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Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

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RETINA SURGICAL 11 Chapter

Fig. 11.17: Choroidal rupture with foveal involvement.

 

Choroidal rupture

 

 

 

 

 

 

Rupture and retraction of the choroid–Bruch’s–RPE complex

 

allows the underlying sclera to be seen as a white streak (Fig.

 

11.17). Alternatively, it may be obscured by subretinal

 

haemorrhage. If there is submacular haemorrhage, discuss

 

urgently with a vitreoretinal surgeon, as some advocate drainage.

 

Otherwise, manage conservatively with review in 2–3 weeks.

 

Ruptured globe

 

 

 

 

 

 

Ruptured sclera is easily missed if haemorrhagic chemosis

 

obscures the view or the injury is posterior. Ask about the

 

mechanism of injury, and previous eye disease or surgery. Gently

 

examine for hypotony, deep or collapsed AC, hyphaema, corneal

 

or lens injury, uveal or vitreous prolapse, vitreous haemorrhage,

 

reduced ocular motility, and VA. Normal IOP does not exclude the

 

diagnosis but normal fundal examination makes posterior scleral

 

rupture from blunt trauma unlikely. If intraocular haemorrhage

 

obscures the view and the index of suspicion is low, ultrasound

 

(USS) may help rule out lens dislocation, retinal detachment,

 

vitreous haemorrhage, and posterior scleral rupture. Avoid USS if

 

penetration is thought likely, as transducer pressure during

 

examination may extrude intraocular tissue (consider CT instead).

 

 

Request plain X-rays if metal orbital or intraocular foreign body

553

 

 

 

Posterior segment trauma

Box 11.3: Primary repair of ruptured globe

1.Explain the procedure and the uncertain, usually guarded prognosis. Subsequent surgery is often required to improve vision or remove the eye. Primary evisceration or enucleation is rarely necessary and only after review by two consultants.

2.Warn the anaesthetist that surgery sometimes takes several hours.

3.Gently insert a lid speculum.

4.Perform a 360º conjunctival peritomy and carefully examine the sclera back to the four vortex veins. Blunt injury often produces rupture at the limbus, under the recti, or through old surgical wounds. This tends to be limited to one wound, but this may be extensive.

5.Consider slinging the recti with 2/0 silk sutures to help position the eye. Recti may need to be temporarily disinserted to access underlying wounds. Measure the muscle’s distance from the limbus before removing and pre-place a double-armed 5/0 Vicryl suture at the anterior muscle border. Reattach after scleral repair.

6.Gently lift prolapsed, nonviable uveal tissue, vitreous, or blood with a dry cellulose sponge and trim flush with the sclera using fine scissors. Avoid excessive vitreous traction. Alternatively, use a vitrector at high cut rate, e.g. 300 cuts/min.

7.Remove any IOFBs visible at the wound opening.

8.Close corneal wounds with interrupted, simple, 10/0 Nylon sutures. Bury knots. It can be difficult to rotate sutures in hypotonous eyes, so start the first bite within the wound margin so that the knot ties within the wound. Close sclera with 8/0 Nylon sutures, conjunctiva with 7/0 Vicryl.

9.It may not be possible to suture very posterior wounds, but these often seal spontaneously after 10 days.

10.Cadaveric sclera is occasionally required to replace missing tissue. Silicone explants can be used if none is available.

11.Once closed, reinflate the eye with intraocular saline and revise any leaking wounds. Cyanoacrylate glue can seal small leaks; dry tissue before applying.

12.Once the globe is secure, examine for conjunctival foreign bodies and eyelid injury.

13.Gently inject subconjunctival antibiotic unless there are open posterior wounds.

554

(IOFB) are possible, but if revealed, use CT to localize. MRI is unsafe with metal FBs. Examination under anaesthesia with conjunctival recession is sometimes required, so keep nil by mouth except for prophylactic ciprofloxacin 750 mg b.d. p.o.. Guard the eye with a plastic shield preoperatively. For repair of ruptured globe, see Box 11.3.

Follow up Day 1 postoperatively, exclude endophthalmitis, retinal detachment, and hypotony. Later complications include phthisis, proliferative vitreoretinopathy with retinal detachment, tissue downgrowth and sympathetic ophthalmia. Rx G. dexamethasone 0.1% 1 hourly by day, Oc. betamethasone nocte, G. ofloxacin 2 hourly, G. atropine 1% o.d. Continue oral antibiotics for 10 days. Review in 1 week. Explain the symptoms of retinal detachment (p. 529) and sympathetic ophthalmia (p. 354).Do not enucleate seeing eyes (even faint perception of light) in an attempt to prevent sympathetic ophthalmia in the undamaged eye, as the visual prognosis is hard to predict and enucleation is not proven to reduce the risk of sympathetic ophthalmia.

Intraocular foreign body

Intraocular foreign body is most commonly caused by metal hammering metal. Signs are similar to penetrating injuries (see Ruptured Globe above) but endophthalmitis is more common

(10%). The decision whether to remove as a primary procedure or subsequently depends on the IOFB size and material, visual potential, surgeon, and patient preference. Discuss with a vitreoretinal surgeon. Endophthalmitis, organic or reactive metal IOFBs (iron/copper) usually require primary removal. Surgery usually involves a three-port pars plana vitrectomy with removal through a sclerotomy. Sometimes a magnet is used to retrieve ferrous IOFBs via a sclerotomy, with or without vitrectomy. Document the IOFB size and send for culture. Preand postoperative management is similar to ruptured globe, but explain the risks of vitrectomy (p. 532). Gas tamponade may be required, so flying may be contraindicated for several weeks.

RETINA SURGICAL 11 Chapter

555

Optometry and general practice guidelines

Optometry and General

Practice Guidelines

General comments

Many patients have a few longstanding vitreous floaters or the occasional flash of light (photopsia), and do not require ophthalmology review. Clues to significant vitreoretinal traction are a sudden increase in the number of floaters or change in the nature of the photopsia, especially flashes of light in the temporal field. Risk factors for retinal detachment (RD) include high myopia, trauma, and previous RD in either eye. In the context of photopsia and floaters, a field defect suggests retinal detachment and blurred vision suggests macular detachment or vitreous haemorrhage. Any of these features warrant same-day ophthalmology review. The commonest differential of photopsia is migraine. Any patient with flashes or floaters should be given a retinal detachment warning.

Optometrists

Acute onset or suddenly changed symptoms of flashes and/or floaters in one eye should be treated as an RD until proven otherwise. Same-day ophthalmology review is required regardless of findings, so dilated fundoscopy by an optometrist

is not therefore required. Anxious patients can be reassured that >90% of cases will not have RD.

Longstanding floaters, or the occasional flash of light should be investigated by the optometrist. Maximal dilation is necessary to view the extreme periphery, therefore use a combination of tropicamide 1%, and phenylephrine 2.5% (after excluding narrow angles, drop allergies, a history of unstable cardiac disease or iris clip intraocular lenses). Warn not to drive until the drops have worn off. Refer abnormalities as detailed below.

General practice

The optometry guidelines also apply, except that many general practitioners will not feel as confident with ophthalmoscopy. If so, then refer chronic mild floaters for routine hospital review. If there are any acute symptoms or features suggesting significant vitreoretinal traction (see above), arrange same-day ophthalmology

556 review.

No referral is required for posterior vitreous detachment or lattice degeneration if these occur in isolation. The following guide to referral urgency is not prescriptive, as clinical situations vary.

Immediate

Macular-on retinal detachment (nil by mouth)

p. 529

Same day

 

Macular-off retinal detachment (nil by month)

p. 529

Posterior vitreous detachment with flashes and

 

floaters

p. 521

Positive Shafer’s sign (pigment cells in vitreous)

p. 521

Vitreous haemorrhage

p. 543

Retinal tear

p. 552

Routine

 

Lattice degeneration with atrophic round holes,

 

but no tears

p. 523

Macular hole

p. 540

Epiretinal membrane

p. 536

References

1.The Diabetic Retinopathy Vitrectomy Study Research Group. Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy. Two-year results of a randomized trial. Diabetic Retinopathy Vitrectomy Study report 2. Arch Ophthalmol 1985; 103:1644–1652.

2.Thanks to Martin Snead of Adenbrooke’s Hospital, Cambridge, for critique.

RETINA SURGICAL 11 Chapter

557

Chapter 12

PAEDIATRICS

History and Examination

Basics Before each consultation, read the notes and decide what questions need to be answered: perform the key parts of the examination first in uncooperative children. Be flexible; for example, it may sometimes be better to examine a child before taking a history. Children (and their carers) are often anxious and it helps to perform the examination in a child-friendly setting, without wearing a white coat. Speak and move gently, and explain what you are going to do. Consider examining the child’s carer or toy first and warn that drops sting. Fundoscopy, retinoscopy, and portable slit lamp examination can sometimes be carried out with the child asleep.

History Note the presenting complaint and birth, family, social, and drug/allergy history. If relevant, draw a family tree (p. 412). Ask if the child attends any other clinics. Ask about hearing and normal developmental milestones.

Vision assessment Acuity develops throughout infancy and does not reach normal adult levels until about the age of 2 years. It may not be possible to obtain accurate acuity assessment of each eye separately until 3–4 years of age.

An age-appropriate vision test should be performed. Log MAR tests are preferable. Check the eye suspected of being the worst first. Observe the child’s response to occlusion. If an eye is densely amblyopic, covering the good eye causes distress.

In an infant with suspected blindness, test the blink response to threat and bright light and see if the child fixes and follows a silent stimulus. Do a spinning baby test. The normal response is tonic deviation of the eyes in the direction of rotation with reflex saccadic movement in the opposite direction. Severe visual impairment due to higher visual pathway damage produces prolonged nystagmus on cessation of rotation (normally only 1–2 beats). Oculomotor apraxia produces tonic deviation without saccades, and characteristic head thrusts are used to break fixation.

Examination Observe the child’s visual attention, alertness, 558 and the presence of any facial abnormality or head posture.

Significant field defects can usually be detected by holding an interesting target straight ahead and then moving a toy in the periphery and seeing if the child looks towards this.

With a torch, examine the conjunctiva, corneal clarity, and pupil reactions. Examine the anterior segment in more detail with a portable slit lamp or direct ophthalmoscope using plus lenses. Infants can be examined on the normal slit lamp by holding them in a prone position when they will extend their neck and can be ‘flown’ into the chin rest.

Look for nystagmus and examine ocular movements. If a squint is suspected, perform cover–uncover, and alternate cover tests to look for manifest and latent deviation, respectively. Examine the pupil response to light and exclude a relative afferent pupil defect (RAPD).

Perform cycloplegic refraction and fundal examination to exclude refractive errors, media opacities, and fundus abnormalities. Document if examination is difficult or incomplete. Use G. cyclopentolate 0.5% under 6 months of age and 1% if older. Some add G. phenylephrine 2.5% in dark eyes or if dilatation is poor.

If adequate cycloplegia is not achieved then use Oc atropine 1% b.d. for 3 days prior to, but excluding, the day of examination to avoid corneal smearing. Atropine drops can be substituted if ointment is unavailable. These do not smear the cornea and can be used on the day of examination, but systemic absorption is higher.

Using a ‘nonstinging’ anaesthetic eyedrop (e.g. proxymetacaine) before dilating drops may reduce discomfort, lacrimation, and future anxiety about eyedrops.

Check the red reflex then start fundoscopy using an indirect ophthalmoscope and a 28 D or 30 D lens (or equivalent), and then a direct ophthalmoscope or higher magnification lens for a more detailed disc examination. Reducing the illumination improves cooperation. In older children, slit lamp biomicroscopy should be possible.

If glaucoma is suspected, check the IOP with an air puff tonometer or Tonopen in younger children who cannot be checked with applanation tonometry.

If cooperation is lost

Casualty : in an emergency situation it is important to obtain as full an examination as possible. Record any relevant tests that were not completed. Explain to the carer what needs to be done and why. Swaddle the child in a blanket then complete the fundus and anterior segment examination.

Clinic : consider ending the consultation and re-booking. Rarely, examination under anaesthetic is required.

12 ChapterTRICS

559

Prescribing glasses

Prescribing Glasses

Background Most infants have 1–3 dioptres (D) of hypermetropia, often with a degree of astigmatism. The hypermetropic refractive error usually emmetropizes by the age of 6–7 years. There is some evidence that fully correcting hypermetropia in a child may reduce emmetropization, so small degrees are not usually corrected and large degrees are usually undercorrected. Anisometropia is a risk factor for the development of amblyopia.

The following are guidelines for the prescription of glasses in children, as situations vary.

Hypermetropia If a child has >4 D of hypermetropia, correct two-thirds of the spherical equivalent, with full correction of any associated astigmatism. Correcting hypermetropia may improve reading in some children with normal distance acuity. Fully correct hypermetropia if the child has a convergent squint.

Myopia Correct myopia if there is reduced vision, which is likely to occur with myopia of − 0.5 D or more. Correcting even small degrees of myopia in a child with intermittent exotropia may substantially improve control of the squint.

Anisometropia Fully correct more than 1 D of anisometropia after age 3 years. Higher degrees will need correcting at younger ages. If there is one nearly emmetropic eye and the fellow is amblyopic and hypermetropic, fully correct the amblyopic eye. If both eyes are hypermetropic with similar vision, give an equal correction to each eye, maintaining the interocular difference, e.g. for + 6 D OD and +3 D OS give +4 D OD and +1 D OS.

Astigmatism Correct 1.50 D or more of astigmatism. Consider correcting smaller degrees in older children if it improves their acuity. Astigmatism is often overestimated in children, secondary to off-axis retinoscopy.

Bifocals Bifocals may be a useful alternative to surgery in children with convergence excess esotropia. They may also be useful in some children, such as those with Down’s syndrome, who may have poor accommodation.

560

Leucocoria

Leucocoria is a white pupil (Fig. 12.1). It is a serious sign that requires urgent referral and assessment. The more common causes include:

Infantile cataract: see next page.

Coats’ disease: page 564.

Persistent hyperplastic primary vitreous: page 565.

Toxocariasis: page 565.

Retinoblastoma: page 407.

Fig. 12.1: Leucocoria in the left eye due to congenital cataract.

12 ChapterTRICS

561

Infantile cataract

Infantile Cataract

Background Bilateral or unilateral lens opacity is historically termed congenital cataract if presumed present at birth. The cumulative incidence by 1 year is 2.5 cases per 10 000 births in the UK. It is bilateral in 66%, with 55% being isolated cataract and 45% associated with other ocular or systemic disorders. Inherited cataract (usually autosomal dominant) accounts for 56% of bilateral lens opacities. Associated ocular anomalies are more common with unilateral cataract, particularly persistent hyperplastic primary vitreous (PHPV), whilst systemic disease usually produces bilateral cataract, with prenatal infection and Down’s syndrome being the commonest.

History and examination Ask the parents about the pregnancy and family history. Check the pupils for an afferent defect. A portable slit lamp makes cataract assessment easier and helps exclude associated anterior segment dysgenesis. The quality of the retinal image on direct or indirect ophthalmoscopy is another measure of severity; if the posterior pole cannot be easily seen visual deprivation is expected. Common cataract morphologies are nuclear, lamellar, anterior polar, posterior subcapsular, posterior with lenticonus, and total lens involvement. Examine the parents, as they may have unrecognized cataract. Other signs include delayed visual development, strabismus, and nystagmus.

Differential diagnosis Consider other causes of leucocoria (see previous page)

Investigations B-scan ultrasonography to assess posterior structures and the globe size (including interocular asymmetry), and biometry if required. Paediatric assessment to exclude systemic causes and associations. Routine investigations include TORCH screen (maternal infection), urinary reducing sugars (galactosaemia), and urinary amino acids (Lowe’s syndrome). Electrodiagnostic testing may be indicated if retinal dysfunction is suspected.

Treatment

Casualty : refer to a specialty clinic the same week, as visually significant unilateral or bilateral cataracts are ideally removed within 6 weeks of birth, to avoid deprivational amblyopia.

Clinic : the decision to operate is made by the parents, after discussion with a surgeon experienced in infant cataract

 

surgery. Bilateral cataracts detected early are treated by

562

lensectomy and anterior vitrectomy, with the resulting aphakia