(S.A. Patney: InteRyc vol 2, 2000, pp 12 - 22)

ARTICLE ON STRABISMUS-SHORT REVIEW

For this issue of the short review article on strabismus I have chosen the subject of "Strabismus resulting from ocular surgery" (iatrogenic?). The reason for the choice of this subject is obvious. Maintenance of goodwill between the patient and the physician is vital. By anticipating certain complications in the postoperative phase we can warn the patient in advance about the possibility of their occurrence so that he is mentally prepared and will not tend to blame the surgeon if some difficult to manage complications do take place. We also have to know how others have managed those complications so that we do not have to go through a long trial and error period.

I therefore consider this an important subject deserving inclusion in this series.

NOTE: This subject will be divided into 3 parts and the first part appearing in this volume of the InteRyc 2000 will deal with complications following cataract surgery.

Strabismus after ocular surgery: Part I

Strabismus is not uncommonly seen after certain types of ocular surgery, the more common ones being the following:

  1. Strabismus after adult cataract surgery
  2. Strabismus after scleral buckling procedures for retinal detachment
  3. Strabismus after valve implant for glaucoma surgery

NOTE: Even non-surgical treatment sometimes leads to strabismus if one of the eyes has been patched for sometime, e.g., for corneal ulcer.

As the population of older generation is increasing and newer techniques are being used in the surgery for cataract, retinal detachment, glaucoma (with episcleral drainage devices) and refractive errors, and new agents for local anesthesia, the complaint of postoperative diplopia has become increasingly frequent.

It is therefore not surprising that strabismus following ocular surgery has been attracting a lot of attention recently. Until about a decade ago nobody except people dealing with the subject of ocular motility paid much attention to it although it was no less common. The general impression is that strabismus occurring after ocular surgery was more common in older days in cases of unilateral aphakia because of aneisokonia making fusion impossible. This does not seem to be true, as patients developing a strabismus after an ocular surgery are quite frequent even as they were a decade or two ago. The reason lies in the fact that there are other causes and precipitating factors apart from aniseikonia for this kind of strabismus. They will be elaborated a little later.

The strabismus following various types of ocular surgery can be of comitant type as well as of incomitant type. Not uncommonly there is pre-existing heterophoria that manifests after surgery, due to various causes.

Following is a short description of each of the above-mentioned types of strabismus.

Strabismus after adult cataract surgery

This type of strabismus can occur after uncomplicated cataract surgery also. More is known about it now than was a decade ago.

Etiology and classification

In fifties, sixties and seventies the two factors mainly blamed for this type of squint were aniseikonia and anisophoria accompanying the use of correction in the form of spectacles or contact lenses.

In eighties and nineties many other factors that cause fusion difficulties, diplopia and strabismus have come to light. To the above-mentioned two factors other names have been added, the most important being the anesthetic toxicity to extraocular muscles and the surgical trauma. They are at present considered the two most important causes of strabismus occurring after adult cataract surgery1, 2, 3, 4, and 5.

Diplopia after adult cataract surgery can be: (a) Transient or (b) Persistent. Also it can be A. Binocular, B. Monocular and C. Combination of the two.

Causes of monocular diplopia may be the following:

  1. Polycoria due to exposed peripheral iridectomy or iridodialysis
  2. Uncorrected refractive errors especially significant degree of astigmatism
  3. Epithelial irregularities
  4. Decentered intraocular lens
  5. Cataract in the other eye

Binocular diplopia

  1. Transient diplopia lasts for a few days to a few weeks. Fortunately it is more common than the persistent diplopia. It is due to one or more of the following several causes, e.g., pre-existing heterophoria becoming temporarily manifest, prolonged effect of local anesthetic, transient anesthetic toxicity, recovering surgical trauma to the orbital soft tissue, prismatic effect of newly acquired spectacles etc.
  2. Persistent diplopia can be caused by one or more of the following conditions6:
  1. Pre-existing disorders including heterophoria/tropia that were not detected before operation due to cataract
  2. Disorders due to prolonged occlusion (and interruption of fusion) caused by cataract
  3. Surgical trauma and myotoxicity caused by the anesthetic
  4. Optical aberrations associated with aphakia and pseudophakia

Persistent diplopia

It is quite an uncomfortable condition that may be unbearable in some people.

The names of various conditions belonging to each of the 4 groups are mentioned in the following text. Hamed6 has beautifully summed them up. The following is a modified classification:

  1. Pre-existing disorders that were not detected before surgery due to the presence of cataract or ones that still exist
  2. Disorders due to prolonged occlusion (and interruption of fusion) caused by cataract
  3. Surgical trauma and myotoxicity caused by the anesthetic
  4. Optical aberrations associated with aphakia and pseudophakia

Some important details have been mentioned under each of the conditions in the classification in the following text.

  1. Pre-existing disorders that were not detected before surgery due to the presence of cataract or ones that still exist:

Heterophoria/tropia: The list of main causes is as follows

  1. Oculomotor nerve palsy/paresis
  2. Any of the various congenital oculomotor anomalies
  3. Myasthenia gravis
  4. Thyroid ophthalmopathy: The affected muscles are more susceptible to myotoxic effects of the anesthetic. Sometimes unsuspected thyroid eye disease becomes manifest by the advent of diplopia after cataract surgery. This happens because of removal of suppression by the improvement in visual acuity. Occasionally the swollen muscles of thyroid myopathy are confused with a muscle swollen and enlarged due to the toxic effect of the anesthetic.
  5. Childhood strabismus and/or amblyopia
  6. Previous surgical trauma, e.g., retinal detachment surgery
  7. Various macular disorders, congenital and acquired

B. Disorders due to prolonged occlusion (and interruption of fusion) caused by cataract:

  1. Sensory strabismus as a result of prolonged occlusion by cataract is now becoming rare because of early operations on immature cataracts. However, it is still seen in cases of longstanding unilateral cataracts7, 8. Johnson and Tillson reported7 24 cases of intractable diplopia in the patients operated for unilateral traumatic cataracts of several years’ duration. They advise caution in the form of testing for fusion preoperatively. They are of the opinion that such patients are worse off after strabismus surgery because by reducing the angle of strabismus the images were brought close together and were difficult to suppress. Such patients should always be warned in advance about the possibility of intractable diplopia. Also one should ask for a history of amblyopia or strabismus in childhood. .... Management: Before advising uniocular occlusion for intractable diplopia prisms should be tried (for maintaining fusion) for at least 6 months.
  2. Pre-existing Amblyopia can give rise to persistent diplopia after cataract surgery by:
  3. Disruption of central fusion: A previously compensated heterophoria or congenital superior oblique (SO) palsy with good or even exceptional fusion ranges may breakdown due to the disruption of central fusion by the presence of cataract. Such patients may develop diplopia after cataract surgery. Old photographs may present evidence of congenital SO palsy by showing the appropriate head tilt.
  4. Injury to the superior oblique tendon/trochlea complex by retrobulbar injection may cause acquired SO palsy.

C. Surgical trauma and myotoxicity caused by the anesthetic:

The role of myotoxicity caused by the local anesthetic is now established. This view is supported by various studies14, 15, 16 and 17. Recently, more and more reports have been appearing in the literature about surgical trauma and anesthetic myotoxicity. Whether this is due to an actual increase in the number of patients in this group or whether more attention is being paid to these cases is anybody’s guess4, 11, 12, and 13.

Currently, the view that holds sway over others is that strabismus is due to an adverse effect of the retrobulbar injection of the anesthetic on extraocular muscles. The effect is due to two main factors: the toxicity of the anesthetic and the trauma to the muscles, nerves and the soft tissue of the orbit. The bridle-suture injury and the subconjunctival gentamycin leading to the inflammation are considered rare causes now. However Gentamycin injected into the muscle or adjacent to it can cause toxicity11.

Such cases were previously blamed on faulty injection technique, trauma to the muscle or the nerve by the injection needle, ischemia of the muscle due to severe swelling or hematoma formation, inflammatory reaction to subconjunctival injection of Gentamycin and bridle suture-trauma to the superior or inferior rectus muscles. However, it is possible that human factor is responsible in some of the cases. This view is supported by several reports that left eye (particularly left inferior rectus) is more often affected54, 55 if the injection is given by right-handed surgeons54 and 55. It is possible that right-handed surgeons find it a little more difficult to give the local anesthetic injection on the left side.

Hamed16 and 17 summarizes the factors that influence the occurrence and degree of myotoxicity by the local anesthetic injection as follows:

  1. The site of injection: Perimuscular, intramuscular, adjacent to the tendon and deep into the muscle belly.
  2. The strength (concentration) of the anesthetic
  3. The amount (volume) injected
  4. Age
  5. The extend of muscle fibre regeneration, which also depends on age
  6. The degree of fibrotic proliferation
  7. The individual’s susceptibility to the anesthetic
  8. Injury to other orbital structures like nerves
  9. Additional injury by hematoma in case of hemorrhage

D. Optical aberrations associated with aphakia and pseudophakia4, 6

The following conditions may be found under this group:

  1. Anisophoria may be found in association with the following:
    1. Anisometropia
    2. Decentration of the IOL
    3. Different segment height in the two eyes
  2. Aniseikonia
  3. Difference in color and brightness perception between the two eyes
  4. Optically induced halos and glare
  5. Changes in depth of focus by surgical alterations in the pupil
  6. Change in the fixation preference or ocular dominance may lead to fixation switch diplopia

Symptomatology

It is of utmost importance to take a thorough history (of patching, prismotherapy and squint surgery) and carry out full orthoptic (ocular motility) examination to detect the presence of pre-existing amblyopia, strabismus and diplopia before cataract surgery.

The most common signs and symptoms reported in the literature1-5, 7, 8, 10, 15, 16, 17 after adult cataract surgery are:

  1. Diplopia
  2. Strabismus and
  3. Restriction of motility
  4. Amblyopia (long standing strabismic, anisometropic or ametropic)

Different combinations of signs seen in the patients depend on the degree and stage of recovery at which they present themselves for consultation. For instance in recent cases the signs of paresis are more likely to be present while in later stages signs of contracture are more common.

Practically all of the sings and symptoms and their causes have already been described under the etiology and classification. Only some of the presenting signs are given below as reported in the literature.

1 Hypotropia is the most common sign.
(a) It is usually the result of inferior rectus contracture consequent upon its paresis due to direct injury or anesthetic myotoxicity.
(b) An acquired superior oblique (SO) tendon (Brown’s) syndrome may result due to injury to the SO tendon-trochlea complex.
(c) The third possibility is an overaction of inferior rectus secondary to a paresis of the direct antagonist, the superior rectus. The latter may result from the same causes (injury and/or anesthetic myotoxicity).
2 Hypertropia is much less common.
(A) It is usually a result of superior rectus contracture
(B) Occasionally caused by inferior oblique contracture, or
(C) May result from a paresis of inferior rectus leading to overaction/contracture of superior rectus muscle
3 Esotropia
A Usually the result of medial rectus contracture
B May be caused by a lateral rectus paresis
4 Exotropia is very rare but can occur as a result of:
A) Lateral rectus contracture, or
B) Medial rectus paresis
5 Ptosis: Rarely, levator muscle is affected resulting in ptosis18. It is rare.
6 Lagophthalmos18 is the consequence of involvement of orbicularis muscle. It is extremely rare.

NOTE: In all the cases the muscle pathology is due to either direct injury by the injection needle, pressure by a hematoma, anesthetic myotoxicity or any of the other less common causes described under etiology.

Some important points are given below:

Optical aberrations associated with aphakia and pseudophakia:

The main conditions responsible are aniseikonia and anisophoria. In fact anisophoria is much more liable to cause problems like diplopia than aniseikonia. In children the visual system is quite pliable and can adapt to rather large differences in the size of the two images. Even in unilateral aphakia evidence of fusion through the center of the lenses has been found provided corrective glasses were prescribed in early childhood19, 20.

But after the cataract surgery when the anisometropia is removed suddenly leading to isometropia, the eyes may find it difficult to once more adapt to the new situation, leading to diplopia due to aniseikonia.

Usually a difference of about 3D or more (sometimes even less) is more likely to lead to anisophoria.

Another condition that has already been named earlier in this chapter and can cause diplopia is the fixation switch. This in fact is a change in the pattern of ocular dominance or preference for fixation with one of the eyes. When one eye has been dominant all through many years and then suddenly the vision in the nondominant eye is increased after cataract surgery, the latter naturally takes over fixation. But despite better vision the previously nondominant eye may not feel comfortable. Hamed has compared this situation with the discomfort felt with a change of handedness21.

To deal with these problems in such patients, if they do not improve with time, two options are there, one improve the vision of the dominant eye to a level better than the pseudophakic eye, by cataract surgery. Or else, switch the dominance back to the previously dominant eye with appropriate lenses by blurring the vision of the pseudophakic eye (having better vision).

Differential diagnosis (See table1)

Table 1:

No.

Differential diagnosis

Confirm by

1

Pre-existing strabismus and amblyopia Orthoptic examination
2 Rule out other causes of strabismus and amblyopia in the elderly. General ophthalmic and neuro-ophthalmic exam.
3 Myasthenia gravis Tensilon (edrophonium) injection test
4 Thyroid eye disease Thyroid function studies
5 Space occupying lesions of the orbit CT scan and/or MRI
6 Preoperative or intraoperative neurovascular events Neuro-ophthalmic exam
7 Retinal lesions as for example foveal* dystopia22, 23 Fundus exam., FFA etc.

* Foveal dystopia (accompanying subretinal neovascular membranes or diabetic macular edema etc.) causes mechanical distortion of the macula leading to displacement of the fovea. Even a small displacement leads to strabismus, sometimes tiny, measuring only 1-2 diopter but causing a disruption of central fusion. The latter in turn leads to a rivalry between central and peripheral fusion. The absence of central fusion as it was (with alignment of retinal points all over the retina, central and peripheral) results in binocular diplopia. Even prisms do not help.

Management of persistent diplopia: Blurring the vision of one eye by lenses or patching gets rid of diplopia.

Management

The main points in the management of post-cataract surgery diplopia are as follows:

  1. Precaution and prevention
  2. Treatment

Precaution and prevention

Prevention of postoperative strabismus and diplopia is understandably the most important part of management. Hamed23 has summarized the various means nicely in the following way:

  1. By looking for, detecting and taking care of sensory motor anomalies of the eyes like anisometropia, amblyopia and strabismus, both paralytic and nonparalytic. Thorough orthoptic examination and management before cataract surgery can do this.
  2. By identifying the nature of obstructions to binocular vision and central fusion and removing them as far as possible.
  3. Each and every patient going in for cataract surgery should be told about the possibility of postoperative diplopia and strabismus, especially in cases with preoperative amblyopia, strabismus, Graves’ ophthalmopathy, myasthenia gravis, longstanding unilateral traumatic cataract and other sensory motor anomalies.
  4. Patients with longstanding unilateral cataracts are more liable to develop postoperative diplopia and therefore need more attention. One way out is to use contact lenses to correct aphakic refractive error instead of intraocular lenses. In case of intractable postoperative diplopia use of contact lenses can be discontinued.
  5. The dominant eye should be operated first if the degree of opacification and other factors are almost equal in both eyes. This is to avoid the problems born of fixation switch or changing of the ocular dominance.
  6. To prevent postoperative diplopia caused by myotoxicity and trauma by retrobulbar injection, the anesthesia should only be given by a person well versed in the orbital anatomy, technique of the injection and the possible complications. Alternatively, the surgery can be carried out under sub-Tenon’s infusion anesthesia, topical anesthesia or general anesthesia.

Treatment

The basic points that must be paid attention are the following:

1 Remove any factors causing asymmetry and disparity of the two eyes in respect to the size of the pupils and clarity, color, size, brightness and depth of the image. They cause unequal and different sensory inputs into the two eyes, resulting in diplopia. To do this, correct the residual refractive error and remove any other factors causing unequal and dissimilar sensory input in the two eyes. These factors have already been mentioned. Some important point are given below:
* Every effort should be made to correct the asymmetry of the two eyes. For instance if a large pupil in one eye is the problem, one can try miotics, failing which, opaque tinted contact lenses can be tried.
*

Some of the most difficult cases to manage are those with long-standing uniocular traumatic cataract with a disrupted and disused central fusion mechanism.

*

Most cases, even the most difficult ones do develop some sort of adaptation as the time goes by, provided the causes of asymmetry have been taken care of. Developing subnormal binocular vision or regaining a weak fusion usually does this. Many a times peripheral fusion holds the two eyes together.

2 Remove (as by surgery) or overcome (as by using prisms) the motor anomaly and misalignment thus removing motor obstacle to fusion.
3 Prismotherapy: Prisms play an important part in the conservative management of postoperative diplopia, especially if the deviation is less than 10 PD. Prisms ground in the glasses or Fresnel prisms are used. For larger deviations Fresnel prisms are better but they become yellowish and allow a slightly hazy vision after sometime. Moreover they are pretty expensive. In a recently reported series of 15 cases of post-cataract surgery vertical strabismus, prisms alone could manage 11 and another with prisms after the angle of deviation was reduced by surgery from 25 PD to 8PD
4 Surgery has to be resorted to if the angle of strabismus is significant. However, the following points should be kept in mind:
* Before deciding on operation every effort should be made to establish the presence of fusion, either with prisms or on the major amblyoscope.
* A thorough ocular motility workout is essential to find out the direction of maximum deviation and the muscles that have contracture or are overacting.
* Weakening the overacting muscles is the procedure of choice.
* Presence of contracture is confirmed by forced duction test.
* A large recession of the muscle with contracture is needed.
* Adjustable sutures may be used25.
5 Denervation: Some surgeons prefer chemical denervation with Botulinum toxin26 for small angle strabismus.
6 If nothing works and the binocular diplopia is intolerable, the only thing for the patient to do is to use a patch in front of the eye with problems and worse vision. However, the patch can be switched over to the other eye for some time every day, say, for two hours to prevent developing or worsening the amblyopia in that eye.

NOTE: This review article will be continued in the InteRyc-volume 2, 2000. The references will be given at the end of the third part in the InteRyc-volume 3, 2000.

 

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