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REGIONAL ANESTHESIA

Neurologic Dysfunction After Major Thoracic Surgery in a Patient with Severe Arteriosclerotic Disease Receiving Epidural Analgesia

Stéphanie Monsel, MD^*, Georges Rodesch, MD, PhD, Pierre-Antoine Laloë, MD^*, Guy Kuhlman, MD^*, and Marc Fischler, MD^*

From the *Service d'Anesthésie, Université Paris Ile-de-France Ouest; and Service de Neuro-Radiologie, Hôpital Foch, Suresnes, France.

Address correspondence and reprint requests to M. Fischler, MD, Service d'Anesthésie, Hôpital Foch, 40 rue Worth, 92151 Suresnes, France. Address e-mail to m.fischler{at}hopital-foch.org.

	Abstract

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We present a patient who underwent pulmonary lobectomy with thoracic epidural analgesia and developed postoperative sensory-motor symptoms of the lower limbs. Radiological investigation indicated ischemia of the conus medullaris as the likely cause. The motor deficit disappeared gradually and the patient was mobilizing independently when discharged on postoperative day 21.

	Introduction

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Major causes of an early neurological complication affecting the lower limbs after neuraxial block include epidural hematoma (estimated incidence between 1:150,000 and 1:220,000) (1) and spinal cord trauma (2). In some cases, spinal stenosis or osteoporosis is considered as possible risk factor (3). This case concerns a patient who presented with postoperative ischemia of the conus medullaris with sensory-motor symptoms of the lower limbs without one of these factors.

	CASE REPORT

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A 76-year-old man underwent left upper lobectomy through a posterolateral thoracotomy. His surgical history included a right inferior lobectomy for lung adenocarcinoma in 1991, an excision of oral cancer in 1993, an aorto-femoral bifurcation graft for aortic aneurysm repair in 1999, and a left carotid endarterectomy in 2001.

The following multiple cardiovascular disease risk factors were identified preoperatively: 50-pack-year history of smoking, poorly controlled hypertension despite triple therapy (ß-adrenergic-blocker, angiotensin converting enzyme inhibitor, and calcium channel blocker) and hypercholesterolemia. On examination, his arterial blood pressure (BP) was recorded at 140/80 mm Hg and symptoms and signs of intermittent claudication of the lower limbs were noted. Preoperative investigations revealed left ventricular hypertrophy with a shortening fraction of 50% (echocardiogram), no coronary artery disease (radionuclide exercise stress testing), and moderate chronic obstructive lung disease.

On the day of surgery, his BP was 180/110 mm Hg on arrival at the operating room. A thoracic epidural catheter was placed before induction of anesthesia at level T5–6 by the paramedian approach without technical difficulty (no pain, paresthesia, or dural puncture). After negative test dose injection of 3 mL of 2% lidocaine with epinephrine, a bolus of 6 mL of ropivacaine 0.375% and 3 mL of sufentanil (15 µg) were administered. Without waiting for the appearance of signs of epidural block, anesthetic induction was achieved with sufentanil, etomidate, and propofol with atracurium for neuromuscular blockade. The trachea was intubated with a left double-lumen endotracheal tube. Anesthesia was maintained with inhaled isoflurane. The patient was placed in the lateral decubitus position.

Hypotension occurred twice without any surgical cause, such as manipulation of the heart or blood loss. The first episode (BP 90/60 mm Hg) occurred 50 min after the epidural injection and lasted for 20 min, despite administration of 18 mg of ephedrine and IV crystalloids. The second episode of hypotension (BP 100/65 mm Hg) occurred 30 min later, lasted <5 min, and did not require administration of any vasopressors. The volume of crystalloids administered during anesthesia was 1750 mL. Tumor excision required ligation of the left intercostal artery near the aorta at level T5. The patient was tracheally extubated in the operating room.

On arrival in the postanesthesia care unit, the patient was normotensive, denied any pain, and had no motor block. Patient-controlled epidural analgesia was started with a background infusion of 5 mL/h of 0.2% ropivacaine and sufentanil (0.75 µg/mL) and fixed bolus of 3 mL with 20-min lockout. A urethral catheter was inserted because of postoperative urinary retention. Thromboembolic disease prophylaxis was started on the sixth postoperative hour with 5000 IU subcutaneous heparin calcium administered every 12 h. No episode of hypotension was noticed during the following period.

The patient began to use the patient-controlled epidural analgesia function 9 h after insertion of the thoracic epidural catheter. Four hours later, he complained of numbness of the left lower limb without motor deficit; a total of 158.5 mg ropivacaine had been infused up to this time. His vital signs were heart rate 63 bpm, BP 125/70 mm Hg, and Spo₂ 98%. The epidural infusion was stopped and the symptoms subsided. On the first postoperative morning (Day 1, D1), the epidural analgesia was restarted at 3 mL/h. In the evening of D1, the patient again reported lower limb symptoms, and bilateral lower limb hypoesthesia was noted, predominantly on the left side. Neurologic examination of the sacral area was not performed. There were no signs of lower limb ischemia. The epidural infusion was stopped again and the catheter was removed 6 h after the last injection of heparin sodium.

Persistence of neurological signs prompted magnetic resonance imaging (MRI) on D2 morning, which excluded an epidural hematoma. However, a high signal area in the conus medullaris on T2-weighted images consistent with ischemia in the arterial territory of the anterior spinal axis at this level was noted (Fig. 1).

View larger version (113K): [in this window] [in a new window]   Figure 1. T2-weighted spinal cord magnetic resonance image. Sagittal view showing a high signal area (arrow) in the conus medullaris consistent with ischemia in the anterior spinal artery distribution.

Steroids and heparin (therapeutic dose) were administered IV. On D3, the patient was admitted to the intensive care unit because of respiratory distress secondary to bronchial obstruction. His respiratory function improved with chest physiotherapy; he did not require ventilatory support. Agitation, however, precluded detailed neurological examination until D6. At that time, moderate bilateral paraparesis mainly in a L5-S1 distribution was diagnosed. No sensory deficit and no sphincter dysfunction were found. A second MRI on D15 found no change.

The patient made a good recovery with gradual reduction of the motor deficit and he was mobilizing independently on discharge at D21. A follow-up MRI was not performed, as the patient recovered completely.

	DISCUSSION

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Several elements linked to the patient, the operation, or the epidural analgesia could be in question in the occurrence of a conus medullaris ischemia. This area, like the upper thoracic cord between T1 and T5, is particularly prone to low flow ischemia ("watershed" areas) (4).

This arteriopathic patient underwent an aorto-femoral bifurcation graft. Postoperative paraplegia after infrarenal abdominal aortic aneurysm repair has an estimated incidence between 0.15% and 0.3% (5). This low figure is probably explained, in part, by the collateral circulation which could compensate for the reduced blood supply to the conus medullaris. This mechanism minimizes conus ischemia under normal circumstances.

Paraplegia rarely complicates a thoracotomy (the rate is 0.08%) (6). Etiologies include arterial embolus in the main supply to the cord (radiculo-medullary artery of the lumbar enlargement [Artery of Adamkiewicz] e.g. (7), costo-vertebral angle hematoma, medullary compression because of foreign body migration (Surgicel®) toward the spinal canal by the inter-vertebral foramen (8–13), vertebral metastases with crush fracture, preoperative or postoperative hypotension (14). Ligation or cauterization of the left T5–6 intercostal artery has recently been reported as the cause of spinal cord ischemia (15); this can be done outside the spinal canal, as in our case, or within it, if tumor excision requires a vertebral resection. Full lateral decubitus positioning of patients for optimal surgical site exposure may also compress spinal vessels, particularly in the presence of spinal stiffness, causing reduced arterial perfusion, or venous compression with subsequent venous hyperpressure in the cord, reduction in medullary perfusion pressure (14), and decreased resorption of cerebrospinal fluid (CSF).

Finally, thoracic epidural analgesia may also have contributed by two mechanisms. Epidural administration of a local anesthetic involves the risk of hypotension (16), with a possible reduction in spinal cord perfusion. An increase in CSF pressure could also reduce conus medullaris perfusion, as described in animal models after an epidural bolus (17,18). This effect is short-lived unless the CSF pressure was high before the bolus (17).

These factors could explain the atypical presentation in this case which corresponds more to postoperative vascular "claudication type" damage to the cord than to a true segmental ischemia. We postulated that, because of the previous abdominal aortic surgery, the main arterial contribution to the cord via the radiculo-medullary artery of the lumbar enlargement was compromised and taken over by a collateral circulation arising from radiculo-pial arteries, and from a more cranially located main radiculo-medullary artery (4). The ligation of the left intercostal artery near the aorta at level T5 (from which a radiculo-medullary artery often arises) may have suppressed this important contribution. Neurologic deficit was probably not due to focal ischemia, as no sulco-commissural or perforating arteries were damaged, but rather to a disequilibrium in the collateral circulation to the cord with symptoms, thus depending on the patient's local and general hemodynamics. Because of the potential collateral circulation of the basket, the MR image distally located on the conus represents trauma in a watershed area and not a fixed irreversible ischemia. Recovery from the symptoms may have been the consequence of the restoration of correct hemodynamic conditions and collateral vascular supply.

In conclusion, we have reported the case of a patient who, after undergoing a thoracotomy with thoracic epidural analgesia, presented with neurological signs consistent with conus medullaris ischemia. No single etiology was found which could explain this complication. Thoracic epidural analgesia was not the likely cause. Intraoperative hypotension may have decreased the perfusion of the poorly vascularized conus medullaris of this arteriopathic patient. The ligation of the left intercostal artery at level T5, which possibly supplied a main source of the cord vascularization in this case, may also have contributed to reducing the arterial perfusion of the distal caudal spinal cord.

	Footnotes

 
Accepted for publication September 21, 2006.

Work should be attributed to the Service d'Anesthésie, Hôpital Foch, Suresnes, Université Paris Ile de France Ouest, France.

	REFERENCES

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1. Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994;79:1165–77.[Free Full Text]
2. Wilkinson PA, Valentine A, Gibbs JM. Intrinsic spinal cord lesions complicating epidural anaesthesia and analgesia: report of three cases. J Neurol Neurosurg Psychiatr 2002;72:537–9.[Abstract/Free Full Text]
3. Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central neuraxial blockades in Sweden 1990–1999. Anesthesiology 2004;101:950–9.[Web of Science][Medline]
4. Lasjaunias P, Berenstein A, Terbrugge K. Spine and spinal cord arteries and veins. In: Lasjaunias P, Berenstein A, ter Brugge KG, eds. Surgical neuroangiography: clinical vascular anatomy and variations. 2nd ed. New York: Springer Verlag, 2001:73–164.
5. Rosenthal D. Spinal cord ischaemia after abdominal aortic operation: is it preventable? J Vasc Surg 1999;30:391–9.[Web of Science][Medline]
6. Attar S, Hankins JR, Turney SZ, et al. Paraplegia after thoracotomy: report of five cases and review of the literature. Ann Thorac Surg 1995;59:1410–15.[Abstract/Free Full Text]
7. Boedeker H, Schmidt J, Zirngibl H. Spinalis-anterior-syndrom nach thoracoabdomineller oesophagusresektion. Eine seltene komplikation. Chirurg 1997;68:902–5.[Web of Science][Medline]
8. Brodbelt AR, Miles JB, Foy PM, Broome JC. Intraspinal oxidised cellulose (surgicel) causing delayed paraplegia after thoracotomy—a report of three cases. Ann R Coll Surg Engl 2002;84:97–9.
9. Iwabuchi S, Koike K, Okabe T, et al. Iatrogenic paraplegia caused by surgicel used for hemostasis during a thoracotomy: report of a case. Surg Today 1997;27:969–70.[Web of Science][Medline]
10. Lovstad RZ, Steen PA, Forsman M. Paraplegia after thoracotomy—not caused by the epidural catheter. Acta Anaesthesiol Scand 1999;43:230–2.[Web of Science][Medline]
11. Short HD. Paraplegia associated with the use of oxidized cellulose in posterolateral thoracotomy incisions. Ann Thorac Surg 1990;50:288–9.[Abstract]
12. Wada E, Yonenobu K, Ebara S, et al. Epidural migration of hemostatic agents as a cause of postthoracotomy paraplegia. Report of two cases. J Neurosurg 1993;78:658–60.[Web of Science][Medline]
13. Walker WE. Paraplegia associated with thoracotomy. Ann Thorac Surg 1990;50:178.[Web of Science][Medline]
14. Bhuiyan MS, Mallick A, Parsloe M. Post-thoracotomy paraplegia coincident with epidural anaesthesia. Anaesthesia 1998;53:583–6.[Web of Science][Medline]
15. Raz A, Avramovich A, Saraf-Lavi E, et al. Spinal cord ischemia following thoracotomy without epidural anesthesia. Can J Anaesth 2006;53:551–5.[Web of Science][Medline]
16. Cashman JN, Dolin SJ. Respiratory and haemodynamic effects of acute postoperative pain management: evidence from published data. Br J Anaesth 2004;93:212–23.[Abstract/Free Full Text]
17. Grocott HP, Mutch WA. Epidural anesthesia and acutely increased intracranial pressure. Lumbar epidural space hydrodynamics in a porcine model. Anesthesiology 1996;85:1086–91.[Web of Science][Medline]
18. Kroin JS, Nagalla SK, Buvanendran A, et al. The mechanisms of intracranial pressure modulation by epidural blood and other injectates in a postdural puncture rat model. Anesth Analg 2002;95:423–9.[Abstract/Free Full Text]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Monsel, S. Articles by Fischler, M. Search for Related Content PubMed PubMed Citation Articles by Monsel, S. Articles by Fischler, M. Related Collections Anesthetic Techniques Complications Regional Anesthesia