The Role of Environmental Factors in the Causation of Sudden Death in Infants: Two Cases of Sudden Unexpected Death in Two Unrelated Infants Who Were Cared for by the Same Babysitter

Abstract

We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly.

Multidrug poisoning involving nicotine and tramadol

“…Though it is one of the most toxic of all poisons, nicotine has caused serious or fatal poisoning only in rare cases that generally involved lethal ingestion of concentrated nicotine solutions and pesticides [25][26][27][28]. Non-fatal cases of unintentional nicotine poisoning reported in literature were mostly caused by children eating cigarettes [29]. The interaction between tramadol and nicotine thus increases CNS depression with an additive effect that might cause severe hypotension and cardiac collapse secondary to hypoxic damage [30].…”

Prenatal exposure to carbon monoxide delays postnatal cardiac maturation

“…In fact, beside cardiomyocytes, 2 central and peripheral neurons may be target of CO-mediated damage as shown by impaired myelin deposition and SNC retardation in the same rat model. 3 Fatal acute CO intoxication at low CO saturation levels (o20%) has been reported for fetuses and infants 45 as fetal hemoglobin has a greater affinity (up to eightfold) for CO than adult hemoglobin. 46 This susceptibility decreases slowly after 6 months as adult hemoglobin synthesis is activated whereas fetal hemoglobin synthesis is deactivated.…”