centers consistently perform high-risk operations, thereby driving up the overall mortality rate for a given region.
The relation between case volume and surgical outcomes in pediatric cardiac surgery has been well documented.2,3However, the explanation for this observation remains controversial. The basis of debate hinges on the question: Do high case volumes lead to better outcomes (“practice makes perfect”), or do superior outcomes attract more referrals, resulting in higher case volume. Our study does not require the validity of either theory. We utilized the volume-outcome relation as the basis for referral regardless of whether high volume is the cause or consequence of better outcomes. We submit that our results are valid independent of the cause of the volume-outcome relationship.
We acknowledge that case volume alone may not be the only indicator for the quality of care in a given hospital. However, higher case volume is associated with hospital characteristics known to result in a better quality of care, such as availability of adequately staffed and equipped operating rooms, intensive care units, cath labs, ancillary services, new technologies, and training programs.4 We believe that most pediatric cardiac specialists would concur there is a need to develop better systems to assess the quality of care for pediatric cardiac services. Until these spe-cific measures of quality are available, case volume will remain the only proven indicator which is available and easily quantifiable.
Finally, we wish to stress that volume and outcome relation is a statistical association yielding the impression that high-volume hospitals generally have better outcomes. As is true for any sta-tistical analysis, there are always outliers. As shown in the scat-terplot in Fig 2 of our paper, there are some low- and medium-volume hospitals that have low mortality rates, some even lower than some high-volume centers. We agree with Smith and Powell that many high-quality programs exist independent of their sur-gical volume. We feel strongly that future research efforts should aim to examine other variables potentially related to outcomes. We hope to engage in such studies in the future to identify the characteristics of high-quality, low-volume hospitals that distin-guish them from other low-volume hospitals with high mortality rates.
Ruey-Kang R. Chang, MD, MPH
Division of Cardiology, Department of Pediatrics Harbor-UCLA Medical Center
Torrance, CA
Thomas S. Klitzner, MD, PhD
Division of Cardiology, Department of Pediatrics UCLA School of Medicine
Los Angeles, CA
REFERENCES
1. Chang R-KR, Klitzner TS. Can regionalization decrease the number of deaths for children undergoing cardiac surgery? A theoretical analysis. Pediatrics.2002;109:173–181
2. Jenkins KJ, Newburger JW, Lock JE, et al. In-hospital mortality for surgical repair of congenital heart defects: preliminary observations of variation by hospital caseload.Pediatrics.1995;95:323–330
3. Hannan EL, Racz M, Kavey RE, Quaegebeur JM, Williams R. Pediatric cardiac surgery: the effect of hospital and surgeon volume on in-hospital mortality.Pediatrics.1998;101:963–969
4. American Academy of Pediatrics Section on Cardiology and Cardiac Surgery. Guidelines for pediatric cardiovascular centers. Pediatrics. 2002;109:544 –549
Attention-Deficit/Hyperactivity Disorder and
Sleep
To the Editor.—
As an epidemiologist who studies attention-deficit/hyperactiv-ity disorder (ADHD), I read with great interest the recent report by Chervin et al1on the association between symptoms of ADHD and sleep-disordered breathing (SDB). I am concerned, however, that their conclusions are preliminary and that the statistical anal-ysis is potentially misleading.
In particular, the conclusion that from 15% to 39% of ADHD
cases may be attributable to SDB cannot be justified at this time. This statistic, the population attributable risk percent, describes the proportion of cases in a population comprised of exposed and nonexposed individuals that is caused by the exposure of interest. As the authors point out, this requires that a causal link be estab-lished between exposure and disease. The presentation of this statistic is premature because it has not been established that SDB is causally related to symptoms of ADHD, and questions regard-ing the validity of the association reported by Chervin et al are raised by methodological limitations.
The authors indicate in the limitations section of their report that the association they found was cross-sectional and did not allow them to demonstrate if SDP preceded the symptoms of ADHD or vice versa. Establishing such a time sequence is a minimal criterion for demonstrating causality. Furthermore, the current state of knowledge regarding sleep problems in ADHD subjects is very sparse and is far from establishing a consistent pattern of results that could reasonably suggest that SDB is caus-ally linked with ADHD or its symptoms. Thus, it was inappropri-ate to calculinappropri-ate and present the population attributable risk per-cent because there is no convincing evidence that SBD is causally related to symptoms of ADHD.
Methodological limitations also raise concerns regarding the validity of the associations reported by Chervin et al. The associ-ation between symptoms of ADHD and SBD is likely to be con-founded by important factors that have been shown to modify the risk for sleeping problems in children with ADHD.2,3Previous studies have shown that comorbidity with anxiety and other dis-ruptive behavior disorders accounts for much of the sleep prob-lems reported by children with ADHD. This research also shows that treatment of ADHD with stimulants impacts the relative risk of sleep problems reported in ADHD samples. Although psychi-atric comorbidity and stimulant therapy may also confound asso-ciation between symptoms of ADHD and SDB, Chervin et al addressed potential confounding by neither of these important factors. Because the estimates of relative risk are likely biased by lack of attention to known confounders, it was inappropriate to use them to calculate the population attributable risk percent.
Identifying the causal risk factors for ADHD and the propor-tion of cases that could be attributable to them is a very important endeavor and is in need of much more research. However, these measures need to be based upon valid estimates of increased risk drawn from a wide database of research if they are to have any impact on public health. If published prematurely, the population attributable risk percent will needlessly confuse clinicians and their patients and could interfere with the delivery of appropriate and better studied treatments.
Eric Mick, ScD
Department of Psychiatry
Massachusetts General Hospital and Harvard Medical School
Boston, MA 02114
REFERENCES
1. Chervin RD, Archbold KH, Dillon JE, et al. Inattention, hyperactivity, and symptoms of sleep-disordered breathing. Pediatrics. 2002;109: 449 – 456
2. Mick E, Biederman J, Jetton J, Faraone SV. Sleep disturbances associated with attention deficit hyperactivity disorder: the impact of psychiatric comorbidity and pharmacotherapy.J Child Adolesc Psyhopharmacol.2000; 10:223–231
3. Corkum P, Moldofsky H, Hogg-Johnson S, Humphries T, Tannock R. Sleep problems in children with attention-deficit/hyperactivity disorder: impact of subtype, comorbidity, and stimulant medication. J Am Acad Child Adolesc Psychiatry.1999;38:1285–1293
In Reply.—
In dismissing the likelihood that sleep-disordered breathing (SDB) does contribute to inattentive and hyperactive behavior (HB), Dr Mick ignores clinical and physiological data, overlooks literature on specific sleep disorders, focuses on nonspecific “sleep problems,” and relies mainly on a lack of longitudinal epidemio-logical studies. Since the first modern description of SDB in chil-dren 26 years ago,1published reports have consistently noted high
frequencies of HB, as well as improvement in HB after treatment for SDB.2–5Similar daytime behavior also is reported in several other primary sleep disorders, as is behavioral improvement after treatment for those conditions.6 –10In controlled experimental set-tings, sleep deprivation causes inattentive behavior and cognitive changes that could contribute to HB.11,12Inattention and hyper-activity are described as important symptoms or consequences of SDB in current sleep textbooks,13,14review articles,15–17national academy courses,18and American Academy of Pediatrics litera-ture reviews19and clinical practice guidelines.20Many sleep re-searchers are now more interested in explaining how, rather than whether, sleep disorders change behavior and underlying cogni-tive processes.21 Animal models and functional imaging have already provided valuable clues.22,23In short, abundant data pro-vide convergent support, if not proof, for the less-than-astonishing hypothesis that interruption of normal brain function during the one third of a child’s existence spent asleep does have important ramifications on brain function during the remaining two thirds. In this context, our recent article24was conservative and re-served rather than premature or misleading. We were careful to point out that our own data do not prove SDB causes HB. We discussed the possibility of a causal relationship only among other potential explanations for the association we identified. We were careful not to imply a causal relationship in the title of the manu-script, an all too common phenomenon even when the study design used precludes definitive identification of cause-and-effect relationships.25,26
The concerns expressed about our methods neglect important considerations from both clinical and epidemiological stand-points. Considerable biological overlap exists among disruptive behavior disorders, and sleep disorders are believed to influence a number of psychiatric conditions in addition to HB, including anxiety.17To have adjusted our results for behavioral outcomes comorbid with HB most likely would have resulted in overadjust-ment, reducing the apparent association between SDB symptoms and HB for reasons that are artificial rather than valid. Adjustment for stimulant use was not necessary: a confounder must be asso-ciated both variables in a relationship, and a physiological expla-nation for how stimulants would increase snoring is not known or readily imaginable. In any case, our previous work showed that adjustment for stimulant use does not eliminate the association between SDB symptoms and HB.27Perhaps Dr Mick was misled by results of his own research, which focused exclusively on sleep-related behavioral issues: sleep walking, dream anxiety, sleep terrors, and 19 nonspecific “sleep problems” such as going to bed willingly, waking up at night, falling asleep easily, fear of sleeping in the dark, talking about pleasant dreams, and smiling while asleep.25The unsurprising conclusion that most of these behavioral problems showed stronger associations with anxiety and stimulants than with ADHD yields no information pertinent to sleep-disordered breathing—which was not mentioned or as-sessed—and hardly identifies “known confounders” of the results we reported. Authors of a previous, similar study of ADHD correlates were careful to point out that their research did not address SDB.28
The concerns about our use of the population attributable risk percent (PARP) confuse what we reported. First, the PARP for the entire sample of 866 children was 15%; the higher figure (39%) applied only to the specific subgroup of 295 boys younger than 8 years old. Second, we did not study ADHD cases, but rather HB as assessed by 2 well-validated measures. The PARP was not men-tioned in the abstract, overemphasized as the main finding, or discussed without redundant reminders that it is contingent on the belief that SDB can contribute to HB. Most clinicians interested in childhood sleep disorders already believe that SDB can promote HB, at least in some cases. Otolaryngologists, for example, fre-quently consider attention deficit to be an indication for adeno-tonsillectomy, a common treatment for childhood SDB.29We pre-sented the PARP with exceptional care so that readers could make an informed decision about its validity, based on their own level of conviction about an underlying cause-and-effect relationship.
As already emphasized in our article,24we agree that more work is needed to prove, quantify, and better define a causal link between SDB and HB. Such work may profit considerably from increased collaboration between epidemiologists and sleep spe-cialists. Our work, including the PARP we calculated, helps to quantify the reward that may accrue from such efforts and thereby helps to motivate needed research. As explained by Dr Mick
himself, in an article published only 1 month before our own, “Even in the absence of a conclusive causal link, estimating how many cases could be attributable to a specific risk factor is often valuable in focusing research and clinical resources.”26
Ronald D. Chervin, MD, MS
Sleep Disorders Center Department of Neurology
University of Michigan, Ann Arbor, MI 48109-0117
REFERENCES
1. Guilleminault C, Eldridge F, Simmons FB. Sleep apnea in eight children. Pediatrics.1976;58:23–30
2. Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome.Lung.1981;159:275–287
3. Guilleminault C, Winkle R, Korobkin R, Simmons B. Children and nocturnal snoring— evaluation of the effects of sleep related respiratory resistive load and daytime functioning.Eur J Pediatr.1982;139:165–171 4. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and
behav-iour in 4 –5 year olds.Arch Dis Child.1993;68:360 –366
5. Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviour and psychological functioning.Eur J Pediatr.1996;155:56 – 62
6. Picchietti DL, Walters AS. Moderate to severe periodic limb movement disorder in childhood and adolescence.Sleep.1999;22:297–300 7. Picchietti DL, England SJ, Walters AS, Willis K, Verrico T. Periodic limb
movement disorder and restless legs syndrome in children with atten-tion-deficit-hyperactivity disorder.J Child Neurol.1998;13:588 –594 8. Walters AS, Mandelbaum DE, Lewin DS, Kugler S, England SJ, Miller
M. Dopaminergic therapy in children with restless legs/periodic limb movements in sleep and ADHD.Pediatr Neurol.2000;22:182–186 9. Dahl RE, Pelham WE, Wierson M. The role of sleep disturbances in
attention deficit disorder symptoms: a case study.J Pediatr Psychol. 1991;16:229 –239
10. Guilleminault C, Pelayo R. Narcolepsy in prepubertal children.Ann Neurol.1998;43:135–142
11. Randazzo AC, Muehlbach MJ, Schweitzer PK, Walsh JK. Cognitive function following acute sleep restriction in children ages 10 –14.Sleep. 1998;21:861– 868
12. Fallone G, Acebo C, Arnedt JT, Siefer R, Carskadon MA. Effects of acute sleep restriction on behavior, sustained attention, and response inhibi-tion in children.Percept Mot Skills.2001;93:213–229
13. Robinson A, Guilleminault C. Obstructive sleep apnea syndrome. In: Chokroverty S, ed.Sleep Disorders Medicine: Basic Science, Technical Con-siderations, and Clinical Aspects. 2nd ed. Boston, MA: Butterworth Heinemann; 1999:331–354
14. Aldrich MS.Sleep Medicine.New York, NY: Oxford University press; 1999
15. Hansen DE, Vandenberg B. Neuropsychological features and differen-tial diagnosis of sleep apnea syndrome in children.J Clin Child Psychol. 1997;26:304 –310
16. Bower CM, Gungor A. Pediatric obstructive sleep apnea syndrome. Otolaryngol Clin North Am.2000;33:49 –75
17. Guilleminault C, Khramtsov A. Upper airway resistance syndrome in children: a clinical review.Semin Pediatr Neurol.2001;8:207–215 18. Hoban TF. Obstructive sleep apnea-hypoventilation syndrome in
chil-dren. Association of Professional Sleep Societies (APSS) Annual Course: Sleep Tales: Pediatric Sleep Medicine 2000. Las Vegas, June 17, 2000. 19. Schechter MS. Technical report: diagnosis and management of
child-hood obstructive sleep apnea syndrome.Pediatrics.2002;109(4) Avail-able at: http://www.pediatrics.org/cgi/content/full/109/4/e69 20. Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep
Apnea Syndrome. Clinical practice guideline: diagnosis and manage-ment of childhood obstructive sleep apnea syndrome.Pediatrics.2002; 109:704 –712
21. Beebe DW, Gozal D. Obstructive sleep apnea and the prefrontal cortex: towards a comprehensive model linking nocturnal upper airway ob-struction to daytime cognitive and behavioral deficits.J Sleep Res.2002; 11:1–16
22. Gozal D, Daniel JM, Dohanich GP. Behavioral and anatomical correlates of chronic episodic hypoxia during sleep in the rat.J Neuroscience. 2001;21:2442–2450
23. Thomas RJ, Rosen BR, Bush G, Kwong KK. Working memory in ob-structive sleep apnea: a functional magnetic resonance imaging study. Society for Neuroscience Abstracts; 2001
24. Chervin RD, Archbold KH, Dillon JE, Panahi P, Pituch KJ, Dahl RE, Guilleminault C. Inattention, hyperactivity, and symptoms of
sleep-LETTERS TO THE EDITOR 851
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disordered breathing.Pediatrics.2002;109:449 – 456
25. Mick E, Biederman J, Jetton J, Faraone SV. Sleep disturbances associated with attention deficit hyperactivity disorder: the impact of psychiatric comorbidity and pharmacotherapy. J Child Adolesc Psychopharmacol. 2000;10:223–231
26. Mick E, Biederman J, Prince J, Fischer MJ, Faraone SV. Impact of low birth weight on attention-deficit hyperactivity disorder.Dev Behav Pe-diatr.2002;23:16 –22
27. Chervin RD, Dillon JE, Bassetti C, Ganoczy DA, Pituch KJ. Symptoms of
sleep disorders, inattention, and hyperactivity in children.Sleep.1997; 20:1185–1192
28. Corkum P, Moldofsky H, Hogg-Johnson S, Humphries T, Tannock R. Sleep problems in children with attention-deficit/hyperactivity disorder: impact of subtype, covmorbidity, and stimulant medication. J Am Acad Child Adolesc Psychiatry.1999;38:1285–1293
29. Weatherly RA, Mai EF, Ruzicka DL, Chervin RD. Adenotonsillectomy in children: indications, practices, and outcomes reported by otolaryn-gologists.Sleep.2000;24 (suppl):A212–A213
PAULING’S ADVICE
“I shall . . . give you a word of advice about how to behave toward your elders.
When an old and distinguished person speaks to you, listen to him carefully and
with respect— but do not believe him. Never put your trust in anything but your
own intellect . . . You must always be skeptical—always think for yourself.”
Linus Pauling quoted in Hager T.Force of Nature. New York, NY: Simon and Schuster; 1995
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DOI: 10.1542/peds.110.4.850
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