Letters to the Editor
Statements appearing here are those of the writers and do not represent the official position of the American Academy of Pediatrics, Inc. or its Committees. Comments on any topic, including the contents ofPediatrics,are invited from all members of the profession: those accepted for publication will not be subject to major editorial revision but generally must be no more than 400 words in length. The editors reserve the right to publish replies and may solicit responses from authors and others.
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Letters should be submitted in duplicate in double-spaced typing on plain white paper with name and address of sender(s) on the letter. Send them to Jerold F. Lucey, MD, Editor, Pediatrics Editorial Office, Fletcher Allen Health Care, Burlington, VT 05401.
Sedation in Emergency Situations
To the Editor.—
The comparative study of 2 sedation protocols for orthopedic emergencies by Kennedy et al1addresses an important issue— how to sedate children for painful procedures both safely and effectively. For many, this study provides some insight into whether these types of procedures may be done with deep seda-tion as safely and effectively as might be accomplished with general anesthesia administered by an anesthesiologist.
In this study, the authors comment, “No subject reached gen-eral anesthesia.” The policy statement of the American Academy of Pediatrics (AAP)2is cited by the authors as distinguishing deep sedation as “responsive to painful stimuli only” and general an-esthesia as “unresponsive to painful stimuli.”
However, no such distinction may be found in these guidelines. In fact, the guidelines state, “Deep sedation and general anesthesia are virtually inseparable for purposes of monitoring.”2 Further-more, the definition of general anesthesia by the AAP’s Commit-tee on Drugs describes a medically controlled state that can be identical to a patient under deep sedation who is both uncon-scious with a complete loss of protective reflexes. By the defini-tions given by the AAP’s Committee on Drugs, general anesthesia can be a state that exists as a subset of patients under deep sedation. And by definition, states of general anesthesia and deep sedation can only be distinguished in a subset of deep sedation cases by consciousness.2Even patients under general anesthesia frequently respond to painful stimuli with cardiorespiratory re-sponses and, infrequently, movement.
Perhaps the authors had in mind a statement by the American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists that states, “Patients whose only re-sponse is reflex withdrawal from painful stimuli are likely to be deeply sedated, approaching a state of general anesthesia, and should be treated accordingly.”3Frequently misinterpreted, this statement neither defines nor distinguishes between deep seda-tion and general anesthesia. It merely serves to establish a road sign warning of the establishment or impending establishment of the general anesthetic state.
The direct observations used by the authors to distinguish general anesthesia from deep sedation are unfounded. Conse-quently, the statement that no subject reached general anesthesia is also unfounded. Given that 2 of 224 patients under “deep sedation” required brief bag-mask ventilation, and roughly 18% of all patients required airway maneuvers such as head tilt, chin lift, and jaw thrust, one wonders how many of these patients really would have been recognized to be under general anesthesia with spontaneous ventilation by most informed practitioners. Indeed, 1 of the patients requiring bag-mask ventilation had apparent la-ryngospasm, often a complication as well as a sign of stage II anesthesia. So although it appears that 2 groups of patients under deep sedation are being compared, it is likely that some individ-uals in 1 or both groups were actually in states of general anes-thesia with spontaneous respiration.
The data presented are useful, presenting outcomes for 2 sed-ative/analgesia techniques. But there exists no accurate means of distinguishing the unconscious, deeply sedated state from the state of general anesthesia. And there should be no such means
until uniform definitions delineate these 2 states. Allusions to such abilities to distinguish between unconscious, deep sedation, and general anesthesia enable sedation providers to have patients enter unrecognized states of general anesthesia with its inherent risks, not those of deep sedation if indeed the 2 are different.
Michael L. Schmitz, MD
Division of Pediatric Anesthesiology, University of Arkansas for Medical Sciences
Arkansas Children’s Hospital Little Rock, AR 72202-3510
REFERENCES
1. Kennedy RM, Porter FL, Miller JP, Jaffe DM. Comparison of fentanyl/ midazolam with ketamine/midazolam for pediatric orthopedic emer-gencies.Pediatrics.1998;102:956 –963
2. American Academy of Pediatrics, Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures.Pediatrics.1992;89: 1110 –1115
3. American Society of Anesthesiologists, Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists.Anesthesiology.1996;84:459 – 471
In Reply.—
We agree with Dr Schmitz that distinguishing deep sedation from general anesthesia is often difficult if not impossible, partic-ularly when sedation is accomplished with ketamine. However, analagous to the clinical assessment for depth of anesthesia in the operating suite, we evaluated specific responses (movement, vo-calization) to a defined stimulus (fracture reduction) as a measure of sedation depth. The goal was to titrate depth of sedation to safely facilitate achievement of 3 goals: fracture reduction, mini-mization of pain with assurance of amnesia, and rapid return to a presedation level of consciousness. In our study we interpreted patients’ levels of sedation as “deep” when they were too sedated to respond to verbal stimulation but cried out, waked to view the procedure, or attempted to push away the orthopedist during the intensely painful fracture reductions.1No patient was unrespon-sive during reduction nor did any patient completely fulfill all 4 of the critical components of anesthesia: amnesia, analgesia, muscle relaxation, and suppression of autonomic reflexes.2
emergency physician instead of an anesthesiologist. For the pur-poses of this study, we interpreted patients’ responses to painful stimuli as an indication that they were not at the level of general anesthesia. The AAP guidelines define “deep sedation” as “a medically controlled state of depressed consciousness or uncon-sciousness from which the patient is not easily aroused,” whereas “general anesthesia” is defined as “a medically controlled state of unconsciousness.” Deep sedation “may be accompanied by a par-tial or complete loss of protective reflexes,” whereas general an-esthesia is “accompanied by a loss of protective reflexes.” Both states are associated with “the inability to maintain a patent air-way independently and respond purposefully to physical stimu-lation or verbal command.”
An important reason for determining the depth of sedation is that it is believed to correlate with the extent of blunting of protective airway reflexes and, consequently, the risk of aspira-tion. Determining the actual extent that protective airway reflexes are blunted during deep sedation is a vexing problem. Unfortu-nately, repeated testing for presence of a “gag reflex,” one pro-posed means to indirectly assess the state of airway reflexes, might stimulate undesired vomiting. We believe that depression of air-way reflexes and respiratory drive correlates well with central nervous system depression when sedation is accomplished with opioids and benzodiazepines. Whether this correlation holds dur-ing sedation with ketamine is unclear. Although depression may occur, respiratory drive appears to be largely intact during deep sedation and general anesthesia with ketamine.4Subclinical aspi-rations during ketamine sedation have been demonstrated,5,6but we are unaware of reports of significant aspiration with use of ketamine alone. Increased reactivity of airway reflexes may even be an explanation for the laryngospasm associated with ketamine use. Consequently, we assume that protective airway reflexes are variably depressed during deep sedation and that careful prepa-ration for and attention to airway management is essential in all patients.
What is the risk of aspiration in our emergency department during these deep sedations of unfasted patients undergoing in-tensely painful procedures? We don’t know. None of the 260 patients in this study nor any of the 339 children undergoing fracture reductions in our retrospective analysis of (admittedly mostly deep) sedations using fentanyl/midazolam7nor any child in more than 2000 subsequent ketamine sedations over the past 8 years in our emergency department has experienced clinical aspi-ration in our emergency department. This is consistent with Green’s report of 1022 ketamine sedations,8 and in contrast to aspiration in 1373 children undergoing general anesthesia for emergency procedures.9We believe this record of safety is in large part attributable to our meticulous attention to patient safety, immediate interventions when adverse effects occur, relatively healthy patients, and lack of invasive airway manipulation.
Carefully titrated deep sedation of children undergoing in-tensely painful emergent or semiemergent procedures in the emergency department is not without risk. However, we believe this humane and psychologically important approach can be safely accomplished with careful preparation and should be avail-able to children.
Robert M. Kennedy, MD* Fran L. Porter, PhD* David M. Jaffe, MD* J. Philip Miller, AB‡
*Department of Pediatrics ‡Division of Biostatistics
Washington University School of Medicine St Louis Children’s Hospital
St Louis, MO 63110-1077
REFERENCES
1. Kennedy RM, Porter FL, Miller JP, Jaffe DM. Comparison of fentanyl/ midazolam with ketamine/midazolam for pediatric orthopedic emer-gencies.Pediatrics.1998;102:956 –963
2. American Society of Anesthesiology. Standards, Guidelines and State-ments.American Society of Anesthesiologists; 1996
3. American Academy of Pediatrics, Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures.Pediatrics.1992;89: 1110 –1115
4. Joly LM, Benhamou D. Ventilation during total intravenous anaesthesia with ketamine.Can J Anaesth.1994;41:227–231
5. White PF, Way WL, Trevor AJ. Ketamine—its pharmacology and ther-apeutic uses.Anesthesiology.1982;56:119 –136
6. Green S, Johnson NE. Ketamine sedation for pediatric procedures: part 2, review and implications.Ann Emerg Med.1990;19:1033–1046 7. Graff KJ, Kennedy RM, Jaffe DM. Conscious sedation for pediatric
orthopedic emergencies.Pediatr Emerg Care.1996;12:31–35
8. Green SM, Rothrock SG, Lynch EL, et al. Intramuscular ketamine for pediatric sedation in the emergency department: safety profile in 1,022 cases.Ann Emerg Med.1998;31:688 – 697
9. Warner MA, Warner ME, Warner DO, et al. Perioperative pulmonary aspiration in infants and children.Anesthesiology.1999;90:66 –71
Child Advocates
To the Editor.—
I would like to comment on Berman’s excellent commentary, “Training Pediatricians to Become Child Advocates.”1The excel-lence of his approach to child advocacy has been proven by the record of the pediatricians of Colorado in influencing public pol-icy regarding children’s health in that state.
Dr Berman makes the point that “theperfectcan too often be the enemy of thegood. . .” He appropriately uses that aphorism in noting that progress toward a goal is most likely to be made in small steps. I should also like to use the same aphorism to note that, lacking a society ofperfectchild advocates, trained as sug-gested by Dr Berman, we should not disdain the help that can be given by [very]goodchild advocates. Ideally, all of us would have had residency training in child advocacy, a number of years in community organizations establishing credibility, and several years of legislative internship. Unfortunately, many chapters of the American Academy of Pediatrics do not have a large cadre (or anyone) trained in this way. That should not deter us from acting on behalf of children.
By following the “approach to child advocacy” specified in Dr Berman’s commentary, sensitive (to incipient signs of success or failure) pediatricians can and will make a difference. In Colorado, I am sure, Dr Berman and other fully trained child advocate-pediatricians have led the way, but in the process they have trained and relied on goodpediatricians from Denver, Greeley, Grand Junction, Boulder, and every other part of the state to support their efforts, to work with state legislators, and to rally their patients’ parents and their communities to their causes.
All of us would be well advised to heed the approach outlined by Dr Berman. However, it is my belief that “one pediatriciancan
make a difference,” whetherperfector merelygood.Not onlycan
we make a difference, but we should. We all should not hide behind a lack of full training and should offer our support to those who are leading the advocacy effort.
Lance A. Chilton, MD, FAAP
Departments of Pediatrics Lovelace Health Systems
and University of New Mexico Albuquerque, NM 87107
REFERENCE
1. Berman S. Training pediatricians to become child advocates.Pediatrics.
1998;102:632– 636
In Reply.—
a pediatrician’s career from residency training through retirement. We should expose all residents to the principles of community service and advocacy in a curriculum just as we expose residents to principles of fluid and electrolyte management and the judi-cious use of antibiotics. We should create opportunities for resi-dents and young pediatricians who want additional child advo-cacy experiences. Developing a cadre of experienced, effective, and knowledgeable child advocates who can work with commit-ted but less experienced pediatric colleagues is appropriate and should not be viewed as an excuse to “deter any of us from acting on behalf of children.”
Stephen Berman, MD
Section of General Academic Pediatrics Children’s Hospital
University of Colorado School of Medicine Denver, CO 80218
Role of Hypothermia in Asphyxia
To the Editor.—
In reference to the article by Gunn et al,1I would like to share the findings of our review on asphyxiated neonates with hypo-thermia. We did a retrospective review (in press) on all term neonates admitted to the neonatal intensive care unit at Sultan Qaboos University Hospital over a period of 2 years (January 1, 1996 to December 31, 1997) with the diagnosis of asphyxia (1-minute Apgar score of,5). The hypothermic asphyxiated neo-nates (temperature,36°C) were noted to have increased mortality (25%) as compared with 0% mortality in normothermic asphyxi-ated neonates. The mean duration of hospital stay in hypothermic asphyxiated neonates was noted to be 12 days as compared with 4 days in normothermic asphyxiated neonates. We concluded that hypothermia increases the risk for mortality and morbidity in term asphyxiated neonates.
The relation between hypothermia and neonatal asphyxia was described 30 years ago.2,3Recently Thoresen et al4advocated the role of hypothermia in hypoxic brain injury in neonates. However, hypothermia is not free of complications.5,6
Shabih Manzar, MD, FAAP
Division of Neonatology Department of Child Health Sultan Qaboos University Hospital PO Box 38, Postal code 123 Al-Khoud, Muscat
Sultanate of Oman
REFERENCES
1. Gunn AJ, Gunn TR, Gunning MI, Williams CE, Gluckman PD. Neuro-protection with prolonged head cooling started before postischemic seizures in fetal sheep.Pediatrics.1998;102:1098 –1106
2. Dunn JM, Miller JA. Hypothermia combined with positive pressure ventilation in resuscitation of asphyxiated newborn.Am J Obstet Gy-necol.1969;104:58 – 67
3. Westin B, Nyberg R, Miller JA, Wedenberg E. Hypothermia and trans-fusion with oxygenated blood in treatment of asphyxia neonatorum.
Acta Pediatr Scand.1962;(suppl)139:1– 80
4. Thoresen M, Wyatt JS. Keeping a cool head, post hypoxic hypother-mia—an old idea revisited.Acta Pediatr.1997;86:1019 –1033
5. Steen PA, Milde JH, Michenfelder TD. The detrimental effects of pro-longed hypothermia and rewarming in the dog.Anesthesiology.1980;52: 224 –230
6. Mann TP, Elliott RIK. Neonatal cold injury due to accidental exposure to cold.Lancet.1957:229 –234
In Reply.—
The findings of Dr Manzar are consistent withmanyprevious observational studies of hypothermia in sick term infants, show-ing a correlation between mortality and hypothermia.1The central limitation of such observational studies however is again seen (ie, that the severity of the infants’ condition is likely to be con-founded with the severity of hypothermia). Furthermore, the
1-minute Apgar scorein isolationis only very weakly associated with asphyxia or outcome.2
Nevertheless, these and previous data reinforce the need for extreme caution in introducing a potentially dangerous treatment into clinical trial.For this reason we took the approach of cooling the head directly, thus lowering the external brain temperature more than that of the body, and into the range of 32°C to 33°C that is likely to be required for effective protection.3In a recent study of the potential adverse effects of hypothermia, we used a cautious stepwise pro-tocol to test the safety of selective head cooling withmildsystemic hypothermia for 3 days in infants with hypoxic-ischemic enceph-alopathy.4In successive groups of term infants, randomized with contemporaneous noncooled infants, we lowered the target rectal temperatures by 0.5°C in each group, starting at 36.060.5°C. No adverse effects from hypothermia or increase in mortality was found compared with the randomized control infants.4,5Although we have recently presented data on infants cooled to rectal tem-peratures of 34.560.5°C, which shows that prolongation of the QT interval may be observed, no arrhythmia or increase in infec-tion occurred.5
Tania R. Gunn, MBChB, MD Alistair J. Gunn, MBChB, PhD
Department of Pediatrics Auckland University Auckland, New Zealand
REFERENCES
1. Gunn T, Outerbridge EW. Effectiveness of neonatal transport.Can Med Assoc J.1978;118:646 – 649
2. Nelson KB, Emery ES III. Birth asphyxia and the neonatal brain: what do we know and when do we know it?Clin Perinatol.1993;20:327–344 3. Gunn AJ, Gunn TR. The ’’pharmacology’ of neuronal rescue with
cere-bral hypothermia.Early Hum Dev.1998;53:19 –35
4. Gunn AJ, Gluckman PD, Gunn TR. Selective head cooling in newborn infants following perinatal asphyxia: a safety study.Pediatrics.1998; 102(4):885– 892
5. Penrice J, Battin M, Gunn T. Head cooling with mild systemic hypo-thermia following birth asphyxia; a safety study. Proceedings of the Annual Scientific Meeting of the Paediatric Society of New Zealand. 1998:19. Abstract
Developmental Care Does Not Alter Sleep and
Development of Premature Infants
To the Editor.—
We read with interest the study by Ariagno et al1reporting the sleep-wake patterns and neurodevelopmental outcomes of very low birth weight infants cared for by the Neonatal Individualized Developmental Care and Assessment Program (NIDCAP). This report is a follow-up to the original randomized, controlled trial conducted by Fleischer et al2where the APIB scores at 42 weeks postconceptional age have already been reported, and are reiter-ated in Table 5 of the article.
In the article by Ariagno et al,1there is a significant loss to follow-up of 12 (34%) of 35 surviving infants by 2 years. There is no indication in this paper of the effect of this loss on randomiza-tion. A comment on extreme outliers of these small groups would be helpful, as one outlier on any of the socioeconomic, health, or perinatal variables could affect outcome with such low subject numbers. There is no statement of the power that this small sample size can afford, which is reflected in the nonsignificantP
values in Table 6.
The study does not have the power to prove or disprove a hypothesis related to the outcome scores of the Bayley Scales of Infant Development (BSID or the BSID-II) at any of the reported ages. Considering the sample, of 11 and 12 respectively in each group, withP5.05 and a power of 80, only an extremely large effect size ofd.1.0 or.15 points could be detected. Thus, the largest difference obtained in this study, 10.3 points (Mental De-velopment Index, BSID-II—24 months: NIDCAP, 80.3 vs control, 70.0) was not significant.
.05 and a power of 80, a sample size of 48 children in each group would have been required.3This would be generous, as a two-tailed test of significance should theoretically be used, should the care prove detrimental. The reported decrease in the developmen-tal indices using the BSID-II is to be expected in view of the recent restandardization of the test.4
The authors are not justified in concluding that “NIDCAP intervention does not result in increased development” based on these small numbers. This outcome is, of course, of great impor-tance but must await a larger, properly designed trial. However, given the demonstrated short-term improvements of reduced hos-pital stay, reduced duration of ventilation, and better weight gain in infants cared for by NIDCAP,2,5 it would be premature to consider discontinuing this form of care, based on this recent article.
Juzer Tyebkhan Kathy Peters
Catherine McPherson Judi Cote´
Developmental Care Committee Neonatal Intensive Care Unit Royal Alexandra Hospital Edmonton, Alberta Canada T5H 3-V9
Charlene Robertson
Neonatal and Infant Follow-up Clinic Glenrose Rehabilitation Hospital
REFERENCES
1. Ariagno RL, Thoman EB, Boeddiker MA, et al. Developmental care does not alter sleep and development of premature infants.Pediatrics.1997; 100(6). URL: http://www.pediatrics.org/cgi/content/full/100/6/e9 2. Fleischer BE, VandenBerg K, Canstantinou J, et al. Individualized
de-velopmental care for very low birth weight premature infants.Clin Pediatr.1995;34:523–529
3. Cohen J. Statistical Power Analysis for the Behavioral Sciences–Revised.
Orlando, FL: Academic Press, Inc; 1997
4. Bayley N.Manual for the Bayley Scales of Infant Development (BSID-II).2nd ed. San Antonio, TX: Psychological Corp; 1993
5. Als H, Lawhon G, Duffy FH, et al. Individualized developmental care for the very low-birth-weight infant: medical and neurofunctional ef-fects.JAMA.1994;272:553–558
In Reply.—
The purpose of our study was simply to determine if the improvement in medical outcomes reported in the group receiv-ing NIDCAP was associated with improved sleep, biorhythm maturation, or better developmental outcome with the Neurobe-havioral Assessment of the Preterm Infant (NAPI) or the Bayley Scales of Infant Development (BSID). None of these measures showed any improvement by NIDCAP. To date, the claim that developmental outcome is improved by NIDCAP has not been established scientifically although we recognize that this is a pop-ular opinion. Furthermore, the limitations or potential adverse effects have not been studied systematically.
Tyebkhan et al are correct to note that the number of subjects in our study was small (n523) and therefore would not allow a robust statistical significance for the BSID. Indeed small sample size has been a serious problem with all of the studies that have been conducted to date to assess the impact of NIDCAP. Never-theless, there was sufficient power in our study to show that there was no difference in sleep or circadian development in the NIDCAP intervention group. It may also be argued that the pur-ported effect of NIDCAP is too small, and thus a large number is required to test the null hypothesis.
Our paper is based on the last 28 infants to be recruited to the original study of 35 infants so there was no bias in the random-ization of subjects. The investigators in this part of the follow-up study were blinded to which infants were in the intervention group. At 24 months 5 infants were lost to follow-up, 3 experi-mental and 2 controls.
We do not suggest that the NIDCAP approach to care be discontinued, but it is important to recognize that reduced time on
mechanical ventilation and reduced hospital stay do not equate to enhanced maturity. It is also important to note that Buehler et al did not find improved medical outcome measures after NIDCAP intervention in infants with a mean gestation of 32 weeks. There was no evidence of a statistically significant weight gain in either of the articles cited in the Tyebkhan et al letter. Often in the clinical environment NIDCAP is referred to as “developmental care,” which is misleading because the data supporting significant short-or long-term developmental effect are lacking.
Finally, our paper has limitations as do all of the previous reports that make an attempt to provide controlled clinical trial data to support the use of NIDCAP. We maintain the position expressed in our paper that systematic controlled multicenter studies are needed to determine if there are medical benefits. If there are such benefits, are they short- or long-term, are they evident in some or in most infants, or are they primarily for very low birth weight infants, ie, ,1250 g? Additionally, it will be important to determine what components of the NIDCAP inter-ventions are effective and which may have no or potential adverse effects.
Ronald L. Ariagno, MD† Majid Mirmiran, MD, PhD*† Janet Constantinou†
†Stanford University School of Medicine Department of Pediatrics
Division of Neonatal and Developmental Medicine Palo Alto, CA 94304
*Netherland Institute for Brain Research Amsterdam, The Netherlands
REFERENCES
1. Ariagno RL, Thoman EB, Boeddiker M, et al. Developmental care does not alter sleep and development of premature infants.Pediatrics.1997; 100(6). URL: http://www.pediatrics.org/cgi/content/full/100/6/e9 2. Fleischer BE, VandenBerg KJ, et al. Individualized developmental care
for very low birth weight premature infants.Clin Pediatr. 1995;34: 523–529
3. Buehler DM, Als H, Duffy FH, et al. Effectiveness of individualized developmental care for low risk preterm infants: behavioral and elec-trophysiologic evidence.Pediatrics.1995;96:923–932
4. Als H, Lawhon G, Duffy FH, et al. Individualized developmental care for the very low birth weight infant: medical and neurofunctional effects.JAMA.1994;272:853– 858
5. Merenstein GB. Individualized developmental care: an emerging new standard for neonatal intensive care units?JAMA.1994;272:890 – 891
Palivizumab (Synagis)—Cohorting Babies to
Reduce Waste
To the Editor.—
This letter is in response to the thoughtful cost analysis in the February 1999 issue ofPediatrics.1
It has been recommended that certain infants at increased risk for severe respiratory syncytial virus (RSV) disease receive Syna-gis on neonatal intensive care unit (NICU) discharge and every 28 days during the RSV season (November through March). The drug comes in 100-mg vials with only a 6-hour limit after recon-stitution and costs approximately $1200/vial. The recommended dose is 15 mg/kg; thus, each vial would cover 6.5 kg of baby weight. In our NICU, we cohort the pending discharges so several infants may receive the Synagis from a single vial. Another exam-ple would be a 4-kg baby receiving 60 mg on an outpatient basis with the balance used for an almost ready to be discharged pre-term infant.
fol-low-up for well child care in the residents’ continuity clinic or in the attendings’ ambulatory clinic are at separate times.
A pharmacist reconstituted the drug in a laminar flow hood and then sequentially drew up and labeled the syringes with each infant’s name. Drug from more than one vial was not mixed. Each vial is used soon after reconstitution.
A similar cohorting was done to a single office by the major health maintenance organization using our facility. We have, thus, been able to have each vial cover 3 to 4 infants in the NICU and 2 to 3 infants on follow-up. This has resulted in a significant reduc-tion in the cost per infant by a factor of 3.
Ruth Andrea Seeler, MD
Michael Reese Hospital Department of Pediatrics
University of Illinois at Chicago College of Medicine Chicago, IL 60616-3390
Beth Schatz, PharmD
Department of Pediatrics Owen Healthcare
University of Illinois College of Pharmacy Chicago, IL 60616
REFERENCE
1. Moler FW, Brown RW, Faix RG, Gilsdorf JR. Comments on palivizumab (Synagis).Pediatrics.1999;103:495
Useful Mnemonic for Remembering the AAP’s
Suggestions for Clinical Violence Prevention and
Management
To the Editor.—
I am writing to share with other pediatricians a mnemonic that I find useful for remembering the core components that the Amer-ican Academy of Pediatrics is suggesting for clinical violence prevention and management.1The mnemonic is ENLiST:
EN: Early Nurturing Li: Limit-setting
S: Screening for risk, and assurance of Safety
T: Treatment of the physical and psychological consequences of violence.
The way this fits in my mind is this: to prevent infections, we immunize; to prevent violence, we enlist. Without the mnemonic, I tend to forget one or another item.
Katherine Kaufer Christoffel, MD, MPH
Department of Pediatrics and Preventive Medicine Northwestern University
REFERENCE
