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Asian Cardiovasc Thorac Ann 2002;10:85-86
© 2002 Asia Publishing EXchange Pte Ltd

CASE STUDY

Spinal Cord Ischemia Associated With Cardiac Arrest

A Kürsat Bozkurt, MD

Department of Thoracic and Cardiovascular Surgery Cerrahpasa Faculty of Medicine University of Istanbul Istanbul, Turkey
A Kürsat Bozkurt, MD Tel: 90 212 560 8187 Fax: 90 212 529 5600 email: akbozkurt{at}yahoo.com Ataköy 5. Kisim A7/40, Istanbul 34750, Turkey.

   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 
Ischemic spinal cord damage from cardiac arrest is rare. A 48-year-old man underwent a straightforward retroperitoneal aortofemoral bypass operation. The following day, he developed cardiac arrest and was resuscitated successfully, but permanent paraplegia was observed soon afterwards.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
CASE REPORT
 DISCUSSION
 REFERENCES
 
Cerebral complications following successful cardio-pulmonary resuscitation are common and well described. However, there are only a few reports of ischemic spinal cord damage resulting from cardiac arrest.1–4


   CASE REPORT
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
DISCUSSION
 REFERENCES
 
A 48-year-old man was admitted because of incapacitating intermittent claudication of the left leg. He had no history of any coexisting disease. His ankle brachial pressure index was 0.26 and angiography revealed left common iliac occlusion. Retroperitoneal aortofemoral bypass with an 8-mm prosthetic graft was performed uneventfully. The aorta was clamped just above the orifice of the inferior mesenteric artery. The patient was extubated in the operating room and transferred to the postanesthetic care unit for a routine overnight stay. The following day, he was hemodynamically stable and was transferred to the surgical ward with palpable left distal pulses. That afternoon, he developed cardiac arrest with no perceptible precipitating cause. Cardiopulmonary resuscitation (CPR) was initiated promptly and monitoring revealed ventricular fibrillation. Full CPR was performed, including several countershocks. Following 45 minutes of CPR, he became stable with blood pressure of 125/80 mm Hg, and he was transferred to the intensive care unit. Serial cardiac isoenzymes and electrocardiograms failed to determine a myocardial infarction. A thorough neurological exami-nation 2 hours after CPR demonstrated that the patient was completely oriented. However, he had no voluntary movement of either lower extremity. Proprioception and vibratory sensation were preserved. Magnetic resonance imaging of the spinal cord was normal (Figure 1Go). Cerebro-spinal fluid (CSF) drainage was contemplated in order to improve the spinal blood flow, but the delayed recognition of paraplegia and already edematous spinal cord precluded CSF drainage. Corticosteroids and mannitol were ad-ministered. Unfortunately, the patient's paraplegia has been permanent throughout the follow-up period of 20 months. He is ambulatory with some form of assistance, and has good bladder and bowel control. A recent spinal magnetic resonance image demonstrated atrophic changes extending from the 9th thoracic vertebra (T9) to the conus medullaris, characterized by pathologic hyperintensity on T2-weighted images, indicating possible Wallerian de-generation of the bilateral corticospinal tracts (Figure 2Go).



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  		Figure 1. Normal magnetic resonance image of the spinal cord taken immediately after resuscitation.

 


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  		Figure 2. Axial T2-weighted image shows pathologic intensities located mostly at the anterior and central portions of the conus medullaris.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
REFERENCES
 
Spinal cord injury remains the most challenging com-plication following thoracoabdominal aortic aneurysm surgery.5 In spite of extensive precautions, the rate of paraplegia or paraparesis is 5.6% at best.6 Consequently, much research has been carried out on the anatomy of the spinal cord, the pathophysiology of aortic crossclamping, and methods of spinal cord protection.5,6 Anterior and posterior spinal arteries supply the spinal cord. The anterior spinal artery supplies the anterior two-thirds of the cord and is usually well developed in the upper thorax. This artery is smaller in the lower chest where some segments are dependent on variable segmental branches from the intercostal and lumbar arteries.6 The artery of Adamkiewicz is the largest of these, and it can arise anywhere from T5 to the 2nd lumbar vertebra.7 Crossclamping of the thoracic aorta renders the spinal cord ischemic and permanent damage may occur after 30 minutes.6 To date, there have been anecdotal reports of nontraumatic spinal cord ischemia following cardio-pulmonary arrest.1–4,7 The most recent report by Idali and colleagues1 described a patient who had cardiac arrest of 15 minutes' duration while undergoing surgery for gangrenous purulent cholecystitis. He became paraplegic postoperatively; however, permanent traumatic damage to one or more critical arteries at the time of hemostatic maneuvers may have been the reason for spinal ischemia rather than the relatively short period of cardiac arrest. The other reported cases fulfilled the criteria of non-ischemic anterior spinal artery syndrome, and resemble the patient in this report.2–4,7

The reason for the rare vascular catastrophe in this case is obscure. It is known that the watershed zone of increased ischemic vulnerability exists near T4. However, the mean level of deficit was found to be at T9 following global ischemia in patients studied by Cheshire and colleagues.7 Individual anatomic variations in the vascular supply to the spinal cord and collateral circulation may be the important factors in selective injury of the cord. Placement of an intrathecal catheter for CSF drainage and applica-tion of intrathecal papaverine in appropriate patients may reverse delayed spinal cord injury.5,8 All reported cases of spinal cord damage following cardiac arrest remained paraplegic during follow-up. Thus, although its effectiveness is not clear yet, it is suggested that CSF drainage with or without intrathecal papaverine adminis-tration be applied in this devastating situation.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 

  1. Idali B, El Mouknia M, Abassi O, Louardi H, Benaguida M. Paraplegia after cardiac arrest. Ann Fr Anesth Reanim 1996;15:199–201.[Medline]

  2. Imaizumi H, Ujike Y, Asai Y, Kaneko M, Chiaba S. Spinal cord ischemia after cardiac arrest. J Emerg Med 1994; 12:789–93.[Medline]

  3. Kim SW, Kim RC, Choi BH, Gordon SK. Non-traumatic ischemic myelopathy: a review of 25 cases. Paraplegia 1988;26:262–72.[Medline]

  4. Rajan RK. Ischemic myelopathy following cardiac arrest. Am Fam Physician 1984;29:221–3.

  5. Svenson LG. New methods of spinal cord protection during operations on the thoracic aorta. In: Franco KL, Verrier ED, editors. Advanced therapy in cardiac surgery. Hamilton, Canada: BC Decker Inc., 1999:311–8.

  6. Coselli JS. Descending and thoracoabdominal aortic aneurysms. In: Edmunds LH, editor. Cardiac surgery in the adult. New York: McGraw-Hill, 1997:1227–44.

  7. Cheshire WP, Santos CC, Massey EW, Howard JF. Spinal cord infarction: etiology and outcome. Neurology 1996; 47:321–31.[Abstract/Free Full Text]

  8. Hill A, Kalman PG, Johnston KW, Vosu HA. Reversal of delayed-onset paraplegia after thoracic aortic surgery with cerebrospinal fluid drainage. J Vasc Surg 1994;20: 315–37.[Medline]





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