Sudden Infant Death Syndrome, Pulmonary Edema, and Sodium Toxicity: A Grounded Theory

Abstract

Sudden Infant Death Syndrome (SIDS) occurs unexpectedly in an otherwise healthy infant with no identifiable cause of death following a thorough investigation. A general hypervolemic state has been identified in SIDS, and fluid in the lungs suggests the involvement of pulmonary edema and hypoxia as the cause of death. The present perspective paper reviews pathophysiological, epidemiological, and dietary evidence in SIDS. A grounded theory is presented that proposes an association of SIDS with sodium toxicity from excessive sodium chloride intake, mediated by noncardiogenic pulmonary edema, hypoxia, and alveolar damage. The peak of SIDS cases occurs in infants 2–4 months of age, who are less efficient in excreting excessive dietary sodium load. Evidence implicating sodium toxicity in SIDS includes increased levels of sodium associated with fever and with inflammatory/immune responses in the lungs. Conditions in near-miss SIDS cases are linked to dysregulated sodium, and increased sodium dietary intake suggests that sodium toxicity from a high-salt diet potentially mediates the association of seasonality and socioeconomic status with SIDS incidence. In addition, exposure to sodium toxicity meets three main criteria of the triple risk model of SIDS. The proposed pathophysiological effects of pulmonary edema related to sodium toxicity in SIDS merit further investigations.

Twelve-Lead ECG, Holter Monitoring Parameters, and Genetic Testing in Brugada Syndrome: Insights from Analysis of Multigenerational Family with a History of Sudden Cardiac Arrest during Physical Activity

“…The majority of BrS patients studied by us did not experience severe symptoms at BrS diagnosis, similarly to BrS patients studied by Probst et al [10]. Moreover, it should be noted that syncope or SCA may be the first manifestation of the disease [38], as in our index case. In most BrS cases, arrhythmic events occur during sleep, resting conditions, or in situations of elevated body temperature [11,28,39], which may also induce BrS ECG changes [26,40,41].…”

“…Detailed investigation was possible in 15 patients included in the study in mean age (at first detailed assessment or performance of SCBT, Figure 5) of 36.0 ± 13.5 years, median 32 (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) years. Females consisted of 26.7% (n = 4).…”