Alveolar septal collapse in the transitional infant lung: a possible common mechanism in sudden unexpected death in infancy.
Sudden unexpected death in infancy (SUDI) is a category used to represent the largest single group of infant deaths. Although there are several theories, the cause of SUDI remains unknown and the mechanism of co-sleeping associated deaths are also undetermined. We investigate a possible biomechanical mechanism which may be common in SUDI and may provide an explanation for the association of the known risk factors for SUDI such as co-sleeping, prematurity, prone sleeping position, overwrapping, overheating and maternal smoking. The neonatal lung has few, if any, true septa but from about four weeks of age, a period of rapid alveolarisation commences. The developing alveolar walls (septae) have little fibre support against surface tension forces as they grow but are supported by a double layer of capillaries. Until the elastin/collagen supporting network is laid down these nascent septal walls are vulnerable to collapse against sac or duct walls during this transitional period. We hypothesise that such collapse will prevent one side of the septa, and the wall it overlays, from alveolar gas exchange and a functional left-right shunt is formed which may result in hypoxia. Furthermore, lung stretch receptors in bronchi running through or adjacent to collapsed regions will be activated, falsely signalling lung inflation to the brain stem with resultant respiratory inhibition, so precipitating further collapse. The process will continue until lung volume falls below residual capacity, when normal tidal breathing efforts will no longer result in significant air flow, even if stretch receptor signals have not produced complete apnoea. Large inspiratory efforts are then required to break the surface tension seal, which damages capillaries to produce petechial haemorrhages. Many epidemiological risk factors for SUDI could influence such a mechanism, leading to the proposal that Alveolar Septal Collapse in Infancy (ASCI) is a core mechanism via which these factors act.
Sebire
N J
NJ
Department of Paediatric Pathology, Camelia Botnar Laboratories, Great Ormond Street Hospital, Great Ormond Street, London WC1N 3JH, UK. sebirn@gosh.nhs.uk
Talbert
D
D
D000402:Airway Obstruction / Q000150:complications / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology; D002986:Clinical Trials as Topic; D019317:Evidence-Based Medicine; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008954:Models, Biological; D015995:Prevalence; D011650:Pulmonary Alveoli / Q000473:pathology* / Q000503:physiopathology*; D001261:Pulmonary Atelectasis / Q000150:complications* / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D013398:Sudden Infant Death / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology*