A squint in childhood is often first recognized or suspected by the
parents when one eye appears to drift inwards or outwards. The majority of childhood squints are convergent (esotropia) and present before the age of 4; some are present at birth. Divergent squints (exotropia) tend to develop a little later.
Double vision is seldom appreciated by the young child because the image from the squinting eye is rapidly suppressed by the brain. This suppression interferes with the normal development of vision resulting in an amblyopic (lazy) eye.
Any suspected squint must be referred for ophthalmological assessment. Amblyopia is a serious but treatable condition.
- Genetic. In most squints there is a failure of the central mechanism governing the development and maintenance of binocular single vision. This failure may be hereditary and is also commonly found where brain damage or mental retardation (e.g. Down's syndrome) exist.
- Refractive errors. In emmetropic eyes the relationship between
accommodation and convergence is balanced but in hypermetropia the extra accommodation required to produce a clear image on the retina may lead to excessive convergence and the development of a squint.
- Ocular. Ocular abnormalities, for example congenital cataract and
retinoblastoma (corner of the retina) may impair central vision in one or
both eyes and prevent the fusion of images and the development of
The appearance of a convergent squint in infants is often caused by broad epicanthic folds but a true squint can be detected by:
- Inspection of the corneal reflexes with a torch light. These are
- The cover test. If the eye fixating an object, such as a small toy, is covered, the squinting eye will move to take up fixation.
The initial steps in the management of a squint are:
- The assessment of visual acuity in each eye.
In very young children an approximation of acuity can be obtained by observing the child's ability to pick up very small objects or follow an oscillating target (the Catford Drum).
- Ophthalmoscopy to exclude ocular disease
- Retinoscopy to determine the presence of any significant refractive error.
Fundus examination and refraction are facilitated by the use of atropine drops to dilate pupil in young children.
- Subsequent steps are:
The provision of glasses, where appropriate, in order to improve
visual acuity or restore a normal balance between accommodation and
convergence. In some squints binocular vision can be restored by
correcting the associated hypermetropia. These are known as accommodative squints.
- If the vision in the squinting eye is defective and cannot be
corrected simply by the provision of glasses amblyopia is present.
Occlusion of the fellow eye forces use of the amblyopic eye and encourages the development of normal visual acuity. Occlusion is most successful when carried out soon after the development of a squint.Little benefit is obtained from occlusion after the age of eight, by which time development of vision is normally complete.
- Squinty surgery is carried out to reduce the angle of squint.
Restoration of full binocular single vision is relatively uncommon with
convergent squints and surgery is usually cosmetic. Ideally it is carried out when amblyopia has been treated and when vision and fixation are equal in both eyes (alternating convergent squint).
The less common divergent squint is frequently intermittent and binocular vision continues to develop normally. Surgery is delayed until the increasing divergence of the eyes causes symptoms.
Stimulus deprivation amblyopia
Optical media opacities, such as cataract or ptosis, cause visual
deprivation and hence amblyopia. These opacities should be removed as
soon as possible.
Anisometropia is present if the refractive errors of the two eyes are
significantly different. The more ametropic eye has a constant blurred
image on the fovea which leads to amblyopia.
The image from the squinting eye is suppressed as mentioned. This
constant suppression leads to amblyopia. It can co-exist with
anisometropic amblyopia, and in fact, the latter might be the cause of the squint itself.
The term 'critical period' is used to describe the period of time that
visual deprivation can cause amblyopia.
In general, the longer the period of visual deprivation, the more likely it is to lead to severe amblyopia.
However, the same length of visual deprivation at a different age leads to a different degree of amblyopia.
The critical period is believed to begin at about 4 months and has maximum sensitivity at 6-9 months; it then declines until the age of 8.
In other words, a short visual deprivation at the age of 6 months can cause profound amblyopia, whilst the same visual deprivation after the age of 8 will not cause amblyopia at all.
This is very important in the management of amblyopia by patching (vide infra)
Removal of the amblyogenic agents, such as ptosis correction and refractive correction.
Patch the good eye, so as the amblyopic eye has a competitive advantage.
If patching is not possible due to poor compliance, atropine eye drop can be used to blur the image on the good eye; however, this treatment is only used as a last resort.
It is important to bear in mind that extensive patching or atropinization can cause amblyopia in the good eye, although fortunately reversal is usually fast.