Branch retinal artery occlusion following cocaine inhalation: Case report and review of the literature
Waleed K Alsarhani1, Abdullah I Almater2, Ahmed M Abu El-Asrar3
1 Department of Ophthalmology, College of Medicine, King Saud University Medical City; Department of Ophthalmology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia
2 Department of Ophthalmology, College of Medicine, King Saud University Medical City, Riyadh, Saudi Arabia
3 Department of Ophthalmology, College of Medicine, King Saud University Medical City; Dr. Nasser Al-Rashid Research Chair in Ophthalmology, College of Medicine, Riyadh, Saudi Arabia
Correspondence Address:
Prof. Ahmed M Abu El-Asrar
Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, P.O. Box: 245, Riyadh 11411
Saudi Arabia
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/meajo.meajo_65_22
Cocaine abuse has been reported to cause devastating systemic and ocular side effects. Retinal vascular occlusion following cocaine abuse has been scarcely reported in the literature. Herein, we are describing a rare case of branch retinal artery occlusion (BRAO) following intranasal cocaine use in a young female. She presented to the emergency department 1 month after having blurred vision in the left eye, which started 1 day after cocaine nasal inhalation. Fundus examination of the left eye showed an inferotemporal BRAO. In conclusion, cocaine should be considered in the differential diagnosis of retinal arterial occlusion in young healthy patients.
Keywords: Branch retinal artery occlusion, cocaine, drug abuse, vascular diseases
Cocaine is a well-known cause of myocardial infarctions and cerebrovascular events.[1] However, central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), and ophthalmic artery occlusion have been scarcely reported with the recreational use of cocaine.[2],[3],[4],[5],[6],[7],[8],[9] In this report, we are describing a case of branch retinal artery occlusion (BRAO) following intranasal cocaine inhalation.
Case ReportA 29-year-old medically healthy female patient presented with blurred vision in the left eye for 1 month, which started 1 day after a nasal cocaine inhalation. She has been a smoker for the past 6 years. Past medical and family histories was negative for any thromboembolic events. The patient denied any history of medication use, including oral contraceptives and intravenous substance abuse. On physical examination, blood pressure on her visit to the ophthalmology clinic was 110/60 mmHg. Visual acuity was 20/20 in the right eye and 20/25 in the left eye. Intraocular pressure was 18 mmHg in both eyes. The anterior segment examination was unremarkable. Fundus examination of the left eye revealed the presence of retinal ischemic whitening along an occluded inferotemporal retinal arteriole sparing the fovea [Figure 1]. Arterial emboli or retinal crystal were not seen in both eyes, and examination of the fellow eye was normal. Fundus fluorescein angiography confirmed the presence of occlusion of the inferotemporal retinal artery of the left eye [Figure 2].
Figure 1: Fundus photography of the left eye depicting an inferotemporal whitening of the inferotemporal retina with an occluded inferotemporal arteryFigure 2: Fundus fluorescein angiography (late venous phase) demonstrating a nonfilling pattern with a leading edge within the inferotemporal arterySystemic workup was normal including full blood count, glucose, erythrocyte sedimentation rate, sickle solubility test, protein C, protein S, factor V Leiden, antithrombin III, antiphospholipid antibodies, blood homocysteine, Venereal Disease Research Laboratory test, rapid plasma reagin, and hemoglobin electrophoresis. Furthermore, echocardiography and carotid Doppler ultrasonography were unremarkable. She was then planned for observation and referral to psychological counseling. However, the patient lost follow-up.
DiscussionIn contrast to older patients, retinal arterial occlusions in young patients are usually secondary to nonembolic causes such as hypercoagulable states.[10] In general, retinal vascular occlusions have been reported in several cases following intranasal cocaine inhalation and once in a cocaine smoker[3],[4],[6],[7],[8][Table 1]. Sleiman et al. reported two cases of CRVO and CRAO in two young healthy chronic intranasal cocaine abusers.[4] Michaelides and Larkin reported a case of CRAO in a generally healthy patient who smoked cocaine regularly.[5] In one case, a macular star was found in a cocaine-induced CRAO, which supports the fact that severe hypertension may play role in the pathophysiology of the disease.[6] In this report, we are describing a case of BRAO following intranasal cocaine use. The patient developed the disease within 1 day of the incident of cocaine abuse. Similarly, previous reports showed that the onset of vascular occlusion may start within 24 h.[2],[3] Wallace et al. reported a case of CRAO in a hypertensive female that occurred 4 hours following the inhalation of cocaine.[3]
Table 1: Cases of retinal vascular occlusions associated with cocaine useCocaine causes inhibition of norepinephrine uptake resulting in vasospasm. Cocaine may indirectly cause vasoconstriction through stimulating endothelin and inhibiting nitric oxide release.[11],[12] Vasospasm is also responsible for cocaine-induced myocardial infarction.[1] Moreover, cocaine may cause severe hypertension that may result in vascular fibrinoid necrosis. Nevertheless, signs of hypertensive retinopathy were not observed in our patient. According to postmortem and in vitro studies, cocaine effects consist of vasoconstriction, endothelial dysfunction and progression of atherosclerosis.[13] In the present case, the absence of a clot on clinical and fluoroscopic examination in the context of a negative systemic workup suggests that the main mechanism for BRAO was vasospasm.
In concluson, retinal vascular occlusion in young patients warrants careful history questioning about substance abuse. Patients refusing to admit illicit drug abuse may make the diagnosis of the underlying etiology challenging; however, this can be overcome with establishing an appropriate patient–doctor relationship.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Acknowledgments
The author would like to thank Vice Deanship of Research Chair, Dr. Nasser Al Rashid Research Chair in Ophthalmology King Saud University.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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