The Society of Pediatric Anesthesia: Fifteenth Annual Meeting, New Orleans, Louisiana, October 12, 2001

The 15th Society of Pediatric Anesthesia Annual Meeting took place in the bayou country, New Orleans, LA, on October 12, 2001. Despite the recent events of September 11th and concerns surrounding air travel, the meeting was well attended and the lecturers well received. The morning session included a series of lectures discussing temperature. Normothermia, hypothermia, and hyperthermia (malignant) were serially discussed. In the first session, Dr. Steven Frank, of the Johns Hopkins Hospital, reviewed temperature regulation in the pediatric patient. He began by reviewing the physiology of temperature regulation. Dr. Frank stated that the hypothalamus integrates afferent information from multiple thermoreceptors throughout the body. The majority (80%) of the information derives from core body receptors and receptors in the hypothalamus itself. The hypothalamus compares the temperature data received from the receptors with a central set point for temperature. In response, efferent information is sent out to alter behavior (seek a warmer or colder environment, change clothing, etc.) and trigger physiologic responses to either conserve heat through shivering and vasoconstriction or enhance cooling through vasodilatation and sweating. In neonates, nonshivering thermogenesis is a major source of heat production but at a high energy expenditure. Dr. Frank went on to discuss the role of anesthesia on thermoregulation. Anesthesia significantly alters thermoregulation in the absence of active warming measures. Inhaled anesthetics provide the most profound decrease in temperature through impaired afferent, central, and efferent mechanisms. The decrease in core temperature during general anesthesia is approximately 1°C for the first 36 min and 1°C/h for the first 1–2 h. Vasoconstriction does not occur until the core temperature approaches 34°C. Dr. Frank presented work by Bissonnette and Sessler suggesting that the thresholds for vasoconstriction in infants and children are quite similar to those reported for adults, but because of the increased surface area/body mass ratio, children lose an increased amount of heat through radiant mechanisms. Stoen and Sessler suggest that higher brain concentrations of inhaled anesthesia reduce the thermoregulating response. Barbiturates induce skin vasodilatation, leading to heat loss, and opioids also impair thermoregulation, but through a more centrally mediated mechanism. Regional anesthetics do not affect central thermoregulation but cause significant vasodilatation, resulting in heat loss, and impair efferent feedback to the brain from peripheral thermoreceptors. The higher the block, the lower the core temperature. The combination of general and regional techniques has a synergistic effect on decreasing temperature, according to Dr. Frank. Active warming techniques have become an important component of anesthetic care. One of the early approaches to maintaining normothermia was the use of warming and humidifying inspired gases. This technique has been found to be suboptimal in adults, because <10% of heat loss occurs through the respiratory tract. In contrast, neonates may benefit from this approach, as demonstrated by Bissonnette and colleagues in 1989. According to Dr. Frank, fluid warming, another commonly applied technology, is a suboptimal approach to warming hypothermic patients. The relatively low flow rates and the maximal fluid temperature of 37°C do not allow for effective temperature gradients. Infusions of large volumes of fluid or blood do benefit from active warming devices. However, if the flow rate is high, the fluid may not have adequate time to warm, and if the flow rate is low, it may lose significant heat in the tubing before it reaches the patient. Dr. Frank recommended devices with countercurrent warming technology, which heats the fluid within the tubing, as a more effective methodology. Passive insulation reduces skin heat loss by upwards of 30% but does not provide effective rewarming. Active warming through forced-air devices appears to be the most effective. It provides better heat transfer than circulating water mattresses and is both less cumbersome and less likely to result in skin overheating, as may occur with radiant heating devices such as overhead warmers. Dr. Frank concluded that maintaining euthermia is an important perioperative goal for children. Because anesthesia alters thermoregulation, anticipating and preventing hypothermia should be an integral part of anesthetic planning. Dr. Bruno Bissonnette, from the Hospital for Sick Children, Toronto, Canada, spoke on the applications of hypothermia in medicine. He began with a historical perspective outlining some of the early, unsuccessful applications of hypothermia in the 1940s for the treatment of cancer and psychosis. He also discussed the “miraculous” use of profound hypothermia, via surface cooling techniques allowing the successful repair of congenital cardiac defects, in the mid 1950s and the subsequent adaptation of hypothermia for therapeutic interventions such as heart surgery, cardiopulmonary resuscitation, and head trauma. Dr. Bissonnette went on to discuss the physiologic basis and cellular effects of hypothermia. At the cellular level, the rate of enzymatic processes is more affected by temperature reductions than routine chemical reactions. Because of this specific effect, organ function such as cerebral metabolism is reduced exponentially with a decrease in temperature. In addition to the metabolic effects of hypothermia, mild to moderate temperature reductions have a beneficial effect on modifying a cascade of events associated with ischemia. This postischemic cascade produces a secondary injury, which is an important focus of hypothermia research as a protective strategy. Dr. Bissonnette discussed the effects of hypothermia on the subcellular mechanisms of brain injury. He began with excitotoxicity. At normothermia, ischemia results in neuronal depolarization, accumulation of intracellular sodium and potassium ions, and, within a few minutes, an accumulation of intracellular calcium. High levels of excitotoxic aminoamines, such as glutamate, facilitate this process. Mild hypothermia has been shown to reduce the release of aminoamines and delay the release of calcium from intracellular stores. This suggests that mild hypothermia may significantly modify ischemic injury. Apoptosis, or programmed cell death, is induced by gene activation after ischemia and traumatic brain injury. According to Dr. Bissonnette, work by Maier and colleagues suggests that experimental models of moderate hypothermia and transient ischemic injury reduce the number of cells dying from apoptosis, but not cells dying from necrosis, therefore partially modifying the extent of brain injury. Astroglial activation is another important factor during neuronal ischemia. The metabolically active astroglial elements are a major source of oxygen free radicals and nitric oxide, which potentiate cerebral cell injury. Moderate hypothermia significantly reduces oxygen free radical production after ischemia. However, the length of postischemic hypothermia needs to be prolonged to achieve a moderate degree of astrocyte protection. Nitric oxide is an important contributor to “oxygen stress” and free radical production. Moderate hypothermia reduced constitutive nitric oxide synthesis activity during the acute phase of ischemia. Constitutive nitric oxide synthesis is preserved during the later phases of brain injury, and inducible nitric oxide, an important mediator of delayed injury, is reduced by hypothermia. White blood cell accumulation occurs immediately after cellular ischemia. Studies have demonstrated that a reduction in white-cell accumulation reduces injury. White cell migration into ischemic tissue appears to be decreased by temperature reductions. Reductions in cytotoxic and vasogenic edema are also reduced by hypothermia. Hypothermia reduces mediators such as leukotriene B4, which induces vasodilatation and lipid peroxidation, thereby modifying cerebral edema and endothelial cell injury. Dr. Bissonnette clearly outlined the measurable benefits of hypothermia, and they are quite dramatic and widespread. Despite these clear benefits, adult clinical studies of hypothermia after traumatic brain injury have not proven beneficial. This surprising and disappointing result may reflect limitations of the study design and a lack of standardized protocols, but still it is disheartening. Complications—increased infection risk, in particular—were more often seen in the patients randomized to hypothermia. Collection of pediatric data is currently ongoing in head trauma patients and those with perinatal asphyxia. Perinatal asphyxia studies are particularly delicate because of the problems of systemic hypothermia in newborn and premature infants. Finally, Dr. Bissonnette discussed the clear detrimental effects of hyperthermia after posttraumatic brain injury. Hyperthermia increases brain contusion volume, and dramatic abnormalities in axonal appearance are present. Multiple experimental models have shown posttraumatic hyperthermia as a major factor in worsening outcomes. Dr. Bissonnette concluded that preventing hyperthermia remains an important therapeutic option after head injury. In the second morning session, Dr. Scott Schulman (Duke University Medical Center) and Barbara Brandom (Pittsburgh Children’s Hospital) discussed malignant hyperthermia (MH). Dr. Schulman discussed the incidence, pathophysiology, clinical features, diagnosis, and treatment of MH. Dr. Brandom discussed the MH registry and provided a few case studies from the registry that highlight some of the difficulty in reaching a clinical diagnosis of suspected MH. According to Dr. Schulman, only 5% of all anesthetics performed in the United States are administered to children, yet 52% of all reported MH cases occur in children. In the pre-dantrolene era, mortality from MH approached 80%. Although significantly reduced in the current era, survival and low morbidity require rapid diagnosis, early intervention, and careful postoperative monitoring. According to Dr. Schulman, the pathophysiology of MH requires an understanding of muscle contraction. At the motor end plate, acetylcholine binds to nicotinic receptors and opens a voltage-gated sodium channel, which depolarizes the muscle membrane, including membrane invaginations called T tubules. Within the T tubules, voltage-gated calcium channels known as dihydropyridine receptors undergo a conformational change that causes a second conformational change of the ryanodine receptor, a transmembrane receptor that releases calcium from the sarcoplasmic reticulum. This calcium release triggers muscle contraction through the interaction of troponin and myosin in the myoplasm. Once contraction is completed, calcium is removed from the myoplasm and pumped back into the sarcoplasmic reticulum. In MH, exposure to triggers, such as succinylcholine and volatile anesthetics, causes a more rapid and sustained increase in myoplasmic calcium. Muscle contracture is vigorous and sustained. The myocyte attempts to restore calcium homeostasis by aggressively pumping calcium back into the sarcoplasmic reticulum. This energy-requiring process creates a dramatic need for adenosine triphosphate and results in hypermetabolism, lactic acidosis, carbon dioxide production, and increased body temperature. Unabated, the acidosis results in cell membrane damage, rhabdomyolysis, hyperkalemia, organ dysfunction, and, ultimately, death. According to Dr. Schulman, the genetic etiologies for MH susceptibility have been defined over the last several years. In approximately 50% of MH cases, an abnormality in the ryanodine receptor has been demonstrated and associated with point mutations in chromosome 19. Other genetic mutations of 1q, 3q, 5q, and 7q and on chromosome 17 have also been identified and are believed to cause abnormalities in the Dr. Schulman reviewed the of MH. the of MH are an increase in and Although not these should the to the of MH. 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