Infections of the upper respiratory tract in cases of sudden infant death

1995 ◽  
Vol 108 (2) ◽  
pp. 85-89 ◽  
Author(s):  
W. J. Kleemann ◽  
A. S. Hiller ◽  
H. D. Tr�ger
PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 531-533
Author(s):  
ALFRED STEINSCHNEIDER

Epidemiological studies repeatedly have demonstrated the importance of a number of variables in affecting the incidence of the sudden infant death syndrome (SIDS).1.2 Characteristically, the peak risk of SIDS is within the second to third month of life, with relatively few cases in the first month of life or after the first year. Another consistent observation is the association between minor upper respiratory tract inflammatory processes(nasopharyngitis) and SIDS: relatively more SIDS victims than controls have had clinical symptoms referable to the upper respiratory tract one to two weeks prior to death. Furthermore, histologic examinations have revealed upper respiratory tract


1974 ◽  
Vol 52 (4) ◽  
pp. 895-898 ◽  
Author(s):  
Barry J. Sessle ◽  
L. Frances Greenwood ◽  
David J. Kenny

During microelectrode penetrations of the solitary tract nucleus and adjacent reticular formation, single neurones were located that discharged in a rhythm that was linked with respiration but that persisted after muscle paralysis. Many of these neurones could be activated from the vagus or upper respiratory tract areas. Some had no demonstrated excitatory input, yet their rhythmic activity could be abolished only by stimulation of nerves innervating the upper respiratory tract. This stimulation also abolished respiration. Such findings emphasize the significance of upper respiratory tract feedback in normal respiratory function and possibly in abnormal conditions such as the 'sudden infant death syndrome.'


PEDIATRICS ◽  
1980 ◽  
Vol 65 (4) ◽  
pp. 713-717
Author(s):  
Jeffrey B. Gould ◽  
Austin F. S. Lee ◽  
Peter Cook ◽  
Suzette Morelock

Having a mild upper respiratory tract infection does not change the sleep state proportions or total sleep time of an infant. However, infants with colds exhibit some sleep state specific alterations in sleep apnea. At 40, 44, and 48 weeks postconception, the number of respiratory pauses of 2 to 4.9 seconds and of 5 to 9.9 seconds duration per 100 minutes of state, during rapid eye movement, and indeterminate sleep are decreased in infants with colds. The absence of this phenomenon at 52 weeks suggests that it is modified by maturation. We hypothesize that the reduction in rapid eye movement and indeterminate sleep apnea is a manifestation of an adaptive response in normal infants, but for infants at risk for the sudden infant death syndrome, this response may be overwhelmed, resulting in increased apnea and, in some instances, sudden infant death.


PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 967-971
Author(s):  
Alfred Steinschneider

The effect of nasopharyngitis on the simultaneous occurrence of prolonged sleep apnea (≥20 seconds in duration) was studied in 26 infants managed at home on an apnea monitor. During the observation period, these infants had a total of 69 illnesses which appeared to represent an upper respiratory tract inflammatory process. In general, the daily frequency of prolonged apneic episodes was significantly greater during nasopharyngitis when compared to comparable time intervals immediately prior to and following the illness. In addition, there was a decrease in the frequency of apneic episodes with increasing postnatal age until the episodes finally ceased to occur during the illnessreleted intervals. Apneic episodes ceased to occur at an earher age for the before- and after-illness intervals than for the time interval during which there were clinical symptoms. Thus, it would appear that infants go through an agerelated phase wherein prolonged apnea occurs during nasopharyngitis but not when free of illness. The implications of these results for the management of infants having prolonged sleep apnea are discussed. In view of the hypothesis that prolonged sleep apnea is part of the physiological process resulting in the sudden infant death syndrome, these results also provide for the prediction that infants who suddenly die in association with nasopharynqitis would do so, in general, at a later age than those who succumb when free of an upper respiratory tract inflammatory tory process.


1998 ◽  
Vol 1 (5) ◽  
pp. 375-379 ◽  
Author(s):  
David M. Parham ◽  
Richard Cheng ◽  
Gordon E. Schutze ◽  
Bradley Dilday ◽  
Rebecca Nelson ◽  
...  

Although respiratory syncytial virus (RSV)-infected infants may present with apnea, the role that RSV plays in sudden infant death syndrome (SIDS) is speculative. To determine whether RSV is associated with bronchiolitis in these patients, we examined histologic sections of lungs from 41 apparent SIDS cases and compared the results with those of enzyme-linked immunofluorescent assay (EIA) from nasal washings. Bronchiolitis was defined by a bronchiolar inflammatory cell infiltrate plus epithelial necrosis. A positive EIA was associated with bronchiolitis in 8 instances, compared with 6 having a positive EIA and negative histology, 14 having a negative EIA and positive histology, and 13 having EIA and histology both negative. These results yield a predictive value of a positive test of 57% and a predictive value of a negative test of 48% ( P > .9 by chi square analysis). Although RSV of the upper respiratory tract may be related to SIDS, our results indicate that EIA of nasal washings is not predictive of bronchiolitis, and we recommend other means of verification of histologic results.


PEDIATRICS ◽  
1978 ◽  
Vol 61 (4) ◽  
pp. 663-664
Author(s):  
Nicholas M. Nenson

Three circumstances may (thinly) be argued to qualify the present writer as an "expert" commentator on the article by Kelly et al. in this issue of Pediatrics (p. 511): first (and nearly 20 years ago), that most humbling of all experiences for the pediatrician, the dismissal from one's office of an apparently healthy 2-month-old infant with a minor upper respiratory tract infection who is brought dead on arrival to one's own hospital not three hours later, the unavailability of any autopsy data (difficult to obtain from unsubsidized pathologists in small suburban hospitals ruled by the coroner system of forensic medicine) forcing the diagnosis of sudden infant death syndrome (SIDS) on bewildered parents and shaken physician; last, participation in a recent task force assembled by the American Academy of Pediatrics in an attempt to generate an omniscient statement to cover the optimal management of a dreaded condition ("near-miss SIDS") whose identification is by definition uncertain and concerning which a minimal base of factual knowledge is only now beginning to accrue.


PEDIATRICS ◽  
1972 ◽  
Vol 50 (4) ◽  
pp. 646-654 ◽  
Author(s):  
Alfred Steinschneider

Little is known of the final physiologic mechanism(s) resulting in SIDS. Five infants participated in this study, three of whom were referred at about 1 month of age because of cyanotic episodes of undetermined etiology. Respirations and eye movements were recorded during several sleep sessions on each patient. In addition, patients were observed on an apnea monitor and a record was kept of the incidence of prolonged apneic episodes (≥ 15 seconds). The laboratory sleep studies revealed frequent periods of apnea (≥ 2 seconds) which (1) decreased in amount after a certain age and (2) were most frequent during REM sleep. All infants had a number of prolonged apneic and cyanotic episodes during sleep, some requiring vigorous resuscitative efforts. Prolonged apnea most often occurred in conjunction with an upper-respiratory tract infection or when frequent apnea was noted in the laboratory. Two of the infants subsequently died of SIDS. These data support the hypothesis that prolonged apnea, a physiological component of sleep, is part of the final pathway resulting in sudden death. It is suggested also, that infants at risk might be identified prior to the final tragic event.


PEDIATRICS ◽  
1971 ◽  
Vol 48 (1) ◽  
pp. 79-82
Author(s):  
C. George Ray ◽  
Nancy M. Hebestreit

A group of 119 unselected cases of the sudden infant death syndrome (SIDS) were studied for evidence of viremia. None of 20 cases studied by standard culture methods yielded virus in the blood, and only 4 of 119 had detectable levels of serum interferon. Coupled with previous studies, the data further suggest that viral infection, if it participates in the ultimate mechanism in SIDS, does not act by means of overwhelming viremia but rather may act locally, possibly in the respiratory tract.


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