Macular infarction in a patient with Toxoplasma ... - BMJ Case Reports

Findings that shed new light on the possible pathogenesis of a disease or an adverse effect

CASE REPORT

Macular infarction in a patient with Toxoplasma retinochoroditis Vinod Kumar, Brijesh Takkar, Parijat Chandra, Atul Kumar Dr Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India Correspondence to Dr Vinod Kumar, [email protected]

SUMMARY Toxoplasma retinochoroditis is one of the commonest causes of infectious posterior uveitis and may lead to occlusive retinitis. We present a case of a patient with Toxoplasma retinochoroditis who developed macular infarction after initial improvement on pharmacotherapy. The potential aetiology and outcome are described.

Accepted 21 December 2015

BACKGROUND Ocular toxoplasmosis can be associated with numerous posterior segment complications such as cystoid macular oedema, retinal detachment, optic atrophy, choroidal neovascularisation, branch artery occlusion, periphlebitis and scleritis.1 We report a case of Toxoplasma retinitis complicated by macular infarction after initial response to medical therapy. Such an occurrence has never been described before.

CASE PRESENTATION A 24-year-old otherwise healthy man had blurring in his right eye 1 month prior to this presentation. He consulted a local ophthalmologist. The visual acuity recorded at that time was 6/18 in the right eye and 6/6 in the left eye. He was diagnosed with Toxoplasma retinochoroditis in his right eye based on clinical presentation (figure 1) and raised IgM antibodies to Toxoplasma on ELISA assays. The patient was advised combination therapy of trimethoprim (160 mg) and sulfamethoxazole (800 mg) along with oral steroids (1 mg/kg body weight). The patient’s vision improved to 6/9 over

3 weeks, when he developed a sudden onset loss of vision and presented at our clinic. There was no history of any other systemic illness or exposure to pets. At presentation, his Best corrected visual acuity (BCVA) was 6/60 in the right eye and 6/6 in the left eye. Anterior segments of both the eyes were unremarkable apart from a relative afferent pupillary defect in the right eye. On fundus examination, the right eye had multiple soft exudates, flame-shaped haemorrhages in the macular area and macular oedema (figure 2A). There was severe attenuation of the arterioles along with inflamed arterioles (figure 2A—black arrow).

INVESTIGATIONS Fundus fluorescein angiography showed capillary non-perfusion along with pruned arterioles in macula leading to severe macular ischaemia (figure 2B). Vessel wall staining was seen in venous phase (figure 2C) while diffuse leakage of dye was noted in late phase (figure 2D). Optical coherence tomography showed inner retinal hyper reflectivity and outer retinal oedema, suggestive of macular ischaemia (figure 3). A diagnosis of macular infarction was made. The patient’s systemic investigations including blood pressure, blood counts, erythrocyte sedimentation rate and renal and liver function tests were all normal. The patient tested negative for HIV.

TREATMENT The patient was advised to continue medical therapy for a further 3 weeks.

OUTCOME AND FOLLOW-UP The patient maintained BCVA of 6/60 in OD until 4 weeks of follow-up.

DISCUSSION

To cite: Kumar V, Takkar B, Chandra P, et al. BMJ Case Rep Published online: [please include Day Month Year] doi:10.1136/bcr-2015212596

Figure 1 Colour fundus photograph of the right eye of the patient at initial presentation showing two active retinochoroditis patches in the inferior part of macula. Fluorescein angiography pictures show early hypofluorescence followed by late staining and leakage.

Macular infarction has been reported with multiple aetiologies including aminoglycoside toxicity, blood cell disorders, vascular disorders, snake bite, haemodialysis and protein-losing enteropathy, among others. The common aetiopathogenesis in all these conditions include a hyperthrombotic state, hypotension and hyperviscosity, which lead to severe macular hypoperfusion and ischaemia, resulting in macular infarction.2 3 Absence of collateral circulation along with the thin long nature of the capillaries in highly metabolically active tissue makes macula vulnerable to such damage.2 Kyrieleis’ vasculitis is a rare condition in which white-yellowish exudates are placed in a beaded pattern within the retinal arteries.4 This kind of arterial involvement is typically seen with

Kumar V, et al. BMJ Case Rep 2016. doi:10.1136/bcr-2015-212596

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Findings that shed new light on the possible pathogenesis of a disease or an adverse effect Figure 2 Colour photograph of the right eye of the patient 1 month after initial presentation. The fundus shows multiple cotton wool spots, flame-shaped haemorrhages in the macular area as well as macular oedema. (A) Black arrow highlights the area of arteriolitis. Early phase fluorescein angiogram (B) of the right eye of the patient 1 month after initial presentation shows a large area of non-perfusion at the macula while venous phase (C) shows vessel wall staining, microvascular abnormalities and pruning of macular arterioles. Late phase angiogram (D) shows diffuse leakage from the affected vessels at posterior pole.

infective necrotising retinitis associated with toxoplasmosis.4 5 Branch retinal arterial occlusion has been described in association with Toxoplasma due to inflammation.6 Kianersi et al7 described a case of ocular toxoplasmosis presenting as macular branch retinal artery occlusion. Our patient had evidence of macular arteriolitis along with macular vascular sclerosis and pruning (figures 2 and 3). Such findings are well explained by necrotising retinitis that is seen with Toxoplasma infestation. To the best of our knowledge, this is the first documented case of macular infarction associated with toxoplasmosis. Figure 3 Spectral domain optical coherence tomography of the right eye of the patient showing hyper-reflectivity of inner retinal layers with oedema of the outer retinal layers.

Competing interests None declared. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES Learning points

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▸ Toxoplasma retinochoroditis is a common cause of infectious posterior uveitis. It is treated by a combination of systemic antibiotics and steroids. ▸ Toxoplasma frequently affects the retinal arterioles, leading to retinal occlusive arteriolitis. ▸ Macular infarction is a rare but dreaded complication of Toxoplasma retinochoroditis. It may be a cause of poor visual outcome in these patients.

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Park YH, Nam HW. Clinical features and treatment of ocular toxoplasmosis. Korean J Parasitol 2013;51:393–9. Subijay S, Varun G, Shikha G, et al. Bilateral macular infarction secondary to haemodialysis in a patient with chronic renal failure. Clin Experiment Ophthalmol 2012;40:e112–13. Subijay S, Shikha G, Yogesh B, et al. An unusual cause of macular infarction: protein-losing enteropathy. Int Ophthalmol 2012;32:519–21. Francés-Muñoz E, Gallego-Pinazo R, López-Lizcano R, et al. Kyrieleis’ vasculitis in acute retinal necrosis. Clin Ophthalmol 2010;4:837–8. Abu El-Asrar AM, Herbort CP, Tabbara KF. Differential diagnosis of retinal vasculitis. Middle East Afr J Ophthalmol 2009;16:202–18. Chiang E, Goldstein DA, Shapiro MJ, et al. Branch retinal artery occlusion caused by toxoplasmosis in an adolescent. Case Rep Ophthalmol 2012;3:333–8. Kianersi F, Ghanbari H, Beni AN, et al. Macular branch retinal artery occlusion as the first manifestation of ocular toxoplasmosis. Retin Cases Brief Rep 2013;7:391–4.


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