,15). During the procedure, the cervical

cord is typically punctured multiple times with a 22-gauge needle electrode, and yet the patient generallydescribes neither pain nor paresthesia (16). In addi-tion, pain reported from dural puncture is rare inclinical practice. This point is also well illustrated inthis case report, as our patient did not complain ofpain despite a clinically obvious dural puncture.

In this case, it is difficult to determine the primarycause of the injury and how a delayed diagnosis as aresult of human error, lack of vigorous neurologicalmonitoring, and uncontrollable environmental condi-tions contributed to the extent of the damage. Clearly,the lack of vigorous neurological monitoring contrib-uted to a delayed diagnosis and possibly reduced theopportunity to correct any reversible defect that mayhave occurred. Thus, vigorous postoperative neuro-logical monitoring should be implemented in all pa-tients receiving neuraxial analgesia. Preoperative re-view of diagnostic imaging of the vertebral columnmay be helpful in delineating the extent of preexistingpathology.

This case reminds clinicians that we should notsimply assume paresthesia will always occur and bereported if a needle encroaches upon the spinal cord.

Although the use of electrophysiological monitoringhas become common practice in spinal surgery (17)and the idea of using electrical stimulation duringepidural needle advancement to provide an additionalmonitoring technique has been recently introduced

(18,19), there is still no clear evidence that direct tho-racic epidural placement can be performed withoutrisk in either awake or anesthetized patients.

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8. Kuker W, Weller M, Klose U, et al. Diffusion-weighted MRI ofspinal cord infarction: high resolution imaging and time courseof diffusion abnormality. J Neurol 2004;251:81824.

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Neuroradiology 2002;44:8517.10. Kawaharada N, Morishita K, Hyodoh H, et al. Magnetic reso-nance angiographic localization of the artery of Adamkiewiczfor spinal cord blood supply. Ann Thorac Surg 2004;78:84651.

11. Simon SL, Abrahams JM, Sean GM, et al. Intramedullary injec-tion of contrast into the cervical spinal cord during cervicalmyelography: a case report. Spine 2002;27:E2747.

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13. Kandel ER. The perception of pain. In: Kandel ER, Schwartz JH,Jessel TM, eds. Principles of neural science. New York:McGraw-Hill Health Professions Division, 2000:47291.

14. Jackson MB, Pounder D, Price C, et al. Percutaneous cervicalcordotomy for the control of pain in patients with pleural me-sothelioma. Thorax 1999;54:238 41.

15. Lahuerta J, Bowsher D, Lipton S, Buxton PH. Percutaneouscervical cordotomy: a review of 181 operations on 146 patientswith a study on the location of pain fibers in the C-2 spinalcord segment of 29 cases. J Neurosurg 1994;80:97585.

16. Pounder D, Elliott S. An awake patient may not detect spinalcord puncture. Anaesthesia 2000;55:194.

17. Raynor BL, Lenke LG, Kim Y, et al. Can triggered electromyo-graph thresholds predict safe thoracic pedicle screw placement?Spine 2002;27:20305.

18. Tsui BC, Wagner A, Cunningham K, et al. Threshold current ofelectrical stimulation in intrathecal space using insulated nee-dles in pediatric patients. Anesth Analg 2005;100:6625.

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1214 CASE REPORTS ANESTH ANALG2005;101:12124