Acquired Problems of the Newborn

Fetal Alcohol Syndrome

The Infant Experiencing Drug Withdrawal (Neonatal Abstinence Syndrome)

The Infant of the Mother with Pregestational or Gestational Diabetes

Preventive Measures

Virtually all controlled clinical trials have demonstrated that effective hand hygiene is responsible for the prevention of health care acquired infection in nursery units. Nursing is directly or indirectly responsible for minimizing or eliminating environmental sources of infectious agents in the nursery. Measures to be taken include implementing Standard Precautions, carefully and thoroughly cleaning the environment and equipment, frequently replacing used equipment (e.g., changing IV tubing per hospital protocol, cleaning resuscitation and ventilation equipment), and appropriately disposing of excrement and linens. Overcrowding must be avoided in nurseries. Guidelines for space, visitation, and general infection control in areas where newborns receive care have been established and published (American Academy of Pediatrics [AAP] & American College of Obstetricians and Gynecologists [ACOG], 2007).

Specific newborn care procedures are intended to prevent infection. These include the instillation of antibiotic ointment in newborns’ eyes 1 to 2 hours after birth, bathing, and cord care (see Chapter 24).

Curative Measures

Breastfeeding or feeding the newborn breast milk from the mother is encouraged. Breast milk provides protective mechanisms (see Chapter 25). Colostrum contains immunoglobulin A (IgA), which offers protection against infection in the GI tract. Human milk contains iron-binding protein that exerts a bacteriostatic effect on E. coli. Human milk also contains macrophages and lymphocytes. The vulnerability of infants to common mucosal pathogens such as respiratory syncytial virus (RSV) can be reduced by passive transfer of maternal immunity in the colostrum and breast milk. Some evidence indicates that early enteral feedings with human milk (trophic or minimal enteral feedings) can be beneficial in establishing a natural barrier to infection in ELBW and VLBW infants (Anderson, Wood, Keller, & Hay, 2011).

Administering medications safely and correctly, taking precautions when performing treatments, and following isolation procedures are important interventions when a newborn has an infection. Monitoring the IV infusion rate and administering antibiotics are the nurse’s responsibility. If the IV fluid the infant is receiving contains electrolytes, vitamins, or other medications, the nurse should check with the hospital pharmacy before adding antibiotics. The antibiotic (or other medication) can be deactivated or can form a precipitate when combined with other substances. To prevent this from occurring, a secondary line of the prescribed solution is attached with a three-way stopcock at the infusion site.

Care must be taken in suctioning secretions from any newborn’s oropharynx or trachea; the secretions can be infected. Routine suctioning is not recommended and can further compromise the infant’s immune status, as well as cause hypoxia and increase ICP. Isolation procedures are implemented as indicated according to hospital policy. Isolation protocols change rapidly, and the nurse is urged to participate in continuing education and in-service programs to remain up to date.

Toxoplasmosis

Toxoplasmosis is a multisystem disease caused by the protozoan Toxoplasma gondii parasite, commonly found in cats, dogs, pigs, sheep, and cattle, with cats being the definitive host. In the United States risk factors for acquisition of toxoplasmosis include exposure to contaminated soil and consumption of raw or undercooked meats or seafood (oysters, clams, or mussels) (Jones, Dargelas, Roberts, Press, Remington, & Montoya, 2009). Changing cat litter is a known risk for toxoplasmosis. The risk of maternal-fetal transmission of acute infection is approximately 40% with the risk of transmission increasing as the pregnancy progresses. However, the earlier in pregnancy that fetal infection occurs, the greater the severity of congenital disease. Because many women are already seropositive for toxoplasmosis, the overall risk of a primary infection in pregnancy is quite low. The diagnosis of toxoplasmosis in the neonate is supported by elevated levels of cord blood serum IgM.

Most neonates infected with T. gondii in utero are asymptomatic at birth, although many will develop chorioretinitis and signs of CNS involvement such as learning disabilities (Cunningham et al., 2010). For some infected neonates, hydrocephalus is the only clinical sign of the disease (Remington, McLeod, Thulliez, & Desmonts, 2006). Up to 30% of infected infants are born with severe manifestations at birth. Clinical features ascribed to T. gondii infection include three key findings (classic triad) first described by Sabin (1942): hydrocephalus or microcephaly, chorioretinitis, and cerebral calcifications (Cunningham et al.). Severe toxoplasmosis is associated with preterm birth, growth restriction, microcephaly or hydrocephaly, microphthalmos, chorioretinitis, CNS calcification, thrombocytopenia, jaundice, and fever. Petechiae or a maculopapular rash also can be evident.

Infants with congenital toxoplasmosis are treated with pyrimethamine, combined with oral sulfadiazine; folic acid supplement is used to prevent anemia. Treatment should be continued for 1 year (AAP Committee on Infectious Diseases, 2009).

Gonorrhea

The incidence of gonococcal infection in pregnant women ranges from 2.5% to 7.3%. Many women with gonorrhea often have a concurrent Chlamydia trachomatis infection (AAP Committee on Infectious Diseases, 2009). After rupture of membranes, ascending infection can result in orogastric contamination of the fetus. The organism can also invade mucosal surfaces such as the conjunctiva (ophthalmia neonatorum), the rectal mucosa, and the pharynx. Contamination can occur as the infant passes through the birth canal, or it may occur postnatally from an infected adult. Neonatal gonococcal arthritis, septicemia, meningitis, vaginitis, and scalp abscesses also can develop.

Eye prophylaxis (e.g., with 0.5% erythromycin ointment) is administered within the first hour after birth to prevent ophthalmia neonatorum (AAP & ACOG, 2007). Eye prophylaxis alone does not prevent systemic infection; therefore, infants with a gonococcal eye infection should receive one dose of ceftriaxone (Gowen, 2007). Infants with systemic gonococcal infection require hospitalization and 7 days of IV antibiotic therapy. Infants rarely die of overwhelming infection in the early neonatal period. With the prophylactic use of silver nitrate or antibiotics, the incidence of gonococcal conjunctivitis is less than 0.5% (Yudin & Gonik, 2006).

Syphilis

Congenital and neonatal syphilis have reemerged in recent years as significant health problems. Rates of congenital syphilis in the United States increased from 8.2 per 100,000 live births in 2005 to 10.1 per 100,000 live births in 2008 (Su, Berman, Davis, & Weinstock, 2010). It is estimated that for every 100 women diagnosed with primary or secondary disease, 2 to 5 infants will contract congenital syphilis. If syphilis during pregnancy is untreated, approximately 50% of neonates born to these women will have symptomatic congenital syphilis. Treatment failure can occur, particularly when treatment is given in the third trimester; therefore, infants born to women treated within 4 weeks of birth should be investigated for congenital syphilis (Woods, 2009). The following factors have been identified as placing the neonate at high risk for congenital syphilis: lack of or late prenatal care, maternal substance abuse, crack cocaine use in the mother or partner, multiple sexual partners, history of STI, poverty, homelessness, and HIV infection.

The fetus is usually infected in utero by transplacental infection, but infection of the amniotic fluid also can occur. The infant can also contract syphilis during contact with an active genital lesion at birth (Ingall, Sanchez, & Baker, 2006). The risk to the fetus and neonate varies according to the stage of maternal infection, with transmission during primary or secondary syphilis being more common. Untreated maternal disease results in stillbirth in 30% to 40% of cases. Prompt maternal treatment will eliminate most fetal infections; however, delayed treatment or a failure to obtain treatment can result in fetal effects that range from minor anomalies to preterm birth or fetal death. Damage to the fetus depends on when in gestation the infection occurred and the time that has elapsed before treatment. Congenital syphilis infection can be asymptomatic at birth in up to two thirds of infected infants. A portion of these infants will become symptomatic in the first 2 years of life, whereas others may take up to 20 years before displaying the effects of congenital infection (Woods, 2009).

Early congenital syphilis can result in prematurity, hydrops fetalis, and failure to thrive. Hepatosplenomegaly and jaundice are common. Hematologic findings include anemia, leukocytosis, and thrombocytopenia. Characteristic bony lesions occur in the long bones, the cranium, and the spine and include osteochondritis, osteomyelitis, and periostitis. Other findings include snuffles (copious clear mucous discharge from the nose), mucocutaneous lesions, edema, and a copper-colored maculopapular dermal rash first noticeable on the palms of the hands, the soles of the feet, and in the diaper area and around the mouth and the anus by the end of the first week of life in untreated infants (Fig. 35-7). Condylomata (elevated wartlike lesions) can be seen on mucous membranes, moist surfaces, or areas of the body affected by friction. Rough, cracked, mucocutaneous lesions of the lips heal to form circumoral radiating scars known as rhagades. Other involvement results in exfoliation (separation, flaking) of nails and loss of hair. Iritis and choroiditis are characteristic of infection of the eyes. The following can be noted: nephrotic syndrome secondary to renal infection; hepatitis with jaundice, lymphadenopathy, and inflammation of the pancreas, the testes, and the colon; and a pseudoparalysis of the extremities. In some infants, signs of congenital syphilis do not appear until late in the neonatal period. In these newborns, early signs such as poor feeding, slight hyperthermia, and snuffles can be nonspecific (Woods, 2009).

Varicella-Zoster

The varicella-zoster virus, responsible for chickenpox and shingles, is a member of the herpes family. Approximately 90% of women in the childbearing years are immune; therefore the risk of infection in pregnancy is low: 5 per 10,000 pregnancies (Gershon, 2006).

Varicella transmission to the fetus can occur across the placenta when the disease is contracted in the first half of pregnancy, but this is relatively infrequent (about 2%). When transmission to the fetus does occur in the early part of pregnancy, the effects on the fetus include limb atrophy, neurologic abnormalities (hydrocephalus or microcephaly), and eye abnormalities (Gowen, 2007).

When maternal infection occurs in the last 3 weeks of pregnancy, 25% of infants born to these mothers will develop clinical varicella (Gershon, 2006). The severity of the infant’s illness will increase greatly if maternal infection occurred within 5 days before or 2 days after birth (Tan & Koren, 2006). The mortality rate in severe illness is 30% (Gershon).

Seroimmune pregnant women exposed to active chickenpox can be given varicella-zoster immune globulin (VZIG), which does not reduce the incidence of infection but should decrease the effects of the virus on the fetus. The immunoglobulin must be given within 72 hours of exposure to be effective.

Infants born to mothers in whom chickenpox develops between 5 days before birth and 48 hours after should be given VZIG at birth because of the risk of severe disease (Tan & Koren, 2006). Acyclovir can be used to treat infants with generalized involvement and pneumonia (Myers, Seward, & LaRussa, 2007).

Term infants exposed to chickenpox after birth will have a mild or no infection if they are born to immune mothers. In those born to nonimmune mothers, chickenpox can develop, but the course is not usually severe. Experts are divided as to whether this group of infants should receive VZIG. Infants born before 28 weeks gestation are at risk regardless of their mother’s status and probably benefit from VZIG if exposed to chickenpox (AAP Committee on Infectious Diseases, 2009).

Hepatitis B Virus

HBV infection during pregnancy is not associated with an increase in malformations, stillbirths, or IUGR; however, approximately 35% of infected fetuses will be born before term (Baley & Toltzis, 2006). The transmission rate of HBV to the newborn ranges from 70% to 90% when the mother is seropositive for both hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) (AAP Committee on Infectious Diseases, 2009).Transmission occurs transplacentally, serum to serum, and by contact with contaminated urine, feces, saliva, semen, or vaginal secretions during birth. Infants are most frequently infected during birth or in the first few days of life. The rate of transmission is highest when the mother contracts the virus in the third trimester or early in the postpartum period (Bradley, 2006). These mothers will be positive for HBsAg. Transmission can occur through breast milk, but antigens also develop in formula-fed infants at the same or a higher rate, thus breastfeeding is not contraindicated. Diagnosis is made by viral culture of amniotic fluid, as well as the presence of HBsAg and IgM in the cord blood or infants serum.

The majority of infants who become HBsAg positive are symptom free at birth, whereas some show evidence of acute hepatitis with changes in liver function. The mortality rate for full-blown hepatitis is 75%. Infants who become carriers are at high risk for chronic hepatitis, cirrhosis of the liver, or liver cancer even years later (Yudin & Gonik, 2006).

Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome

Approximately 6000 pregnant women infected with HIV give birth each year in the United States. Due to the success of preventive strategies during pregnancy, the incidence of mother-to-child transmission has been reduced to approximately 1% to 2%. Universal HIV testing for all pregnant women allows for early identification and treatment of HIV-positive women during pregnancy, which decreases the risk of transmission to the fetus. Other strategies to prevent neonatal HIV infection include administration of antiviral medications during pregnancy and labor to women who are infected with the virus, administration of antiretrovirals to neonates for 6 weeks, and elective cesarean birth for women with HIV viral loads greater than 1000 copies per ml. In the United States, an additional strategy is the total avoidance of breastfeeding (AAP Committee on Pediatric AIDS, 2008)

Transmission of HIV from the mother to the fetus can occur transplacentally at various gestational ages. The risk of infection in an infant born to an HIV-positive mother (not treated) is approximately 12% to 40%. Transmission most often occurs during birth. Globally, approximately one third to one half of cases of mother-to-child transmission occur through breastfeeding (AAP Committee on Infectious Diseases, 2009).

Diagnosis of HIV infection in the neonate is complicated by the presence of maternal IgG antibodies that cross the placenta after 32 weeks of gestation. The most accurate test for newborns and infants younger than 18 months is the HIV-1 deoxyribonucleic acid (DNA) PCR assay, which is performed on neonatal blood, not cord blood (AAP Committee on Infectious Diseases, 2009). Follow-up testing for infants born to HIV-positive mothers is recommended at several intervals within the first year of life.

Typically the HIV-infected neonate is asymptomatic at birth. Early-onset illness (i.e., virus detected within 48 hours of birth) is attributed to prenatal infection. These infants develop opportunistic infections (Candida and Pneumocystis jiroveci pneumonia) and experience rapid progression of immunodeficiency that often results in death during the first 1 to 2 years of life.

The remainder of infants seroconvert over a period of months to years. By 1 year of life, the vast majority of perinatally infected infants show signs of infection. Some children infected at birth show no signs of disease 8 to 10 years later. The age of onset of symptoms predicts the length of survival.

The presenting signs and symptoms of HIV infection vary from severe immunodeficiency to nonspecific findings such as growth failure, parotitis, and recurrent or persistent upper respiratory tract infections. In the first year of life, lymphadenopathy and hepatosplenomegaly are common. The infant can have fever, chronic diarrhea, chronic dermatitis, interstitial pneumonitis, persistent thrush, and acquired immunodeficiency syndrome (AIDS)–defining opportunistic infections. Common secondary opportunistic infections include pneumonia, candidiasis, CMV, cryptosporidiosis, herpes simplex or herpes zoster, and disseminated varicella.

Although it is rare for an infant to be born with symptoms of HIV infection, all infants born to seropositive mothers should be presumed to be HIV positive until proven otherwise. Management begins by implementing Standard Precautions. Measures should also be taken to protect the infant from further exposure to maternal blood and body fluids. In the United States, breastfeeding is avoided completely if the mother is HIV positive. Regimens for the prevention of HIV transmission include antepartum, intrapartum, and neonatal treatment with highly active retroviral therapy (HAART).

The goal in the administration of antivirals is the suppression of the virus to undetectable concentrations; the available antiviral drugs do not, however, cure the child’s disease. HIV diagnosis in the neonatal period combined with aggressive antibiotic treatment of opportunistic infections has the potential to prolong survival in children (AAP Committee on Infectious Diseases, 2009). Studies of HIV symptoms in children treated in the era of HAART show a significant decrease in the incidence of secondary opportunistic infections (Nesheim, Kapogiannis, Soe, Sullivan, Abrams, Farley, et al., 2007).

Counseling regarding the care of the mothers themselves, the family’s care of the infant, and future pregnancies should be provided. The risk for transmission among members of the same household is minimal. Social services are required in these cases. If the parent chooses to keep the infant, home health care may be arranged. For more information and updated information, parents are referred to the National AIDS Hotline—1-800-342-AIDS.

In the United States, breastfeeding by the HIV-positive mother is contraindicated; however, in developing countries, the risks versus benefits in relation to number of infant deaths attributed to poor sanitary conditions and availability of an appropriate food supply for infants are considered. The World Health Organization (2010) recommends that HIV-positive mothers who are taking antiretroviral medications should breastfeed for at least 12 months. For those who do not have access to ARV therapy, exclusive breastfeeding for 6 months is recommended. After 6 months, complementary foods are introduced and breastfeeding is continued until a safe, nutritional diet without breastmilk can be provided for the infant (WHO, UNICEF, UNFPA, UNAIDS, 2010).

The family must be counseled about vaccinations. All HIV-1–exposed infants should receive routine immunizations. There are specific guidelines for those with confirmed HIV infection (CDC, 2009a). It is usually safe to administer all inactivated vaccines to HIV-1–infected children. In the absence of severe immunosuppression, children with HIV-1 can receive varicella vaccine (CDC, 2009a).

Rubella Infection

Since the rubella vaccination program was begun in 1969, cases of congenital rubella infection have been reduced significantly; however, it is still seen occasionally in the newborn. Vaccination failures, lack of compliance, and the migration of nonimmunized persons result in periodic outbreaks of rubella, also known as German measles.

The risk of a congenitally infected infant varies with the gestational age of the fetus when maternal infection occurs. Abnormalities are most severe if the mother contracts the virus during the first trimester and rare if the disease occurs after that time (Cooper & Alford, 2006).

More than two thirds of infected infants show no apparent symptoms at birth, but sequelae can develop years later. Hearing loss, the most common result, appears to be progressive after birth. Congenital rubella syndrome includes cataracts or glaucoma, hearing loss, and cardiac defects (pulmonary artery stenosis, patent ductus arteriosus, or coarctation of the aorta). Multiple other abnormalities also are present, including IUGR, microphthalmia, hypotonia, hepatosplenomegaly, thrombocytopenic purpura, dermatoglyphic abnormalities, bony radiolucencies, microcephaly, and brain wave abnormalities. Severe

infection can result in fetal death. Delayed effects of infection manifest as thyroid dysfunction, diabetes mellitus, growth hormone deficiency, myocarditis, and glaucoma (Baley & Toltzis, 2006).

Cytomegalovirus Infection

CMV infection during pregnancy can result in miscarriage, stillbirth, or congenital or neonatal cytomegalic inclusion disease (CMID). It is the most common cause of congenital viral infections in humans, occurring in 40,000 newborns in the United States every year. Maternal-fetal transmission of CMV virus occurs in approximately one third of mothers with a primary CMV infection during pregnancy (Edwards, 2006).

The neonate with classic, full-blown CMID typically displays IUGR and has microcephaly, seizures, hypotonia, and lethargy. The neonate also has a rash, jaundice, and hepatosplenomegaly (Fig. 35-8). Anemia, thrombocytopenia, and hyperbilirubinemia are common (Malm & Engman, 2007). Intracranial, periventricular calcification often is noted on x-ray films. Mortality rates in symptomatic infants are 20% to 30%, with death resulting from hepatic failure, DIC, or secondary bacterial infection (Edwards, 2006). Congenital CMV can cause a variety of neurologic problems such as mental retardation, autism, learning disabilities, hearing loss, visual impairment, or blindness (Malm & Engman, 2007). Most (90%) affected infants are asymptomatic at birth (Kenneson & Cannon, 2007), although there is a 5% to 15% risk that they will develop later sequelae such as hearing loss and learning disabilities (Edwards). Hearing loss can be present at birth or may not be apparent until after the first year of life. The hearing loss is often progressive. Chorioretinitis, microcephaly, mental retardation, and neuromuscular deficits can occur by 2 years of age. Some children are at risk for a defect in tooth enamel, resulting in severe caries (Edwards).

Elevated levels of cord blood IgM are suggestive of disease. The virus can be isolated from urine or saliva of the newborn. Differential diagnoses include other causes of jaundice, syphilis (positive Venereal Disease Research Laboratory [VDRL] findings), toxoplasmosis (positive Sabin-Feldman dye test result), hemolytic disease of the newborn (positive Coombs’ test reaction), or coxsackievirus infection (positive culture).

CMV can be transmitted through breast milk while the mother has acute CMV infection. CMV infections acquired after birth are often asymptomatic and have no sequelae. Exceptions to this occur in preterm infants in whom postnatal acquisition of CMV can result in pneumonia, hepatitis, thrombocytopenia, and long-term neurologic sequelae.

Treatment of the infected newborn with ganciclovir is effective in decreasing neurologic sequelae, in particular sensorineural hearing loss. There is some evidence that administration of CMV-specific human immunoglobulin to the pregnant woman with primary CMV infection can help protect the fetus (Schleiss, 2008).

Herpes Simplex Virus

HSV infections among newborns are being diagnosed more frequently and are estimated to occur in as many as 1 in 3,000 to 1 in 20,000 births (AAP Committee on Infectious Diseases, 2009). The neonate can acquire the virus through transplacental infection, ascending infection by way of the birth canal, direct contamination during passage through an infected birth canal, or direct transmission from infected personnel or family (Malm, 2009).

Transplacental transmission of HSV infection to the neonate can occur during maternal infection; however, an ascending transcervical infection first involves the intact fetal membranes, causing chorioamnionitis. Transcervical infection can be accelerated by the use of internal fetal monitoring. The scalp electrodes break the fetal skin barrier and increase the risk of infection.

Congenital infection is rare and characterized by in utero destruction of normally formed organs. Affected infants are growth restricted and have skin lesions and scarring. They have severe psychomotor delays, with intracranial calcifications, microcephaly, hypertonicity, and seizures. They have eye involvement, including microphthalmos, cataracts, chorioretinitis, blindness, and retinal dysplasia. Some infants have patent ductus arteriosus, limb anomalies, and recurrent skin vesicles, with a short life expectancy.

HSV is most often transmitted from mother to neonate through viral shedding during passage through the birth canal. The risk of infection during vaginal birth in the presence of genital herpes has not been clearly delineated. It may be as high as 50% with active primary infection at term (Prober, 2008). Primary maternal infections after 32 weeks of gestation have a higher risk for the fetus and newborn than recurrent infections (Baley & Toltzis, 2006). If the mother is shedding HSV virus as a result of reactivated infection, the risk of transmission is only about 2% (AAP Committee on Infectious Diseases, 2009). This is possibly related to passive intrauterine immunity to herpes. Clinical and laboratory features associated with neonatal herpes include maternal primary HSV infection, vaginal birth, preterm birth, neonatal seizures, elevated liver enzymes, vesicular rash, and elevated CSF counts (Caviness, Demmler, & Selwyn, 2008). In approximately 70% of women whose infants have HSV infection, there are no symptoms or history of infection although serologic testing reveals evidence of herpesvirus (Baley & Toltzis, 2006).

Postnatal acquisition of the virus and spread within a nursery have been documented by DNA analysis. Parents have been implicated in neonatal infections. There also is concern regarding symptomatic and asymptomatic shedding among hospital personnel. Nursery personnel with cold sores should practice strict hand hygiene and wear a mask, but no evidence indicates that they should be removed from the nursery unless they have a herpetic whitlow (primary HSV infection of the terminal segment of a finger) (Baley & Toltzis, 2006).

Clinically, neonatal HSV infections are classified as disseminated infection (22%), CNS disease (34%), or localized infection of the skin, eye, or mouth (SEM) (40%) (Baley & Toltzis, 2006). Although the incubation period for HSV is 1 to 7 days, the onset of symptoms varies with the type of infection (Malm, 2009).

Disseminated infections are sepsis-like and can involve virtually every organ system, but primarily the liver, the adrenal glands, and the lungs are involved. By 5 to 11 days of age affected infants show signs of bacterial sepsis or shock. Death often results within 1 week of the onset of symptoms and is related to respiratory failure, pneumonitis, DIC with shock, and CNS complications (Baley & Toltzis, 2006; Malm, 2009).

In CNS disease, blood-borne seeding of the brain results in multiple lesions of cortical hemorrhagic necrosis. It also can occur alone or in association with oral, eye, or skin lesions. Brain involvement usually manifests in the second to fourth weeks of life. Skin lesions are apparent in 60% to 70% of the infants, and the CSF of less than 50% will reveal the virus. The presenting manifestations include lethargy, poor feeding, irritability, and local or generalized seizures. If untreated, the mortality rate in CNS disease approaches 50% with the vast majority of survivors experiencing severe sequelae such as microcephaly and blindness (Baley & Toltzis, 2006).

Localized HSV infections most often occur with skin findings or rarely with isolated oral cavity lesions (Fig. 35-9). Without treatment, CNS or disseminated disease develops in 70% of the infants with skin vesicles. Ocular involvement, which can occur alone, can be secondary to either HSV-1 or HSV-2. Ocular disease may not be discovered for months. Microphthalmos, cataracts, optic atrophy, and corneal scarring can result from chorioretinitis, keratitis, and retinal hemorrhage (Baley & Toltzis, 2006).

Gloves should be worn when caregivers are in contact with these infants. The neonate’s eyes, oral cavity, and skin are inspected carefully for the presence of any lesions. Cultures are obtained from the mouth, the eyes, and any possible lesions. Circumcision, if performed, is delayed until the infant is ready to be discharged. The infant can be discharged with the mother if the infant’s cultures are negative for the virus. As long as no suspicious lesions are present on the mother’s breasts, breastfeeding is allowed. For the infant at risk, prophylactic topical eye ointment (vidarabine) is administered for 5 days for prevention of keratoconjunctivitis. No current recommendations exist for prophylactic systemic therapy; each case should be considered individually. Blood, urine, and CSF specimens should be cultured when indicated clinically. If herpetic lesions first occur after 6 weeks of life, the risk of dissemination and severe illness is very low (Baley & Toltzis, 2006).

Therapy includes general supportive measures, as well as treatment with acyclovir. Duration of treatment is 21 days for infants with disseminated or CNS disease and 14 days for the skin-eye-mouth form of the disease (Malm, 2009). Continuing therapy is required in case of recurrence. When there is ocular involvement, ophthalmic ointment should be administered simultaneously (AAP Committee on Infectious Diseases, 2009).

Parvovirus B19

Parvovirus B19 is well known in older children as “fifth disease” or “slapped cheek illness” because of the characteristic facial appearance of the affected child. During pregnancy, infection can result in miscarriage, fetal anemia, hydrops fetalis, IUGR, and stillbirth. Vertical transmission of the parvovirus to the fetus occurs in about one third of maternal infections (de Jong, de Haan, Kroes, Beersma, Oepkes, Walther, et al., 2006) and the overall fetal loss rate after infection is about 5% to 10% (Tolfvenstam & Broliden, 2009).

The virus can be isolated from amniotic fluid, fetal blood, or tissues using DNA PCR assay. Viral load is not predictive of fetal morbidity and mortality (Cunningham et al., 2010).

There are no specific antiviral medications to treat parvovirus B19 infection and there is no vaccine. If a pregnant woman is confirmed with the infection, the fetus should be closely monitored for the development of fetal hydrops using serial ultrasound examinations (Tolfvenstam & Broliden, 2009). Protocols for intrauterine management have not been well developed, but intrauterine transfusion to treat anemia is the only currently accepted therapy (de Jong et al., 2006). There is insufficient evidence about the long-term effects of parvovirus (Cunningham et al., 2010).

Enterovirus

Enteroviruses include poliovirus, coxsackievirus, and echovirus. Nonpolio enteroviruses are among the most common viruses that infect humans. Enteroviral infections in the newborn account for about 10% of all reported cases of enterovirus infection in the United States (Khetsuriani, Lamonte, Oberste, & Pallansch, 2006). Group B coxsackieviruses and echovirus 11 are the serotypes most commonly affecting neonates and can be transmitted transplacentally or through exposure to maternal blood or secretions during birth. The risk of transmission is increased with maternal enterovirus illness around the time of birth and a lack of maternal antibodies to the specific type of enterovirus. Antenatal transmission increases the risk of severe disease and death (Tebruegge & Curtis, 2009).

The onset of infection following perinatal transmission is usually within 1 to 2 weeks after birth. Usual presenting symptoms are fever, irritability, lethargy, and poor feeding; rash, respiratory symptoms and gastrointestinal symptoms also can occur. Clinical manifestations can be severe and include myocarditis, meningitis, respiratory distress, and hepatitis. Deaths are usually due to multiorgan involvement (Tebruegge & Curtis, 2009; Wikswo, Khetsuriani, Fowlkes, Zheng, Penaranda, Verma, et al., 2009).

Currently there is no vaccine or any treatment approved by the U.S. Food and Drug Administration (FDA) for nonpolio enteroviruses. Immunoglobulin is sometimes used to treat symptomatic infants. Pleconaril is under investigation as a treatment for enteroviral infection in neonates and infants (Tebruegge & Curtis, 2009).

Group B Streptococci

GBS infection is a leading cause of neonatal morbidity and mortality in the United States (CDC, 2009d). The practice of giving prophylactic antibiotics to women in labor who are GBS positive has significantly reduced the incidence and severity of early-onset GBS infection in the newborn (Yudin & Gonik, 2006). In the United States, the incidence of early onset neonatal GBS infection is 0.4 per 1000 live births and the incidence of late-onset (after 7 days of age) infection is 0.3 per 1000 live births (CDC, 2009d).

Early-onset GBS infection in the neonate usually occurs in the first 7 days of life but most commonly manifests in the first 24 hours after birth. Risk factors for the development of early-onset GBS include low birth weight, preterm birth, rupture of membranes of more than 18 hours, maternal fever, previous GBS infant, maternal GBS bacteriuria, use of intrauterine fetal monitoring, maternal age less than 20 years, and Hispanic or African-American ethnicity. Early-onset disease usually results from vertical transmission from the birth canal and manifests as systemic infection or respiratory illness that mimics the symptoms of severe respiratory distress. The infant can rapidly develop pneumonia, shock, or meningitis. The mortality rate for early-onset infection is approximately 4%, with higher rates among preterm infants (AAP Committee on Infectious Diseases, 2009; Cunningham et al., 2010).

Late-onset GBS infections occur between 1 week and 3 months of age, with an average age at onset of 24 days. Infection can result from vertical transmission or from health care acquired infection or community exposure. Of infants with late-onset GBS, 30% develop meningitis (Edwards, Nizet, & Baker, 2006). Mortality rates are less than for early-onset infection. Survivors often have neurologic damage (Cunningham et al., 2010).

For newborns with suspected GBS infection, the usual treatment is ampicillin in combination with an aminoglycoside. If GBS is identified as the cause of infection, penicillin G alone can be given (AAP Committee on Infectious Diseases, 2009). Figure 35-10 provides a sample algorithm for the management of a neonate whose mother received intrapartum antibiotics for prevention (IAP) of group B streptococcal disease in the newborn or suspected chorioamnionitis.

Escherichia coli

E. coli is responsible for approximately 40% of cases of neonatal sepsis and 80% of cases of neonatal meningitis in the United States (AAP Committee on Infectious Diseases, 2009). It is found in the gastrointestinal tract soon after birth and makes up the bulk of human fecal flora. E. coli can cause a variety of neonatal infections, including omphalitis, diarrheal illness, pneumonia, peritonitis, urinary tract infections, and meningitis. Risk factors for the development of E. coli infections in the newborn include preterm birth, low birth weight, maternal infection, prolonged rupture of membranes, and septic or traumatic birth (AAP Committee on Infectious Diseases).

Neonates most often acquire E. coli from the maternal birth canal or rectum during birth, although it also can be hospital acquired through person-to-person transmission or from the hospital environment. Exposure to E. coli can result in no infection, infection without illness, gastroenteritis, or rarely, septicemia. Symptoms can appear within the first 24 hours after birth or several weeks later. Clinical signs of E. coli sepsis are relatively nonspecific and include fever, temperature instability, apnea, cyanosis, jaundice, hepatomegaly, lethargy or irritability, vomiting, abdominal distention, and diarrhea.

The usual treatment for E. coli infection in the newborn is ampicillin or an extended spectrum cephalosporin and an aminoglycoside. Treatment is continued for 1 to 14 days for bacteremia and 21 days for meningitis (AAP Committee on Infectious Diseases, 2009). Use of ampicillin in labor as prophylaxis against GBS disease has not been found to increase the risk of early-onset E. coli infection (Schrag, Hadler, Arnold, Martell-Cleary, Reingold, & Schuchat, 2006) but can result in more virulent E. coli disease resulting from ampicillin-resistant organisms (Bizzaro, Dembry, Baltimore, & Gallagher, 2008).

Staphylococcus aureus

Most staphylococcal infections in the newborn develop within the first few days after birth and involve the skin and soft tissue. Conjunctivitis, presenting with purulent eye discharge, is also a common manifestation of S. aureus infection. Skin lesions are typically small vesicles or pustules that are easily treated with topical antimicrobial agents. The skin lesions can appear as large fragile bullae containing clear or purulent fluid. These bullae rupture easily and leave moist, red, denuded areas of skin. A more severe bullous eruption due to staphylococcal infection is scalded skin syndrome characterized by widespread bullous lesions that easily rupture; fever and irritability are also present (Narendran & Hoath, 2006). S. aureus can cause serious problems such as abscesses, osteomyelitis, endocarditis, and septic arthritis. Breaks in the skin from IV catheters or scalp electrodes present an opportunity for the development of S. aureus abscesses. Colonization of the maternal genital tract with S. aureus is not uncommon although the potential for vertical transmission to the neonate is unclear (Andrews, Schelonka, Waites, Stamm, Cliver, & Moser, 2008). The major sources of colonization by S. aureus are the hands of medical and nursing personnel.

Although most strains of S. aureus are sensitive to semisynthetic penicillins, there are increasing concerns about methicillin-resistant strains (Gorwitz, 2008). MRSA has caused outbreaks of hospital-acquired infection in neonatal intensive care units and hospital nurseries (Fortunov, Hulten, Hammerman, Mason, & Kaplan, 2006).

Listeriosis

Listeriosis, caused by Listeria monocytogenes, is primarily a foodborne infection that can cause maternal and neonatal illness. Globally it is one of the three major causes of neonatal meningitis (Posfay-Barbe & Wald, 2009). The incidence of neonatal listeriosis in the United States is reported to be approximately 8.6 per 100,000 live births (CDC, 2009b). Although it is relatively uncommon and probably underdiagnosed, it occurs more frequently among pregnant women and those who are older or immunocompromised. Mother-to-child transmission occurs transplacentally, through ascending infection, or during birth. Prenatal infection causes chorioamnionitis or endometritis and should be suspected in cases of brown-stained amniotic fluid. It can also cause miscarriage, preterm birth, and stillbirth. Two forms of neonatal listeriosis are recognized: early onset and late onset. Signs of early-onset infection are present at birth or in the first 1 to 2 days. Manifestations of infection are sepsis-like symptoms, acute respiratory distress, pneumonia, and more rarely, meningitis or myocarditis. With severe infection the infant can have granulomatosis infantiseptum which is a widely disseminated granuloma, causing an erythematous rash with pale papules and abscesses in the liver, lungs, brain, kidneys, spleen, adrenal glands, and GI system. (Posfay-Barbe & Wald, 2009). Late-onset listeriosis is more insidious and usually manifests as meningitis. Listeriosis in the newborn is treated with ampicillin and an aminoglycoside (AAP Committee on Infectious Diseases, 2009).

Chlamydia Trachomatis

Chlamydia trachomatis, the most common reportable sexually transmitted infection in the United States, causes neonatal conjunctivitis (25% to 50% of exposed infants) and pneumonia (5% to 20% of exposed infants). Neonatal infection is acquired by newborns in approximately half of all vaginal births by infected mothers and is known to occur in some infants born by cesarean with intact membranes (AAP Committee on Infectious Diseases, 2009). Chlamydial infection in pregnancy has also been suggested as a cause of early and late pregnancy loss, stillbirth, premature labor, and postpartum endometritis (Yudin & Gonik, 2006).

Neonatal chlamydial conjunctivitis (congestion and edema), with minimal discharge, develops within a few days to several weeks after birth and usually lasts 1 to 2 weeks. If untreated, it can progress to chronic follicular conjunctivitis with conjunctival scarring and corneal microgranulations.

Chlamydial pneumonia usually has a gradual onset, between 4 and 11 weeks of age, beginning with rhinorrhea and progressing to tachypnea and coughing (Yudin & Gonik, 2006). Signs may be quite subtle and often go unrecognized. It is speculated that pneumonia can occur as a result of movement of the organism from the conjunctiva into the lower respiratory tract; however, conjunctivitis is not a prerequisite to pneumonia.

Chlamydial conjunctivitis is treated with oral erythromycin or ethylsuccinate for 14 days. The recommended treatment for chlamydial pneumonia is oral azithromycin for 3 days or a 14-day regimen of erythromycin or ethylsuccinate. Erythromycin administration in infants younger than 6 weeks has been associated with an increased risk of infantile hypertrophic pyloric stenosis; therefore, parents should be educated regarding the symptoms of the condition (feeding intolerance, projectile vomiting, and abdominal distention) (AAP Committee on Infectious Diseases, 2009).

Candidiasis

Candida infections, formerly known as moniliasis, can occur in the newborn. Candida albicans, the organism usually responsible, can cause disease in any organ system. It is a yeastlike fungus (producing yeast cells and spores) that can be acquired during birth from a maternal vaginal infection; by person-to-person transmission; or from contaminated hands, bottles, nipples, or other articles. It usually is a benign disorder in the neonate, often confined to the oral and diaper regions (Wilson & da Cunha, 2007).

Candidal diaper dermatitis appears on the perianal area, inguinal folds, and lower portion of the abdomen. The affected area is intensely erythematous, with a sharply demarcated, scalloped edge, frequently with numerous satellite lesions that extend beyond the larger lesion. The source of the infection is through the GI tract. Treatment is an antifungal ointment, such as nystatin (Mycostatin) or miconazole 2% (Monistat), applied with each diaper change. The infant also can be given an oral antifungal preparation to eliminate any GI source of infection (Wilson & da Cunha, 2007).

Oral candidiasis (thrush, or mycotic stomatitis) is characterized by the appearance of white plaques on the oral mucosa, gums, and tongue. The white patches are easily differentiated from milk curds; the patches cannot be removed and tend to bleed when touched. In most cases, the infant does not seem to be in discomfort from the infection. A few infants seem to have some difficulty swallowing.

Infants who are sick, debilitated, or receiving antibiotic therapy are more susceptible to thrush. Those with cleft lip or palate, neoplasms, and hyperparathyroidism seem to be more vulnerable to mycotic infection.

The objectives of management are to eradicate the causative organism, to control exposure to C. albicans, and to improve the infant’s resistance. Interventions include maintenance of scrupulous cleanliness to prevent reinfection (nursing personnel, parents, others). Careful hand hygiene is always essential. Clean surfaces should be provided for neonates. Proper cleanliness of the equipment and environment is essential. If the infant is breastfeeding, the mother also is treated with a topical antifungal preparation such as nystatin applied to the nipples.

For the infant, topical application of 1 ml nystatin over the surfaces of the oral cavity four times a day, or every 6 hours, is usually sufficient to prevent spread of the disease or prolongation of its course. Several other drugs can be used, including amphotericin B (Fungizone), clotrimazole (Lotrimin, Mycelex), fluconazole (Diflucan), or miconazole (Monistat, Micatin) given intravenously, orally, or topically. To prevent relapse, therapy should be continued for at least 2 days after the lesions disappear. Gentian violet solution can be used in addition to one of the antifungal drugs in chronic cases of oral thrush; however, the former does not treat GI candida and can irritate the oral mucosa.

Infants who are breastfed can acquire thrush from the mother. If the mother is colonized, treatment for mother and infant is recommended. Breastfeeding can continue even if the mother is receiving systemic antifungal medications.

Caffeine

Caffeine is a mild CNS stimulant that is consumed on a regular basis by more than 85% of adults and children and 68% of pregnant women in the United States (Frary, Johnson, & Wang, 2005). Coffee is the primary source of caffeine for most Americans, although caffeine is also found in tea, chocolate, colas, energy drinks, guarana, and mate (a tea consumed primarily in South America).

The average half-life of caffeine ranges from about 3 to 7 hours with individual variation in metabolism related to genetic and environmental factors. During the second and third trimesters of pregnancy, caffeine metabolism is slowed due to hormonal influences. Caffeine readily crosses the placenta and is distributed to all fetal tissues. Because of immature liver function, fetuses metabolize caffeine very slowly.

Although caffeine has not been implicated as a teratogen in humans, there are concerns about caffeine consumption during pregnancy. The effects of caffeine seem to be dose dependent; that is, the risk increases with greater caffeine consumption. High maternal intake of caffeine (more than 200 to 300 mg/day) increases the risk of miscarriage and low birth weight (Higdon & Frei, 2006; Weng, Odouli, & Li, 2008).

The American Dietetic Association recommends that caffeine intake in pregnant women should not exceed 300 mg/day (Kaiser & Allen, 2008). The March of Dimes more conservatively recommends no more than 200 mg/day for women who are pregnant or are planning to become pregnant (March of Dimes, 2010).

Selective Serotonin Reuptake Inhibitors

Antidepressant medication is the mainstay treatment for maternal depression with selective serotonin reuptake inhibitors (SSRIs) being the first line of pharmacotherapy. Commonly prescribed SSRIs include citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline (Cunningham et al., 2010). The American College of Obstetricians and Gynecologists (2008) published guidelines for the use of psychiatric medications in women who are pregnant and breastfeeding. All medications that have been studied are known to cross the placenta and are transferred in breast milk. Their use should be determined by a risk/benefit analysis of the risks to the fetus/neonate with use of the medication weighed against risks of not treating the mother’s psychiatric condition. Risks of nontreatment include noncompliance with prenatal care, poor nutrition, substance abuse, and interference with maternal-infant bonding (ACOG).

Based on current evidence, the ACOG (2008) has concluded that the absolute risk of any congenital abnormality associated with maternal SSRI use is small. However, certain medications carry greater risk than others. Because of the risk of cardiac defects associated with maternal paroxetine treatment, the ACOG (2008) warns that paroxetine use should be avoided during pregnancy and in women considering pregnancy. There have also been reports linking paroxetine use to other anomalies such as omphalocele, craniosynostosis, and anencephaly.

Fetal exposure to SSRIs predisposes the neonate to a behavioral syndrome resembling neonatal abstinence syndrome. Symptoms include irritability, agitation, tremors, nasal congestion, tachypnea, emesis, and diarrhea. This syndrome is usually mild and lasts for no longer than 2 days. In rare cases the syndrome is severe with seizures, hyperpyrexia, excessive weight loss, and respiratory problems (Cunningham et al., 2010). Persistent pulmonary hypertension in the newborn (PPHN) has been reported in infants who were exposed to maternal SSRIs after 20 weeks of gestation; the risk for PPHN was 6 to 12 per 1000 births (Chambers, Hernandez-Diaz, Van Marter, Werler, Louik, Jones, et al., 2006).

For parents who are concerned about maternal use of psychiatric medications and the fetal or neonatal effects, the nurse can direct them to the following websites: REPROTOX (www.reprotox.org) and TERIS (http://depts.washington.edu/terisweb) (ACOG, 2008).

Nursing Care

Planning for care of the infant born to a substance-abusing mother presents a challenge to the health care team. Parents are included in the planning for the newborn’s care and for the care and support of the mother and her newborn at home. A multidisciplinary approach includes home health or community resource personnel (e.g., regulatory agencies such as child protective services).

Education and social support to prevent the abuse of drugs provide the ideal approach. However, given the scope of the drug abuse problem, total prevention is an unrealistic goal.

Nursing care of the drug-dependent neonate involves supportive therapy for fluid and electrolyte balance, nutrition, infection control, and respiratory care. Swaddling, holding, reducing stimuli, and feeding as necessary can be helpful in easing withdrawal (see the Nursing Care Plan: The Infant Experiencing Drug Withdrawal [Neonatal Abstinence Syndrome]). Specific suggestions for providing care to infants experiencing withdrawal are listed in the Box 35-4.

Pharmacologic treatment is usually based on the severity of withdrawal symptoms, as determined by an assessment tool (see Fig. 35-13). When indicated, medications are given as ordered. Neonatal tincture of opium (0.4 mg/ml of morphine equivalent), phenobarbital, and, less commonly, paregoric may be used to control symptoms. Treatment may be needed for 2 weeks or more.

The issue of breastfeeding in this population is a difficult one. Although breast milk remains the optimal source of nutrition for these infants, care must be taken to avoid exposing the infant to additional drugs through the breast milk. According to the AAP Committee on Drugs (2001), nursing mothers should not ingest drugs of abuse including amphetamine, cocaine, heroin, marijuana, and phencyclidine because they are hazardous to the breastfeeding infant and to the mother.

Drug dependence in the neonate is physiologic, not psychologic. Thus a predisposition to dependence later in life is not believed to be a factor. However, the psychosocial environment in which the infant is raised may create a tendency to addiction.

The mother requires considerable support. Her need for and her abuse of drugs can result in a decreased capacity to cope. The infant’s withdrawal signs and decreased consolability stress her coping abilities even further. Family members also need support as they assist in caring for the infant. Home health care, treatment for addiction, and education are importantconsiderations. Sensitive exploration of the woman’s options for the care of her infant and herself and for future fertility management may help her see that she has choices. This approach helps communicate respect for the new mother as a person who can make responsible decisions.