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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