Year : 1995 | Volume
: 43 | Issue : 4 | Page : 201--209
Complications of cataract surgery
Madhukar K Reddy
From L.V Prasad Eye Institute, Road No. 2, Banjara Hills, Hydrabad 500 0034, India
Madhukar K Reddy
From L.V Prasad Eye Institute, Road No. 2, Banjara Hills, Hydrabad 500 0034
|How to cite this article:|
Reddy MK. Complications of cataract surgery.Indian J Ophthalmol 1995;43:201-209
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Reddy MK. Complications of cataract surgery. Indian J Ophthalmol [serial online] 1995 [cited 2019 Jun 18 ];43:201-209
Available from: http://www.ijo.in/text.asp?1995/43/4/201/25254
Over the years, the technique of cataract surgery has evolved into a safe and successful procedure for visual rehabilitation of the cataract blind. The conversion from intracapsular cataract extraction (ICCE) to extracapsular cataract extraction (ECCE), advent of microsurgery, availability of fine suture materials, affordable high-quality intraocular lens implants and vitrectomy instrumentation have significantly decreased the complications of cataract surgery.
In this article, the diagnosis, treatment and prevention of intraoperative and postoperative complications of cataract surgery are discussed. Early recognition and prompt treatment of these problems can minimize the risk of ocular morbidity.
I. INTRAOPERATIVE COMPLICATIONS
I.A. Anaesthesia-Related Complications
I.A.I. Globe Perforation
Globe perforation is a relatively common complication with retrobulbar anaesthesia when compared to peribulbar anaesthesia. The incidence of this complication is reported as none in a series of 2,000 cases with peribulbar anaesthesia to three in a series of 4,000 cases with retrobulbar blocks, although individual cases have been reported with peribulbar anaesthesia. This complication has potential for severe injury to the retina and occurs more frequently in highly myopic eyes.
Diagnosis: The diagnosis of globe perforation may be suspected by the presence of hypotony, poor red reflex and vitreous haemorrhage.
Treatment: In cases with dense cataract, cataract extraction should be performed with peribulbar anaesthesia. The postoperative management should include examination of the retina to assess the extent of retinal damage and, argon laser barrage photocoagulation or cryopexy for retinal breaks, if necessary.
If perforation of the eye is suspected and the cataract is not dense, cataract surgery should be postponed.Cryopexy or photocoagulation should be done as soon as possible to close the perforation site.
Accidental injection of lidocaine into the vitreous has been shown to have no associated visual loss.
Prevention: Globe perforation can be prevented by moving the needle to and fro after insertion into the orbital tissue. If the whole globe moves, it means that either the coats of the globe are incarcerated or the needle has passed through the coats and the tip is in the vitreous. In such situations, the needle should be withdrawn and injection of the anaesthetic agent into the eye be refrained.
I.A.2. Retrobulbar Haemorrhage
Retrobulbar haemorrhage is one of the commonest complications of ocular retrobulbar anaesthesia with an incidence rate of 1 to 3%. Here, the tip of the needle perforates one of the orbital vascular channels, resulting in accumulation of blood in the orbital spaces. One of the complications of retrobulbar haemorrhage is occlusion of central retinal artery.
Diagnosis: Retrobulbar haemorrhage is detected by increasing proptosis, tightness of the lids, conjunctival chemosis and elevated intraocular pressure (IOP).
Treatment:Retrobulbar haemorrhage is managed by postponing surgery for at least one week. Raised IOP can be managed by lateral canthotomy and antiglaucoma medication. The eye must be patched to prevent exposure keratitis.
Prevention: The use of blunt needles and the technique of peribulbar anaesthesia can decrease the incidence of retrobulbar haemorrhage.
I.B. Surgery-Related Complications
I.B.I. Positive Vitreous Pressure
Positive vitreous pressure occurs due to poor akinesia, inadvertent pressure on the globe, proptosis, eyelid abnormalities, myopia and in children due to low scleral rigidity. Here, the lens-iris diaphragm is pushed forward towards the cornea, on opening the globe. This makes any intraocular manipulation risky.
Diagnosis: If positive vitreous pressure is present, the iris tends to prolapse through the wound and shallowing of the anterior chamber occurs. In patients with high positive vitreous pressure, horizontal corneal stress lines are seen extending from one end of the section to the other.
Treatment: In cases with mild positive vitreous pressure, injection of viscoelastic material into the eye and partial closure of the wound can help in cortical aspiration and intraocular lens (IOL) implantation.
Prevention: Positive vitreous pressure can be avoided by giving a good preoperative massage and making the eye soft. Preoperative administration of intravenous mannitol or oral glycerol helps to dehydrate the vitreous, thereby decreasing vitreous upthrust.
In cases where the lens-iris diaphragm opposes the cornea, the wound can be closed. If surgery is continued with IOL implantation or cortical aspiration, inadvertent posterior capsular rupture or endothelial damage, or both, can occur. Cataract extraction with IOL implantation can be performed safely at a later date with adequate precaution.
I.B.2. Posterior Capsular Dehiscence or Zonular Dialysis
The incidence of posterior capsular rupture is in large part a function of the experience and skill of the surgeon. The incidence should probably be below 5%.
Posterior capsular tears occur most commonly during cortical clean-up but can also occur during expression of the nucleus, removal of the anterior capsular flaps and polishing of the posterior capsule.
Diagnosis:Intraoperative diagnosis of posterior capsular dehiscence or zonular dialysis can be made by visualization of the torn ends of the posterior capsule with or without mushrooming of the vitreous in the anterior chamber. The presence of vitreous in the anterior chamber is an indicator of posterior capsular rent or zonular dialysis.
Treatment: In patients with a posterior capsular rent or zonular dialysis involving less than a third of the periphery at any position, IOLs can be placed with the haptics placed away from the rent or dialysed area and their stability checked. If any instability exists, these lenses can be sutured to the scleral margin [Figure:1]. If vitreous is present in the anterior chamber or wound, a meticulous anterior vitrectomy should be performed.
Patients with posterior capsular dehiscence or zonular dialysis during intraocular lens implantation surgery can be managed by the following techniques:
a) In patients with a central posterior capsular rent with adequate rim all around, a sulcus-fixated IOL can be implanted. In an envelope capsulotomy, the anterior capsular flap can be used for support, if necessary.
b) In patients with a capsular rent or zonular dialysis extending to more than 1/3 of the periphery inferiorly, a multiflex anterior chamber IOL can be implanted.
c) In patients with a capsular rent or zonular dialysis superiorly involving upto half of the periphery, a scleral-fixated IOL can be implanted. An IOL with prolene haptics or a single-piece IOL with an eye in the haptic can be placed with the leading haptic in the sulcus inferiorly and the trailing haptic sutured to the sclera superiorly with 10-0 prolene suture [Figure:1]. The tip of the sutured prolene haptic should be heat cauterized to prevent slippage of the knot by creating a bulbous end. This technique of scleral fixation of the IOL causes minimal intraoperative trauma.
Prevention: Posterior capsular dehiscence or zonular dialysis can be minimised by keeping the Simcoe cannula as far as possible parallel to the posterior capsular plane and by avoiding blind aspiration of the anterior chamber and anterior capsular tags.
I.B.3. Vitreous Prolapse
Loss of vitreous causes significant ocular morbidity and its appropriate management is an important aspect of cataract surgery. The incidence of vitreous loss in the practice of a skilled cataract surgeon performing intracapsular cataract extraction should be approximately 3% and that in extracapsular cataract extraction should be lower.
The vitreous may be present in the anterior chamber preoperatively due to various causes or intraoperatively due to posterior capsular dehiscence, zonular dialysis or disruption of anterior hyaloid face in intracapsular extraction.
Diagnosis: Vitreous prolapse is diagnosed by the presence of vitreous in the anterior chamber (which may occlude the port of the aspirating cannula), distortion of the pupil, presence of vitreous in the wound and the accompanying posterior capsular rent or zonular dehiscence.
Treatment: In the event of vitreous prolapse, the aim of vitrectomy is to prevent vitreous incarceration in the corneoscleral section and adhesion of vitreous to the corneal endothelium.
To achieve this, an automated vitrectomy is the best method. A vitrectomy probe without an in-built irrigation port is preferred in order to prevent churning of the vitreous. A separate irrigation cannula should be used. The cutting rate of the vitrector should be high (approximately 300 cuts/min) and the vacuum should be low (approximately 100-150 mm Hg) to prevent traction on the vitreous base. An alternative technique with cellulose sponge may be used to hold the vitreous strands and an angled Vannas scissors or De Wecker's scissors may be used to cut the stretched vitreous at the pupillary margin. A vitreous-free anterior chamber is indicated by a round pupil, falling back of the iris and formation of a single bubble on air injection.
Prevention: Preoperative softening of the globe is the best method to prevent vitreous loss. Adequate lid and globe anaesthesia and minimal external pressure on the globe can decrease the incidence of vitreous loss.
I.B.4. Expulsive Haemorrhage
Expulsive haemorrhage, though a rare complication, is discussed here because of its potential for visual loss. As reported, the incidence of expulsive haemorrhage is approximately 0.2%.
Histopathologic studies have shown expulsive haemorrhage to result as a consequence of rupture of the posterior ciliary arteries. The exact pathogenesis of expulsive haemorrhage is not known. However, glaucoma, hypertension, generalised arteriosclerosis and myopia are associated with this condition.
Diagnosis:Expulsive haemorrhage is recognised by an increasing positive vitreous pressure, leading to vitreous loss and ultimate extrusion of the retina caused by subchoroidal haemorrhage. The subchoroidal haemorrhage manifests as disappearance of red glow, as seen with coaxial illumination.
Treatment: Early recognition of expulsive haemorrhage is imperative and immediate closure of the wound with silk or nylon sutures (preferably 8-0) is necessary to prevent retinal extrusion and loss of the eye. The subchoroidal haemorrhage gradually resolves over a period of time.
Prevention: The incidence of expulsive haemorrhage can be decreased by ensuring a preoperative soft eye, treating hypertension adequately and controlling IOP preoperatively, if raised.
I.B.5. Descemet's Detachment
Descemet's detachment commonly occurs during an attempt to enter the globe without proper visualization. This results in inadvertent entry of the instrument between the Descemet's membrane and stroma, leading to detachment of the Descemet's membrane.
Diagnosis: The presence of an opalescent rolled up membrane near the section should alert the surgeon to the possibility of detachment of the Descemet's membrane.
Treatment: A small Descemet's detachment extending about 1 or 2 mm into the cornea can be left as such. A wider Descemet's detachment along the section would need full-thickness suturing of the cornea including the Descemet's membrane.
Placement of a large air bubble or viscoelastic material within the anterior chamber facilitates opposition of the Descemet's membrane to the stroma. In case of extensive Descemet's detachment involving the visual axis, full-thickness radial corneal sutures in the mid-periphery would help hold the Descemet's membrane against the stroma until healing occurs [Figure:2].
Prevention:Detachment of Descemet's membrane can be minimized by careful insertion of instruments into the anterior chamber through adequate incisions and with good visualization.
I.B.6. Wound Malapposition
A well-apposed water-tight wound is necessary for adequate postoperative healing. An irregular or jagged wound or loose sutures usually result in a leaking wound at the end of surgery.
Diagnosis: The wound should be checked with a cellulose sponge or cotton swab for any wound leak. Gentle pressure over the posterior lid of the wound confirms the water tightness of wound closure.
Treatment: Meticulous wound closure needs adequate number of sutures to prevent a wound leak. The sutures should be: (1) radial to help in better wound apposition; (2) deeply placed to appose the cut ends of Descemet's membrane; and (3) approximately equally spaced to cover the length of the wound. The suture bite should be approximately 0.5 mm on the corneal side and 0.75 mm on the scleral side. The suture knots should be pulled flushed with the scleral surface or buried after close trimming to prevent postoperative irritation of the eye. Jagged wound margins need extra sutures to oppose the wound adequately.
II. EARLY POSTOPERATIVE COMPLICATIONS
II.A. Postoperative Examination
II.A.l. Shallow Anterior Chamber
The common causes of shallow anterior chamber are wound leak, pupillary block and choroidal detachment.
II.A.l. (a) Wound Leak
A leaking wound commonly manifests as a shallow or flat chamber with a soft eye.
Diagnosis: On slit-lamp biomicroscopic examination with cobalt blue filter after fluorescein instillation, a wound leak can be demonstrated better (Seidel's test). An eye with a slow leak has a deep to shallow anterior chamber, whereas an eye with a brisk leak has a shallow to flat anterior chamber with corneal stromal oedema due to hypotony.
Treatment: For a slow leak, pressure patch or soft bandage contact lens application can help to oppose the wound edges and seal the wound. In case of failure to seal the wound in 48 hours or in a wound with a brisk leak and wound malapposition, the wound should be resutured under topical or peribulbar anaesthesia. Preoperative massage should be avoided. Addition of hyaluronidase helps diffuse the anaesthetic agent.
II.A.l. (b) Pupillary Block
A pupillary block can be caused by anterior hyaloid face, exudate or anterior chamber IOL optic, especially in patients who have undergone intracapsular cataract extraction. Pupillary block can also occur despite a peripheral iridectomy which may be lamellar or blocked by vitreous.
Diagnosis: Pupillary block can be diagnosed by a shallow anterior chamber with raised intraocular pressure.
Treatment: Administration of intravenous mannitol (1 gm/kg) and oral acetazolamide help decrease intraocular pressure and along with cycloplegics release the pupillary block, occasionally. Pupillary block can also be released by a YAG laser peripheral iridotomy. In case of failure, a peripheral iridectomy would be the next treatment of choice.
II.A.1. (c) Choroidal Detachment
The exact aetiology of choroidal detachment is not known. It is not clear as to whether hypotony causes choroidal detachment or vice-versa.
Diagnosis: A choroidal detachment manifests as a shallow anterior chamber and soft eye without a wound leak. A B-scan would reveal the choroidal detachment.
Treatment: Majority of choroidal detachments usually resolve spontaneously within three weeks of onset of the disease.
II.A.2. Iris Prolapse
Iris prolapse can result from inadequate wound closure, accidental trauma, or raised intraocular pressure.
Diagnosis: Postoperatively, the iris tissue may be found in the wound with or without a shallow anterior chamber and a peaked pupil.
Treatment: In cases of iris prolapse of less than 48 hours duration, the iris tissue can be reposited. In cases of more than 48 hours duration, the iris tissue can be excised. Peribulbar or retrobulbar anaesthesia is necessary for iris manipulation. Sutures adjacent to the iris prolapse should be opened, the iris reposited or abscised and the wound resutured.
Prevention: Adequate wound closure, as described earlier in the article, can decrease the incidence of iris prolapse to a certain extent.
II.A.3. Postoperative Uveitis
Postoperative uveitis commonly occurs in patients who have undergone hypermature cataract extraction, patients with past history of uveitis, or in children with an increased fibrin exudation from the iris.
Diagnosis: There is an increased anterior chamber cellular reaction and flare, with or without presence of coagulum in the anterior chamber and rarely a hypopyon. If not treated immediately and adequately, postoperative uveitis could lead to endothelial damage, occlusion of the pupil, coating of the intraocular lens with inflammatory debris and cystoid macular oedema.
Treatment: Postoperative uveitis should be managed with frequent instillation of topical corticosteroids. The frequency of instillation may be tapered according to clinical response, such as, betamethasone sodium 0.1% every half hour or less, depending on the severity of inflammation with steroid ointment cover at night. Administration of cycloplegics is mandatory. Cycloplegics such as cyelopentolate hydrochloride 1% twice daily (in mild postoperative uveitis) and atropine sulphate 1% thrice daily (in severe postoperative uveitis) are recommended. Systemic steroids (oral prednisolone 1 to 2 mg/kg) should be started in cases of severe postoperative uveitis.
Sometimes postoperative uveitis can be very severe with dense exudate around the intraocular lens, presence of hypopyon and absence of red glow, mimicking infectious endophthalmitis, The differentiating features of postoperative uveitis are less pain, minimal lid oedema and conjunctival congestion/chemosis and a brighter red reflex compared to infectious endophthalmitis. Initial treatment with frequent instillation of topical steroids and a close monitoring for worsening of the symptoms are recommended. If worsening of symptoms occurs within 6 to 12 hours, a diagnosis of infectious endophthalmitis should be entertained. A vitreous biopsy should be done and the appropriate management protocol should be followed in conjunction with a vitreoretinal surgeon.
Prevention: Cataract extraction as far as possible should be done in a quiet eye and if surgery has to be performed when ocular inflammation is present, steroid cover is recommended.
II.A.4. Infectious Endophthalmitis
The reported incidence of endophthalmitis after cataract extraction is in the range of 0.05 to 0.5%.
Infectious endophthalmitis most commonly occurs due to intraocular microbial contamination from the patient's skin, preocular tear film and ocular adnexa. The commonly isolated organisms are Staphylococcus epidermidis, Staphylococcus aureus, Streptococcus species followed by gram-negative bacteria.
Diagnosis: Postoperative complaints of severe pain with lid oedema, conjunctival congestion, chemosis and hypopyon or exudates in the anterior chamber, dull or absent fundal glow should arouse suspicion of infectious endophthalmitis. A B-scan may reveal vitreous opacities indicating vitreous involvement. Endophthalmitis caused by a less virulent microorganism can manifest insidiously as chronic uveitis.
Treatment: Co-management with a vitreoretinal surgeon is mandatory. A diagnostic vitreous tap or vitrectomy should be done and the vitreous sample should be subjected to microbiologic investigation. Based on the culture results, topical and systemic antimicrobial agents should be prescribed.
Prevention: The incidence of this devastating complication can probably be reduced by preoperative decontamination of ocular surface with antimicrobial agents and by following strict asepsis such as use of sterile gloves, instruments and intraocular irrigating fluids.
II.A.5. Corneal Oedema
Postoperatively, corneal oedema can be localized or diffuse.
Diagnosis: Postoperative localized stromal and/or epithelial oedema, especially in the superior half of the cornea indicates intraoperative trauma. On slit-lamp examination, corneal stromal oedema is seen as an area of corneal swelling with underlying Descemet's folds. Raised intraocular pressure manifests as diffuse microcystic epithelial oedema, which is best visualized by retroillumination. Postoperative corneal stromal oedema could also indicate pre-existing endothelial pathology as in Fuch's endothelial dystrophy.
Treatment: Corneal oedema secondary to intraoperative trauma and consequent inflammation heals in most cases with topical 0.1% betamethasone or dexamethasone sodium, the frequency of instillation depending upon the severity of the oedema. In patients with diffuse epithelial oedema, tonometry should be performed and if IOP is raised the condition should be treated with topical and/or systemic antiglaucoma medication.
II.A.6. Retained Lens Material
Inadequate aspiration of the cortex, especially behind the iris at the 12 o'clock position, is the commonest cause of retained lens material after cataract surgery.
Treatment: In cases with minimal cortical matter, the anterior segment inflammation can be treated medically with topical steroids and cycloplegics. In cases with significant cortical residue, surgical removal is essential.
II.B. Postoperative Follow-up Visit at 1 Week
The common complications following cataract surgery at the 1 week follow-up visit are anterior uveitis, iris incarceration in the wound and sometimes a persistent wound leak. The management of these complications has been discussed earlier in this article.
II.C. Postoperative Follow-up Visit at 6 Weeks
The common complications following cataract surgery at the six weeks follow-up visit are suture-induced astigmatism and post-refraction subnormal vision.
II.C.l. Suture-Induced Astigmatism
Tight sutures lead to with-the-rule astigmatism due to steepening of the cornea in the vertical meridian. Occasionally, loose sutures intraoperatively or wound slippage after suture removal lead to against-the-rule astigmatism.
Diagnosis: Suture-induced astigmatism is usually diagnosed by retinoscopy and confirmed by keratometry or computerized corneal topography.
Treatment: If sutures are tight and deeply placed, they may be cut and left buried. If sutures are tight, superficial and causing irritation, they should be removed. Sutures should be released after checking the wound for healing (i.e., adequate vascularization of the surgical wound). In cases where the wound is not well healed, removal of sutures can lead to dehiscence of the wound. It is advisable to remove all sutures instead of selective removal of tight sutures as this leads to shift in astigmatism. Refractive correction of the eye 1 to 2 weeks after sutures removal is appropriate. If the residual stable astigmatism is high, gas permeable contact lens wear or surgical correction is advised.
II.C.2 Post-Refraction Subnormal Vision
Subnormal vision after refractive correction can occur due to several causes. The common causes are media opacities, retinal pathology and optic disc abnormalities.
II.C.2. (a) Media Opacities
A pre-existing corneal scar or epithelial keratopathy, e.g., due to a dry eye, can cause significant diminution of visual acuity. In addition, a preexisting posterior capsular opacity can obstruct the visual axis and prevent full recovery of vision. Vitreous opacification due to vitreous haemorrhage, prior uveitis or advanced asteroid hyalosis can lead to decreased visual acuity.
Diagnosis: Decreased vision due to media opacities can be differentiated from retinal pathology by interferometry. If visual acuity improves on interferometry, a diagnosis of opacification of media is made.
Treatment: Corneal pathology responsible for diminished vision should be managed appropriately. If a posterior capsular opacity is present, a YAG laser capsulotomy can be performed to improve vision. Intraoperatively, if the posterior capsule is thick and potentially not treatable by laser capsulotomy, a primary posterior capsulotomy should be performed. In case of vitreous opacities, a vitrectomy should be done in consultation with a vitreoretinal surgeon, if necessary.
II.C.2. (b) Retinal Pathology
The common retinal causes of decreased vision are cystoid macular oedema, diabetic retinopathy, age-related macular degeneration, macular degeneration secondary to retinitis pigmentosa or myopia and macular holes.
Diagnosis: Cystoid macular oedema is diagnosed clinically by a postoperative decrease in vision and macular oedema with a 90-D lens or indirect ophthalmoscopy. It can be confirmed by fundus fluorescein angiography.
Diminished vision in diabetic retinopathy may be due to macular oedema, vitreous haemorrhage, preretinal fibrosis or retinal detachment. Age-related macular degeneration manifests as macular drusen or subretinal vascularization.
Treatment: Retinal pathology should be managed appropriately with the help of a vitreoretinal surgeon. In cases with myopia, the peripheral retina should be examined for retinal degeneration or breaks. Retinal breaks or thinning should be managed appropriately by cryopexy or laser photocoagulation.
II.C.2. (c) Optic Nerve abnormalities
The common optic nerve abnormalities responsible for decreased vision after cataract surgery are primary optic atrophy, anterior ischaemic optic neuropathy or glaucomatous optic atrophy in presence of normal intraocular pressure (low-tension glaucoma).
III. LATE POSTOPERATIVE COMPLICATIONS
Late postoperative complications can manifest as decreased vision without red eye and decreased vision with red eye (Flowchart).
III.A. Decreased Vision Without Red Eye
Decreased vision without red eye could be due to change in refraction, posterior capsule opacification, cystoid macular oedema and retinal detachment.
III.A.1. Change in Refraction
Post-cataract surgery wound healing causes gradual regression of with-the-rule astigmatism and can manifest as diminished vision requiring a repeat refraction and spectacle prescription.
III.A.2 Posterior Capsule Opacification
Thickened posterior capsule is a common cause of decreased vision following cataract surgery. The decrease in visual acuity is more with proliferation of epithelial cells (Elschnig's pearls) than with fibrosis of the capsule. Posterior capsule opacification can be treated with YAG laser capsulotomy, preferably six months after surgery, after stabilization of the blood-ocular barrier. In case of non-availability of YAG laser, surgical capsulotomy may be done. However, surgical capsulotomy carries the risks of an intraocular surgical procedure. YAG laser capsulotomy should begin with minimal power and an adequate opening should be created, at least encompassing the pupillary area in the undilated position.
III.A.3. Cystoid Macular Oedema
Various authors have reported approximately a 1% incidence of clinical cystoid macular oedema following ECCE with posterior chamber IOL implantation. These studies included patients who underwent ECCE with posterior chamber IOL implantation and had an intact posterior capsule and visual acuity of 6/12 or worse. Cystoid macular oedema commonly occurs 1 to 3 months after cataract surgery.
Cystoid macular oedema occurs as a result of leakage of fluid into the macula from perifoveal retinal capillaries. Other causes such as local prostaglandin release, ultraviolet light exposure and vitreous traction have also been implicated.
Diagnosis: The most common and often the only symptom of cystoid macular oedema is decreased vision. Clinically, several cysts are seen with a 90-D lens within the central macular region. Diagnosis of cystoid macular oedema is confirmed by fluorescein angiography.
Treatment: Topical steroid eye drops approximately six times daily may help stabilize the blood-ocular barrier. In addition, oral indomethacin in a dose of 75 mg/day, 50 mg/day and 25 mg/day for two weeks each is recommended. Systemic acetazolamide has also been shown to decrease cystoid macular oedema.
The reported incidence of rhegmatogenous retinal detachment following cataract extraction is 1 to 3%. The risk factors for retinal detachment are high myopia, intraoperative vitreous loss, intracapsular cataract extraction, prior retinal detachment in the fellow eye and YAG laser capsulotomy in high myopes (axial length more than 25 mm).
Diagnosis: Recent onset of floaters, flashes of light, sudden visual loss and a hypotonous eye should arouse suspicion of retinal detachment. An indirect ophthalmoscopic examination and a confirmatory ultrasonographic evaluation is needed.
Treatment: Surgical apposition of the detached retina to the choroid is done with the help of a vitreoretinal surgeon.
Prevention: Patients with predisposition to retinal detachment should undergo a peripheral retinal examination preoperatively, at the 6-week postoperative follow-up visit and thereafter at yearly intervals.
III.B. Red Eye With Decreased Vision
Red Eye with decreased vision could be due to loose sutures, rebound uveitis, chronic irritable eye, epithelial downgrowth and bullous keratopathy.
III.B.1. Loose Sutures
Complaints of congestion, discharge and irritation of the ocular surface may indicate loose or broken sutures. These sutures should be removed to provide comfort to the patient.
III.B.2. Rebound Uveitis
Rebound inflammation of the anterior segment of the eye manifests as conjunctival congestion, anterior chamber cells and flare. Rebound uveitis can be treated with topical steroid drops and tapered accordingly.
III.B.3. Chronic Irritable Eye
Chronic inflamed eyes could be due to vitreous strands or iris incarceration in the wound. If anterior uveitis is present, the eye should be treated with topical steroids and cycloplegics and, if the inflammation persists, surgical release of the iris or vitreous from the wound should be done.
III.B.4. Epithelial Downgrowth
Epithelial downgrowth is a rare complication probably occurring in less than 0.1% of cases following cataract surgery. Epithelial downgrowth into the anterior chamber is a result of inadequate wound closure or healing.
Diagnosis: Epithelial downgrowth is seen as an opalescent membrane with scalloped margins on the iris or on the endothelial surface. It gradually progresses in some cases causing a chronic anterior chamber inflammation and in the later stages leads to intractable glaucoma (due to occlusion of the trabecular meshwork) and consequent loss of the eye.
Treatment: Anterior segment inflammation is treated by topical steroids and raised intraocular pressure is managed medically and/or surgically. Anterior segment resection of the involved area is curative in the early stages but unfortunately most cases are unsuccessful.
Prevention: A careful closure of the wound at the time of surgery and of any persisting wound leaks would decrease the incidence of epithelial downgrowth.
III.B.5. Bullous Keratopathy
Bullous keratopathy can occur due to pre-existing endothelial pathology, significant intraoperative endothelial damage, chronic inflammation leading to endothelial cell loss and inappropriate IOL design. Endothelial touch can also lead to endothelial attrition and consequent bullous keratopathy.
Diagnosis: Clinically, bullous keratopathy presents as stromal oedema with overlying epithelial oedema, which initially manifests as blurred vision early in the morning and improving later in the day. Chronic corneal oedema leads to scarring.
Treatment: Bullous keratopathy can be treated symptomatically by hypertonic agents (ointment or eye drops) or a bandage contact lens may be fitted. Cautery of the denuded epithelial surface by heat or multiple stromal punctures may help adhesion of the epithelium to the scarred surface and prevent occurrence of bullous lesions. A penetrating keratoplasty would be the definitive treatment leading to symptomatic relief and visual improvement.
Cataract surgery is one of the commonest surgical procedures performed. Postoperative complications though inevitable, adequate preventive measures such as timely diagnosis and appropriate management of complications can decrease ocular morbidity. Peribulbar anaesthesia, preoperative soft eye, decontamination of the conjunctival sac with povidone-iodine, adequate vitrectomy in patients with vitreous loss, pre- and postoperative peripheral retinal evaluation in patients with myopia, adequate wound closure and awareness of occurrence of cystoid macular oedema are emphasized to reduce the incidence complications following cataract surgery.