Etiology and Pathology

At present, the etiology of SIDS remains a mystery. It is not even clear whether SIDS has a single cause, has several causes, or is the result of a combination of factors working together.

Before the medical profession took an interest in the sudden, unexplained deaths of infants in the eighteenth century, people attributed the demise of these children to accidental suffocation in bedclothes, or to accidental smothering and overlaying by sleeping parents. Less charitable people accused parents or nursemaids of infanticide. These theories persisted throughout the nineteenth and early and mid-twentieth centuries concomitantly with medical theories that ascribed sudden infant deaths to an enlarged thymus or a thymic condition (see the History section for more on this). Since the 1940s, when researchers took a renewed interest in the etiology of sudden unexplained infant deaths, medicine has proposed numerous theories to explain why these children die.

When medical examiners in the 1940s and 1950s tested the blood of infants who had died suddenly and inexplicably, they often found fulminant infections that could easily have caused death. For the next several years, bacterial and viral infections were considered a major cause of sudden infant deaths. But when those deaths from infection were weeded out, there still remained a large number for which pathologists could find no infectious agents. Researchers then found other possible causes of death, including the following: powerful allergic reactions to cow's milk, to house dust mites, or to some unidentified allergen; botulism, beginning in 1976 when a number of infants infected with Clostridium botulinum were discovered in California; a severe, undetected respiratory viral infection; a response to vaccination against childhood diseases; overheating; hypothermia; high sodium in the blood; deficiency of a trace element like magnesium, zinc, copper, calcium, selenium, or manganese; a vitamin deficiency; and high or low levels of thyroid hormones. Some physicians reiterated the old view that a proportion of parents committed infanticide. Further research into these and other proposed etiologies continues.

Most current research relates the "final pathway" of SIDS to a malfunctioning or immaturity of the respiratory or cardiovascular system. Etiologic theories under consideration include preexisting hypoxia, heart conduction problems (arrhythmias), and apnea (Culbertson et al. 1988; Schwartz, South-all, and Valdes-Dapena 1988; Guntheroth 1989). Evidence indicates that children who die of SIDS possess physical risk factors such as small size, slower growth rate, fatty changes in the liver, and thymic changes campatible with previous infection. These risk factors are not specific to SIDS but, like the social factors listed in the Epidemiology section, reflect increased risk to all infant deaths. When a young patient possesses what Abraham Bergman (1986) calls a "critical mass" of these physical and social factors, all that is needed is a trigger to cause SIDS to occur. "Something must happen during sleep to tip the balance," he speculates, because virtually all SIDS deaths occur during sleep. The nature of that trigger is the mystery of SIDS.

SIDS leaves few pathological footprints in its young victims' bodies. Postmortem examination reveals little for the physician to use in understanding the pathology of the condition. The very definition of SIDS incorporates this fact, stating that negative postmortem findings help to classify an infant's cause of death as SIDS. Pathologists studying large numbers of SIDS cases have, over the years, noted only a few consistent postmortem findings that might at some time help explain the nature of SIDS. These include, according to one SIDS researcher (Guntheroth 1989), "intrathoracic pete-chiae, patchy pulmonary edema and emphysema," indicative of respiratory problems; "histopathology suggesting pre-existing hypoxia, such as changes in pulmonary arteries and right ventricle, smaller thymus, extra-medullary erythropoiesis, increased peri-adrenal brown fat cells, [and] enlarged adrenal chromaffin cells"; and neuropathological changes such as "astroglial proliferation in brain stem, leu-komalacia, and delayed loss of dendritic spines in reticular substance," consistent with underdevelopment or a subtle chronic disorder. The pathological changes so far discovered fail to provide enough information for medical scientists to understand the etiology or mechanism behind SIDS deaths.

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