Where have all the pediatric anesthesiology fellows gone in the USA? Anesthesiology fellowship trends.

BACKGROUND: Recent consternation over the number of unfilled Pediatric Anesthesiology fellowship positions in the United States compelled us to assess the change in the ratio of Pediatric Anesthesiology fellows to the number of graduating anesthesiology residents over the 14-year period between 2008 and 2022. We also sought to report the total ratio of anesthesiology fellows to graduating residents and trends in the annual number of fellowship applicants relative to the number of Accreditation Council for Graduate Medical Education (ACGME)-accredited anesthesiology fellowship positions by specialty. METHODS: We used publicly available resources, including ACGME Data Resource Books, National Resident Matching Program (NRMP) data, San Francisco (SF) Match data, and American Board of Medical Specialties (ABMS) data, to determine the ratio of anesthesiology fellows to graduating anesthesiology residents and to compare the number of fellowship applicants to fellowship positions for Adult Cardiothoracic Anesthesiology, Critical Care Anesthesiology, Obstetric Anesthesiology, Pain Medicine and Pediatric Anesthesiology. RESULTS: Since 2008, the ratio of ACGME-accredited anesthesiology fellows to graduating residents increased from 0.36 in 2008 (2007 residency graduates) to 0.59 in 2022 (2021 residency graduates) and the ratio of Pediatric Anesthesiology fellows to graduating residents remained relatively stable from 0.10 to 0.11. The number of unmatched positions in Pediatric Anesthesiology increased from 17 in 2017 to 86 in 2023, and all ACGME-accredited fellowships had more positions available than applicants in 2023. CONCLUSION: In the USA, while the ratio of Pediatric Anesthesiology fellowship graduates to anesthesiology residency graduates remained relatively constant from 2008 to 2022, this is likely a lagging indicator that has not yet accounted for the recent decrease in fellowship applicants. These findings refute prior estimates for a surplus in Pediatric Anesthesia supply in the USA and have significant implications for the future.

Anesthesia and Developing Brains: Unanswered Questions and Proposed Paths Forward.

Anesthetic agents disrupt neurodevelopment in animal models, but evidence in humans is mixed. The morphologic and behavioral changes observed across many species predicted that deficits should be seen in humans, but identifying a phenotype of injury in children has been challenging. It is increasingly clear that in children, a brief or single early anesthetic exposure is not associated with deficits in a range of neurodevelopmental outcomes including broad measures of intelligence. Deficits in other domains including behavior, however, are more consistently reported in humans and also reflect findings from nonhuman primates. The possibility that behavioral deficits are a phenotype, as well as the entire concept of anesthetic neurotoxicity in children, remains a source of intense debate. The purpose of this report is to describe consensus and disagreement among experts, summarize preclinical and clinical evidence, suggest pathways for future clinical research, and compare studies of anesthetic agents to other suspected neurotoxins.

Analysis of 1478 Cases of Hypospadias Repair: The Incidence of Requiring Repeated Anesthetic Exposure as Well as Exploration of the Involvement of Trainees on Case Duration.

BACKGROUND: Recently, there has been significant focus on the effects of anesthesia on the developing brain. Concern is heightened in children <3 years of age requiring lengthy and/or multiple anesthetics. Hypospadias correction is common in otherwise healthy children and may require both lengthy and repeated anesthetics. At academic centers, many of these cases are performed with the assistance of anesthesia and surgical trainees. We sought to identify both the incidence of these children undergoing additional anesthetics before age 3 as well as to understand the effect of trainees on duration of surgery and anesthesia and thus anesthetic exposure (AE), specifically focusing on those cases >3 hours. METHODS: We analyzed all cases of hypospadias repair from December 2011 through December 2018 at Texas Children's Hospital. In all, 1326 patients undergoing isolated hypospadias repair were analyzed for anesthesia time, surgical time, provider types involved, AE, caudal block, and additional AE related/unrelated to hypospadias. RESULTS: For the primary aim, a total of 1573 anesthetics were performed in children <3 years of age, including 1241 hypospadias repairs of which 1104 (89%) were completed with <3 hours of AE. For patients with <3 hours of AE, 86.1% had a single surgical intervention for hypospadias. Of patients <3 years of age, 17.3% required additional nonrelated surgeries. There was no difference in anesthesia time in cases performed solely by anesthesia attendings versus those performed with trainees/assistance (16.8 vs 16.8 minutes; P = .98). With regard to surgery, cases performed with surgical trainees were of longer duration than those performed solely by surgical attendings (83.5 vs 98.3 minutes; P < .001). Performance of surgery solely by attending surgeon resulted in a reduced total AE in minimal alveolar concentration (MAC) hours when compared to procedures done with trainees (1.92 vs 2.18; P < .001). Finally, comparison of patients undergoing initial correction of hypospadias with subsequent revisions revealed a longer time (117.7 vs 132.2 minutes; P < .001) and AE during the primary stage. CONCLUSIONS: The majority of children with hypospadias were repaired within a single AE. In general, most children did not require repeated AE before age 3. While presence of nonattending surgeons was associated with an increase in AE, this might at least partially be due to differences in case complexity. Moreover, the increase is likely not clinically significant. While it is critical to maintain a training environment, attempts to minimize AE are crucial. This information facilitates parental consent, particularly with regard to anesthesia duration and the need for additional anesthetics in hypospadias and nonhypospadias surgeries.

Observed and calculated cerebral critical closing pressure are highly correlated in preterm infants.

BACKGROUND: Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow ceases. Preterm ABP is low and close to CrCP. The diastolic closing margin (diastolic ABP minus CrCP) has been associated with intraventricular hemorrhage in preterm infants. CrCP is estimated from middle cerebral artery cerebral blood flow velocity (CBFV) and ABP waveforms. However, these estimations have not been validated due to a lack of gold standard. Direct observation of the CrCP in preterm infants with hypotension is an opportunity to validate synchronously estimated CrCP. METHODS: ABP and CBFV tracings were obtained from 24 extremely low birth weight infants. Recordings where diastolic CBFV was zero were identified. The gold standard CrCP was delineated using piecewise regression of ABP and CBFV values paired by rank ordering and then estimated using a published formula. The measured and estimated values were compared using linear regression and Bland-Altman analysis. RESULTS: Linear regression showed a high degree of correlation between measured and calculated CrCP (r2 = 0.93). CONCLUSIONS: This is the first study to validate a calculated CrCP by comparing it to direct measurements of CrCP from preterm infants when ABP is lower than CrCP.

Sedation and the Food and Drug Administration Warning: What a Pediatric Gastroenterologist, Hepatologist, and Pancreatologist Should Know.

Pediatric gastroenterologists recommend and perform a range of procedures requiring sedation and anesthesia in young children. A recent warning from the US Food and Drug Administration (FDA) states that "repeated or lengthy use of general anesthetics and sedation drugs during surgeries or procedures in children younger than 3 years or in pregnant women during their third trimester may affect the development of children's brains." 1 As it relates to time, the FDA warning details risks of "procedures lasting longer than 3 hours or if multiple procedures are required." Pediatric gastroenterologists and related specialists should be aware of the warning and its relevance to their patients.

Results of a phase 1 multicentre investigation of dexmedetomidine bolus and infusion in corrective infant cardiac surgery.

BACKGROUND: Dexmedetomidine (DEX) is increasingly used intraoperatively in infants undergoing cardiac surgery. This phase 1 multicentre study sought to: (i) determine the safety of DEX for cardiac surgery with cardiopulmonary bypass; (ii) determine the pharmacokinetics (PK) of DEX; (iii) create a PK model and dosing for steady-state DEX plasma levels; and (iv) validate the PK model and dosing. METHODS: We included 122 neonates and infants (0-180 days) with D-transposition of the great arteries, ventricular septal defect, or tetralogy of Fallot. Dose escalation was used to generate NONMEM® PK modelling, and then validation was performed to achieve low (200-300 pg ml-1), medium (400-500 pg ml-1), and high (600-700 pg ml-1) DEX plasma concentrations. RESULTS: Five of 122 subjects had adverse safety outcomes (4.1%; 95% confidence interval [CI], 1.8-9.2%). Two had junctional rhythm, two had second-/third-degree atrioventricular block, and one had hypotension. Clearance (CL) immediately postoperative and CL on CPB were reduced by approximately 50% and 95%, respectively, compared with pre-CPB CL. DEX clearance after CPB was 1240 ml min-1 70 kg-1. Age at 50% maximum clearance was approximately 2 days, and that at 90% maximum clearance was 18 days. Overall, 96.1% of measured DEX concentrations fell within the 5th-95th percentile prediction intervals in the PK model validation. Dosing strategies are recommended for steady-state DEX plasma levels ranging from 200 to 1000 pg ml-1. CONCLUSIONS: When used with a careful dosing strategy, DEX results in low incidence and severity of adverse safety events in infants undergoing cardiac surgery with cardiopulmonary bypass. This validated PK model should assist clinicians in selecting appropriate dosing. The results of this phase 1 trial provide preliminary data for a phase 3 trial of DEX neuroprotection. CLINICAL TRIALS REGISTRATION: NCT01915277.

Elevated arterial blood pressure after superior cavo-pulmonary anastomosis is associated with elevated pulmonary artery pressure and cerebrovascular dysautoregulation.

BACKGROUND: Elevated arterial blood pressure (ABP) is common after superior bidirectional cavopulmonary anastomosis (BCPA). The effects of elevated ABP after BCPA on cerebrovascular hemodynamics are unknown. We sought to determine the relationship between elevated ABP and cerebrovascular autoregulation after BCPA. METHODS: Prospective, observational study on infants with single-ventricle physiology after BCPA surgery. Continuous recordings of mean ABP, mean cavopulmonary artery pressure (PAP), near-infrared spectroscopy measures of cerebral oximetry (regional cerebral oxygen saturation (rSO2)), and relative cerebral blood volume index were obtained from admission to extubation. Autoregulation was measured as hemoglobin volume index (HVx). Physiologic variables, including the HVx, were tested for variance across ABP. RESULTS: Sixteen subjects were included in the study. Elevated ABP post-BCPA was associated with both, elevated PAP (P<0.0001) and positive HVx (dysautoregulation; P<0.0001). No association was observed between ABP and alterations in rSO2. Using piecewise regression, the relationship of PAP to ABP demonstrated a breakpoint at 68 mm Hg (interquartile range (IQR) 62-70 mm Hg). Curve fit of HVx as a function of ABP identified optimal ABP supporting robust autoregulation at a median ABP of 55 mm Hg (IQR 51-64 mm Hg). CONCLUSIONS: Elevated ABP post-BCPA is associated with cerebrovascular dysautoregulation, and elevated PAP. The effects, of prolonged dysautoregulation within this population, require further study.

Impaired cerebral autoregulation and elevation in plasma glial fibrillary acidic protein level during cardiopulmonary bypass surgery for CHD.

BACKGROUND: Cerebrovascular reactivity monitoring has been used to identify the lower limit of pressure autoregulation in adult patients with brain injury. We hypothesise that impaired cerebrovascular reactivity and time spent below the lower limit of autoregulation during cardiopulmonary bypass will result in hypoperfusion injuries to the brain detectable by elevation in serum glial fibrillary acidic protein level. METHODS: We designed a multicentre observational pilot study combining concurrent cerebrovascular reactivity and biomarker monitoring during cardiopulmonary bypass. All children undergoing bypass for CHD were eligible. Autoregulation was monitored with the haemoglobin volume index, a moving correlation coefficient between the mean arterial blood pressure and the near-infrared spectroscopy-based trend of cerebral blood volume. Both haemoglobin volume index and glial fibrillary acidic protein data were analysed by phases of bypass. Each patient's autoregulation curve was analysed to identify the lower limit of autoregulation and optimal arterial blood pressure. RESULTS: A total of 57 children had autoregulation and biomarker data for all phases of bypass. The mean baseline haemoglobin volume index was 0.084. Haemoglobin volume index increased with lowering of pressure with 82% demonstrating a lower limit of autoregulation (41±9 mmHg), whereas 100% demonstrated optimal blood pressure (48±11 mmHg). There was a significant association between an individual's peak autoregulation and biomarker values (p=0.01). CONCLUSIONS: Individual, dynamic non-invasive cerebrovascular reactivity monitoring demonstrated transient periods of impairment related to possible silent brain injury. The association between an impaired autoregulation burden and elevation in the serum brain biomarker may identify brain perfusion risk that could result in injury.

Effect of Anesthesia on the Developing Brain: Infant and Fetus.

The potential for commonly used anesthetics and sedatives to cause neuroapoptosis and other neurodegenerative changes in the developing mammalian brain has become evident in animal studies over the past 15 years. This concern has led to a number of retrospective studies in human infants and young children, and some of these studies observed an association between exposure to general anesthesia as an infant, and later neurobehavioral problems in childhood. This association is particularly evident for prolonged or repeated exposures. Because of the significant growth of fetal interventions requiring sedation and analgesia for the fetus, or because of maternal anesthetic effects, this concern about anesthetic neurotoxicity is relevant for the fetus. The potential for anesthetic neurotoxicity is the most important clinical and research problem in the field of pediatric anesthesiology. This review will first briefly summarize the rapid brain growth and development in the fetus and neonate. Next, animal model data of anesthetic neurotoxicity in the fetus and neonate will be presented, followed by a review of recent human clinical anesthetic neurotoxicity trials. Finally, the rationale for studying dexmedetomidine as a potential neuroprotectant agent in anesthetic neurotoxicity will be reviewed along with study design for two human clinical trials involving dexmedetomidine.

Elevated Diastolic Closing Margin Is Associated with Intraventricular Hemorrhage in Premature Infants.

OBJECTIVE: To determine whether the diastolic closing margin (DCM), defined as diastolic blood pressure minus critical closing pressure, is associated with the development of early severe intraventricular hemorrhage (IVH). STUDY DESIGN: A reanalysis of prospectively collected data was conducted. Premature infants (gestational age 23-31 weeks) receiving mechanical ventilation (n = 185) had ∼1-hour continuous recordings of umbilical arterial blood pressure, middle cerebral artery cerebral blood flow velocity, and PaCO2 during the first week of life. Models using multivariate generalized linear regression and purposeful selection were used to determine associations with severe IVH. RESULTS: Severe IVH (grades 3-4) was observed in 14.6% of the infants. Irrespective of the model used, Apgar score at 5 minutes and DCM were significantly associated with severe IVH. A clinically relevant 5-mm Hg increase in DCM was associated with a 1.83- to 1.89-fold increased odds of developing severe IVH. CONCLUSION: Elevated DCM was associated with severe IVH, consistent with previous animal data showing that IVH is associated with hyperperfusion. Measurement of DCM may be more useful than blood pressure in defining cerebral perfusion in premature infants.

The Ontogeny of Cerebrovascular Pressure Autoregulation in Premature Infants.

Our objective was to quantify cerebrovascular autoregulation as a function of gestational age (GA) and across the phases of the cardiac cycle. One hundred eighty-six premature infants, with a GA range of 23-33 weeks, were monitored using umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. Autoregulation was quantified as a moving correlation coefficient between systolic arterial blood pressure (ABP) and systolic FV (Sx); mean ABP and mean FV (Mx); diastolic ABP and diastolic FV (Dx). Autoregulation was compared across GAs for each aspect of the cardiac cycle. Systolic FV was pressure-passive in infants with the lowest GA, and Sx decreased with increased GA (r = -0.3; p < 0.001). By contrast, Dx was elevated in all subjects, and showed minimal change with increased GA (r = -0.06; p = 0.05). Multivariate analysis confirmed that GA (p < 0.001) and the "closing margin" (p < 0.01) were associated with Sx. Premature infants have low and almost always pressure-passive diastolic cerebral blood FV. Conversely, the regulation of systolic cerebral blood FV by autoregulation was manifested in this cohort at a GA of between 23 and 33 weeks.

The Diastolic Closing Margin Is Associated with Intraventricular Hemorrhage in Premature Infants.

Premature infants are at an increased risk of intraventricular hemorrhage (IVH). The roles of hypotension and hyperemia are still debated. Critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. When diastolic ABP is equal to CrCP, CBF occurs only during systole. The difference between diastolic ABP and CrCP is the diastolic closing margin (DCM). We hypothesized that a low DCM was associated with IVH. One hundred eighty-six premature infants, with a gestational age (GA) range of 23-33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity for 1-h sessions over the first week of life. CrCP was calculated linearly and using an impedance model. A multivariate generalized linear regression model was used to determine associations with severe IVH (grades 3-4). An elevated DCM by either method was associated with IVH (p < 0.0001 for the linear method; p < 0.001 for the impedance model). Lower 5-min Apgar scores, elevated mean CBF velocity, and lower mean ABP were also associated with IVH (p < 0.0001). Elevated DCM, not low DCM, was associated with severe IVH in this cohort.

The Ontogeny of Cerebrovascular Critical Closing Pressure.

Premature infants are at risk of vascular neurological insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to quantify CrCP as a function of gestational age (GA). One hundred eighty-six premature infants with a GA range of 23-33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. CrCP was calculated using an impedance model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. CrCP increased significantly with GA (r = 0.47; slope = 1.4 mmHg/week gestation), an association that persisted with multivariate analysis (p < 0.001). Higher diastolic ABP and higher GA were associated with increased CrCP (p <0.001 for both). CrCP increases significantly at the end of the second and beginning of the third trimester. The low CrCP observed in premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Training residents and fellows in paediatric cardiac anaesthesia.

The significant increase in complex anaesthetic care for infants, children, adolescents, and adults with CHD has given rise to specialized fellowship training programs. Specialized paediatric cardiac anaesthesia training for residents and fellows has advanced significantly since the 1970's, when there a handful of programs. With the advent of formal paediatric anaesthesia fellowship programs in the U.S., more specialized training became available in the 1990's and early 2000's. In the past decade, increasing numbers of second year advanced fellowships in paediatric cardiac anaesthesia have been organized; today in North America there are 18 programs with 25 positions. Standardized recommendations for case numbers and curriculum have been devised and are widely available via journal publications.

Ontogeny of cerebrovascular critical closing pressure.

BACKGROUND: Premature infants are at risk of vascular neurologic insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to determine the ontogeny of CrCP. METHODS: Premature infants (n = 179) with gestational age (GA) from 23-31 wk had recordings of ABP and middle cerebral artery flow velocity twice daily for 3 d and then daily for the duration of the first week of life. All infants received mechanical ventilation. CrCP was calculated using an impedance-model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. The association between GA and CrCP was determined in a multivariate analysis. RESULTS: The median (interquartile range) CrCP for the cohort was 22 mm Hg (19-25 mm Hg). CrCP increased significantly with GA (r = 0.6; slope = 1.4 mm Hg/wk gestation), an association that persisted with multivariate analysis (P < 0.0001). CONCLUSION: CrCP increased significantly from 23 to 31 wk gestation. The low CrCP observed in very premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

The association between brain injury, perioperative anesthetic exposure, and 12-month neurodevelopmental outcomes after neonatal cardiac surgery: a retrospective cohort study.

BACKGROUND: Adverse neurodevelopmental outcomes are observed in up to 50% of infants after complex cardiac surgery. We sought to determine the association of perioperative anesthetic exposure with neurodevelopmental outcomes at age 12 months in neonates undergoing complex cardiac surgery and to determine the effect of brain injury determined by magnetic resonance imaging (MRI). METHODS: Retrospective cohort study of neonates undergoing complex cardiac surgery who had preoperative and 7-day postoperative brain MRI and 12-month neurodevelopmental testing with Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III). Doses of volatile anesthetics (VAA), benzodiazepines, and opioids were determined during the first 12 months of life. RESULTS: From a database of 97 infants, 59 met inclusion criteria. Mean ± sd composite standard scores were as follows: cognitive = 102.1 ± 13.3, language = 87.8 ± 12.5, and motor = 89.6 ± 14.1. After forward stepwise multivariable analysis, new postoperative MRI injury (P = 0.039) and higher VAA exposure (P = 0.028) were associated with lower cognitive scores. ICU length of stay (independent of brain injury) was associated with lower performance on all categories of the Bayley-III (P < 0.02). CONCLUSIONS: After adjustment for multiple relevant covariates, we demonstrated an association between VAA exposure, brain injury, ICU length of stay, and lower neurodevelopmental outcome scores at 12 months of age. These findings support the need for further studies to identify potential modifiable factors in the perioperative care of neonates with CHD to improve neurodevelopmental outcomes.

Anesthesia for the patient with congenital heart disease presenting for noncardiac surgery.

PURPOSE OF REVIEW: To summarize recent publications emphasizing the changes in the population of patients with congenital heart disease and trends in the anesthetic and perioperative care of these patients presenting for noncardiac procedures. RECENT FINDINGS: It has been reported that children with congenital heart disease presenting for noncardiac surgery are at an increased anesthetic risk. This risk has become better defined. The patients at highest risk are infants with a functional single ventricle and patients with suprasystemic pulmonary hypertension, left ventricular outflow tract obstruction or dilated cardiomyopathy. Familiarity with the physiology and perioperative implications of the stages of single ventricle palliation is critical. The anesthetic approach, monitoring, conduct of surgery and postoperative care and outcomes are variable in this patient population. Recent literature reflects the growing number of children with ventricular assist devices and the management of these patients for noncardiac procedures. Cardiac imaging modalities provide diagnostic information, and strategies for reducing anesthetic risk for these procedures are of great interest. Pharmacologic trends and the application of technology are reviewed. SUMMARY: The identification of high-risk patients, multidisciplinary decision-making and planning and careful anesthetic management and monitoring are critical for optimizing outcomes in children with congenital heart disease presenting for noncardiac procedures.

Neuroprotective strategies in anesthesia-induced neurotoxicity.

Over the past 20 years, hundreds of preclinical studies of the developing central nervous system have been published concluding that the common γ-aminobutryic acid and N-methyl-d-aspartate binding anesthetic agents cause neuroapoptosis and other forms of neurodegeneration. Some clinical studies, including controlled trials, both prospective and ambidirectional in design, indicate an association between any exposure (single or multiple) to anesthesia and surgery at a young age, generally less than 3-4 years, and later behavioral and neurodevelopmental problems. A consideration of neuroprotective strategies is important, as scientists and clinicians alike ponder methods to potentially improve the neurodevelopmental outcomes of the millions of infants and children who undergo surgery and anesthesia annually around the world. This review will address plausible neuroprotective strategies and include alternative anesthetics, neuroprotective nonanesthetic drugs, and physiologic neuroprotection.

The effect of obesity on the ED(95) of propofol for loss of consciousness in children and adolescents.

INTRODUCTION: Anesthesiologists face a dilemma in determining appropriate dosing of anesthetic drugs in obese children. In this study we determined the dose of propofol that caused loss of consciousness in 95% (ED(95)) of obese and nonobese children as determined by loss of eye lash reflex. METHODS: Forty obese (body mass index [BMI] > 95th percentile for age and gender) and 40 normal weight (BMI 25th to 84th percentile) healthy ASA 1 to 2 children ages 3 to 17 years presenting for surgical procedures were studied using a biased coin design. The primary endpoint was loss of lash reflex at 20 seconds after propofol administration. The first patient in each group received 1.0 mg/kg of IV propofol, and subsequent patients received predetermined propofol doses based on the lash reflex response in the previous patient. If the lash reflex was present, the next patient received a dose increment of 0.25 mg/kg. If the lash reflex was absent, the next patient was randomized to receive either the same dose (95% probability) or a dose decrement of 0.25 mg/kg (5% probability). The ED(95) and 95% confidence intervals (CI) were calculated using isotonic regression and bootstrapping methods respectively. RESULTS: The ED(95) of propofol for loss of lash reflex was significantly lower in obese pediatric patients (2.0 mg/kg, approximate 95% CI, 1.8 to 2.2 mg/kg) in comparison with nonobese patients (3.2 mg/kg, approximate 95% CI, 2.7 to 3.2 mg/kg), P ≤ 0.05. DISCUSSION: A simple approach to deciding what dose of propofol should be used for induction of anesthesia in children ages 3 to 17 years is to first establish the child's BMI on readily available gender-specific charts. Obese children (BMI >95th percentile for age and gender) require a lower weight-based dose of propofol for induction of anesthesia, than do normal-weight children.