Pediatric emergency medicine trisk 646

Symptoms

Signs

Respiratory
Increased work of breathing
Cough
Cyanosis

Cardiac
Pallor

Gastrointestinal
Poor feeding
Vomiting
Diarrhea
Skin and musculoskeletal
Hypothermia
Fever
Jaundice
Floppiness
Neurologic
Lethargy
Irritability
Seizures
Laboratory abnormalities
CBC
High WBC count
Low WBC count
High ANC

Tachypnea
Desaturations
Hyperventilation
Respiratory distress (grunting, flaring,
retractions)
Apnea
Tachycardia
Bradycardia
Hypotension
Poor capillary refill
Shock
Abdominal distention
Ileus

Low temperature
High temperature
Hypotonia
Petechiae
Rash
Full anterior fontanelle
Hypertonia or hypotonia
Meningismus (occasional)
Electrolytes: metabolic acidosis,
hypernatremia, hyponatremia
Liver function tests: hyperbilirubinemia (direct
or indirect)


Low ANC (neutropenia)
High immature to total

WBC (>0.2)
Thrombocytopenia
CRP: elevated
Blood sugar: hyperglycemia
Hypoglycemia Coagulation
studies: DIC
WBC, white blood cells; DIC, disseminated intravascular coagulopathy; ANC, absolute neutrophil count.

Triage Considerations. Any symptomatic neonate should be assessed for the
possibility of neonatal sepsis. Neonates should be triaged urgently due to the
potential for rapid deterioration. Shock and respiratory distress demand emergent
treatment and initiation of resuscitation. Rapid establishment of intravenous
access and urgent antibiotic therapy are needed. Meningitis can present in a
similar fashion and could be part of the systemic infection.
Clinical Assessment. History of GBS colonization in the mother,
chorioamnionitis, prolonged rupture of membranes, maternal postpartum
antibiotic use, or presence of maternal symptoms of infection (fever, rash, or
URI) may raise clinicians’ suspicion of early infection. Presence of sick contacts,
CHD, and prematurity are risk factors that may be elicited in late-onset disease.
Physical examination may be notable for hypothermia or fever and may reveal a
localized source of infection (e.g., pneumonia, meningitis, septic arthritis,
herpetic rash, NEC, or omphalitis). However, examination findings are usually
nonspecific ( Table 96.7 ). Neonates with signs of shock should be presumed to
have neonatal sepsis but should also be evaluated for coarctation of the aorta and
cardiogenic shock. Clinicians can attempt to narrow diagnosis by history and
physical examination to a specific cause, however, this can be very difficult.
Complete blood count with differential will reveal leukocytosis or leukopenia,
and may also show neutropenia, elevated immature to total white blood cell
(WBC) ratio above 0.20 (calculated as immature cells [bands + myelocytes +
metamyelocytes] divided by total neutrophils). C-reactive protein (CRP) is an

acute phase reactant that becomes elevated 6 to 8 hours after infection. It reaches
peak around 24 hours after initiation of infection and can be used to monitor
response to treatment, and optimize duration of treatment. Other acute phase
reactants and cytokines are being studied as markers of disease including
procalcitonin and interleukin (IL)-6, IL-8, tumor necrosis factor-alpha, and


granulocyte colony–stimulating factor but are not commonly used clinically.
CBC, CRP, and other nonspecific markers are useful indicators of disease. None
of these tests alone or in combination are sensitive enough to be used solely to
exclude the diagnosis of bacterial infection.
Definitive diagnosis is isolation of a specific pathogen from a normally sterile
site, such as blood, urine, or CSF culture. Blood samples for culture should be at
least 1 mL to allow for identification of low levels of bacteremia. A catheterized
urine specimen or suprapubic aspiration for urinalysis and urine culture is
recommended for all infants since ascending infection can lead to bacteremia.
CSF will show elevation in WBC count (20 to 30 cells/μL definitive), high
protein, and/or low glucose in bacterial infections. HSV encephalitis may
demonstrate elevated CSF protein only. CSF Gram stain may show presence of
bacteria. Lumbar puncture prior to antibiotic administration is recommended for
all neonates due to high incidence of meningitis (23%) in cases of bacteremia and
up to 30% of neonates may have a negative blood culture even in the presence of
bacterial meningitis. Lumbar puncture can be deferred if the infant has
hemodynamic instability but should be performed as soon as the infant is stable.
Infants should be placed on cardiorespiratory monitors during the lumbar
puncture procedure. Traumatic results should be interpreted with care. Correction
of CSF WBC count according to the RBC count in traumatic taps does not
improve the ability to diagnose meningitis. Clinicians should avoid this
correction and presume meningitis until the CSF culture results are available.
Other specific testing can be done (e.g., HSV CSF PCR, liver function tests, and

CSF enteroviral PCR) if specific pathogens are suspected. CXR can be helpful if
the neonate has respiratory or cardiac symptoms but is not routine.
Management. Any neonate with concern for bacterial or serious viral infection
should be admitted to the hospital. Initial management should include placing the
infant on cardiorespiratory monitoring, with vital sign monitoring and clinical
reassessments. Normal saline boluses may be given in cases of hypoperfusion and
shock. Blood pressure stabilization with pressors may be needed. In some cases
hydrocortisone may be required. Hypothermia should be corrected by gradual
warming of the baby. Hypoglycemia and electrolyte abnormalities should also be
corrected. Oxygen, humidified nasal cannula, or other respiratory support may be
needed for neonates with apnea or respiratory distress.
Antibiotics should be given as soon as possible. Whenever feasible, cultures
should be obtained before starting antibiotics. Obtaining cultures and starting
antibiotics are a priority. Lumbar puncture may be delayed if the baby is unstable.


Intravenous ampicillin and an aminoglycoside are recommended for early-onset
sepsis. For full-term infants less than 7 days of age, 200 to 300 mg/kg/day of
ampicillin, intravenously, in three divided doses is the recommended dose; for
newborns beyond 7 days of age, 300 mg/kg/day, intravenously, in four divided
doses is recommended. Cefotaxime can be added for better CNS penetration if
gram-negative meningitis is suspected or if renal dysfunction precludes the use of
an aminoglycoside. Ceftriaxone should be avoided in neonates due to possibility
of exacerbating hyperbilirubinemia as a result of bilirubin displacement from
albumin, and the possibility of precipitating sludging in the gall bladder.
Intravenous vancomycin should be considered in neonates who have been at
home and exposed to community-acquired Staphylococci. Intravenous
vancomycin and an aminoglycoside are recommended for empiric therapy of lateonset sepsis until isolation of the specific pathogen occurs; at which time
antibiotic therapy can be tailored accordingly. Acyclovir should be considered if
there is suspicion for herpes simplex infection (suspicious vesicular rash,

transaminitis, or history of exposure). Doses and intervals of antibiotics and
antivirals can vary according to postgestational age, renal function, and liver
function. For an expanded discussion on fever in children 1 to 3 months of age,
please refer to Chapter 31 Fever .

Pneumonia in the Newborn
Neonatal pneumonia, similar to neonatal sepsis, can occur early (within the first
72 hours of life) or late (after 1 week of life). Early-onset pneumonia occurs as a
result of vertical transmission during the perinatal period, possibly through
aspiration of infected amniotic fluid or chorioamnionitis. Although Group B
streptococcal infection is the most common pathogen, other organisms similar to
those causing early sepsis can be responsible for infection (bacteria, viruses, and
fungi). Chlamydia trachomatis is also acquired perinatally. The long incubation
period in neonates causes infants to present around 2 to 4 weeks of age with an
insidious onset of a staccato cough without fever or wheezing. Infants who pass
through a vaginal canal infected with C. trachomatis have a 3% to 16% risk of
developing pneumonia. Tuberculosis and syphilis can also cross the placenta to
infect the fetus.
Late-onset pneumonia occurs as a result of horizontal transmission from the
infant’s surrounding environment; Streptococcus pneumoniae is the most
common organism. Other etiologic agents that cause late-onset sepsis are also
implicated in development of pneumonia. Acute respiratory failure and rapidly
evolving pneumonia can occur as a result of Bordetella pertussis infection in