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Despite the common occurrence of insect stings and local and systemic allergic reactions,1 there are few reports of optic neuropathy or stroke following bee or wasp stings and, to our knowledge, there has been no report of both cerebral infarction and optic neuropathy occurring in the same patient after such an event. We report on a middle aged woman who sustained both a stroke and ischaemic optic neuropathy after multiple bee stings.
A 57 year old white woman reported being stung by 30–40 bees, identified as Africanised honey (killer) bees, in the back of her neck, head, right eye, face, and right arm. She was treated with intravenous antihistamines and antiemetics at a local emergency room and released.
Two days later, the patient experienced a severe headache with nausea and vomiting and noticed a left homonymous visual field loss. She went to see her primary doctor and while there became unresponsive, leading to hospitalisation. Head computed tomography (CT) showed a right occipital ischaemic infarct.
Shortly thereafter, the patient experienced acute nausea and vomiting with neck rigidity and was readmitted. A head CT scan and brain magnetic resonance image (MRI)/magnetic resonance angiography (MRA) were performed showing a large right temporo-occipital haemorrhagic infarct (fig 1A, B). An ocular examination revealed best corrected visual acuity (BCVA) of 20/20-1 right eye and 20/30-2 left eye at distance and 20/20 right eye and 20/200 left eye at near, with left homonymous hemianopia, a left inferior altitudinal defect, and bilateral arcuate defects (fig 1C) with bilateral haemorrhagic disc oedema.
Past medical and surgical history are significant only for controlled arterial hypertension and pseudophakia.
Neuro-ophthalmic examination 5 weeks after her sting episode showed BCVA of 20/15 right eye and 20/25 left eye at distance and 20/20 right eye and 20/30+1 at near. Amsler grid and automated perimetry showed a left homonymous hemianopic defect with a right inferior arcuate defect and a left inferior altitudinal defect.
Pupil examination showed isocoria with a 0.3–0.6 log unit relative afferent pupillary defect in the left eye. Motility was unremarkable, as was anterior segment both eyes. Intraocular pressures were 20 mm Hg right eye and 18 mm Hg left eye. Funduscopic examination showed bilateral disc oedema with pallid swelling superiorly and temporally in both eyes and peripapillary haemorrhage and cotton wool spots in both eyes consistent with anterior ischaemic optic neuropathy (AION). Both maculas were unremarkable without exudative changes. Both retinas were flat with normal vasculature out to the periphery.
Three months after the sting event, the patient reported some improvement of peripheral vision, and repeat visual fields improved slightly inferiorly but were otherwise unchanged. Both optic discs were now flat and showed superior temporal pallor with corresponding nerve fibre layer dropout.
In their literature review of five cases and report of two additional cases of optic neuropathy occurring after bee and wasp sting, Maltzman, et al2 describe common characteristics, such as acute to subacute onset of symptoms, moderate to severe visual loss followed by significant recovery (except in one case of a sting directly to the eye); oedematous and haemorrhagic optic discs, and central or caecocentral scotomas. Although our patient had subacute vision loss associated with haemorrhagic disc oedema, her case differs because of minimal recovery of vision and altitudinal visual loss consistent with an ischaemic neuropathy, rather than a transient optic neuritis.
Seven cases of wasp and bee sting associated cerebral infarction were found in the literature.3–9 Reported neurological complications included seizure, hemiparesis, aphasia, apraxia, dysarthria, ataxia, and coma, none of which were experienced by our patient. None of these patients had a full eye examination, although in one patient8 a right homonymous superior quadrantanopia was demonstrated (table 1).
The pathophysiology explaining the associated stroke is unknown. Hypotension caused by anaphylaxis may certainly induce cerebral and optic nerve ischaemia; however, this was not documented in our case. Similar to acute myocardial infarction after hymenoptera stings, it has been suggested that vasoconstriction secondary to mediators released after the sting, aggravated by exogenous adrenaline, and platelet aggregation also contribute to cerebral ischaemia.8 Bee venom itself contains histamine, thromboxane, leucotrienes, and other vasoactive and inflammatory mediators. In our patient, we postulate that the systemic immune mediated reaction to the bee sting caused vasoconstriction and a prothrombotic state with subsequent ischaemia leading to both the stroke and AION. In addition, a neuropharmacological (sympathetic) mechanism of endothelial permeability involving the cerebral vasculature with a concurrent systemic thrombogenic or immune response has also been postulated.5,6
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