Figure 11-6 Old left orbital floor fracture with inferior rectus muscle entrapment. Note limitation of elevation of the left eye and pseudoptosis from enophthalmos. The eyelids are elevated manually in the bottom row.
Initially, a hypertropia due to weakness of the inferior rectus muscle without entrapment is managed with observation, because the weakness may improve with time. If recovery is not complete within 6–12 months of the injury and there is at least a moderate degree of active force, resection of the affected muscle can be performed. If the hypertropia is large, the procedure can be combined with recession (with or without an adjustable suture) of the ipsilateral superior rectus muscle. Alternatively, recession of the contralateral inferior rectus muscle, with or without the addition of a posterior fixation suture (fadenoperation), can be used to limit the fellow eye’s downgaze movement and match the duction deficiency of the injured eye. A substitute to match the infraduction limitation is a combined recession and resection of the contralateral inferior rectus muscle. Transposition of the ipsilateral medial and lateral rectus muscles to the inferior rectus muscle (inverse Knapp procedure) may be necessary for treatment of complete chronic inferior rectus muscle palsy. Whether or not prior orbital surgery has been performed to release entrapped tissues, partial restriction persists in many cases even though imaging studies may show no residual entrapment. This restriction can limit the success of surgery.
Other Comitant Vertical Tropias
Other disorders that feature a hypertropia that does not change significantly from right to left gaze include innervational problems, such as superior division (partial) palsy of the third cranial nerve; and mechanical disorders such as thyroid eye disease, congenital fibrosis of the extraocular muscles, and orbital tumors. A long-standing superior oblique palsy may also develop a spread of comitance. These topics are discussed elsewhere in this volume and in other BCSC Sections.
Dissociated Vertical Deviation
Dissociated vertical deviation (DVD) is an innervational disorder found in more than 50% of patients with infantile strabismus (esotropia or exotropia). There are 2 explanations for the origin of DVD. One theory is that it is the result of mechanisms to compensate for latent nystagmus, with the oblique muscles playing the principal role. An alternative theory suggests that deficient fusion allows the primitive dorsal light reflex, which is prominent in other species, to emerge.
Brodsky MC. Dissociated vertical divergence: a righting reflex gone wrong. Arch Ophthalmol. 1999;117(9):1216–1222. Guyton DL. Ocular torsion reveals the mechanisms of cyclovertical strabismus: the Weisenfeld lecture. Invest Ophthalmol Vis
Sci. 2008;49(3):847–857.
Clinical Features
DVD usually presents by age 2 years, whether or not the horizontal deviation has been surgically corrected. Either eye slowly drifts upward and outward, with simultaneous extorsion, when occluded or during periods of visual inattention (Fig 11-7). Some patients attempt to compensate by tilting the head, for reasons that still have not been conclusively identified.
Figure 11-7 Dissociated vertical deviation, left eye. A, Straight eyes during binocular viewing conditions. B, Large left hyperdeviation immediately after the eye is covered and then uncovered. C, Left eye drifts back down toward midline. Note that the right eye does not adopt a hypotropic position when the left eye drifts back to the midline.
In bilateral or unilateral DVD, the vertical movement usually predominates, but sometimes the principal dissociated movement is one of abduction (dissociated horizontal deviation or DHD). DVD is usually bilateral but is frequently asymmetric. It may occur spontaneously (manifest DVD) or only when 1 eye is occluded (latent DVD). In addition to DHD, latent nystagmus and horizontal strabismus are often associated with DVD. These entities are manifestations of deficient binocular vision.
Measurement of DVD is difficult and imprecise. In one method, a base-down prism is placed in front of the upwardly deviating eye while it is behind an occluder. The occluder is then switched to the fixating lower eye. The prism power is adjusted until the deviating eye shows no downward movement to refixate. Results are similar when a red Maddox rod is used to generate a horizontal line for the dissociated higher eye while the other eye fixates on a small light; vertical prism power is adjusted to eliminate the separation of the light and the line. Each eye is tested separately in cases of bilateral DVD.
Management
Treatment of DVD is indicated if the deviation is noticeable (generally more than 6Δ–8Δ) and occurs frequently during the day. Changing fixation preference using optical penalization is effective mostly in unilateral or highly asymmetric bilateral DVD. Since DVD is a cause of OEAd, distinguishing it from overaction of the inferior oblique muscles is important because the surgical approaches to these 2 conditions are different in most cases.
Surgery on the vertical muscles often improves the condition but rarely eliminates it. Recessions of the superior rectus muscle, ranging from 6 to 10 mm according to the size of the hypertropia, can be