Visual Loss Following Indirect Trauma: A Diagnostic Dilemma

TL;DR

A case of vision loss after indirect trauma shows how traumatic optic neuropathy and Purtscher's retinopathy can be diagnosed and treated with imaging and timely intervention.

Contribution

This paper presents a rare case combining traumatic optic neuropathy and Purtscher's retinopathy, emphasizing diagnostic challenges and the role of multimodal imaging.

Findings

Multimodal imaging, including OCT, aids in diagnosing Purtscher's retinopathy alongside traumatic optic neuropathy.

Early treatment with intravenous methylprednisolone improved visual acuity and retinal findings.

Combination of clinical signs and imaging confirmed the dual diagnosis of TON and Purtscher's retinopathy.

Abstract

Monocular vision loss from indirect trauma can result in damage to the optic nerve, retina, or surrounding structures, often occurring without direct injury to the eye. In some cases, overlapping conditions can complicate the diagnosis. We present a case of monocular vision loss following indirect trauma, caused by traumatic optic neuropathy (TON) and Purtscher's retinopathy, emphasizing the diagnostic challenges encountered. A 28-year-old gentleman with no underlying medical conditions, who was involved in a motor vehicle accident and developed a sudden onset of central scotoma in his left eye three days later. His left visual acuity was hand movement, and 6/6 in the right eye. Left eye presented a positive relative afferent pupillary defect (RAPD), with reduced red saturation and light brightness. Anterior segment and intraocular pressure were unremarkable. Dilated fundus examination showed disc hemorrhage, peripapillary cotton wool spots (CWS), and swollen retinal nerve fibre layers surrounding the disc. Minimal dot-blot hemorrhage seen at the macula. Amsler’s grid and Bjerrum visual field test showed central scotoma. Optical coherence tomography (OCT) showed retinal thickening and oedema, with a hyperreflective band at the inner nuclear layer and at the perifoveal region, like paracentral acute middle maculopathy (PAMM). The right eye was unremarkable. Contrast computed tomography (CT) of the brain and orbit ruled out intracranial bleeding, cerebral oedema, and skull fracture. The patient was initially treated as left TON, as no other associated injuries with potential embolic etiologies, such as long bone fractures or chest compressions, suggested Purtscher’s retinopathy. He was treated with a three-day course of megadose intravenous methylprednisolone. On day 2 of treatment, left eye visual acuity improved to 6/18. We then re-evaluated OCT and noticed PAMM, which is suggestive of Purtscher’s retinopathy. Subsequently, his left visual acuity regained 6/6. Peripapillary CWS and hemorrhages diminished, with improvement seen on OCT and Bjerrum. This case highlights the clinical presentation of indirect TON combined with Purtscher’s retinopathy. Multimodal imaging, such as OCT, provides more information, which is helpful in diagnosing Purtscher’s retinopathy. Early recognition and management are crucial in optimizing visual outcomes and addressing the complex nature of such traumatic injuries.

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