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ADDICTION AND VISION LOSS

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Title: ADDICTION AND VISION LOSS


1
ADDICTION AND VISION LOSS
  • Bruce Kastner, M.S., O.D.,
  • Clinical Coordinator,
  • CBVI

2
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/side-ef
    fects/chloroquine.html
  • Steel, JR, Cockcroft, JR an Ritter, JM, Blind
    drunk alcoholic pancreatitis and loss of
    vision. Postgrad Med J (1993) 69, 151-152.

3
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

4
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

5
NORMAL RETINA
6
RETINAL STRUCTURES
7
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)

8
TESTING FOR TOXICITY
  • CBC (rule out macrocytic anemia associated with
    alcoholism)
  • Serum vitamin B12
  • Serum folate
  • Screening for metal toxicity (lead)

9
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

10
METHANOL TOXICITY
MRI on day 15 after methanol intoxication. (a)
T2-weighted 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.
  • Edema secondary to increased pressure

11
METHANOL TOXICITY
  • MRI on day 15 after methanol intoxication. (a)
    T2-weighted 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.

12
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

13
PATHOPHYSIOLOGY CASE STUDY
  • Alcoholic pancreatitis with delirium
  • Treatment with parenteral vitamins
  • Sedated with intravenous chlormethiazole
  • Rehydrated with physiological saline
  • BP 140/80
  • Next day delirium resolved
  • Normal temperature
  • BP stabile
  • Oriented and rational
  • completely blind

14
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

15
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

16
MACULAR TESTING
  • Color testing Ishihara plates
  • Automated visual fields

17
ADDITIONAL TESTING
18
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

19
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?

20
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/pa
rt2.htm http//www.opt.indiana.edu/ce/syspharm/par
t2.htm)
21
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)
22
TALC RETINOPATHY
23
TALC RETINOPATHY
24
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
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