HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Donna E. Maziak Robert J. Ginsberg Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shamji, M. F. Articles by Pon, R. Search for Related Content PubMed PubMed Citation Articles by Shamji, M. F. Articles by Pon, R. Related Collections Cerebral protection

Ann Thorac Surg 2003;76:315-321
© 2003 The Society of Thoracic Surgeons

---

Review

Circulation of the spinal cord: an important consideration for thoracic surgeons

^a Division of Thoracic Surgery, The Ottawa Hospital, General Campus, Ottawa, Ontario, Canada
^b Division of Thoracic Surgery, University Health Network, Toronto General Hospital, Toronto, Ontario, Canada
^c Division of Thoracic Surgery, Yale University Medical Centre, New Haven, Connecticut, USA

^* Address reprint requests to Dr Maziak, The Ottawa Hospital, General Campus, 501 Smyth Road, 6NW-6354, Ottawa, ON K1H 8L6, Canada
e-mail: dmaziak{at}ohri.ca

	Abstract

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
The spinal cord has significant thoracic arterial watershed areas rendering it vulnerable to intraoperative ischemic damage, clearly mandating a need for postoperative neurologic monitoring. Mechanisms of hypoperfusion include aortic cross-clamping, rib retraction, intercostal artery interruption, and costovertebral junction bleeding. We report cases of primary lung cancer resection, resection of pulmonary metastasis adherent to the thoracic aorta, resection of cartilaginous tumor with chest wall invasion, and esophagomyotomy for achalasia—all complicated by postoperative paraplegia. We review spinal cord circulation, describe mechanisms and patterns of neurologic dysfunction of susceptible watershed areas, and outline roles of preoperative spinal angiography and intraoperative evoked potentials.

	Introduction

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
Thoracic surgery poses a rare, yet tragic threat to spinal cord circulation. Iatrogenic intraoperative spinal cord ischemic injury is multifactorial, with mechanisms including perioperative hypotension, acute thromboembolic episodes, aortic cross clamping, increased cerebrospinal fluid pressure, and interruption or compression of intercostal arterial supply [1]. Most of the literature surrounds hypoperfusion pursuant to repair of aortic aneurysms and coarctation [2–4], but other thoracic operations involving the posterior mediastinum such as esophagectomy or posterior chest wall resection and resection of neurogenic tumors pose a real risk to spinal cord circulation [5, 6]. Although manifest signs identify the infarcted level and region of the cord, ascertaining the site of the vascular lesion is difficult because of variability in regional arterial supply. The anatomy of spinal cord circulation and its marked variation must be appreciated and the postoperative clinical presentations must be clarified for appropriate follow-up care.

Paraplegia after repair of the thoracic aorta is a recognized risk, with a reported incidence rate of about 5% [7], but it is less frequent after nonaortic chest surgery. The incidence of paraplegia after posterolateral thoracotomy is estimated at 0.08% [6] although reported incidence may be prone to underestimation because of postoperative sedation and analgesia, which delay identification of neurologic dysfunction. We report on 6 patients who suffered such iatrogenic deficit after thoracic operations.

	Case 1: chest wall resection

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 62-year-old woman presented with an operable right lower lobe primary non–small cell lung cancer extending posteriorly to the chest wall between the sixth and eighth ribs. An en-bloc resection of the involved lobe and the chest wall was performed without the use of epidural anesthesia. Significant bleeding was noted from the sixth intercostal artery and arrested by electrocauterization. The patient was noted to have paraplegia with sensory deficit at T8 level in the early postoperative period. Computed tomography (CT) scan ruled out intraspinal bleeding and spinal cord compression from an epidural blood clot. No neurologic recovery was noted while the patient was in the hospital or at the 10-month follow-up.

	Case 2: chest wall resection

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 65-year-old man presented with an operable primary malignant tumor in the superior segment of the right lower lobe of the lung. At thoracotomy, the surgical team deemed it necessary to perform a lobectomy and an en-bloc posterior chest wall resection of the fifth to seventh ribs inclusive, requiring disarticulation from the thoracic vertebrae. An epidural catheter was not used for postoperative pain control. Paraplegia with sensory deficit caudal to T7 was noted in the early postoperative period. A CT scan ruled out intraspinal bleeding and spinal cord compression from an epidural blood clot. Recovery was complicated by postoperative pneumonia and the patient died of acute respiratory distress syndrome on the 5th postoperative day.

	Case 3: resection of pulmonary metastasis adherent to descending thoracic aorta

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 69-year-old woman with a remote history of endometrial carcinoma was found to have an asymptomatic solitary pulmonary metastasis in the superior segment of the left lower lobe of the lung. The tumor deposit was located peripherally and was found to be adherent to the descending thoracic aorta. The aorta was cross-clamped for 15 minutes above and below the area of involvement for safe resection and aortic Gore-Tex (W.L. Gore and Assoc, Flagstaff, AZ) patch reconstruction in a normothermic patient. No intercostal arteries were sacrificed during the procedure. Neither systemic heparinization nor a temporary aortic shunt was used. Epidural catheter was not inserted for postoperative pain control. In the recovery room, the patient was noted to have paraplegia below level T8. Functional recovery was absent until her death from ARDS 30 days after her operation.

	Case 4: resection of a malignant cartilaginous tumor in the posterior chest

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 64-year-old man presented with an asymptomatic, right posterior mediastinal mass initially thought to be a neurogenic tumor. At operation, the lesion was determined to be a chondrosarcoma involving the posterior portions of the third and fourth ribs, the adjoining third and fourth costovertebral joints, and the periosteum of the respective vertebral bodies. All gross tumor material was removed with neither severe local bleeding nor systemic hypotension. The tumor was found to spread along the T3 and T4 nerve roots, and an inadvertent dural tear was repaired to prevent cerebrospinal fluid leak. Immediately postoperatively the patient was noted to have paraplegia and loss of sensation below the nipples (T5). At spinal exploration through laminectomy, neither direct injury to the spinal cord nor significant local bleeding was found. No functional recovery was noted by the 4-year follow-up.

	Case 5: distal esophagomyotomy for achalasia

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 25-year-old man was undergoing an operation for relief of dysphagia caused by achalasia. An epidural catheter had been inserted for postoperative pain control. During the performance of the left thoracotomy (sixth interspace), the intercostal vessel was injured at the posterior end of the incision deep to the erector spinalis muscle. Hemostasis was achieved by electrocautery. Thereafter, the operation proceeded with no complication. Postoperatively, paraparesis developed along with sensory deficit below the level of T10. A CT scan suggested the possibility of extradural compression with laminectomy demonstrating abnormal dural blood vessels but no hematoma or other compression. Some functional recovery has been noted, although accompanied by mild persistent lower limb spasticity after follow-up at 2 years.

	Case 6: right lower lobectomy

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
A 56-year-old man was undergoing a right lower lobectomy for stage I carcinoma of the lung. During the posterolateral thoracotomy incision through the sixth rib, some bleeding occurred at the posterior end of the interspace—possibly the result of injury to branches of the sixth intercostal artery. The area was cauterized and packed with oxycellulose. After completion of the routine lobectomy, the oxycellulose was removed but the bleeding persisted. A small strip of oxycellulose was left in the intercostal space to control the bleeding. The patient did well for 18 hours, after which he developed paresthesias in his feet. Over the next 6 hours paraplegia and anesthesia developed below the T7 dermatome. An emergent magnetic resonance imaging (MRI) of the spine revealed extrinsic compression, and T6-T7 laminectomy was performed with removal of the oxycellulose from the extradural space. Recovery was to full function, although the patient had some spasticity on discharge. The patient was lost to follow-up.

	Comment

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 
These cases and a literature review prompted this current review of the importance of spinal cord circulation to the general thoracic surgeon.

Anatomy
The spinal cord receives blood from three longitudinal channels: one anterior spinal artery (ASA) and two posterior spinal arteries (PSA). The ASA is a midline vessel that lies on, but does not penetrate, the anterior fissure and supplies blood to the anterior two thirds of the spinal cord [8, 9]. The ASA is formed at the level of the foramen magnum by fusion of the anterior spinal branches of the vertebral arteries. Although originally described [10] and often still cited [11, 12] as discontinuous, the ASA has been portrayed in more recent studies as continuous but with an ongoing heavy dependence on segmental supply [13, 14]. The PSAs are medial to the nerve roots and originate from the posterior inferior cerebellar arteries, but still receive segmental supply. They are normally continuous rostral to caudal and supply the posterior third of the spinal cord [11]. Arteriolar-sized vessels from the ASA and the PSAs form a pial plexus that constitutes the vaso corona that provide limited anastomosis [12] between the longitudinal vessels.

Feeding arteries from the thoracic aorta provide an interrupted segmental supply to the ASA and PSAs [14]. The basic configuration of this regional supply involves dorsal branches of the posterior intercostal artery in each hemithorax. These vessels enter the neural foramen, penetrate the dural root sleeve, and branch to bone, meninges, and neurons. In the thoracic region, spinal arteries bifurcate to form the anterior and posterior radicular branches that connect with the ASA and PSAs [2]. These paired segmental arteries are patent at every level in the human embryo, but most will involute during development leaving a variable adult spinal circulation [15]. Two points are important about the adult segmental arterial blood supply of the spinal cord: that only one of the paired segmental arteries at the levels mentioned will be dominant with the other vestigial, and that the blood from the dominant arteries provides important segmental supply to maintain ASA perfusion [12]. Normally two small radicular branches supply the cord between C8 and T9; the remainder of the spinal cord is supplied largely by the arteria radicularis magna (artery of Adamkiewicz) with minor contribution from an infrarenal radicular artery [12, 14]. The artery of Adamkiewicz, originating from the left in 80% of the population [16], arises from T5-T8 in 15% of cases, T9-T12 in 75%, and L1-L2 in 10% [14]. Only a few radicular arteries persist in the adult leaving precarious supply, with watershed areas prone to ischemic damage around the levels of T1, T5, and T8-T9 [11, 17]. Because the PSAs are continuous and have more consistent segmental supply [12], most vascular lesions will cause anterior cord dysfunction.

Venous drainage of the spinal cord has a similar distribution to arterial supply. Batson’s plexus is arranged as an intraspinal longitudinal system composed of anterior and posterior spinal veins running medially and laterally fed by segmental radicular veins [11]. These arise from an internal vertebral venous plexus in the epidural space that communicates through the intervertebral foramina with the external vertebral plexus closely related to the vertebral bodies [18]. Blood passes to the vertebral, intercostal, and lumbar veins and ultimately through the hemiazygous and azygous systems to the inferior vena cava [19]. An important difference between spinal cord veins and their systemic counterparts is the absence of veins to uniformly direct blood flow, thereby potentially allowing for seeding of infection, particulate emboli, or neoplastic cells.

Pathophysiology
Neurologic deficit after thoracic surgery can be divided into changes in arterial supply, obstruction to venous outflow, and direct damage from use of epidural analgesia. The operations, presentations, investigations, and outcomes of our patients are summarized in Table 1, to accompany the discussion of pathophysiology below.

As we found, the mechanism of ischemic injury can be highly variable: prolonged hypoxia from rib retraction during thoracotomy and posterior sectioning of intercostal vessels for chest wall resection may have damaged the susceptible watershed areas of the spinal cord. Aortic cross-clamping can cause direct reduction of spinal cord perfusion, and resection of a metastasis adherent to the aorta may injure the artery of Adamkiewicz or other segmental supply of the ASA and the PSAs. A tumor infiltrating the ribs and into the nerve root might divert blood flow away from the spinal cord in the T4 watershed area for its own growth through neoangiogenesis. Other mechanisms of such injury in nonaortic thoracic surgery are worthy of note: by simple proximity of the pleural cavity to the dura through the intervertebral foramina, the extent of posterior dissection of the posterolateral thoracotomy and use of electrocautery to achieve hemostasis are both associated with accidental trauma to the vessels supplying the spinal cord vasculature and direct damage to the cord. Mobilization of the esophagus during blunt dissection may sever vessels that unknowingly also feed the spinal cord. Routine ligation of intercostal vessels, particularly in the setting of extensive aortic or esophageal disease, also carries the risk of irreversibly damaging vessels that provide critical blood supply to the anterior spinal artery [6, 21]. Oxidized cellulose is recognized as a definite hazard believed to act by physical phenomenon as demonstrated in our sixth case. Saturated with blood, the oxycellulose swells to aid in clot formation; this enlarging gelatinous substance can also migrate through intervertebral foramina into the limited space of the spinal canal. The increased epidural pressure causes spinal cord compression and associated catastrophic, albeit potentially correctable, neurologic deficit [22].

Venous outflow obstruction is rare but produces cord edema and progressive neuronal dysfunction with or without concomitant hemorrhage [23]. Typical presentation is hemorrhagic infarction with sudden and rapidly progressive motor, sensory, or autonomic dysfunction over days to weeks, frequently accompanied by back pain. The pattern of injury is more typical of a centrally located cord lesion [19]. The rarer, nonhemorrhagic presentation is slowly progressive over weeks to months and less often associated with pain. Lesions are discrete, peripherally located, and often associated with vascular malformations [23]. Dural arteriovenous fistulas and associated arachnoid fibrosis may cause intramedullary hypertension with ensuing Foix–Alajouanine syndrome [24], characterized by lower limb spasticity, sensory deficit, and loss of sphincter control.

The increasing popularity of thoracic epidural analgesia for postoperative acute pain control merits comment. The patient is afforded an effective means of postoperative pain management with minimal risk of neurologic sequelae. The possibilities of direct damage to the spinal cord, systemic hypotension leading to ischemic damage, and epidural hematoma leading to compressive damage are mechanisms by which permanent neurologic damage may occur [25]. Despite these theoretical risks, permanent neurologic complications from epidural analgesia are estimated to occur at a maximum risk of 0.07%, with neurologic damage from bleeding complications occurring in only 1 in 150,000 patients [25].

Neurologic manifestations
The signs of spinal cord ischemia are highly variable, ranging from transient ischemic attacks to autonomic dysfunction to extensive motor deficits and paresthesias [11]. Specific individual presentation indicates the area of neuronal malfunction, but as understood from the discussion above, the affected site may be distant from the vascular lesion.

The vascular anatomy predisposes the presentation of the anterior two-thirds syndrome resulting from insufficient ASA supply. This pattern reflects bilateral disease of the spinal cord generally sparing the dorsal columns. All motor, sensory, and autonomic functions are lost below the level of the lesion, leaving a paraplegic patient with severe weakness, sphincter paralysis, and loss of pain and temperature sensation with notable preservation of intact proprioception and vibration sensation [11, 26]. Most often, this situation occurs with a loss of lower arterial supply, the watershed zone of which can involve the spinal cord several levels superior [14].

Recalling that at any given level, the central portion of the cord is a watershed zone, a central cord syndrome may result after prolonged hypotension [27]. This gray matter disorder involves the crossing spinothalamic tracts near the central canal. The expected pattern is one of segmental findings: loss of pain and temperature sensation, loss of tendon reflexes, segmental atrophy and weakness; and may include long tract signs (spastic weakness, brisk reflexes, Babinski response, urinary urgency) below the lesion. Identification of a sensory level on the trunk facilitates localization of the damage and useful markers are at the nipples (T4) and umbilicus (T10). Infarction at T9 and T10 paralyzes the lower and spares the upper abdominal muscles, creating upward movement of the umbilicus with abdominal wall contraction.

Neurogenic shock is a presentation of autonomic dysfunction arising from malperfusion at or above T6 [11]. From a cardiovascular perspective, the patient is effectively sympathectomized and relative bradycardia, hypotension [28], and hypothermia [11] manifest distributive shock in the setting of unopposed parasympathetic discharge. Additionally, urologic consequence of detrusor hyperreflexia and striated and smooth sphincter dyssynergia may ensue [29].

Therapy
Postoperative detection of neurologic deficit constitutes an emergency, and the surgeon should be aware of the above-delineated etiologies of such presentation. Neurosurgical consult with emergent CT or MRI are necessary to rule out lesions with potential surgical remedy—CT may demonstrate hematoma or vertebral fracture and MRI helps detect compressive or demyelinating lesions [11]. Early changes associated with spinal cord infarction are best appreciated with MRI [30]. Functional recovery is poor even when emergency exploratory laminectomy reveals a compressing element [18] and reversal of ischemia due to critical vessel interruption is not viable as the exact vessels requiring implantation cannot currently be identified accurately [1].

Prevention
Preoperative identification and preservation of the artery of Adamkiewicz may help avoid spinal cord ischemia, although having radiographic evidence of this highly variable artery’s level of origin remains of questionable advantage. Visualization can be accomplished by magnetic resonance angiography in approximately 70% of patients and has demonstrated benefit in the repair of thoracic aortic aneurysms as spinal cord complications fall from between 3% and 5% of patients to none recorded [31]. Conversely, other studies report a very low incidence of paraplegia after aortic repair performed with intentional sacrifice of all involved arteries [4, 32, 33], obviating the benefit of any such investigation. Of equal importance are the recognition of precarious watershed areas in adult spinal cord circulation and the paucity of segmental feeding radicular arteries in the thorax. Knowledge of the arterial supply can allow for more protective cross-clamping techniques and care to revascularize intercostal arteries at the originating and neighboring levels. Mineo and coworkers [34] proposed the use of radiographic study in select groups of patients such as elderly patients with generalized arteriosclerosis undergoing esophageal dissection. Djurberg and Haddad [5] suggested that certain high-risk patients should be identified if procedures require positioning that may cause radicular artery compression by osteophytes at the intervertebral foramen. Grillo [35] proposed the routine use of thoracic aortography for assessing spinal cord blood supply in the thorax before resecting posterior mediastinal neurogenic tumors arising between T6 and T12. However, no studies have compared the risks of these techniques with the benefit conferred.

The role of intraoperative monitoring is also undergoing clarification. Two groups of researchers have proposed somatosensory-evoked potentials and motor-evoked potentials during aortic surgery to detect the onset of spinal dysfunction and allow for rapid revascularization or decompression [36, 37]. Such clearly effective studies are currently used to reduce neurologic deficit during orthopaedic surgery for scoliosis correction by Harrington rod insertion [38], and debate continues as to the benefit conferred by motor-evoked potentials [39] as spinal cord ischemia affects anterior horn cells not tested by conventional somatosensory-evoked potentials. Neurologic complications of nonaortic thoracic surgery are rarer and no benefit has been demonstrated with this technique.

In the setting of aortic repair, several techniques and pharmacologic agents have been explored to minimize potential ischemic damage. While of questionable relevance to the general thoracic surgeon’s practice, an awareness of ongoing research in the field of postthoracotomy paraplegia prevention may help prepare surgeons for anticipated future techniques. Hypothermia reduces oxygen consumption of neural tissue by approximately 5% per degree drop [40] between 37°C and 22°C, prolonging the tolerance of the spinal cord to ischemia [41]. Although this practice may permit reimplantation of transected intercostal arteries, the technique remains controversial because patients in whom the arteries were sacrificed generally have more extensive aortic disease that demanded the prolonged cross-clamping [1]. Rabbit studies have demonstrated that elevated pre-ischemia glucose levels lead to a higher incidence of paraplegia after aortic occlusion [42], thereby mandating close monitoring of blood glucose and use of intravenous fluids devoid of glucose during procedures. Increased substrate supply results in lactic acid accumulation potentiating a less favorable intracellular environment. Expeditious surgery with short aortic cross-clamping time [43] and limiting the use of the bipolar cautery may decrease the risk of transecting spinal cord arterial supply. Minimizing oxidized cellulose packing with meticulous removal of material prior to closure [22] may prevent extrinsic compression. No studies have been performed to validate the effectiveness of the latter two suggestions.

Use of an opiate antagonist combined with cerebrospinal fluid drainage increases spinal cord blood flow and perfusion pressure. This strategy has demonstrated benefit on neurologic function in patients undergoing repair of thoracic and thoracoabdominal aneurysms [44]. Corticosteroid use for membrane stabilization, free-radical scavenging, and immune system modulation [12] are under investigation, with encouraging results from early canine studies [45, 46]. More recently, use of 21-aminosteroids, potent scavengers of peroxyl radicals and superoxide species that lack mineralocorticoid and glucocorticoid activity, have demonstrated reduced spinal cord ischemia in rabbit models [47]. Calcium-channel blockers also have equivocal evidence with opposing studies showing excellent prevention of spinal cord ischemia from use of nimodipine within 30 minutes of injury [48] and no significant difference [49]. Other agents showing early promise in animal studies include chloroquine and colchicine [50] by inhibiting mononuclear phagocyte function; anti-CD18 antibody [51] by attenuating leukocyte adherence to the endothelium; hypothermic adenosine [52] by limiting free-radical production, neutrophil adherence to the endothelium, and calcium influx into neurons; and intrathecal papaverine [53] as a potent vasodilator of the ASA.

Thoracic surgery poses a threat to spinal cord vasculature and this tragic outcome warrants a clear understanding of the spinal cord circulation and its susceptibility to ischemic damage. The cases presented herein outline a variety of ways in which thoracic surgery can adversely affect the spinal cord circulation. Our experience demonstrates that aortic cross-clamping, chest wall resection, esophageal surgery, tumors invading into nerve roots, and the thoracotomy incision itself all warrant appropriate caution to preserve intercostal artery anatomy, particularly in the watershed areas. The role of selective motor- and somatosensory-evoked potentials and spinal angiography in high-risk surgical procedures (eg, large neurogenic tumors and vertebral resections) needs further investigation and elaboration—the former to intraoperatively identify neurologic deficit, and the latter to establish an anatomical roadmap for surgery.

	References

Top Abstract Introduction Case 1: chest wall... Case 2: chest wall... Case 3: resection of... Case 4: resection of... Case 5: distal esophagomyotomy... Case 6: right lower... Comment References

 

1. Laschinger J.C., Izumoto H., Kouchoukos N.T. Evolving concepts in prevention of spinal cord injury during operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1987;44:667-674.[Abstract]
2. Patersnak B.M., Boyd D.P., Ellis F.H. Spinal cord ischemia after procedures on the aorta. Surg Gynecol Obstet 1972;135:29-34.[Medline]
3. Brewer L.A., Fosburg R.G., Mulder G.A., Verska J.J. Spinal cord complications following surgery for coarctation of the aorta. J Thorac Cardiovasc Surg 1972;64:368-380.[Medline]
4. Griepp R.B., Ergin M.A., Galla J.D., et al. Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta. J Thorac Cardiovasc Surg 1996;112:1202-1215.[Abstract/Free Full Text]
5. Djurberg H., Haddad M. Anterior spinal artery syndrome: paraplegia following segmental ischaemic injury to the spinal cord after oesophagectomy. Anaesthesia 1995;50:345-348.[Medline]
6. Attar S., Hankins R.J., Turney Z.P., Kreasna J.M., McLaughlin S.G. Paraplegia after thoracotomy: report of five cases and review of the literature. Ann Thorac Surg 1995;59:1410-1416.[Abstract/Free Full Text]
7. Cambria R.P., Davison J.K., Carter C., et al. Epidural cooling for spinal cord protection during thoracoabdominal aneurysm repair: a five-year experience. J Vasc Surg 2000;31:1093-1102.[Medline]
8. Svensson L.G., Klepp P., Hinder R.A. Spinal cord anatomy of the baboon—comparison with man and implications for spinal cord blood flow during thoracic aortic cross-clamping. S Afr J Surg 1986;24:32-34.[Medline]
9. Sliwa J.A., Maclean I.C. Ischemic myelopathy: a review of spinal vasculature and related clinical syndromes. Arch Phys Med Rehabil 1992;73:365-372.[Medline]
10. Lazorthes G., Gouaze A., Zadeh J.O., et al. Arterial vascularization of the spinal cord: recent studies of anastomotic substitution pathways. J Neurosurg 1971;35:253-262.
11. Cheshire W.P., Santos C.C., Massey E.W., Howard J.F. Spinal cord infarction: etiology and outcome. Neurology 1996;47:321-330.[Abstract/Free Full Text]
12. Gharagozloo F., Larson J., Dausmann M.J., Neville R.F., Jr., Gomes M.N. Spinal cord protection during surgical procedures on the descending thoracic and thoracoabdominal aorta: review of current techniques. Chest 1996;109:799-809.[Free Full Text]
13. Biglioli P., Spirito R., Roberto M., et al. The anterior spinal artery. The main arterial supply of the human spinal cord—a preliminary anatomic study. J Thorac Cardiovasc Surg 2000;119:376-379.[Free Full Text]
14. Domisse G.F. The blood supply of the spinal cord: a critical vascular zone in spinal surgery. J Bone Joint Surg 1974;56B:225-235.
15. Moore K.L., Persaud T.V.N. The developing human: clinically oriented embryology, 6th ed Philadelphia: WB Saunders, 1998.
16. Svensson L.G., Rickards E., Coull A., et al. Relationship of spinal cord blood flow to vascular anatomy during thoracic aortic cross-clamping, and shunting. J Thorac Cardiovasc Surg 1986;91:71-78.[Abstract]
17. Alleyne C.H., Cawley C.M., Shengelaia G.G., Barrow D.L. Microsurgical anatomy of the artery of Adamkiewicz and its segmental artery. J Neurosurg 1998;89:791-795.[Medline]
18. Gillilan L.A. Veins of the spinal cord: anatomic details, suggested clinical applications. Neurology 1970;20:860-868.[Abstract/Free Full Text]
19. Heller S.L., Meyer R.J., Russell E.J. Spinal cord venous infarction following endoscopic sclerotherapy for esophageal varices. Neurology 1996;47:1081-1085.[Abstract/Free Full Text]
20. Szilagyi D.E., Hageman J.H., Smith R.F., Elliott J.P. Spinal cord damage in surgery of the abdominal aorta. Surgery 1978;83:38-56.[Medline]
21. Koning H.M., Koster H.G., Niemeijer R.P. Ischaemic spinal cord lesion following percutaneous radiofrequency spinal rhizotomy. Pain 1991;45:161-166.[Medline]
22. Short D.H. Paraplegia associated with the use of oxidized cellulose in posterolateral thoracotomy incisions. Ann Thorac Surg 1990;50:288-290.[Abstract]
23. Kim R.C., Smith H.R., Henbest M.L., Choi B.H. Nonhemorrhagic venous infarction of the spinal cord. Ann Neurol 1984;15:379-385.[Medline]
24. Hughes J.T. Venous infarction of the spinal cord. Neurology 1971;21:794-800.[Free Full Text]
25. Giebler R.M., Scherer R.U., Peters J. Incidence of neurologic complications related to thoracic epidural catheterization. Anesthesiology 1997;86:55-63.[Medline]
26. Foo D., Rossier A.B. Anterior spinal artery syndrome and its natural history. Paraplegia 1983;21:1-10.[Medline]
27. Wagner R., Jagoda A. Spinal cord syndromes. Emerg Med Clin North Am 1997;15:699-711.[Medline]
28. Low P.A., Dyck P.J. Pathologic studies and the nerve biopsy in autonomic neuropathies. In: Low P.A., ed. Clinical autonomic disorders. Boston: Little Brown, 1993:331-334.
29. Kaplan S.A., Chancellor M.B., Blavas J.G. Bladder and sphincter behavior in patients with spinal cord lesions. J Urol 1991;146:113-117.[Medline]
30. Yuh W.T.C., Marsh E.E., Wang A.K., et al. MR imaging of spinal cord, and vertebral body infarction. Am J Neuroradiol 1992;13:145-154.[Abstract]
31. Yamada N., Okita Y., Minatoya K., et al. Preoperative demonstration of the Adamkiewicz artery by magnetic resonance angiography in patients with descending or thoracoabdominal aortic aneurysms. Eur J Cardiothorac Surg 2000;18:104-111.[Abstract/Free Full Text]
32. Acher C.W., Wynn M.M., Hoch J.A., Kranner P.W. Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement. J Vasc Surg 1998;27:821-830.[Medline]
33. Biglioli P., Spirito R., Poqueddu M., et al. Quick, simple clamping technique in descending thoracic aortic aneurysm repair. Ann Thorac Surg 1999;67:1038-1043.[Abstract/Free Full Text]
34. Mineo T.C., Cristino B., Ambrogi V. Paraplegia after surgery of the thoracic esophagus. J Thorac Cardiovasc Surg 1998;116:653.[Free Full Text]
35. Grillo G.C. Combined approach to "dumbell" intrathoracic and intraspinal neurogenic tumors. Ann Thorac Surg 1983;36:402-407.[Abstract]
36. Cunningham J.N., Laschinger J.C., Merkin H.A., et al. Measurement of spinal cord ischemia during operations on the thoracic aorta: initial clinical experience. Ann Surg 1982;196:285-296.[Medline]
37. de Haan P., Kalkman C.J. Spinal cord monitoring: somatosensory- and motor-evoked potentials. Anesthesiol Clin North Am 2001;19:923-945.[Medline]
38. Nuwer M.R., Dawson E.G., Carlson L.G., et al. Somatosensory evoked potential spinal cod monitoring reduces neurologic deficits after scoliosis surgery: results of a large multicenter survey. Electroencephalogr Clin Neurophysiol 1995;96:6.[Medline]
39. Owen J.H., Bridwell K.H., Grubb R., et al. The clinical application of neurogenic motor evoked potentials to monitor spinal cord function during surgery. Spine 1991;16(suppl):S385.[Medline]
40. Hagerdal M., Harp J., Nilsson L., et al. The effect of induced hypothermia on oxygen consumption in the rat brain. J Neurochem 1975;24:311.[Medline]
41. Robertazzi R.R., Cunningham J.N. Intraoperative adjuncts of spinal cord protection. Semin Thorac Cardiovasc Surg 1998;10:29-34.[Medline]
42. Drummond J.C., Moore S.S. The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia in the rabbit. Anesthesiology 1989;70:64-70.[Medline]
43. Katz N.M., Blackstone E.H., Kirklin J.W., et al. Incremental risk factors for spinal cord injury following operation for acute traumatic aortic transection. J Thorac Cardiovasc Surg 1981;81:669-674.[Abstract]
44. Acher C.W., Wynn M.M., Hoch J.R., et al. Combined use of cerebrospinal fluid, and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994;19:236-246.[Medline]
45. Weaver C.E., Jr., Marek P., Park-Chung M., Tam S.W., Far D.H. Neuroprotective activity of a new class of steroidal inhibitors of the N-methyl-D-aspartate receptor. Proc Natl Acad Sci USA 1997;94:10450-10454.[Abstract/Free Full Text]
46. Laschinger J.C., Cunningham J.N., Cooper M.M., et al. Prevention of ischemic spinal cord injury following aortic-cross-clamping: use of corticosteroids. Ann Thorac Surg 1984;38:500-506.[Abstract]
47. Braughler J.M., Pregenzer J.F., Chase R.L. Novel aminosteroids as potent inhibitors of iron dependent lipid peroxidation. J Biol Chem 1987;262:10438-10440.[Abstract/Free Full Text]
48. Schittek A., Bennink G.B., Cooley D.A., et al. Spinal cord protection with intravenous nimodipine: a functional and morphologic evaluation. J Thorac Cardiovasc Surg 1992;104:1100-1105.[Abstract]
49. Lyden P.D., Zivin J.A., Kochler A., et al. Effects of calcium channel blockers on neurologic outcome after focal ischemia in rabbits. Stroke 1988;19:1020-1026.[Abstract/Free Full Text]
50. Giulian D., Robertson C. Inhibition of mononuclear phagocytes reduces ischemic injury in the spinal cord. Ann Neurol 1990;27:33-42.[Medline]
51. Clark W.M., Madden K.P., Rothlein R., et al. Reduction of central nervous system ischemic injury in rabbits using leukocyte adhesion antibody treatment. Stroke 1991;22:877-883.[Abstract/Free Full Text]
52. Rudolphi K.A., Schubert P., Parkinson F.E., et al. Neuroprotective role of adenosine in cerebral ischemia. Trends Pharmacol Sci 1992;13:439-445.[Medline]
53. Svensson L.G., Von Ritter C.M., Groeneveld H.T., et al. Cross-clamping of the thoracic aorta: influence of aortic shunts, papaverine, calcium channel blockers, allopurinol and superoxide dismutase on spinal cord blood flow and paraplegia in baboons. Ann Surg 1986;204:38-47.[Medline]

This article has been cited by other articles:

				A. Raz, A. Avramovich, E. Saraf-Lavi, M. Saute, and L. A. Eidelman Spinal cord ischemia following thoracotomy without epidural anesthesia: [Ischemie de la moelle epiniere a la suite d'une thoracotomie sans anesthesie peridurale]. Can J Anesth, June 1, 2006; 53(6): 551 - 555. [Abstract] [Full Text] [PDF]

				J. Flores, T. Kunihara, N. Shiiya, K. Yoshimoto, K. Matsuzaki, and K. Yasuda Extensive deployment of the stented elephant trunk is associated with an increased risk of spinal cord injury J. Thorac. Cardiovasc. Surg., February 1, 2006; 131(2): 336 - 342. [Abstract] [Full Text] [PDF]

				J. F. Bruzzi, M. Remy-Jardin, D. Delhaye, A. Teisseire, C. Khalil, and J. Remy Multi-Detector Row CT of Hemoptysis RadioGraphics, January 1, 2006; 26(1): 3 - 22. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Donna E. Maziak Robert J. Ginsberg Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shamji, M. F. Articles by Pon, R. Search for Related Content PubMed PubMed Citation Articles by Shamji, M. F. Articles by Pon, R. Related Collections Cerebral protection