Pediatric emergency medicine trisk 102

that a significant apneic episode has not occurred, the patient can be discharged
after appropriate counseling of the parents and arrangements for close follow-up.
The evaluation of a young child with apnea, however, rarely will be so
straightforward. If historical information indicates that significant apnea has
occurred, the infant can be at risk for a recurrence of this potentially lifethreatening event. An aggressive search for an underlying cause is necessary and
may include laboratory studies, lumbar puncture, chest radiograph, and EKG.
Hospital admission should be arranged for observation and further diagnostic
evaluation.
A significant apneic episode in the absence of systemic disease leaves the
emergency physician in a quandary. There may not be an explanation for the
event that satisfies the physician or the anxious parents. Thus, referral to an
available specialist or center may be required. There is considerable practice
variation in the inpatient evaluation and management of an ALTE. The approach
that is usually pursued is designed to identify known causes of primary apnea. It
generally includes in-hospital observation with monitoring, a chest radiograph,
and/or an EKG. More significant events warrant further evaluation. This may
include an evaluation of the CNS with an electroencephalogram (EEG), and in
some cases, a sleep study. Gastroesophageal reflux is often recognized clinically.
Barium swallow can help identify anatomic abnormalities but are not reliable for
the diagnosis of reflux. Esophageal probes to measure pH and intraluminal
impedance are rarely required, but can be utilized during hospitalization if the
diagnosis is unclear. An ultrasound can identify hydrocephalus or intraventricular
hemorrhage, though a CT or MRI would be indicated if inflicted head injury is
suspected. Home cardiorespiratory monitoring is beyond the scope of emergency
practice, but is not routinely recommended. It is for this reason the AAP
recommends utilizing BRUE guidelines to minimize practice variation.
In many instances, a thorough history and careful physical examination will
suggest that a significant apneic event has not occurred and that there is no
serious underlying illness. In this situation, the emergency physician should
reassure and educate the family before discharging the patient. The parents also
should be given specific instructions regarding indications for another emergent

ED visit and a close follow-up visit to a primary care provider.
Suggested Readings and Key References
Eichenwald EC; Committee on Fetus and Newborn, American Academy of
Pediatrics. Apnea of prematurity. Pediatrics 2016;137(1).


Regenbogen E, Zhang S, Yang J, et al. Epidemiological trends among preterm
infants with apnea. A twelve-year database review. Int J Pediatr
Otorhinolaryngol 2018;107:86–92.
Tieder J, Altman R, Bonkowsky J, et al. Management of apparent life-threatening
events in infants: a systematic review. J Pediatr 2013;163:94–99.
Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief resolved unexplained events
(formerly apparent life-threatening events) and evaluation of lower-risk infants.
Pediatrics 2016;137:e1–e32.


CHAPTER 15 ■ ACUTE ATAXIA
JACLYN N. KLINE, LUCA BARTOLINI

INTRODUCTION
Ataxia is defined as impaired coordination of voluntary movements, usually
caused in children by cerebellar dysfunction or, less frequently, vestibular or
proprioceptive afferent dysfunction. While uncommon, acute ataxia in children is
important to recognize, because an early diagnosis may have significant
therapeutic implications. Ataxia is usually associated with other signs of
neurologic dysfunction, and the three most common causes of acute ataxia in
children are: (1) Acute postinfectious cerebellar ataxia, (2) Drug ingestion, and
(3) Guillain–Barré syndrome (GBS) and its variants (Table 15.1 ).

HOW TO DIAGNOSE ATAXIA ON NEUROLOGIC

EXAMINATION
Ataxia can manifest as abnormal timing of contraction of agonist/antagonist
muscles (dysrhythmia) and abnormal movement trajectory, resulting in frequent
overshooting and overcorrecting (dysmetria).
Symptoms and signs often relate to the anatomic location of the cerebellum
that is affected by the underlying process. Gait and truncal ataxia are observed in
diffuse processes and those involving the cerebellar vermis. Gait ataxia is the
most common presentation and consists of a wide-based gait with inability to
walk without support, especially on tandem gait. When the deficit is more evident
with the eyes closed, sensory or vestibular causes should be considered. Young
children may just refuse to ambulate.
Lesions in the cerebellar hemispheres or peduncles are associated with
ipsilateral limb ataxia. Appendicular ataxia, caused by lesions in the lateral
hemispheres of the cerebellum that leads to ataxic movements in the extremities,
can be unmasked by performing the rapid alternating movement, finger tapping,
and finger-to-nose tests, especially if the examiner’s finger is held at the extreme
of the patient’s reach and moved unpredictably. Similarly, heel-to-shin test can be
done for the lower extremities, but generally requires more cooperation and is
rarely feasible in younger patients. Overshoot can also be observed when the
patient is asked to suddenly raise his outstretched arms from their lap to the level
of the examiner’s hand. This also allows detection of postural tremor, which is
also a cerebellar sign. Examination can be affected by the presence of upper or


lower motor neuron signs, since weakness can easily be mistaken for ataxia or the
two signs may coexist. A very useful test that requires little strength to be
performed and can help differentiate weakness from ataxia is done by asking the
patient to follow one of the creases of her thumb with her index finger. Truncal
and appendicular ataxia may coexist in the presence of large lesions or diffuse
processes.

Eye movement abnormalities in cerebellar dysfunction may be more difficult to
detect; nystagmus is often present, and saccades may under- or overshoot the
target. Also, speech can be affected, with irregular changes in volume and rate
(scanning speech).
Ataxia can result from lesions outside of the cerebellum, when the cerebellar
afferent or efferent pathways are disrupted, for example by a lesion in the pons, or
by lesions in the posterior column - medial lemniscal pathway, which result in
positive Romberg sign and loss of joint position sense.

DIFFERENTIAL DIAGNOSIS AND ROLE OF IMAGING AND
LABORATORY TESTS
While several diseases can manifest with ataxia (Table 15.2 ), the most common
cause of acute ataxia in children with normal mental status is acute
postinfectious cerebellar ataxia . This condition is usually observed in toddlers
(60% of patients in large series were aged between 2 and 4 years) and is
characterized by a prodrome of nonspecific viral illness followed after days or up
to 2 to 3 weeks by ataxia. The clinical course is usually benign, with full return to
baseline within 8 months in 70% of children. This remains a clinical diagnosis, as
imaging and CSF analysis are usually unremarkable; sometimes, especially in
younger patients where the examination may not be entirely reliable, brain MRI
and lumbar puncture (LP) should be considered to rule out other causes, such as
acute disseminated encephalomyelitis (ADEM—see below), because of potential
treatment implications.
In a child with ataxia and abnormal mental status , urgent brain imaging (plain
CT head or, ideally, brain MRI if available without significant delay) is
warranted, and LP should be considered. Imaging, particularly MRI, allows the
clinician to rule-out brain tumors, demyelinating conditions, cerebellitis, and
stroke. CSF pleocytosis (>5 cells/mm3) may be observed in different conditions
and while bacterial meningitis is unlikely in an ataxic child without fever or
meningismus, viral meningoencephalitis remains a possibility, especially if the

pleocytosis is primarily lymphocytic.