Goals of Treatment
The goals of treatment are to recognize which children may be at higher risk for bacteremia than the general
pediatric population (e.g., asplenic children, children with central venous catheters [CVCs], neutropenic children)
and to be cognizant of the most common organisms causing bacteremia seen in a given region. Thus, knowledge of
local antibiotic resistance patterns is critical for the ED physician.
Clinical Considerations
Clinical recognition: Children at highest risk for bacteremia are under 2 years of age. For meningococcus, biphasic
peaks occur: one during infancy and a second during adolescence. Thus, algorithms for fever management focus
heavily upon young children due to higher incidence at this age and because the signs of occult bacteremia are
difficult to discern. In many tertiary care centers, the children at highest risk for bacteremia and sepsis are children
with indwelling CVC, neutropenia, or short gut. These children may have baseline tachycardia from anemia,
making triage recognition more problematic.
Triage considerations: Recognition of abnormal vital signs (e.g., tachycardia, hypothermia) and signs of poor
perfusion are critical for rapid initiation of resuscitation in the ED. Given the variation in normal vital sign ranges
through the pediatric age spectrum, recognition can be facilitated if alerts are built into electronic health records.
Clinical assessment: Several studies have attempted to stratify the risk of bacteremia and other serious bacterial
infections in febrile children. Table 94.2 describes clinical and laboratory predictors of serious bacterial infection
in young children.
Management: Empiric antibiotic management depends upon knowledge of the most common causes of
bacteremia in a community. While there has been a decline in pneumococcal isolates causing occult bacteremia,
there have been increases in the rates of penicillin- and cephalosporin-resistant pneumococcal isolates. As such, if
there is concern for invasive pneumococcal disease, initiating treatment with vancomycin and a third-generation
cephalosporin (cefotaxime or ceftriaxone) would be appropriate. In the event that the isolate is cephalosporin
susceptible, a cephalosporin would be a much more effective bactericidal drug than vancomycin. However, if
resistance to a cephalosporin is present, then the child is receiving a drug to which the isolate retains susceptibility.
This regimen would also provide coverage for the most common other causes of bacteremia and sepsis in
immunocompetent children outside the neonatal period. If staphylococcal disease is suspected, children could
receive nafcillin as well; in the event that they have methicillin-susceptible S. aureus (MSSA), nafcillin is far more
bactericidal than vancomycin. In immunocompromised hosts, the causes of bacteremia are more diverse, and
antipseudomonal coverage should be considered a priori. In addition, these children may also be at higher risk for
antibiotic-resistant organisms from prior antibiotic exposure(s). Reviewing prior culture data to evaluate for a
history of infection with drug-resistant organisms can help optimize ED-based management. Empiric coverage
with vancomycin and an antipseudomonal beta-lactam (e.g., cefepime, ceftazidime, piperacillin/tazobactam) may
be considered.
TABLE 94.1
MOST COMMON CAUSES OF PEDIATRIC OCCULT BACTEREMIA IN THE POSTPNEUMOCOCCAL CONJUGATE VACCINE ERA
OTHER SYSTEMIC INFECTIOUS EMERGENCIES
Goals of Treatment
The goals of treatment are to rapidly identify children at risk for some less common pathogens that can result in
fulminant infection and to plan an empiric treatment course while awaiting diagnostic testing.
CLINICAL PEARLS AND PITFALLS
If rickettsial disease is suspected based upon epidemiologic risk factors and clinical presentation,
doxycycline should be started immediately.
Doxycycline is the treatment of choice for the most deadly rickettsial disease in the United States,
Rocky Mountain spotted fever (RMSF); this is true for all age groups (including children younger than
8 years of age).
The “classic” triad for RMSF of fever, headache, and a rash is present in approximately 60% of
cases.
Babesiosis presents with symptoms similar to malaria, but in a child who lacks a travel history to a
malaria-endemic region. Treatment is similar to that for malaria.
Asplenic patients are at highest risk for babesiosis complications.
TABLE 94.2
CLINICAL AND LABORATORY PREDICTORS OF SERIOUS BACTERIAL INFECTION
Toxic Shock Syndrome
Toxic shock syndrome (TSS) is characterized by severe, prolonged shock and is caused by toxins produced by S.
aureus or GAS. TSS presents with the sudden onset of high fever, vomiting, and watery diarrhea. Pharyngitis,
headache, and myalgias may also occur, and oliguria rapidly develops. Within 48 hours, the disease progresses to
hypotensive shock. The patient has a fever, usually 39° to 41°C (102.2° to 105.8°F); a diffuse, erythematous
maculopapular rash; and hyperemia of the mucous membranes. In almost one-half of cases of streptococcal TSS,
no portal of entry is identified, or only minor, nonpenetrating skin trauma is identified in retrospect. The Centers
for Disease Control and Prevention (CDC) definitions of TSS are described in
e-Table 94.1 . Laboratory
findings include leukocytosis with a left shift, thrombocytopenia, transaminitis, elevated creatinine, elevated
creatinine kinase, myoglobinuria, and coagulopathy. Complications can include acute respiratory distress
syndrome (seen in over one-half of patients), acute kidney injury occurs in almost all children (creatinine elevation
precedes hypotension), and disseminated intravascular coagulation. The initial diagnosis is clinical. The following
laboratory tests should be obtained from all children suspected of having TSS: CBC, platelet count, PT, PTT, D dimer, electrolytes, blood urea nitrogen (BUN), creatinine, AST, alanine aminotransferase (ALT), and creatinine
kinase. Cultures of the blood, urine, stool, throat, and vagina serve to isolate S. aureus and to rule out other
infectious causes of shock. A lumbar puncture (LP) is often required to exclude bacterial meningitis, assuming a
child is not unstable or coagulopathic. The management of TSS is the same as that for shock caused by other
organisms (see Chapter 10 Shock ). Broad-spectrum antibiotics (vancomycin and ceftriaxone) are indicated for
patients who are hemodynamically unstable, while those who are less ill may have treatment limited to an
antistaphylococcal agent. Many authorities recommend the addition of clindamycin, which inhibits the toxin.
Rickettsial Diseases
The most severe endemic rickettsial disease in the United States is RMSF, caused by Rickettsia rickettsii.
Transmitted by dog and wood ticks, RMSF is found in the southeastern United States and most cases present
during the spring and summer months. Fever, headache, and a rash are considered the characteristic triad of RMSF,
but are found in only 60% of cases. The rash begins as a maculopapular rash on the wrist and ankles and
progresses centrally, later becoming petechial. Laboratory findings include thrombocytopenia, hyponatremia, and
transaminitis. Multisystem involvement is seen with this systemic vasculitic condition, and the high mortality rate
(up to 80% in untreated patients) usually is attributable to disseminated intravascular coagulation and shock. As a
consequence, treatment with doxycycline should begin immediately if RMSF is suspected, without awaiting
confirmatory diagnostics (acute and convalescent serologies). Doxycycline use has been shown to decrease
morbidity and mortality over the second-line drug, chloramphenicol, and doxycycline also treats ehrlichiosis,
which can present with symptoms similar to RMSF. Doxycycline is the preferred treatment for RMSF in children
of all ages, unless a child has a severe doxycycline allergy.
Babesiosis
Babesiosis is caused by Babesia microti, an intraerythrocytic parasite whose symptoms mimic those of malaria in
persons who lack a travel history to a malarial-endemic region. Babesiosis is seen in the northeastern and upper
Midwestern United States; it is transmitted by the same Ixodes ticks that transmit Lyme disease and has also been
transmitted via blood transfusion. Symptoms include fever and influenza-like illness; signs can be minimal, but in
more severe cases, tachypnea, hypotension, icterus, and mild hepatosplenomegaly can be seen. Disease can be
severe in asplenic patients, who have very high parasite burdens. The diagnosis is made by thick and thin blood
smears demonstrating the organism’s classic Maltese cross form within erythrocytes. Treatment is azithromycin
with atovaquone or clindamycin with quinine for 7 to 10 days. Exchange transfusion may be needed for patients
with parasitemia above 10%.
CNS INFECTIOUS EMERGENCIES
Meningitis, Bacterial
CLINICAL PEARLS AND PITFALLS
The most common causes of meningitis in the first month of life are GBS and gram-negative rods;
beyond the first month of life, the most common etiologies are pneumococcus and meningococcus.
The “classic” signs and symptoms of meningitis, including nuchal rigidity, are insensitive in infancy.
The Gram stain of the cerebrospinal fluid (CSF) should be used to broaden, but not to narrow, empiric
antibiotic selection.
Empiric antibiotic therapy should comprise bactericidal agents that cross the blood–brain barrier. For
neonates, ampicillin and either cefotaxime or ceftriaxone can be used. For infants and older children,
vancomycin (for enhanced pneumococcal coverage) and either cefotaxime or ceftriaxone (for
meningococcal coverage) should be utilized.
In neonates and young infants with a CSF pleocytosis, addition of acyclovir (20 mg/kg every 8 hours)
is reasonable until herpes simplex virus (HSV) is excluded.
Current Evidence
The most common causes of bacterial meningitis by age are listed in Table 94.3 . In the first month of life,
Escherichia coli and GBS are usually isolated; Listeria monocytogenes, a gram-positive rod, accounts for 1% to
3% of the cases. Between 30 and 60 days of age, GBS continues to be recovered frequently, followed by S.
pneumoniae and Neisseria meningitidis; Hib occurs rarely. After the first 2 months of life, S. pneumoniae and N.
meningitidis cause the majority of meningeal infections; Haemophilus influenzae remains a consideration
primarily among children not immunized with conjugated Hib vaccine. Salmonella, an uncommon etiologic agent
in the United States, should be suspected in the first few months of life if meningitis occurs in association with
gastroenteritis. The incidence of acute bacterial meningitis has declined in the last three decades due to widespread
use of the Hib and polyvalent pneumococcal conjugate vaccines.