Small intestinal mucosal abnormalities in post-perinatal deaths.

Examination of small intestinal mucosa from cases of post-perinatal death in Sheffield between September 1980 and September 1981 showed mucosal changes before death in 18 of 78 cases (20%). There was no significant difference in prevalence between explained and unexplained deaths, nor was there any positive association with viral isolation from the small intestine. The lesion was much more common in males than females and showed a strong association with bottle feeding--no infant wholly breast fed showed an enteropathy. There was a low incidence of symptoms referrable to the gastrointestinal tract among affected infants, and no appreciable evidence of failure to thrive, as reflected by the postmortem body weight, was present. Mucosal changes of the small intestine in cases of sudden infant death syndrome have previously been reported and attributed to heatstroke. Although the finding of similar lesions in infants who died explicably does not appear to support this view, overheating is difficult to exclude as most of the explained deaths with a mucosal lesion occurred at home

Carbon monoxide concentrations in infant deaths.

Carboxyhaemoglobin measured in 50 infant deaths showed no significant difference between home and hospital deaths nor between explained and unexplained deaths. Carbon monoxide toxicity is unlikely to have an important role in the pathogenesis of sudden infant deaths. The generally low carboxyhaemoglobin concentrations are probably due to endogenous production

Sudden infant death and cytomegalovirus inclusion disease.

Four infants, apparently thriving and without clinical evidence of disease, died suddenly at ages ranging from 2 to 6 months. Inclusions bearing cells pathognomonic of cytomegalovirus infection were shown microscopically in a small number of extraneural organs. In view of the lack of associated tissue destruction on microscopy and the apparent well being of the infants before death whether the function of these organs had been impaired to any important degree was questionable: such limited disease, consequently, could not have contributed substantially to the cause of death. The brainstem, on the other hand, consistently showed small numbers of glial nodules. Damage to strategically located neurones associated potentially with the organisation of vital function was a possible basis of sudden death. Alternatively, the small number of glial nodules may have represented a residue of previous more severe brainstem disease, which had possibly started while the baby was in the uterus