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The Sudden Infant Death Syndrome in Hospitalized Babies


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sopharyngeal swabs remained positive. Whether

or not the bacteremia was the primary source of


is probably unanswerable. However, its

early clearing, the lack of histological evidence of


in any


at autopsy,



pres-ence of GB-BHS organisms with inflammatory

reaction in ears and meninges strongly suggest the

nasopharynx as the portal of entry for the

menin-gitis, and the bacteremia to be secondary and

brief-lived. It is likely the infant acquired the

dlis-ease in utero or during passage through the birth

canal, with ultimate lodging of the organism in the

middle ear. This middle ear infection was the

like-ly portal of entry for the organism into the

memn-ges. This mechanism has been put forward to

explain neonatal meningitis caused by .other

or-ni1#{176} The middle ear pathway could also be

operant in cases of late onset meningitis where the


has been



or during




for the meninges

charac-teristic for most late-onset GB-BHS infections

may well be determined by a middle ear portal of

entry, and its late onset is probably related to the

serological subtype, as has been shown previously

by Franciosi and associates.4 Although this report

concerns an isolated observation of a case of

GB-BHS meningitis preceded by an otitis media and


it could




atten-tion is paid to the middle ear, especially since

oti-tis media in the neonate is frequently overlooked

by clinicians and not specifically looked for by




this report, a premature black male infant

was found at autopsy to have bilateral otitis

media, mastoiditis, and suppurative meningitis

due to group B beta-hemolytic streptococcus

(GB-BHS). The pathogenetic pathway proposed

for this early onset meningitis is of importance in

late onset meningitis. This patient clearly

demon-strates the critical importance of examining

mid-cUe ear and mastoid, both clinically and at

autop-sy, in the neonate colonized with this organism.

RuFIN0 EaliocILi, M.D.


Perinatal Research Laboratory


of Pathology

and Pediatrics


of Alabama

Medical Center

Birmingham, Alabama

ADDRESS FOR REPRINTS: (R.C.) Department of Pa-thology, University of Alabama Medical Center, University Station, Birmingham, Alabama 35294.


1. Baker, C, J., and Barret, F. F. : Transmission of group B streptococci among parturient women and their neonates. J. Pediat., 83:919, 1973.

2. Baker, C. J., Barret, F. F., Gordon, R. C., and Yow, M.D.: Suppurative meningitis due to streptococci of Lancefleld group B: A study of 33 infants. J. Pedi-at., 82:724, 1973.

3. Barton, L. L., Feigin, R. D., and Lins, R.: Group B beta-hemolytic streptococcal meningitis in infants. J. Pediat., 82:719, 1973.

4. Franciosi, R. A., Knostman, J. D., and Zimmerman, R. A.: Group B streptococcal neonatal and infant infections. J. Pediat., 82:707, 1973.

5. Eickhoff, T. C., Klein, J. 0., Daly, A. K., Ingall, D., and Finland, M.: Neonatal sepsis and other infections due to group B beta-hemolytic streptococci. N. Eng. J. Med., 271:1221, 1964.

6. McCracken, G. H.: Group B streptococci: The new chal-lenge in neonatal infections. J. Pediat., 82:703, 1973.

7. Quirante, J., and Cassady, C.: Group B beta-hemolytic

streptococcal sepsis in the newborn. Clin. Res.,

20: 104, 1972.

8. Quirante, J., Ceballos, R., and Cassady, G.: Group B beta-hemolytic streptococcal infections in the newborn. Amer. J. Dis. Child., to be published. 9. Blanc, W. A.: Amniotic infection syndrome:

Pathogene-sis, morphology, and significance in circumnatal mortality. Clin. Obstet. Gynec., 2:705, 1959. 10. Hemsath, F. A.: Intrauterine and neonatal otitis: A study

of seven cases including a case of otitic meningitis. Arch. Otolaryng., 23:78, 1936.

11. McLellan, M. S., Strong, J.P., Johnson, Q. R., and Dent,

J. H.: Otitis media in premature infants: A histo-pathologic study. J. Pediat., 61:53, 1962.

The Sudden




in Hospitalized


“Ifinfant.s die because, while passing through a period of increased physiological vulnerability, some critical combination ofintriric and extrinsic factors proves lethal, then It would be strange if

death occurs only in the course of minor and not major illnesses. Is it possible that sudden unex-plained death does happen in hoital, but is not


as such


the major diagnosis L judged to be the cause ofdeath, or do the resuscita-tive measures which are readily available prevent it?”

This provocative question, posed in an

edito-nal in late 1971,1 drew a response from Raphael,

who submitted rather convincing evidence of an

instance of sudden unexplained infant death in a




the extent

to which

the SIDS occurs in hospitalized babies remains ob-scure.

The number of infant-months of risk in hospital

would seem to be the critical variable for

estimat-ing the degree to which the SIDS might be

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ed to occur in such a setting. During the period

1970 to 1972, the Children’s Orthopedic Hospital

in Seattle admitted 2,344 babies between 7 and



of age on admission.



of stay

in hospital averaged 4.5 days. These babies,

there-fore, incurred 352


of hospital

expo-sure during




be considered

at risk

to the SIDS during the three-year period: (2,344)


= 352 infant-months.

For the same period in King County,

Washing-ton, the average annual SIDS incidence rate

equalled 2.9/1,000 live births. Altogether, 150

cases occurred.



of these


fell in the age range of


to 180 days (5.75 mo).

From these data, the average number of

infant-months of risk incurred to produce a single case

outside of hospital can be calculated: (1,000 live

births) (5.75 months of life during which an infant

is susceptible)/2.9 deaths per 1,000 live births =

1,983 infant-months per one SIDS case.

From these calculations, the length of time



at risk in hospital

is approximately


sixth the value computed for nonhospitalized

babies: 352/ 1983 0. 18. One can infer,

there-fore, that if the number of admissions, the average

length of stay, and the incidence remain constant,

one SIDS case might be expected to occur at the





17 years


so. Some



to 1970 one

of us (J.B.B.)






in the

afore-mentioned editorial and decided to record in

detail any such episodes. A review of 144 autopsy

reports of infants between 7 and 364


of age,

collected during the period 1970 to 1972 (which

represent slightly more than one half of all infants

who died in King County), disclosed two


of probable SIDS which involved hospitalized


In the first instance, a 4-month-old, white, male

infant with transposition of the great vessels had a







after birth. Subsequently, cyanosis recurred, and

the baby was readmitted to the hospital on


9, 1970,





of the




inter-vention was deferred because of fever,

accompan-ied by symptoms and signs referable to the upper

respiratory tract, which began on the fourth

hos-pita! day and persisted until he was unexpectedly

found dead on the 17th hospital day. On

patholog-ical examination, the septostomy was narrowed,

but not to a degree sufficient to account for the


of the





pete-chiae suggested a diagnosis of SIDS.

The second case involved a 3#{189}-month-old

white male admitted to a hospital on February 28,

1971, because of intermittent vomiting and failure

to thrive. He was found apneic 12 hours after

ad-mission. During the resuscitation effort, a

general-ized seizure occurred which did not respond to

treatment with anticonvulsants. The infant was

pronounced dead 30 hours after admission. The

findings at autopsy were compatible with a

diag-nosis of SIDS.

The death in each instance was officially

certi-fled as attributable to a cause other than SIDS;

but, in fact, each would seem to be a case of

the SIDS in a hospitalized infant with major


The observed two cases, within the time frame

under consideration, represents a relative risk to

hospitalized babies that is 11 times that for

non-hospitalized babies in the same locale (two

ob-served versus 0.18 expected). This observation

seems biologically reasonable, even though the

numbers upon which it is based are small and,

therefore, potentially deceptive statistically.

Re-lative risk aside, the extent of the SIDS in hospitals

will be low simply because of the short span of

time spent by infants in hospital during the age of

maximum susceptibility.

The search of autopsy files also revealed two

in-stances in which apparently lifeless infants were

rushed to hospital where resuscitation measures,

though partially successful initially, finally failed.

These, therefore, were SIDS deaths with onset at

home and death in hospital. One of these was a

2#{189}-month-old white male infant whose pulse

re-turned after resuscitation in the emergency room

of a small suburban hospital. Because of lack of

spontaneous breathing, the infant was transferred

to the Children’s Orthopedic Hospital where,

de-spite mechanical ventilation over a six-hour

pe-nod, death occurred. Pathological findings were

consistent with a diagnosis of SIDS. The other

in-stance involved a 5-month-old male infant who

was found unresponsive in his crib one morning

and rushed to hospital where, after a few hours, he

developed seizures. These abated with

anticon-vulsant therapy, but he remained comatose until

the fifth hospital day, when he died. On

postmor-tem examination, cerebral swelling and other

findings compatible with prolonged hypoxia were

the only findings, and a diagnosis of SIDS seemed

the most probable.

Finally, an additional record indicated that an

ostensibly healthy 2-month-old child, whose

de-mise was a typical SIDS episode, was discovered

at autopsy to have an atrial septal defect, atresia

of the inferior vena cava, and assorted minor

con-genital defects. This death was officially certified

as one due to congenital heart disease, but the

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postmortem record indicated that SIDS was the

probable cause.

From the experiences cited, we submit that the

sudden infant death syndrome does occur in

hospi-tal, but rarely, because of the relatively short time

periods susceptible infants are so confined. The

SIDS also occurs during major, as well as minor,

illness. Finally, resuscitation efforts in hospital

often fail. We have no way of knowing how often

they succeed, however.




with the assistance of E. A. BENSON

Departments of Epidemiology and


University of Washington

Seattle, Washington

ADDRESS FOR REPRINTS: (D.R.P.) Department of Epi-demiology, University of Washington, Seattle, Washington 98195.


1. Sudden deaths in infants (editorial). Lancet, II: 1070, 1971.

2. Sudden deaths in infants (letter to the editor). Lancet, 1:325, 1972.


Pure Red Cell


in Identical


Congenital aregenerative anemia is a relatively

uncommon disease first described by Blackfan and

Diamond in the late 9301 The condition usually

begins in early infancy as a normochromic,

nor-mocytic anemia with decreased red cell

precur-sors in the bone marrow and normal numbers of

thrombocytes and leukocytes. With the exception

of a few patients undergoing Spontaneous

remis-sion, patients required repeated transfusions until

steroids became available.

Over the past forty years several hundred cases

of this disease have been reported with

specula-tion regarding the etiology. Occasional families

have been described with two or three involved

members, suggesting genetic transmission. We

have recently observed a set of twins with the

un-common disease.


RB. and SB. are 2#{189}-year-old male twins who were well until a bout of diarrhea when a local physician found RB. to have a hemoglobin level of 9.8 gm/100 ml. When the brother was found to have a hemoglobin level of 8.5 gm/ 100 ml, they were given iron orally (4 to 5 mg/kg) for two weeks. Despite this therapy the hemoglobin levels fell to

6.2 and 7.6 gm/100 ml, with reticulocyte counts of 0.3% and

0.5%, respectively. The white blood cell counts were 6,500 and 12,200/cu mm, with normal differentials and platelet counts were 400,000 and 355,000, respectively. The children were referred for further evaluation. There was no previous treatment with antibiotics, exposure to poisons, lead, or other medications; no history of pica could be obtained. The twins had been adopted on the eighth day of life after a nor-mal neonatal period. They are the product of a gravida 1, para 2, aborta 0, 18-year-old mother, who was said to be in good health with no difficulties during the pregnancy. No other family history is available. Hemoglobin levels at birth

were 21.5 and 19.3 gm/100 ml, and at one month oflife had

fallen to 10.8 and 10.4, respectively. There were no further hemoglobin determinations. No history of bleeding tenden-cies, hematemesis, black stools, or recurrent infections could be obtained.

Physical examinations of both twins were normal with the exception of height, weight and head circumferences which were within the third to tenth percentiles. Both were ex-tremely pale. Radii and ulni were present with no abnor-malities of the upper extremity.

Laboratory determinations of the twins are compared in Table I. Both twins were blood type A, D-positive, Kell-neg-ative; dermatoglyphics showed identical patterns. Kar-yotypes of each showed normal 46 chromosomes with no in-creased chromosomal breaks noted. X-ray films of the chest were normal. Bone marrow specimens were obtained from the anterior iliac crest of each twin with myeloid:erythroid (M:E) ratios of 2:1 and 26:1. Both bone marrows were quite cellular with erythroid precursor elements markedly de-pressed in both. The myeloid elements were normal in distri-bution and megakaryocytes were plentiful.

The patients were transfused with whole blood and given 2 mg/kg of prednisone daily. Three months later both pa-tients receive steroids on alternate days, have reticulocyte counts of 1.5% and 1.1% and hemoglobin levels of 13.8 and

12.9 gm/100 ml.


Many theories have been advanced concerning

the etiology of pure red cell hypoplasia. The

possi-bility of an inborn error of erythropoiesis has been

suggested by Diamond et al.2 Altman and Miller

proposed an abnormality of tryptophan

metabo-lism after they observed an increase in anthranilic

acid in the urine of patients with congenital

hypo-plastic anemia.7 These tryptophane metabolites

have been measured by others who have failed to

show any consistent elevation.81#{176}

After Burgert in 1954 described the occurrence

of this disease in two brothers, the familial nature

of the disease became of interest. The hypothesis

that Blackfan-Diamond anemia is genetically

transmitted as an autosomal dominant gene was

advanced by the observations of Forare3 (1963)

and Mott et al.4 (1969), both of whom described

two healthy fathers who had anemic children

from each of two different women. The vertical

transmission of this disease from mother to

daugh-ter was first documented by Falter and Robinson5

(1972) and recently substantiated by Hamilton,6

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Donald R. Peterson, J. Bruce Beckwith and E. A. Benson

The Sudden Infant Death Syndrome in Hospitalized Babies


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Donald R. Peterson, J. Bruce Beckwith and E. A. Benson

The Sudden Infant Death Syndrome in Hospitalized Babies


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American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

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been published continuously since 1948. Pediatrics is owned, published, and trademarked by the

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