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Ann Thorac Surg 1996;62:1532-1534
© 1996 The Society of Thoracic Surgeons


Case Report

Spinal Cord Infarct After Arterial Switch Associated With an Umbilical Artery Catheter

Robert P. Lemke, MD, Nnanake Idiong, MD, Saad Al-Saedi, MD, Niels G. Giddins, MD, Cameron Ward, MD, Andrew Hamilton, MD, Lois Hawkins, MN, Betty J. Hancock, MD, Jonah N. K. Odim, MD, PhD

Variety Children's Heart Center, Winnipeg, Manitoba, Canada

Accepted for publication June 4, 1996.


    Abstract
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Paraplegia after an open heart operation in a neonate is a rare complication. We report a case of a infant in whom paraplegia developed after a successful arterial switch operation for transposition of the great arteries. The infant was monitored and resuscitated in the preoperative period with umbilical arterial and venous catheter tips located in the midthoracic region. He likely suffered a clinically silent thromboembolic event predisposing him to a localized hemorrhagic infarction during the repair.


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Spinal cord lesions in neonates after cardiopulmonary bypass are extremely rare despite the performance of increasingly more complex neonatal congenital heart operations. In this report, we describe a term infant in whom paraplegia developed after a successful arterial switch operation for transposition of the great arteries. This neonate had undergone preliminary resuscitation and monitoring with umbilical arterial (UAC) and venous catheters (UVC).

A 3.3-kg male infant, born at term after an uneventful pregnancy and delivery, became cyanotic at 3 hours of age. The patient was started on a regimen of intravenous prostaglandin, intubated because of respiratory failure, and transferred to our institution for evaluation.

Physical examination revealed normal heart sounds, no murmurs, and normal peripheral pulses. A neurologic assessment demonstrated normal primitive and deep tendon reflexes with normal tone and movement of all four limbs. A UAC and a UVC were inserted with catheter tips positioned at the level of the fourth and tenth thoracic vertebrae, respectively (Fig 1Go). Cross-sectional echocardiography revealed D-transposition of the great arteries.



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Fig 1. . Chest roentgenogram illustrating the level of the tips of both umbilical arterial and venous catheters.

 
A balloon atrial septostomy was performed at 2 days of life. Concurrent angiography confirmed that the coronary ostia arose from their appropriate facing sinuses. Prostaglandin administration was discontinued and mechanical ventilation weaned to extubation. The UAC and UVC were removed at 3 days of age. He remained stable with movement in his lower limbs until definitive operative repair at 5 days of age.

Under continuous low-flow (50 mL•kg-1•min-1) hypothermic (16°C) perfusion, the infant underwent an arterial switch operation. The circulation was arrested for 6 minutes to repair the atrial septum. The aortic cross-clamp time was 90 minutes. During rewarming normal sinus rhythm was easily established. There was bleeding at the neo-aortic reconstruction site, which abated with local pressure and administration of blood product components. The patient remained hemodynamically stable throughout. Total time on bypass was 3 hours 43 minutes.

Sternal closure was delayed until the sixth postoperative day, when relaxants and sedation were lifted and initial inotropic support (12 µg•kg-1•min-1 of dopamine, 2 µg•kg-1•min-1 of nitroglycerin, and 7.5 µg • kg-1•min-1 of amrinone) had been weaned. There was neither significant hypotension nor anemia in the postoperative period. There were no arrhythmias.

After discontinuation of muscle relaxants, the patient became more alert and active. But he was noted to have flaccid lower extremities with absent deep tendon and plantar reflexes. Urine dribbled continuously from the urethra, and he had an absent anal wink. Magnetic resonance imaging revealed enlargement and increased signal intensity characteristic of a hemorrhagic infarct in the tenth thoracic to first lumbar region of the spinal cord (Fig 2Go).



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Fig 2. . Magnetic resonance image of the spinal cord identifying enlargement and increased signal intensity within the cord proximal to the conus, consistent with hemorrhagic infarction.

 
Within 4 weeks the patient was voiding spontaneously. A voiding cystourethrogram done at 7 weeks of age revealed poor bladder emptying but no signs of vesicouretal reflux. The child's neurologic examination was unchanged at discharge. At follow-up, 6 months later, he had a normally functioning heart and return of proximal hip flexion.


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After cardiopulmonary bypass, spinal cord infarction and paraplegia is almost unheard of in neonates despite an increasing number of definitive complex congenital heart repairs undertaken in these critically ill patients. In an anecdotal report, Amitay and associates [1] described an infant with paraplegia 8 days after uneventful repair of a hypoplastic aortic arch. These signs were attributed to postoperative anemia not corrected due to parental religious convictions. Amitay and associates speculated that decreased oxygen carrying capacity exacerbated an obligate ischemia produced by aortic cross-clamping, which led to the delayed-onset spinal cord syndrome. No incidence of spinal cord injury was noted in a large series of 171 patients undergoing arterial switch prospectively randomized to hypothermic arrest or low-flow bypass support. Moreover, at 1-year follow-up, there was only a higher incidence of seizures and subtle delayed motor development in the circulatory arrest group [2].

On the other hand, the use of UACs has a known, albeit rare association with neonatal spinal cord ischemia [38]. The proposed mechanism of cord ischemia appears related to thromboembolism of the segmental artery supplying the thoracolumbar spinal cord. Clinically silent thromboses have been demonstrated using aortography in 95% of infants with UACs [5]. Furthermore, there are reports of infarction of other major organs such as the intestine and kidneys associated with the position of UAC catheter tips in sick newborns. Despite widespread use of UACs, cord infarction is presumably rare because of variable collateral blood supply. Indeed, there is a great deal of variability in the patterns and degrees of cord infarction in experimental animals when selected vessels are ligated under tightly controlled conditions [8]. We surmise that this cord was predisposed to a localized hemorrhagic infarction during the surgical repair because of an unrecognized preoperative ischemic insult related to the use of umbilical vessel catheters. We further speculate that the combination of an indwelling UAC and UVC in the inflow and outflow vascular territories subserving the midthoracic spinal cord may have compromised blood flow and increased the potential for thromboembolic occlusion of the blood supply to the anterior spinal artery. The diagnosis of cord infarction and paraplegia in this case was delayed because of a period of postoperative muscle relaxation due to an open chest.

With the widespread use of umbilical vessel catheters in newborns and the increasing trend toward earlier definitive repair of complex congenital heart defects in neonates, the use of peripheral arterial lines may prevent this rare but devastating complication of local spinal cord hemorrhagic infarction.


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Address reprint requests to Dr Odim, Department of Cardiothoracic Surgery, Emory Clinic, 1365 Clifton Rd, NE, Atlanta, GA 30322.


    References
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 Footnotes
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 References
 

  1. Amitay M, Welch RW, Byrne PJ, Robertson MA, Penkoske PA. Neonatal spinal cord syndrome associated with hypoplastic aortic arch and anemia. Ann Thorc Surg 1993;56:568–70.[Abstract]
  2. Bellinger DC, Jonas RA, Rappaport LA, et al. Developmental and neurologic status of children after heart surgery with hypothermic circulatory arrest or low flow cardiopulmonary bypass. N Engl J Med 1995;332:550–5.
  3. Aziz EM, Robertson AF. Paraplegia: a complication of umbilical artery catheterization. J Pediatr 1973;82:1051–2.[Medline]
  4. Krishnamoorthy KS, Fernandez RJ, Todres ID, De Long GR. Paraplegia associated with umbilical artery catheterization in the newborn. Pediatrics 1976;58:443–5.[Abstract]
  5. Haldeman S, Fowler GW, Ashwal S, Schneider S. Acute flaccid neonatal paraplegia: a case report. Neurology 1983;33:93–5.[Abstract/Free Full Text]
  6. Brown MS, Phibbs RH. Spinal cord injury in newborns from use of umbilical artery catheters: report of two cases and a review of the literature. J Perinatol 1989;8:105–10.
  7. Singer R, Joseph K, Gilai AN, Meyer S. Nontraumatic, acute neonatal paraplegia. J Pediatr Orthop 1991;11:588–93.[Medline]
  8. McCormick PC, Stein BM. Functional anatomy of the spinal cord and related structures. Neurosurg Clin North Am 1990;1:469–89.




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