Indian Journal of Ophthalmology

: 2004  |  Volume : 52  |  Issue : 2  |  Page : 95--7

Major ocular complications after organ transplantation.

P Lanzetta, P Monaco 

Correspondence Address:
P Lanzetta

How to cite this article:
Lanzetta P, Monaco P. Major ocular complications after organ transplantation. Indian J Ophthalmol 2004;52:95-7

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Lanzetta P, Monaco P. Major ocular complications after organ transplantation. Indian J Ophthalmol [serial online] 2004 [cited 2022 Aug 9 ];52:95-7
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Organ transplantation has evolved over the years. Renal transplantation has become a very successful and routine procedure. Heart transplantation is a mainstay of therapy for patients of heart failure. In liver transplantation, significant improvements in both patient and graft survival have been made during the last decade. With near optimal rates of early transplant patient and allograft survivals, the focus has shifted to the alleviation of medical complications that can improve outcomes. Pharmacologic immunosuppression has played a major role in the advancement of organ transplantation. However, immunosuppression has been shown to carry the risk of systemic diseases and other problems.

Visual loss is a rare but potentially devastating complication of organ transplantation. Postoperative therapy with steroids, cyclosporine, tacrolimus, other immunosuppressants and conditioning chemotherapeutic drugs have been associated with the development of cataract, ocular surface disorders, retinopathies and neurotoxic phenomena.

Corticosteroid cataract is a common complication that occurs frequently in spite of the use of cyclosporine, and is similar to the azathioprine era. The incidence of corticosteroid cataract after renal transplantation varies from more than 60% to 78%.[1],[2] Total body irradiation is also a major risk factor for the development of cataract.[3] In general, a reduction in the total dose of corticosteroid during the first year has no influence on cataract occurrence.[2] Increased intraocular pressure due to the intake of corticosteroids is seen in about 10% of patients receiving renal transplantation and postoperative corticosteroid therapy.[1] Systemic corticosteroids may also either aggravate or cause idiopathic central serous chorioretinopathy with multifocal serofibrinous retinal pigment epithelial detachments and retinal detachment in patients who become symptomatic after renal transplantation.[4] Central serous chorioretinopathy has also been described after bone marrow transplantation and the use of systemic corticosteroids and cyclosporine.[5] Patients undergoing renal, heart, and heart-lung transplantation may develop loss of vision caused by serous retinal detachment associated with geographic zones of leopard-spot pattern of clumping of orange retinal pigment epithelium and retinal pigment epithelium depigmentation in the posterior fundi of both eyes.[6] Oral corticosteroids, cyclosporine, and azathioprine, singly or in combination, may be of pathogenetic importance.[4],[5],[6],[7]

Ischaemic retinal microvasculopathy and visual loss after renal transplantation and bone marrow transplantation in patients treated with cyclosporine alone or conditioned with total body irradiation, busulfan, and/or cyclophosphamide have been documented.[3],[4],[5],[6],[7],[8],[9],[10],[11],[12][13],[14] Cyclosporine alone may be responsible for capillary/arteriolar damage.[13] In some studies, estimates of the incidence of retinal microvasculopathy were biased by ascertainment of only symptomatic cases.[9] The true incidence may be higher. In a prospective study, 46% of transplant patients with ischaemic fundi were asymptomatic.[11] Bone marrow transplant retinopathy occurs, on average, within 6 months of bone marrow transplantation. The earliest reported case of bone marrow transplant retinopathy was 3 months and the longest latent period was 25 months. The development of bone marrow transplant retinopathy is not influenced by age, gender, or race of the transplant recipients.[11],[12],[13],[14] Between 10% and 28% of patients who receive the cyclosporine experience some type of neurotoxic adverse event.[15] The case of a bone marrow transplant recipient who developed blindness 22 months after bone marrow transplant has been reported, where neuroretinal damage without microvascular retinopathy was suggested, without excluding an optic nerve lesion.[8] Cyclosporine has been implicated in the development of optic nerve head oedema in some cases associated with pseudotumour cerebri,[14],[15],[16],[17],[18] and as a cause of cortical blindness.[19] Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of cyclosporine.[15] The disc oedema resolves when the cyclosporine dose is decreased or discontinued.[14] The disc oedema occurs on average about 150 days after bone marrow transplant, which is similar to the latent period for the development of the retinopathy.[14] After allogenic bone marrow transplant, about 1% of patients may develop transient unilateral or bilateral sixth nerve palsies and bilateral ptosis. Cyclosporine, possibly together with ganciclovir may represent the promoting factor.[20]

Tacrolimus is a relatively new immunosuppressive agent that is particularly indicated in liver transplantation and bone marrow transplantation. Preclinical toxicity studies in rats showed that tacrolimus may cause cataract due to an accumulation of sorbitol in the lens secondary to the diabetogenic effect of the drug. It is supposed that cataract would not develop with tacrolimus if diabetic parameters are under control.[21] Tacrolimus, like cyclosporine, may have a direct neurotoxic effect.[22] Acute cortical blindness has been reported occurring 5-47 days following bone marrow transplantation and after liver transplantation.[23],[24],[25] Reversibility within few weeks after discontinuation of tacrolimus is generally observed. A case of bilateral anterior ischaemic optic neuropathy 3 months after liver transplantation has been reported in a patient on tacrolimus therapy. Clinical features resembled ischaemic optic neuropathies. Deterioration of vision and bilateral optic atrophy occurred despite discontinuation of the tacrolimus.[22]

Major ocular complications due to immunosuppresant or conditioning chemotherapeutic drugs may also be influenced by other unknown underlying acquired of inherent conditions.

In conclusion, the incidence of ocular complications such as cataract or increased intraocular pressure due to immunosuppression may be relevant. Although more severe cases may occur less frequently, their implication on possible severe visual loss suggests that patients using immunosuppressants after organ transplantations should undergo routine ophthalmologic evaluation especially during the first year of therapy. Patients scheduled for organ transplantation and postoperative immunosuppressant therapy should receive visual acuity measurement, complete eye examination, automated perimetry, and color fundus photography before and every three months after transplantation for the first two years. Ancillary examinations should be performed in selected cases if indicated.


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