Seizures - Case 19-1: 8-Day-Old Girl
Seizures - Case 19-1: 8-Day-Old Girl: Excerpt from Pediatric Complaints and Diagnostic Dilemmas
I. History of Present Illness
An 8-day-old girl presented to the emergency department after an episode of
irregular, rapid breathing followed by stiffening of her body and shaking of
her extremities that lasted several seconds. On arrival, the infant was
lethargic, cyanotic, and bradycardic with minimal spontaneous respirations. She
underwent emergency endotracheal intubation and received multiple boluses of
normal saline, with improvement in her perfusion and heart rate.
She then had a generalized seizure and received intravenous lorazepam.
Ampicillin and cefotaxime were administered after a blood culture was obtained.
According to the family, she had fed poorly that day and had been sleeping more
than usual. The infant had been afebrile and had had normal stooling and urine
output. There was no vomiting, diarrhea, or rashes. There were no ill contacts.
II. Past Medical History
The infant weighed 3,400 g at birth and was the product of a full-term
gestation. She was born by spontaneous vaginal delivery after an uncomplicated
pregnancy. Maternal serology was negative. The infant
's postnatal course was remarkable only for mild jaundice that did not require
phototherapy. The mother denied a history of genital HSV infection. There was
no family history of seizures.
III. Physical Examination
T, 39.0°C; RR, 20/min; HR, 180 bpm; BP, 86/45 mm Hg; SpO2, 100% in room air
Weight, 25th percentile; head circumference, 50th percentile
Examination revealed a mechanically ventilated infant. She was sedated but
withdrew in response to painful stimuli. The fontanel was bulging. There were
no head lacerations or skull depressions. The sclerae were anicteric, and the
pupils were 1.5 mm and symmetrically reactive. There were no cardiac murmurs,
and the femoral pulses were weakly palpable. The lungs were clear to
auscultation. The abdomen was soft, and the umbilical stump was well healed
without erythema or discharge. There were two pustules in the perineal area.
IV. Diagnostic Studies
Laboratory results were as follows: sodium, 132 mEq/L; potassium, 3.3 mEq/L;
chloride, 99 mEq/L; bicarbonate, 23 mEq/L; glucose, 73 mg/dL; calcium, 8.9
mg/dL; and magnesium, 2.1 mg/dL. The complete blood count revealed 8,000
WBCs/mm
3, including 33% band forms, 18% segmented neutrophils, 35% lymphocytes, and 10%
monocytes. The hemoglobin and platelet count were normal. On cerebrospinal
fluid (CSF) examination, there were 879 WBCs/mm
3 (48% segmented neutrophils, 19% lymphocytes, and 33% monocytes) and 1,739 red
blood cels/mm
3; no organisms were seen on Gram staining. The CSF glucose concentration was 36
mg/dL, and the protein concentration was 400 mg/dL. CSF was sent for bacterial
culture and detection of HSV by polymerase chain reaction (PCR). There were no
abnormalities on chest radiograph.
V. Course of Illness
In the intensive care unit, the patient received ampicillin, gentamicin, and
acyclovir. A head computed tomogram (CT) was normal, and the patient
's neurologic examination improved quickly over the next day. She was extubated
on the second day of hospitalization but required replacement of the
endotracheal tube due to multiple episodes of apnea. Electroencephalography
(EEG) revealed status epilepticus. Sustained seizure control was observed only
after the addition of phenobarbital and phenytoin. Because HSV was not detected
in the CSF by PCR, acyclovir was discontinued. Growth of an organism from the
CSF on the third day of hospitalization guided additional therapy.
Discussion: Case 19-1
I. Differential Diagnosis
Seizures are a feature of almost all brain disorders in the newborn. The time of
onset of the first seizure is helpful in determining the cause. The causes of
neonatal seizures that occur after the first 72 hours of life include
intracranial infection, intracranial hemorrhage, metabolic abnormalities,
developmental defects, and drug withdrawal. Intracranial infections occur in 5%
to 10% of neonatal seizures, and after 72 hours of life group B streptococci
and
Listeria monocytogenes are common bacterial causes. Seizures with HSV typically occur during the second
week of life, and 30% of infected infants present with a vesicular rash.
Intracranial hemorrhages are frequently associated with hypoxic-ischemic or
traumatic birth injury. Intraventricular hemorrhages principally occur in the
premature infant, and subarachnoid and subdural hemorrhages usually occur in
the term infant. Metabolic abnormalities include disturbances of glucose,
calcium, magnesium, and sodium. Hypocalcemia is associated with low birth
weight, asphyxia, maternal diabetes, transient neonatal hypoparathyroidism, and
microdeletions of chromosome 22q11. Other metabolic abnormalities include
inborn errors of metabolism, especially aminoacidurias, because protein and
glucose feedings have been initiated. Aberrations of brain development are
usually related to a disturbance of neuronal migration such as lissencephaly,
pachygyria, or polymicrogyria. Passive addiction of the newborn and drug
withdrawal may involve narcotic-analgesics (methadone), sedative-hypnotics
(shorter-acting barbiturates), cocaine, alcohol, or tricyclic antidepressants.
In the case described, the results of CSF analysis were suggestive of
intracranial infection, but interpretation of the Gram stain was misleading.
II. Diagnosis
The diagnosis is meningitis due to L. monocytogenes, a gram-positive rod. On the fourth day of hospitalization, the organism was
noted to have only intermediate susceptibility to ampicillin. The patient was
switched to intravenous vancomycin, and gentamicin was continued. CSF from the
lumbar puncture, repeated on the sixth day of hospitalization, was sterile.
Head CT was repeated on the eighth day of hospitalization and revealed
bilateral frontal, parietal, and temporal lobe infarcts but no
ventriculomegaly. Mechanical ventilation was required until the ninth day of
hospitalization. The infant was discharged after 21 days of antibiotic therapy.
III. Incidence and Epidemiology
L. monocytogenes, a motile gram-positive rod, was first isolated in 1926 during an investigation
of epidemic perinatal infection among a colony of rabbits. It is a common
veterinary pathogen that causes meningoencephalitis in sheep and cattle. It is
widespread in the environment and is found commonly in soil and decaying
vegetation. Many foods are contaminated with this organism; it has been
recovered from raw vegetables, fish, poultry, unpasteurized milk, and certain
types of cheese. The organism has been isolated from the stools of 5% of
healthy adults, and higher rates of recovery have been reported for household
contacts of patients with clinical infection. Infection in humans is uncommon
but occurs most frequently in neonates, pregnant women, and elderly or
immunosuppressed patients. Approximately 30% of all
L. monocytogenes infections occur in neonates.
IV. Clinical Presentation
Neonatal L. monocytogenes infection, like group B streptococcal infection, manifests in both an early- and
a late-onset form. Clinical manifestations of
L. monocytogenes infection are similar to those of other neonatal bacterial infections. Signs of
infection include temperature instability, respiratory distress, irritability,
lethargy, and poor feeding. In early-onset disease, transplacental transmission
after maternal bacteremia or ascending spread from vaginal colonization leads
to intrauterine infection with
L. monocytogenes. Preterm labor is common among infants with early-onset L. monocytogenes infection; length of gestation is less than 35 weeks in approximately 70% of
cases. There is often evidence of an acute febrile maternal illness, with
symptoms of fatigue, arthralgias, and myalgias preceding delivery by 2 to 14
days. Blood cultures are positive for
L. monocytogenes in 35% of mothers of infants with early-onset listeriosis.
Early-onset infection classically develops within the first or second day of
life. Bacteremia (75%) and pneumonia (50%) are usually seen with early-onset
infection. Meningitis is seen in 25% of early-onset cases. In severe infection,
a granulomatous rash is associated with disseminated disease (granulomatosis
infantisepticum). The mortality rate, including stillbirths, is 40% for
early-onset infection. In late-onset infection, modes of transmission unrelated
to maternal carriage may be involved. Late-onset infection develops during the
second to eighth week of life. The most common form
of L. monocytogenes infection over this period is meningitis, which is present in approximately 95%
of cases. Bacteremia (20%) and pneumonia (10%) are less common. Mortality of
late-onset infection is generally low (15%) if the infection is diagnosed early
and treated appropriately.
A nosocomial outbreak occurred when nine newborn infants were bathed in mineral
oil contaminated with
L. monocytogenes. The affected infants developed bacteremia (two cases), meningitis (two cases),
or both (five cases); one infant died. Signs of infection developed within 1
week after exposure to the mineral oil.
V. Diagnostic Approach
Lumbar puncture. Isolation of the organism from culture of CSF is the only reliable means of
diagnosing meningitis due to
L. monocytogenes. The finding of short, sometimes coccoid, gram-positive rods on microscopic
examination of the CSF strongly supports the diagnosis of
L. monocytogenes meningitis. However, because of the low concentration of organisms, most (60%)
Gram-stained smears of CSF from infants with
L. monocytogenes meningitis do not reveal bacteria, as occurred with the infant in this case.
Furthermore,
L. monocytogenes sometimes does not stain clearly as gram positive. In such cases, variable
decoloration on Gram staining may cause the organism to appear as a
gram-negative rod and be confused with
Haemophilus influenzae, especially with long-standing disease or when the patient has received prior
antibiotics. In other instances,
Listeria has been mistaken for Streptococcus pneumoniae or for Corynebacterium spp. CSF glucose is normal in more than 60% of cases. Mononuclear cells
predominate in one third of cases.
Additional studies. PCR probes and antibodies to listeriolysin O, the major virulence factor of the
organism, have not proved useful for acute diagnosis of invasive disease.
VI. Treatment
Ampicillin is the preferred agent in the treatment of L. monocytogenes infections. Based on synergy studies in vitro and in animal models, most authorities suggest adding gentamicin to ampicillin
for the treatment of meningitis due to
L. monocytogenes. There appears to be partial synergy with combinations of ampicillin or
vancomycin with rifampin. Vancomycin alone has been used successfully in a few
penicillin-allergic adult patients, but others have developed listerial
meningitis while receiving the drug. Trimethoprim-sulfamethoxazole is effective
for penicillin-allergic patients but should not be used in neonates because of
the concern of bilirubin toxicity. Cephalosporins are not active against
L. monocytogenes. Once susceptibility studies become available, changes in therapy may be
necessary. Treatment of
L. monocytogenes meningitis should continue for a minimum of 3 weeks.
Corticosteroids should be avoided, if possible, because impairment of cellular
immunity due to corticosteroid therapy is a major risk factor for the
development of listeriosis. A maternal history of a previous infant with
perinatal listeriosis is not an indication for intrapartum antibiotics.
VII. References
1. Bortolussi R, Schlech WF III. Listeriosis. In: Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant. Philadelphia: WB Saunders, 2001;1157–1177.
2. Lorber B. Listeriosis. Clin Infect Dis 1997;24:1–11.
3. Schuchat A, Lizano C, Broome CV, et al. Outbreak of neonatal listeriosis
associated with mineral oil.
Pediatr Infect Dis J 1991;10:183–189.
4. Southwick FS, Purich DL. Mechanisms of disease: intracellular pathogenesis
of listeriosis.
N Engl J Med 1996;334:770–776.
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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