Constant Exotropia (XT) Flashcards
What are the risk factors for strabismus?
- Low birth weight < 2.5kg
- <37wks Gestation (premature)
- Head circumference >37cm = 36% higher risk
- XT more strongly associated with congenital abnormalities 22% malformations or chromosomal abnormalities
- Constant XT associated with schizophrenia
What’s the aetiology of XT?
Less certain, as there’s not a centre of divergence but with ET we know there is a centre of convergence. This makes understanding why XT’s happen more complicated. The reasons above are the theories as to why we have these.
- Anomalous Position of Rest = weak control
- Anatomical - Orbits shaped differently (wider) or wider IPD
- Refractive Error - Myopia, not as clear as the hypermetropia and ET relationship but in Asian cultures where Myopia is more common, XT is also more common
- Innervational Imbalance
What is Innervational Imbalance in XT?
Hypertonicity of Divergence /
Divergence excess where distance fixation > Nr
Convergence Insufficiency /
Convergence weakness where near fixation > Dist
Hypertonicity of Divergence / Convergence Insufficiency -
Non-specific (basic XT) where exotropia near equals XT distance
What’s the typical mode of onset for an XT?
X –> Intermittent XT –> Constant XT
= potential for BSV
Rarely constant XT from birth (Infantile XT)
= no BSV potential
Why might an XT increase?
Progression to increasing exotropia
- Decreased tonic convergence with age
- Development of suppression
- Reducing accommodation with age
- Increased divergence of the orbits with age
If someone has a primary constant XT, what do we need to check?
Check it’s not secondary (sensory)
Check it’s not a consecutive XT
Check BSV potential to see if it’s a decompensated X
Check for associated neurological conditions
What tests would you perform on a patient with an XT?
CT
VA – Amblyopia if child, test using crowded LogMAR
BSV tests – simultaneous perception, sensory & motor fusion, stereopsis
Measure size of deviation – PCT, Maddox Rod(?)
OM – V patterns are common in constant XT as are A patterns which will be overactions of certain muscles
CBA
PAT test with Fresnel prisms to see if a responder or non-responder to prisms/surgery (If they have ARC they will “eat up” prisms to return to original angle = prism non-responder)
If no BSV potential = PODT
Why do we need to test abnormal BSV to see how well established it is?
Prism adaptation in Abnormal BSV:
Give the prism that correct the angle of deviation onto the fovea to see if they can have potential for fusion, if they “eat up” the prism or re-diverge the abnormal connections are well established, however if not then can proceed to correct deviation. More common in those with stronger BV such as stereo and in small angle strabismus.
What area would it be stimulating? Temporal retina stimulated
Fovea cones get less and less as you go further out and therefore less chance of binocular connections being established.
What are the potential outcomes to this case?
Example - Post-op diplopia test
CT 1/3 m & 6m Mod RXT
PCT 1/3 m & 6m 35PD XT
Synoptophore obj angle = -18 degrees, subj angle not possible with peripheral slides R suppression
Post-op diplopia test 1/3m & 6m
- Suppresses to 35 PD BI then homonymous diplopia with increasing prisms
- Suppresses to 25 PD BI then heteronymous diplopia with prisms to 35PD, homonymous diplopia with prisms ≥40PD
- No diplopia with correcting / overcorrecting BI prisms to 60PD
Consider under or overcorrecting due to change in tone with age and IPD widening. Can tailor surgery (mm)
When do we do no further treatment in XT?
No further treatment if:
- Small angle
- No symptoms
- ARC
- Patient declines it
What surgery do we do in constant XT?
- MR Resect & LR Recession (unilateral)
- Bilateral LR Recession (if Dist > Nr significantly)
- 3 muscles when it’s a large angle >40PD
How much surgery do we do in an XT LR recession?
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