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

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Presentation on theme: "ADDICTION AND VISION LOSS Bruce Kastner, M.S., O.D., Clinical Coordinator, CBVI."— Presentation transcript:

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

2 ACKNOWLEDGMENTS Spalton, Atlas of Clinical Ophthalmology, 3 rd Edition, 2005 Onofrey, Ocular Therapeutics Handbook, 2 nd Edition, 2005 Kunimoto, Danitkar, and Makar, The Wills Eye Manual, 4 th Edition, 2004 EyeRounds.org effects/chloroquine.html Steel, JR, Cockcroft, JR an Ritter, JM, Blind drunk: alcoholic pancreatitis and loss of vision. Postgrad Med J (1993) 69,

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 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 bloodbrain barrier. METHANOL TOXICITY 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 bloodbrain 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 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:

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:

22 TALC RETINOPATHY

23

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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