The use of various drugs for recreational purposes is widespread, has various triggers and is apparent in all ages and socioeconomic groups. Statistics from the NHS Information Centre1 show that majority of drug misuse complications arise in individuals 16 to 34 years old, with cannabis being the most commonly used drug among young people, even after this drug was reclassified from a class C to a class B drug. More than £900 million has been invested by the Home Office since 2003 to establish the Drugs Intervention Programme which incorporates a partnership working across the criminal justice system, primary healthcare professionals and a range of drug treatment or rehabilitation services.2

Optometrists are health care providers that can sit at the forefront of detecting early ocular signs and diagnosing drug-related ocular complications. This review will concentrate on the effect on ocular health of some common addicting substances, such as alcohol and tobacco but also cannabis, ecstasy, LSD (lysergic acid diethylamide), meth, heroin and cocaine.

Alcohol

Alcohol is a legal addictive substance that is only second to water in the sheer volume consumed by humans. It not only affects the nervous system but it also has a large number of adverse ocular effects. These include;

  • paralysis and jerky pursuit movements of extraocular muscles
  • downbeat nystagmus
  • paralysis of accommodation
  • decreased visual discrimination
  • miosis with a reduced or absent reaction to light
  • visual field defects
  • decreased intraocular pressure (IOP)
  • optic neuritis
  • arcus senilis
  • toxic neuropathy.

Dry eye, cataract, refraction changes, transient amblyopia, jaundice (due to liver damage) and high IOP in glaucoma patients has also been described.3 However, a definite link between age-related macular degeneration (AMD) and alcohol consumption was not established.4 Beside its effects on the central nervous system, the ability to drive is affected after alcohol consumption also due to its effects on oculomotor functioning, even at a non-intoxicating dose.5

Both smooth pursuit and saccade eye movements are impaired or decrease across the visual field by 25% if blood ethanol concentrations reach ranges of 60 to 100mg/dl. Law enforcement officials in the US use the horizontal gaze nystagmus test (HGN) to identify cases of driving under the influence (DUI). The results of this test need, however, to be validated using an on-the-spot alcohol breath test and is also administered in association with Walk-and-Turn (WAT) and One-Leg Stand (OLS) tests.6 The usefulness of HGN for DUI convictions in court is, nevertheless, criticised. Other variables, such as the presence of various medical conditions, the effects of fatigue and fear, inter-observer variability in testing speed and view angles, could all have an effect on the results.7

It is important to mention here a new trend in alcohol consumption among young individuals, the so-called ‘eyeballing’, which represents direct pouring of alcohol onto the eye surface. This new trend occurs in association with binge drinking and multiple substance abuse.8 Through this method, users achieve a ‘quick high’; however, it is expected that immediate and potentially very damaging effects can also occur. Indeed, pain, blurred vision, conjunctival injection (figure 1), corneal ulcers, scars and blindness have been reported after this type of alcohol use.8

Figure 1: Conjunctival injection after ‘eyeballing’

This issue was also highlighted by a BBC3 documentary in 2011 ‘Ready, Steady, Drink’. The president of the UK College of Optometrists at that time also featured in that documentary saying: ‘By putting vodka, or in fact any alcohol, in your eye actually means you are stripping away the very delicate layer of skin on the surface of the eye which is there to protect it. Alcohol is used during surgery for this very purpose during certain surgical eye procedures, so it is extremely dangerous to expose your eyes to this yourself. Repeated direct exposure to alcohol could cause permanent corneal scarring and potential loss of vision.’9

Health care providers, including optometrists should be aware of this new method of alcohol administration when examining young adults that come to the emergency room with such ocular changes and behaviour that points towards possible intoxication with alcohol.

Tobacco smoking

There are about 7,000 toxic compounds in tobacco, including nitric oxide, carbon monoxide, hydroquinone and formaldehyde. Smoking is a known risk factor for ocular diseases such as;

  • age-related macular degeneration (AMD)
  • ocular surface disease
  • cataract
  • diabetic retinopathy (figure 2)
  • thyroid associated orbitopathy.

In addition, smoking has also been shown to enhance the effect of genetic susceptibility with regards to the presence and development of AMD.10 Nevertheless, only a small proportion of smokers (less than 10% in the UK) are aware that smoking has a negative effect on their ocular health.11 Recent studies also show that smokers have a higher risk of suffering from ocular inflammatory diseases.

Figure 2: Diabetic retinopathy (maculopathy)

Ocular ischaemia can also be a regular occurrence among smokers, as platelet activation increases the likelihood of thrombosis and vasoconstriction through α-adrenergic vascular receptors are stimulated by nicotine.12 In the buildup of hypoxic conditions, an increase in free fatty acids and low-density lipoproteins levels can accelerate atherosclerosis posing a greater possibility of vaso-occlusive diseases. In association with excessive alcohol consumption, chronic smoking can lead to toxic optic neuropathy with signs of colour vision impairment, gradual bilateral blurring of vision, central scotoma, disc oedema and optic disc atrophy.13

Community optometrists could play an important role in increasing the awareness of the harmful effects of smoking on the general and ocular health. They can also provide information on various campaigns and treatment plans that include smoke cessation. However, at the moment, despite an increased involvement in promoting general health, the level of optometrists’ contribution to the fight against smoking is low.

A study performed in 2016 showed that teaching smoking cessation to UK optometry students is patchy and practical training for delivering evidence-based behavioural support interventions in clinical practice is almost nonexistent.14 The authors concluded that in the UK available materials, such as those developed by the National Centre for Smoking Cessation and Training (see ncsct.co.uk) designed to provide training on established, evidence-based, competencies for smoking cessation, can be easily used for training optometry students with possible high impact on their future practice.

Cannabis

Cannabis is one of the most widely used recreational drugs in the world and this psychoactive substance is usually smoked for obtaining a sedative influence upon the central nervous system. The ocular side effects of cannabis that occur after long term drug use are;

  • visual hallucinations
  • colour vision defects (objects having yellow or violet tinge, sensitive colour perception and coloured flashing lights)
  • nystagmus
  • general ocular irritation
  • decreased accommodation
  • decreased dark adaptation
  • pupil anomalies (miosis and anisocoria)
  • diplopia
  • impaired oculomotor co-ordination
  • intermittent esotropia
  • decreased lacrimation
  • blepharospasm
  • decreased IOP (figure 3)
  • decreased vision.

In chronic users there was a general increase in basal lacrimation, increase in photosensitivity, decrease in dark adaptation, increase in pupil constriction, decrease in Snellen acuity and an increase in IOP.15

Figure 3: Cannabis may act as an ocular hypotensive

Medical use of cannabis appeared first in China, 5,000 years ago when was recommended for malaria, constipation, rheumatic pains, childbirth and as an analgesic.16 In 19th century, WB O’Shaughnessy, an Irish scientist and physician, prescribed cannabis as a muscle-relaxant, anticonvulsant, analgesic and anti-emetic, thus marking the first use of cannabis as medicine in the UK. After that, in early 1800s cannabis was available in the UK over the counter. However, its life for such purpose was short and it was outlawed in 1928 by ratification of the 1925 Geneva Convention on the manufacture, sale and movement of dangerous drugs.17

Nevertheless, dispensation for special cases still exist. Closely related compounds, Δ9-tetrahydrocannabinol (Δ9-THC), cannabichromene (CBC), cannabigerol (CBG), cannabinol (CBN) and cannabidiol (CBD) were later discovered and THC is available on prescription in the UK for treatment of nausea and vomiting after chemotherapy in special cases. In 1971 it has been shown that the use of cannabinoids can lower the IOP.18 Topical administration of WIN-55-212-2, a synthetic cannabinoid, also showed IOP reduction in glaucoma patients in a time and dose dependent manner.19

Neuroprotective effects on the retinal ganglion cells have also been reported. Nevertheless, the use of such substances in glaucoma treatment is controversial. Their interactions with other medication used by the patients for their co-morbidities are not sufficiently researched. In addition, due to its addictive effects and the effects on systemic blood pressure that could negatively influence the perfusion of an already damaged optic nerve, such is the case in glaucoma, use of marijuana for glaucoma, is not presently supported.20

Methylenedioxymethamphetamine (ecstasy)

Methylenedioxymethamphetamine (MDMA), more commonly known as the party drug ecstasy, acts on the central nervous system by increasing the release of neurotransmitters such as noradrenaline, serotonin and dopamine.21 Systemic side effects of this drug include;

  • headache
  • loss of appetite
  • dry mouth
  • muscular tension
  • hyperthermia
  • cerebral oedema
  • tachycardia
  • hypertension
  • intracerebral haemorrhage
  • blurred vision.

At the ocular level, a common complaint in most ecstasy users is blurred vision.22 Due to increased serotonin release, ecstasy misuse can also induce acute onset angle closure and transient myopia. Other adverse reactions, such as retinal haemorrhages with sudden loss of vision and vascular occlusions23 occur secondary to drug-induced systemic hypertension. Other ocular effects are diplopia and abnormal ocular motility due to cranial nerve palsies secondary to cerebral oedema.24

Lysergic Acid Diethylamide (LSD)

The illicit use of lysergic acid diethylamide (LSD) is known for its potent hallucinogenic effects. Ocular side effects commonly reported by users are;

  • visual hallucinations
  • image distortion
  • colour intensification
  • colour vision defects
  • pupil mydriasis
  • decreased dark adaptation
  • decreased vision.

Decreased accommodation, photophobia, abnormal electroretinogram (ERG) and visually evoked response (VEP), increased frequency and amplitude of physiological nystagmus after oral administration of LSD and palinopsia, a condition of prolonged afterimages usually associated with destructive lesions of the parieto-occipital cortex, have also been mentioned as a consequence of LSD ingestion.25

Mothers using LSD while pregnant can give birth to children suffering from congenital cataract, iris coloboma, microphthalmos, corneal opacities, persistent hyperplastic primary vitreous (PHPV), retinal and optic disc abnormalities and anophthalmia.26

Figure 4: Early necrotising scleritis

Amphetamines

Crystal methamphetamine (crystal meth) belongs to a class of amphetamines used around the world as a potent CNS stimulant. Meth is a highly addictive drug and its common ways of administration include intranasal inhalation, smoking and intravenous injections. Crystal meth use has many ocular manifestations including;

  • keratitis
  • corneal ulcerations and scarring,27 depending upon the purity of the drug sample and the method of administering the drug
  • episcleritis
  • scleritis (figure 4)
  • panophthalmitis and endophthalmitis.28

Through its sympathomimetic effects, crystal meth induces elevated blood pressure and vasoconstriction. These vascular problems can increase the risk of central retinal artery occlusions (figure 5), intraretinal haemorrhages29 as well as drug-induced stroke with secondary ocular complications. Injected crystal meth can also result is retinal vasculitis and crystalline retinopathy from the impurities that built up in the vascular layers of the retina.

Figure 5: Inferior branch retinal artery occlusion. Occlusions can result from cocaine abuse

Cocaine

Cocaine and crack cocaine have very high levels of ocular side effects. This is probably due to their sympathomimetic and vasoconstrictor effects. The following have all been reported in association with this drug;

  • acute angle closure glaucoma
  • decreased vision
  • colour vision defects
  • visual hallucinations
  • photosensitivity
  • reduced pupil reaction to light and mydriasis
  • paralysis of accommodation
  • exophthalmos
  • optic neuritis and optic atrophy
  • madarosis
  • iritis.

Cocaine-induced central retinal artery occlusions and retinal haemorrhages have also been reported. Therefore, optometrists should consider cocaine abuse as a significant risk factor for young healthy patients with retinal vascular occlusions or any retinal vascular manifestations for that matter. In addition, intranasal use of cocaine can have an injurious effect on ocular tissues, resulting in reduced corneal sensitivity, corneal ulcers, corneal oedema and superficial punctuate keratopathy. Sachs et al30 suggested exposure of impurities found in crack cocaine lead to corneal neurotrophic keratitis, and this nerve damage in turn depresses the corneal sensation and reduces blink rate.

As crack cocaine is alkaline in nature, direct toxic effects via smoke particles result in low grade chemical burns damaging the corneal epithelial plasma membrane and microvilli, allowing secondary microbial growth and infections. In some extreme cases of intranasal cocaine use, loss of the nasal septum can extend to the bony walls of the orbit which in turn relates to the onset of optic neuropathies accompanied by lacrimal duct obstruction and orbital cellulitis.31

Drug-induced cerebrovascular haemorrhages can instigate defects in ocular motility and visual acuity. A case study reported a 35-year-old cocaine user with a midbrain haemorrhage which resulted in bilateral internuclear ophthalmoplegia (INO), bilateral ptosis, convergence-retraction nystagmus (with limited upgaze) and pupils non-reactive to light.32 Strokes secondary to crack cocaine (figure 6) use have also been related to INO and trochlear nerve palsy resulting in abnormal ocular motility.

Figure 6: Stroke may result from abuse of recreational drugs – a superior left homonymous quadranopia post-stroke

Medical use of cocaine

Cocaine has been used as anaesthetic from 1884 when Carl Holler, an Austrian ophthalmologist used cocaine drops for eye surgery. It was subsequently used as a cure for toothache, surgery on throat and nose, even for shyness in children. Presently, cocaine hydrochloride is still used in topical anaesthesia for minor surgical procedures. Cocaine is also used as 10% drops in the diagnosis of Horner’s syndrome, a disorder characterised by an interruption at any point along the oculosympathetic pathway.

Through blocking the re-uptake of norepinephrine released at neuromuscular junctions of the iris dilator muscle, cocaine helps differentiate between a normal eye from one affected by Horner’s. Following instillation of cocaine in a normal eye, the pupil will dilate; but in Horner syndrome, the pupil dilates poorly because little or no norepinephrine is being released.

Diacetylmorphine (heroin)

Heroin belongs to the group of opiates and is usually injected21 but reports of transconjunctival administration also exist.33 The most intense phase of heroin effects, the ‘rush’, takes place shortly after intake. Ocular side effects associated with heroin misuse include:

  • pupil miosis with poor reaction to light (withdrawal symptoms include pupil mydriasis and anisocoria)
  • reduced accommodation
  • strabismus
  • downbeat nystagmus
  • toxic INO
  • abnormal ocular motility
  • Horner’s syndrome
  • visual loss
  • candidal chorioretinitis
  • episcleritis
  • endophthalmitis.

Dias34 investigated the correlation of blue-purple colour deficiencies in heroin addicts but concluded there was no correlation between the level of severity of colour deficiency and amount of heroin used. Diplopia and abnormal ocular motility also occurs in heroin withdrawal. Treatment for withdrawal symptoms of heroin may require prismatic corrections, botulinum toxin or surgical intervention.

Example of ophthalmic drug misuse

It is well known that ocular drugs can be a hidden poison, due to their systemic side effects. However, little is known about ophthalmic medication used for intoxication purposes. Recently, there have been reports (especially coming from Eastern Europe, Italy, Turkey and Kazakhstan) on intravenous injection of tropicamide, mainly in opiate addicts that want to attenuate their withdrawal symptoms.35

Tropicamide use in this way was associated with complications such are cardiovascular toxicity, headache, nausea and psychosis. The users, however, report that tropicamide enhances the effect of heroin and delays the symptoms of withdrawal. The use of tropicamide in multi-drug users is a new trend that is spreading fast.36 Health care professionals should be aware of this new drug use, recognise it in their patients and consider this danger when prescribing them as therapies.

Discussion

In accordance to the College of Optometrists, the role of the optometrist is to provide a professional service to maintain sight and health, treating patients’ needs with common courtesy and sensitivity without infringing on patient confidentiality.37 Good optometric practice means the optometrist is at the forefront in offering immediate advice, being familiar with the types of drug referral programmes, and through general practitioner (GP) referrals, utilise counselling services available in the local community to help treat the patient.

It is important for the optometrist or ophthalmologist to be aware of the potential risks and signs associated with drug abuse. The easiest way to recognise a problem of drug abuse is when a patient admits to the addiction during the general history and symptoms check. If the patient’s ocular pathology is concurrent with illicit drug misuse, an immediate referral to the patient’s GP must be in place, with due consent from the patient.

In addition, another point to raise here is: what should be the practitioner’s attitude if a patient shows up for an eye exam while intoxicated? There are no clear guidelines to state whether a practitioner should or should not see a patient that looks under the influence of alcohol. This is a very complicated decision because either attitude can have important consequences on the patient’s health but also legal implications. If an emergency intervention is necessary, the practitioner also needs to assess the ability of the patient to consent to any investigation or treatment. However, one always needs to act in the best interest of the patient. In the General Optical Council’s and Association of British Dispensing Opticians’ codes of conduct it is stated that practitioners ‘shall always place the welfare of the public, who require their professional services, before all other considerations’.

They also need to make an appropriate referral in case the patient needs it. This means the patient needs to be examined and managed regardless of their condition. In a very informative article on such situations, Malone and Friedman (2005)38 published some important guidelines on dealing with drunkenness. This information has been adapted in table 1.

Table 1: Attitude when dealing with intoxicated patients

When judging a patient as intoxicated, however, one also has to be aware of other possibilities. Smelling like alcohol, for example can also be found in ketoacidosis and erratic behaviour is part of the clinical picture of hypoglycaemia in diabetic patients, both very dangerous medical emergencies that optometrists should know how to recognise. In addition, epilepsy, brain injury and Alzheimer’s are also conditions that can mimic intoxication. Therefore, when not sure, ask for medical history or look for prescriptions and any medical alert bracelets or cards.

Preventive optometry, a concept known since 1950,39 if applied correctly and widely, is a practice of a great value that could provide a way to intervene at a disease stage when less dramatic medical measures are needed. Therefore, any effort should be done to train our existing and future practitioners beyond their current practice and get them involved in more prevention and early health care interventions at the primary care level.

Dr Doina Gherghel is a lecturer in ophthalmology at the School of Life and Health Sciences, Aston University. Gurudutt Sidhu is an optometrist practicing in the Midlands.

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