ADDICTION AND VISION LOSS

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ADDICTION AND VISION LOSS

• Bruce Kastner, M.S., O.D.,
• Clinical Coordinator,
• CBVI

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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.

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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

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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

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NORMAL RETINA
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RETINAL STRUCTURES
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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)

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TESTING FOR TOXICITY

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

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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

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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

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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.

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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

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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

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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

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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

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MACULAR TESTING

• Color testing Ishihara plates

• Automated visual fields

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ADDITIONAL TESTING
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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

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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?

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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)
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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)
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TALC RETINOPATHY
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TALC RETINOPATHY
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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