“Delayed” sudden infant death syndrome

Molander, N; Brun, Arne

doi:10.1097/00000433-198309000-00016

Cited by 5 publications

(4 citation statements)

References 0 publications

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“…5) introduced into distal airways and alveoli rendered vulnerable by cardiovascular collapse led to acute bronchopneumonia in some cases. The failure of acute bronchopneumonia to increase in severity with protracted survival intervals is similar to findings of Molander and Brun who identified bronchopneumonia, which they described as ''extensive,'' ''in all parts of the lungs,'' ''advanced,'' and ''widespread'' in all four of their cases with differing survival intervals [30]. Finally, neither the presence nor the severity of acute bronchopneumonia correlated with postmortem culture results.…”

Section: Pathologic Findings In Delayed Sidssupporting

confidence: 81%

Delayed death in sudden infant death syndrome: A San Diego SIDS/SUDC Research Project 15-year population-based report

Krous

Haas

Chadwick

et al. 2008

Forensic Science International

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Section: Pathologic Findings In Delayed Sidssupporting

confidence: 81%

Delayed death in sudden infant death syndrome: A San Diego SIDS/SUDC Research Project 15-year population-based report

Krous

Haas

Chadwick

et al. 2008

Forensic Science International

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“…This gives an incidence for AL of 0.4611 000 live births and a SIDS incidence of 0.9411 000 live births. Of the SIDS cases seven were 'delayed SIDS' (9). The ratio boys : girls was 1.4 : 1 for SIDS and 1.6 : 1 for AL.…”

Section: Resultsmentioning

confidence: 95%

“…SIDS was defined according t o Beckwith (8), i.e., 'the sudden death of any infant or young child which is unexpected by history, and in which a thorough postmortem examination fails to demonstrate an adequate cause for death', with addition of 'delayed SIDS' (9), i.e., infants who were found lifeless and were resuscitated but who later died in the intensive care unit, and in whom no plausible explanation to the event other than SIDS was obtained. Autopsy was performed in all SIDS cases.…”

Section: Materials a N D Methodsmentioning

confidence: 99%

The Epidemiology of Sudden Infant Death Syndrome and Attacks of Lifelessness in Sweden

et al. 1987

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Infants who died showing the syndrome of sudden infant death (SIDS) and infants who survived attacks of lifelessness (AL) were examined in a prospective epidemiological multicentre study over 24 months covering close to 40% of all births in Sweden. Seventy SIDS cases and 34 cases of AL were observed, giving an incidence for SIDS of 0.94/1000 and for AL of 0.46/1000. This SIDS incidence is higher than that observed during the seventies. The boy/girl ratio was 1.4:1 for SIDS and 1.6:1 for AL. The age distribution for AL resembled that for SIDS. Similarities were also seen with regard to place of occurrence. Sixty per cent of the SIDS cases occurred during the daytime/evening. Twenty-nine per cent of the infants with AL had more than one apneic spell during the three-day-period around the attack, indicating a period of respiratory instability, but only 12% had such spells later on. None of the infants who had had AL died from SIDS. The possible relationship between AL and SIDS is discussed.

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“…Naturgem~ig wurde vor allem die Region der Atemzentren, also der Hirnstamm, untersucht und auf Gliosen als Folgezustand nach Hypoxie geachtet (Ambler et al [1]; Becker und Takashima [4]; Kelly und Shannon [12]; Molander und Brun [17]; Naeye [18]; Takashima et al [22]). Naturgem~ig wurde vor allem die Region der Atemzentren, also der Hirnstamm, untersucht und auf Gliosen als Folgezustand nach Hypoxie geachtet (Ambler et al [1]; Becker und Takashima [4]; Kelly und Shannon [12]; Molander und Brun [17]; Naeye [18]; Takashima et al [22]).…”

Section: Einlcitungunclassified

Periventrikul�re fettige Metamorphose der Neuroglia ? Ein morphologisches Substrat beim SIDS

Missliwetz

Reiter

Zoder³

1986

Z Rechtsmed

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In 7 of 15 cases of sudden infant death syndrome (SIDS), distinct periventricular fatty metamorphosis of the neuroglia could be demonstrated by a histological staining technique. None of the six children (under 1 year of age) used as a control group whose cause of death was not SIDS showed this morphological change. Thin-layer chromatographic analysis of the lipids accumulated in the glial cells in SIDS established a high amount of esterified cholesterol whereas the content of esterified cholesterol in the control group was low. We presume that fatty metamorphosis of the neuroglia represents the morphological substrate of a metabolic disorder of the sensitive, immature glia of the periventricular white cerebral matter caused by various kinds of damage.

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“Delayed” sudden infant death syndrome

Cited by 5 publications

References 0 publications

Delayed death in sudden infant death syndrome: A San Diego SIDS/SUDC Research Project 15-year population-based report

Delayed death in sudden infant death syndrome: A San Diego SIDS/SUDC Research Project 15-year population-based report

The Epidemiology of Sudden Infant Death Syndrome and Attacks of Lifelessness in Sweden

Periventrikul�re fettige Metamorphose der Neuroglia ? Ein morphologisches Substrat beim SIDS

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