Consumption of cannabis and cocaine: correct mix for arterial occlusions

Abstract

We present a case of a young Afro-Caribbean man who presented with sudden unilateral loss of vision due to central retinal artery occlusion. He was a cocaine and cannabis abuser for 6 years. Acute central retinal artery occlusion at such a young age is unusual. We discuss the possible pathogenesis and treatment options for acute retinal artery occlusion, due to suspected cocaine and cannabis abuse, and present our experience of its management.

BACKGROUND

This case is important because:

• Central retinal artery occlusion is uncommon in young people

• There is no previous report of cannabis and cocaine user having sudden vision loss due to a similar cause. Although there are reports of acute arterial occlusion leading to myocardial infarction

• It is important to be aware of the acute risk of abuse of cocaine and cannabis. Treating patients early with aspirin may limit the damage. There is a theoretical possibility that the occlusion in our patient could be reversed by aspirin.

CASE PRESENTATION

A 24-year-old Afro-Caribbean man presented with sudden loss of vision in his right eye (RE) for 12 h. His vision was hand movements in the right and 6/4 in the left. He was not forthcoming with the history of drug abuse, but on specific questioning he admitted to smoking cocaine and using intranasal cocaine about 7 h before his sudden loss of vision. He was a cannabis and cocaine user for 6 years. He used cocaine only once in the past 2 months but he was a regular cannabis user, smoking cannabis 5–6 times a day. Alcohol consumption was 24 units per week.

INVESTIGATIONS

There was decreased right acuity with relative afferent pupillary defect. The anterior segments were normal. Fundus examination revealed whitening of the retina at the posterior pole with a cherry red spot in the macula. These changes are evident in fig 1, consistent with a diagnosis of right central retinal artery occlusion (CRAO). Intraocular pressure was 12 mm Hg in both eyes. Immediate intravenous acetazolamide improved the patient’s vision, enabling him to count fingers at a distance of 1 metre. Rebreathing and ocular massage were also initiated without any appreciable benefit after half an hour. The full blood count, blood sugar, liver functions, kidney functions, erythrocyte sedimentation rate (ESR), C reactive protein (CRP), lipid profile, haemoglobinopathy, antinuclear antibody (ANA), protein C, free protein S, antithrombin, activated partial thromboplastin time (APTT), international normalised ration (INR), and fibrinogen were normal. Electrocardiography, echocardiography, carotid ultrasonography, and cardiovascular examination were normal.

Figure 1.

Central retinal artery occlusion of the right eye, whitening of the retina, and cherry red spot at the fovea.

TREATMENT

The patient was asked to continue oral acetazolamide 250 mg four times a day for 2 days, topical timolol 0.5% twice a day in his right eye for 36 h, and latanoprost 0.05% at night in his right eye for 2 days to keep intraocular pressures low. He was commenced on oral aspirin 75 mg once a day.

OUTCOME AND FOLLOW-UP

The patient’s vision the next day stayed at counting fingers at a distance of 1 metre. Two months later, his visual acuity was 6/60. This notable improvement in vision is remarkable but we do not expect any further improvement. He says he had stopped using cocaine and is trying to stop smoking cannabis.

DISCUSSION

To the best of our knowledge this is the first case of CRAO associated with cocaine and cannabis abuse in a relatively healthy young male. There has been no previously published report of ocular side effects associated with the combined use of cannabis and cocaine. Retinal vascular occlusions in a young adult is devastating and frustrating. They are infrequent and usually associated with systemic disorders.¹

Cocaine abuse is on the increase and so is the realisation and reporting of its potential to cause serious vascular occlusions. They are common in people on large doses of drug intravenously. Postulated mechanisms include: inhibition of uptake of norepinephrine by adrenergic nerve endings causing vasoconstriction of small vessels; and platelet activation, α granule release, and microaggregrate formation causing thromboembolic events.² Common complications include myocardial infarction, cardiac arrhythmias, central nervous system (CNS) disturbances (seizures/strokes), and peripheral vascular disease, although renal and intestinal ischaemia can also occur. Vasospasm due to cocaine causing ischaemia can potentially be reversed by timely administration of vasodilators such as nifedipine. Newborns exposed to maternal cocaine use in utero have been found to have deep intraretinal haemorrhages signifying chronic ischaemia. Ocular adverse effects include ischaemic optic neuropathy, central and branch retinal and vein occlusions,^3–6 chorioretinal infarction, and talc/microtalc retinopathy.

Vascular complications of cannabis use include cerebrovascular events, and cardiac and peripheral vascular ischaemia. Proposed aetiologic mechanisms include vasospasm, arteritis,⁷ and systemic hypotension with impaired autoregulation. Cannabis smoking produces peripheral vascular disease due to arteritis, CNS symptoms, cardiac death, and, less commonly, renal and pulmonary manifestations. Cannabis arteritis was first described in 1960, and subsequent reports have found the arteritis to parallel cannabis use.⁸

In our patient, we believe long term cannabis use was responsible for the arteritis and cocaine use caused platelet microaggregrates, producing the right mixture for retinal arterial occlusion. There is one report of sudden coronary arterial occlusion with use of cocaine and cannabis in a young healthy adult male resulting in sudden death.⁹ Although there are previous reports of CRAO with intranasal, intravenous or smoking of cocaine alone, there is no case of CRAO with combined use of cocaine and cannabis. We feel it is important to identify combined drug abuse and their interactions. There is evidence to suggest that arterial occlusion in these settings can benefit from the early institution of antiplatelet drugs. We therefore tried the use of early low dose aspirin 75 mg once a day¹⁰ not only to increase ocular perfusion but also to prevent CNS and coronary complications. Other treatments that have been tried to overcome cocaine and cannabis occlusions include iloprost,¹¹ a synthetic analogue of prostacyclin PGI2 for peripheral vascular disease, heparin, and thrombolysis.

In the current scenario of rising drug abuse with cannabis and cocaine, health care professionals in all specialities and at all levels should be made aware of the potential of these drugs to cause sudden arterial occlusions in young adults without an identifiable source or overt cardiovascular risk factors. This may have implications in their management.

It is not routine to give aspirin in acute management of central retinal artery occlusions which are commonly caused by atherosclerosis, cholesterol emboli or calcium. We feel that it may be possible that early institution of aspirin can protect these young adults from irreversible visual loss in a setting of CRAO resulting from cannabis and cocaine use.

LEARNING POINTS

• The role of aspirin in the management of central retinal artery occlusion, where there is a history of cocaine intake, needs to be evaluated.

• Cocaine and cannabis abuse can cause central retinal artery occlusion.

• Combined use of cannabis and cocaine can produce more dramatic arterial occlusions.