Studies have shown that infants born through elective cesarean section may be at greater risk for SIDS.

Sudden infant death syndrome (SIDS) is the unexpected, sleep-related death of an apparently healthy infant of 1 year or less in age. The death cannot be explained by disease, accident, abuse, or homicide. One suspected cause of SIDS is sleep apnea. In support of this, autopsies of infants that have died of SIDS reveal physiological evidence that frequent episodes of apnea had been occurring for some time before the death. Many infants who have died of SIDS have petechiae, small pinpoint-shaped hemorrhages, scattered on the surface of the heart, lungs, and thymus. Scientists believe that the petechiae may have resulted from the effort involved in gasping as an infant struggled to breathe after an apneic episode. Other autoptic support for apnea^1-3 is the finding that the arcuate nuclei (located on the medulla oblongata) are smaller than normal in infants that have died of SIDS. Scientists believe that these nuclei play a role in respiration. Additionally, scientists note that the cells of the arcuate nuclei do not bind properly to serotonin, which may affect transmission of signals controlling respiration and, in turn, result in apnea. Because of the suspected role of sleep apnea in SIDS, infants are considered at greater risk for SIDS if they have symptoms of obstructive sleep apnea, central apnea, cyanosis, choking, and gagging. Interestingly, central apneas, pauses, mixed apneas, and tachypnea are more common in infants born by cesarean section than in infants born vaginally. These respiratory alterations are more pronounced if the infant is delivered by an elective cesarean section.⁴ Investigations into the breathing patterns of cesarean-born infants are leading scientists to consider that this method of birth may place an infant at greater risk for SIDS.

Prior to birth, a fetus’ vital functions (eg, gas exchange) are fully supported by the mother. This dependence abruptly stops with birth, at which point an infant begins to maintain its own functions. One function—respiration—has undergone much study; yet scientists remain unclear as to what triggers continuous respiration in a neonate immediately after its birth. One speculation focuses on the postbirth clamping of the umbilical cord.^5,6 Once the cord is clamped, factors such as prostaglandin E2, which had inhibited respiratory motions in utero, are no longer supplied by the mother. Decreased levels of the factors mean decreased respiratory inhibition, which in turn allows continuous respiration to begin after birth. A second speculation looks at the interplay between oxygen and cord clamping. Once an infant’s dependence on maternal oxygen is blocked by clamping the cord, the presence of oxygen in the atmosphere stimulates an infant to breathe.⁷ A third speculation is that physiological effects of skin cooling (eg, increased electrocortical activation) after birth trigger respiration.⁸ A fourth speculation is that somatic stimulation triggers respiration.⁹

The Evidence Is In
Results of animal studies suggest that it is primarily somatic stimulation occurring with the force of uterine contractions during labor which triggers respiration. For example, during a three-part study, Ronca and Alberts¹⁰ investigated the role of compression, cooling, and umbilical cord clamping on respiration in neonatal rats. In the first two parts of the study, rats were externalized from the uterus but remained attached to the mother by the umbilical cord. They were then subjected to one of the three conditions. Afterwards, they were delivered by cesarean birth.

The first part of the experiment compared the individual effects of compression (simulated labor contraction), cooling, and umbilical cord clamping on respiration. For compression, the researchers used a latex balloon to apply a pressure of 15 mm Hg for a 20-second period once every minute. The fetuses were compressed in this fashion for 15 minutes. For cooling, the researchers exposed a second group of externalized fetuses to an air temperature of 26.0° centigrade (78.8° Fahrenheit; normal rat temperature is about 37.5° centigrade [99.5° Fahrenheit]). For umbilical cord clamping, the researchers used a microvascular clamp to block umbilical cord blood flow in a third group of fetuses.

Ronca and Alberts found that the neonatal rats that had been in the compression group had the highest rate of respiration immediately after birth. The respiratory rate increased from about 5 breaths/min to about 20 breaths/min during the hour in which this group of rats were observed. The rats that had undergone cooling had a significantly reduced respiration rate immediately after birth (about 1–2 breaths/min) and had a smaller increase in the rate of respiration to about 3–4 breaths/min by 1 hour. All rats in the umbilical cord clamping group died within an hour of observation. From this, Ronca and Alberts concluded that somatic stimulation plays a significant role in triggering respiration in a neonate.

In the second part of the experiment, using a different group of fetuses, Ronca and Alberts compared the effect of different combinations of the conditions. The first group of fetuses underwent clamping only; the second group, clamping and cooling; the third group, clamping and compression; and the fourth group (simulated birth group), clamping, cooling, and compression. As in the previous experiment, all of the occlusion-only neonates died within 1 hour of birth. In the second group (clamping and cooling), only 23% of the rats were breathing by 1 hour. In the third and fourth groups, which both involved compression, 100% of the rats were breathing by 1 hour. Again, this points to the importance of somatic stimulation in triggering respiration.

In the third part of the study, Ronca and Alberts compared the respiratory pattern of rats from the second part of their study that had undergone simulated birth (ie, compression, cooling, and cord clamping) to the respiratory pattern of rats that had been born vaginally. They found that the respiratory rate of both groups of rats immediately after birth was virtually the same: The rats delivered by simulated birth breathed at a rate of 21 breaths/minute; the vaginally born rats, 29 breaths/minute. By the end of 1 hour, the breathing rate had increased similarly in both groups: The simulated-birth group breathed at a rate of about 43 breaths/min; the vaginal birth group, 34 breaths/min. From these results, Ronca and Alberts concluded that, although the combined effect of compression, cooling, and clamping has virtually the same respiratory effect as a vaginal birth in a neonate, it is physical stimulation (compression) that is most needed to trigger respiration after birth. The physical stimulation that occurs with a vaginal birth is absent in an infant delivered by cesarean section.

Why and When Cesarean
A mother may undergo cesarean section electively or as the result of an emergency. In an elective cesarean section, no labor takes place. This option may be chosen for several reasons, such as to avoid the risk of labor-induced uterine rupture if a mother has undergone previous cesarean sections; as a personal lifestyle choice; or if mother has tocophobia (severe fear of labor). An emergency cesarean section, on the other hand, takes place after labor has begun. It is performed in cases of fetal distress; prolonged, unprogressive labor; breech birth; or if the mother’s life is in danger. Although labor is aborted in an emergency cesarean, even a short duration of labor seems to stabilize a neonate’s respiration after birth.

Bader et al⁴ were the first to study the consequences of an elective cesarean section on neonatal breathing patterns. They compared the respiratory patterns of infants born by elective cesarean with those of infants that had been born by an emergency cesarean section. The elective group were born at approximately the 38th week of pregnancy, whereas the emergency group was born at approximately the 40th week of pregnancy. All the infants were considered term. (The criteria for full term is birth during the 38th-42nd week of pregnancy.)

The researchers collected polysomnographic information for 2 hours on infants 26-36 hours old. Polysomnography revealed that infants in the elective cesarean group had: 1) significantly more respiratory events in quiet sleep than did the emergency group (5.3 events versus 1.8 events, respectively); 2) more central apneas during quiet sleep (2.8 apneas versus 0.7 apnea); 3) longer duration of central apneas during quiet sleep (6.4 seconds versus 2.5 seconds); 4) more mixed apneas (2.2 apneas versus 0.6 apnea); and 5) mixed apneas lasting for longer duration (13.3 seconds versus 5.5 seconds).

Because other researchers have noted that infants born at or before the 37th week of pregnancy tend to have more respiratory events than full-term infants, Bader et al acknowledge that the increased respiratory events in the elective group may have resulted from their slightly younger age at birth.⁴ To counter this potentiality, the researchers performed multivariate analysis (with gestational age treated as the independent variable) to determine whether the earlier birth in the elective group had impacted their results. Multivariate analysis also revealed that the elective cesarean group had an increased number of mixed apneas with longer durations and an increased number of central apneas of longer duration in quiet sleep. Based on these results, Bader et al believe that the short duration of labor that had occurred before the emergency cesarean section resulted in improved respiration in neonates after birth.

Reducing the Risk
The altered respiration of cesarean-born infants may result in their being placed in a neonatal intensive care unit (NICU) for monitoring. One type of monitoring—pulse oximetry—detects apnea in NICU infants by measuring changes in oxygen saturation (Sao2). In pulse oximetry, a probe (which is typically placed on an infant’s foot) passes a wavelength of red light (approximately 660 nm) and a wavelength of infrared light (approximately 940 nm) through skin tissue onto a photoreceptor. The red wavelength is more readily absorbed by deoxygenated hemoglobin (deoxyhemoglobin) and the infrared wavelength is more readily absorbed by oxygenated hemoglobin (oxyhemoglobin). The ability of deoxyhemoglobin and oxyhemoglobin to absorb the red and infrared wavelengths changes as the former gains oxygen molecules and the latter loses oxygen molecules. This change in the absorption of red and infrared is converted by a mathematical algorithm into a number to represent the percentage of blood oxygen saturation.

Since a low Sao2 can be evidence that an infant is having an episode of apnea, a pulse oximeter can be programmed to sound an alarm if it detects a low blood oxygen level (for example, if the Sao2 falls below 90%). Once alerted to the drop in Sao2, NICU workers can ideally take immediate action such as stimulation, cardiopulmonary resuscitation, etc to avert the apnea and potentially avoid a case of SIDS.

A Johns Hopkins University¹¹ epidemiological study also found that infants delivered by cesarean section have an increased risk of dying of SIDS than an infant born vaginally. This risk may be a consequence of the earlier gestational age at which an elective cesarean section occurs or it may be a consequence of lack of somatic stimulation during a cesarean section. Both factors can result in increased episodes of apnea, which may potentially be a prelude to SIDS.

Since apneas are more common in cesarean-born infants (and especially so in elective cesarean-born infants), physicians may need to consider using home apnea monitors on infants delivered by cesarean section. Ideally, an apnea monitor could prevent an infant’s apnea from progressing to SIDS. The monitor sounds an alarm if it detects a prolonged episode of apnea, hypoxia, or bradycardia, at which point parents can arouse their infant or do cardiopulmonary resuscitation if necessary.

Physicians may also need to consider delaying the due date of an elective cesarean to the 40th to 42nd week (rather than at the 38th to 39th week). Some research shows that term infants born in the 38th to 39th week range have more apneas than those born in the 40th to 42nd week range. Delaying an elective cesarean due date could allow an infant’s respiratory system to mature, thereby resulting in a more stable breathing pattern after birth.

More studies are needed that investigate the connection between SIDS and cesarean birth. Future studies may reveal whether simulating compression in an infant after a cesarean section would result in more stabilized breathing after birth and whether simulating compression would reduce the risk of an infant’s dying of SIDS after being born by cesarean section. Learning such information could potentially save many infants’ lives.

Regina Patrick, RPsgT, is a contributing writer for RT.

References
1. Kinney HC, Myers MM, Belliveau RA, et al. Subtle autonomic and respiratory dysfunction in sudden infant death syndrome associated with serotonergic brainstem abnormalities: a case report. J Neuropathol Exp Neurol. 2005;64(8):689-94.
2. Filiano JJ. Arcuate nucleus hypoplasia in sudden infant death syndrome: a review. Bio Neonate. 1994;65(3-4):156-9.
3. Kinney HC, Randall LL, Sleeper LA, et al. Serotonergic brainstem abnormalities in Northern Plains Indians with the sudden infant death syndrome. J Neuropathol Exp Neurol. 2003;62(11):1178-91.
4. Bader D, Riskin A, Paz E, et al. Breathing patterns in term infants delivered by cesarean section. Acta Paediatr. 2004;93(9):1216–20.
5. Adamson SL, Kuipers IM, Olson DM. Umbilical cord occlusion stimulates breathing independent of blood gases and pH. J Appl Physiol. 1991;70(4):1796-1809.
6. Jansen AH, Chernick V. Fetal breathing and development of control of breathing. J Appl Physiol. 1991;70(4):1431-46.
7. Togari H, Sobajima H, Suzuki S. Oxygen and reduced umbilical blood flow trigger the first breath of human neonates. Acta Paediatr Jpn. 1992;34(6):660-2.
8. Gluckman PD, Gunn TR, Johnston BM. The effect of cooling on breathing and shivering in unanesthetized fetal lambs in utero. J Physiol. 1983;343:495-5063.
9. Moss IR, Condorelli S, Scarpelli EM. The progressive onset of spontaneous and induced fetal breathing. Respir Physiol. 1981;45(3):299-308.
10. Ronca AE, Alberts JR. Simulated uterine contractions facilitate fetal and newborn respiratory behavior in rats. Physiol Behav. 1995;58(5):1035-41.
11. Sanghavi DM. Epidemiology of sudden infant death syndrome (SIDS) for Kentucky infants born in 1990: maternal, prenatal, and perinatal risk factors. J Ky Med Assoc. 1995;93(7):286-90.