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There is a myriad of changes that can be produced in the eye by toxic drugs ranging from mild/no symptoms to severe loss of vision from endophthalmitis. The routes of administration include oral ingestion, smoking, nasal inhalation, intravenous injection, topical application or application to other mucosal surfaces. It is important to recognize certain clinical signs and symptoms in the eye produced by these toxins. This article describes in brief some of the ocular effects of commonly abused drugs. For identification of a particular poisoning, in addition to the clinical presentation, pulse, blood pressure, respiration and body temperature, pupillary size, pupillary reaction to light, ocular convergence and nystagmus can be useful indicators of the type of drug the patient is exposed to. Unmasking these features help the clinician in an early and accurate diagnosis of the offending drug as well as timely management.
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© 2019 Indian Journal of Medical Research, published by Wolters Kluwer - Medknow for Director-General, Indian Council of Medical Research
There are numerous illicit drugs or chemicals
causing unwanted physiological changes in our body.
Several of these may have ophthalmic effects. It is
important from an ophthalmologist’s point of view to
have knowledge regarding the effects of these illicit
drugs on the eye. Understanding their adverse effects
on the eye can aid in early diagnosis and initiating
appropriate treatment. The routes of administration
of these drugs include oral ingestion, smoking, nasal
inhalation, intravenous injection, topical application
or application to other mucosal surfaces1. The changes
that can be produced in the eye by toxic drugs range
from mild/no symptoms to severe loss of vision and
endophthalmitis resulting in a permanent loss of sight.
Intravenous drug abuse can lead to microemboli in
retinal microcirculation leading to retinal ischaemia2,3.
Spread of microorganisms (including Candida,
Aspergillus, Bacillus, Staphylococcus, Pseudomonas,
Klebsiella, etc.) to the eye through blood stream due
to contaminated needles can lead to endogenous
endophthalmitis2,3. Several drugs which dilate the pupil
can lead to angle-closure glaucoma in predisposed
patients with narrow angles4. Often such patients
present to the emergency team or to a physician in the
acute setting. Recognition of subtle ophthalmic signs
in a patient who does not have the whole manifestation
of symptoms due to a particular drug abuse can be
benecial. This review describes some of the ocular
effects of commonly abused drugs.
Quick Response Code:
Review Article
Indian J Med Res 150, September 2019, pp 228-238
DOI: 10.4103/ijmr.IJMR_1210_17
Illicit drugs: Effects on eye
Deepika Dhingra, Savleen Kaur & Jagat Ram
Department of Ophthalmology, Advanced Eye Centre, Postgraduate Institute of Medical Education & Research,
Chandigarh, India
Received July 25, 2017
There is a myriad of changes that can be produced in the eye by toxic drugs ranging from mild/no
symptoms to severe loss of vision from endophthalmitis. The routes of administration include oral
ingestion, smoking, nasal inhalation, intravenous injection, topical application or application to other
mucosal surfaces. It is important to recognize certain clinical signs and symptoms in the eye produced
by these toxins. This article describes in brief some of the ocular eects of commonly abused drugs. For
identication of a particular poisoning, in addition to the clinical presentation, pulse, blood pressure,
respiration and body temperature, pupillary size, pupillary reaction to light, ocular convergence and
nystagmus can be useful indicators of the type of drug the patient is exposed to. Unmasking these features
help the clinician in an early and accurate diagnosis of the oending drug as well as timely management.
Key words Alcohol - blurred vision - cannabinoids - illicit drugs - methanol - ophthalmology - opiates - retinopathy - smoking - toxins
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Alcohol abuse is emerging as a major public-health
problem in India and more than half of all alcohol
drinkers fall into the category of hazardous drinking5.
Alcohol intake in short term leads to dilated pupils,
slower pupillary reaction, diplopia, night vision
disturbances6,7, decreased contrast sensitivity,
congested eyes, twitching of eyelid (myokymia) due to
excessive intake and nystagmus. Alcohol intake may
impair the vision or orientation to visuospatial stimuli
due to the various mechanisms. Alcohol intoxication
can also impair mesopic rod and cone temporal
processing pathways8. The mean subfoveal choroidal
thickness increases during the rst hour after alcohol
consumption and decreases during the next two hours9.
Chronic intake of alcohol can cause external
ophthalmoplegia (due to thiamine deciency), toxic
amblyopia and age-related macular degeneration
(ARMD). Ethanol is detected in tears, and it decreases
tear lm volume, disturbs tear lm structure10, increases
tear hyperosmolarity11, induces increased expression of
inammatory cytokines12, and vitamin A deciency and
all these factors combined lead to dry eyes. Chronic
alcoholism changes the conjunctival ora by increased
colonization of Staphylococcus aureus bacteria which
along with associated dry eye is responsible for higher
rates of keratitis in alcoholics13.
Intake of alcohol with other abusive agents is also
common, and a cocktail of drugs can lead to a multitude
of changes in the eye which are often unpredictable
(Fig. 1). Alcohol dependence can be associated with
other addictive disorders, among which nicotine
dependence is most common in about 80-90 per
cent of the patients14. Coexistent use of smoking and
alcohol is known to cause tobacco-alcohol amblyopia,
the cause of which is hypothesized to be either
because of these substances themselves or nutritional
deciency associated with the abuse. The prevalence
of toxic optic neuropathy among alcohol addicts
might be underestimated. A pilot study on a group of
alcoholic patients reported 13 per cent prevalence of
bilateral typical optic neuropathy in males, but about
20-40 per cent of patients had incomplete forms of
optic neuropathy with or without visual impairment
which was unilateral and caused impaired colour
vision15. Hence, screening of these patients for early
detection of toxic optic neuropathy is essential. Early
identication can lead to timely preventive measures
and abstinence from drug abuse as well as vitamin
Eye thermal signatures as a test to detect alcohol
In a sober person, temperature of sclera and iris is
the same, but with alcohol intoxication, temperature of
sclera increases compared to the iris because of denser
blood vessel network over the sclera, and thermal
signature of eye with infrared imaging may provide
rst assessment tool to detect alcohol drunkenness16.
The acute effects of alcohol seldom need treatment
as these subside with time. The treatment of Wernicke’s
encephalopathy is a medical emergency, and mainstay
of treatment is intravenous hydration and thiamine.
Fig. 1. Unpredictable and unwanted consequences of combination of alcohol with other drugs. A 24 yr old male with a visual acuity of 6/6
in both eyes with normal pupillary reactions but 45 prism dioptre of exotropia in the right eye with full extraocular movements in all gazes.
Patient presented with binocular diplopia for 4-5 months following intake of marijuana and alcohol. On the basis of multiple infarcts on
magnetic resonance imaging brain, a diagnosis of reversible cerebrovascular spasm syndrome was made.
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Magnesium sulphate is also used to reduce the potential
for seizures. Chronic thiamine supplementation may
be required to reverse the external ophthalmoplegia17.
Cigarette smoking is one of the most common and
the most alarming health problem today. It can affect
multiple structures in the body as well as the eye due
to chemical toxicity and free radical-related oxidative
damage. Nicotine has been reported to cause alteration
of the conjunctival ora, irritation, redness, dry eye,
ocular surface inammation and meibomian gland
dysfunction18-20. Tear lm breakup time is decreased
which is suggestive of unstable tear lm. Schirmer’s test
may be normal, lower or even higher because of unstable
tear lm and reex tearing18,21. Smoking also increases
the risk of squamous metaplasia of bulbar conjunctiva
and conjunctival intraepithelial neoplasia21,22. Corneal
wound healing is delayed in smokers, increasing the
risk of keratitis and poor healing of epithelial defect or
ulcer23. Some studies have shown reduced endothelial
cell count or a decrease in hexagonality of endothelial
cells24,25. The only benecial effect on the cornea has
been an accelerated collagen cross-linking leading to
improved corneal biomehanics26.
Smoking increases the risk of cataract formation
including nuclear and posterior subcapsular cataract
(PSC)27. It has a higher association with nuclear cataract
compared to PSC, but it does not increase the risk of
cortical cataract28,29. The City Eye Study29, a nine year
prospective study conducted to know the association
between lens opacities and risk factors has shown the
relative risk for nuclear lens opacity of 2.6 for past
heavy smokers and 2.9 for present heavy smokers.
Risk of development of ARMD is also increased
in genetically susceptible individuals who smoke.
Smoking has been shown to increase the risk of
polypoidal choroidal vasculopathy (3 times more than
non-smokers) and choroidal neovascular membrane
due to ARMD (4 times more than non-smokers)30.
According to The Blue Mountains Eye Study31, current
smokers have four times greater risk of late ARMD
than non-smokers. Smoking along with alcohol also
predisposes the patient to ARMD.
Regarding effects of smoking on intraocular
pressure (IOP), studies have shown variable results.
The Blue Mountains Eye Study showed no relationship
of IOP with smoking32. However, some studies have
shown higher mean IOP in smokers independent of
corneal biomechanics33. The mechanism of raised
IOP has been proposed to be vasoconstriction and rise
in episcleral venous pressure due to smoking, thus
increasing the risk of glaucoma32. Smoking increases the
risk of development of thyroid-associated orbitopathy,
and it is associated with its progression and poor
response to treatment34,35. Ophthalmologists should
advise patients with thyroid-associated orbitopathy to
abstain from smoking.
There is doubtful association between smoking
and non-arteritic anterior ischemic optic neuropathy
(NAION). One study has shown that smoking increases,
and its cessation reduces the risk of NAION36. Hayreh
et al37 did not show any association with smoking.
Smoking with/without alcohol leads to dysfunction
of electron transport chain of mitochondria leading
to cell death with damage to papillomacular bundle
because of combined toxic cyanide and formic acid
levels along with nutritional deciency of vitamin B12,
folate, thiamine, etc38,39. It is initially manifested as a
change in colour vision and later on causes progressive
decline in visual acuity leading to a central xation
scotoma. However, visual loss usually does not go
beyond 20/400 and does not lead to blindness. Optic
nerve may be normal or hyperemic in early stages, and
later, there may be temporal pallor of disc40. Visual
eld shows central or centrocaecal scotoma.
Methanol intake in the form of an adulterated drink
can lead to metabolic acidosis (due to toxic metabolite
formic acid). Symptoms include headache, dizziness,
nausea, vomiting, abdominal pain and blurred vision.
The onset of symptoms is usually delayed for 12-24 h.
In severe poisoning, dyspnoea, coma, convulsion and
blindness may occur41. Fatal dose can be as little as
30 ml and blindness can occur with as little as 10 ml42.
Fundus may be normal in case with visual impairment
and retrobulbar neuritis. Optic neuropathy can be
present in the form of hyperemic optic disc oedema
followed by optic disc pallor and cupping if not treated
on time. The cause of optic neuropathy is considered
to be mitochondrial dysfunction and progressive
demyelination in acute stage followed by retrograde
degeneration of optic nerve axons leading to optic
disc cupping and pallor43. In a case report, methanol
intoxication has been shown to cause bilateral multifocal
extrafoveal retinal pigment epithelial detachments
along with optic neuritis44. Methanol has also been
shown to cause effects on outer retina including retinal
pigment epithelium and photoreceptors45.
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It includes gastric lavage, ethanol/fomepizole
(aldehyde dehydrogenase enzyme inhibitors),
haemodialysis to remove toxic metabolites, folinic
acid to enhance the metabolism of formic acid,
sodium bicarbonate for acidosis, correction of vitamin
deciencies and use of intravenous steroids for optic
disc oedema46. A retrospective case series of 37 patients
with visual disturbance after methanol poisoning
reported that 62 per cent patients completely recovered,
14 per cent recovered partially, 11 per cent had partial
recovery followed by deterioration to blindness and
14 per cent had complete blindness47. A study on
predictors of visual outcome in methanol poisoning
has found acidosis at presentation to be a stronger
predictor of nal visual acuity48. An inverse relationship
has been found between serum methanol levels at
presentation and nal visual acuity. Initial pH <7.2
was associated with lesser improvement in visual
acuity. Early presentation and treatment may not affect
the visual outcome, especially in a case of severe
Role of erythropoietin
There are many studies on the use of erythropoietin
for methanol poisoning because of its ability to reduce
the neuronal apoptosis, reduction in inammatory
response and its neuroregenerative properties.
Intravenous erythropoietin 10000 IU twice a day
for three days has been shown to improve the visual
outcome dramatically in patients already receiving
supportive measures and intravenous steroids.
However, whether it is efcacious when given alone,
needs further studies49. A study evaluated the effect of
steroids plus erythropoietin versus steroids alone and
found that patients with steroids plus erythropoietin
showed deterioration in visual acuity at two months.
The conclusion is that protective effect of erythropoietin
may be strong at the beginning of intervention, but it
is probably transient50. Another study on efcacy of
intravitreal erythropoietin in late-stage optic neuropathy
did not nd any benecial or detrimental effect, but its
effect in early stage is still to be determined51.
The active compound is tetrahydrocannabinol
(THC), and route of intake can be smoking or
oral ingestion. The effects of smoked cannabinoid
begin within minutes and usually last for 1-3 h. It
leads to euphoria, short attention span and red eyes.
With oral ingestion, concentration peaks occur at
about 1-3 h52. Cannabis intake leads to conjunctival
injection53, dilated pupils54, reduced accommodation
amplitude55,56 and impaired oculomotor function in
chronic users. Impaired oculomotor function can
manifest in the form of increase in latency to initiate
saccades, impairment in processing of saccades and
impaired visuospatial working memory57, and smooth
pursuit eye tracking performance58. Because of high
lipid solubility of THC, it accumulates in fat cells.
When used continuously, it is slowly distributed out of
the cells. Its metabolites can be detected in urine for
one day to a week or longer after acute use, depending
on the amount smoked59. A case of conjugate deviation
of the eyes due to cannabis intoxication was reported
which lasted for six weeks60. The reported effects of
the drugs can last longer sometimes without detectable
levels in urine. Fig. 2 highlights the pupillary side
effects of marijuana. Cannabis decreases IOP, but it is
not suitable for medical purpose for glaucoma because
of short duration of action (3-4 h) and its addiction
properties. For being effective, it must be smoked 6-8
times a day which can lead to dependence and patients
develop tolerance with time61.
Fig. 2. Dilated pupils in both eyes (A) and sluggishly reacting on
direct and consensual reexes (B and C) as well as near reex (D)
in a 25 yr old male patient with a history of smoking marijuana.
Patient presented with a one week history. Pilocarpine one per cent
drops were described to relieve symptoms.
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Opiates include numerous substances such as
morphine (naturally occurring), heroin (semisynthetic),
meperidine and methadone (synthetic derivatives)
and prescription opioids including hydrocodone,
oxycodone, pentazocine and fentanyl.
Routes of intake
The routes of intake for morphine include oral,
intravenous, intramuscular, rectal, epidural and
intrathecal. Morphine tablets can be injected, and
opium can be smoked. Heroin intake can be in the form
of smoking, snorting, or intravenous and subcutaneous
administration. Black tar heroin is usually dissolved,
diluted and injected. These drugs act through the opioid
receptors μ, κ, δ, and cause a decrease in the pupillary
size and in the velocity of constriction to light stimulus,
and dilatation after the light stimulus is removed62.
The effect usually starts in 15-60 min and lasts for 3-5
h. Miosis by morphine is due to an excitatory action
on the Edinger-Westphal nucleus of the oculomotor
nuclear complex63. The effect on pupil diameter in
dependent and non-dependent individuals varies
because of the development of tolerance in dependents.
A study on the effect of heroin has found that pupillary
constriction starts in 15 min and persists for at least two
hours in non-dependent individuals whereas dependent
individuals show recovery from pupillary constriction
after 15 min64. Therapeutic doses of morphine increase
accommodative power and decrease IOP in normal and
glaucomatous eyes65,66.
The triad of coma, pupillary constriction and
depressed respiration suggests opioid poisoning.
Intravenous heroin and morphine abuse can cause
downbeat nystagmus, transient disturbance of eye
xation, saccadic intrusions and oscillations, lasting
for 10-15 min67. Intravenous abuse can also lead
to microembolism in the retinal vasculature and
endophthalmitis. Acute-onset esotropia can be seen in
about 30 per cent of individuals following withdrawal
of heroin which is manifested as an acute onset of
binocular diplopia with impaired convergence68.
Neurological investigations are normal in such patients.
Hence, clinicians should be aware of this condition
due to drug use and avoid unnecessary and extensive
neurological investigations68.
Diffuse retinal ischaemia and disc
neovascularization with intravenous use of crushed
oxymorphone have been reported which is intended to
be used as an oral opioid analgesic. It has also been
associated with thrombotic thrombocytopenic purpura
(TTP). Hence, any patient with TTP like illness and
retinal ndings should be questioned regarding drug
abuse, and urine testing should be done69. To detect
recent use of opioids, a useful test is the nalorphine
test70. Two to four milligrams of nalorphine is injected
subcutaneously, and the pupillary dilation is observed
within 30 min. Narcotic users show dilation of pupils
whereas in patients who are non-opiate users or have
not used narcotics recently, pupillary constriction will
be observed70. During the withdrawal states of opioids,
mydriasis or anisocoria can occur.
Commonly abused stimulants include
cocaine, amphetamine, methamphetamine, and
3,4-methylenedioxymethamphetamine (MDMA,
ecstasy); in increasing order of potency cocaine
< amphetamines < methamphetamine < MDMA.
Other psychostimulants include cyclazodone,
4-methylaminorex and prescription stimulants.
Cocaine can be ingested orally, and combined opioid
and cocaine abusers, use it as intravenous injection. It
is often used with alcohol. With freebase inhalation,
effects occur within 4-6 sec and lasts for 5-7 min only.
When the powder is sniffed, effects are produced
within 1-3 min and last for about 30 min. Cocaine
causes dilated pupils because of inhibition of reuptake
of norepinephrine. In high concentrations, it may
cause cycloplegia, and in chronic users, exophthalmos
and retraction of upper eyelid can occur56. A case of
severe sinusitis following intranasal cocaine abuse
was reported which spread to the orbit leading to optic
neuropathy and orbital apex syndrome71. Cocaine users
can also present with complications like supercial
punctate keratitis, epithelial defects and ulcers because
of contamination through eye rubbing or retrograde
passage of the substance through the nasolacrimal
duct by snifng, as well as direct toxic effects from
substance smoke72. Conjunctival lesions and chronic
red eye have been reported with the transconjunctival
use of crystallized heroin73.
It increases the production of dopamine in the
brain and activates reward centres of the brain giving
a sense of euphoria soon after taking the drug and
causes aggressiveness, anxiety and dilated pupils.
It is known to cause crystalline retinopathy by
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intranasal methamphetamine use74. Retinal vascular
occlusive disease can also occur with cocaine and
methamphetamine75,76. Psychostimulants act on
dopamine receptors in the brain. These enhance
the activity of sympathetic nervous system leading
to increased pulse rate, respiratory rate and blood
Cyclazodone (n-cyclopropylpemoline)
It is a novel stimulant drug which produces
stimulating and focus-enhancing effects similar to
dexamphetamine by increasing release of dopamine,
noradrenaline and serotonin. Its ocular and visual effects
are less consistent and usually occur at higher doses in
the form of pupillary dilatation and brightness alterations
which manifest as change in the level of perceived
brightness i.e., surroundings may appear darker and
gloomier or brighter77. Transformations may also occur
rarely with high doses which manifest as smooth and
uid-like transitions of an object in various shapes.
It is a stimulant drug with its action similar to
amphetamine and available in powder and tablet forms.
It is abused because of its stimulant and euphoric
effects. The unwanted effects include agitation,
nausea, tachycardia, restlessness and dilated pupils78.
Currently, its availability is limited, and hence, it is
abused less frequently.
Prescription stimulants
Prescription stimulants include amphetamines,
methylphenidate for attention-decit hyperactivity
disorder and nasal decongestants such as
pseudoephedrine, phenylephrine, promethazine,
phenylpropanolamine and oxymetazoline. These drugs
can also be abused/misused, and drug effects on eye can
occur in the form of pupil dilatation and precipitation of
angle-closure glaucoma in predisposed individuals with
narrow angles79. Anecdotal case of anisocoria in a patient
on oral decongestant pseudoephedrine for sinusitis in
which anisocoria occurred because of the absence of
pupil dilatation in one eye with latent form of Horner’s
syndrome has been described79. Promethazine because
of anticholinergic property and phenylpropanolamine
due to sympathomimetic activity have been reported to
cause acute angle-closure glaucoma80.
Saturday night retinopathy
It has been described in patients with heavy
drug abuse (alcohol, iv heroin/ methadone) which
is characterized by unilateral vision loss along with
proptosis and ophthalmoplegia after heavy intravenous
drug abuse. It occurs because of unconsciousness
following heavy drug abuse and patient sleeping in
abnormal posture with continuous pressure on the orbit
leading to orbital congestion and ophthalmic/central
retinal artery occlusion. It may also be associated
with peroneal nerve palsy of lower limb81. Orbital
congestion and proptosis improve with time, but visual
prognosis is poor.
This group includes lysergic acid diethylamide
(LSD), psilocybin, phencyclidine (angel dust) and
mescaline. These drugs can cause hallucinations,
recklessness, sleeplessness, slurred speech,
hyperarousal of the central nervous system (CNS),
loss of coordination and pupil dilation. LSD ‘trip’
typically lasts for 6 to 18 h. The effects of psilocybin
and mescaline are similar to those of endogenous
serotonin and can last for 8 to 12 h82. There have been
no systematic studies on dynamic measures of light
reex after the intake of these drugs.
Phencyclidine does not cause changes in pupil size
but often causes horizontal and vertical nystagmus in
intoxicated states83. A case of phencyclidine-induced
oculogyric crisis with involuntary conjugate upwards
deviation of eyeballs was reported, the rest of the
ocular and systemic examinations were normal and
patient improved with diphenhydramine84. Dystonia
can be improved with anticholinergics/antihistaminics.
Poppers maculopathy
Poppers belong to a group of alkyl nitrites and are
used as recreational drugs in the form of inhalation.
Popper use has been found to cause visual impairment
due to photoreceptor damage because of an increase
in cyclic guanosine monophosphate (cGMP) leading
to disruption of inner segment-outer segment (IS-OS)
junction in the fovea85. Some improvement of vision
may occur on cessation of drug use and using oral
lutein. It has been found more in HIV patients/who are
on sildenal/proteinase inhibitor. The pathogenesis is
not exactly known. It has been postulated to be due to
sildenal/proteinase inhibitor use which also increases
cGMP similar to poppers and probably enhances the
photoreceptor damage86. Another study suggested that
poppers maculopathy might be caused by photic injury
because of its similarity on clinical examination as
a small yellow spot at the fovea and IS-OS junction
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Central nervous system (CNS) depressants
Barbiturates and benzodiazepines
Benzodiazepines are commonly self-administered
by addicts, sometimes to ameliorate withdrawal from
heroin, alcohol or to weaken the side effects of cocaine
or methamphetamine intoxication. Addicts may also
combine these drugs with heroin, marijuana or alcohol to
enhance their effects. The short- and intermediate-acting
barbiturates are lethal if taken more than 10 times a
single therapeutic dose. Benzodiazepines are non-lethal
unless combined with alcohol or other CNS-depressant
drugs. The symptoms of benzodiazepine overdose
include drowsiness, slurred speech, ataxia, horizontal
gaze nystagmus, hypotension, coma, respiratory
depression and cardiorespiratory arrest88. Some patients
can have severe allergies such as anaphylaxis and
angioedema89,90. Flumazenil is indicated for reversing
the sedative effect of benzodiazepines and for treatment
in a benzodiazepine overdose91. The treatment has
to be done under the supervision of a psychiatrist.
Large doses of barbiturates can cause decreased pulse
rate, shallow breathing and dilated/normal pupils.
Common ocular manifestations are disturbances of
ocular movements, including decreased convergence,
paresis of extraocular muscles or nystagmus. Pupillary
response is variable although hippus and sluggish
pupillary reaction can be seen92. Subnormal vision
or bilateral blindness has been reported in patients
recovering from coma caused by barbiturates93. Ptosis
is common in habitual barbiturate users94. There is no
antidote to reverse barbiturates action.
It is a CNS depressant with sedative-hypnotic action
on gamma aminobutyric acid (GABA) A receptor and is
used for insomnia. It has addiction potential, but unlike
barbiturates, it does not cause respiratory depression.
It can have visual and ocular effects at high doses.
Visual effects can occur in the form of double vision,
hallucinations and visual disconnection. It is known to
cause generalized purpura due to thrombocytopenia,
and its ocular effects can include conjunctival95 and
retinal haemorrhages96. Pupil size and reaction usually
are not affected, but dilated pupils can occur at very
high doses97.
Gamma hydroxybutyrate (GHB)
It is a depressant drug with its actions on its own
receptor in brain and GABA B receptor and is used
by club goers for its euphoric action, body builders
for probable action on growth hormone boost and
as a date rape drug. It is available as powder and
taken in liquid/oral form and can be mixed with any
alcoholic/non-alcoholic drink. It can cause blurred
vision, visual disturbances with difculty in focusing.
Due to its tendency to cause dependency, withdrawal
symptoms have been reported in the form of 6th nerve
palsy, nystagmus and Wernicke-Korsakoff syndrome98.
Wernicke-Korsakoff is proposed to be due to thiamine
deciency and gets ameliorated with thiamine
In utero use of abusive drugs
A study on infants born to drug-misusing mothers
who were prescribed methadone in pregnancy for opioid
dependence, found abnormal visual development in
infants in the form of strabismus (25%, 10-fold higher
than in normal children), decreased visual acuity
(22%), nystagmus (11%) and ve-fold higher risk of
failing in six-month visual assessment99. Exposure to
opiates and/or benzodiazepines during pregnancy may
cause infantile nystagmus in child100. Foetal alcohol
syndrome is associated with optic nerve hypoplasia,
strabismus and decreased saccadic velocity83. Opioids
and polysubstance abuse in mothers has been found
to be associated with poor visual acuity and binocular
visual functions compared to control groups even if
they are detoxied during pregnancy101.
Intoxicated patients are more prone to road side
accidents/assaults. Alcohol-related ocular injuries
have been found to be associated with severe globe
rupture with high incidence of adnexal injuries and
were associated with worse visual outcome and higher
rates of evisceration102. Among addicts, polydrug use
is very common; so, variable ocular and systemic
effects can be seen due to combined mechanisms.
Treatment from ophthalmologist point of view is as per
the effect of drug, e.g., for pupillary effects - mydriatic
or miotics; for ocular surface diseases including dry
eyes and conjunctival hyperaemia - tear substitutes
and topical steroids may be required; and for
accommodation - convergence dysfunction, refractive
correction to be prescribed until the effect of abusive
drug subsides.
Tables I and II summarize the ocular manifestations
of commonly abused drugs. For identication of
poisoning, clinical presentation, pulse, blood pressure,
respiration, body temperature, pupillary size, pupillary
reaction to light, ocular convergence and nystagmus
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can be useful indicators of the type of drug the patient
is exposed to103 (Table II).
The use of illicit drugs is a public health concern.
Identication of ophthalmic side effects of these drugs
is crucial for timely diagnosis and management of these
cases. Not only is it essential for the general physician
to use the ophthalmic signs for early diagnosis but also
for the ophthalmologist to timely refer and treat the
patient. Early recognition can go a long way in visual
rehabilitation of these patients.
Financial support & sponsorship: None.
Conicts of Interest: None.
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Table I. Frequent ophthalmic or visual manifestations and most commonly abused drugs causing them
Ocular/visual manifestations Suspected drugs
Diplopia Alcohol, phencyclidine, barbiturates, heroin
Corneal anaesthesia, keratitis Phencyclidine, cocaine
Dry eye Alcohol, nicotine
Mydriasis Cocaine, methamphetamine, lysergic acid diethylamide, marijuana
Miosis Heroin
Hippus/indistinct pupillary response Barbiturates
Non-arteritic optic neuropathy Nicotine
Age-related macular degeneration Alcohol, nicotine
Retinal venous occlusion, intraretinal haemorrhage Cocaine, methamphetamine, opioids
Talc retinopathy Methamphetamine, heroin
Toxic optic neuropathy Nicotine, methanol
Nystagmus Phencyclidine, barbiturates, morphine
Impaired oculomotor function Cannabinoids
Palinopsia Lysergic acid diethylamide
Thyroid orbitopathy Nicotine
Raised intraocular pressure Smoking nicotine
Decreased intraocular pressure Cannabinoids
Source: Refs 1, 20, 21, 34, 35, 67
Table II. Summary of effects of abusive drugs on ocular motility and pupil
Ocular adverse effects Marijuana Narcotic analgesics Hallucinogens CNS depressants CNS stimulants Phencyclidine
Pupils Dilated/normal Constricted Dilated Normal Dilated Normal
Pupillary reaction to light Normal Slow/none Normal Slow Slow Normal
HGN Not present Not present Not present Present Not present Present
VGN Not present Not present Not present Possibly present Not present Usually present
Lack of ocular convergence Present Not present Not present present Not present Present
CNS, central nervous system; HGN, horizontal gaze nystagmus; VGN, vertical gaze nystagmus
Source: Refs 54, 62, 66, 103
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... Other precipitating factors for pinpoint pupil also do not typically resemble opioid overdose in the nonsurgical context. 22 For patients who received naloxone but did not have cardiac arrest and who had a dispatch concern consistent withalthough not specific to-opioid overdose ("breathing problem," "sick person," "unknown problem/man down," "ingestion/poisoning," or "unconscious/fainting"), 12 we used an ML model (described in the following section) to designate suspected opioid overdoses (category 4). ...
Objectives Tracking nonfatal overdoses in the escalating opioid overdose epidemic is important but challenging. The objective of this study was to create an innovative case definition of opioid overdose in North Carolina emergency medical services (EMS) data, with flexible methodology for application to other states’ data. Methods This study used de-identified North Carolina EMS encounter data from 2010-2015 for patients aged >12 years to develop a case definition of opioid overdose using an expert knowledge, rule-based algorithm reflecting whether key variables identified drug use/poisoning or overdose or whether the patient received naloxone. We text mined EMS narratives and applied a machine-learning classification tree model to the text to predict cases of opioid overdose. We trained models on the basis of whether the chief concern identified opioid overdose. Results Using a random sample from the data, we found the positive predictive value of this case definition to be 90.0%, as compared with 82.7% using a previously published case definition. Using our case definition, the number of unresponsive opioid overdoses increased from 3412 in 2010 to 7194 in 2015. The corresponding monthly rate increased by a factor of 1.7 from January 2010 (3.0 per 1000 encounters; n = 261 encounters) to December 2015 (5.1 per 1000 encounters; n = 622 encounters). Among EMS responses for unresponsive opioid overdose, the prevalence of naloxone use was 83%. Conclusions This study demonstrates the potential for using machine learning in combination with a more traditional substantive knowledge algorithm-based approach to create a case definition for opioid overdose in EMS data.
... 90 Illicit drug use and depression involving cannabis, heroin, fentanyl, ketamine, cocaine, methamphetamine, and "ecstasy" (methylenedioxymethamphetamine) may also be a part of the patient profile that can cause ocular side effects from hemianopia and corneal anesthesia to cranial nerve palsies. 32,91,92 Patients may also use herbal remedies for the treatment or management of psychiatric disorders, although there is a lack of double-blind randomized controlled studies to demonstrate a clear efficacy, and such remedies may have unknown drug-drug interactions and interactions with metabolic enzymes. 93,94 Future clinical therapeutics are being developed to improve the selectivity of the therapeutics used in the treatment and management of anxiety and depression. ...
Full-text available
Paul A Constable, Dalia Al-Dasooqi, Rhiannon Bruce, Mallika Prem-Senthil Caring Futures Institute, College of Nursing and Health Sciences, Flinders University, Adelaide, AustraliaCorrespondence: Paul A Constable, Flinders University, GPO Box 2100, Adelaide, 5001, South Australia, Australia, Tel + 61 8 7221 8398, Email This review of commonly prescribed psychotropic drugs aims to update the clinician on possible ophthalmic side effects that may include dry eye, diplopia, mydriasis, and cataracts. This review summarizes our current knowledge of known ocular side effects of psychotropic drugs based on reviews, case reports, case-control studies, a case series, and cross-sectional observational studies reported in the recent literature. The review covers disorders related to depression, anxiety, and stress which are commonly encountered within society and can have debilitating impacts on an individual’s quality of life that may require chronic therapeutic management. The main medications used in the treatment and management of these conditions typically target receptors, metabolic enzymes, or transport pumps that alter the pre- and/or post-synaptic levels of neurotransmitters such as serotonin, norepinephrine, dopamine, gamma-aminobutyric acid, and opioids to improve mood and/or relieve pain and anxiety. Novel non-therapeutic options are undergoing clinical trials, and some patients may seek alternative therapies or have associated substance abuse issues to alleviate their symptoms. This review summarizes some of the clinical signs of depression and the main therapeutic options and their reported ocular side effects which may be pertinent today given the rise in use of psychotropic medications used to manage depression, anxiety, and stress.Keywords: drugs, ocular, psychotropic, side effects
Full-text available
L'examen neurologique est un aspect important de la pratique infirmière en soins critiques. Au sein de cet examen, l'évaluation des pupilles peut fournir des informations vitales chez la personne gravement malade. À la salle d'urgence spécifiquement, les infirmier.ères jouent un rôle déterminant dans l'identification de changements subtils au niveau de la taille, la symétrie, la réactivité pupillaire ou tout autre signe de détérioration neurologique chez la personne nouvellement admise. En dépit de l'importance de l'évaluation des pupilles à la salle d'urgence, il n'existe actuellement aucune norme pour guider cette pratique au sein de la profession infirmière. Le but de cet article est de décrire les composantes essentielles de l'évalua-tion des pupilles à la salle d'urgence ainsi que les facteurs et troubles neurologiques pouvant l'influencer afin d'outiller les infirmier.ères à l'égard de cette pratique.
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Homogeneously depigmented sclerae have long been proposed to be uniquely human—an adaptation to enable cooperative behaviour by facilitating interpersonal coordination through gaze following. However, recent evidence has shown that deeply pigmented sclerae also afford gaze following if surrounding a bright iris. Furthermore, while current scleral depigmentation is clearly adaptive in modern humans, it is less clear how the evolutionarily intermediate stages of scleral pigmentation may have been adaptive. In sum, it is unclear why scleral depigmentation became the norm in humans, while not so in sister species like chimpanzees, or why some extant species display intermediate degrees of pigmentation (as our ancestors presumably did at some point). We created realistic facial images of 20 individually distinct hominins with diverse facial morphologies, each face in the (i) humanlike bright sclera and (ii) generalised apelike dark sclera version. Participants in two online studies rated the bright-sclera hominins as younger, healthier, more attractive and trustworthy, but less aggressive than the dark-sclera hominins. Our results support the idea that the appearance of more depigmented sclerae promoted perceived traits that fostered trust, increasing fitness for those individuals and resulting in depigmentation as a fixed trait in extant humans.
Purpose: To compare visual evoked potential (VEP) components in normal individuals and those with long-term methamphetamine and crystal methamphetamine use. Methods: In this study, monocular pattern-reversal VEPs were recorded in 40 methamphetamine and crystal methamphetamine users and 38 normal individuals. Visual stimuli were high-contrast (99%) checkerboard patterns at 15 and 60 min of arc with a reversal rate of 1.53 reversals per second. Results: A significant difference was seen between the two groups for the P100 peak time for the 60 min of arc checks (p = 0.002, d = 0.75, 4.61% higher peak time in the addicted group) and the 15 min of arc checks (p = 0.004, d = 0.73, 4.78% higher peak time in the addicted group). However, other VEP components were not significantly different between the two groups. Conclusions: The higher P100 peak time at both 15 and 60 min of arc in methamphetamine-dependent users reveals that VEPs are highly sensitive for the diagnosis of retinal and visual pathway lesions.
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Homogeneously depigmented sclerae have long been proposed to be uniquely human - an adaptation to enable cooperative behaviour by facilitating interpersonal coordination through gaze following. However, recent evidence has shown that deeply pigmented sclerae also afford gaze following if surrounding a bright iris. Furthermore, while current scleral depigmentation is clearly adaptive in modern humans, it is less clear how the evolutionarily intermediate stages of scleral pigmentation may have been adaptive. In sum, it is unclear why scleral depigmentation became the norm in humans, while not so in sister species like chimpanzees, or why some extant species (presumably as our ancestors did at some point) display intermediate degrees of pigmentation. We created realistic facial images of 20 individually distinct hominins with diverse facial morphologies, each face in the (i) humanlike bright sclera and (ii) generalised apelike dark sclera version. Participants in two online studies rated the bright-sclera hominins as younger, healthier, more attractive and trustworthy, but less aggressive than the dark-sclera hominins. Our results support the idea that the perceptual affordances of more depigmented sclerae increased perceived traits that fostered trust, increasing fitness for those individuals and resulting in depigmentation as a fixed trait in extant humans.
Clinical relevance Considering the significant relationship between methamphetamine abuse and some anterior segment indices, methamphetamine abuse should be considered in differential diagnosis especially in the case of angle closure glaucoma. Background To investigate the effect of inhaled methamphetamine (meth) and crystal methamphetamine (crystal meth) on the quantitative indices of the cornea and anterior chamber using pentacam and anterior segment optical coherence tomography. Methods In this cross-sectional study, the participants were (crystal) meth addicts living in Zahedan. The participants were transported to the examination site to undergo imaging and optometric tests. Pentacam and anterior segment optical coherence tomography imaging were then conducted so as to evaluate corneal and anterior chamber quantitative indices. Results A total of 42 (crystal) meth addicts and 42 healthy subjects with matching age and gender were examined. Out of 42 subjects in the case group, 6 were female and 36 were male (mean age: 35.7 ± 8.6 years). The mean dose of drug used was 0.0074 ± 0.0034 g, and the mean duration of drug use was 6.9 ± 2.6 years (5–12 years). Based on the images of both devices, corneal curvature was significantly steeper in both meridians of anterior and posterior surfaces compared to the control group (p = 0.01). Among the anterior chamber parameters, the anterior chamber depth and volume were lower in the cases than the controls (p < 0.01). However, the lens rise was higher in addicts than controls (p = 0.01). Conclusion Quantitative changes in corneal and anterior segment indices including dilated pupils, shallower anterior chamber depth and higher lens rise in addicted cases compared to the control group may precipitate the risk of closed-angle in these individuals.
The eye, with its distinctive anatomy, not only reflects a wide variety of diseases in life but also undergoes a myriad of post-mortem changes. Consequently, the eye has long been an area of interest in forensic science, primarily for the estimation of post-mortem interval and therefore the time of death and also for assistance in ascertaining the cause of death. There has been significant progress in the knowledge of ophthalmic forensic science using new technologies which have allowed further possibilities to arise where understanding of this field can assist the forensic pathologist. This review aims to highlight the current knowledge which exists in this field and also to identify important avenues for further investigation. Post-mortem changes of the eye along with its current applications and challenges will be discussed. These include the important areas of post-mortem iris biometrics, pupil size correlation with post-mortem interval, use of point-of-care technology on vitreous humor, and the use of ophthalmic imaging in pediatric abusive head trauma.
Autopsy is often the only way of obtaining material for histological study from conditions such as age-related macular degeneration or various retinopathies. It is also a valuable source that allows the study of the eye in various systemic or multisystem diseases. If systemic hypertension is uncontrolled this leads to retinal vascular ischaemia usually by way of microinfarcts. Fibrinoid necrosis may be seen in choroidal vessels. Sclerokeratitis may be seen in rheumatoid arthritis, various vasculitides and other autoimmune diseases such as systemic lupus erythematosus. Deposits of leukaemia and lymphoma are usually seen in the choroid and haemorrhages may also occur. Retinitis pigmentosa is frequently only studied at the late stage where there is bone spicule pigmentation with sparing of the macular region. A common feature in syndromic retinal degeneration appears to be abnormalities in the cilia. Metabolic deficiencies may also affect the eye. These include lysosomal storage disorders, peroxisomal storage disorders, lipofuscinosis and aminoacidopathies. Mitochondrial disorders also occur. The effects of demyelinating disease such as multiple sclerosis may also be seen in the eye.
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Aim: To evaluate the whether intravitreal erythropoietin (EPO) administration has any beneficial or adverse effect in patients with late-stage optic neuropathy (ON) or not. Methods: The study examined 16 eyes of 16 patients who had late-stage ON and ≥1/20 best-corrected visual acuity (BCVA) in their affected eye. There were nonarteritic ischemic ON in 10 (62.5%) eyes, traumatic ON in 4 (25.0%) eyes and methanol-induced ON in 2 (12.5%) eyes. Using pars plana approach, 2000 IU/0.2 ml EPO was administered intravitreally with a 30-gauge needle. Injections were administered three times with 6-week intervals. We compared the differences in the BCVA, intraocular pressure (IOP), retinal nerve fiber layer (RNFL) thickness, pattern visual evoked potentials (p-VEP) and pattern electroretinography (p-ERG) parameters performed at initial examination and final visits. Results: The mean age of the patients was 52.38 ± 12.00 years; 2 (12.50%) of them were female, and 14 (87.50%) of them were male. The mean BCVA levels of 16 patients with optic atrophy were 1.12 ± 0.25 logMAR at the initial examination and 1.08 ± 0.26 logMAR at the final visit (p = 0.102). There was no statistically significant difference between the initial and final RNFL thicknesses, IOP values, p-ERG or p-VEP responses. Conclusions: Intravitreal EPO injections have no beneficial or detrimental effect on the late stage of ON. Further studies are necessary to compare our results in patients with ON in earlier stages.
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Purpose The aim of this study was to explore the relationship between chronic cigarette smoking and meibomian gland dysfunction (MGD). Methods This study enrolled 322 smokers with MGD and 2067 non-smokers with MGD. All enrolled subjects were tested in the following sequence: Ocular Surface Disease Index (OSDI), tear film breakup time (TBUT), corneal fluorescein staining (CFS), Schirmer I test (SIT)and finally slit-lamp microscope examination of lid margin abnormalities, meibomian gland expression as well as meibum. Results Compared with the MGD patients without smoking, the MGD patients with smoking had significantly increased scores of lid margin abnormality and meibum (P<0.01 for each comparison). No significant difference was noted in OSDI, TBUT, CFS, SIT or the score of Meibomian gland expressibility between the smokers and non-smokers (P>0.05 for each comparison). In the smokers, the smoking index was significantly correlated with the scores of lid margin abnormality (Both sexes, R = 0.19, P<0.01; Male, R = 0.18, P<0.01) and meibum (Both sexes, R = 0.29, P<0.01; Male, R = 0.20, P<0.01), whereas it was not significantly correlated with OSDI, TBUT, CFS, SIT or score of Meibomian gland expressibility (P>0.05 for each comparison). Conclusion The findings of this study suggest chronic smoking might be associated with MGD.
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We aimed to investigate the effect of alcohol abuse on the conjunctival flora. The cases were evaluated as two groups. The study group consisted of 55 heavy-drinking males diagnosed with alcohol abuse, while the control group consisted of 55 males without a history of alcohol abuse. Samples were taken from the inferior fornix conjunctiva with sterile cotton-tipped swabs (Amies transport medium) for culture. The samples were inoculated into blood agar, chocolate agar, eosine methylene blue agar and Saboraud-Dextrose agar (Oxoid/UK) with the dilution method. The microorganisms that grew in study group subjects were Coagulase Negative Staphylococcus (CNS) in 30 (54.5%), Staphylococcus aureus in 14 (25.5%), Moraxella spp. in 3 (5.5%), Streptococcus spp. in 3 (5.5), Bacillus spp. in 3 (5.5%), Corynebacterium spp. in 3 (5.5%), Candida spp. in 3 (5.5%), Haemophilus spp. in 2 (3.6%), Acinetobacter spp. in 2 (3.6%), Neisseria spp. in 1 (1.8%) and Micrococcus spp. in 1 (1.8%). The results for control group were CNS in 31 (56.4%), Bacillus spp. in 7 (12.7%), S. aureus in 5 (9.1%), and Corynebacterium spp. in 2 (3.6%). Moraxella spp., Streptococcus spp., Candida spp., Haemophilus spp., Acinetobacter spp., Neisseria spp. and Micrococcus spp. microorganisms grew in the conjunctival flora samples of the study group but not in the control group. S. aureus colonization was significantly higher in the study group than the control group (p < 0.05). The S. aureus colonization rate was statistically significantly higher in the study group. Some microorganisms only grew in the conjunctival flora samples of the study group. These findings indicate that the conjunctival flora in persons with chronic alcoholism is different than the normal population.
The Oxford Handbook of Acute Medicine is the essential guide to the management of the acutely ill patient. It features expanded material on practical procedures and new information on common presentations.
This title is a practical and comprehensive guide to the management of the acutely ill patient. It is a single source to the most up-to-date therapies and protocols. It presents the most recent treatment guidelines and evidence-based content that is up-to-date with the recent advances in clinical medicine. Topics covered include cardiac emergencies, respiratory emergencies, gastroenterological emergencies, renal emergencies, shock, neurological emergencies, infectious diseases, emergencies in human immunodeficiency virus, diabetes and endocrine emergencies, haematological emergencies, rheumatological emergencies, dermatological emergencies, psychiatric emergencies, drug overdoses, and practical procedures in acute medicine.
Purpose: Following methanol intoxication, optic nerve neuropathy may occur which is currently treated by different therapeutic regimens. Erythropoietin (EPO) has recently been introduced as a good therapeutic option in methanol-induced optic neuropathy. The aim of the current study was to evaluate the efficacy of EPO in improvement of the visual disturbances in methanol-intoxicated patients. Materials and methods: In a case-control study, all patients who had referred to our toxicology center with confirmed diagnosis of methanol toxicity were considered to be included. Of them, those who had referred with visual disturbances, survived, and their visual disturbances had not improved after hemodialysis were entered. Cases received EPO and corticosteroids while controls only received corticosteroids. They were then compared regarding their visual outcome. Results: All five patients in the control group mentioned that after discharge, their visual acuity had improved while in the cases, three mentioned visual improvement, two mentioned their visual acuity had deteriorated after discharge, two mentioned no change in their visual acuity and three mentioned that their visual acuity had first improved but then deteriorated with a mean 2-month interval period. In fundoscopic evaluations, two controls had normal fundospcopy while 8 cases had abnormal fundoscopy (P = 0.055). Conclusion: Protective effect of EPO on methanol-induced optic nerve may be strong at the beginning of the intervention but is probably transient.
Objectives: The effects of smoking on central corneal thickness (CCT), corneal endothelial cell density (ECD), and morphology were evaluated in otherwise healthy subjects. Methods: The study included 103 current smokers and 106 healthy nonsmoking subjects without any eye disease apart from refractive errors. Endothelial cell density, percentage of hexagonality, and coefficient of variation (CV) in cell size were measured using noncontact specular microscopy. Central corneal thickness was measured by ultrasound pachymetry. Results: The mean age of participants in the nonsmoker group was 31.4 ± 5.1 years (18-60) and 33.0±9.1 years (18-58) in the current smoker group. The mean CCT value was 523.7±34 μm in the nonsmoker group and 518.5±37 μm in the smoker group. The mean ECD, CV, and percentage of hexagonality values were 2,881±293.7 cells per square millimeter, 32.5±6%, and 56.6±11% in the nonsmoker group, and 2,681±323.9 cells per square millimeter, 33.4±5%, and 55.5±10% in the smoker group, respectively. Although there was no difference between the groups in terms of CCT, CV, and percentage of hexagonality values, a significant difference was determined in the case of ECD values[ZERO WIDTH SPACE][ZERO WIDTH SPACE] (P<0.001). The smoker group comprised 67 light smokers (65.0%) and 36 (35.0%) heavy smokers. Between these groups, there was no statistically significant difference in the mean values of CCT, ECD, CV, and the percentage of hexagonality. Conclusions: Although cigarette smoking has no effect on cell polymorphism and polymegethism, the results suggest that smoking reduces endothelial cell count.
Marijuana has been shown to lower intraocular pressure (IOP) but with limited duration of action and numerous adverse effects. Use of marijuana to lower IOP as a means of glaucoma treatment would require frequent use throughout the day, leading to significant adverse effects, possible progression toward Cannabis Use Disorder (CUD), and/or withdrawal symptoms. The treatment of glaucoma based on the cannabis plant or drugs based on the cannabinoid molecule should be considered carefully before being prescribed. Considerations should include the adverse physical and psychological adverse effects, including substance abuse. Currently, the deleterious effects of marijuana outweigh the benefits of its IOP-lowering capacity in most glaucoma patients. Under extremely rare circumstances, a few categories of glaucoma patients may be potential candidates for treatment with medical marijuana. Further studies on alternate routes and more focused means of cannabinoid molecule delivery to the eye for glaucoma treatment are needed.