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Infant Cardiac Surgery: Keeping a Cool Head

Kurth, C. Dean M.D.; Steven, James M. M.D.

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DURING the past 15 yr, the survival rate of children born with congenital heart disease has improved dramatically. With the improved survival rate, attention is being directed to morbidity, especially neurologic impairment, which affects 5–25% of the survivors. 1 As with the survival rate, improvements in neurologic outcome probably will result from many factors. The observations in the article by Bissonnette et al.2 in this issue of Anesthesiology have the potential to make an impact on neurologic outcome.
Neurologic impairment in congenital heart disease clearly is multifactorial in origin. It may originate before, during, or after surgery, as a result of genetic defects or hypoxia–ischemia. The brain contains several types of cells that vary in sensitivity to hypoxic–ischemic death. In the immature brain, neurons and oligodendricytes in the neocortex, hippocampus, and striatum are most vulnerable. 3
Ischemia and reperfusion injure these cells through several biochemical reactions. An example is glutamate binding to the N-methyl-d-aspartate receptor, which increases the amount of intracellular calcium and subsequently activates proteases, phospholipases, DNAases, free radical generation, and so forth. These reactions, in turn, injure the organelles. At this point, the injured cells are dysfunctional but not yet dead. Organelle injury subsequently triggers a host of biochemical and genetic reactions, which ultimately decides their fate: death or recovery. With recovery, organelle repair occurs and neurologic function returns to normal. Cell death may occur as a result of apoptosis or necrosis. 4 In apoptosis, cell death is orchestrated, involving the activation of specific genes and enzymes through which cells neatly break up into membrane-packaged bits for removal by resident macrophages. Cell death by necrosis, in contrast, is uncontrolled, involving catalysis and membrane rupture, spilling cellular contents that cause inflammation and secondary injury. Whether a cell undergoes apoptosis or necrosis after ischemia depends on many factors. For example, mild to moderate ischemia tends to cause apoptosis, whereas severe ischemia causes necrosis.
In the brain, the amount of time from hypoxic–ischemic injury to death ranges from days to weeks. 4,5 This gives ample time to initiate neuroprotective therapies but also necessitates that they continue well after the ischemic injury. Hypothermia is the only proven neuroprotective therapy for infant heart surgery. Hypothermia confers neurologic protection in large part because it slows the activity of the enzymes and receptors involved in the biochemical reactions that injure the cell. 6 Although the effect of a few degrees of hypothermia on a single enzyme or receptor is minimal, the cumulative inhibition on the many enzymes and receptors involved with cell injury yields a profound effect. Conversely, a few degrees of hyperthermia can markedly increase hypoxic–ischemic cell death. 7
Many reports have shown that neurologic impairment can occur during infant heart surgery as a result of ischemia related to cardiopulmonary bypass (CPB) and total circulatory arrest. However, in clinical studies, the correlation between neurologic impairment and circulatory arrest duration is weak, and, in animal studies, neurologic impairment does not occur until circulatory arrest is prolonged (> 60 min) outside the duration of customary clinical practice. 1,3 These observations point to the importance of factors other than CPB and circulatory arrest in neurologic impairment, suggesting a role for the vulnerable early postoperative period, in which hemodynamics tend to deteriorate, as well.
Although hypothermia represents the mainstay of cerebral protection during infant cardiac surgery, brain temperature is not measured but inferred from other core body temperatures, typically from the nasopharynx, rectum, and esophagus. Normally, brain temperature is 0.5–1°C more than core temperature, and, within the brain, the temperature of deep regions (e.g., the caudate) is 0.5–1°C more than that of superficial regions (e.g., the neocortex). 8,9 These temperature differentials increase by several degrees during CPB cooling—up to 5°C in some subjects. 9,10 Because brain temperature differences of 3–4°C influence neurologic outcome after ischemia, it is hypothesized that subjects with large temperature differences are at greatest risk of neurologic impairment, either from insufficient brain cooling or from excessive brain rewarming. To test this hypothesis, a clinically practical method to measure brain temperature is needed, as well as a description of brain temperature postoperatively, when cellular ischemic injury is evolving and treatable.
Bissonnette et al.2 have provided this needed information. These authors threaded a thermocouple through a catheter, for which the tip was located in the jugular bulb, in children undergoing cardiac surgery using hypothermic CPB. They recorded jugular bulb venous temperature and core body temperatures during surgery and for 6 h postoperatively. They observed jugular bulb venous temperature at the end of CPB as 36.9 ± 1.4°C, increasing at 6 h postoperatively to 39.6 ± 0.8°C. Although the study was ended after 6 h, jugular bulb venous temperature in all subjects had not reached a plateau, indicating the possibility of higher cerebral hyperthermia. The jugular bulb venous temperature was similar to core temperatures at the end of CPB and increased after surgery 2 or 3°C more than core temperatures. These observations suggest that cerebral hyperthermia of sufficient magnitude and duration to influence outcome after ischemic injury develops regularly after infant cardiac surgery. Hemodynamic deterioration also occurs at 6 h postoperatively, rendering the injured brain cells vulnerable to further ischemic injury.
This observation raises many questions. First, does jugular bulb venous temperature reflect brain temperature? No study directly addresses this. However, the authors make a strong case that, if anything, it would underestimate brain tissue temperature. Second, did the authors’ perioperative temperature management contribute to the development of cerebral hyperthermia? At their institution, management revolved around rectal temperature. Some institutions use this strategy, whereas others measure temperatures from a combination of sites because rectal temperature lags behind these temperature sites, rendering its estimation of core temperature inaccurately low. Thus, the use of rectal temperature alone to guide rewarming may predispose patients to hyperthermia. Yet, in the study by Bissonnette et al., 2 hyperthermia did not develop at the core sites during CPB rewarming, but rather hours afterward, despite surface cooling in those patients with core hyperthermia, making this possibility unlikely.
The observations of Bissonnette et al.2 will hopefully spur clinical studies to address the role of brain temperature and postoperative care in neurologic impairment after infant heart surgery.
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References

1. Bellinger DC, Jonas RA, Rappaport LA, Wypij D, Wernovsky G, Kuban KCK, Barnes PD, Holmes GL, Hickey PR, Strand RD, Walsh AZ, Helmers SL, Constantinou JE, Carrazana EJ, Mayer JE, Hanley FL, Castaneda AR, Ware JH, Newburger JW: Developmental and neurologic status of children after heart surgery with hypothermic circulatory arrest or low-flow cardiopulmonary bypass. New Engl J Med 1995; 332: 549–55

2. Bissonnette B, Holtby HM, Davis AJ, Pua H, Gilder FJ, Black M: Cerebral hyperthermia in children after cardiopulmonary bypass. A nesthesiology 2000; 93: 000–000

3. Kurth CD, Priestley M, Golden J, McCann J, Raghupathi R: Regional patterns of neuronal death after deep hypothermic circulatory arrest in newborn pigs. J Thorac Cardiovasc Surg 1999; 118: 1068–77

4. MacManus JP, Linnik MD: Gene expression induced by cerebral ischemia: An apoptotic perspective. J Cereb Blood Flow Metab 1997; 17: 815–32

5. Schulz JB, Weller M, Moskowitz MA: Caspases as treatment targets in stroke and neurodegenerative diseases. Ann Neurol 1999; 45: 421–9

6. Busto R, Globus MYT, Dietrich D, Martinez E, Valdes I, Ginsberg MD: Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. Stroke 1989; 20: 904–10

7. Wass CT, Lanier WL, Hofer RE, Scheithauer BW, Andrews AG: Temperature changes of ≥1°C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia. A nesthesiology 1995; 83: 325–35

8. Baker MA: Brain cooling in endotherms in heat and exercise. Ann Rev Physiol 1982; 44: 85–96

9. Kurth CD, O’Rourke MM, O’Hara IB, Uhr B: Brain cooling efficiency with alpha-stat and pH-stat cardiopulmonary bypass in newborn pigs. Circulation 1997; 96 (suppl II): II-358–63

10. Stone JG, Young WL, Smith CR, Solomon RA, Wald A, Ostapkovich REPT, Shrebnick PA: Do standard monitoring sites reflect true brain temperature when profound hypothermia is rapidly induced and reversed. A nesthesiology 1995; 82: 344–51

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Keywords:
Cardiopulmonary bypass; pediatric anesthesia; temperature management; temperature regulation.

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