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ischemic stroke due to vertebral artery dissection is traumatic in half of cases and
often presents with ataxia, headache, vomiting, cranial nerve deficits, and
hemiparesis. Rarely, cerebral sinovenous thrombosis can manifest with isolated
cerebellar venous infarction.
On rare occasions, ataxia can be part of the initial clinical manifestations of
opsoclonus-myoclonus syndrome, often associated with neuroblastoma.

FIGURE 15.1 Acute ataxia diagnostic pathway.

MANAGEMENT CONSIDERATIONS
Posterior fossa masses and cerebellar edema due to stroke or cerebellitis may
manifest with signs of ICP, often associated with ataxia, altered mental status, and
other neurologic signs. In these instances, consideration of the increased ICP
must be foremost. Deferring LP in a child with concern for increased ICP is
imperative to prevent herniation and its potential morbidity and mortality. If there
is any concern clinically for a mass, hemorrhage, or other space occupying CNS
lesion, imaging should precede LP. If a child is found to have increased ICP,
treatment with hypertonic saline or mannitol and other acute neurologic
precautions should be undertaken (see Chapter 97 Neurologic Emergencies ).
Consultation with neurology and/or neurosurgery may be warranted.
Treatment for GBS or its variants is mostly supportive, and in up to 10% to
20% of cases may require ventilator support. Children with reduced vital capacity
(≤20 mL/kg) generally progress to respiratory failure. This needs to be evaluated


early in the emergency department through pulmonary function testing (in
cooperative children) and close clinical monitoring for fatigue and other clinical
signs of impending failure. Most children will recover with immunomodulatory
therapy (intravenous [IV] immunoglobin, or plasma exchange [PLEX] in more
severe cases), however, recovery times vary and can take months to a year in
some patients. Definitive treatment will require collaboration with critical care


and neurology.
Randomized trials for the treatment of ADEM are lacking, but general
consensus indicates that high-dose IV methylprednisolone (30 mg per kg per day,
maximum 1,000 mg per day) should be initiated early and given for 5 days,
usually followed by an oral taper over 4 to 6 weeks. IV Ig (2 g per kg over 2 to 5
days) is often considered as a second-line agent in cases poorly responsive to
steroids. PLEX is reserved for refractory and particularly severe cases. Prompt
initiation of treatment usually results in excellent outcome, with full recovery in
the majority of cases within days or weeks.
Suggested Readings and Key References
Caffarelli M, Kimia AA, Torres AR. Acute ataxia in children: a review of the
differential diagnosis and evaluation in the emergency department. Pediatr
Neurol 2016;65:14–30.
Thakkar K, Maricich SM, Alper G. Acute ataxia in childhood: 11-year experience
at a major pediatric neurology referral center. J Child Neurol 2016;31(9):1156–
1160.


CHAPTER 16 ■ BREAST LESIONS
JONATHAN ORSBORN, RAKESH D. MISTRY

INTRODUCTION
Most breast lesions in children and adolescents are benign and self-limited, and
patients and their families will generally benefit from reassurance that neoplastic
diseases of the breast are extremely rare in all pediatric age groups. This chapter
focuses on the diagnostic approach to the variety of breast lesions, and discusses
the management of common etiologies that pediatric emergency physicians are
likely to encounter.

DIFFERENTIAL DIAGNOSIS

Breast lesions in children are typically divided into the following categories:
infections, benign cysts or masses, malignant masses, abnormal nipple secretions,
lesions associated with pregnancy and lactation, and miscellaneous causes,
including both anatomic and physiologic entities ( Table 16.1 ). A complete
history and physical examination narrow the differential diagnosis and usually
provides sufficient information to guide management. With few exceptions, most
breast lesions require little diagnostic testing in the emergency department (ED)
and typically can be managed with supportive care and occasionally, outpatient
referral to an appropriate specialist. The commonly encountered disorders ( Table
16.2 ) are almost always benign, but consideration must be given to potentially
life-threatening processes ( Table 16.3 ).

Breast Infections
Infection in the breast may take the form of a mastitis, cellulitis, or abscess. The
incidence of breast infection occurs bimodally, with the early peak in the neonatal
age group and the later, more common, peak in postpubertal females. Neonatal
breast infection (mastitis neonatorum) most frequently presents in the first few
weeks of life, commonly resulting from infection of the already enlarged breast
bud produced by intrauterine maternal estrogen stimulation. As a result, mastitis
neonatorum is more likely to occur in full-term, as opposed to premature infants.
The most common infecting organism is Staphylococcus aureus in >75% of
cases, although gram-negative enterics, anaerobes, group A or group B
streptococci may be isolated. More recent studies have demonstrated an increased
incidence of community-associated methicillin-resistant S. aureus (CA-MRSA).


The clinical presentation of neonatal breast infection is characterized by local
signs of inflammation, such as edema, erythema, and warmth. Fever is present in
just 22% to 38% of cases. Traditionally, the evaluation of even well-appearing
infants with neonatal mastitis included blood, urine, and potentially CSF cultures;

however, there is scant evidence supporting this degree of diagnostic workup.
There is growing evidence that demonstrates little correlation between blood,
urine, or CSF cultures and causative organisms of mastitis or breast abscess.
Therefore, for well-appearing infants with localized mastitis, one may consider
culture of purulent discharge, if present, and forgoing further evaluation for
invasive infection. Empiric antibiotic coverage for S. aureus including CAMRSA active agents should be initiated. Infants managed as outpatients require
strict return precautions and close follow-up with PCP. Although uncommon in
neonatal mastitis, infants with signs of systemic illness have potential for invasive
infections, including bacteremia, osteomyelitis, and pneumonia. Therefore, a
complete sepsis evaluation is indicated. For hospitalized infants, initial ED
therapy consists of empiric broad-spectrum intravenous antibiotic for S. aureus ,
streptococcal organisms, and gram-negative enterics. These antibiotic regimens
include vancomycin plus a third-generation cephalosporins for gram-negative
coverage. Subsequent antibiotic therapy is guided by culture and sensitivity
results. If there is concern for breast abscess, incision and drainage should be
done by a surgeon to minimize harm to developing breast tissue.
Breast infection in postpubertal females is classified as lactational or
nonlactational. Nonlactational mastitis/breast abscess is rare but can develop in
the central or peripheral regions of the breast from introduction of skin bacteria
into the ductal system. Infections in the central region of breast, proximal to the
nipple, are more likely in the setting of obesity, nipple piercings, or poor hygiene,
while peripheral mastitis is more likely to be associated with trauma or systemic
illness. Other predisposing factors for mastitis include previous radiation therapy,
foreign body, sebaceous cysts, hidradenitis suppurativa, and trauma to the
periareolar area. Signs and symptoms of infection include local erythema,
warmth, pain, and tenderness and purulent nipple discharge. Systemic signs,
including fever, are less commonly present. Organisms commonly implicated in
this age group include both methicillin-sensitive and resistant S. aureus,
streptococcal species, Enterococcus, Pseudomonas species, and anaerobic
organisms such as Bacteroides species.

Recommended treatment for mastitis in the postpubertal female includes
initiation of anti-staphylococcal oral antibiotic therapy and warm compresses.
Instruct patients to keep the area clean and dry, to wear a clean cotton bra, and to



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