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COMMENTARIES

Opinions expressed in these commentaries are those of the authors and not necessarily those of the American Academy of Pediatrics or its Committees.

Thoughts of a Plastic Surgeon

A

s a recently retired plastic and reconstructive surgeon, I have some thoughts I wish to share with the pediatric community that I believe will be to the benefit of both our specialties and our patients. As I have closed my office, I am not encour-aging referrals or soliciting patients.

I believe that there are 2 conditions seen by pedi-atricians that are underreferred to plastic surgeons. The first of these is gynecomastia. These young males are exquisitely sensitive to their abnormal breast development. They frequently will ask that their parents not be in the room when they are ex-amined. Their female-appearing chest significantly affects their activities, as they avoid situations where they might have to remove their shirts.

Often these boys/young men are overweight. I feel there are 2 reasons for this. By being hefty, the chest appears to be that of a “fatty” rather than being female in appearance. That is better-accepted in the eyes of their peers. I actually believe that many in-tentionally gain weight for this reason. Further, as they tend to avoid exercise and athletics where they would be forced to remove their shirts, either in the competition or in the shower room, these boys tend to be more sedentary than normal, and therefore in poorer physical shape.

I realize that many cases of gynecomastia will spontaneously involute. If this has not occurred by the start of high school (age 14 to 15), then a referral for evaluation is indicated, especially in a patient you have observed for a few years, or in a boy who is greatly bothered by the condition despite your reas-surances that there is no health risk or gender-related question. In those cases, there is no medical treat-ment option.

Operation is a straightforward procedure, with re-moval of the excess breast and/or fat, either by an open approach using an incision within the areola or via liposuction with only 1 or 2 small stab wounds on each side. This is an outpatient procedure, done ei-ther under local with sedation or a short (1.5-hour) general anesthetic, depending on the individual pa-tient. Insurance will often cover this procedure, an indication that the insurance companies, which often try to find any plausible reason not to pay for a service, do not consider this to be cosmetic in nature. The patients are virtually universally overjoyed with the results of operation.

The second condition is that of prominent ears. I know that in our age of political correctness, there is a tendency to strive to accept everyone as they are, but these children are the butt of jokes and made fun of by others. Terms as “loving cup ears” and “Dumbo ears” readily bring a recognizable image to mind. The head reaches close to adult size by about age 5, and if the ears are unduly prominent at that time, they will remain so.

Correction of prominent ears is again a rather stan-dard procedure. It takes only about 30 to 45 minutes per side, and is done as an outpatient. Older children may be done under local anesthesia (especially girls). The complication rate of the procedure is quite low, and even if perfect symmetry is not achieved, simply having the ears within the range of normal satisfies these patients. If the ears do not attract attention, that is enough for them.

The American Medical Association-approved def-inition of cosmetic surgery is the modification of a structure that has no functional impairment and that a reasonable individual would feel falls within the range of normal. While the correction of prominent ears is closer to cosmetic in nature, again, even the insurance companies will often consider that it is a correction of a developmental anomaly. I personally do not favor cosmetic procedures such as liposuction or breast augmentations in teenagers, but feel that these 2 entities fall into another category. I offer these thoughts for your consideration and, I believe, to the benefit of your patients.

Robert J. Wilensky, MD

Washington, DC 20016

Reducing Medical Error Through

Systems Improvement: The

Management of Febrile Infants

ABBREVIATION. SBI, serious bacterial infection.

W

orry about avoiding the disaster of over-whelming bacterial sepsis in a young fe-brile infant has cost many a pediatrician sleepless nights. Which infant is destined to become

Received for publication Sep 20, 1999; accepted Oct 21, 1999.

Reprint requests to (R.J.W.) 2807 Battery Place NW, Washington, DC 20016. E-mail: robertjwilensky@erols.com

PEDIATRICS (ISSN 0031 4005). Copyright © 2000 by the American Acad-emy of Pediatrics.

Received for publication Jun 2, 1999; accepted Nov 15, 1999.

Reprint requests to (J.G.) Clinical Effectiveness Program, Children’s Hospi-tal, Boston, 300 Longwood Ave, Boston, MA 02115. E-mail: glauber@a1. tch.harvard.edu

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critically ill and which will recover in a few days from a trivial viral infection without treatment? Un-able to predict reliably the course of febrile illnesses, pediatricians often select the option of treating many infants to benefit a few.

Faced with the inefficiency and risks of universal treatment of febrile infants, several investigators have developed strategies to identify low-risk infants who could be safely observed without antibiotics.1–3

These approaches use various clinical and laboratory criteria that are applied prospectively to an eligible population of febrile infants. In research settings, the best of these protocols can reliably discriminate be-tween high-risk infants who warrant inpatient ad-mission and antibiotic therapy, and low-risk infants who can safely be managed conservatively with close outpatient observation.

Can these evidence-based risk assessment proto-cols be applied successfully outside the research set-tings in which they were developed? A recent study by Baker and colleagues4in Pediatrics suggests that

such strategies should be pursued with caution. In particular, the study confirms the importance of er-ror in medicine and the need to improve systems of care if we are to safely reduce cost and improve outcomes.

The authors report the performance of the Phila-delphia protocol in guiding the treatment of a con-secutive sample of 422 febrile infants presenting to the emergency department of the Children’s Hospi-tal of Philadelphia. The study yielded 2 important, yet discordant, findings:

1. The Philadelphia protocol performed reliably in identifying as high-risk all infants with serious bacterial infection (SBI).

2. Overall 6.6% of infants were treated contrary to the clinical course dictated by the protocol, expe-riencing both overtreatment and undertreatment. Twenty-one (6.5%) of 321 high-risk infants were treated as low-risk and 7 (7%) of 101 low-risk infants were treated as high-risk. Further, 3 (7%) of the 41 infants ultimately proven to have SBI were not empirically treated with antibiotics, even though the protocol designated them as high-risk (Table 1).

The first of these observations addresses the issue of the efficacy of the screening test: under ideal cir-cumstances, divorced from real-world problems, how did the test perform? The second finding ad-dresses effectiveness: what actually happened when the test was implemented in a real clinical setting? In everyday practice errors occurred, leading some

low-risk infants to receive antibiotics unnecessarily and, more importantly, 7% of high-risk infants to not be treated.

How important is an error rate of 7%? Although the authors minimize the importance of this error rate because no adverse outcomes occurred, the in-fants escaped injury more by chance than by intent. If the protocol designates 75% of a hypothetical co-hort of 10 000 febrile infants high-risk, misclassifying 7% will lead to 525 high-risk infants not receiving empiric antibiotics. Of the remaining 2500 low-risk infants, 175 will be hospitalized and treated unnec-essarily. If 10% of febrile infants have SBI, misclassi-fying 7% will leave 70 infected infants untreated. Harm to at least some infants will be nearly inevita-ble.

Harm from incorrect medical care is, in fact, com-mon and well-documented in the health services research literature. Brennan and colleagues5reported

that 3.9% of 30 000 hospitalized patients whose med-ical records were subjected to retrospective review experienced an adverse event. On chart review, 27.6% of these adverse events were attributed to negligence and therefore were preventable. Seventy percent of adverse events arising in the emergency department were deemed preventable.6The national

death toll from preventable medical errors is the equivalent of 3 jumbo jets crashing every 2 days.7

More individuals die annually in this country from medical error than from traffic accidents. The logical conclusion is that error in medicine is a major public health concern.

The salient question is, then, what is responsible for the error rate in our health care delivery systems? We have been slow in health care to recognize that errors are an intrinsic performance characteristic of complex systems. Systems, by encompassing defined processes, are perfectly designed to create the results that are achieved.8 If we understand the relevant

systems, we can begin to explore the vulnerable pro-cesses that cause error and endeavor to correct them through systems redesign.

This systems-oriented analysis of unintended out-comes differs from the traditional method of ad-dressing error in medicine. Old-style peer review and quality assurance programs attempt to reduce error by: 1) increasing physician vigilance and, 2) identifying physician outliers. Increased physician vigilance, it is hoped, will lead to flawless perfor-mance. This hope is evidenced by the authors’ prop-osition:

“Had the managing physicians paid closer attention . . . all management breaches that resulted in delayed administration of antibiotics would have been avoided.”

When flawless performance is achievable through vigilance error presumably results from a decrement of attentiveness or diligence. Quality assurance em-ploys the social mechanism of feedback, exhortation, or blame to restore vigilance to erring physicians. As stated by Donabedian,9quality assurance seeks to:

“. . . identify and correct the most serious failures in care and, by doing so, to create an environment of watchful concern that motivates everyone to do better.”

TABLE 1. Effectiveness of Philadelphia Protocol in the Man-agement of Febrile Infants

Number Managed in Accordance With Protocol Number Managed Out of Accordance With Protocol Percentage Managed Out of Accordance With Protocol

Low-risk infants 94 7 6.9

High-risk infants 321 21 6.5

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Health care professionals are already highly mo-tivated to provide careful and competent care. Watchful concern typifies the attitude of health care professionals. Yet highly motivated, skilled, and dedicated professionals can, do, and will make er-rors. The authors observe that errors were evenly distributed among 13 of the 18 emergency depart-ment physicians. This observation argues against the outlier assumption of quality assurance, namely that a few bad apples can be identified as the principal source of errors. Instead the implication is that the 7% failure rate is a function of the system of care, not of individual vigilance or motivation. Nonetheless the authors “advocate continued performance of quality assurance initiatives to prevent such occur-rences.”

It is doubtful that quality assurance initiatives will prevent recurrences. Continued quality assurance in-itiatives are a component of the system that performs at a 7% failure rate. Is this the level of quality that we wish to assure?

Substantial reductions in the error rate in medicine will occur only when we first acknowledge that hu-man error is inevitable. Errors must be acknowl-edged and studied when they occur so that vulner-able processes and flawed systems of care can be identified and repaired. It is inexcusable and epide-miologically unsound to wait for adverse events to occur. Errors and near-misses provide the data for a systematic approach to preventing adverse events. Experts in error-proofing health care systems appro-priately regard errors as treasures.10 Blaming those

who commit errors is counterproductive because it encourages staff to hide errors.

Errors often result from misapplication of a cogni-tive strategy that is beneficial in most circumstances. Stress, fatigue, and distraction increase the likelihood that such cognitive mishaps will occur. Conse-quently, robust systems anticipate common cogni-tive errors and build in safeguards to identify and counteract them before vital processes are impacted. The authors report the decision points that com-monly led to protocol violation. They cite the failure to recognize abnormalities in the peripheral blood white cell count as the most common source of error. Yet, they do not ask the next scientific question: “Why should this be?” and then “What redesign would make that error less likely?” A variety of causal hypotheses are plausible. One may speculate that relevant lab results may simply have been over-looked. Perhaps laboratory delays in reporting dif-ferential counts led to premature assignment of pa-tients to a specific risk group and therapeutic course. Additionally the immature-to-total neutrophil ratio typically requires physician calculation, which may prove fallible in the distracting environment of the emergency department. Possible solutions might therefore be to decrease lab turnaround for this class of patients or have the lab calculate the ratio and report outlying values in bold type. The analysis of the sources of error will naturally lead to specific intervention and improvement strategies. These strategies may range in complexity and breadth, each appropriate in a given context. Only through

contin-ued monitoring of performance and testing of rem-edies will one be able to conclude whether the inter-ventions are successful.

The Baker study is valuable both because it simul-taneously informs how we might practice medicine and reveals how medicine is actually practiced. The physicians whose performance is reported correctly treated 93% to 94% of patients. This performance evidences diligence and expertise unlikely to be aug-mented by greater effort. However if the other 6% to 7% of patients are to enjoy the therapeutic benefit of the protocol, systems must be redesigned that antic-ipate and avert cognitive errors.

The potential for the Philadelphia protocol, or any other evidence-based guideline, to improve the lives of patients rests on the capability of the health care system to deliver the care as intended. The gap be-tween intended care and received care will not be bridged solely through focused, dedicated individ-ual effort, but will also require different methods that focus on systems. We must recognize that error is an expected product of any human process, identify the predictable sources of error, and then strive to design systems robust enough to intercept and prevent er-ror. Error-proofing is far more powerful than exhor-tation. This effort must be guided by a clear vision of the level of quality that we wish to deliver.

James Glauber, MD*

Donald A. Goldmann, MD‡

*Clinical Effectiveness Program ‡Department of Quality Improvement Children’s Hospital, Boston

Boston, MA 02115

Charles J. Homer, MD, MPH

National Initiative for Children’s Healthcare Quality Boston, MA

Donald M. Berwick, MD, MPP

Institute for Healthcare Improvement Boston, MA

ACKNOWLEDGMENT

This work was supported in part by Grant T32 HS00063 from the Agency for Health Care Policy and Research.

REFERENCES

1. Baker MD, Bell LM, Avner JR. Outpatient management without antibi-otics of fever in selected infants.N Engl J Med.1993;329:1437–1441 2. Jaskiewicz JA, McCarthy CA, Richardson AC, et al. Febrile infants at

low risk for serious bacterial infection—an appraisal of the Rochester criteria and implications for management.Pediatrics.1994;94:390 –396 3. Baraff LJ, Bass JW, Fleisher GR, et al. Practice guidelines for the

man-agement of infants and children 0 to 36 months of age with fever without source.Pediatrics.1993;92:1–12

4. Baker MD, Bell LM, Avner JR. The efficacy of routine outpatient man-agement without antibiotics of fever in selected infants.Pediatrics.1999; 103:627– 631

5. Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events in hospitalized patients.N Engl J Med.1991;324:370 –376

6. Leape LL, Brennan TA, Laird N, et al. The nature of adverse events in hospitalized patients.N Engl J Med.1991;324:377–384

7. Leape LL. Error in medicine.JAMA.1994;272:1851–1857

8. Deming WR.Out of Crisis.Cambridge, MA: Massachusetts Institute for Technology; 1982

9. Donabedian A. The quality of care: how can it be assessed?JAMA.

1988;260:1743–1748

10. Blumenthal D. Making medical errors into “medical treasures.”JAMA.

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Lyme Disease Vaccine: Good for

Dogs, Adults, and Children?

ABBREVIATIONS. LD, Lyme disease; Osp A, outer surface pro-tein A; ELISA, enzyme-linked immunosorbent assay.

I

n 1977, Steere and colleagues1described a

myste-rious disease (in 39 children and 12 adults) char-acterized by a rash and followed by arthritis. Most patients came from the communities of Lyme and Old Lyme, Connecticut, thus, the name Lyme disease (LD). Over the next 2 decades most of the mysteries of LD were solved and vaccines have been developed.2– 8 LD is caused by the tick-borne

spiro-cheteBorrelia burgdorferi. Infection is clinically diag-nosed by the pathognomonic rash, erythema mi-grans, or positiveB burgdorferiserology with specific objective rheumatologic, neurologic, or cardiac find-ings.2,3Patients can get LD more than once.4LD can

be successfully treated with 3 to 4 weeks of oral amoxicillin or doxycycline. An exception is meningi-tis, which requires 2 weeks of intravenous ceftriax-one.2,3During 1993 through 1997, a mean of 12 451

cases of LD per year were reported to the Centers for Disease Control and Prevention,5 which may only

represent 10% of actual cases.6In Connecticut, 30% of

LD cases occur in children ages 1 through 18 years old with the highest risk group being those children aged 5 through 9 years (Connecticut Department of Public Health Statistics, 1998). Most cases of LD come from the high-risk states of Connecticut, Delaware, Maryland, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin and the moderate-risk states of Maine, Massachusetts, Minnesota, New Hampshire, and Vermont.5,8Families living in or

vis-iting these endemic areas frequently ask physicians for advice about how to decrease their risk of acquir-ing LD.

The most logical approach to prevent LD would be to prevent tick bites. Preventive measures include the following: 1) using tick repellent (and reapplying it every 1 to 2 hours while outside); 2) wearing light-colored clothing to highlight ticks (and remov-ing ticks before they bite); 3) long sleeves and long pants tucked into socks (to hide the skin from ticks); 4) daily tick checks and removing attached ticks (a tick needs to be attached for ⬎24 hours to cause infection); and 5) antibiotic prophylaxis of tick bites (this is usually not recommended).8,9These

preven-tive measures may be difficult to follow and their efficacies are unknown.10

The only way to prevent Lyme disease that has been proven in prospective studies is vaccination. In 1990, a whole-cell inactivated B burgdorferi vaccine was licensed for use in dogs. For veterinary licen-sure, the vaccine studies were only required to

dem-onstrate a persistent antibody response without ob-vious toxicity. Dogs manifest LD by fever, lameness, and swelling of their carpi (wrists) and tarsi (ankles). In a postlicensure 20-month study, LD developed in 211 (4.7%) of 4498 unvaccinated dogs versus 20 (1%) of 1969 vaccinated dogs.11The cost of the veterinary

LD vaccine is $6.70/dose. The initial series is 2 doses followed by yearly boosters. There is now a second LD vaccine for dogs. Because LD is treatable in dogs, there is disagreement among veterinarians with re-spect to using the vaccines.12,13

Because whole-cell vaccines may cause severe lo-cal reactions in humans, a recombinant immuno-genic B burgdorferiprotein (outer surface protein A, [Osp A]) was chosen for human trials. Antibodies to Osp A killB burgdorferiin the tick and are not effec-tive after infection is established.14

In 1998, the results of a large adult Osp A vaccine trial were published.15 The vaccinations were given

at 0, 1, and 12 months. In the tick season after the 3 immunizations, LD developed in 66 (1.2%) of 5467 placebo recipients versus 16 (0.3%) of 5469 vacci-nees—76% efficacy. In 1999, an Osp A vaccine was licensed for use in patients 15 to 70 years old and costs $61.25/dose. The Advisory Committee on Im-munization Practices has recommended5that the LD

vaccine be “considered” for persons (ages 15 to 70 years old) who live, work, recreate, or travel in high-or moderate-risk areas.

A pilot study of Osp A vaccine in children 5 to 15 years old was published in 1999.16 The vaccine was

highly immunogenic and well-tolerated. Efficacy was not part of this trial. A large pediatric study of immunogenicity and tolerability (not efficacy) has just been completed and, if the results are similar to the pilot study, the Osp A vaccine could be licensed for use in children before the 2001 tick season. The adult efficacy trial15required skin biopsies and

mul-tiple serologies to definitively diagnose LD, which could not be done on children, thus, efficacy in chil-dren has not been studied.

What are the downsides to the Osp A vaccine? First, Osp A resembles the human red blood cell antigen h LFA-1. h LFA-1 is a possible autoantigen for persistent Lyme arthritis17 that occurs in a small

percentage of patients with LD. Could repeated Osp A vaccinations induce autoimmune arthritis in sus-ceptible humans? This has not occurred but postvac-cine surveillance is ongoing.18 Second, the LD

vac-cine efficacy from the adult trials is only 76%. Initially it was thought that 2 Osp A vaccinations would give maximum efficacy. After 2 Osp A injec-tions approximately 50% of adults have protective Osp A antibody levels; after 3 injections approxi-mately 90% of adults have protective levels. There are data that after 4 injections ⬎95% of adults have protective levels.19 Maximum efficacy may not be

reached in adults until after 4 Osp A injections. There are also data that the first 3 injections can be given in accelerated schedules at 0, 1, and 3 months20or 0, 1,

and 6 months.21 Thus, the shortest and most

effica-cious schedule including boosters has not yet been defined. Lastly, after vaccination, patients may have a positiveB burgdorferiserology. The test affected by

Received for publication Feb 29, 2000; accepted Feb 29, 2000.

Reprint requests to (H.M.F.) Department of Family Medicine, University of Connecticut Health Center, Farmington, CT 06030-1406. E-mail: feder@nso2.uchc.edu

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vaccination is the enzyme-linked immunosorbent as-say (ELISA) while the Western blot interpretation is not affected. There are ELISA tests under develop-ment that are not positive after vaccination.22

If the Osp A vaccine gets licensed for children, who should get it? Some families are so worried about LD that they don’t want to wait for the vaccine to be licensed. A few adults actually vaccinated themselves with the whole-cell dog vaccine before the Osp A vaccine was available. However, vaccina-tion should not be done before licensure, and wor-ried parents need to have the risks of LD put in perspective. Furthermore, the LD vaccine should not replace tick avoidance behavior, as the vaccine does not protect against the other tick-borne infections— ehrlichiosis and babesiosis. If the Osp A vaccine gets licensed for children, it would make sense to use it for families living in high LD endemic areas who want to decrease their childrens’ risk of acquiring LD. For families making short visits to LD endemic areas, or living in low-risk, endemic areas, physi-cians will have to decide about vaccination on a case-by-case basis. If postlicensure surveillance es-tablishes the safety of Osp A vaccine in a large num-ber of patients and if its efficacy is demonstrated to be ⬎95%, then these narrow recommendations for using the LD vaccine should broaden.

Henry M. Feder, Jr, MD

Departments of Pediatrics and Family Medicine Connecticut Children’s Medical Center

Hartford, CT 06106

University of Connecticut Health Center Farmington, CT 06030-1406

REFERENCES

1. Steere AC, Malawista SE, Snydman DR, et al. Lyme arthritis: an epi-demic of oligoarticular arthritis in children and adults in three Connect-icut communities.Arthritis Rheum.1977;20:7–17

2. Rahn DW, Malawista SE. Lyme disease: recommendations for diagnosis and treatment.Ann Intern Med.1991;114:472– 481

3. Feder HM Jr, Hunt MS. Pitfalls in the diagnosis and treatment of Lyme disease in children.JAMA.1995;274:66 – 68

4. Gerber MA, Shapiro ED, Burke GS, et al. Lyme disease in children in Southeastern Connecticut.N Engl J Med.1996;335:1270 –1274 5. Centers for Disease Control and Prevention. Recommendations for the

use of Lyme disease vaccine.MMWR Morb Mortal Wkly Rep. 1999;48(RR-7):1–26

6. Marwich C. Guarded endorsement for Lyme disease vaccine.JAMA.

1998;279:1937–1938

7. Lyme disease vaccine.Med Lett.1999;41:29 –30, 46

8. American Academy of Pediatrics, Committee on Infectious Diseases. Prevention of Lyme disease.Pediatrics.2000;105:142–147

9. Shapiro ED, Gerber MA, Holabird NB, et al. A controlled trial of antimicrobial prophylaxis for Lyme disease after deer-tick bites.N Engl J Med.1992;327:1769 –1773

10. Steigbigel RT, Benach JL. Immunization against Lyme disease—an im-portant first step.N Engl J Med.1998;339:263–164

11. Levy SA, Lissman BA, Ficke C. Field performance studies ofBorrelia burgdorferibacterin in three veterinary practices in borreliosis endemic areas.J Am Vet Med Assoc.1992;202:1834 –1838

12. Levy SA. Why I vaccinate dogs against Lyme disease.Perspect Vet Med Compendium.1997:1268 –1271

13. Littman MP. Why I don’t use Lyme disease vaccines.Perspect Vet Med Compendium.1997:1269 –1275

14. Wormser GP. Prospects for a vaccine to prevent Lyme disease in hu-mans.Clin Infect Dis.1995;21:1267–1274

15. Steere AC, Sikand VK, Meurice F, et al. Vaccination against Lyme disease with recombinantBorrelia burgdorferiouter-surface lipoprotein A with adjuvant.N Engl J Med.1998;339:209 –215

16. Feder HM Jr, Beran J, Van Hoecke C, et al. Immunogenicity of a recombinantBorrelia burgdorferiouter surface protein A vaccine against Lyme disease in children.J Pediatr.1999;135:575–579

17. Gross DM, Forsthuber T, Tary-Lenmann M, et al. Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis.

Science.1998;281:703–706

18. Dickman S. Possible cause found for Lyme arthritis.Science.1998;281: 631– 632

19. Parenti DL. Dear doctor letter. Collegeville, PA: Smith Kline Beecham; 1999

20. Parenti DL, Schoen RT, Sikand VK, et al. Evaluation of reactogenicity of LYMErix recombinant L Osp A vaccine against Lyme disease.Clin Infect Dis.1998;27:1053. Abstract 708

21. Van Hoecke C, Lebacq E, Beran J, Parenti D. Alternative vaccination schedules (0, 1, 6 months versus 0, 1, 12 months) for a recombinant Osp A Lyme disease vaccine.Clin Infect Dis1999;28:1260 –1264

22. Gomes-Solecki M, Wormser G, Yang X, Glass JD, Luft BJ, Dattwyler RJ. A serodiagnostic assay for the Lyme disease vaccine era.Clin Infect Dis.

1999;29:1005. Abstract 248

SHOCKING NEWS

. . . From birth through late adolescence, the brain appears to add billions of new cells, literally constructing its circuits out of freshly made neurons as children and teenagers interact with their environments. In adulthood, the process of adding new cells slows down but does not stop. Mature circuits appear to be maintained by new cell growth well into old age.

Blakeslee S. A decade of discovery yields a shock about the brain.New York Times.January 4, 2000

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DOI: 10.1542/peds.105.6.1330

2000;105;1330

Pediatrics

Robert J. Wilensky

Thoughts of a Plastic Surgeon

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DOI: 10.1542/peds.105.6.1330

2000;105;1330

Pediatrics

Robert J. Wilensky

Thoughts of a Plastic Surgeon

http://pediatrics.aappublications.org/content/105/6/1330.1

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Figure

TABLE 1.Effectiveness of Philadelphia Protocol in the Man-agement of Febrile Infants

References

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