Choreoathetosis in infants following cardiac surgery with deep hypothermia and circulatory arrest

Brunberg, James A.; Doty, Donald B.; Reilly, Edward L.

doi:10.1016/s0022-3476(74)80607-4

Cited by 83 publications

(24 citation statements)

References 13 publications

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“…l79l8 In most patients with cerebrovascular accidents, open heart surgery had been performed. [19][20][21][22] Hypotension during extracorporal perfusion, microemboli, or air trapping are of pathogenetic irn~0rtance.l~ However, in one series of patients with Fallot's tetralogy and BlalockTaussig shunts, a high percentage of cases were found to have cerebrovascular infarcts at autopsy.19 This corresponds with our findings that in 2 of 5 children with cortical infarcts the lesion occurred following an aortopulmonary shunt operation.…”

Section: Discussionsupporting

confidence: 61%

Improved neurological outcome following early anatomical correction of transposition of the great arteries

Veelken¹,

Grävinghoff²,

Keck³

et al. 1992

Clinical Cardiology

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Summary: The incidence of neurological residuals following anatomical correction of transposition of the great arteries (d-TGA) has not been described so far. Clinical examination, EEG recordings, and computed tomography (CT) scans were carried out in a consecutive series of 38 children with d-TGA surviving anatomic corrective surgery. The patients were classified into one of three groups according to the type of operation: 15 patients after twostage approach (TSA) (Stage 1: pulmonary artery banding + aortopulmonary shunt; Stage 2: anatomic correction); 12 patients with primary anatomic correction within the first 2 weeks of life (early switch, ES); 11 patients with primary anatomic correction later in infancy (later switch, LS). In 26 patients (68%) we found no abnormalities on neurologic examination, CT scan, or EEG. Four patients suffered from spastic hemiplegia, 3 of these had cortical brain damage visible on CT scan, and 3 had focal epilepsy as well. In 2 otherwise clinical normal patients cortical infarction could be seen on a CT scan. Thus, in 5 cases (13% of 38 patients) cerebral infarcts were diagnosed by CT scan. The cortical vascular infarction was seen in 4 patients after TSA and in 1 after LS. In 6 patients we found other neurological abnormalities. Early anatomic correction in patients with d-TGA reduces the risk of cortical vascular infarction.

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Section: Discussionsupporting

confidence: 61%

Improved neurological outcome following early anatomical correction of transposition of the great arteries

Veelken¹,

Grävinghoff²,

Keck³

et al. 1992

Clinical Cardiology

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“…Thus, the histopatholog ical outcome of the brain damage, as assessed after 7 days It has been known for a long time that moderate to deep hypothermia increases the tolerance of the brain to ischemic insults (e.g., Hirsch et aI., 1957;Rosomoff, 1959;Boyd and Connolly, 1961; Siebke et aI., 1975; Haneda et aI., 1986). This increase in tolerance has been extensively exploited in the clinic (Fay, 1959;Brunberg et al, 1974; Spetzler et aI., 1988). To take an extreme example, by reducing the brain temperature to 5-8°C, White and associ ates (1973) were able to interrupt brain circulation for 60 min in primates.…”

mentioning

confidence: 99%

“…This increase in tolerance has been extensively exploited in the clinic (Fay, 1959;Brunberg et al, 1974;Spetzler et aI., 1988). To take an extreme example, by reducing the brain temperature to 5-8°C, White and associ ates (1973) were able to interrupt brain circulation for 60 min in primates.…”

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confidence: 99%

The Influence of Mild Body and Brain Hypothermia on Ischemic Brain Damage

Minamisawa

Nordström

Smith

et al. 1990

J Cereb Blood Flow Metab

323

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Summary: The influence of brain and body temperature on ischemic brain damage, notably on the density and distribution of selective neuronal vulnerability, was stud ied in SPF-Wistar rats subjected to 15 min of forebrain ischemia induced by bilateral occlusion of the common carotid arteries combined with arterial hypotension (50 mm Hg) in a room air environment. In one group of ani mals, the body temperature was maintained at 37°C but no attempt was made to prevent heat losses from the ischemic brain; i. e. , the head was not heated during isch emia. Under those conditions the temperature of the cau doputamen and at a subcutaneous site over the skull bone spontaneously fell to � 32°C. In four other groups, both the rectal and the subcutaneous skull temperatures were maintained at 38, 37, 35, and 33°C during the ischemia. Our results confirm those recently reported when brain temperature was varied during 20 min of ischemia, with body temperature kept constant. Thus, the histopatholog ical outcome of the brain damage, as assessed after 7 days It has been known for a long time that moderate to deep hypothermia increases the tolerance of the brain to ischemic insults (e.g., Hirsch et aI., 1957;Rosomoff, 1959;Boyd and Connolly, 1961; Siebke et aI., 1975; Haneda et aI., 1986). This increase in tolerance has been extensively exploited in the clinic (Fay, 1959;Brunberg et al., 1974; Spetzler et aI., 1988). To take an extreme example, by reducing the brain temperature to 5-8°C, White and associ ates (1973) were able to interrupt brain circulation for 60 min in primates. In patients, hypothermia of such magnitude allows surgical intervention of a type that could not be tolerated at normal temper atures. The procedure has apparently no untoward effects on postischemic brain function. 365of recovery, was strongly temperature dependent. Whereas ischemia at 37-38°C consistently caused neuro nal necrosis in the hippocampus, neocortex, and caudo putamen, spontaneous cooling of the brain during isch emia at a rectal temperature of 37°C significantly reduced the ischemic damage. Intentional lowering of temperature to 35°C markedly reduced and to 33°C virtually prevented neuronal necrosis in some but not all of the regions stud ied. While damage to the caudoputamen was extremely temperature sensitive, that affecting the CA 1 sector of the hippocampus, and particularly the lateral reticular nu cleus of the thalamus, was less so. Our results suggest that whatever biochemical events are responsible for se lective neuronal vulnerability, they are temperature sen sitive; however, since there are differences in sensitivity between different parts of the brain, more than one mech anism may be involved. Key Words: Cerebral ischemia Hypothermia-Neuronal damage.In 1962, Hirsch and Muller published an exten sive series of experimental results that suggested that even very small differences in brain tempera ture affect the neurological and histopathological outcome of complete global ischemia. The authors, who conducted their experiments ...

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“…Most of the reports on postoperative neurologic abnormalities, such as seizures, choreoathetosis, and impaired mental development, relate to the adverse effects of the low flow or circulatory arrest on the brain [3][4][5][16][17][18]. However, analysis of these reports shows that maximal and thorough cooling of the brain is done by maintaining or increasing the rate of perfusion prior to institution of low flow or circulatory arrest.…”

Section: Commentsmentioning

confidence: 99%

Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

et al. 1998

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Choreoathetosis, seizures, and impaired mental development continue to occur in children undergoing cardiopulmonary bypass (CPB) and profound hypothermia with or without circulatory arrest. Although there is some evidence that the hypothermia itself may be causing these neurologic problems, skepticism remains because of lack of evidence from experimental studies simulating the clinical setting. In this experimental study, we examined the effect of profound and moderate hypothermia on the brain while maintaining normal flow rates during CPB. Ten adult mongrel dogs equally divided into two groups were anesthetized and subjected to CPB and varying levels of hypothermia (group 1, < or = 15 degreesC; group 2, < or = 2 degreesC). Both groups were kept at the desired temperature for 1 hour prior to rewarming and discontinuation of CPB. The dogs were euthanized 4-6 weeks later and neuropathologic studies were performed. The mean CPB flow rates during cooling and at the desired rectal temperature were comparable in both groups: group 1, 108 +/- 10 ml/kg/min versus 106 +/- 7 ml/kg/min in group 2 (p = NS) and 95 +/- 12 ml/kg/min in group 1 versus 101 +/- 5 ml/kg/min in group 2 (p = NS). Because of the difference in temperature between the two groups, the mean cooling time (onset of CPB to desired rectal temperature) was longer in group 1 (70 +/- 14 minutes) than in group 2 (28 +/- 11 minutes, p = 0.007). Hence, the total mean CPB time was also longer in group 1 (198 +/- 25 minutes) than in group 2 (143 +/- 13 minutes, p = 0.002). The lowest mean blood and rectal temperature achieved in group 1 were 11 +/- .9 degreesC and 12 +/- 1 degreesC versus 29 +/- .4 degreesC (p < 0.001) and 30 +/- .6 degreesC (p = 0.001), respectively, in group 2 (p = 0.001). Neuronal loss and degeneration was noted in all dogs in group 1 ranging from 2 to 8 cells per 1000 cells counted compared to none in group 2 (p = 0.05). These lesions occurred in both the basal ganglia and the cortex, although they were more marked in the caudate when compared to the cortex and cerebellum. Both in the cortex and in the caudate, neuronal loss was more marked around the capillaries. We conclude that the use of profound hypothermia of < or =15 degreesC and maintenance of normal flow rates during cooling at this temperature for 1 hour produces neuronal loss and degeneration in the brain. These lesions being more marked around capillaries points to the vulnerability of the neurons, probably because of their high lipid content to injury from the cold perfusate.

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Choreoathetosis in infants following cardiac surgery with deep hypothermia and circulatory arrest

Cited by 83 publications

References 13 publications

Improved neurological outcome following early anatomical correction of transposition of the great arteries

Improved neurological outcome following early anatomical correction of transposition of the great arteries

The Influence of Mild Body and Brain Hypothermia on Ischemic Brain Damage

Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

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