acquired hearing loss whose loss could not have been detected as neonates, exclusion of those children from the denominator would have resulted in an even higher percentage classifiable as HRR/ ICN, particularly if one referred to the most recent (1994) version of the HRR.7Finally, in the United Kingdom study11cited later by Dr Grosse and colleagues, which involved a total of 53 781 new-borns, 70% (37/53) of the infants eventually identified as having moderate to profound bilateral sensorineural hearing loss had high-risk factors and/or were in special/ICNs. I stand by my statement that most of the infants with sensorineural hearing impairment detectable in the newborn period will be found by screening only newborns who meet HRR criteria and/or are ad-mitted to an ICN.12
The statement that “intervention by age 6 months is important to ensure normal language development” refers to the study by Yoshinaga-Itano and colleagues,13 limitations of which I have discussed previously.14The study consisted of a nonrandomized comparison, some of its findings seem counterintuitive, and its authors considered its results suggestive rather than indicative of a cause-and-effect relationship.
Dr Grosse and colleagues express agreement with concerns that Bess and I have raised about adequacy of facilities and follow-up, about the need for greater public awareness, and particularly about the impact of false-positive identifications. Unfortunately, those concerns appear to be receiving little more than lip service in the drive to implement universal screening.
Once again, I refer the interested reader to a previously pub-lished exchange of correspondence (Pediatrics. 1994;94:948 –963) that provides a comprehensive summary of arguments for and against universal newborn hearing screening. A more recent ex-change (Pediatrics. 1999;104:351–355) adds new details. It seems likely that the arguments will continue to be voiced until such time as the issue is settled one way or the other by an appropri-ately designed and executed study or, less rationally and far more expensively, by the cumulative weight of favorable or unfavorable experience.
Jack L. Paradise, MD
Department of Pediatrics University of Pittsburgh School of Medicine and
Children’s Hospital of Pittsburgh Pittsburgh, PA 15213-2583
REFERENCES
1. Bess FH, Paradise JL. Universal screening for infant hearing impairment: not simple, not risk-free, not necessarily beneficial and not presently justified.Pediatrics.1994;93:330 –334
2. Bess FH, Paradise JL. Reply to letters concerning universal screening for infant hearing impairment.Pediatrics.1994;94:959 –963
3. MMWR. Serious hearing impairment among children aged 3–10 years—Atlanta, Georgia, 1991–1993. MMWR Morb Mortal Wkly Rep.
1997;46:1073–1076
4. Mauk GW, White KR. Giving children a sound beginning: the promise of universal newborn hearing screening.Volta Rev.1995;97:5–32 5. Mutton P. Early identification of deaf babies.Lancet.1998;352:1951–1952 6. Stein LK. Factors influencing the efficacy of universal newborn hearing
screening.Pediatr Clin North Am.1999;46:95–105
7. Joint Committee on Infant Hearing. 1994 position statement.Pediatrics.
1995;95:152–156
8. Elssmann SF, Matkin ND, Sabo MP. Early identification of congenital sensorineural hearing impairment.Hear J.1987;40:13–17
9. Joint Committee on Infant Hearing. 1982 position statement.Pediatrics.
1982;70:496 – 497
10. Mauk GW, White KR, Mortensen LB, Behrens TR. The effectiveness of screening programs based on high-risk characteristics in early identifi-cation of hearing impairment.Ear Hear.1991;12:312–319
11. Wessex Universal Neonatal Hearing Screening Trial Group. Controlled trial of universal neonatal screening for early identification of perma-nent childhood hearing impairment.Lancet.1998;352:1957–1964 12. Paradise JL. Universal newborn hearing screening: should we leap
before we look?Pediatrics.1999;103:670 – 672
13. Yoshinaga-Itano C, Sedey AL, Coulter DK, Mehl AL. Language of early-and later-identified children with hearing loss. Pediatrics. 1998;102: 1161–1171
14. Paradise JL. Reply to letters concerning universal newborn hearing screening: should we leap before we look?Pediatrics.1999;104:354 –355
Cardiopulmonary Resuscitation in Very Low
Birth Weight Infants
To the Editor.—
We read with interest the recent manuscript entitled “Cardio-pulmonary Resuscitation in the Very Low Birth Weight Infant: The Vermont Oxford Network Experience.”1The authors should be commended for pursuing a complex clinical issue. However, there are significant deficiencies in study design and data analysis that limit the interpretation and significance of the data.
Briefly, as background information, the birth of an infant is associated with abrupt cessation of the fetomaternal circulation with subsequent rapid and profound physiologic changes involv-ing both the cardiac and respiratory systems. Failure of either system to adapt will result in cardiorespiratory compromise and the need for resuscitation. Two cardinal events appear critical in the genesis of compromised cardiorespiratory adaptation and the subsequent need for intensive resuscitation (CPR). These events include failure to establish a functional residual capacity (FRC) and the presence of impaired placental gas exchange as evidenced by profound fetal acidemia (umbilical cord arterial pH ⱕ7.00 [2,31]). Failure to establish a FRC may be secondary to ineffective or improper ventilation or an abnormal underlying pulmonary state, eg, pulmonary hypoplasia, pulmonary immaturity, etc. In-deed, we previously documented the prominent association be-tween improper or ineffective ventilatory support and the need for CPR.4The presence of asphyxia may be suspected when there is an associated sentinal event, eg, abruptio placentae, but often is clinically inapparent in the delivery room.5Recovery after CPR is in part influenced by the cause of the cardiorespiratory compro-mise, the duration of the precipitating event, the establishment of effective ventilation, and restoration of spontaneous circulation (ROSC) with establishment of coronary perfusion pressure.
To briefly illustrate the importance of the above issues, we present data on infants⬍1500 g birth weight who received CPR (n⫽21), ie, chest compression only (n⫽17) and additionally epinephrine (n⫽4) for the years 1996 –1998. It should be noted that in cases of uncertain prognosis (birth weight⬍600 g) CPR is not pursued in our delivery room (DR) in all cases. Moreover, prophylactic surfactant is not administered in the DR. The per-centage of infants receiving CPR by birth weight is shown in Table 1.
The percentage of infants requiring chest compressions is com-parable to the Vermont Oxford Network experience. However, the percentage of infants requiring epinephrine is markedly less. Cur-rent National Resuscitation Program (NRP) guidelines are fol-lowed in our institution; however, we stress the importance of ventilation in ROSC.
This may in part explain the less frequent use of epinephrine. The perinatal characteristics and short-term outcome of the 21 infants are illustrated in Table 2.
The data highlight several important points that are crucial when assessing the efficacy of CPR including: 1) the duration of CPR which was significantly longer for infants who died, 270⫾ 231 versus 43⫾32 seconds (P⫽.0004) for all survivors, and even shorter for those survivors without severe IVH 30⫾12 seconds; 2) lethal conditions incompatible with life which included pulmo-nary hypoplasia, complex heart disease (unknown in the DR) and
TABLE 1. DR-CPR by Birth Weight
BW (G) n DR-Cardiac
Compression %
Epinephrine %
501–750 80 7.5% (1.25%)
751–1000 103 6.7% 0
1001–1250 146 2.7% 0
1251–1500 196 2.0% 3 (1.5%)
DR-CPR indicates delivery room resuscitation; BW, birth weight; G, grams.
trisomy 18; and 3) ineffective or improper ventilatory support, ie, a misplaced endotracheal tube that complicated the resuscitation in at least 4 cases.
This and additional relevant information lacking from the Ox-ford-Vermont data included: 1) the outcome of infants with a 1-minute Apgar score of 0 or 1 alone, or as compared to infants with an Apgar score ofⱖ2; 2) the number of infants who received prophylactic surfactant in the DR that may have complicated cardiorespiratory adaptation; and 3) the absence of important clinical data, ie, the presence or absence of asphyxia. In addition, it is noteworthy that of the 1595 infants of birth weight 501–1500 g, 670 (42%) had a 1-minute Apgar scoreⱖ2 and 367 infants (19%) had a scoreⱖ3. Did these latter infants really require chest com-pressions? The authors fail to comment on the potential neuropro-tective influence of antenatal glucocorticoids, ie, decreased inci-dence of intraventricular hemorrhage, which was administered to 33% of the mothers of infants who received DR-CPR. Because neither the timing and/or number of cranial ultrasound scans performed is provided, cases of late hemorrhage and/or cystic periventricular leukomalacia (PVL) may have been missed. De-spite this limitation, it is very bothersome that 7.8% of infants who received DR-CPR had evidence of PVL that was double the antic-ipated 3.9% incidence in the group of infants without CPR. The diagnosis of PVL is synonymous with poor neurodevelopmental outcome.
Despite these inherent weaknesses, the data are important vis-a`-vis the antenatal counseling of parents as to the potential for CPR in the DR, ie, 10% for the tiniest infants (⬍750 g) versus 2% for the larger infants (⬎1250 g). Given the rarity of asphyxia in this patient population, ineffective ventilation and failure to establish a FRC should be the primary concern for those infants with persistent bradycardia. For the tiniest infants, pulmonary imma-turity is the most likely explanation in most cases. The duration of CPR would appear to be the most useful clinical determinant of short and long adverse outcome, an observation consistent with data from other patient population groups, ie, children and adults.
Myra Wyckoff, MD Jeffrey Perlman, MB
Department of Pediatrics
University of Texas Southwestern Medical Center Dallas, TX 75235
REFERENCES
1. Finer NN, Horbar JD, Carpenter JH. Cardiopulmonary resuscitation in the very low birth weight infant: the Vermont Oxford Network expe-rience.Pediatrics.1999;104:428 – 434
2. Vyas H, Field D, Milner AD, Hopkin IE. Determinants of the first inspiratory volume and functional residual capacity at birth.Pediatr Pulmonol.1986;2:189 –193
3. American College of Obstetricians and Gynecologists.Assessment of Fetal and Newborn Acid-Base Studies.Washington, DC: American College of Obstetricians and Gynecologists; 1989:1– 4. ACOG Technical Bulletin No. 127
4. Perlman JM, Risser RR. Cardiopulmonary resuscitation in the delivery room: associated clinical events. Arch Pediatr Adolesc Med.1995;149: 20 –25
5. King TA, Jackson GL, Josey AS, et al. The effect of profound umbilical artery acidemia in term neonates admitted to a newborn nursery. J Pediatr.1998;132:571–572
In Reply.—
We thank Drs Wyckoff and Perlman for their correspondence regarding our manuscript. In their letter they emphasize the need to establish a functional residual capacity (FRC) shortly after delivery, discuss some of the shortcomings of the data presented in our manuscript, and review their own experience with DR-CPR. We are pleased that our paper has stimulated others to review their own experience and provide additional information, which may be of clinical importance.
Wyckoff and Perlman discuss events related to poor cardiopul-monary adaptation at birth. We agree that impaired placental gas exchange predisposes infants, especially extremely very low birth weight (VLBW) infants, to poor adaptation, but, as has been previously pointed out, cord pH per se is often inadequate to explain a poor transition at birth or subsequent neonatal events.1 Other factors including the arterial base deficit and Apgars may be more predictive of neonatal outcome. The failure to establish spontaneous breathing or to make effective respiratory efforts may delay the development of an adequate FRC and the use of larger, longer breaths during resuscitation may be effective in promoting the development of FRC.2In addition, previously com-promised fetuses are often intolerant of labor and delivery. We agree that prompt and effective resuscitation, including the early and effective establishment of FRC, is essential to maximize intact TABLE 2. Selected Perinatal Events/Factors in Infants Receiving DR IR (1996 –1998)
Patient No.
BW GA 1 Minute
Apgar
5 Minute Apgar
Duration Cord pH
Clinical Morbidity Outcome
1.* 1470 28 1 3 600 7.14 HIE Died
2.* 1300 30 0 0 600 7.14 Trisomy 18 Died
3.* 695 25 1 1 480 7.28 Pulm. Hypoplasia Died
4.* 1320 29 1 1 430 7.22 Sepsis Died
5.⫹ 1045 26 4 6 180 7.32 C.H.D., Heart Block Died
6.⫹⫹ 720 27 3 7 180 7.29 C.L.D. Died
7.⫹⫹ 660 26 2 2 180 7.25 Severe IVH Died
8. 850 27 1 3 60 – Pulm Hypoplasia Died
9. 880 26 1 6 30 7.10 Pulm Hypoplasia Died
10. 748 25 1 7 30 7.33 Severe IVH Died
11. 1058 27 0 3 120 7.25 TWIN, Severe IVH Dev. delay
12.⫹⫹ 786 27 1 1 90 6.82 Severe IVH Dev. delay
13. 894 25 1 6 30 – TWIN, Severe IVH Dev. delay
14. 776 27 2 6 30 6.99 Antenatal PVL Dev. delay
15. 783 29 1 4 45 7.09 CLD Intact at discharge
16.⫹⫹ 1170 30 2 1 45 7.29 CLD Intact at discharge
17. 1310 31 1 6 30 6.96 HMD Intact at discharge
18. 1068 27 2 7 30 7.33 HMD Intact at discharge
19. 516 25 1 3 30 7.08 CLD Intact at discharge
20. 800 25 1 4 15 7.30 CLD Intact at discharge
21. 636 26 1 5 15 7.10 CLD Intact at discharge
BW indicates birth weight; GA, gestational age; min, minute; duration, duration of CPR; HIE, hypoxic ischemic encephalopathy; CHD, complex heart disease; IVH, intraventricular hemorrhage; PVL, periventricular leukamalacia; CLD, chronic lung disease; HMD, hyaline membrane disease; dev, neurodevelopment.
* Received epinephrine;⫹developed bradycardia at 5 minutes;⫹⫹variable heart rate includingⱖ100 beats/minute related to endotra-cheal tube difficulties and ineffective ventilation.
LETTERS TO THE EDITOR 619
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recovery. In addition, the reflex response by the premature infant to positive pressure ventilation appears to be important in im-proving tidal exchange and establishing and FRC.3Such reflex responses may be inhibited by degrees of asphyxia during labor. Wyckoff and Perlman indicate that certain information was lacking from our review. To facilitate the use of the Vermont Oxford Network database at a large number of neonatal units, the database has been limited a set of core data items. Asphyxia is not a data item in the database. The timing of surfactant therapy was not an item in the database during the time period of the study, but has been subsequently added and is now routinely collected. We indicated the percentage of all the infants whose mothers received antenatal steroids, but limited our discussion to the as-pects of resuscitation and neonatal outcome. Wyckoff and Perl-man mistakenly indicate that steroids were “administered to 33% of mothers of infants who received DR-CPR.” As shown in Table 1 of our report, 33% of the 497 infants weighing 401 to 500 g and 64% of the 27 210 infants weighing 501 to 1500 g were exposed to antenatal steroid therapy.4We did not report steroid exposure separately for the infants who received DR-CPR.
We specifically limited our discussion of PVL because were not able to review the neuroanatomic evaluations and their timing as stated on page 432.4We were also concerned about the overall incidence of PVL, but because we could not evaluate the extent of this abnormality, we refrained from further comment. Until our review, there was no suggestion that infants⬍750 g at birth would survive if they required DR-CPR. Our efforts were directed at determining the proportion of infants who survived with and without evidence of neuromorbidity. However, our study did not evaluate long-term neurodevelopment.
A recent study has evaluated VLBW infants who survived following DR-CPR and has shown that intact survival occurred in 70% of the 15 survivors who were assessed. In that study at least 1 CPR survivor with white-matter injury was neurodevelopmen-tally normal.5We welcome further data which demonstrate that intact neonatal survival can occur after DR-CPR, and note that 2 of the 6 infants⬍750 g shown by Wyckoff and Perlman survived apparently intact.
Wyckoff and Perlman have provided information from a 4-year period from their own institution. They report that during this period 21 (4%) of 525 infants weighing 501 to 1500 g received CPR. This is similar to the overall rate of cardiac compressions of 4.8% that we reported. Furthermore, 11 (52%) of their 21 infants sur-vived and only 3 of the 11 survivors had evidence of severe IVH. This is consistent with our findings. The difference in the propor-tion of infants receiving epinephrine during resuscitapropor-tion is not surprising because our report is based on data for⬎1600 resusci-tations at 196 centers whereas theirs is a single center report. Clearly, there is marked variation among units in DR practice including the use of epinephrine. For instance, in 1998 there were 4654 infants weighing 501 to 750 g treated at the 295 neonatal intensive care units (NICUs) participating in the Vermont Oxford Network that year. Overall, 9% of these infants received epineph-rine in the DR. However, there was marked variation among centers; with 25% of NICUs having a 0% rate for this treatment and 25% of NICUs having rates⬎17%.6
Wyckoff and Perlman indicate that they follow NRP guidelines at their institution and stress the importance of ventilation and the ROSC. They report 3 infants who received 180 seconds of DR-CPR, at least 1 of whom had this intervention initiated at 5 minutes, and none of these infants received epinephrine. These authors have commented that infants with Apgar scores ofⱖ2 at 1 minute were unlikely to require compressions. Although we agree and so stated in the manuscript on page 431,4it is of interest to us that 6 of their 21 infants who received chest compressions had an Apgar at 1 minute of 2 or greater. We believe that their information supports our belief that current practices of neonatal resuscitation are variable and do not always follow the teachings of the AAP/ AHA NRP.7As we stated in our “Conclusion,” “Further informa-tion is urgently required regarding the indicainforma-tions, applicainforma-tion, and longer-term neurodevelopmental outcome of DR-CPR so that we may fully assess its role in the initial treatment of these fragile infants.” We hope that our report will stimulate additional re-search on the issue of DR-CPR for VLBW infants.
Neil N. Finer, MD
Department of Pediatrics
University of California, San Diego School of Medicine
San Diego, CA 92103-8774
Jeffrey D. Horbar, MD
University of Vermont College of Medicine Vermont Oxford Network Burlington, VT 05401
REFERENCES
1. Sehdev HM, Stamilio DM, Macones GA, Graham E, Morgan MA. Pre-dictive factors for neonatal morbidity in neonates with an umbilical arterial cord pH less than 7.00.Am J Obstet Gynecol.1997;177:1030 –1034 2. Vyas H, Milner AD, Hopkin IE, et al. Physiologic responses to pro-longed and slow rise inflation in the resuscitation of the asphyxiated newborn infant.J Pediatr.1981;99:635
3. Hoskyns EW, Milner AD, Boon AW, Vyas H, Hopkin IE. Endotracheal resuscitation of preterm infants at birth.Arch Dis Child.1987;62:663– 666 4. Finer NN, Horbar JD, Carpenter JH. Cardiopulmonary resuscitation in the very low birth weight infant: the Vermont Oxford Network expe-rience.Pediatrics.1999;104:428 – 434
5. Finer NN, Tarin T, Vaucher YE, Barrington K, Bejar R. Intact survival in extremely low birth weight infants after delivery room resuscitation.
Pediatrics.1999:104(4). URL: http://www.pediatrics.org/cgi/content/ fall/104/4/e40
6. Vermont Oxford Network,Vermont Oxford Network 1998 Database Sum-mary.Burlington, VT: Vermont Oxford Network; 1999
7. Bloom RS, Cropley C and the AHA/AAP Neonatal Resuscitation Pro-gram Steering Committee.Textbook of Neonatal Resuscitation.Dallas, TX: American Heart Association; 1994
First Urinary Tract Infections in Swedish
Children
To the Editor.—
In their epidemiologic analysis of first urinary tract infections (UTIs) in Swedish children, Jakobsson et al1make the observation that UTI rates varied seasonally and declined over the 2-year study period. The authors do note that such rate trends are bio-logically implausible, but fail to acknowledge several method-ologic sources of bias that may have distorted their results.
A single, mid-study population estimate was selected as the denominator for all rates, despite a 5% decline in the base popu-lation (children⬍2 years of age) in a single year. If this decline is attributable to a drop in the birth rate, then the person-month contribution of newborns may have declined 10% over the 24-month study period. Given such a rapid decline in the age group at greatest risk for UTI, a fixed population denominator appears to be an inappropriate denominator for the calculation and compar-ison of annual rates.
By using a fixed denominator for all rates, the study analysis also fails to account for the gradual attrition of some 2300 children from the study population over 2 years. This declining denomi-nator occurs because the authors have studied only “first” UTIs. By definition, children with UTI contribute no additional person-time to the at-risk population beyond their dates of diagnosis.
The most important source of bias is the striking seasonality of births in Sweden—where monthly birth indices are at least 30% higher in spring than early winter.2,3 As a result, rates for any illness associated with early infancy can be expected to show substantial seasonal fluctuation. The importance of adjusting for season of birth is illustrated in a recent analysis of seasonal risks for sudden infant death syndrome in Sweden.4
Taken together, these factors suggest that simple monthly or annual counts of UTIs (numerator data) may not fairly represent true incidence. Accurate denominator data are needed. If the authors would consult available birth and census data, it should be possible to calculate age-specific, person-time denominators for each month of the study period. This would permit calculation of
DOI: 10.1542/peds.106.3.618
2000;106;618
Pediatrics
Myra Wyckoff and Jeffrey Perlman
Cardiopulmonary Resuscitation in Very Low Birth Weight Infants
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