A comparison of respiratory symptoms and inflammation in sudden infant death syndrome and in accidental or inflicted infant death.

Upper respiratory infection and pulmonary inflammation are common in sudden infant death syndrome, but their role in the cause of death remains controversial. Controlled studies comparing clinical upper respiratory infection and inflammation in sudden infant death syndrome with sudden infant deaths caused by accidents and inflicted injuries (controls) are unavailable. Our aim was to compare respiratory inflammation and upper respiratory infection within 48 hours of death and postmortem culture results in these two groups. A retrospective analysis of upper respiratory infection and pathologic variables in the trachea and lung of 155 infants dying of sudden infant death syndrome and 33 control infants was undertaken. Upper respiratory infection was present in 39% of sudden infant death syndrome cases and 40% of control cases. Upper respiratory infection was more likely to have occurred in association with more severe lymphocytic interstitial pneumonitis when sudden infant death syndrome cases and control cases were combined ( P=.04). Proximal and distal tracheal lymphocytic infiltration was more severe in control cases than in sudden infant death syndrome cases ( P=.01 and.01, respectively). Lymphocytic infiltrations of the bronchi, bronchioles, and pulmonary interstitium were similar between groups. Bronchial associated lymphoid tissue was more prominent in control cases ( P=.04). Cultures were positive in 80% of sudden infant death syndrome cases, 78% of which were polymicrobial. Among control cases, 89% were positive, with 94% being polymicrobial. This study confirms that microscopic inflammatory infiltrates in sudden infant death syndrome are not lethal.

Infanticide: is its incidence among postneonatal infant deaths increasing?: an 18-year population-based analysis in California.

The decline in the incidence of sudden infant death syndrome (SIDS) and recent recommendations regarding the differentiation of SIDS and child abuse has generated speculation that some cases of infanticide were misdiagnosed as SIDS. The aims of this study were to determine the change in incidences and proportions of postneonatal deaths from all causes, SIDS, and infanticide in California over an 18-year interval encompassing years before and after the Back to Sleep campaign. Selected postneonatal mortality data from 1981 through 1998 obtained from the California Department of Health Services were analyzed and graphically displayed. The total postneonatal mortality and incidence of SIDS deaths per 100,000 live births decreased 45% and 66%, respectively, during the study interval; the incidence of infanticide remained low. The ratio of infanticide to SIDS increased from 4.3 per 100 in 1981 to 10.2 per 100 in 1998. Infanticide deaths, as a percentage of the total number of postneonatal deaths, increased slightly from the first to the second half of the study interval but never rose above 3.2%. It is concluded that this increased percentage is due to a decrease in SIDS deaths and not to an actual increase in infanticide deaths.

Medial smooth muscle thickness in small pulmonary arteries in sudden infant death syndrome revisited.

Increased relative medial thickness (RMT) of smooth muscle in small pulmonary arteries, peripheral extension of smooth muscle into the alveolar wall arteries, and right ventricular hypertrophy (RVH), in response to purported prolonged hypoxia, have been reported in sudden infant death syndrome (SIDS). Prone sleep position, an important risk factor for SIDS, predisposes infants to hypoxia from airway obstruction or rebreathing. Since publication of the earlier pulmonary artery studies, the SIDS definition has been expanded, and sudden infant death investigational protocols have been implemented. Our aims in this study were to (1) compare RMT in preacinar arteries (PA), intra-acinar arteries accompanying small airways (SIA), and alveolar wall arteries (AW) in SIDS infants and controls; (2) correlate RMT with postmortem variables; (3) determine if peripheral extension occurred more often in SIDS infants than in controls; and (4) determine if RVH occurred in SIDS. Movat-stained sections from standardized tissue blocks taken prospectively from the apex of the right upper lobe from 88 SIDS cases and 17 controls were evaluated using a computer-assisted digitizing system with images obtained from a microscope with an attached video camera. When adjusted for age, the RMT values for the SIA arteries were significantly greater in controls, while the PA and AW arteries were not statistically different between the SIDS cases and controls. Peripheral medial smooth muscle extension did not differ between the groups, and RVH was not seen in SIDS cases. Given the recent identification of brain stem abnormalities interfering with protective cardiorespiratory responses against acute life-threatening hypoxia perhaps precipitated by prone sleeping, our data suggest that SIDS is an acute event not preceded by recurrent or prolonged apnea and hypoxia.