Pediatr Cardiol 13:100-103, 1992
Pediatric Cardiology 9 Springer-Verlag New York Inc. 1992
A s y m p t o m a t i c S u b c l a v i a n Steal S y n d r o m e in C h i l d r e n F o l l o w i n g C a r d i a c Surgery: A P o t e n t i a l H a z a r d with R e - o p e r a t i o n ? Michael O. Gayle, C. Anthony Ryan, Kathy Pauw, and Patricia Penkoske Pediatric Intensive Care Unit, Departments of Pediatrics, Pathology and Cardiothoracic Surgery, University of Alberta Hospitals, Edmonton, Alberta, Canada
SUMMARY. We describe a case of fatal hypoxic--ischemic encephalopathy, leading to brain death following the modified Fontan procedure in a child with asymptomatic subclavian steal syndrome (SSS). This patient's brain death was most likely multifactorial in view of his postoperative course. However, we believe that the presence of the SSS contributed to the abnormal cerebral circulation during surgery and postoperatively, leading to brain death. The presence of SSS in patients undergoing an open-heart procedure may be a risk factor for cerebral ischemia or brain death. KEY WORDS: Subclavian steal syndrome - - Fontan - - Brain death
Performance of a Blalock-Taussig (BT) (subclavian-pulmonary artery) anastomosis for treatment of congenital heart disease may lead to the vascular anatomy of the Subclavian steal syndrome (SSS) after either the classic [10] or modified [1] procedure. SSS in patients following the BT shunt procedure is usually due to occlusion of the proximal subclavian artery, but this may also occur secondary to severe stenosis of the innominate artery. Cerebral vascular symptoms in children with SSS are uncommon [16] because of the presumably intact circle of Willis in over 50% of children [2]. However, early [17] and late cerebral ischemic symptoms do occur [13] in children who were initially asymptomatic from their SSS. We report a case of severe cerebral ischemia leading to brain death following the Fontan procedure in a child with asymptomatic SSS, which we presume was acquired after his initial BT shunt.
Case Report A 5-year-old boy, diagnosed to have cyanotic congenital heart disease at birth, had a cardiac catheterization performed which revealed a univentricular atrioventricular connection with a large morphologic left ventricle supporting the pulmonary artery. A d d r e s s offprint requests to: Dr. Michael O. Gayle, 2C3.89 Walter Mackenzie Centre, University of Alberta Hospitals, Edmonton, Alberta T6G 2R7, Canada.
There was severe valvar and subvalvar pulmonary stenosis and an anterior outlet chamber supporting the aorta. The ventricular septal defect was large and nonrestrictive. There was left atrioventricular valve atresia, a patent ductus arteriosus, and a left aortic arch. He had a right BT shunt and a Blalock-Hanlon procedure performed as a newborn and a left BT shunt at 2 years of age. One and a half years after his left BT shunt, a left chest mass was noted on chest x-ray. Investigations of ~his mass, which proved to be a seroma, included a cardiac catheterization which revealed severe stenosis of the right innominate artery resulting in an SSS from the left vertebral to the right vertebral, which then supplied the right BT shunt (Figs. 1 and 2). On review of the patient's history, there were no symptoms of vertebrobasilar ischemia. The patient subsequently had ligation of both BT shunts and a modified Fontan procedure under cardiopulmonary bypass (CPB) using a membrane oxygenator (Sci-Med 1500, Minneapolis, Minnesota) with arterial line filters and hypothermia (core temp 25~ for a period of 3 h and 10 min with an aortic cross clamp time of 33 min. No intraoperative cerebral monitor device was used during CPB. He was admitted postoperatively to the Pediatric Intensive Care Unit (PICU). In the PICU, the patient's temperature was 37.5~ heart rate 130 beats/min, BP 130/60 mmHg (mean arterial pressure [MAP] 77), central venous pressure (CVP) 12 mmHg, and left atrial pressure (LAP) 6 mmHg. The pupils were equal in size and reacted sluggishly to light. Sedation was maintained with an infusion of morphine sulphate (30 mcg/kg/h). Clinically, he was in a low cardiac output state, which was treated with infusions of dopamine (10 mcg/kg/min), neosynephrine (0.8 mcg/kg/min), nitroglycerine (1.0 mcg/kg/min), and calcium chloride. Muscle relaxation was maintained with pancuronium bromide. On the first postoperative day he was noted to have spontaneous movements of his limbs in between doses of muscle relaxants, which were
Gayle et al.: Subclavian Steal Syndrome
101
m Artery
& : Catheters
Fig. 1. Retrograde injection of dye at junction of left carotid and subclavian arteries.
~Rt.
CarotidArtery
h I) Rt. Pulmonary Artery f
/
given every 1-2 h. These movements were unassociated with hemodynamic or pupillary changes and were not considered to be seizure activity. Deterioration in cardiac output with elevations of CVP to 28 mmHg and hypotension (MAP 52 mmHg) occurred by the third postoperative day. After cessation o1' morphine and pancuronium bromide, subsequent neurological examination revealed opening of eyes to deep pain but not to commands, breathing spontaneously, and moving all limbs. By the fourth postoperative day, his neurological examination indicated that he was responding to verbal commands by moving his upper limbs. However, he had progressive generalized edema in the head and neck region, despite diuretic therapy. Cardiac function appeared to stabilize by the fifth postoperative day with mean CVP 14 mmHg and MAP 65 mmHg. Pupils were reactive to light and there were attempts at eye opening to verbal commands. Later his pupils increased in size to 6 mm, and
Fig. 2. Follow through of same injection, visualizing right carotid artery, BT shunt (white arrows), and pulmonary artery (black arrow).
gradually became unreactive despite hyperventilation to keep his Pco2 below 30 mmHg. Further examination revealed no evidence of cortical activity or brainstem reflexes. Temperature, electrolytes, glucose, and serum ammonia were normal. A repeat examination 8 h later confirmed brain death and an electroencephalogram was isoelectric. A computerized tomography (CT) of the head showed diffuse cerebral edema (Fig. 3). After discussions with the family, life support was discontinued. An autopsy, the brain weighed 1570 g (expected weight for age and sex 1300 g, SD 20 g). Macroscopically, there was generalized cerebral and cerebellar swelling with bilateral transtentorial and transforaminal herniation of cerebellar tonsils with focal necrosis. Coronal sections of the cerebrum confirmed the presence of marked to generalized symmetrical swelling associated with compression of the lateral and third ventricles. There was no shift within the midline or regions of normal mottling or softening of the cerebral cortex. Transverse sections of the cerebel-
102
Fig. 3. CT scan demonstrates generalized supratentorial hypodensity of diffuse brain swelling and very small (slit-like) ventricles.
lure revealed diffuse swelling associated with focal softening of the tips of the cerebellar tonsils. The preoperative catheterization findings of severe stenosis of the mid segment of right innominate artery proximal to the anastomosis of the righ~ BT shunt was confirmed.
Discussion
Obstructive lesions of the aortic arch and great vessels predispose to a variety of alterations of normal hemodynamic patterns. The combination of proximal subclavian artery obstruction with retrograde flow in the ipsilateral vertebral artery define the SSS [13]. Accompanying ischemic neurological or upper extremity symptomatology completes the full clinical picture. The symptom patterns are frequently episodic, being related to activity of the upper extremity. Children are often asymptomatic and SSS phenomenon may be an incidental finding, as our patient demonstrated. Neurological sequelae following CPB, including seizures and strokes, may occur in as many as 14% of adult [3] and 2-25% of childhood survivors [9]. While preexisting neurological disorders and abnormal cerebral circulation [4] are present in some children with congenital heart disease, the major cause of neurological morbidity and mortality is thought to be related to the alterations in cerebral blood flow and metabolism associated with CPB [8]. The Fontan procedure is a complex operation involving prolonged CPB, and would be expected to be associated with significant neurological sequelae including death [11, 15]. In a retrospective study, neurological deaths accounted only for 2 (6%) of 32 deaths in 102 children who underwent the Fontan procedure [12].
Pediatric Cardiology Vol. 13, No. 2, 1992
The patient presented in this case report died from tonsillar and cerebellar herniation secondary to cerebral ischemia. This cerebral ischemia could be as a result of alterations in cerebral flow and metabolism and/or air or particulate emboli during CPB [14]. It has been shown that both children [14] and adults [7] have reduced cerebral perfusion during CPB for major cardiac surgery. However, transcranial Doppler ultrasonography studies during CPB in adult patients with severe carotid stenosis suggest normal to increased cerebral blood flow with no increased risk of neurological sequelae [I 8]. There have been no similar studies in children with obstructive lesions of the aortic arch or carotid artery. It is possible that in our patient further decrease in cerebral blood flow could have occurred during CPB as a result of the combination of innominate artery stenosis and SSS. In the postoperative period, our patient had elevated right atrial pressures which would be transmitted to his jugular venous system with subsequent inadequate cerebral perfusion pressure [5], leading to cerebral hypoperfusion. In addition, with the presence of SSS, the brain could lose its blood supply from the left vertebral artery in addition to a potentially important portion of the carotid and contralateral vertebral artery flow [16]. We believe the combination of cerebral hypoperfusion during CPB and the above postoperative factors resulted in this patient having cerebral ischemia with resultant cerebral edema and raised intracranial pressure with subsequent brain death. The microscopic findings in the brain at autopsy indicating no evidence of asymmetrical ischemic changes is not surprising, as there are ample collateral vessels in the pediatric brain [16]. The risk of death following the Fontan procedure is increased with elevated post-repair right atrial pressure, hypertrophy of the ventricular main chamber, and possibly age [12]. We would suggest in view of our present case, an additional risk factor for patients undergoing Fontan or other open-heart procedures could be the presence of an underlying asymptomatic SSS. Vascular reconstructive surgery, as described elsewhere [6, 13], could be indicated at the time of the open-heart procedure, if the SSS is recognized angiographically before surgery. References I. Agarwal KC, Ali Khan MA, Marbey ML (1984) Pulmonary and subclavian steal phenomenon following modified Blalock-Taussig shunt. Am Heart J 108:1567-1570 2. Alpers BJ, Pawray RG, Paddison RM (1959) Anatomical studies of the circle of Willis in normal brain. Arch Neurol Psychiatr 81:409-418
Gayle et al.: Subclavian Steal Syndron~e
3. Andersen K, Waeben J, Jusum B, et al. (1985) Non-pulsatile cardiopulmonary bypass disrupts the flow metabolism couple in the brain. J Thorac Cardiovasc Surg 90:570-579 4. Benson LN, Freedom RM, Wilson GJ, et al. (1986) Cerebral complications following balloon angioplasty of coarctation of the aorta. Cardiovasc Intervent Radiol 9:184-186 5. Dean JM, Rogers MC, Traystman RJ (1987) Pathophysiology and clinical management of the intracranial vault. In Rogers MC (ed) Textbook o f pediatric intensive care 1987. Williams & Wilkins, Baltimore, pp 535-536 6. De Sobregrau RC, Lopez Collado M, Matas Docampo M, et al. (1986) Surgery of the innominate artery. J Cardiovasc Surg 27:31-37 7. Editorial (1989) Brain damage and open-heart surgery. Lancet 2:364-366 8. Ferry C (1987) Nem-ologic sequelae of cardiac surgery in children. A m J Dis Child 141:309-312 9. Ferry PC (1990) Neurologic sequelae of open-heart surgery in children. Am J Dis Child 144:369-373 10. Fogler GM Jr, Shah KD (1965) Subclavian steal in patients with Blalock-Taussig anastomosis. Circulation 31:241 11. Fontan F, Baudet E (1971) Surgical repair of tricuspid atresia. Thorax 26:240-248 12. Kirklin JK, Blackstone EH, KMin JW, et al. (1986) The
103
13.
14.
15.
16.
17.
18.
Fontan operation. Ventricular hypertrophy, age and date of operation as risk factors. J Thorac Cardiovasc Surg 92:1021-1028 Kurlan R, Krall RL, Deweese JA (1984) Vertebrobasilar ischemia after total repair of tetralogy of fallot: Significance of subclavian steal created by Blalock-Taussig anastomosis (Vertebrobasilar ischemia after correction of Tetralogy of Fallot). Stroke 15:359-362 Lundar T, Lindberg H, Lundegaard KF, et al. (1987) Cerebral perfusion during major cardiac surgery in children. Pediatr Cardiol 8:161-165 Mathews K, Bale JF, Clark EB, et al. (1986) Cerebral infarction complicating Fontan surgery for cyanotic congenital heart disease. Pediatr Cardiol 7:161-166 Midgley FM, McClenathan JE (1977) Subclavian steal syndrome in the pediatric age group. Ann Thorac Surg 24:252257 Narto H, Kurokawa K, Kanno T, et al. (1973) Status epilepticus and cortical blindness due to subclavian steal syndrome in a girl with Blalock's operation. Surg Neurol 1:46-49 Von Reutern GM, Hetzel A, Burnbaum D, Schlosse V (1988) Transcranial Doppler ultrasonography during cardiopulmonary bypass in patients with severe carotid stenosis or occlusion. Stroke 19:674-680
Pediatric Cardiology 9 Springer-Verlag New York Inc. 1992
A s y m p t o m a t i c S u b c l a v i a n Steal S y n d r o m e in C h i l d r e n F o l l o w i n g C a r d i a c Surgery: A P o t e n t i a l H a z a r d with R e - o p e r a t i o n ? Michael O. Gayle, C. Anthony Ryan, Kathy Pauw, and Patricia Penkoske Pediatric Intensive Care Unit, Departments of Pediatrics, Pathology and Cardiothoracic Surgery, University of Alberta Hospitals, Edmonton, Alberta, Canada
SUMMARY. We describe a case of fatal hypoxic--ischemic encephalopathy, leading to brain death following the modified Fontan procedure in a child with asymptomatic subclavian steal syndrome (SSS). This patient's brain death was most likely multifactorial in view of his postoperative course. However, we believe that the presence of the SSS contributed to the abnormal cerebral circulation during surgery and postoperatively, leading to brain death. The presence of SSS in patients undergoing an open-heart procedure may be a risk factor for cerebral ischemia or brain death. KEY WORDS: Subclavian steal syndrome - - Fontan - - Brain death
Performance of a Blalock-Taussig (BT) (subclavian-pulmonary artery) anastomosis for treatment of congenital heart disease may lead to the vascular anatomy of the Subclavian steal syndrome (SSS) after either the classic [10] or modified [1] procedure. SSS in patients following the BT shunt procedure is usually due to occlusion of the proximal subclavian artery, but this may also occur secondary to severe stenosis of the innominate artery. Cerebral vascular symptoms in children with SSS are uncommon [16] because of the presumably intact circle of Willis in over 50% of children [2]. However, early [17] and late cerebral ischemic symptoms do occur [13] in children who were initially asymptomatic from their SSS. We report a case of severe cerebral ischemia leading to brain death following the Fontan procedure in a child with asymptomatic SSS, which we presume was acquired after his initial BT shunt.
Case Report A 5-year-old boy, diagnosed to have cyanotic congenital heart disease at birth, had a cardiac catheterization performed which revealed a univentricular atrioventricular connection with a large morphologic left ventricle supporting the pulmonary artery. A d d r e s s offprint requests to: Dr. Michael O. Gayle, 2C3.89 Walter Mackenzie Centre, University of Alberta Hospitals, Edmonton, Alberta T6G 2R7, Canada.
There was severe valvar and subvalvar pulmonary stenosis and an anterior outlet chamber supporting the aorta. The ventricular septal defect was large and nonrestrictive. There was left atrioventricular valve atresia, a patent ductus arteriosus, and a left aortic arch. He had a right BT shunt and a Blalock-Hanlon procedure performed as a newborn and a left BT shunt at 2 years of age. One and a half years after his left BT shunt, a left chest mass was noted on chest x-ray. Investigations of ~his mass, which proved to be a seroma, included a cardiac catheterization which revealed severe stenosis of the right innominate artery resulting in an SSS from the left vertebral to the right vertebral, which then supplied the right BT shunt (Figs. 1 and 2). On review of the patient's history, there were no symptoms of vertebrobasilar ischemia. The patient subsequently had ligation of both BT shunts and a modified Fontan procedure under cardiopulmonary bypass (CPB) using a membrane oxygenator (Sci-Med 1500, Minneapolis, Minnesota) with arterial line filters and hypothermia (core temp 25~ for a period of 3 h and 10 min with an aortic cross clamp time of 33 min. No intraoperative cerebral monitor device was used during CPB. He was admitted postoperatively to the Pediatric Intensive Care Unit (PICU). In the PICU, the patient's temperature was 37.5~ heart rate 130 beats/min, BP 130/60 mmHg (mean arterial pressure [MAP] 77), central venous pressure (CVP) 12 mmHg, and left atrial pressure (LAP) 6 mmHg. The pupils were equal in size and reacted sluggishly to light. Sedation was maintained with an infusion of morphine sulphate (30 mcg/kg/h). Clinically, he was in a low cardiac output state, which was treated with infusions of dopamine (10 mcg/kg/min), neosynephrine (0.8 mcg/kg/min), nitroglycerine (1.0 mcg/kg/min), and calcium chloride. Muscle relaxation was maintained with pancuronium bromide. On the first postoperative day he was noted to have spontaneous movements of his limbs in between doses of muscle relaxants, which were
Gayle et al.: Subclavian Steal Syndrome
101
m Artery
& : Catheters
Fig. 1. Retrograde injection of dye at junction of left carotid and subclavian arteries.
~Rt.
CarotidArtery
h I) Rt. Pulmonary Artery f
/
given every 1-2 h. These movements were unassociated with hemodynamic or pupillary changes and were not considered to be seizure activity. Deterioration in cardiac output with elevations of CVP to 28 mmHg and hypotension (MAP 52 mmHg) occurred by the third postoperative day. After cessation o1' morphine and pancuronium bromide, subsequent neurological examination revealed opening of eyes to deep pain but not to commands, breathing spontaneously, and moving all limbs. By the fourth postoperative day, his neurological examination indicated that he was responding to verbal commands by moving his upper limbs. However, he had progressive generalized edema in the head and neck region, despite diuretic therapy. Cardiac function appeared to stabilize by the fifth postoperative day with mean CVP 14 mmHg and MAP 65 mmHg. Pupils were reactive to light and there were attempts at eye opening to verbal commands. Later his pupils increased in size to 6 mm, and
Fig. 2. Follow through of same injection, visualizing right carotid artery, BT shunt (white arrows), and pulmonary artery (black arrow).
gradually became unreactive despite hyperventilation to keep his Pco2 below 30 mmHg. Further examination revealed no evidence of cortical activity or brainstem reflexes. Temperature, electrolytes, glucose, and serum ammonia were normal. A repeat examination 8 h later confirmed brain death and an electroencephalogram was isoelectric. A computerized tomography (CT) of the head showed diffuse cerebral edema (Fig. 3). After discussions with the family, life support was discontinued. An autopsy, the brain weighed 1570 g (expected weight for age and sex 1300 g, SD 20 g). Macroscopically, there was generalized cerebral and cerebellar swelling with bilateral transtentorial and transforaminal herniation of cerebellar tonsils with focal necrosis. Coronal sections of the cerebrum confirmed the presence of marked to generalized symmetrical swelling associated with compression of the lateral and third ventricles. There was no shift within the midline or regions of normal mottling or softening of the cerebral cortex. Transverse sections of the cerebel-
102
Fig. 3. CT scan demonstrates generalized supratentorial hypodensity of diffuse brain swelling and very small (slit-like) ventricles.
lure revealed diffuse swelling associated with focal softening of the tips of the cerebellar tonsils. The preoperative catheterization findings of severe stenosis of the mid segment of right innominate artery proximal to the anastomosis of the righ~ BT shunt was confirmed.
Discussion
Obstructive lesions of the aortic arch and great vessels predispose to a variety of alterations of normal hemodynamic patterns. The combination of proximal subclavian artery obstruction with retrograde flow in the ipsilateral vertebral artery define the SSS [13]. Accompanying ischemic neurological or upper extremity symptomatology completes the full clinical picture. The symptom patterns are frequently episodic, being related to activity of the upper extremity. Children are often asymptomatic and SSS phenomenon may be an incidental finding, as our patient demonstrated. Neurological sequelae following CPB, including seizures and strokes, may occur in as many as 14% of adult [3] and 2-25% of childhood survivors [9]. While preexisting neurological disorders and abnormal cerebral circulation [4] are present in some children with congenital heart disease, the major cause of neurological morbidity and mortality is thought to be related to the alterations in cerebral blood flow and metabolism associated with CPB [8]. The Fontan procedure is a complex operation involving prolonged CPB, and would be expected to be associated with significant neurological sequelae including death [11, 15]. In a retrospective study, neurological deaths accounted only for 2 (6%) of 32 deaths in 102 children who underwent the Fontan procedure [12].
Pediatric Cardiology Vol. 13, No. 2, 1992
The patient presented in this case report died from tonsillar and cerebellar herniation secondary to cerebral ischemia. This cerebral ischemia could be as a result of alterations in cerebral flow and metabolism and/or air or particulate emboli during CPB [14]. It has been shown that both children [14] and adults [7] have reduced cerebral perfusion during CPB for major cardiac surgery. However, transcranial Doppler ultrasonography studies during CPB in adult patients with severe carotid stenosis suggest normal to increased cerebral blood flow with no increased risk of neurological sequelae [I 8]. There have been no similar studies in children with obstructive lesions of the aortic arch or carotid artery. It is possible that in our patient further decrease in cerebral blood flow could have occurred during CPB as a result of the combination of innominate artery stenosis and SSS. In the postoperative period, our patient had elevated right atrial pressures which would be transmitted to his jugular venous system with subsequent inadequate cerebral perfusion pressure [5], leading to cerebral hypoperfusion. In addition, with the presence of SSS, the brain could lose its blood supply from the left vertebral artery in addition to a potentially important portion of the carotid and contralateral vertebral artery flow [16]. We believe the combination of cerebral hypoperfusion during CPB and the above postoperative factors resulted in this patient having cerebral ischemia with resultant cerebral edema and raised intracranial pressure with subsequent brain death. The microscopic findings in the brain at autopsy indicating no evidence of asymmetrical ischemic changes is not surprising, as there are ample collateral vessels in the pediatric brain [16]. The risk of death following the Fontan procedure is increased with elevated post-repair right atrial pressure, hypertrophy of the ventricular main chamber, and possibly age [12]. We would suggest in view of our present case, an additional risk factor for patients undergoing Fontan or other open-heart procedures could be the presence of an underlying asymptomatic SSS. Vascular reconstructive surgery, as described elsewhere [6, 13], could be indicated at the time of the open-heart procedure, if the SSS is recognized angiographically before surgery. References I. Agarwal KC, Ali Khan MA, Marbey ML (1984) Pulmonary and subclavian steal phenomenon following modified Blalock-Taussig shunt. Am Heart J 108:1567-1570 2. Alpers BJ, Pawray RG, Paddison RM (1959) Anatomical studies of the circle of Willis in normal brain. Arch Neurol Psychiatr 81:409-418
Gayle et al.: Subclavian Steal Syndron~e
3. Andersen K, Waeben J, Jusum B, et al. (1985) Non-pulsatile cardiopulmonary bypass disrupts the flow metabolism couple in the brain. J Thorac Cardiovasc Surg 90:570-579 4. Benson LN, Freedom RM, Wilson GJ, et al. (1986) Cerebral complications following balloon angioplasty of coarctation of the aorta. Cardiovasc Intervent Radiol 9:184-186 5. Dean JM, Rogers MC, Traystman RJ (1987) Pathophysiology and clinical management of the intracranial vault. In Rogers MC (ed) Textbook o f pediatric intensive care 1987. Williams & Wilkins, Baltimore, pp 535-536 6. De Sobregrau RC, Lopez Collado M, Matas Docampo M, et al. (1986) Surgery of the innominate artery. J Cardiovasc Surg 27:31-37 7. Editorial (1989) Brain damage and open-heart surgery. Lancet 2:364-366 8. Ferry C (1987) Nem-ologic sequelae of cardiac surgery in children. A m J Dis Child 141:309-312 9. Ferry PC (1990) Neurologic sequelae of open-heart surgery in children. Am J Dis Child 144:369-373 10. Fogler GM Jr, Shah KD (1965) Subclavian steal in patients with Blalock-Taussig anastomosis. Circulation 31:241 11. Fontan F, Baudet E (1971) Surgical repair of tricuspid atresia. Thorax 26:240-248 12. Kirklin JK, Blackstone EH, KMin JW, et al. (1986) The
103
13.
14.
15.
16.
17.
18.
Fontan operation. Ventricular hypertrophy, age and date of operation as risk factors. J Thorac Cardiovasc Surg 92:1021-1028 Kurlan R, Krall RL, Deweese JA (1984) Vertebrobasilar ischemia after total repair of tetralogy of fallot: Significance of subclavian steal created by Blalock-Taussig anastomosis (Vertebrobasilar ischemia after correction of Tetralogy of Fallot). Stroke 15:359-362 Lundar T, Lindberg H, Lundegaard KF, et al. (1987) Cerebral perfusion during major cardiac surgery in children. Pediatr Cardiol 8:161-165 Mathews K, Bale JF, Clark EB, et al. (1986) Cerebral infarction complicating Fontan surgery for cyanotic congenital heart disease. Pediatr Cardiol 7:161-166 Midgley FM, McClenathan JE (1977) Subclavian steal syndrome in the pediatric age group. Ann Thorac Surg 24:252257 Narto H, Kurokawa K, Kanno T, et al. (1973) Status epilepticus and cortical blindness due to subclavian steal syndrome in a girl with Blalock's operation. Surg Neurol 1:46-49 Von Reutern GM, Hetzel A, Burnbaum D, Schlosse V (1988) Transcranial Doppler ultrasonography during cardiopulmonary bypass in patients with severe carotid stenosis or occlusion. Stroke 19:674-680
