Telephone Advice: To Charge or Not to Charge, That Is the Question

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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.

Telephone Advice: To Charge

or Not to Charge, That Is

the Question

T

he article in the April 1998 issue of Pediatrics electronic pages by Kirkland and Copeland1 _is an excellent documentation of an important problem in clinical pediatrics. Its focus is on a sub-specialty practice, but its implications are for all of us who are practicing clinical pediatrics in today’s eco-nomic environment. Documentation exists that a large portion of a clinician’s day is spent on the telephone,2,3_{and our patients expect telephone} avail-ability of their pediatrician as a major component of how they choose their “pediatric provider.”4

In our practice of three full-time and one part-time pediatricians, we receive an average of 10 500 to 13 000 calls per year during office hours. In addition, our nursing staff handles;15 000 calls per year. Last year, we joined a newly established triage system, provided by our local children’s hospital for after-hours calls. They answered 3883 calls last year at a cost of $11 652. The cost will increase to $17 500 for the same number of calls this year to cover the actual cost of the service. When I started practice, my part-ners explained to me that telephone advice is “bun-dled” in the fee of the office visit. Since then, how-ever, the telephone has replaced the extended family as a dispenser of practical information, triage, and emergency advice. Reimbursement of this service on a fee-for-service basis seems appropriate, but has not been deemed compensable by most insurance com-panies. With the advent of capitation and “reduced

negotiated payments,” insurance companies

usurped this “phone medicine” as part of the bun-dled payment, and it has become a “giveaway” rather than a compensated service, a giveaway that the practicing pediatrician did not realize was being donated. The fear of doing danger to the physician– patient relationship does not seem warranted, be-cause the “new” pediatrics is not allowing the per-manent medical home to develop, when many families change offices every January or July because their employer changes insurance plans. The old brake on the after-hours call included a personal relationship with “their doctor” not “their provider.” The telephone practice of medicine is not a new phenomenon. It was first described inLancetin 1879.5

The tradition that physicians do not charge for tele-phone advice and consider it a professional courtesy has grown since then, but recent changes in the prac-tice environment should prompt a reexamination of this free service as perhaps an anachronism from which we should advance.6_{Pediatricians working on} salary or on “capitation” are being reimbursed. Those of us in conventional practice should look around carefully and evaluate to whom we are ex-tending this free expertise. The value of this tele-phone advice and triage is enormous and its com-pensation needs to be established by the pediatric community and those it serves.

The work by Kirkland and Copeland1_thoughtfully describes the establishment of a reimbursement sys-tem. It would be of benefit to assess access and acceptance of such a system in a conventional pedi-atric practice.

Kurt Metzl, MD

Department of Pediatrics

University of Missouri–Kansas City School of Medicine

Kansas City, MO 64114

REFERENCES

1. Kirkland JL, Copeland KC. Telephone charges and payments in the diabetes clinic.Pediatrics1998:101(4). URL: http://www.pediatrics.org/ cgi/content/full/101/4/e2

2. Bergman AB, Dassel SW, Wedgewood RJ. Time motion studies of practicing pediatricians.Pediatrics. 1966;38:254 –263

3. Hessel SJ, Haggerty RJ. General pediatrics: a study of practice in the mid-1960s.J Pediatr. 1968;73:271–279

4. Deisher RW, Engel WL, Spielholz R, Standfast SJ. Mothers’ opinions of their primary care.Pediatrics.1965;35:82–90

5. Practice by telephone.Lancet. 1879:819

6. Fisher GR III. Telemedicine and the payment system.PA Med.1995; 32–34

Apnea of Prematurity and Risk

for SIDS

ABBREVIATION. SIDS, sudden infant death syndrome.

T

he premature infant is at increased risk to die of sudden infant death syndrome (SIDS).1 Al-though the overall risk in Los Angeles County in 1996 was 1.5 per 1000 live births, that for the baby

Received for publication Feb 5, 1998; accepted Apr 2, 1998.

Reprint requests to (K.M.) University of Missouri–Kansas City School of Medicine, 930 Carondelet, Suite 302, Kansas City, MO 64114.

Received for publication May 1, 1998; accepted Aug 4, 1998.

Reprint requests to (J.E.H.) Women’s and Children’s Hospital, 1240 N Mission Rd, Los Angeles, CA 90033.

PEDIATRICS Vol. 102 No. 4 October 1998 969

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born before 37 weeks’ gestation was approximately five times as high. This increased risk has been rec-ognized for many years, yet the reasons remain ob-scure. It would be highly desirable to be able to identify the individual infant who is at greatest risk within the group. Without information as to cause, this has proven impossible thus far. A number of efforts have been made to identify subpopulations of premature infants in whom the risk is greater. Only one factor has been reliably associated with risk, and that is gestational age.2 _{This has been true in all} studies reporting weeks of gestation, and the associ-ation is inverse. The shorter the gestassoci-ational interval, the more immature the infant is at birth. The more immature the infant, the higher the risk is that the infant will die of SIDS. In our nursery follow-up clinic where we see infants after discharge whose birth weight was ,1500 g, corresponding to a gestational age of#32 weeks, the risk increases to 1 per 100.

Apnea of prematurity, which occurs while the in-fant is in the nursery and usually disappears by 36 weeks’ gestation, also is associated with maturity, the incidence being highest in the least mature in-fants.3 _{It has been tempting to consider the infant} with apnea in the nursery to be at higher risk for SIDS after discharge. This approach seemed particu-larly attractive when the sleep apnea theory as the cause of SIDS was widely accepted. A number of programs for pneumography studies at discharge with home monitoring schedules based on the re-sults have been recommended and actively pursued. This has been true even though the criteria that were developed from term infants were never verified, and no clinical studies have demonstrated a reduction in SIDS in monitored infants. I believe it is time to look at the facts published during the last several years.

The most reliable and reproducible information we have about SIDS comes from epidemiologic stud-ies. The largest and most detailed study of risk fac-tors was conducted by the National Institute of Child Health and Human Development and results pub-lished in theAnnals of the New York Academy of Science

in 1988.4_{SIDS cases were obtained from six centers} representing;10% of live births for the total United States. Cases were matched with two control groups of surviving infants, control group A by age alone, and control group B by birth weight and race as well as age. When SIDS infants were compared with those in control group A, it was not surprising that new-born apnea appeared as the strongest risk factor. This observation proved misleading when SIDS infants were compared with those in control group B, which included equal numbers of low birth weight infants. Here, the effect disappeared entirely, leading to the conclusion that apnea of prematurity is related to birth weight but is not a risk factor for SIDS. This finding is corroborated by our own follow-up study of low birth weight infants referred to above. Although the incidence of SIDS was increased, we could find no relationship between SIDS and apnea of prematurity or the need for ventilation in the nursery.

When cardiorespiratory recordings are performed at or near discharge of the premature infant, an increased number of events can be seen in the

re-cordings compared with those of term infants.5 Ap-nea, periodic breathing, and brief episodes of brady-cardia identified on 4- to 24-hour polysomnograms have been implicated as risk factors for SIDS. This is despite the fact that in all published studies, no cor-relation has been found between recorded events and apnea of prematurity, between recorded events and apparent life-threatening events, or, most impor-tantly, between recorded events and SIDS. In 1982, David Southall and associates in England published results from a large study of discharge recordings from 1157 preterm infants.6_{Five of these infants} sub-sequently died of SIDS, and none had had suspicious findings on their recordings at discharge from the nursery. A number of studies of cardiorespiratory behavior in preterm infants both at and after dis-charge from the nursery found increased events of apnea, especially obstructive apnea, and bradycar-dias.5_{This is of considerable interest in} understand-ing the behavior of these infants, but has been shown convincingly not to identify infants at increased risk for SIDS. Only one published article has reported an increase in SIDS deaths in infants with bronchopul-monary dysplasia.7 _{This finding has not been} repli-cated in the literature and is not supported by our own experience.

Surprisingly, little information is available about cardiorespiratory behavior in preterm infants after discharge from the nursery. Investigators with the Collaborative Home Infant Monitoring Evaluation (CHIME), a multicenter study supported by the Na-tional Institute of Child Health and Human Develop-ment, are utilizing event recorders in the home. They recently have presented preliminary data that appar-ently normal prematures have prolonged apnea with obstruction and oxygen desaturation in the home.8_The significance of these findings is not yet clear.

Home monitoring of premature infants is not in-dicated for risk of SIDS. There is no evidence that monitoring is effective, and there are no criteria available including the history of apnea of prematu-rity to identify the infant who is more likely to die. This opinion is well summarized in a consensus statement issued by the National Institute of Child Health and Human Development on the subject of home monitoring for risk of SIDS.9_{I believe it is past} time to discontinue the practice of obtaining cardiore-spiratory recordings to identify risk for SIDS in the premature infant and recommending home monitoring based on the findings.

Joan E. Hodgman, MD

Department of Pediatrics

University of Southern California School of Medicine Los Angeles, CA 90033

REFERENCES

1. Bergman AB, Ray CG, Pomeroy MA, et al. Studies of the sudden infant death syndrome in King County, Washington, III. Epidemiology. Pedi-atrics. 1972;49:860 – 870

2. Kraus JF, Borhani NO. Postneonatal sudden unexpected death in California: a cohort study.Am J Epidemiol. 1972;95:497–510

3. Henderson-Smart DJ. The effect of gestational age on the incidence and duration of recurrent apnea in newborn babies.Aust Pediatr J. 1981;17: 273–276

4. Hoffman HJ, Damus K, Hillman L, et al. Risk factors for SIDS: results of

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the National Institutes of Health and Human Development SIDS coop-erative epidemiological study. In: Schwartz PJ, Southall DP, Valdes-Dapena M, eds.The Sudden Infant Death Syndrome: Cardiac and Respira-tory Mechanisms.Ann NY Acad Sci. 1988;533

5. Barrington KF, Finer N, Li D. Predischarge respiratory recordings in very low birth weight newborn infants.J Pediatr. 1966;129:934 –940 6. Southall DP, Richards JM, Rhoden KJ, et al. Prolonged apnea and

cardiac arrhythmias in infants discharged from neonatal intensive care units: failure to predict an increased risk for sudden infant death syndrome.Pediatrics. 1982;70:844 – 851

7. Werthammer J, Brown ER, Neff RK, et al. Sudden infant death syn-drome in infants with bronchopulmonary dysplasia.Pediatrics.1982;69: 301–304

8. Ramanathan R, Corwin M, Hunt CE, et al. Preterm infants have pro-longed apnea with obstruction and associated oxygen desaturation at home.Pediatr Res. 1997;41:171A

9. Consensus Statement: National Institutes of Health Consensus Devel-opment Conference on Infantile Apnea and Home Monitoring; Septem-ber 29 to OctoSeptem-ber 1, 1986.Pediatrics. 1987;79:292–299

Xylitol Sugar and Acute

Otitis Media

I

n this month’s Pediatrics1 _{and in an article} pub-lished previously in the British Medical Journal,2 Uhari and associates of Finland have suggested that xylitol sugar is effective in preventing acute otitis media. The studies tackle the difficult issue of determining the effect of a targeted prevention on the incidence of a disease as complex and multifac-torial in its etiology as acute otitis media. The key finding is that xylitol, given as a gum to older chil-dren and as a syrup to younger chilchil-dren, decreased the incidence of acute otitis media and the use of antibiotics by approximately one third in both stud-ies. The criteria for the randomization, blinding of observers, and diagnosis of otitis media can be quib-bled with but are unlikely to invalidate this impres-sive and consistent finding in both studies. This is very good news at a time when antibiotic use and consequent antibiotic resistance are increasing rapidly.3 At this point, one should ask, “What is xylitol, what was the rationale for trying xylitol in Finland, and why might it work?” Xylitol is a 5 carbon sugar alcohol found in many plant materials, including raspberries and plums. It has been used as a sweet-ening substitute. It is absorbed slowly, and in dos-ages of 30 to 40 g per day can cause osmotic diarrhea. (The dosage in this study was 10 g per day, with no excess gastrointestinal complaints in the treatment arm.) Xylitol-containing gum has been widely ex-plored as a means of decreasing the incidence of dental caries, with a presumed mechanism of action being the inhibition of growth of Streptococcus mu-tans.4_{Xylitol is not a carbon source for most bacteria.} In addition, bacteriologic work showed that xylitol inhibited the growth of S pneumoniae, although not

other major bacterial causes of acute otitis5_{— hence,} the rationale and presumed mechanism of action for the use of xylitol in the Finnish studies.

The mechanism of action may not be as simple as inhibition of growth of S pneumoniae. The study in the British Medical Journalcould demonstrate no ef-fect on pneumococcal carriage.2_{The xylitol} concen-tration in the posterior nasopharynx, the entry point for middle ear colonization, is surely lower than that in the mouth, where the effect on caries was estab-lished.6 _{The chewing of gum was attractive as a} mechanism that might lead to opening of the eusta-chian tube and equalization of middle ear pressure. However, xylitol was equally effective when given as a syrup to the younger children. An osmotic effect of xylitol might be postulated. Suffice it to say that we do not have a biologically plausible mechanism of action, which is always disturbing when advocating a new therapy.

What do these two studies tell us about our future management of otitis? No single set of studies in an area as complex as otitis media is going to define the appropriate use of a novel intervention.

Some of the limitations of the clinician’s ability to extrapolate from this study are inherent in its design. Both studies examined the effect of xylitol in the day care setting on children whose mean age ranged from 2 to 5 years. The effectiveness and tolerance of the compound have not been assessed in the peak age for otitis media, which is 6 to 18 months.7_Xylitol was administered five times a day, which is difficult to translate into a practical regimen. The studies were performed in children at no special risk of otitis. A critical question is whether the treatment would be as effective in the subset of children with recurrent otitis. Given the complexity of the regimen, it would be more applicable in children who have identified themselves by having recurrent otitis me-dia. There also are differences between the ethnic and racial populations in Finland and those in the United States. Might these influence the outcome and interpretation of the study? An additional con-founding variable is that a high percentage of chil-dren in Finland have had adenoidectomies as part of their otitis management, .20% at age 2 and 30% at age 5, in the current study. The intervention ap-peared safe and compliance was good over a rela-tively brief period of enrollment—2 or 3 months. Can this compliance be sustained, and will xylitol resis-tance develop? Bacteria that adapt to growth in xy-litol have been described.8

A final critical question is the availability of xylitol in the United States. Xylitol compounds are used widely in gums in Europe. However, the pharmacy at Vanderbilt University Medical Center could iden-tify no source of either xylitol gum or syrup that might be suitable for initiating a regimen similar to that used in Finland. Xylitol is a regulated food ad-ditive under the Food and Drug Administration reg-ulations, as described in the Code of Federal Regula-tions.9_{Xylitol may be used safely in foods for special} dietary uses, provided the amount used is not greater than that required to produce its intended effect. Xylitol also can be used to replace dietary

Received for publication Jul 22, 1998; accepted Jul 24, 1998.

Reprint requests to (P.F.W.) Department of Pediatrics, Division of Infectious Diseases, D7235 Medical Center North, Vanderbilt Medical Center, Nash-ville, TN 37232-2581.

COMMENTARIES 971

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DOI: 10.1542/peds.102.4.969

1998;102;969

Pediatrics

Kurt Metzl

Telephone Advice: To Charge or Not to Charge, That Is the Question

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DOI: 10.1542/peds.102.4.969

1998;102;969

Pediatrics

Kurt Metzl

Telephone Advice: To Charge or Not to Charge, That Is the Question

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