Pediatric emergency medicine trisk 148

by vascular or neoplastic changes in the midbrain, increased intracranial pressure
(ICP), large anterior midline craniofacial tumors (e.g., nasopharyngeal
carcinoma), otitis media (OM) with involvement of the petrous portion of the
sphenoid (Gradenigo syndrome), and any abnormality that involves the cavernous
sinus. An abnormality of the sixth cranial nerve will cause a reduction in
ipsilateral abduction ( Fig. 28.2 ) resulting in a possible ipsilateral esotropia.
The fourth cranial nerve innervates the superior oblique muscle. It is the only
cranial nerve that completely decussates and has a dorsal projection over the
midbrain. This position renders the fourth cranial nerve particularly vulnerable to
blunt head trauma, one of the most common causes of fourth nerve palsy. The
fourth cranial nerve also has a relatively long intracranial course, which makes it
susceptible to increased ICP and parenchymal shifts caused by cerebral edema. It
also runs through the cavernous sinus. Fourth cranial nerve palsy may be
congenital but asymptomatic for several years during childhood until the brain is
no longer able to compensate. Acquired or congenital palsy of this cranial nerve
causes the eyes to become misaligned vertically (ipsilateral hypertropia). Patients
with congenital fourth cranial nerve paresis compensate by tilting their head to
the ipsilateral side, which allows for a rebalancing of the eye muscles such that
alignment may be achieved. Old photographs may demonstrate this tilt. Facial
asymmetry can also be seen after years of this compensatory tilting. Ophthalmic
consultation is usually needed to differentiate between congenital and acquired
palsy.
The third cranial nerve supplies the remaining four extraocular muscles. It is
involved with downgaze, upgaze, and adduction. Parasympathetic innervation to
the pupil (see Chapter 29 Eye: Unequal Pupils ) and innervation to the eyelid
muscle (levator palpebrae) are also carried in the third cranial nerve. A complete
third cranial nerve palsy results in an eye that is positioned down (from the
remaining action of the unaffected superior oblique muscle) and out (from the
remaining action of the unaffected lateral rectus muscle) with ipsilateral ptosis
and ipsilateral pupillary dilation ( Fig. 28.3 ). Because the third cranial nerve
divides into a superior and an inferior division just as it enters the orbit from the

cavernous sinus and because the fibers to individual muscles are segregated
within the nerve throughout its course, partial third cranial nerve palsies may
occur with or without ptosis and/or pupillary dilation. This may leave the patient
with complex strabismus, which is best left to the ophthalmology consultant. The
differential diagnosis of third cranial nerve palsies is summarized in Chapter 29
Eye: Unequal Pupils .

Muscle Restriction


The action of a muscle may also be impaired by restriction. The muscle can
become infiltrated with substances that might restrict its action or cause fibrosis.
Children with hyperthyroid eye disease (e.g., Graves) can have enlarged, tight eye
muscles, which along with infiltrate to the periorbital fat, contribute to proptosis.
An eyeball may be restricted in its movements by tumors or infection in and
around the globe. Orbital tumors, cellulitis, or abscesses that cause restriction
may be associated with proptosis or a displacement of the entire eyeball, either
vertically or horizontally. With blunt trauma to the eyeball, the globe may be
translocated posteriorly, causing increased intraorbital pressure that may result in
a “blowout” fracture of the bony orbital wall. When an orbital wall fracture
occurs, the muscle or surrounding tissues that run along that wall may become
entrapped within that fracture, tethering the eyeball so the eye cannot look in the
direction opposite the fracture. Children with orbital floor or medial orbital wall
fractures are prone to entrapment of the inferior or medial rectus muscles,
respectively. This may not be noticeable until eye movements are attempted. For
example, fractures of the orbital floor may entrap the inferior rectus muscle,
tethering the eye downward and thereby restricting upgaze ( Fig. 28.4 ). Less
commonly, the eye may have a limitation of movement in the direction of the
fracture. Orbital wall fractures may also be associated with enophthalmos, in
which the eye appears to be sunken in the orbit, or proptosis caused by retroorbital hemorrhage. All patients with orbital fractures must receive a complete

ophthalmic examination to rule out accompanying ocular injury. The most
common fracture involves the inferior and/or medial walls of the orbit. The lateral
wall is rarely fractured. Fracture of the superior wall (orbital roof) is particularly
worrisome because it may allow communication between the orbit and the
subfrontal intracranial space.


FIGURE 28.1 Normal extraocular muscle anatomy.

Strabismus With Intact Eye Muscle Function
The remaining types of strabismus fall into the category where eye muscle
function is normal (i.e., nonparetic and nonrestrictive). These problems are not
emergent. The eyes may be misaligned as a result of failure of the brain to use
both eyes simultaneously in a coordinated fashion (idiopathic), a need for
corrective lenses, or the presence of poor vision in one eye. Uncorrected
farsightedness (hyperopia) can result in accommodative esotropia, which may
have an acute onset, usually between the ages of 1 and 6 years, with the
misalignment often worse at near viewing. Uncorrected nearsightedness (myopia)
can result in exotropia, especially when the patient views in the far distance. Both
types of misalignment may be treated with corrective lenses.
Checking the vision in both eyes (see Chapter 123 Ophthalmic Emergencies )
is essential in all cases of strabismus along with full examination of eye
movements to rule out the presence of uncorrected refractive error or a poorly
seeing eye. The latter may be due to serious eye problems such as retinoblastoma
or cataract. Of note, strabismus is the second most common presenting sign of
retinoblastoma after leukocoria.


TABLE 28.1
EXTRAOCULAR MUSCLES

Muscle a
Medial rectus

Cranial nerve

III (inferior
division)
Inferior rectus
III (inferior
division)
Lateral rectus
VI
Superior rectus
III (superior
division)
Superior oblique IV
Levator palpebrae III (superior
c
division)
a Inferior

Action b

Eye position in
palsy

Adduction

Exotropia

Downward gaze

Hypertropia

Abduction
Upward gaze

Esotropia
Hypotropia

Downward gaze
Eyelid

Hypertropia
Ptosis (lid)

oblique not included for simplicity. Isolated palsy of the inferior oblique is extremely rare.
in the horizontal or vertical field only. Cyclorotatory movements not included.
c By definition, not truly an extraocular muscle.
b Action