|Year : 1981 | Volume
| Issue : 4 | Page : 419-423
Complications after intraocular lens implants
Daljit Singh, Shamindar Kumar, Arun Verma, Ashok Bajaj
Department of Ophthalmology, Medical College, Amritsar, India
Department of Ophthalmology, Medical College, Amritsar
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Singh D, Kumar S, Verma A, Bajaj A. Complications after intraocular lens implants. Indian J Ophthalmol 1981;29:419-23
|How to cite this URL:|
Singh D, Kumar S, Verma A, Bajaj A. Complications after intraocular lens implants. Indian J Ophthalmol [serial online] 1981 [cited 2020 Jun 3];29:419-23. Available from: http://www.ijo.in/text.asp?1981/29/4/419/30944
Intraocular lens implants though very useful for solving optical, social and psychological problems of many of the aphakes, themselves create a number of problems of their own. Therefore it is essential that such problems be properly understood with regards to their aetiology, prevention and management. The trivial postoperative complications occuring after routine cataract surgery assume dangerous proportions if the eye has received an intraocular lens implant.
The complications may be considered as early, those occurring sooner or later, and late complications.
| Early complications|| |
The early complications include pupillary block, shallow anterior chamber, striate keratitis and precipitates on the implant.
1. Shallow anterior chamber and pupillary block:
A shallow anterior chamber may be caused by a leakage from the wound, choroidal detachment, migration of air behind the implant and by pupillary block.
The frequent and intensive use of corticosteroids in the implant cases increases the chances of leakage. This can be prevented by making a clean incision, properly apposed with multiple stitches and preferably covered by a conjunctival flap. In the event of leakage, it is essential to apply extra stitches without any delay, so that the endothelial touch by the implant is avoided.
In our series of 150 cases, a three plane flange incision under a conjunctival flap with 3 to 6 corneoscleral stitches was used. We encountered shallow anterior chamber due to leakage in 2 cases. Both of them - recovered spontaneously in 12 hours time. There was one case of shallow anterior chamber in whom the air had gone behind the implant; change of head posture brought the air into the ante-r rior chamber and deepened it.
There was no case of choroidal detachment in our series.
Pupillary block is caused when the pupillary area is blocked by the implant and the peripheral iridectomy is blocked by lens matter, air, blood, vitreous or by the haptic of the implant. Pupillary block may be overcome by discontinuation of miotics and careful administration of mydriatics. If these measures fail, as early additional peripheral iridectomy should be performed.
In the excitement of intraocular lens implantation, a peripheral iridectomy may cony letely be forgotten, resulting in a pupillary block. Not only peripheral iridectomies have to be remembered, but also their patency should be checked during operation. In one of our cases, we forgot to do iridectomy during operation. The patient had just reached the ward when the mistake was discovered.
The patient was promptly recalled into the operation theatre and the much needed iridectomy was performed.
In two cases, both of them having irisplane implants, the single iridectomy done was blocked by the haptic of the implant. An additional peripheral iridectomy in each case deepened the anterior chamber without any further trouble. I/V Pentothal sodium was used in these cases.
2. Striate keratitis
Excellent instruments are being used all over the world for lens implantation. There are instruments which not only hold the implant but also irrigate the anterior chamber at the same time, thus minimising the endothelial rub. This goes a long way to prevent striate keratitis. The excessive use of normal saline for irrigation, also increases the incidence of striate keratitis. Unfortunately the really useful implant instruments are not being made in this country. In their absence, the implant can be introduced under an air bubble, thus avoiding to some extent the endiothelial rub. It is a pity that the more physiologic solutions like balanced-salt-solution (BSS) is not being made by any firm in India for use by ophthalmologists. Such a solution would be an ideal irrigatirg solution and would prevent striate keratitis in most cases.
3. Precipitates on the implants
The precipitates may be pigmented or greyish white in colour. The former are derived from the pigment epithelium of the iris whereas the latter are either lens material or the result of excessive uveal reaction. The greyish white deposits first appear on the pins of the implant loops. A careful watch should be kept on the transparency of the anterior chamber and the surface of the implant, during the postoperative period.
| Complications that may occur sooner or later|| |
Under this heading we may include uveitis, dislocation of the implant, and cystoid macular oedema (CME).
It is universally known that the postoperative reaction after implant surgery is minimum in blue eyes and more severe in brown and black eyes. The reaction may range from mild to very severe. It usually starts about 24 to 48 hours, when the effect of subconjunctival injection of dexamethasone, given at the end of surgery has disappeared. This is the time to recognize the onset of uveitis and to start intensive steroid therapy. However, it should be remembered that a certain amount of reaction is essential for the fixation of Binkhorst's two loop implant that is put after extracapsular extraction. The severe reaction is manifested by the haziness of the anterior chamber, the clouding of the cornea, the appearance of greyish white deposits on the pins of the implant loops, by the collection of exudates behind the lens implant and by hypopyon formation. The appearance of exudates is sometimes so quick as to take the surgeon by surprise. Fortunately the severe uveal reaction can quickly be brought under control by frequent instillation of steroid drops, subconjunctival injections and ora therapy.
Severe uveal reaction was common in our early cases. Such reactions have not beer allowed to occur in our later cases. Now the incidence of severe reaction is about 3 to 4%.
The fixation of the implant is the major concern of the implant surgeon. The mode of fixation depends upon the type of the implant, the types of cataract extraction and the amount of post operative reaction. It is essential to put miotics in the eye regularly till implant fixation is achieved. Discontinuation of pilocarpine. erroneous administration of mydriatic and the pupil dilatation at night may cause dislocation. The dislocation may further be added by the movement of the air bubble, the kick of the vitreous gel or by trauma.
It is surprising how large implants manage to pass through apparently small pupils. We have made calculations from models that a 9 mm iris plane lens can slip through the pupil when the pupillary diameter is just 6.5 mm. A Binkhorst's 4 loop lens (diameter 8 mm) can dislocate through a 5.4 mm pupil. The detailed findings of this study will be presented elsewhere. Suffice to say, that a slightly dilated pupil, aided by the pressure of an air bubble in a deep anterior chamber are the ideal conditions for dislocation in the immediate post operative period.
Majority of the Binkhorst's type implants can be repositioned medically and by a suitable tilt of the head, failing which it may be essential to interfere surgically.
In the early part of our study we have been quick to remove the dislocated implants. Lately, the dislocations in the immediate post operative period have been very infrequent and have been managed non-surgically. However, there were two cases of late dislocation where the implants had to be removed. One implant was removed at the request of the patient. The other had to be removed because of repeated dislocations, despite proper repositioning by medical means every time.
2. Cystoid macular oedema (C.M.E.) ;
The possibility of cystoid macular oedema should be considered if the pin-hole visual acuity decreases during early postoperative period or if the corrected visual acuity decreases during the later period.
According to Colenbrander there is a relationship of macular oedema with the duration of operation. Progressive macular oedema starts to develop from the moment the eye is opened until it is closed again. According to Jaffe the incidence of clinically apparent and definite cystoid oedema without fluoresein angiography is 3%. As compared to routine intracapsular cataract extraction, cystoid macular oedema is not significantly high in the implant group (Osher). Binkhorst and Worst have also shown the incidence of CME to be 3% in their series of cases. CME has a tendency for spontaneous recovery.
We have encountered clinical cystoid macular oedema in 2 cases in the immediate postoperative period and five late cases in a series of 150 cases. The cases were given steroid therapy and all of them recovered. One case of late cystoid macular oedema developed severe vitreous haemorrhage 2 months after the resolution of macular oedema. CME is often associated with small haemorrhages. The cause of haemorrhage in this case could not be identified and the patient is recovering.
| Late complications|| |
The late complications include endothelial corneal dystrophy (ECD), iris atrophy and retinal detachment.
1. Endothelial corneal dystropy (ECD)
It is the most dreaded and important complication of lens implantation. Its various stages are
A. Local epithelial oedema near the incision or the anterior loop tips of iris clip lens.
B. Striate keratitis with incipient corneal oedema.
C. Generalised corneal oedema.
D. Bullous keratopathy, epithelial bullae.
Miller & Dohlman described its etiology as decompensation of aqueous pump function of endothelium. The later stages manifest themselves if promoting factors were already present e.g. Fuch's endothelial dystrophy. Major operative and postoperative complications also play an important part in promoting this condition. The main cause of ECD however is the intermittent or continuous contact
of implant with corneal endothelium brought about by incorrect size & shape of implant or its dislocation. The incidence of ECD may be decreased by minimising surgical trauma.
It is very important to examine the corneal endothelium by slit lamp microscopy in order to assess the endothelial vitality before subjecting the eye to surgery. In this connection it should be remembered that implant surgery tend to be more traumatic than other surgery.
ECD is resistant to any therapy including extraction of the implant. Penetrating kerato plasty is the only rational treatment to attempt and this is even safer when the lens implant is in situ.
In our series we observed endothelial corneal dystrophy in three cases. The implants had to be removed in these cases. visual results were poor.
2. Iris atrophy
Iris atrophy may be present in the form of pressure atrophy of the iris tissue or local atrophy of the pigment epithelium. In most cases, however, gonioscopy does not reveal any greater amount of pigmentation in the angle of pseudophakic than of aphakic eyes. This means that pigmentation is mainly caused by loss of pigment during surgery and not by loop friction.
In our series, two cases developed iris atrophy about 1½ years after operation. The iris atrophy in these cases were in the form of localised loss of pigmentation near the pupillary margin. Both these cases upto date have good vision and the implant is in place. The implant used in these cases was Binkhorst's two loop type.
3. Retinal detachment
Retinal detachment is mainly seen in implantation after intracapsular cataract extraction of senile cataract The incidence of retinal detachment according to Jaffe is 1.87%. This is comparable to the incidence of retinal detachment following uneventful cataract surgery without implantation.
In our series of 150 cases we did not encounter retinal detachment in any case.
There were two cases of severe iritis and one case of vitritis in the late postoperative period in our series. All these cases were successfully treated by intensive steroid therapy.
| References|| |
Binkhorst, C.D., 1973, Trans. Amer. Acad. Ophthalmol Otolaryngol; 77:589.
Binkhorst, C.D. and Leonard, P.A.M., 1967, Amer. J. Ophthalmol 64:947.
Binkhorst, C.D. and Leonard, P.A.M., 1968, Perspect. Ophthalmol 1:195.
Colenbrander, M.C., 1974, Quoted by Binkhorst C.D., 1973, Trans. Amer. Acad. Ophthalmol Otolaryngol 77:589.
Duke-Elder, S., 1969, System of Ophthalmology, Vol. II, P. 280, Henry Kimpton, London.
Jaffe, N.S., 1972, Cataract Surgery and its complications P. 417, C. V. Mosby, St. Louis.
Jaffe, N.S., 1976, Trans. Amer. Acad. Ophthalmol Otolaryngol 81:133.
Miller, D. and Dohlman, C.H., 1970, Trans: Amer. Acad. Ophthalmol. Otolaryngol 74:369.
Osher, M.S., 1976, Ophthalmol Surg 7:71.
Singh, D. and Singh, M., 1977, Proc. All India Ophthalmol. Soc.
Worst, J.G.F., 1974, Eye, E,N, Monthly: 25:37.