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Exotropia Kenneth W 8 Exotropia Kenneth W. Wright xodeviations are quite common, and they are not necessa- Erily pathological. A small intermittent exotropia is normal in most newborns, as 70% of normal newborns have a transient exodeviation that resolves by 2 to 4 months of age.1 Another type of exodeviation that is considered normal is a small exophoria, usually less than 10 prism diopters (PD). Most normal adults have a small exophoria when fully dissociated. Exodeviations are controlled with our innate strong fusional convergence, typi- cally measuring 30 PD or more. The most common form of divergent strabismus is intermittent exotropia, which probably accounts for more than 90% of all exodeviations. Table 8-1 lists the different categories of pathological exodeviations, with the one most frequently occurring listed first. INTERMITTENT EXOTROPIA Intermittent exotropia is a large phoria that is intermittently controlled by fusional convergence. Unlike a phoria, intermit- tent exotropia spontaneously breaks down into a manifest exotropia (Fig. 8-1). Clinical Features Intermittent exotropia is usually first observed by the parents in early childhood or late infancy as an infrequent drifting or squinting of one eye. 12 Patients with intermittent exotropia tend to manifest their deviation when they are tired, have a cold or the flu, or when they are daydreaming. Adult patients will often become exotropic after imbibing alcoholic beverages or taking sedatives. 266 chapter 8: exotropia 267 TABLE 14.1. Classifications of Exodeviations. Intermittent exotropia (common) Convergence insufficiency (common) Sensory exotropia (common) Congenital exotropia (rare) Signs of intermittent exotropia include blurred vision, asthenopia, visual fatigue, and, rarely, diplopia in older children and adults. Many patients with intermittent exotropia have pho- tophobia (squinting to bright light). Photophobia was originally thought to be a way for eliminating diplopia or confusion, but Wiggins and von Noorden have shown that the photophobia may not be related to diplopia avoidance.39 As a rule, during the phoric phase of intermittent exotropia, the eyes are perfectly aligned and the patient has bifoveal fusion with excellent stereoacuity ranging between 40 and 50 s arc. This excellent bifoveal fusion develops because the eyes are well aligned in early infancy when the critical binocular cortical con- nections are being established. A minority of patients with inter- mittent exotropia are primary monofixators and do not develop normal bifoveal fusion with good stereopsis. Rarely a patient will even have significant amblyopia. The poor fusion in these cases is associated with a predominance of the tropia phase. During the tropia phase of intermittent exotropia, patients will show large hemiretinal or regional suppression of the temporal retina.26,30 Anomalous retinal correspondence in the tropia phase and normal retinal correspondence in the phoria phase have been demon- strated in some patients with intermittent exotropia.4,38 Natural History The natural history of intermittent exotropia remains obscure, as there are no longitudinal prospective studies and only a few retrospective studies of untreated intermittent exotropia. Von Noorden found that 75% of 51 untreated patients showed pro- gression over an average follow-up period of 3.5 years, whereas 9% worsened and 16% improved.36,38 Hiles et al.,20 in their study of 48 patients, found no significant change in the deviation after an average of 11 years follow-up, and 2 patients progressed to a constant tropia. The most we can say about the natural history is that, in the majority of cases, intermittent exotropia does not get better; it either stays the same or progresses. If the tropic phase increases, patients may develop dense suppression and, 268 handbook of pediatric strabismus and amblyopia A B FIGURE 8-1A–B. (A) Patient with intermittent exotropia and straight eyes in the phoric phase. Patient has 40 s arc stereoacuity. (B) Occlusion of the right eye disrupts fusion and manifests the exotropia. Under the occluder, the right eye is deviated temporally. over time, may progress to a constant exotropia with loss of fusional potential. Classifications Intermittent exotropia has been classically categorized into three subtypes based on the difference between the distance chapter 8: exotropia 269 C FIGURE 8-1C. (C) Occluder is removed and the right eye is deviated temporally, showing the exotropia. Patient is in the tropic phase and suppresses right eye. deviation and the near deviation. These three “older” classic cat- egories are (1) basic, (2) pseudodivergence excess, and (3) true divergence excess. It is important to note that the older termi- nology uses the term divergence excess, and pseudodivergence excess is only descriptive as to the difference of the deviation distance versus near; it is not meant to imply a mechanism for the distance–near disparities. The mechanism for the dis- tance–near disparities seen in patients with intermittent exotropia is most likely caused by superimposed overconver- gence on the basic exodeviation. These convergence mecha- nisms include tonic fusional convergence (tenacious proximal fusion),22 accommodative convergence (AC/A ratio), and proxi- mal convergence (instrument convergence). BASIC INTERMITTENT EXOTROPIA With this type of exotropia, there is no significant distance–near disparity, and the distance deviation is within 10 PD of the near deviation. Patients with a basic deviation have normal conver- gence, so their deviation is essentially the same for distance and near. 270 handbook of pediatric strabismus and amblyopia PSEUDODIVERGENCE EXCESS This is an exodeviation that is measured larger for distance fix- ation than near fixation by brief alternate cover testing (distance 10 PD greater than near); however, with prolonged monocular occlusion (patch test for 30–60 min), the near deviation increases and becomes similar to the distance deviation (within 10 PD). For example, an exodeviation measures 30 PD in the distance and 10 PD at near to alternate cover testing. One eye is patched for 30 min, and now the patient measures 30 PD in the distance and 25 PD at near. This change occurs because patients with pseudodivergence excess have increased tonic near fusional convergence that dissipates slowly after monocu- lar occlusion. Prolonged monocular occlusion of 30 to 60 min is required in these patients to dissipate tonic near fusional con- vergence and disclose the full latent deviation (see Patch Test, below). The relatively brief period of monocular occlusion that occurs with alternate cover testing is not enough to break up the tonic near fusional convergence and disclose the full deviation at near. Surgery is performed for the full distance deviation. Pseudodivergence excess is quite common. More than 80% of patients with an apparent divergence excess actually have pseudodivergence excess, as the near deviation will increase to within 10 PD of the distance deviation after the patch test.5,22,37 PATCH TEST (OCCLUSION TEST) The patch test consists of placing an occlusive patch over one eye for at least 30 to 60 min, then measuring the deviation without letting the patient restore binocular fusion. The idea is to totally suspend all tonic fusional convergence by occluding one eye, forcing the full latent deviation to become manifest. When performing the patch test, be sure the patient does not peek around the patch and regain fusion before the deviation is measured. To measure the deviation, first cover the unpatched eye with a paddle occluder, then remove the patch and measure the deviation with alternate cover testing. This method ensures the patient will not sneak a peek with both eyes and reestablish fusion before the deviation is measured. TRUE DIVERGENCE EXCESS In these cases, the distance deviation is greater than the near deviation by more than 10 PD, even after performing the patch chapter 8: exotropia 271 test. For example, the distance deviation would measure 30 PD, near deviation 10 PD and, after a 30-min patch test, the distance deviation would be 30 PD and the near deviation 15 PD. This author and Eugene De Juan (Los Angeles, CA) studied the cause of true divergence excess at the Wilmer Clinic at Johns Hopkins Hospital in Baltimore in 1981. They found that most of the patients with true divergence excess had a high AC/A (accom- modative convergence/accommodation) ratio as determined by a ϩ3.00 add after a 60-min patch test. The patch test relaxes tonic fusional convergence, and the ϩ3.00 add relaxes accom- modation. The high AC/A ratio patients do not show an increase in the near exotropia to the patch test, but the near deviation increases dramatically with a ϩ3.00 near add.40 In a similar study, Kushner22 found approximately 60% of patients with a true divergence excess had a high AC/A ratio and 40% had a normal AC/A ratio. The group with a high AC/A ratio was prone to postoperative overcorrection (75% overcorrection) at near if the distance measurement is used as the surgical target angle. The 40% of true divergence excess patients with a normal AC/A ratio had relatively good results using the distance measure- ment. Patients with true divergence excess are a difficult group to surgically correct as they are prone to having a consecutive esotropia at near, and some will require bifocals or additional surgery. Following is a summary of the causes of overconver- gence that produce true divergence excess. CAUSES OF TRUE DIVERGENCE EXCESS HIGH AC/A RATIO This condition occurs when the distance deviation is larger than the near deviation even after the patch test, but the near devia- tion increases close to the distance deviation with a ϩ3.00 add. High AC/A ratio intermittent exotropia has normal tonic fusional convergence but has a high AC/A ratio that causes the distance–near disparity. Surgery is usually performed for a deviation somewhere between the distance and near deviation measured without near add. Some of these patients require bifocals after surgery if there is an esotropia at near.
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