Kathryn A. Mun˜oz, PhD, MPH Merck & Co, Inc
Blue Bell, PA
Susan M. Krebs-Smith, PhD, MPH, RD Rachel Ballard-Barbash, MD, MPH Applied Research Branch
Division of Cancer Control and Population Sciences National Cancer Institute
Bethesda, MD
Linda E. Cleveland, MS, RD Food Surveys Research Group
Beltsville Human Nutrition Research Center Agricultural Research Service
US Department of Agriculture Riverdale, MD
REFERENCES
1. Mun˜oz KA, Krebs-Smith SM, Ballard-Barbash R, Cleveland LE. Food intakes of US children and adolescents compared with recommenda-tions.Pediatrics.1997;100:323–329
SIDS or Murder?
To the Editor.—
In his commentary in the January 1997 issue ofPediatrics,1Dr
Bergman stated his concern that the much-publicized conviction of Waneta Hoyt for causing the deaths of her five children, deaths previously attributed to the sudden infant death syndrome (SIDS), might provoke a “return to the aura of suspicion that surrounded SIDS deaths in the past.” We agree, but still believe that informa-tion excluding the possibility of child abuse should have been provided for the cases reported inPediatrics electronic pagesof the same month under the title “Environmental Risk Factors Associ-ated with Pediatric Idiopathic Pulmonary Hemorrhage and He-mosiderosis in a Cleveland Community.”2In that article, Montana
and colleagues2describe the epidemiologic investigation of a
clus-ter of 10 infants who during 1993 to 1994 had illnesses of sudden onset at home with evidence of acute pulmonary hemorrhage that was confirmed by the demonstration of alveolar iron-laden mac-rophages (sidemac-rophages) 3 to 6 weeks later. Five infants had re-current acute episodes, all after leaving the hospital and some within 48 hours of returning home. One child died. These cases differed from a control series in various respects, but on the basis of exceptionally high incidence of water damage in the case
in-TABLE 3. Percentage of Population Meeting the Recommendations for the Five Food Guide Pyramid Groups Over Three Consecutive Days According to Age, Gender, Race/Ethnicity, and Poverty Level, 1989 –1991 CSFII
Characteristics N Grain Vegetable Fruit Dairy Meat
Recommendations 6–11 Servings 3–5 Servings 2–4 Servings 2–3 Servings 5–7 Ounces#
% (SE)
Males and females, 2–19 y 3307 36 (1.5) 38 (1.6) 28 (1.8) 54 (1.8) 31 (1.6)
Males
2–5 y 429 39 (3.4) 26 (3.6) 41 (4.0) 65 (4.2) 25 (3.1)
6–11 y 599 36 (3.5) 35 (2.7) 28 (3.3) 73 (3.1) 23 (2.8)
12–19 y 618 42 (3.8)* 50 (3.9) 17 (2.4) 45 (3.4)† 49 (3.3)†
Females
2–5 y 416 34 (3.7) 28 (3.3) 41 (3.9) 63 (4.2) 25 (3.3)
6–11 y 573 35 (3.1) 34 (3.7) 34 (3.8) 68 (3.0) 26 (3.4)
12–19 y 672 31 (3.0) 46 (3.4) 19 (2.4) 22 (2.8) 32 (2.9)
Race/Ethnicity
White, non-Hispanic 2248 38 (1.7) 36 (2.0) 29 (2.0) 58 (2.1) 28 (2.0)
Black, non-Hispanic 550 31 (3.9) 47 (4.2)‡ 23 (4.1) 40 (4.0)§ 39 (4.4)‡
Hispanic 393 28 (4.4) 40 (6.3) 26 (5.5) 48 (5.4) 37 (4.7)
Poverty Index Ratio
,131% 1723 37 (1.9) 40 (2.2) 22 (1.9) 47 (2.1) 33 (1.7)
131–350% 1183 37 (2.3) 39 (2.6) 28 (2.5)\ 55 (2.8)\ 30 (2.9)
.350% 401 34 (2.9) 36 (3.7) 34 (3.6)** 56 (3.7) 31 (3.7)
# Recommendation used for 2- to 3-year-olds consuming,6.7 mJ per day is 3 ounces. * P,.05; male versus female for same age category; † P,.01.
‡ P,.05; white versus black or Hispanic; § P,.01.
\P,.05; poverty index ratio,131% versus 131%–150% or.350%; ** P,.01.
TABLE 6. Nutrient Intakes Associated With Selected Patterns of Intake by Children, 1989 –1991 CSFII
Nutrient Total
(n53307)
Pattern of Intake
GVFDM (n525)
GvfDm (n5195)
gVfDm (n5185)
gVfdm (n5189)
gvFDm (n5150)
gvfDm (n5386)
gvfdm (n5378)
Energy (mJ) 7.4 (.11) 10.8 (1.94) 7.9 (.21) 8.3 (.34) 6.6 (.18) 6.9 (.22) 6.8 (.18) 5.0 (.17) Total fat* 34.7 (.23) 36.4 (1.30) 35.8 (.64) 36.0 (.54) 35.2 (.50) 31.9 (.65) 35.7 (.45) 33.6 (.53) Discretionary fat* 25.5 (.23) 26.9 (1.40) 27.9 (.63) 28.2 (.62) 26.8 (.52) 23.9 (.78) 27.4 (.39) 24.5 (.57) Added sugars* 15.1 (.35) 11.6 (1.76) 14.2 (.76) 13.9 (.76) 18.3 (.74) 13.5 (1.14) 15.0 (.74) 20.2 (1.03) Vitamin A** 128 (4.3) 209 (24.2) 153 (7.8) 162 (11.8) 86 (7.6) 153 (10.9) 140 (5.3) 74 (4.7) Vitamin C** 184 (5.0) 315 (49.4) 162 (19.9) 182 (10.7) 129 (7.7) 262 (17.6) 149 (10.9) 102 (4.7) Vitamin B6** 110 (1.8) 163 (23.3) 114 (4.5) 128 (4.5) 85 (3.8) 123 (6.2) 112 (3.7) 70 (3.0) Folate** 228 (5.0) 382 (41.5) 265 (11.2) 266 (13.3) 147 (11.2) 291 (19.8) 243 (9.8) 128 (6.4) Calcium** 94 (1.5) 138 (11.6) 131 (4.1) 119 (3.5) 57 (2.0) 121 (7.6) 117 (2.1) 51 (1.5) Iron** 112 (2.5) 160 (26.0) 146 (9.0) 122 (6.4) 82 (3.5) 120 (7.4) 112 (4.9) 67 (3.1)
Zinc** 84 (1.2) 112 (10.8) 91 (3.8) 93 (3.4) 65 (2.4) 85 (4.4) 87 (2.1) 55 (2.5)
Fiber (g) 11.8 (0.2) 19.0 (3.3) 11.5 (0.5) 14.6 (0.6) 10.7 (0.4) 11.4 (0.5) 9.8 (0.3) 7.0 (0.2)
G indicates grains; V, vegetables; F, fruit; D, dairy; M, meat. Capital letters indicate that the recommendation was met for the identified food group.
* Percent energy; ** Percent 1989 RDA.
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fants’ homes it has been suggested in another publication that the fungus Stachybotrys atramight have been responsible.3A
retro-spective study by the coroner’s office of 172 infant deaths in the same county during approximately the same time period revealed nine infants (5%) with intrapulmonary siderophages indicating previous pulmonary hemorrhage.3
We have recently reported4the identification of abundant
in-traalveolar siderophages in the lungs of two pairs of siblings who had previous hospital admissions for apparent life-threatening events (ALTEs) before dying suddenly at home. Imposed suffo-cation in the context of “Munchausen syndrome-by-proxy” child abuse was suspected and the mother of one pair and a babysitter for the other pair were convicted of causing their deaths. Bleeding from the mouth or nose was observed during 6 of 10 previous ALTEs suffered by these children and three surviving infants who had been in the same care. Since our publication, we have found excess intraalveolar siderophages in the lungs of a third pair of siblings who died in suspicious circumstances. The six deaths were in four widely separated geographic locations in New Zea-land, a country where the environmental conditions affecting the Cleveland cluster are rare and toxigenicStachybotrys atrahas not been identified.
A working party reporting to the British Paediatric Association on the evaluation of suspected imposed upper airway obstruction noted that “commonly there is some blood-stained discharge from the nose or mouth.”5The individual case histories of the Cleveland
cases were not presented, but the listed symptoms (abrupt cessa-tion in crying, limpness, pallor and/or color change followed by acute hemoptysis, lethargy, grunting, and respiratory failure) and pulmonary infiltrates in chest radiographs have also been de-scribed in cases of imposed suffocation.5,6The occurrence of
fur-ther episodes when the children returned home is typical of the Munchausen syndrome-by-proxy scenario.
The finding of intraalveolar siderophages was presented in evidence by Professor J. A. Emery at a 1991 British trial for the murder of an infant that resulted in the conviction of a man whose attempts at smothering another infant had been documented by video.7 We note particularly that the nine Cleveland deaths in
which pulmonary hemosiderosis was found during the coroner’s retrospective investigation included two resulting from homicide, one child who had a recent history of abuse and two siblings.3The
same retrospective study found pulmonary siderophages in 6 of 117 deaths attributed to SIDS (5%), an incidence comparable with our finding of siderophages in 4.4% of 158 infants diagnosed with SIDS.4A distinction has to be made between intraalveolar
sid-erophages and the more common finding in SIDS cases of hemo-siderin deposits in the lung interstitium.8
We do not suggest that the presence of intraalveolar sideroph-ages is specific for previous imposed suffocation, but if no other explanation is provided by the clinical history or other necropsy findings, then there should be further inquiry into the possibility. Imposed suffocation is not excluded by the data presented on the Cleveland cases in which the consistent acute presentation in early infancy and clinical course differ from the insidious onset in later childhood and progression in most cases of idiopathic pulmonary hemosiderosis.9
D. M. O. Becroft, MD, FRCPA
Department of Obstetrics and Gynaecology National Women’s Hospital
Auckland 3, New Zealand B. K. Lockett, MB, ChB, FRCPA Pathology Department
Palmerston North Hospital Palmerston North
New Zealand
REFERENCES
1. Bergman AB. Wrong turns in sudden infant death syndrome research. Pediatrics.1997;99:119 –120
2. Montan˜a E, Etzel RA, Allan T, Horgan TE, Dearborn DG. Environmen-tal factors associated with pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community.Pediatrics.1997;99(1). URL:http://www.pediatrics.org/cgi/content/full/99/1/e5
3. Centers for Disease Control and Prevention. Update: pulmonary hemorrhage/hemosiderosis among infants—Cleveland, Ohio 1993–1996.MMWR.1997;46:33–35
4. Becroft DMO, Lockett BK. Intra-alveolar pulmonary siderophages in sudden infant death: a marker for previous imposed suffocation. Pathology.1997;29:60 – 63
5. Bamford FN, MacFadyen UM, Meadow SR, et al.Evaluation of Suspected Imposed Upper Airway Obstruction: Report of a Working Party.London, England: Royal Society of Medicine Press; 1994
6. Meadow R. Suffocation, recurrent apnea, and sudden infant death. J Pediatr.1990;117:351–357
7. Regina v Stout.Crown Court, Exeter, England 1991
8. Byard RW, Stewart WA, Telfer S, Beal SM. Assessment of pulmonary and intrathymic hemosiderin deposition in sudden infant death syn-drome.Ped Pathol Lab Med.1997;17:275–282
9. Heiner DC. Pulmonary hemosiderosis. In: Chernick V, Kendig EE, eds. Disorders of the Respiratory Tract in Children.5th ed. Philadelphia, PA: WB Saunders Co; 1990:498 –509
In Reply.—
We appreciate the concern of Drs Becroft and Lockett that it is important to attempt to exclude the possibility of child abuse for cases of idiopathic pulmonary hemorrhage. Nonaccidental trauma should always be considered and worked up in cases that present with symptoms that can be seen with abuse and in which the diagnosis is made by an exclusion process (such as the diagnosis of an acute life-threatening event [ALTE]). All of the initial 10 Cleveland cases came into the pediatric intensive care unit, a clinical setting where abuse is seen frequently and considered high in the differential diagnosis. The depth to which it was considered in each of these 10 cases in Cleveland was a clinical decision based on a careful social and medical assessment of the patient and family. Although abuse was considered, and in many cases screened for with objective testing, in none of the 10 infants was there sufficient suspicion to alert the child protection author-ities (as required by law).
We recognize that suffocation is extremely difficult to exclude absolutely. However, we feel that it is highly unlikely that im-posed airway obstruction is the explanation for the outbreak of pulmonary hemorrhage in Cleveland. As we described in our article, the homes of the 10 infants with pulmonary hemosiderosis were clustered in one part of the city, a finding that led us to strongly consider the possibility that environmental risk factors in the homes may have played a role. Temporal clustering has also occurred in Cleveland; since January 1, 1993, 24 infants have been treated for idiopathic pulmonary hemorrhage at the Rainbow Babies and Childrens Hospital, while only 3 infants and children with this diagnosis had been treated at that hospital over the previous 10 years. Such marked geographic and temporal cluster-ing might not be expected if the infants had been victims of abuse. In addition, although recurrence is frequently observed in abuse cases,1only 1 of the 24 infants had previously had an ALTE. Before
home environmental factors were identified as possible causal factors, 8 infants returned to their original home environments after discharge from the hospital; 5 of these 8 had recurrent hemorrhages. Subsequently, 16 infants with idiopathic pulmonary hemorrhage have not returned to the original home environment; only 2 of these 16 have had recurrent pulmonary hemorrhages. This provides additional evidence that the physical environment, rather than the caregiver, was a strong risk factor for recurrent hemorrhage.
Furthermore, the extent of pulmonary hemorrhage in most of these infants was much more than one would expect from the petechial hemorrhages described in human and experimental an-imal suffocation.2Respiratory failure requiring ventilator support
occurred in 17 of the 24 infants; half of these infants required blood transfusions. The extent of intrathoracic petechial hemorrhages in sudden infant death syndrome has been noted2to be greater than
that seen with imposed airway obstruction. The six coroner cases of pulmonary hemosiderosis had such massive intraalveolar he-mosiderin-laden macrophages that the Prussian blue staining of the lung sections was readily evident to the naked eye, without the necessity of microscopic examination. Although the 117 SIDS cases were distributed across the entire county, these 6 cases were limited to the same geographic cluster area where all but 4 of the patients with idiopathic pulmonary hemorrhage lived, an area of census tracts that accounts for only 20% of the county population. We agree that the presence of intraalveolar “siderophages”
does not imply a specific cause of bleeding. (Note: It takes 36 to 48 hours for macrophages to convert red cell iron from bleeding into hemosiderin.3) Nevertheless, because the finding of recurrent
bleeding in an infant may suggest certain causes of death, we recommend that Prussian blue staining be performed on lung sections in all cases of unexpected infant deaths. On the other hand, it is premature to suggest that the presence of intraalveolar hemosiderin-laden macrophages is indicative of infanticide. Be-cause environmental mycologists have foundStachybotrys charta-rumin New Zealand and because this toxigenic fungus and its toxigenic cousin Memnoniella echinatawere well-known in Aus-tralasia for rotting canvas during World War II,4we suggest that
this be considered when caring for or studying infants with idio-pathic pulmonary hemorrhage in Australasia as well.
Ruth A. Etzel, MD, PhD Eduardo Montan˜a, MD, MPH
Centers for Disease Control and Prevention Atlanta, GA 30341
Dorr G. Dearborn, PhD, MD Paul G. Smith, DO
Michael D. Infeld, MD Beverly B. Dahms, MD
Cindie Carroll-Pankhurst, PhD
Case Western Reserve University School of Medicine
Cleveland, OH 44106
REFERENCES
1. Meadow R. Suffocation, recurrent apnea, and sudden infant death. J Pediatr.1990;117:351–357
2. Beckwith JB. Intrathoracic petechial hemorrhages: a clue to the mecha-nism of death in sudden infant death syndrome?Ann N Y Acad Sci. 1988;533:37– 47
3. Sherman JM, Winnie G, Thomassen MJ, Abdul-Karim FW, Boat TF. Time course of hemosiderin production and clearance by human pul-monary macrophages.Chest.1984;86:409 – 411
4. Sui RG.Microbial Decomposition of Cellulose.New York, NY: Reinhold; 1951
INVISIBLE IDIOTS NEED INTELLIGENT MONITORS
As computers become more deeply embedded as the underlying performers of
a wide variety of social and organizational tasks, they are also growing more and
more invisible. It is all too easy to forget that they are also idiots, having no
information other than what was programmed into them. And they are no more
capable of understanding or predicting indirect and long-term consequences than
were their designers or programmers. They require constant, intelligent, and
informed monitoring.
Rochlin GI.Trapped in the Net.Princeton, NJ: Princeton University Press; 1997.
Submitted by Student
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DOI: 10.1542/peds.101.5.953
1998;101;953
Pediatrics
D. M. O. Becroft and B. K. Lockett
SIDS or Murder?
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D. M. O. Becroft and B. K. Lockett
SIDS or Murder?
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