Transcript ADDICTION AND VISION LOSS

ADDICTION AND VISION
LOSS
Bruce Kastner, M.S., O.D.,
Clinical Coordinator,
CBVI
ACKNOWLEDGMENTS
Spalton, Atlas of Clinical Ophthalmology, 3rd Edition,
2005
Onofrey, Ocular Therapeutics Handbook, 2nd Edition,
2005
Kunimoto, Danitkar, and Makar, The Wills Eye Manual,
4th Edition, 2004
EyeRounds.org
http://www.opt.indiana.edu/ce/syspharm/part2.htm
http://www.kellogg.umich.edu/theeyeshaveit/sideeffects/chloroquine.html
Steel, JR, Cockcroft, JR an Ritter, JM, “Blind drunk:
alcoholic pancreatitis and loss of vision.” Postgrad Med J
(1993) 69, 151-152.
OCULAR STRUCTURES
Cornea – clear, anterior-most
Iris – Colored, contains pupil
Anterior chamber – between cornea and lens
Lens – focuses light onto retina
Posterior chamber – between lens and retina
Retina – photoreceptors; converge to form optic
nerve
Optic Nerve – sends signal to brain for
perception
OCULAR STRUCTURES
Retina – 10 layers
– Macula – most sensitive part of retina –
Responsible for best resolution (20/20, color vision
and central vision)
– Photoreceptors
Rods = peripheral vision, black and white, 20/400
Cones = central vision, color, 20/20
NORMAL RETINA
RETINAL STRUCTURES
VISION LOSS DUE TO TOXICITY
Toxic optic neuropathy – differential
diagnosis
– Tobacco/alcohol abuse
– Severe malnutrition (thiamine deficiency) –
Vitamin B1 deficiency
– Pernicious anemia (problem with B12
absorption)
– Toxic (cloramphenicol, ethambutol, isoniazid,
digitalis, chloroquine, streptomycin, lead, etc)
TESTING FOR TOXICITY
CBC (rule out macrocytic anemia
associated with alcoholism)
Serum vitamin B12
Serum folate
Screening for metal toxicity (lead)
OPTIC NEUROPATHY
Damage to the optic nerve due to any cause
Most recognized cause: methanol intoxication.
– Victim usually mistakes or substitutes methanol for ethyl alcohol.
– Blindness occurs with drinking as little as one ounce
– Initial nausea and vomiting followed by respiratory distress,
headache and vision loss starting 12 hours after consumption
– Ethylene glycol (component of antifreeze) is toxic to the entire
body causing permanent neurological and ophthalmic loss
Increased intracranial pressure causes swelling of the optic
nerve and cerebral edema
TREATMENT FOR METHANOL AND ANTIFREEZE
TOXICITY IS ETHANOL CONSUMPTION
METHANOL TOXICITY
Edema secondary to increased pressure
METHANOL TOXICITY
MRI on day 15 after methanol intoxication. (a) T2weighted image showed high signal abnormalities in
bilateral basal ganglia (arrows), frontal, and occipital
subcortical white matter (arrowheads), consistent with
oedematous change. (b) T2-weighted image showed
oedematous change involving bilateral optic tracts and
optic radiations (arrows). High signal oedematous
change was also noted in the optic disc of left eye
(arrowheads). (c) T1-weighted image showed slightly
high signal component in bilateral basal ganglia,
indicating the haemorrhage (arrows). (d) T1-weighted
image with gadolinium administration showed marginal
enhancement in bilateral putamen, indicating breakdown
of the blood−brain barrier.
PATHOPHYSIOLOGY
Methanol is metabolized in the liver and
converted to formic acid (toxic) resulting in
systemic metabolic acidosis
Onset of vision loss and central nervous system
effects are delayed for 12-24 hours,
corresponding to the time for methanol to be
converted to its toxic metabolites
Laboratory testing can take one day to complete,
so toxicity is not usually diagnosed in the ER
Best treatment: gastric lavage, treatment of the
metabolic acidosis and competitive inhibition of
methanol oxidation by ethanol or methypyrazole
PATHOPHYSIOLOGY – CASE STUDY
Alcoholic pancreatitis with delirium
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Treatment with parenteral vitamins
Sedated with intravenous chlormethiazole
Rehydrated with physiological saline
BP 140/80
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Next day: delirium resolved
Normal temperature
BP stabile
Oriented and rational
“completely blind”
PATHOPHYSIOLOGY – CASE STUDY
Reason for original visit – “blurred vision”
– Denied drinking methylated spirits
– Normal pupillary reflex
– Ophthalmoscopy revealed cotton wool spots (infarcts
– similar to that associated with hypertension) with a
cherry red spot in the macula OD (evidence of toxicity
and loss of macular function)
– Admitted to abusing drugs up to 2 years previously
and shared needles
– Blood work: (-) HIV; (-) lupus erythematosus
– Ultrasound of abdomen: enlarged pancreas
PATHOPHYSIOLOGY – CASE STUDY
Minimal improvement in vision one month
after diagnosis
Etiology of pancreatic retinopathy
uncertain: granulocyte aggregates
(activated by the complement system)
versus fat emboli result in vascular
occlusions
Retinal treatment is conservative – limited
to observation and supportive care
MACULAR TESTING
Color testing –
Ishihara plates
Automated visual
fields
ADDITIONAL TESTING
TESTS TO DETERMINE TYPE OF
TOXICITY
Color vision
Electrodiagnostic testing
– ERG – electroretinogram (tests layers of
retina)
– VEP – tests entire visual pathway to occipital
lobe
Visual field
– Amsler (specific for macula – central)
– Automated field
DRUG TOXICITY
44 y/o female with acute onset of paracentral scotomas (visual
field loss around the central field) in right eye (corresponded
directly to Amsler grid findings) – What should be tested?
TAMOXIFEN MACULOPATHY
Tamoxifen (Nolvadex, Emblon, Noltam, Tamofen) is an anti-estrogen used
to treat breast carcinoma. It has few systemic side-effects at a traditional normal dose
of 20 to 40mg/day. Current dosages prescribed today may be even less, reducing the
prevalence of side-effects. Vortex keratopathy and optic neuritis can rarely occur,
which usually is reversible on cessation of therapy. Retinotoxicity presents as multiple
superficial yellow crystalline ring-like deposits at the macula, that can cause visual
acuity loss (Figure 29).
(Source: http://www.opt.indiana.edu/ce/syspharm/part2.htm
http://www.opt.indiana.edu/ce/syspharm/part2.htm)
ANTIMALARIAL TOXICITY
Chloroquine (Nivaquine, Avlocor) and Hydroxychloroquine (Plaquenil)
are used in treating malaria and rheumatological disorders
(i.e. rheumatoid arthritis, lupus). Excess of 300g cumulative oral dose
(250mg/day for 3 years) significantly increases risk of maculopathy.
Hydroxychloroquine has less maculopathy risk than chloroquine,
and as such is typically the preferred medication to prescribe (Figure 26).
Source: http://www.kellogg.umich.edu/theeyeshaveit/side-effects/chloroquine.html)
TALC RETINOPATHY
TALC RETINOPATHY
CONCLUSIONS
IV drug users are susceptible to emboli which
deprive retinal structures of oxygen secondary to
talc which is added to “cut” the drug. Cortical
damage can also occur, but the emboli tend to
travel downstream to the smaller vessels where
they lodge
Alcohol abuse results in death of retinal
structures –
– Loss may be sudden and irreversible if methanol is
ingested
– Loss may be gradual, permanent with sustained
nutritional amblyopia secondary to ethanol abuse.
This is generally caused by lack of vitamins