Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

Fig. 13.21. Synoptophore.

3.Preoperative orthoptic exercises. These are given after the correction of amblyopia to overcome suppression.

4.Squint surgery. It is required in most of the cases to correct the deviation. However, it should always be instituted after the correction of refractive error, treatment of amblyopia and orthoptic exercises.

Basic principles of squint surgery. These are to weaken the strong muscle by recession (shifting the insertion posteriorly) or to strengthen the weak muscle by resection (shortening the muscle).

Type and amount of muscle surgery. It depends upon the type and angle of squint, age of patient, duration of the squint and the visual status. Therefore, degree of correction versus amount of extraocular muscle manipulation required cannot be mathematically determined. However, roughly 1 mm resection of medial rectus (MR) will correct about 1°-1.5° and 1 mm recession will correct about 2°-2.5°. While 1 mm resection and recession of lateral rectus (LR) muscle will correct 1°-2°. The maximum limit allowed for MR resection is 8 mm and recession is 5.5 mm. The corresponding figures for LR muscle are 10 mm and 8 mm, respectively.

5.Postoperative orthoptic exercises. These are required to improve fusional range and maintain binocular single vision.

Fig. 13.22. Optical principle of synoptophore.

INCOMITANT SQUINT

It is a type of heterotropia (manifest squint) in which the amount of deviation varies in different directions of gaze. It includes following conditions:

1.Paralytic squint,

2.‘A’ and ‘V’ pattern heterotropias,

3.Restrictive squint.

PARALYTIC STRABISMUS

It refers to ocular deviation resulting from complete or incomplete paralysis of one or more extraocular muscles.

Etiology

The lesions may be neurogenic, myogenic or at the level of neuromuscular junction.

I. Neurogenic lesions

1.Congenital. Hypoplasia or absence of nucleus is a known cause of third and sixth cranial nerve palsies. Birth injuries may mimic congenital lesions.

2.Inflammatory lesions. These may be in the form of encephalitis, meningitis, neurosyphilis or peripheral neuritis (commonly viral). Nerve trunks may also be involved in the infectious lesions of cavernous sinus and orbit.

3.Neoplastic lesions. These include brain tumours involving nuclei, nerve roots or intracranial part of the nerves; and intraorbital tumours involving peripheral parts of the nerves.

4.Vascular lesions. These are known in patients with hypertension, diabetes mellitus and atherosclerosis. These may be in the form of haemorrhage, thrombosis, embolism, aneurysms or vascular occlusions. Cerebrovascular accidents are more common in elderly people.

5.Traumatic lesions. These include head injury and direct or indirect trauma to the nerve trunks.

6.Toxic lesions. These include carbon monoxide poisoning, effects of diphtheria toxins (rarely), alcoholic and lead neuropathy.

7.Demyelinating lesions. Ocular palsy may occur in multiple sclerosis and diffuse sclerosis.

II. Myogenic lesions

1.Congenital lesions. These include absence, hypoplasia, malinsertion, weakness and musculofacial anomalies.

2.Traumatic lesions. These may be in the form of laceration, disinsertion, haemorrhage into the muscle substance or sheath and incarceration of muscles in fractures of the orbital walls.

3.Inflammatory lesions. Myositis is usually viral in origin and may occur in influenza, measles and other viral fevers.

4.Myopathies. These include thyroid myopathy, carcinomatous myopathy and that associated with certain drugs. Progressive external ophthalmoplegia is a bilateral myopathy of extraocular muscles; which may be sporadic or inherited as an autosomal dominant disorder.

III. Neuromuscular junction lesion

It includes myasthenia gravis. The disease is characterised primarily by fatigue of muscle groups, usually starting with the small extraocular muscles, before involving other large muscles.

Clinical features

Symptoms

1.Diplopia. It is the main symptom of paralytic squint. It is more marked towards the action of paralysed muscle. It may be crossed (in divergent squint) or uncrossed (in convergent squint). It may be horizontal, vertical or oblique depending on the muscle paralysed. Diplopia occurs due to formation of image on dissimilar points of the two retinae (Fig. 13.23).

Fig. 13.23. Diplopia.

2.Confusion. It occurs due to formation of image of two different objects on the corresponding points of two retinae.

3.Nausea and vertigo. These result from diplopia and confusion.

4.Ocular deviation. It is of sudden onset.

Signs

1.Primary deviation. It is deviation of the affected eye and is away from the action of paralysed muscle, e.g., if lateral rectus is paralysed the eye is converged.

2.Secondary deviation. It is deviation of the normal eye seen under cover, when the patient is made to fix with the squinting eye. It is greater than the primary deviation. This is due to the fact that the strong impulse of innervation required to enable the eye with paralysed muscle to fix is also transmitted to the yoke muscle of the sound eye resulting in a greater amount of deviation. This is based on Hering’s law of equal innervation of yoke muscles.

3.Restriction of ocular movement. It occurs in the direction of the action of paralysed muscles

4.Compensatory head posture. It is adopted to avoid diplopia and confusion. Head is turned towards the direction of action of the paralysed muscle, e.g., if the right lateral rectus is paralysed, patient will keep the head turned towards right.

5.False projection or orientation. It is due to increased innervational impulse conveyed to the paralysed muscle. It can be demonstrated by asking the patient to close the sound eye and then to fix an object placed on the side of paralysed muscle. Patient will locate it further away in the same direction. For example, a patient with paralysis of right lateral rectus will point towards right more than the object actually is.

Pathological sequelae of an extraocular muscle palsy

In all cases of extraocular muscle palsy, certain sequelae take place after some time. These occur more in paralysis due to lesions of the nerves than the lesions of muscles. These include:

1.Overaction of the contralateral synergistic muscle.

2.Contracture of the direct antagonist muscle.

3.Secondary inhibitional palsy of the contralateral antagonist muscle.

For example, in paralysis of the right lateral rectus muscle there occurs (Fig 13.24):

Overaction of the left medial rectus,

Contracture of the right medial rectus and

Inhibitional palsy of the left lateral rectus muscle.

Clinical varieties of ocular palsies

1.Isolated muscle paralysis. Lateral rectus and superior oblique are the most common muscles to be paralysed singly, as they have separate nerve supply. Isolated paralysis of the remaining four muscles is less common, except in congenital lesions.

2.Paralysis of the third cranial nerve. It is of common occurrence. It may be congenital or acquired. Clinical features of third nerve palsy (Fig. 13.25 A and B) include:

Fig. 13.24. Pathological sequelae of the right lateral rectus muscle paralysis.

A

B

Fig. 13.25. A patient with third cranial nerve paralysis showing: A, ptosis; B, divergent squint.

Ptosis due to paralysis of the LPS muscle.

Deviation. Eyeball is turned down, out and slightly intorted due to actions of the lateral rectus and superior oblique muscles.

Ocular movements are restricted in all the directions except outward.

Pupil is fixed and dilated due to paralysis of the sphincter pupillae muscle.

Accommodation is completely lost due to paralysis of the ciliary muscle.

Crossed diplopia is elicited on raising the eyelid.

Head posture may be changed if pupillary area

remains uncovered.

3. Double elevator palsy. It is a congenital condition caused by third nerve nuclear lesion. It is characterised by paresis of the superior rectus and the inferior oblique muscle of the involved eye.

4.Total ophthalmoplegia. In this condition all extraocular muscles including LPS and intraocular muscles, viz., sphincter pupillae, and ciliary muscle are paralysed. It results from combined paralysis of third, fourth and sixth cranial nerves. It is a common feature of orbital apex syndrome and cavernous sinus thrombosis.

5.External ophthalmoplegia. In this condition, all extraocular muscles are paralysed, sparing the intraocular muscles. It results from lesions at the level of motor nuclei sparing the Edinger-Westphal nucleus.

6.Internuclear ophthalmoplegia. In this condition there is lesion of the medial longitudinal bundle. It is the pathway by which various ocular motor nuclei are linked. Internuclear ophthalmoplegia is characterised by: defective action of medial rectus on the side of lesion, horizontal nystagmus of the opposite eye and defective convergence.

Investigations of a case of paralytic squint

A. Evaluation for squint

Every case of squint should be evaluated utilising the tests described on page 327-329. Additional tests

required for a case of paralytic squint are :

1.Diplopia charting. It is indicated in patients complaining of confusion or double vision. In it patient is asked to wear red and green diplopia charting glasses. Red glass being in front of the right eye and green in front of the left. Then in a semi-dark room, he is shown a fine linear light from a distance of 4 ft. and asked to comment on the images in primary position and in other positions of gaze. Patient tells about the position and the separation of the two images in different fields. Fig. 13.26 shows diplopia charting in a patient with right lateral rectus palsy.

2.Hess screen test. Hess screen/Lees screen (Fig. 13.27) test tells about the paralysed muscles and the pathological sequelae of the paralysis, viz., overaction, contracture and secondary inhibitional palsy.

The two charts are compared. The smaller chart belongs to the eye with paretic muscle and the larger to the eye with overacting muscle (Fig. 13.28).

3.Field of binocular fixation. It should be tested in patients with paralytic squint where applicable, i.e., if patient has some field of single vision. This test is performed on the perimeter using a central chin rest.

Fig. 13.28. Hess chart in right lateral rectus palsy.

4.Forced duction test (FDT). It is performed to differentiate between the incomitant squint due to paralysis of extraocular muscle and that due to mechanical restriction of the ocular movements. FDT is positive (resistance encountered during passive rotation) in cases of incomitant squint due to mechanical restriction and negative in cases of extraocular muscle palsy.

B. Investigations to find out the cause of paralysis

These include orbital ultrasonography, orbital and skull computerised tomography scanning and neurological investigations.

Paralytic vs. non-paralytic squint

Differences between paralytic and non-paralytic squint are depicted in Table 13.2.

Management

1.Treatment of the cause. An exhaustive investigative work-up should be done to find out the cause and, if possible, treat it.

2.Conservative measures. These include: wait and watch for self-improvement to occur for a period of 6 months, vitamin B-complex as neurotonic; and systemic steroids for non-specific inflammations.

3.Treatment of annoying diplopia. It includes use of occluder on the affected eye, with intermittent use of both eyes with changed headposture to avoid suppression amblyopia.

4.Surgical treatment. It should be carried out in case the recovery does not occur in 6 months. Aim of treatment is to provide a comfortable field of binocular fixation, i.e., in central field and lower quadrants. The principles of surgical treatment involve strengthening of the paralysed muscle by resection; and weakening of the overacting muscle by recession.

‘A’ AND ‘V’ PATTERN HETEROTROPIA

The terms ‘A’ or ‘V’ pattern squint are labelled when the amount of deviation in squinting eye varies by more than 10° and 15°, respectively, between upward and downward gaze.

‘A’ and ‘V’ esotropia. In ‘A’ esotropia the amount of deviation increases in upward gaze and decreases in downward gaze. The reverse occurs in ‘V’ esotropia. ‘A’ and ‘V’ exotropia. In ‘A’ exotropia the amount of deviation decreases in upward gaze and increases in downward gaze. The reverse occurs in ‘V’ exotropia.

Clinical presentations

A and V pattern heterophoria essentially refer to vertically incomitant horizontal strabismus. Thus, the horizontally comitant esotropias and exotropias (described on page 324-326) may be associated with A or V patterns.

RESTRICTIVE SQUINT

In restrictive squint, the extraocular muscle is not paralysed but its movement is mechanically restricted. Restrictive squints are characterized by a smaller ocular deviation in primary position in proportion to the limitation of movement and a positive forced duction test (i.e., a restriction is encountered on passive rotation) (see page 334).

Common causes of restrictive squint are :

Duane’s retraction syndrome,

Brown’s superior oblique tendon sheath syndrome,

Strabismus fixus,

Dysthyroid ophthalmopathy (see page 390), and

Incarceration of extraocular muscle in blow-out fracture of the orbit (see page 397).

1. Duane’s retraction syndrome

It is a congenital ocular motility defect occurring due to fibrous tightening of lateral or medial or both rectus muscles. Its features are:

Limitation of abduction (type I) or adduction (type II) or both (type III).

Retraction of the globe and narrowing of the palpebral fissure on attempted adduction.

Eye in the primary position may be orthotropic, esotropic or exotropic.

2.Brown’s superior oblique tendon sheath syndrome

It is congenital ocular motility defect due to fibrous tightening of the superior oblique tendon. It is characterized by limitation of elevation of the eye in adduction (normal elevation in abduction), usually straight eyes in primary position and positive forced duction test on attempts to elevate eye in adduction.

3. Strabismus fixus

STRABISMUS SURGERY

Surgical techniques

1.Muscle weakening procedures include recession, marginal myotomy and myectomy.

2.Muscle strengthening procedures are resection, tucking and advancement.

3.Procedures that change direction of muscle action. These include (a) vertical transposition of horizontal recti to correct ‘A’ and ‘V’ patterns (b) posterior fixation suture (Faden operation) to correct dissociated vertical deviation; and (c) transplantation of muscles in paralytic squints.

Steps of recession (Fig. 13.29)

1.Muscle is exposed by reflecting a flap of overlying conjunctiva and Tenon’s capsule.

2.Two vicryl sutures are passed through the outer quarters of the muscle tendon near the insertion.

3.The muscle tendon is disinserted from the sclera with the help of tenotomy scissors.

4.The amount of recession is measured with the callipers and marked on the sclera.

5.The muscle tendon is sutured with the sclera at the marked site posterior to original insertion.

6.Conjunctival flap is sutured back.

It is a rare condition characterised by bilateral fixation of eyes in convergent position due to fibrous tightening of the medial recti.

Fig. 13.29. Technique of recession.

Steps of resection (Fig. 13.30)

1.Muscle is exposed as for recession and the amount to be resected is measured with callipers and marked.

2.Two absorbable sutures are passed through the outer quarters of the muscles at the marked site.

3.The muscle tendon is disinserted from the sclera and the portion of the muscle anterior to sutures is excised.

4.The muscle stump is sutured with the sclera at the original insertion site.

5.Conjunctival flap is sutured back.

NYSTAGMUS

It is defined as regular and rhythmic to-and-fro involuntary oscillatory movements of the eyes.

Etiology

It occurs due to disturbance of the factors responsible for maintaining normal ocular posture. These include disorders of sensory visual pathway, vestibular apparatus, semicircular canals, mid-brain and cerebellum.

Features of nystagmus

It may be characterised by any of the following features:

Fig. 13.30. Technique of resection.

1.It may be pendular or jerk nystagmus. In pendular nystagmus movements are of equal velocity in each direction. It may be horizontal, vertical or rotatory. In jerk nystagmus, the movements have a slow component in one direction and a fast component in the other direction. The direction of jerk nystagmus is defined by direction of the fast component (phase). It may be right, left, up, down or rotatory.

2.Nystagmus movements may be rapid or slow.

3.The movements may be fine or coarse.

4.Nystagmus may be latent or manifest.

Types of nystagmus

I. Physiological nystagmus

1.Optokinetic nystagmus. It is a physiological jerk nystagmus induced by presenting to gaze the objects moving serially in one direction, such as strips of a spinning optokinetic drum. The eyes will follow a fixed strip momentarily and then jerk back to reposition centrally to fix up a new strip. Similar condition occurs while looking at outside things from a moving train.

2.End-point nystagmus. It is a fine jerk horizontal nystagmus seen in normal persons on extreme right or left gaze.

3.Physiological vestibular nystagmus. It is a jerk nystagmus which can be elicited by stimulating the tympanic membrane with hot or cold water. It forms the basis of caloric test. If cold water is poured into right ear the patient develops left jerk nystagmus (rapid phase towards left), while the reverse happens with warm water, i.e., patient develops right jerk nystagmus. It can be remembered by the mnemonic ‘COWS’ (Cold– Opposite, Warm–Same).

II. Sensory deprivation (ocular) nystagmus. It may occur in following forms:

1.Congenital pendular (ocular) nystagmus. It is a horizontal slow pendular nystagmus usually associated with sensory deprivation due to reduced central visual acuity. Its common causes are congenital cataract, congenital toxoplas-mosis, macular hypoplasia, aniridia, albinism, optic nerve hypoplasia and Leber’s congenital amaurosis.

2.Acquired ocular nystagmus. It occurs in monocular adults when they develop decreased

visual acuity in the only seeing eye. It is a pendular nystagmus.

3.Miner’s nystagmus. It is a rapid rotatory type of nystagmus which occurs in coal mine workers. It probably results from fixation difficulties in the dim illumination.

III. Motor imbalance nystagmus

1.Congenital jerk nystagmus. It is a hereditary nystagmus of unknown etiology which persists throughout life. It is bilateral, horizontal jerk nystagmus with rapid phase towards the lateral side. It is not present during sleep.

2.Latent nystagmus. It is not present when both eyes are open. It appears when one eye is covered. It is a jerk nystagmus with rapid phase towards the uncovered eye.

3.Spasmus nutans. It is characterised by fine pendular horizontal nystagmus associated with head nodding and abnormal head posture. It appears in infancy and self-resolves by the age of 3 years.

4.Peripheral vestibular nystagmus. It occurs due to diseases of the eighth nerve or vestibular end organ. The nystagmus is jerky, fine, rapid and horizontal-rotatory.

5.Central vestibular nystagmus. It may be of the following types:

(a)Upbeat nystagmus. In primary position of gaze, the fast component is upward. It is usually seen in lesions of central tegmentum of brain stem.

(b)Down beat nystagmus. In primary position of gaze the fast component is downward. It is usually associated with posterior fossa diseases and is typical of compression at the level of foramen magnum. It is a common feature of cerebellar lesions and Arnold Chiari syndrome.

(c)Periodic alternative nystagmus: It is a jerk nystagmus which shows fluctuations in amplitude and direction. It may occur due to vascular or demyelinating brain stemcerebellar lesions.

6.Gaze-paretic nystagmus. It is a slow horizontal jerk nystagmus due to upper brain stem dysfunction.

7.Convergence retraction nystagmus. It is a jerk nystagmus with bilateral fast component towards the medial side. It is associated with retraction of the globe in convergence.

8.See-saw nystagmus. In it, one eye rises up and intorts, while the other shifts down and extorts. It is usually associated with upper brain stem lesions.

9.Nystagmus blockage syndrome. It is a rare condition in which sudden esotropia develops in infancy to dampen the horizontal nystagmus.

NYSTAGMOID MOVEMENTS

There are ocular movements which mimic nystagmus. These include:

1.Ocular flutter occurs due to interruption of cerebellar connection to brain stem. It is characterized by horizontal oscillation and inability to fixate after change of gaze.

2.Opsoclonus refers to combined horizontal, vertical and/or torsional oscillations associated with myoclonic movement of face, arms and legs. It is seen in patients with encephalitis.

3.Superior oblique myokymia is characterized by monocular, rapid, intermittent, torsional vertical movements (which are best seen on slit-lamp examination).

4.Ocular bobbing refers to rapid downward deviation of the eyes with slow updrift. It occurs due to pontine dysfunctions.

APPLIED ANATOMY

Gross anatomy

Structure

Glands of eyelid

Blood supply

Nerve supply

CONGENITAL ANOMALIES

ANOMALIES IN THE POSITION OF LASHES AND LID MARGIN

Trichiasis

Entropion

Ectropion

Symblepharon

Ankyloblepharon

Blepharophimosis

APPLIED ANATOMY

GROSS ANATOMY

The eyelids are mobile tissue curtains placed in front of the eyeballs (Fig. 14.1). These act as shutters protecting the eyes from injuries and excessive light. These also perform an important function of spreading the tear film over the cornea and conjunctiva and also help in drainage of tears by lacrimal pump system. Parts of eyelid. Each eyelid is divided by a horizontal furrow (sulcus) into an orbital and tarsal part.

Position of lids. When the eye is open, the upper lid covers about one-sixth of the cornea and the lower lid just touches the limbus.

Canthi. The two lids meet each other at medial and lateral angles (or outer and inner canthi). The medial canthus is about 2 mm higher than the lateral canthus. Palpebral aperture. It is the elliptical space between the upper and the lower lid. When the eyes are open it measures about 10-11 mm vertically in the centre and about 28-30 mm horizontally.

The lid margin. It is about 2-mm broad and is divided into two parts by the punctum. The medial, lacrimal portion is rounded and devoid of lashes or glands.

Fig. 14.1. Gross anatomy of the eyelid.

The lateral, ciliary portion consists of a rounded anterior border, a sharp posterior border (placed against the globe) and an intermarginal strip (between the two borders). The grey line (which marks junction of skin and conjunctiva) divides the intermarginal strip into an anterior strip bearing 2-3 rows of lashes and a posterior strip on which openings of meibomian