Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

elevated IOP. Most cases are mild and are observed. If there is moderate to severe visual loss and or optic neuropathy, admit and consider urgent lateral cantholysis, orbitotomy, and evacuation of the haematoma. Formal bony orbital decompression may rarely be required. Consider the following, after consultation with an orbital surgeon, if there is no response to surgical decompression: mannitol (0.5–2 g/kg i.v. over 30–60 minutes), acetazolamide (500 mg i.v.), high-dose corticosteroids (e.g. methylprednisolone i.v. 0.5–2 g b.d.). Consider prophylactic antibiotics in cases associated with sinus fracture. Monitor visual and orbital function regularly (up to 2–3 times a day), depending on the response to treatment.

■Superior orbital fissure syndrome Severe impact to the lateral wall may produce oedema, haemorrhage, or bony compression of adjacent soft tissues with subsequent ophthalmoplegia (cranial nerves III, IV, VI), ptosis (III), mydriasis, efferent

pupillary defect (III), loss of accommodation (III), and V1 sensory loss (including cornea). Management includes highdose corticosteroids, e.g. i.v. methylprednisolone for 48 hours (up to 8 g/day in 1–2 divided doses or infusion), then prednisolone 1 mg/kg/day rapidly reducing (beware steroid side effects and contraindications, p. 343). Reduction of significantly displaced fractures may be considered. Superior orbital fissure syndrome may also occur with orbital apex tumours, granulomas, and idiopathic orbital inflammation

(p. 91).

■Orbital apex syndrome This consists of superior orbital fissure syndrome with optic neuropathy. Management includes highdose steroids (as above) and bony decompression.

■Orbital foreign bodies These occur in up to 3% of orbital trauma. A clear history of penetrating trauma may not be forthcoming, especially in children. Look for small entry wounds. Request CT, or MRI if organic matter is suspected. Avoid MRI if metallic objects are suspected. Beware intracranial and intraocular penetration. Removal is indicated if organic (e.g. wood), copper containing, infective (e.g. associated with an abscess, discharging sinus), or for a functional deficit (e.g. optic neuropathy, ocular motility disturbance).

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Eye socket disorders

Eye Socket Disorders

Post-enucleation socket syndrome (PESS) Caused by an absent or small implant following enucleation or evisceration; attempted correction with a large, heavy prosthesis may result in poor prosthetic retention, rotation, and instability. Clinical features form the mnemonic, PESS: P tosis, Enophthalmos, deep upper lid Sulcus, lower lid Sag (Fig. 3.15). Patients may also develop upper lid entropion with lagophthalmos.

Consider a larger artificial eye, but this may worsen lower lid sag, retention, and stability problems. If no implant is palpable, augment volume with a secondary ball implant. If an implant is present, exchange for larger ball implant, add orbital floor implant (e.g. silicone, Medpor, cranial bone graft), or autogenous material to the socket and/or postseptal upper lid sulcus (e.g. dermis-fat, micro-fat graft).

Discharge is a common and often minor problem, relating mainly to the presence of the prosthesis. Regular prosthetic care, including polishing, helps reduce proteinaceous surface biofilm. Evert the lid to exclude giant papillary conjunctivitis, and if present treat with topical steroids, e.g. G. Maxitrol q.d.s. for 1 month. Exclude exposed sutures or implants – these generally require removal of exposed material (± later reinsertion of implant or graft). True socket infection is rare and relates to bacterial contamination at the time of implant insertion, implant exposure, and host factors e.g. prior radiotherapy, diabetes or immunosuppression.

Implant exposure generally relates to inadequate surgical implantation. Failure to widely open the posterior orbital space and dragging of anterior tissues leads to insufficiently posterior placement. Restitution of dragged tissues further shallows the

implant. Other factors include poor host conditions (e.g. prior radiotherapy), insufficient socket lining (limiting closure over implant), disproportionately small, bony socket (e.g. prior radiotherapy, microphthalmos/anophthalmos), and possibly use of nonabsorbable sutures.

Poor prosthetic motility is common after eye removal ± orbital implantation, especially in horizontal gaze (shorter fornices). It is less common after evisceration than enucleation.

Distinguish motility of the socket (often poor after trauma, multiple surgeries) from that of the prosthesis. Optimize prosthetic fitting and volume augmentation. The use of pegged implants may improve motility but has a high complication rate ( ≈50%), e.g. granuloma, exposure, infection, peg extrusion, ‘clicking’ noise, poor prosthesis retention.

ORBIT 3 Chapter

Procedures

Procedures

Box 3.1: Enucleation

1.Obtain fully informed consent and agreement from two consultant ophthalmologists. Mark the side.

2.Avoid if there is endophthalmitis, as infection may spread to the orbit and brain.

3.Surgery is usually performed under GA, but retrobulbar LA with sedation is possible.

4.Confirm the side by examining the eyes, notes, and consent form.

5.Perform 360˚ peritomy using spring scissors and blunt dissect Tenon’s capsule from the globe.

6.Preplace 5/0 Vicryl in the recti near their insertion, then disinsert. Disinsert obliques (may reattach the inferior oblique)

7.Divide the optic nerve using enucleation scissors or snare. Gently handle the eyes with ocular tumours to minimize the risk of seeding. Send the eye for histopathology.

8.Obtain central retinal artery haemostasis using bipolar cautery and pressure.

9.Select an implant, typically 22 mm size. Acrylic is much cheaper than other choices. For implants other than porous polyethylene (Medpor), a wrap (e.g. Vicryl mesh) is required for muscle attachment. Donor sclera is generally avoided because of the risk of prion transmission.

10.Insert the implant behind posterior Tenon’s capsule using a ‘notouch’ technique, e.g. insert into a surgical glove finger and glide into place through a hole cut in the end of the finger.

11.Suture the recti to the implant/wrap using the preplaced sutures.

12.Close Tenon’s capsule (interrupted 5/0 Vicryl) and conjunctiva (continuous 7/0 Vicryl).

13.Insert the largest possible conformer into the fornices, leaving 2–3 mm lagophthalmos. Apply antibiotic ointment.

Box 3.1: Enucleation—cont’d

14.Apply a pressure dressing for 5–7 days and prescribe broadspectrum antibiotics, e.g. cephalexin 250 mg p.o. q.d.s. 7 days.

15.Review in 5–7 days. Early complications include orbital haemorrhage, oedema, and infection. Late complications include postenucleation socket syndrome, implant extrusion, exposure or malposition, and lining deficiency (p. 104).

16.Refer for an ocular prosthesis in 3–4 weeks.

Box 3.2: Evisceration

1.Consent, precautions, anaesthesia and peritomy are similar to enucleation (Steps 1–5 above).

2.Perform a 360˚ limbal keratectomy (blade then spring scissors).

3.Remove the intraocular contents using a metal scoop.

4.Carefully debride all uveal tissue with a cotton bud. Avoid alcohol as this may cause scleral necrosis. Cauterize the vortex veins and any bleeding vessels.

5.Split sclera diagonally across the macula into two halves (each with two recti attached).

6.‘Islandize’ the optic nerve with a small scleral rim. This prevents neuroma.

7.Insert an unwrapped implant into the posterior orbit via a ‘glide’. As per enucleation, avoid the implant contacting the surgeon or lids. Unlike enucleation, an implant wrap is not required.

8.Close the sclera (5/0 Vicryl) with a 4–5 mm overlap, avoiding closure under tension over the implant.

9.See ‘Enucleation’, points 12–16.

Optometry and General

Practice Guidelines

Infection of the skin and the eye is not uncommon, but it is important to distinguish minor soft tissue infection from preseptal cellulitis, and especially orbital cellulitis (infection behind the orbital septum). Reduced visual acuity, eye movements, diplopia, and proptosis suggest orbital cellulitis.

Orbital cellulitis requires immediate referral to a specialist to exclude lifeor vision-threatening complications. Commence

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Optometry and general practice guidelines

broad-spectrum intravenous antibiotic therapy (cefuroxime, and in patients over 10 years old, metronidazole) immediately, before investigation or referral. This measure may be sight and life saving.

Orbital trauma also requires urgent assessment; small penetrating entry points may be hard to detect or absent. Exclude and stabilize other injuries to head, neck, and spine before arranging ophthalmic review.

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

Immediate

References

1.Mourits MP, et al. Clinical activity scores as a guide in the management of patients with Graves’ ophthalmopathy. Clin Endocrinol (Oxf) 1997; 47(1):9–14.

2.Werner SC. Modification of the classification of the eye changes of Graves’ disease: recommendations of the Ad Hoc Committee of the American Thyroid Association. J Clin Endocrinol Metab 1977; 44(1):203–204

History and examination

History and Examination

History Key symptoms include redness, surface irritation, itch, discharge, watering, conjunctival swelling, and mildly blurred vision if the tear film is disturbed. More severe visual loss may indicate corneal or other disease.

Examination Systematically examine the lid margin and position, lashes, meibomian gland orifices, punctae, fornices, tarsal plates, tear film, limbus, cornea, and conjunctiva. Note and ideally draw the following:

■Conjunctival injection (hyperaemia): may be diffuse or localized.

■Subconjunctival haemorrhage: may be fine punctate haemorrhages, larger blotches, or a solid sheet.

■Discharge: note if serous or watery (viral, toxic aetiology), mucopurulent (bacterial conjunctivitis), or stringy (allergic).

■Chemosis: oedematous conjunctiva appears milky and may swell beyond the lid margins.

■Follicles: focal lymphoid hyperplasia over the tarsus produces rounded, avascular, whitish-grey centres with small vessels encircling the base (Fig. 4.1). Differentiate from papillae.

■Papillae: inflammatory exudates accumulate in the fibrous layer, heaping the conjunctiva into mounds. There is a central tuft of vessels (Fig. 4.2). When small, papillae produce a

Fig. 4.2: Papillae (Courtesy of DH Verity).

Fig. 4.3: Pseudomembrane (Courtesy of DH Verity).

smooth velvety appearance. ‘Giant papillae’ have a cobblestone appearance. At the limbus, giant papillae appear as gelatinous mounds, usually in the palpebral aperture.

■Pigment: assess the extent and whether this is associated with increased conjunctival thickness.

■Pseudomembrane: coagulated exudate that adheres to the tarsal or forniceal conjunctiva. It is easily peeled off and the

DISEASE EYE EXTERNAL 4 Chapter