An Ocular Review on Commonly Used Substances

doi:10.62055/98001619Cv

INTRODUCTION

According to the Substance Abuse and Mental Health Service Administration 2024 report, 73.6 million people used illicit drugs in the past year in the United States, which includes marijuana, cannabis, cocaine, heroin, hallucinogens, inhalants, methamphetamine, stimulants, tranquilizers, sedatives, and pain relievers.¹ In the same report, 48.4 million people aged 12 years and older had a substance abuse disorder.¹

Eye care providers can and should play a role in screening for ocular sequelae of substance use. Recreational substances can contribute to vision loss, ocular pain, and dysfunction of ocular motility, as well as systemic life-threatening side effects. An accurate and timely diagnosis of ocular manifestations secondary to substance use is essential to ensure proper treatment and management for patients with a history of substance abuse. Although tobacco and alcohol are commonly used substances, the ocular effects of tobacco and alcohol were beyond the scope of this paper. This review will summarize the literature on substances reported more frequently by patients, from this writer’s perspective, and on substances whose ocular effects have been investigated more frequently in the literature. Specifically, cocaine, crack cocaine, heroin, cannabis, hallucinogens, and alkyl nitrites will be discussed in relation to the eye. The objective of this review is to provide a summary of the ocular sequelae of these substances and to provide proper education and management to these patients.

METHODS

A broad literature search was conducted in the PubMed database to identify primary research and review publications reporting on the prevalence, descriptions, systemic and ocular side effects, and other characteristics of substances. The search terms included “recreational substances and eye”, “recreational drugs and eye,” “cocaine and eye,” “crack cocaine and eye,” “heroin and eye,” “cannabis and eye,” “hallucinogens and eye,” and “poppers and eye.” This article summarizes the findings and results of these articles.

DISCUSSION

COCAINE

According to the 2024 National Survey on Drug Use and Health in the United States, approximately 4.3 million people, age 12 and over, used cocaine.¹ Cocaine is a schedule II drug, derived from coca leaves. The appearance of cocaine is a fine, white, crystalline powder that is typically used via insufflation or intravenous injection. Cocaine is typically used for its effects of euphoria, extreme energy, mental alertness and hypersensitivity.² The chronic use of cocaine will result in an increase of dopamine in the brain, causing a euphoric sensation. Cocaine prevents the recycling of dopamine, resulting in large amounts of dopamine to accrue, which in turn will reinforce the need for more cocaine and drug-taking behaviors.³ With the continued use of cocaine, the brain’s reward system may adapt and eventually become less sensitive to its effects. This results in people taking stronger and more frequent dosing of cocaine, in an attempt to feel the same high and to obtain relief from withdrawal.³ Short-term adverse effects of cocaine include irritability, paranoia, and tremors, whereas long-term effects include loss of smell from chronic insufflation, HIV risk with intravenous injection, and movement disorders.³ Overdosing on cocaine can cause heart attacks, strokes, seizures and sometimes death.³ The most common ocular side effects from cocaine use include talc retinopathy, decreased blink rate, dacryocystorhinostomy complications, and chorioretinal infarction.

Talc Retinopathy

To increase profits and extend supply, cocaine is often mixed with other substances such as talcum powder, cornstarch or flour.³ Talcum powder, or talc, can cause complications when injected intravenously. When a cocaine and talc mixture is injected intravenously into the bloodstream, particles can embolize to the lung and cause capillary occlusion.^3-4 The capillary occlusion can then result in pulmonary hypertension with collateral vessel formation. Eventually, the collateral vessels allow the emboli to bypass the lungs and enter the heart.⁴ From the heart, the emboli can be pumped to various organs, including the eye. This embolization of talc to the eye almost always occurs with intravenous injection, but can also occur with chronic insufflation, although rare.⁴

Once talc deposits in the retina, it is then defined as talc retinopathy, and typically remains indefinitely.³ Talc retinopathy appears as tiny white or yellow crystalline deposits concentrated in the central posterior pole and can be viewed with a fundus lens in combination with a slit lamp biomicroscope, as pictured in Figure 1.⁴ Most talc emboli will deposit in the inner layers of the posterior retinal and choroidal circulation because of the dense capillary network and the greater blood flow to these areas.³ Talc can also lodge into the peripheral retinal vessels, causing areas of nonperfusion which can eventually cause neovascularization. Evidence of nonperfusion can manifest as retinal hemorrhages, cotton wool spots, microaneurysms, and neovascularization.^3-4 Neovascularization secondary to talc retinopathy can appear in a sea-fan formation, which is atypical compared with neovascularization from other more common vascular etiologies.^3-4

 

Patients with talc retinopathy will usually have no symptoms, since the most common ocular manifestation is the presence of talc particles in the posterior pole. However, in more unusual cases, patients may have a mild decrease in vision secondary to microvascular occlusion due to talc embolization in the arterioles. As a result, patients may be symptomatic for small scotomas in areas of nonperfusion.

A fluorescein angiography is indicated if neovascularization is suspected, otherwise talc retinopathy can be monitored with yearly eye exams.^3-4 More importantly, the presence of talc in the retina can serve as a reminder to the clinician that talcum powder can also embolize to other organs of the body. Specifically, talc granulomas have been found in the lungs, liver, kidneys and lymph nodes.^3-4 If talc retinopathy is diagnosed, a referral to the patient’s primary care physician is warranted for a pulmonary work-up to rule out talc granuloma formation in the lungs.³

Decreased Blink Rate

Chronic use of cocaine is associated with a reduction in dopaminergic D2 receptor density in the striatum, which can result in a reduction in blink rate due to an increase in dopaminergic malfunction.⁵ A chronic decreased blink rate from cocaine use may, in turn, contribute directly to dry eye.

Dacryocystorhinostomy (DCR) complications

With chronic insufflation of cocaine, significant damage to the nasal septum can result.⁶ This becomes significant if a dacryocystorhinostomy is indicated, as a DCR attempts to create a new path for tears to drain between the eyes and nose and may be indicated in a patient with a nasolacrimal duct obstruction symptomatic for epiphora. A dacryocystorhinostomy may not be possible if nasal perforations or necrotic lesions secondary to cocaine insufflation are too severe. Referral to an otorhinolaryngologist may be necessary to manage ulcerous and necrotic lesions within the nose secondary to cocaine insufflation.⁶

Chorioretinal Infarction

Cocaine blocks the reuptake of norepinephrine, dopamine and serotonin, resulting in increased heart, respiratory and metabolic rates, and higher blood pressure and body temperature.⁷ Direct vasoconstriction of vascular smooth muscle can contribute to myocardial infarction, cardiac arrhythmias, and central nervous system disorders.⁸ Like many other diseases, the systemic adverse effects of cocaine may first be identified following a funduscopic ocular examination.

Severe retinal vasospasm secondary to cocaine abuse can result in decreased ocular perfusion and subsequent vision loss. Ocular signs of cocaine-induced vasospasm are typically bilateral and symmetric. Signs include the presence of cotton wool spots, retinal hemorrhages and chorioretinal ischemia.⁹ Depending on the location of infarction and hemorrhages, visual symptoms from cocaine induced vasospasm may or may not include reduced visual acuity. In these cases, vision loss may spontaneously resolve. However, since quinine is commonly used to cut cocaine, vasospasm may also be the result of quinine ocular toxicity.¹⁰ A thorough social history can play an important role in timely management and treatment for patients who may present with bilateral ocular signs.

CRACK COCAINE

Crack cocaine is a more pure alkaloid form of cocaine, but they share the same systemic effects.² Similar to cocaine, crack cocaine can be insufflated or injected intravenously, but it is almost always inhaled or smoked.² There are many adverse effects of crack cocaine, but the most common ocular sequela is corneal epithelial defects known as “crack eye syndrome.” Talc retinopathy, decreased blink rate, dacryocystorhinostomy complications, and chorioretinal infarction, discussed with the use of cocaine, can also be observed with the use of crack cocaine.

Crack Eye Syndrome

In 1989, McHenry and colleagues discovered a pattern of corneal epithelial defects in patients with a history of crack cocaine use and labeled the condition crack eye syndrome.^11-12 The corneal epithelial changes secondary to crack cocaine include a spectrum ranging from superficial punctate keratopathy to microbial keratitis. Two major subtypes were classified: infectious and non-infectious crack eye syndrome.¹¹ Although the exact pathophysiology of crack eye syndrome has not yet been determined, there are some suspected mechanisms. It has been hypothesized that the smoke from inhaling crack cocaine results in irritation, consequently causing rubbing of the eyes which in turn can cause epithelial devitalization and eventually epithelial defects.¹² Epithelial damage and defects can also occur secondary to the alkalinity of crack cocaine resulting in a low-grade chemical burn.¹² A decrease in corneal sensation is common secondary to cocaine’s effect on blink rate.⁵ It is possible that chronic and repeated crack cocaine exposure could devitalize the corneal nerves, leading to decreased neurogenic support of corneal epithelial integrity, and over time, crack cocaine users could develop a neurotrophic keratitis.¹² Ocular signs of crack eye syndrome include a broad spectrum of corneal epithelial changes; attentive management is vital to preserve vision.

Treatment for crack eye syndrome commonly involves the use of broad-spectrum fortified antibiotics, but it is dependent on the severity of the presentation.^11-12 Hospitalization should be considered, given that crack cocaine users often have poor adherence to treatment and a poor ability to keep follow-up appointments. A corneal ulcer or epithelial defect in the absence of a history of contact lens wear, trauma, surgery, predisposing keratopathy or an immunocompromised state should prompt an eye care practitioner to consider crack eye syndrome as a possible diagnosis.¹¹

As an eye care provider, patients with a history of cocaine or crack cocaine use should always be referred to a primary care physician to rule out embolization of talcum powder to other organs. In addition, consider a referral to an otorhinolaryngologist if any complications of the tear duct arise, especially if a dacryocystorhinostomy is warranted. Crack eye syndrome should always be ruled out in patients with persistent corneal epithelial defects and a history of cocaine use. In addition to a history of systemic vascular disease, in patients with bilateral vascular changes, history of cocaine use should also be ruled out. A table of ocular signs and relevant systemic implications of cocaine use are summarized in Table 1.

HEROIN

Among people ages 12 and older, approximately 556,000 people used heroin in the past year, according to the National Survey.¹ Heroin is a Schedule I drug, derived from the seed pod of the opium poppy plant found in Asia, Mexico, and Colombia. Heroin is a white or brown powder that is typically used via insufflation, inhalation or intravenous injection.¹³ Heroin is typically used for the effects of euphoria and clouded mental functioning.¹³ Short-term adverse effects include itching, nausea, and dry mouth. Long-term effects include loss of smell from chronic insufflation, HIV risk with intravenous injection, infection of the heart, and liver or kidney disease.¹³ Overdosing on heroin can cause slowed or stopped breathing, and sometimes death.¹³ There are many ocular effects of heroin, but endophthalmitis is the most common. Talc retinopathy, discussed with the use of cocaine and crack cocaine, can also be observed with the use of heroin.

Heroin-Induced Endophthalmitis

Many patients with a history of heroin use have a positive Candida albicans culture in the oropharynx.¹⁴ Prior to intravenous use, the addition of an acid is necessary to dissolve the heroin, making it more suitable for injection.¹⁵ In many cases, lemon juice is used since it is easily acquired; however, the growth of the fungus Candida albicans may flourish in the lemon juice.¹⁵ C. albicans contamination and infection from impure filtering techniques can eventually lead to fungal endophthalmitis.

The most common symptoms of endophthalmitis in heroin users are indistinct vision, redness and pain in one eye that do not manifest until at least one week after the last intravenous injection.¹⁵ Visual acuity will vary, but it is typically always reduced.¹⁵ Treatment for endophthalmitis secondary to heroin use includes fluconazole or amphotericin B injection prior to and after a vitrectomy. Suspected endophthalmitis should always be referred to a specialist for immediate treatment and management due to its visually devastating consequences.

Although talc retinopathy is not as commonly seen with heroin use, talc retinopathy is also a possible ocular sign with an extensive history of heroin use. A table of ocular signs and relevant systemic implications of heroin use is summarized in Table 1.

 

CANNABIS

Among people ages 12 and older, according to the 2024 National Survey, approximately 20.6 million people used cannabis in the United States.¹ Cannabis remains classified as a Schedule I drug, despite recent legalization in certain states. Cannabis is derived from the Cannabis sativa or Cannabis Indica plant.¹⁶ It appears as a dry, shredded green or brown mixture of stems and leaves and is typically used via inhalation or ingestion.¹⁶ Cannabis is typically used for the effects of euphoria, pain relief and drowsiness.¹⁶ Short-term effects of cannabis include impaired body movement or memory, and an increase in appetite.¹⁶ Long-term effects include changes to the nervous system and a negative impact on brain development.¹⁶ The most common ocular effects are corneal changes, visuomotor changes and a decrease in intraocular pressure.

Cannabinoids, produced by the resin of the cannabis plant, are responsible for Cannabis’ medical, physical and psychotropic properties.¹⁷ There are different sources of cannabinoids; phytocannabinoids are found within the cannabis plant, and endogenous cannabinoids are produced intracorporeally. The endogenous cannabinoids, or endocannabinoid system, assist in regulating mood, memory and stress by binding to cannabinoid receptors located throughout the body.¹⁷ With the ingestion of cannabis, competition arises between endocannabinoids and phytocannabinoids for the activation of cannabinoid receptors. Phytocannabinoids are further classified into different types, including cannabidiol (CBD) and tetrahydrocannabinol (THC). Cannabidiol is responsible for cannabis’ neurologic and bioactive reactions, whereas tetrahydrocannabinol is the main psychoactive element and is responsible for causing mind-altering effects.¹⁷

Corneal Changes Secondary to Cannabis Use

The corneal endothelium contains abundant cannabinoid receptors. In a study by Polat et al, a significant decrease in corneal endothelial cell density was found in cannabinoid users compared to those who were not using cannabis.¹⁸ The loss of endothelial cells was linked to cannabinoid toxicity. This association can provide important information about the ocular sequelae of decreased corneal endothelial cell density, such as corneal edema or an increased risk of endothelial decompensation during ocular surgery. However, some research has proven cannabinoids to be effective in reducing corneal pain and inflammation by activating receptors involved in the cannabinoid pathway.¹⁹ Research remains ongoing in terms of the potential benefits and risks to the cornea regarding cannabis use.

Visuomotor Changes Secondary to Cannabis Use

Cannabis is able to produce acute effects on perception, cognition, and behavior through its interaction with an endogenous cannabinoid receptor system that is distributed across the central nervous system.²⁰ According to Huestegge et al, chronic cannabis consumption is associated with an increase in sentence reading times, fixation duration, an increase in the rate of regressive saccades and a decrease in reading comprehension.²⁰ They concluded that chronic cannabis use is related to adverse long-term effects on reading, and overall, chronic cannabis use can result in degraded performance involving visuomotor control, including spatial navigation.²⁰

Decrease in Intraocular Pressure Secondary to Cannabis Use

Another important and potentially relevant clinical application of cannabis is its effect on intraocular pressure. Numerous studies have found a 20-30% reduction in intraocular pressure associated with inhalation of cannabis.²¹ The duration of intraocular pressure reduction after smoking cannabis lasts approximately 3-4 hours, and there is a dose-related response, with the peak action of intraocular pressure reduction occurring approximately 2 hours after inhalation.²¹ Tetrahydrocannabinol (THC) was found to be responsible for the decrease in intraocular pressure.²² Cannabidiol (CBD), contrarily, was found to cause an increase in intraocular pressure.²² According to Passani et al, topical cannabis was found to produce no reduction in intraocular pressure; oral administration of cannabis resulted in a moderate intraocular pressure reduction; inhalation of cannabis provided a greater intraocular pressure reduction compared to oral ingestion; and intravenous administration of cannabis provided the most significant intraocular pressure reduction.²³

There are several hypotheses regarding the pathophysiology of intraocular pressure reduction from cannabis use. Cannabinoids may inhibit calcium influx through presynaptic channels, thus reducing noradrenaline release in the ciliary body and decreasing the production of aqueous humor.²³ Cannabinoids may also act as vasodilators in the anterior uvea, improving aqueous humor uveoscleral outflow.²⁹ More recent studies have also demonstrated possible neuroprotective properties of cannabinoids via the inhibition of glutamic acid.²³ The pathophysiology behind the reduction in intraocular pressure caused by cannabis continues to be extensively studied. Discussion of cannabis use, especially with patients who have glaucoma, is common during an eye examination. It is important to understand that CBD is commonly used by those suffering from post-traumatic stress disorder and for the management of pain, but it can negatively impact glaucoma due to the potential increase in intraocular pressure. Unlike THC, CBD acts as a negative allosteric modulator at CB1.²² Since CBD is an antagonist of the cannabinoid receptor (CB1), this can cause an increase in IOP. Although research with mice models has demonstrated this relationship, further research is warranted to truly understand the relationship between CBD and IOP.

As an eye care provider, it is important to note the relationship between intraocular pressure and cannabis use. It is important to consider communication between physicians who are prescribing CBD for those suffering from PTSD and/or for pain management because of the potential increase in IOP from CBD use. It is also important to educate patients regarding the negative impact cannabis may have on reading comprehension and reading efficiency. This doctor-patient discussion will play a particularly important role with the increasing number of states that have legalized cannabis use. Further studies are warranted to rule out cannabis’ effect on the cornea. A table of ocular signs and relevant systemic implications of cannabis use are summarized in Table 2.

 

HALLUCINOGENS

Among people aged 12 and older, according to the National Survey, approximately 10.4 million people used hallucinogens in the United States.¹ Synthetically created hallucinogens are a Schedule I drug. Hallucinogens are usually in tablet or paper form and can be ingested, inhaled, insufflated or injected intravenously.²⁴ Hallucinogens are typically used for the effects of intensified feelings or sensory experiences.²⁴ Short-term side effects of hallucinogens include increased heart rate, increased body temperature and seizures, where long-term effects include persistent psychosis and memory loss.²⁴ There are many ocular effects resulting from the use of hallucinogens, but the most common is solar retinopathy.

Solar Retinopathy Secondary to Hallucinogen Use

Those under the influence of hallucinogens, specifically lysergic acid diethylamide (LSD), are typically attracted to bright and colorful objects due to their sense of a heightened degree of awareness.²⁵ The sun is one of the more common bright objects that those taking LSD tend to focus on. Solar retinopathy causes a lesion secondary to the thermal effects of the sun’s visible and infrared radiation.²⁵ In addition, LSD and other hallucinogens tend to cause a mild dilation of the pupil, which can result in a higher concentration of light energy being delivered to the macula.

Vision loss resulting from solar retinopathy can vary depending on the degree of exposure. Ocular signs include a small, red or pigmented, depressed lesion at the fovea. Disruption to the outer retinal layers is more easily seen with optical coherence tomography imaging, as depicted in Figure 2. Educating patients regarding the risk of sungazing while taking hallucinogens is important to prevent visually devastating consequences. A table of implications of hallucinogen use relevant to eye care providers is summarized in Table 3.

 

ALKYL NITRITES

Alkyl nitrites, more commonly referred to as poppers, are a type of chemical sometimes used to treat heart conditions or chest pain.²⁶ They are typically sold under other names such as poppers, purple haze or liquid gold.²⁶ Poppers are a strong-smelling, colorless liquid packaged in small bottles and typically inhaled. Poppers are typically used for the effects of euphoria, muscle relaxation and sensation boost.²⁶ Short-term effects of alkyl nitrites include headaches from vasodilation, while long-term effects include serious cardiovascular complications when mixed with phosphodiesterase-5 inhibitors.²⁶ There are many ocular effects of alkyl nitrites, but the most common is maculopathy.

Poppers cause an increase in nitric oxide, which has a negative impact on zeaxanthin macular pigment and can result in photoreceptor apoptosis.^27-28 Nitric oxide increases intracellular cyclic guanosine monophosphate levels, which eventually can lead to photoreceptor apoptosis.^27-28 Ocular symptoms include blurred vision, fluctuating vision, central scotomas and photophobia.²⁸ Ocular signs include an alteration of photoreceptors in the fovea, most notably observable with optical coherence tomography (OCT) (Figure 3), and sometimes a yellow-white lesion may be present at the macula during fundus examination.^27-28 Ocular signs and symptoms can present soon after inhalation or after many years of use. Visual recovery will depend on the dose as well as the chronicity of use.²⁷ Most patients will have a complete spontaneous resolution of signs and symptoms within six months of cessation.²⁹ Poppers maculopathy can range from a subtle alteration in photoreceptors, such as depicted in Figure 3, to a more significant foveal disruption, such as seen in solar retinopathy. In the presence of reduced vision and a mild or moderate disruption to the photoreceptors, a thorough social history is warranted to rule out maculopathy secondary to poppers use. The implications of alkyl nitrite use relevant to eye care providers are summarized in Table 3.

 

 

CONCLUSION

With the proper knowledge, an eye care provider can diagnose ocular disease secondary to drug use and also play a role in educating patients on resources regarding the prevention of substance use. The Substance Abuse and Mental Health Services Administration (SAMSHA) helpline, 1-800-662-4357, is meant for those or friends of those who are suffering with drug addiction and should be made known to patients who may be experiencing any drug abuse or addiction. In addition to the helpline, information regarding naloxone should be made known to patients and their families. Naloxone is able to quickly restore breathing if it has stopped or slowed secondary to an opioid overdose and will not cause harm if given to someone who is not overdosing on an opioid. This gives an individual enough time to bring a person who may be suffering from an opioid overdose to the closest emergency room for more advanced life support. There are many community centers across America that provide free training to those interested in obtaining and administering naloxone. It is recommended that healthcare providers carry naloxone in their offices.

Recreational substances can contribute to vision loss, ocular pain, dysfunction of ocular motility, as well as systemic life-threatening side effects. A thorough social history in combination with ocular examination findings can assist in discovering a patient’s use of substances. This discovery can potentially save a patient’s vision or even life. The eye is a part of a multi-organ system, and understanding the ocular effects of substances is vital to the care of patients.

 

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