Overview of Mortality and Morbidity

Chapter 87 Overview of Mortality and Morbidity

The risk for mortality in fetuses and neonates is very high around the time of birth. The perinatal period is most often defined as the period from the 28th wk of gestation through the 7th day after birth. The neonatal period is defined as the 1st 28 days after birth and may be further subdivided into the very early (birth to less than 24 hr), early (birth to <7 days), and late neonatal periods (7 days to <28 days). Infancy is defined as the 1st year after birth.

Perinatal mortality is influenced by prenatal, maternal, and fetal conditions and by circumstances surrounding delivery. Perinatal deaths are associated with intrauterine growth restriction (IUGR); conditions that predispose the fetus to asphyxia, such as placental insufficiency; severe congenital malformations; and overwhelming early-onset neonatal infections (Table 87-1). The major causes of neonatal mortality are prematurity/low birthweight (LBW) and congenital anomalies. Mortality is highest during the 1st 24 hr after birth. Neonatal mortality (4.27/1,000 in 2008) accounts for about two thirds of all infant deaths (deaths before 1yr of age). Neonatal and postneonatal mortality rates in the USA have declined or remained stable (Fig. 87-1). Factors related to the decline in mortality include improved obstetric and neonatal intensive care management with a significant reduction in birthweight-specific neonatal mortality (Fig. 87-2). Further reduction in neonatal mortality will depend on prevention of preterm delivery and LBW, prenatal diagnosis and early management of congenital anomalies, and effective diagnosis and treatment of diseases that result from adverse factors during pregnancy, labor, and/or delivery (see Table 87-1). In the USA each year, approximately 6 million pregnancies, 4 million live births, 19,000 neonatal deaths, and 28,000 infant deaths occur. Ten per cent of births are to teenage women between the ages of 15 and 19 yr, a proportion that has been decreasing for about 35 yr (Fig. 87-3). Births to girls 10-14 yr, very young mothers who are at great social and medical risk, declined substantially over this period. The proportion of deaths to unmarried women was 40.6% in 2008, the highest ever in U.S. history.

Figure 87-1 Fetal and neonatal mortality rates (MR) in the USA for the selected years 1990, 2005, and 2006 (final) and 2007 (preliminary). a, data not available; EFMR, early fetal deaths (20-27 wk of gestation) per 1000 live births plus specified fetal deaths; LFMR, late fetal deaths (≥28 wk of gestation) per 1000 live births plus specified fetal deaths; NMR, neonatal deaths per 1000 live births; PNMR, postneonatal deaths per 1000 live births.

(From Heron M, Sutton PD, Xu J, et al: Annual summary of vital statistics: 2007, Pediatrics 125:4–15, 2010.)

Figure 87-2 Neonatal mortality, by birthweight categories, for black (filled circles) and white (open circles) infants in the United States. Solid lines denote data for 1989; dashed lines are for 1997. Data shown are for births of newborn infants weighing <2,250 g only.

(From Demissie K, Rhoads GG, Ananth CV, et al: Trends in preterm birth and neonatal mortality among blacks and whites in the United States from 1989 to 1997, Am J Epidemiol 154:307–315, 2001.)

Figure 87-3 Birthrates for teenagers by age, USA, final for 1980-2006 and preliminary for 2007.

(From Hamilton BE, Martin JA, Ventura SJ: Births: preliminary data for 2007, Natl Vital Stat Rep 57:12:1–23, 2009.)

Infant mortality rates (deaths occurring from birth to 12 mo per 1,000 live births) vary by country; in 2008, rates were lowest in Hong Kong (1.8/1,000 births), moderate in the USA (6.6/1,000), and highest in developing countries (30-150/1,000). Medical, socioeconomic, and cultural factors influence perinatal and neonatal mortality. Preventive variables such as health education, prenatal care, nutrition, social support, risk identification, and obstetric care can effectively reduce perinatal, neonatal, and infant mortality. A number of reasons can explain in part the relatively higher infant mortality in the USA than in other countries. There is evidence of differential reporting of live births versus fetal deaths or stillbirths among countries. Many countries do not report as live births those of infants as mature as up to 27 wk if they die early after birth. The reporting of vital events in the USA is more complete than in many countries, including developed countries. This situation in part explains the larger proportion of LBW/preterm infants in the USA than in other countries. Increases in recorded preterm live births, especially of the most immature infants (<500 g BW) in the USA, result in increases in both neonatal and infant mortality rates. Nonetheless, continuing health care disparities in part account for the higher infant mortality rate in the USA. Infants of African-American women continue to have a high infant mortality rate (13.6/1000), which is more than twice the rates of infants of white (5.6/1000) and Hispanic mothers (5.5/1000).

In the USA, ∼50% of infant deaths in 2008 were due to four conditions (classified according to the International Classification of Diseases, 10th revision): congenital malformations (20.1%), disorders relating to prematurity and unspecified LBW (16.9%), sudden infant death syndrome (SIDS) (8.2%), and newborns affected by maternal complications of pregnancy (6.3%). LBW (as a result of preterm delivery and/or IUGR) is a major determinant of both neonatal and infant mortality rates and, together with congenital anomalies (cardiac, central nervous system, respiratory), contributes significantly to childhood morbidity. In developing countries, LBW/prematurity, birth asphyxia, and infections are the major causes of infant deaths.

The LBW rate (infants weighing ≤ 2,500 g at birth each year) in the USA increased from 6.6% to 8.2% between 1981 and 2008, whereas the very low birthweight (VLBW) rate (infants weighing ≤1,500 g at birth) increased from 1.1% to 1.46% of all births. In the past decade, LBW has increased among white infants, mainly because of a rise in the number of multiple births (often associated with assisted reproduction) (Fig. 87-4). Nonetheless, LBW and VLBW rates remain highest among black infants. Reasons for the racial disparity in LBW remain unclear. Despite advances in prenatal and obstetric care, racial disparity in birthweight persists, thus suggesting the need for novel prevention programs. Furthermore, although preterm LBW survival is better among black neonates (see Fig. 87-2), overall neonatal and infant mortality rates remain highest among blacks (Fig. 87-5), even for infants born to extremely low-risk mothers (married, aged 20-34 yr, ≥13 yr of education, adequate prenatal care, no medical risk factors, no alcohol or tobacco use during pregnancy). A reduction in the racial disparity in mortality is an important public health issue reflected in Healthy People 2010, the U.S. national health objectives for the year 2010.

Figure 87-4 Preterm birthrates, USA, final for 1990-2006 and preliminary for 2007.

(From Hamilton BE, Martin JA, Ventura SJ: Births: preliminary data for 2007, Natl Vital Stat Rep 57:12:1–23, 2009.)

Figure 87-5 Infant mortality rates by race and ethnicity, 2002. In 2002, the infant mortality rate was highest for infants of non-Hispanic black mothers. Infants of Hawaiian, Native American, and Puerto Rican mothers also had high rates. The lowest rates were observed for infants of Cuban and Chinese mothers. Additional birth data are available at www.cdc.gov/nchs/births.htm.

(Adapted from Mathews TJ, Menacker F, MacDorman MF: Infant mortality statistics from the 2002 period linked birth/infant death data set. www.cdc.gov/nchs/data/nvsr/nvsr53/nvsr53_10.pdf. Accessed April 26, 2010.)

LBW is caused by preterm birth, IUGR, or both. The predominant cause of LBW in the USA is preterm birth, whereas in developing countries, the cause is more often IUGR. Although IUGR does not appear to further increase the risk of mortality in preterm infants, both morbidity and mortality are increased in term growth-restricted infants. VLBW infants are most often premature (<37 wk of gestation), although IUGR may also complicate their early delivery. Even though VLBW occurs in only 1-2% of all infants in the USA, their births represent a large proportion of the neonatal and infant mortality as well as of infants with both short- and long-term complications, including neurodevelopmental handicaps. The etiology of preterm birth is complex, multifactorial, and not completely understood. Causes include maternal diseases such as severe preeclampsia requiring elective delivery, premature rupture of membranes, uterine abnormalities, placental bleeding (abruptio, previa), multiple-fetus gestation, drug misuse, maternal chronic illnesses, fetal distress, and infection. A complex interaction can be noted among infection, inflammation, and both preterm premature rupture of membranes and preterm birth. Infectious antecedents include maternal urinary tract infection, chorioamnionitis, bacterial vaginosis, and upper and lower genitourinary tract infection with a variety of agents (Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, Gardnerella vaginalis, and group B streptococcus). Preconceptional dietary folate supplementation may effectively reduce the rate of spontaneous preterm birth. In many cases, the cause of preterm delivery is unknown. The number of late preterm births (34-36 wk) has increased owing in part to elective deliveries; late preterm neonates are also at increased risk for morbidity and mortality. If possible, elective delivery should be delayed until ≥39 wk.

Although 99% of births occur in hospitals, only 80-85% of pregnant women receive ideal prenatal care in the 1st trimester. Many women who receive inadequate prenatal care are at risk for perinatal complications. Barriers to prenatal care include lack or insufficiency of money or insurance to pay for care; poor coordination of services, including language and cultural issues; and inadequate effective education about the importance of prenatal care. Successful and adequate provision of high-quality prenatal care requires competent health care professionals and coordination of services among physicians’ offices, clinics, community hospitals, specially regionalized programs for high-risk mothers and infants, and tertiary care centers. Regional perinatal programs should provide continuing education and consultation in both the community and the referral center and transportation for pregnant women and newborn infants to appropriate hospitals; they should also include a regional hospital with facilities, equipment, and personnel for obstetric and neonatal intensive care (Table 87-2).

Table 87-2 LEVELS OF IN-HOSPITAL PERINATAL CARE

From American Academy of Pediatrics, American College of Obstetricians and Gynecologists: Guidelines for perinatal care, ed 5, Elk Grove Village, IL, 2002, American Academy of Pediatrics.

Fetal deaths slightly exceed neonatal deaths in their contribution to perinatal mortality. The fetal mortality rate in the USA has been declining steadily during the last two decades and decreased to 6.2/1000 in 2004. Obstetricians and maternal-fetal medicine subspecialists have a central role in reducing perinatal mortality and morbidity. The overall decrease in fetal death has been due to a reduction in late fetal deaths (≥28 wk). Intrapartum fetal deaths have declined more than antepartum fetal deaths, reflecting improvements in care during labor and delivery. It is important to emphasize the ability to predict the maturity and functional reserve of a fetus both before and during labor so that fetuses and infants at greatest risk can be identified as early as possible. The obstetrician and pediatrician must interact effectively to anticipate perinatal problems and take prompt preventive and therapeutic measures.

Postneonatal mortality refers to deaths between 28 days and 1yr of life. Historically, these infant deaths were due to causes outside the neonatal period, such as SIDS, infections (respiratory, enteric), and trauma. With the advent of modern neonatal care, many VLBW and preterm infants who would have died in the 1st mo of life now survive the neonatal period only to succumb to the sequelae listed in Table 87-3. This delayed neonatal mortality is an important contributor to postneonatal mortality and explains its lack of decline during the last years.

Table 87-3 MORBIDITIES AND SEQUELAE OF PERINATAL AND NEONATAL ILLNESS

BPD, bronchopulmonary dysplasia; CMV, cytomegalovirus.

Late preterm infants are at risk for hypothermia, hypoglycemia, respiratory distress, apnea, jaundice, feeding difficulties, dehydration, and suspected sepsis. They are also at risk of having rehospitalizations. Even term infants born at 37 and 38 wk by cesarean section are at increased risk for respiratory distress syndrome, transient tachypnea of the newborn, suspected sepsis, hypoglycemia, need for ventilatory support, and admission to the neonatal intensive care unit (NICU) (Table 87-4).

For the most immature infants at the limit of viability (22-25 wk gestation), decision-making about care is a complex process that involves the physician, other health professionals, and the family. The challenge for all premature infants is not only to improve survival but also to reduce short-term complications and improve long-term neurodevelopmental outcome. Adverse neurodevelopmental sequelae include cerebral palsy, seizures, hydrocephalus requiring a shunt, blindness, deafness, and cognitive impairment. The risk of an adverse outcome increases with decreasing gestational age at birth. Higher birthweight, female gender, singleton birth, and antenatal steroids reduce the risk of neurodevelopment impairment or death. Early morbidity and prognostic variables that contribute to adverse neurodevelopmental outcomes include intraventricular hemorrhage, periventricular leukomalacia, necrotizing enterocolitis requiring extensive bowel resection, neonatal infection, and bronchopulmonary dysplasia. Many studies have documented the impact of adverse social and family risk factors on poor outcome.

High-risk infants must be monitored after discharge so that neurodevelopmental impairment is detected as early as possible and to ensure that children and families receive any interventions indicated and adequate support to optimize long-term outcome. At school age, former VLBW and preterm infants have poorer physical growth, cognitive function, and school performance. Although disadvantages may persist into adulthood, data now suggest that there may be cognitive improvement throughout childhood.