Geographic and race/ethnicity factors play an ad-
ditional role in increasing the relative risks. SIDS
rates increase during cold weather months, in eco-
nomically poor countries, and in infants of black race
or Native-American ethnicity. Worldwide, groups
such as Gypsy, Maori, Hawaiian, and Filipino also
have increased SIDS rates.
Pathologic Findings
Extensive work has been done in an attempt to
determine distinguishing pathological abnormalities
that if present at autopsy would definitively identify
SIDS as the cause of death. While there are findings
that are commonly present at autopsy, no gross ana-
tomical or microscopic abnormalities have been
found that are distinct to SIDS. Nevertheless, a thor-
ough postmortem (autopsy) examination demon-
strating the absence of a causative abnormality is
crucial to the diagnosis of SIDS. Especially important
is not missing evidence of child abuse such as signs of
(1) suffocation, (2) blunt trauma to the head, ribs, or
extremities, and (3) retinal hemorrhages seen in
shaken baby syndrome.
Commonly described findings in the central ner-
vous system include: (1) increase in brain weight, pre-
sumably due to disordered development of the brain,
(2) delayed myelination (maturation) of nerve cells,
(3) gliosis (scarring) of brain-stem cells, (4) areas of
leukomalacia (degeneration of brain tissue that oc-
curred weeks to months earlier), and (5) abnormal
dendritic spine density in selected areas of the brain
stem. Evidence of chronic oxygen deprivation—such
as persistence of brown fat around the adrenal glands,
red blood cell production in the liver, and gliosis of
the brain stem—add support to the theory that ab-
normal respiratory regulation may be the mechanism
underlying SIDS.
Mechanism (Pathophysiology)
Current thinking regarding the mechanism of
SIDS is focused on disordered regulation of the car-
diorespiratory systems. The primary area of physio-
logical regulation in humans is within the brain stem,
which is located anatomically at the base of the brain.
Abnormal findings on autopsy (as described in the
above section), combined with clinical observations of
abnormal regulatory control, support the view that
delayed maturation or disruption of brain stem func-
tion results in the infant’s lack of ability to respond
when breathing and circulation patterns are insuffi-
cient to maintain life.
Several areas of respiratory regulation have been
studied. Abnormalities of breathing patterns—such
as recurrent brief apneic episodes, prolonged apneic
An infant sleeping in a car seat attached to a Sudden Infant Death
Syndrome (SIDS) monitor. There are documented incidences of
SIDS occurring even when the infants were being properly
monitored, the machinery was fully functioning, and the
resuscitative efforts were started promptly and correctly. This
suggests that while abnormal breathing patterns are found in
infants who subsequently die of SIDS, this is probably not the
primary mechanism. (David H. Wells/Corbis)event, and periodic breathing—have been observed
in infants who later died of SIDS. The ability to elec-
tronically monitor and record breathing patterns in
infants sparked enthusiasm for screening and moni-
toring of infants felt to be at high risk for SIDS.
However, experience has proven this interven-
tion is not reliable in detecting which infants with ab-
normal breathing patterns will actually subsequently
die of SIDS. In addition, multiple false alarms from
the monitoring equipment resulted in high noncom-
pliance rates in the home setting.
Diminished respiratory responsiveness to exces-
sive buildup of carbon dioxide (hypercarbia) or to ex-
cessively low levels of oxygen (hypoxia) has also been
found in infants at risk for SIDS. Nevertheless, the
ability to discriminate between these infants andSUDDEN INFANT DEATH SYNDROME 395