Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Box 6.3: Anterior vitrectomy (Fig. 6.22)

1.Be familiar with the anterior vitrector before it is required; know how to set up the machine.

2.A bimanual method is preferred by many to limit hydration and further vitreous prolapse. Separate the 20-gauge cutter from the infusion. If there is minimal vitreous prolapse, perform a ‘dry’ vitrectomy (no infusion), maintaining the AC with viscoelastic. Otherwise, insert the infusion cannula via a side port.

3.Check the vitrector is cutting and aspirating in BSS before using in the eye; if the vitrector blows bubbles, the tubes are incorrectly connected.

4.Insert the vitrector via a corneal section. A pars plana approach 3.5 mm behind limbus is an alternative for experienced surgeons. Set at low vacuum but avoid low cut rates.

5.Place the cutter tip through the PCT and hold steady just behind the capsule, with the cutting port facing anteriorly and visible at all times.

6.Vitreous is difficult to visualize; use pupil asymmetry and iris movement to betray residual vitreous. Intracameral fluorescein (2

drops of 2% unpreserved fluorescein in 2 mL BSS) can be used to stain prolapsed vitreous for easy detection (triamcinolone suspension has also been used for this purpose).

7.Minimize further vitreous loss: avoid shallowing the AC, tamponade with viscoelastic each time before resuming anterior vitrectomy, and lower the bottle height to reduce vitreous hydration. Keep the vitrectomy to the least required to clear the AC to the plane of the PCT and minimize capsular loss.

8.Suture all wounds to ensure positive AC pressure and to decrease the potential for vitreous migration to the wounds.

may include age >65 years, atherosclerosis, anticoagulation (warfarin, aspirin), tachycardia, hypertension, Valsalva manoeuvre, myopia, unstable AC, glaucoma, uveitis, and previous ocular surgery. Early recognition is critical. Look for a sudden shallowing of the AC with positive posterior pressure and iris prolapse. Selfsealing wounds of small incision surgery usually limit the bleed – never convert to ECCE as there is a high risk of expulsion of the intraocular contents. Deepen the AC if possible and close the eye immediately. Examine the fundus on the table for dark choroidal elevation. Give intravenous 20% mannitol (1 mg/kg over 30 minutes) on the table. If the bleed is limited, surgery may be

SURGERY CATARACT 6 Chapter

Intraoperative complications

completed after waiting at least 30 minutes for the blood to clot. Early drainage via a sclerostomy is controversial and should not be attempted if inexperienced. Postoperatively, arrange a vitreoretinal opinion to exclude RD and consider late drainage of a large suprachoroidal haemorrhage when the clot liquefies. Small haemorrhages may do well but the visual prognosis is usually poor.

Anterior capsule tears/discontinuous capsulorrhexis

Radial capsulorrhexis tears risk extending to the equator and the posterior capsule. To prevent losing a peripherally tearing capsulorrhexis, ensure the AC is fully formed with viscoelastic and attempt to redirect the tearing forces towards the centre by gripping the capsule as close to the tearing point as possible. If the capsulorrhexis is lost under the iris, try to visualize the endpoint by retracting the iris with the second instrument or an iris hook. Rescue may also be possible by starting a new tear in the opposite direction to include the deviation. If rescue is not feasible, an experienced surgeon may proceed with ‘gentle’ phako in the presence of a single tear: use gentle and minimal hydrodissection; avoid overinflation (or collapse) of the AC; use slow bimanual rotation of the nucleus; employ chop techniques and careful cortical aspiration. If the IOL is placed in the bag, position the haptics perpendicular to the tear, or else insert in the sulcus.

If phako is too risky, complete the rhexis and convert to extracapsular extraction.

temporal iridectomies). Ensure the corneal wound is well sutured at the end of surgery.

Corneal phako burn

The phako tip heats significantly when emulsification continues without flow of irrigation fluid, resulting in a thermal corneal burn at the main incision, compromising wound integrity and causing significant astigmatism (Fig. 6.24). Wounds frequently require multiple sutures to remain watertight. Phako burns are much less likely using burst mode or hyper-pulse (‘cool phaco’).

Causes include:

■Obstruction to flow by viscoelastic: this results in ‘smoke’ (emulsified viscoelastic) appearing at the phako tip. Ensure adequate aspiration of viscoelastic before starting phako.

■Wound too tight, constricting the infusion sleeve. Enlarge the wound appropriately.

Fig. 6.24: Phako burn. (Courtesy of G. S. Bhermi.)

SURGERY CATARACT 6 Chapter

Postoperative complications

Postoperative Complications

Although highly successful, modern phako surgery is not without complications (Table 6.4). See page 237 for anaesthetic complications and page 260 for the management of intraoperative complications.

Elevated intraocular pressure Postoperative IOP elevation is common and usually self-limiting. Some surgeons routinely prescribe prophylactic acetazolamide 250 mg p.o. stat postoperatively, repeated at 6 hours. Causes of raised IOP include retained viscoelastic, overpressurized AC on completion of surgery, inflammation, preexisting glaucoma, posterior capsule (PC) rupture, and vitreous loss. Less common causes include pupil block (p. 325) and malignant glaucoma (p. 317). Short-term topical IOP lowering agents and/or systemic acetazolamide is usually successful in treating elevated IOP. Late (>2 weeks, typically 4–6 weeks) postoperative IOP rise after uncomplicated surgery is usually secondary to steroid response (p. 310) – stop steroids and use a topical NSAID (or G. rimexolone 1%) if required. Exclude chronic inflammation and retained lens matter.

Wound leak Prevention is better than cure! Causes include poor wound construction, phako burn, inadequate suture closure, and postoperative trauma. If the AC remains deep, observe or insert a bandage contact lens. If there is persistent or brisk leak, iris prolapse, flat AC or excess against-the-wound astigmatism, return to theatre to re-suture wound.

Postoperative iris prolapse This may be avoided with well-constructed, self-sealing wounds or adequate suture closure in those at risk (shallow AC, ‘floppy iris’ in those on tamsulosin (Flomax), intraoperative prolapse, risk of rubbing eye postoperatively). G. pilocarpine 4% in the early postoperative period may reduce minor incarceration but surgery is usually required if the iris is prolapsed through the wound. Reposition viable iris if not epithelialized (<48 hours), excise any nonviable tissue, and suture the wound. Intensive topical steroids and antibiotic are required to reduce the risk of severe inflammation or infection.

Decentred, subluxed, or unstable intraocular lens This may be asymptomatic, or result in reduced bestcorrected vision, dysphotopsia, diplopia, glare, uveitis-glaucoma hyphaema syndrome. Causes include loss of capsular support (anterior rhexis tear, PC tear, zonular dehiscence), asymmetric haptic placement, and pupil capture (if rhexis larger than optic or sulcus PCIOL). According to symptoms and signs, management is by early or late IOL repositioning, PCIOL exchange with or without fixation (iris or scleral), or replacement with an ACIOL. Minimize intervention if the endothelial count is low and beware the eccentric pupil (c.f. IOL subluxation). An IOL dislocated into the vitreous does not necessarily require retrieval but may be removed via a vitrectomy if the mobile lens gives troublesome symptoms. Refer routinely for vitreoretinal review.

Corneal decompensation Risk factors include preexisting endothelial compromise (symptomatic diurnal variation in vision, guttatae, pachymetry > 630 μm) and intraoperative endothelial trauma. Exclude postoperative IOP rise. To minimize endothelial cell loss, use highly retentive viscoelastic protection, reduce phako energy with pulse, burst, or cool phako mode, and use chop techniques. Allow at least 3 months for resolution of oedema and assess vision and pachymetry before considering corneal graft surgery. Consider interim treatment with topical hypertonic

saline (G. sodium chloride 5% q.d.s. or Oc. sodium chloride l0% nocte).

Rhegmatogenous retinal detachment The reported incidence after uncomplicated phako surgery ranges from 0.2– 3.6% (average 0.7%). The excess risk in the first 10 years is probably 5.5, with most occurring in the first year. The risk is increased with PC rupture or vitreous loss (4.5–13-fold), high myopia (10-fold), peripheral lattice degeneration, ocular trauma, or previous retinal detachment. Some studies show increased risk in myopic males compared to females.

Refractive surprise See page 230.

SURGERY CATARACT 6 Chapter

269

Postoperative complications

Cystoid macular oedema See page 492.

Endophthalmitis See page 382.

Posterior capsular opacification (PCO) The most common complication (<10% at 2 years) occurring months to years after cataract surgery due to proliferation and migration of residual lens epithelial cells across the PC. Symptoms include gradual blurring, glare, or reduced contrast sensitivity. PCO may be asymptomatic. Exclude coexisting disease accounting for visual loss. Patient-, surgical-, and IOL-related factors influence the risk of developing PCO.

■Patient factors : young age (virtually 100% occurrence in children) and uveitis.

■Surgical factors : in the bag IOL fixation and 360° overlap of the capsulorrhexis margin onto the anterior optic surface provide biomechanical barriers to posterior lens epithelial cell migration. Good cortical clean-up reduces the risk but routine anterior or posterior capsule polishing may not.

■IOL factors : barriers to cell migration include square-edged optic and contact between the optic and posterior capsule (facilitated by angled haptics; large optic diameter; convex posterior optic surface; bioadhesive IOL material, e.g. hydrophobic acrylic c.f. silicone or PMMA).

Treatment involves Nd:YAG laser posterior capsulotomy (Box 6.4 and Fig. 6.25) or rarely surgical removal.

Box 6.4: Nd:YAG posterior capsulotomy

1.Consent.

Benefit : Improve VA and contrast sensitivity, reduce glare, improve view of the fundus for management of posterior segment disease.

Risk : IOP rise, inflammation, IOL pitting (not usually visually significant unless in the visual axis); subluxation or posterior dislocation of the IOL (especially silicone plate haptic IOLs). Rarely bleeding, iris damage, endophthalmitis (release of

loculated bacteria), corneal decompensation, macular oedema (less likely if capsulotomy is delayed ≥3 months postoperatively);

retinal detachment (up to 4.1% within 4 years, excess risk 3.9), especially if axial length >24 mm.

2.Check the pupil position and visual axis on the slit lamp before dilating the pupil.

3.Instil topical anaesthetic before applying a capsulotomy contact lens (e.g. Abraham lens).

4.Set the laser to a single pulse. Defocus by +1.50 D. Minimize

laser energy: start with ≤1 mJ, increase the power until sufficient to open the capsule (rarely need >2.5 mJ). Focus on or just behind capsule with the helium–neon aiming beam.

5.Start peripherally to avoid pitting the IOL in the visual axis. Aim to clear the visual axis to the largest physiological mydriatic pupil size or more if a clear peripheral fundal view is important, e.g. diabetic retinopathy. An inverted-’U’ (horseshoe) opening avoids the potential of pitting in the visual axis (unlike a cruciate opening) and minimizes ‘floaters’ (unlike full-‘circular’ capsulotomy). Treating areas under tension allows the capsule to spring apart, minimizing the number of shots (and total energy) required. Usually requires 30–40 shots.

6.For prophylaxis against post-YAG IOP spike, instil 1 drop apraclonidine 1% before and after treatment. Alternatively, a single dose of oral acetazolamide SR 250 mg may be given. Check IOP 1 hour post laser.

7.To minimize inflammation, prescribe a short course of topical steroid, e.g. G. dexamethasone 0.1% q.d.s. 5–7 days.

8.Warn about new floaters, and distinguish from retinal detachment symptoms.

Follow-up is not routinely required, but patients with raised IOP at 1 hour despite prophylactic treatment should be monitored for glaucoma.

SURGERY CATARACT 6 Chapter

Optometry and general practice guidelines

Optometry and General

Practice Guidelines

General comments

Age-related cataracts produce a gradual reduction in acuity. The diagnosis is seldom difficult using slit lamp examination. The red reflex is often altered when viewed with a direct ophthalmoscope, although nuclear sclerotic cataracts may be less evident than cortical lens opacities or posterior subcapsular cataracts. If the vision deteriorates below the patient’s requirements and they would like to discuss surgery, then arrange routine referral. Direct referral by optometrists using local guidelines is increasingly favoured in the UK.

Optometrists

■If symptoms are disproportionate to VA using standard highcontrast charts, check contrast sensitivity, low-contrast VA, and glare sensitivity. These may give a better indication of ‘real world’ visual function.

■Where possible, include the following when referring:

1.Visual symptoms attributable to cataract, including the effect on the patient’s desired lifestyle, occupation, and driving.

2.Any known ocular comorbidity.

3.Up-to-date spectacle refraction and best corrected VA in each eye.

4.Any relevant medical or social history and any special circumstances.

General practitioners

■Remember the cataractogenic effect of long-term corticosteroid use (including eye drops, face cream, oral or inhaled steroids).

■Consider reduced VA as a cause of falls in the elderly.