Pediatric emergency medicine trisk 569

TABLE 94.10
EVALUATION OF A CHILD WITH SUSPECTED ENCEPHALITIS OR MENINGOENCEPHALITIS
All suspected cases
CSF

Cell count and differential, protein/glucose, bacterial culture, HSV PCR, enteroviral PCR
Consider holding CSF in the laboratory for additional diagnostic studies (see below)
Serum
CBC, chemistries, blood cultures, EBV/CMV serologies, HIV, HSV PCR, Bartonella
serologies, Mycoplasma serologies
Other
Enteroviral PCR (respiratory, stool), PCR of respiratory specimens
Specific risk factor or features
Tuberculosis risk
Should be suspected in any child with CSF pleocytosis and a high CSF protein and/or low
factors
CSF glucose: chest radiograph (abnormal in approximately 90% of children with
tuberculosis meningitis; tuberculin skin test; interferon gamma release assay; gastric
aspirate or sputum for acid-fast culture; CSF PCR for Mycobacterium tuberculosis
Immunocompromised Acid-fast culture for tuberculosis, cryptococcal antigen (serum, CSF), human herpesvirus
6 and 7, JC virus, Toxoplasma serum IgG; cultures for Listeria monocytogenes, VZV
PCR, histoplasmosis serologies/urinary antigen
Sexually active
Summer/fall

Winter

RPR/VDRL for syphilis
West Nile IgM (CSF, serum), Arboviral panel (CSF, serum), and serologies for other
geographically appropriate arboviruses (e.g., St. Louis, La Crosse, and the equine
encephalitides)

Serologies for Rickettsia rickettsii (Rocky Mountain spotted fever) and ehrlichiosis as
well as Borrelia burgdorferi (Lyme disease) if in the appropriate geographic region
Influenza PCR

Raw or unpasteurized Toxoplasma IgG, serologies for Coxiella, culture for Listeria monocytogenes, evaluation
food products
for Gnanthostoma if history of travel to Southeast Asia or Latin America
Animal exposures
Rabies (bites from unimmunized dogs/cats or contact with bats or wild carnivores),
Bartonella (cat scratches or bites from cat fleas), LCMV (exposure to rodent urine or
feces)
Ticks
Insect contact

Swimming in
brackish or
stagnant water
Travel history

Serologies or PCR for Rickettsia rickettsii, Ehrlichia chaffeensis, Anaplasma, Borrelia
burgdorferi
Serologies for equine encephalitides, St. Louis encephalitis, Japanese encephalitis, West
Nile virus, La Crosse virus and smear for malaria (if appropriate travel histories) for
mosquito contact; Bartonella bacilliformis serologies (sandflies); trypanosomiasis
serologies (tsetse flies)
Wet mount for Naegleria fowleri

Vesicular rash

Serologies for fungal infections endemic in certain regions; consider early consultation

with an infectious diseases specialist. Infections more common outside industrialized
nations are discussed in the section on Infections in Returned Travelers
PCR of lesion for HSV, VZV

Diarrhea and seizure
CSF eosinophilia

Stool for bacterial culture (Shigella, E. coli ) and for rotavirus PCR
Baylisascaris (raccoon roundworm) serologies

CSF, cerebrospinal fluid; HSV, herpes simplex virus; PCR, polymerase chain reaction; CBC, complete blood count; EBV, Epstein–Barr virus; CMV,
cytomegalovirus; HIV, human immunodeficiency virus; VZV, varicella zoster virus; RPR, rapid plasma reagin; VDRL, venereal disease research
laboratory; LCMV, lymphocytic choriomeningitis virus.
From Tunkel AR, Glaser CA, Bloch KC, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of
America. Clin Infect Dis 2008;47:303–327, by permission of the Oxford University Press.


Other CNS Infections
Goals of Treatment
The goal is to rapidly identify infections which may result in intracranial extension, and to recognize that the
empiric antibiotic selection in these cases must include antibiotics that are both bactericidal and achieve adequate
CNS penetrance.
CLINICAL PEARLS AND PITFALLS
The most common comorbidity in children with brain abscesses is congenital heart disease.
Staphylococci and streptococci are the most common organisms isolated.
One common regimen to treat suspected CNS invasion from contiguous structures is the combination
of vancomycin, ceftriaxone or cefotaxime, and metronidazole, all at meningitic doses. If multiply
resistant gram-negative organisms have been isolated from a child previously, empiric meropenem
can be considered after consultation with infectious diseases.
Fewer data exist for other antibiotics (e.g., piperacillin-tazobactam, ampicillin-clavulanate) crossing

the blood–brain barrier.
Brain Abscesses
Brain abscesses can result from contiguous spread from head and neck infections (e.g., mastoiditis, sinusitis,
odontogenic) or from direct seeding from septic emboli, most commonly in children with congenital heart disease.
The latter remains the most common risk factor for pediatric brain abscesses. The most common organisms are
streptococci (aerobic and anaerobic streptococci, GAS, and pneumococcus) and S. aureus, followed by fungal
(primarily Aspergillus ) and Enterobacteriaceae. Early symptoms are nonspecific and can include fever, malaise,
vomiting, and headache. The most common signs are focal neurologic deficits (particularly cranial nerve VI),
papilledema, meningeal signs, hemiparesis, and ataxia, although symptoms will vary by abscess location (cerebral
hemisphere is the most common location) and size. Mental status changes are late signs with ominous prognoses.
LP rarely yields an organism, and blood cultures infrequently are positive. ED-based diagnosis can be made by
contrast CT of the brain, although magnetic resonance imaging (MRI) will better delineate brainstem and
cerebellar abscesses. Early neurosurgical intervention is critical. Empiric antibiotics should be broad-spectrum
antibiotics with CNS penetrance covering staphylococci, streptococci, and anaerobes. One regimen would be
vancomycin, cefotaxime, and metronidazole, all at meningitic doses. Standard precautions should be used.

Acute Flaccid Paralysis
Acute flaccid myelitis (AFM) has historically been caused by polio, transmitted via the fecal–oral route. Polio is
now only endemic in Afghanistan and Pakistan. More recently, other enteroviruses (A71, D68), adenovirus,
herpesviruses, and flaviviruses have been causing AFM on an every-other-year pattern. A prodromal upper
respiratory tract infection, with or without pyrexia, is often noted within 4 weeks of the development of acuteonset extremity weakness. MRI shows gray matter spinal cord lesions and a CSF pleocytosis often is noted. The
differential diagnosis includes acute transverse myelitis and Guillain–Barré syndrome. In addition to routine
studies on CSF, PCR for enteroviruses, EBV, CMV, HSV, and arboviruses should be considered.
Sinusitis
Sinusitis is an inflammation of the paranasal sinuses. While the ethmoid and maxillary sinuses are present at birth,
the frontal and sphenoid sinuses do not develop until children are school aged. The most common etiologies mimic
those causing acute otitis media and include pneumococcus, nontypeable H. influenzae, Moraxella, and GAS. The
most common signs and symptoms of acute sinusitis are listed in e-Table 94.3 . Children with chronic sinusitis
can have milder, more indolent symptoms, such as cough that is often worse when the child is supine and
rhinorrhea; pyrexia is less common in this group of children, and physical examination often is normal. The

diagnostic criteria are summarized in
e-Table 94.4 . Complications of sinusitis include orbital cellulitis, brain
abscess, epidural or subdural empyema, and cavernous sinus thrombosis.
Most sinusitis is managed solely with medical therapy in the outpatient setting. Amoxicillin (80 to 90
mg/kg/day) remains the mainstay of therapy; a 10-day course is recommended for most cases of uncomplicated
acute sinusitis. Two- to 3-week courses may be needed for chronic sinusitis or for immunocompromised or


chronically ill children with acute sinusitis. Inpatient therapy should be considered for toxic-appearing children,
those with facial swelling, or children with suspected or confirmed intracranial extension. The AAP
recommendations for sinusitis treatment are summarized in e-Table 94.5 . Standard precautions should be used.
Mastoiditis
Mastoiditis, an infection of the mastoid air cells, is a rare complication of acute otitis media. The most common
organism is pneumococcus, followed by S. aureus, GAS, and Pseudomonas; historically, Hib has also been
implicated. The most common signs are fever, ear proptosis, and postauricular redness, pain, and swelling; the
tympanic membrane is usually erythematous and bulging. Complications can include intracranial extension of the
abscess, damage to the facial nerve, labyrinthitis, bacteremia, and osteomyelitis. The diagnosis is confirmed by CT
of the temporal bone. Tympanocentesis cultures reflect etiology of mastoiditis in approximately 50% of cases.
Treatment is a combination of medical and surgical management. Empiric antibiotics should target streptococci
and staphylococci. In regions where MRSA and penicillin-resistant pneumococci are common, a reasonable
regimen would include vancomycin and a third-generation cephalosporin. Standard precautions should be used.
Orbital Cellulitis
Orbital cellulitis is an infection posterior to the orbital septum caused primarily by S. aureus, streptococci,
pneumococcus, and nontypeable H. influenzae. The most common signs are fever, proptosis, limited ocular range
of motion, pain with eye motion, chemosis, and an afferent pupillary defect. Blood cultures should be obtained; LP
should be considered for young infants and for children with signs of meningitis. Contrasted CT of the orbit and
brain confirms the diagnosis and allows for evaluation for intracranial extension, which would alter antibiotic
management. Many children with uncomplicated orbital cellulitis are managed medically; however, early
consultation with surgical subspecialists would be advised. Empiric antibiotic selection should cover the same
organisms as for mastoiditis; if intracranial extension is not evident on CT, substitution of vancomycin for

clindamycin can ease the transition of a child from parental to an entirely oral regimen after clinical improvement
even if an isolate is not recovered. Indications for operative management include intracranial extension, visual
loss, or optic nerve dysfunction. Standard precautions should be used.
Botulism
Botulism is a neurotoxic disorder caused by Clostridium botulinum that causes a descending flaccid paralysis. The
most common pediatric manifestation is infantile botulism, most common in children under 6 months of age,
caused by ingestion of spores; botulism is the reason that honey is not recommended for infants. Affected infants
have decreased movement, bulbar nerve palsies, expression-less facies, loss of head control, and descending
hypotonia. Diagnosis is confirmed by isolation of toxin or spores from stool. The mainstay of treatment is
supportive therapy; intubation may be necessary. Infants with botulism should immediately receive botulism
immune globulin (BabyBIG) intravenously. Antibiotics are not indicated for infantile botulism, and
aminoglycosides may worsen the toxin’s paralytic effects. Older patients with wound botulism after penetrating or
crush trauma should receive penicillin or metronidazole after receiving an equine-derived Heptavalent Botulinum
Antitoxin (HBAT). Standard precautions should be used.
TABLE 94.11
TETANUS PROPHYLAXIS FOR PATIENTS WITH WOUNDS OR BITES

Tetanus
Tetanus is caused by another neurotoxin in the Clostridium family, Clostridium tetani. Spores are ubiquitous in the
environment and can contaminate wounds of unimmunized or underimmunized persons. Neonatal tetanus is most


common in developing nations where infants are unprotected because of the lack of maternal immunity. Local
tetanus refers to muscle spasms in areas contiguous to the wound, and can result in generalized tetanus (lockjaw),
with trismus, risus sardonicus, and generalized muscle spasming. The differential diagnosis includes hypocalcemia
and drug reactions. Tetanus is a clinical diagnosis; culture yield is poor. Treatment is tetanus immune globulin
(TIG), with some infiltrated around the wound and the rest administered intramuscularly. Metronidazole
(preferred) or penicillin for 10 to 14 days also is needed. The recommendations for ED management of tetanus
prophylaxis are described in Table 94.11 . It is important that the ED physician asks about tetanus vaccination, as
opposed to assuming that children are up to date on this immunization; a recent national surveillance study found

that only 72% of toddlers were appropriately immunized. Standard precautions should be used.

NECK INFECTIOUS EMERGENCIES
Cervical Lymphadenitis
CLINICAL PEARLS AND PITFALLS
The most common organisms causing cervical lymphadenitis are staphylococci and streptococci.
However, thorough travel and exposure histories should be taken to evaluate for less common
etiologies.
Signs of inflammation also can help differentiate among the causes of localized infectious
lymphadenopathy. Nontender adenopathy should lead the clinician away from most pyogenic causes,
and should increase the index of suspicion for viral upper respiratory infections (URIs) or
mycobacterial disease, depending upon the duration of illness.
Current Evidence
Cervical lymphadenitis is a bacterial infection of the lymph nodes in the neck. This condition must be
distinguished from lymphadenopathy, an enlargement of one or more lymph nodes that occurs with viral
infections, or as a reaction to bacterial disease in structures that drain to the nodes. The most common etiologies
are listed in e-Table 94.6 (see also Chapter 47 Lymphadenopathy ).
Goals of Treatment
Clinical outcomes for children with lymphadenitis include limiting the use of CT among patients with
uncomplicated bacterial lymphadenitis.
Clinical Considerations
Clinical recognition: The child with cervical lymphadenitis is usually noted to have swelling in the neck. If
sufficiently old, he or she will complain of pain. Fever occurs only occasionally, more often in children younger
than 1 year. The infected node may vary in size from 2 cm to more than 10 cm. Initially, it has a firm consistency,
but fluctuance develops in about 25% of the infected nodes. The skin overlying the node becomes erythematous,
and there may be associated edema. Children with nontuberculous mycobacterial infections may have nontender
adenopathy with violaceous discoloration of the overlying skin.
Triage considerations: Children with lymphadenitis should be promptly assessed for deep neck infections and
for infections that may affect the airway. Lymphadenitis should be considered in the differential diagnosis of a
child with a painful neck mass. Associated toxic appearance or pain out of proportion to the examination may

imply a deeper extension of the infection and demand emergent surgical consultation and empiric broad-spectrum
antibiotic therapy.
Clinical assessment: The WBC count is usually normal but may be elevated in the younger, febrile child.
Aspiration of the node often identifies the organism by both Gram stain and culture, even if fluctuance is not
appreciated. Children with infections from Mycobacterium tuberculosis usually react to the TST and may have
findings compatible with tuberculosis seen on chest radiograph. Complications of bacterial adenitis are unusual.
Organisms such as S. aureus and group A streptococci (GAS) can spread locally if unchecked. A draining sinus
tract may develop in untreated children with atypical mycobacterial adenitis. Recurrence of infection suggests a
local anatomic abnormality (e.g., branchial cleft cyst laterally or thyroglossal duct cyst in the midline) or
immunocompromising conditions such as chronic granulomatous disease.