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Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

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minutes improves neuromuscular transmission and improves function).

Congenital cases : work-up for a possible neurological aetiology.

Hess chart : Figure 13.5.

Treatment

Treat amblyopia in children <8 years old (p. 589). Prisms may help in isolated muscle cases.

Surgery only achieves a limited area of binocular single vision at best. The main aim is to improve the appearance. Residual diplopia can be treated with an occlusive contact lens.

1.Exotropia with hypotropia : large lateral rectus recession, and resection of medial rectus with supraplacement of the insertions. Consider recessions of contralateral synergists.

2.Mainly exotropia : large lateral rectus recession and resection of medial rectus with temporary traction sutures. Nasal transposition of the vertical rectus muscles.

3.Superior division : Knapp procedure for hypotropia.

4.Inferior division : inverse Knapp for hypertropia on depression.

Follow–up Review isolated pupil-sparing cases at 1 week, then monthly. Expect improvement in presumed microvascular cases and arrange CT or MRI if not evident in 6–12 weeks, or if any aberrant regeneration occurs.

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Left eye

Rect.sup. Obl.inf.

 

Rect.sup.

Obl.inf.

 

Rect.ext.

Rect.ext.

Rect.int.

Rect.int.

 

Rect.inf.

Obl.sup.

 

Rect.inf.

 

 

Obl.sup.

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Obl.inf.

 

 

up

Right eye

Rect.s.

 

Obl.inf.

Rect.sup.

 

Rect.int.

Rect.int.

Rect.ext.

Rect.ext.

 

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Obl.sup.

 

 

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Green before right eye

3rd nerve palsy

Fig. 13.5: Hess chart of a total right third nerve palsy. This shows the primary deviation with the right eye exotropic and hypotropic (right lateral rectus and superior oblique functioning). The right affected eye has the smaller field and is markedly constricted in the fields of action of the affected muscles (right superior, medial and inferior recti and inferior oblique). The large left field shows the secondary deviation and overactions of the contralateral synergists (Sherrington’s law).

4th Nerve Palsy

Background May be unior bilateral, congenital (abnormal superior oblique tendon/trochlea) or acquired (head trauma; trochlear/orbital injury; ENT surgery; sinus infections, or vascular). May also be idiopathic or associated with hypertension and diabetes, or more rarely demyelination, giant cell arteritis, tumours, and aneurysms.

Symptoms Vertical diplopia ± torsional and horizontal components.

Signs A left superior oblique palsy may have a head tilt ± slight face turn to right, with chin depression. Cover testing shows left hyperdeviation, greater for near, with slight esodeviation. Excyclotorsion may be present. Hyperdeviation and diplopia increase in dextrodepression but this is less common in congenital cases. Torsional diplopia is maximum on laevodepression. The Bielschowsky head tilt test (p. 587) may show a positive result – an increased hyperdeviation on head tilt left – but not all practitioners feel it is reliable.

History and examination Diplopia is a presenting sign in acquired cases – usually vertical, on depression and to one side; diplopia may also have horizontal and tilted components. In congenital cases diplopia is less common as a presenting symptom. Such cases may present at any age because of signs of decompensating or abnormal head posture (AHP) noticed by others.

Investigations

Full orthoptic testing including vertical fusion range.

Synoptophore.

Hess chart : Figure 13.6.

Blood tests : fasting glucose. ESR and CRP if age > 50 years.

CT or MRI : request if age <50 years and no diabetes or hypertension, or if failure to improve after 6 weeks. Image urgently via neurologists if there are other signs, including cranial nerve palsies.

Differential diagnosis

Congenital versus acquired : acquired cases are more likely to experience diplopia, especially with subjective torsion, have binocular single vision, and normal (6 dioptres) vertical fusion range. Congenital cases may have contralateral facial

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Left eye

Rect.sup. Obl.inf.

 

Rect.sup.

Obl.inf.

 

Rect.ext.

Rect.ext.

Rect.int.

Rect.int.

 

Rect.inf.

Obl.sup.

 

Rect.inf.

 

 

Obl.sup.

Green before left eye

Obl.inf.

 

 

up

Right eye

Rect.s.

 

Obl.inf.

Rect.sup.

 

Rect.int.

Rect.int.

Rect.ext.

Rect.ext.

 

Obl.sup.

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Obl.sup.

 

 

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Green before right eye

4th nerve palsy

Fig. 13.6: Hess chart showing a left fouth nerve palsy. This shows the primary deviation of a small left hypertropia. The smaller left field shows greatest constriction in the field of action of the superior oblique. The left fields also shows a small overaction of the unopposed ipsilateral antagonist – left inferior oblique. The right field shows the larger secondary deviation – right hypotropia (Hering’s law) and the greatest enlargement is in the field of action of the right inferior rectus (contralateral synergist – Sherrington’s law), and a slight underaction of the right superior rectus (secondary inhibitional palsy of contralateral antagonist).

hypoplasia, a large vertical fusion range (but not always), and often have a longstanding AHP which can be seen in old photographs.

Unilateral versus bilateral : assume bilateral until proved otherwise. Bilaterality is suggested by a ‘V’ esodeviation, a

right over left in laevodepression and left over right in dextrodepression (may be very asymmetrical), and 10 degrees of excyclotorsion on the synoptophore in depression.

Other diseases : consider myasthenia gravis, skew deviation, and orbital disease.

Treatment

Medical : prisms (and/or AHP) may control small deviations. Joining the vertical diplopia often allows patients to then fuse a remaining slight horizontal deviation, if present. Prisms

cannot join torsional diplopia. Treat any amblyopia in children <8 years (p. 589).

Surgery : options for hyperdeviation include:

1.Ipsilateral inferior oblique weakening if <15 prism dioptres in primary position.

2.Superior oblique tendon tuck if superior oblique underaction exceeds inferior oblique overaction, particularly in congenital cases.

3.Ipsilateral superior rectus recession.

4.Contralateral inferior rectus recession.

For bilateral acquired cases perform bilateral Harado-Ito procedure to correct torsion first.

Follow–up

All patients are seen every 1–2 months whilst being monitored for stability/recovery.

Unilateral cases of vascular origin usually recover within 6 months. Congenital cases, as the deviations tend to be larger, often require surgery as do large unrecovered vascular or more frequently bilateral traumatic superior oblique palsies. Small unrecovered deviations with vertical/horizontal diplopia can be managed long-term by incorporating prisms into spectacles.

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6th nerve palsy

6th Nerve Palsy

Background Several possible causes include:

Adults : microvascular (particularly if aged >50 years, hypertensive, or diabetic), MS, neoplasm, head trauma, infection (bacterial or viral), raised intracranial pressure, and idiopathic.

Children : similar to adults except microvascular causes are unlikely. Transient 6th nerve palsies may occur in neonates. ‘Benign 6th nerve palsy of childhood’ may occur 1–3 weeks after a febrile viral illness.

Symptoms Horizontal diplopia greater looking to the affected side and in the distance. Diplopia may be constant in total 6th nerve palsy.

Signs Patients may have a head turn to the same side, limited abduction, and esodeviation most easily detected with cover test and a distant target, comparing findings in extreme left and right gaze. Nuclear lesions are accompanied by a gaze palsy to the same side because of involvement of the conjugate gaze mechanism. Pontine lesions may be accompanied by a 7th nerve palsy, and cavernous sinus disease is often accompanied by 3rd , 4th and trigeminal division of 5th nerve palsies. Look for bilaterality.

History and examination See page 612.

Investigations

Orthoptic testing : a prism cover test (PCT) in right and left gaze at distance quantifies incomitance and is useful diagnostically and preoperatively. There is usually motor fusion and stereopsis at near.

Hess chart : Figure 13.7.

Blood tests : fasting glucose. ESR and CRP if >50 years old.

MRI and CT: request if age <50 years and no diabetes or hypertension, or if failure to improve after 6 weeks. Image urgently via a neurologists if there are other signs, including other cranial nerve palsies.

Management Most microvascular palsies and childhood postviral palsies resolve spontaneously, so offer prisms or, for large very incomitant deviations, occlusion. If stable and symptomatic after more than 6 months, consider surgery. The selected operation depends on the abduction status (check with

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Left eye

Rect.sup. Obl.inf.

 

Rect.sup.

Obl.inf.

 

Rect.ext.

Rect.ext.

Rect.int.

Rect.int.

 

Rect.inf.

Obl.sup.

 

Rect.inf.

 

 

Obl.sup.

Green before left eye

Obl.inf.

 

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Right eye

Rect.s.

Obl.inf. Rect.sup.

Rect.int. Rect.int. Rect.ext. Rect.ext.

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Green before right eye

Fig. 13.7: Hess chart of a left lateral rectus palsy. The left smaller field in the affected eye shows a small esotropia in the primary position; there is greatest constriction in the field of action of the left lateral rectus. The right field shows a larger secondary esotropia in the primary position (Hering’s law); the greatest enlargement is in the field of action of the right medial rectus (contralateral synergist – Sherrington’s law).

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6th nerve palsy

diagnostic botulinum toxin to medial rectus). If there is abduction beyond the midline, the palsy is incomplete, so perform medial rectus recession and lateral rectus resection. If not, the palsy is complete, so undertake transposition of the vertical recti to the lateral rectus border and botulinum toxin to the ispilateral medial rectus. Treat bilateral palsies like unilateral ones, but these often need second-stage surgery.

Follow–up Monitor for stability or recovery. Review every 1–2 months. Unilateral cases of vascular origin usually recover within 6 months. If recovery does not take place, smaller unrecovered deviations can be managed long-term by incorporating prisms into spectacles. Larger/very incomitant deviations may require surgery.

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Optometry and General

Practice Guidelines

General comments

All children under the age of 5 years with suspected strabismus and amblyopia should be assessed by an orthoptist. However, those who are older than 5 years may be seen initially by a community optometrist. The risk of amblyopia and strabismus is increased in children with a family history of squint, amblyopia or a high refractive error (particularly hypermetropia), and children born prematurely or with developmental delay.

Optometrists

Preschool children who are found to have abnormal amounts of hypermetropia (>+3.5 dioptres), or anisometropia (>1.0 dioptre), or astigmatism (>1.5 dioptres) are at risk of developing strabismus and amblyopia. To prevent this, a spectacle correction is required. If in doubt about management, discuss with a Hospital Eye Service.

General practice

Never delay referral for suspected squint as it is very rare for a child to ‘grow out of it’. Squint or limited eye movements due to trauma, even when the eye does not appear inflamed, should be seen the same day. Childhood refractive errors (without squint) are usually treated by an optometrist experienced in refracting children.

The following guide to referral urgency is not prescriptive, as clinical situations vary.

Same day

3rd nerve palsy with pupil involvement

p. 612

Orbital blow-out fractures

p. 101

6th nerve palsy with papilloedema (refer to neurology)

p. 618

Urgent (within 1 week)

 

Sudden onset of squint with diplopia in a child

 

>5 years

p. 585

Sudden onset of double vision

p. 585

Squint with other neurological symptoms or signs

p. 585

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Optometry and general practice guidelines

Routine

Disorders of accommodation and convergence

p. 599

Childhood squints with full ocular movements

p. 585

Adults, without diplopia, requesting squint surgery

 

for cosmetic improvement

p. 585

Long-standing squints with increasing angle of

 

deviation

p. 585

Amblyopia

p. 589

Suspected squint

p. 585

Refractive errors (see comments above)

p. 560

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