Pediatric emergency medicine trisk 647

neonates born to mothers not previously exposed to pertussis or with inadequate
vaccination. These neonates will not have passive immunity from maternal
antibodies. It can present either as an early- or late-onset pneumonia after contact
with an infected family member or sibling.
Neonates with pneumonia present with respiratory distress and increase in
nasal and respiratory secretions. Signs and symptoms similar to neonatal sepsis
can be nonspecific ( Table 96.7 ). Viral infection with RSV, influenza,
parainfluenza viruses, adenovirus, and metapneumovirus can produce a similar
presentation. Apnea is a common presentation in RSV infection.
All neonates with suspected pneumonia should receive a complete workup,
including CBC, CRP, blood, urine, and CSF cultures. CXR may show patchy
infiltrates with air bronchograms, diffuse haziness, or lobar or segmental
consolidation. Pleural effusions are common but CXRs may also be normal in
15% of cases. CXR in babies with C. trachomatis may show hyperinflation with
infiltrates. Nasopharyngeal aspirates can be sent for direct immunofluorescence
or PCR to diagnose chlamydial pneumonia.
Neonatal pneumonia should be differentiated from other pulmonary etiologies
(pneumothorax) and nonpulmonary etiologies of respiratory distress (e.g.,
choanal atresia, tracheoesophageal fistula, CHD, and metabolic etiologies).
Empiric treatment with broad-spectrum antibiotics is indicated similar to
neonatal sepsis. Supportive treatment including intravenous fluids, correction of
electrolyte disturbances, and respiratory support should be initiated as needed.
Therapy should be tailored according to the organism. Oral erythromycin or
azithromycin is indicated for chlamydial infection. Mothers and their partners
should also be treated. Infants born through a vaginal canal infected with
chlamydia are at high risk of contracting pneumonia or conjunctivitis. They
should be observed for emergence of signs and symptoms. Efficacy of antibiotic
prophylaxis is unknown.

Urinary Tract Infections in the Newborn
UTIs occur in 0.1% to 1% of neonates. They are more common in uncircumcised

males because of limited retraction and increased bacterial burden in the foreskin.
This holds true up to 1 year of age, after which the incidence is higher in females.
E. coli is responsible for 50% to 80% of UTIs. E. coli has increased virulence
factors that facilitate adherence and propagation of the organisms. Other gramnegative bacteria can be etiologic agents but gram-positive organisms may also
contribute. Infectious spread to the urinary system can occur hematogenously
from bacteremia (30% of cases) or from an ascending infection. Twenty to 50%


of neonates who develop a UTI will have a congenital abnormality of the
genitourinary tract that facilitates stasis of urine or propagation of bacteria (e.g.,
hydronephrosis, posterior urethral valves, ectopic ureter, duplication of the
collecting system, renal dysplasia). VUR may be the only abnormality. Signs and
symptoms are similar to those of neonatal sepsis ( Table 96.7 ). Fever and poor
feeding are the most common presenting symptoms. Direct hyperbilirubinemia,
prolonged jaundice, or new onset of jaundice in a newborn after 8 days of life is
suspicious for a UTI. One percent to 2% of babies with UTI will develop
meningitis. Neonates suspected of having a UTI should undergo a full sepsis
workup including blood, urine, and CSF cultures. Urinalysis alone for diagnosis
of UTI lacks specificity and sensitivity. Infants frequently void, which does not
allow for an adequate concentration of nitrites or leukocyte esterase to form in the
urine. Urine culture should be obtained by catheterization or suprapubic
aspiration and not from a bagged specimen. Presence of more than 10,000
colony-forming units/mL in a catheterized urine culture with positive urinalysis
or dipstick is significant. Neonates should be admitted for observation and
intravenous antibiotics after obtaining cultures.

Other Viral Infections of the Newborn
Neonates often develop specific viral infections that have characteristic
manifestations different from bacterial infection. The goal of treatment is to
determine differences between these viral infections and neonatal sepsis. Often

this is not possible until after admission and testing.
CLINICAL PEARLS AND PITFALLS
Sixty percent to 80% of mothers who transmit HSV to their newborns
have not had a history of a prior genital infection.
Consider HSV in neonates who have abnormal liver function tests.
Enteroviral infections are more severe in the neonate than children
resulting in meningitis, acute fulminant hepatitis, and heart failure from
myocarditis.
Consider sending enteroviral PCR from a CSF sample in babies with
signs and symptoms of neonatal sepsis and high liver functions.

Neonatal Herpes Simplex Virus Infection
Neonatal HSV disease can result from infection with HSV-1 or HSV-2. It is still
very rare, occurring in only 1:3,200 deliveries. Infection occurs through vertical


transmission in utero (congenital infection) (5%), or while passing through an
infected birth canal (intrapartum) (85%), or from contact with infected oral
secretions (postpartum) (10%).
Maternal HSV infection can be described as first-episode primary infection,
first-episode nonprimary infection, and recurrent infection. First-episode primary
infections occur in mothers who have never been previously exposed to infection.
First-episode nonprimary infections occur when a mother has had HSV-1
previously and then becomes infected with HSV-2 (or vice versa) since HSV-1
and HSV-2 share significant cross reactivity. Recurrent maternal infection implies
that the mother has had a previous exposure and has formed protective antibodies
that are conveyed to the baby but is having a reactivation.
Recurrent infections are responsible for 50% of the cases of neonatal HSV
because recurrent maternal outbreaks occur more commonly than primary
infections. However, primary infections are more severe in nature than recurrent

episodes due to the absence of maternal antibodies and shedding of higher
quantities of HSV for longer periods of time. About 30% of pregnant women will
have serologic evidence of HSV-2, the majority without prior history of
symptoms or infection.
Complete perinatal history may reveal the occurrence of genital outbreaks
before or shortly after birth. History of contact with a person who has had cold
sores or presence of breast lesions in breast-feeding mothers may be helpful.
Maternal history of a genital infection is often unclear due to the possibility of
asymptomatic or subclinical infections. It is estimated that 60% to 80% of women
whose infants develop HSV do not have a prior history of genital infection or
symptoms. Mothers with a history of recurrent HSV infection have a 2% chance
of transmitting infection to their newborn at delivery during active shedding. The
chance of transmission increases to 57% in first-episode primary maternal
infection and 25% in first-episode nonprimary infection. History may also reveal
the presence of risk factors such as a primary infection, vaginal delivery,
prolonged rupture of membranes (>4 to 6 hours), use of fetal scalp electrode, or
disruption of the skin during vacuum extraction.
HSV disease in neonates is usually symptomatic. It can present in two forms:
(a) Congenital HSV infection from an in utero transmission (characterized by
vesicular skin lesions, or scarring, neurologic lesions [microcephaly,
hydranencephaly, intracranial calcifications, hypertonicity, or seizures] and ocular
findings [chorioretinitis, microphthalmia, cataracts, or optic atrophy]) or (b)
neonatal HSV, which may present 2 to 3 weeks after discharge from the newborn
nursery.


Neonatal HSV, like neonatal sepsis, can have nonspecific symptoms ( Table
96.7 ). Neonatal HSV classically produces three presentations (skin, eyes, mouth
[SEM] [45%], CNS disease [30%], or disseminated HSV [25%]). Fever occurs in
30% of neonates with HSV, whereas 20% present with hypothermia. While HSV

is uncommon, the overall incidence of HSV in febrile neonates is approximately
1%. Neonates presenting with fever, irritability, and CSF pleocytosis should be
worked up for HSV disease, particularly if seizures occur.
SEM disease presents with vesicular eruptions usually 10 to 12 days after birth.
Clusters of vesicles appear on the skin and mucous membranes without
involvement of any other organ system, particularly the scalp for neonates born
with cephalic presentations. Herpetic keratitis can lead to corneal scarring.
CNS disease presents with mucocutaneous lesions that appear around 17 to 19
days, as well as neurologic manifestations (seizures, bulging anterior fontanelle,
and lethargy). Absence of skin lesions does not rule out CNS disease; 30% to
60% of infants with CNS disease do not have mucocutaneous lesions.
Neonates with disseminated disease typically present at about 10 to 12 days
with septic shock. These infants have the worst prognosis. Multiple organ
systems involvement produces acute hepatitis, respiratory distress, pneumonia,
pleural effusions, adrenal disease, neurologic manifestations, pneumatosis
intestinalis, and disseminated intravascular coagulopathy. Again, absence of skin
lesions (up to 40%) does not exclude disseminated disease.
Neonates suspected of having HSV disease should undergo a full sepsis
workup including CBC, urinalysis and urine culture, blood culture, liver
functions, lumbar puncture, and HSV cultures. Isolation of HSV by culture
(blood, CSF, and surface cultures) (swabbing the conjunctiva, mouth,
nasopharynx, and ending with the rectum then placing swabs in one viral media
containing tube) remains the definitive diagnostic method. HSV cultures can be
obtained from skin lesions. Diagnosis of HSV can also be confirmed by PCR
from CSF samples. CSF PCR for HSV should be accompanied by surface
cultures. CSF will show mild pleocytosis with abundant mononuclear cells,
elevated protein level, normal glucose concentration, and a negative Gram stain.
Infants suspected of having any form of HSV disease, even SEM, should have a
lumbar puncture performed. Blood HSV PCR can also be obtained but not
enough data are available to recommend its routine use. Liver functions may

show elevated alanine aminotransferase (ALT). Electroencephalogram (EEG)
may show nonspecific findings but occasionally temporal lobe seizures may be
seen. Transfer of maternal antibodies makes serologic tests in neonates difficult to
interpret and therefore not useful.