Pediatric emergency medicine trisk 150

subtle reductions in extraocular movement, ophthalmology consultation is most
likely appropriate.
Of note, depending on the patient’s age and clinical circumstance, some
children may not cooperate fully with portions of the examination. If a child will
not follow an examiner’s target but will fix on the examiner, the examiner can ask
the parent to gently move the patient’s head to each side and then up and down.
The examiner can also guide the child by putting one hand on the child’s head (
Fig. 28.2 ), although care must be used to avoid heightening the patient’s anxiety.
As the patient continues to look straight ahead when the head is being turned, the
eyes are moving passively in reference to the head and orbit. When the head is
turned to the left, the eyes move into right gaze to maintain fixation straight ahead
( Fig. 28.2 ). If the head is tilted up, the eyes are moved into relative downgaze.
Essentially, this is the “doll’s eye” maneuver used in the assessment of comatose
patients. If the eyes move symmetrically and fully on passive movement of the
head, this rules out the presence of a neurogenic or restrictive problem with the
same accuracy as if the patient had voluntarily followed a target.
After these ophthalmologic exam maneuvers, computed tomography (CT) scan
of the orbit with both coronal and axial views is the imaging modality of choice
when there is limited extraocular motility in patients in whom orbital fracture is
suspected (see Chapters 107 Facial Trauma and 114 Ocular Trauma ).
The causes of pediatric strabismus are summarized in Tables 28.2 to 28.4 . The
first considerations ( Figs. 28.4 and 28.6 ) are neurogenic palsies and restrictive
strabismus. Myasthenia gravis and thyroid eye disease can mimic virtually any
strabismus with deficiency of extraocular movement and must always be
considered in the differential diagnosis in any pattern of ocular misalignment.
Myasthenia may cause intermittent strabismus and variable ptosis, whereas
thyroid disease causes retraction of the upper lid. The pupils are not involved in
either condition.

ESOTROPIA EMERGENCIES
Figure 28.7 summarizes the approach to a patient with esotropia and exotropia.

Patients with a restrictive or neurogenic esotropia (deficiency of abduction) may
adopt an abnormal head position to place the eyes in the position of best
alignment to avoid double vision. By turning the face in the direction of the
deficiency (e.g., right face turn for right sixth nerve palsy) when looking straight
ahead, the eyes align and appear straight ( Fig. 28.2 ). The patient’s head must be
held in the straight up position to notice that the affected eye is actually crossed.


TABLE 28.2
DIFFERENTIAL DIAGNOSIS OF STRABISMUS a
Neurogenic palsies
III Cranial nerve palsy (partial or complete)
IV Cranial nerve palsy
VI Cranial nerve palsy
Traumatic extraocular muscle palsy
Myasthenia gravis
Internuclear ophthalmoplegia
Skew deviation
Restrictive strabismus
Orbital wall fracture
Orbital hemorrhage, tumor, infection, or abscess
Thyroid eye disease
Nonthyroid extraocular muscle infiltration (e.g., metastasis)
Orbital cellulites
Nonneurogenic nonrestrictive strabismus
Idiopathic childhood strabismus
Strabismus caused by refractive errors (e.g., accommodative esotropia)
Sensory strabismus (unilateral visual loss)
a Not

listed in order of frequency.


TABLE 28.3
COMMON CAUSES OF STRABISMUS a
Esotropia
Congenital infantile or acquired (with or without farsightedness), nonparalytic,
nonrestrictive
Long-standing unilateral visual loss
Medial orbital wall fracture
VI Cranial nerve palsy
Exotropia
Nonparalytic nonrestrictive idiopathic childhood exotropia
Long-standing unilateral visual loss
III Cranial nerve palsy
Hypertropia
Dissociated vertical deviation (a nonparalytic nonrestrictive childhood
deviation)
Idiopathic over action or the inferior oblique muscle (affected eye rises in
adduction)
Inferior or superior orbital wall fracture
IV Cranial nerve palsy: congenital or acquired
Hypotropia
Brown syndrome (tight superior oblique tendon)
Inferior or superior orbital wall fracture
a Not

listed in order of frequency.

TABLE 28.4
LIFE-THREATENING CAUSES OF STRABISMUS a
Intracranial mass
Elevated intracranial pressure
Myasthenia gravis
Orbital tumor
Orbital cellulitis
a Not

Head trauma
Neoplastic infiltration of extraocular muscles
Meningitis
Superior orbital wall fracture
Retinoblastoma causing visual loss

listed in order of frequency.

Esotropia following orbital trauma may be due to lateral rectus injury,
hemorrhage, and medial or lateral wall fracture. Fracture of the medial orbital
wall may cause entrapment and restriction of the medial rectus. Fracture of the
lateral wall—usually part of a tripod fracture that involves the zygoma and
inferior lateral wall—may cause orbital hemorrhage that would displace the eye
medially.
The presence of proptosis suggests an orbital process. A lateral orbital tumor or
abscess can push the eye toward the nose or restrict abduction. Any infiltrative
process that involves the eye muscles may also cause esotropia through
restriction. Orbital cellulitis, with or without abscess formation, can cause any
type of misalignment including esotropia. A contrast CT scan of the orbit with
coronal and axial views is the diagnostic procedure of choice in these situations.