BASICS
DESCRIPTION
Characteristic retinopathy with small, intraretinal, whitish yellow, refractile deposits in patients who abuse intravenous drugs, especially those made from crushed tablets or powder (1)[B]
RISK FACTORS
Occurs in patients of any age
PATHOPHYSIOLOGY
• Drug addicts crush oral medications such as methylphenidate hydrochloride (Ritalin) or methadone hydrochloride and create an aqueous suspension for intravenous injection.
• Oral medications contain talc (hydrous magnesium silicate) as an inert filler.
• After intravenous administration, talc particles embolize to the pulmonary vasculature.
• With chronic intravenous drug abuse, collateral vasculature forms in the lung and allows talc particles to enter the systemic circulation.
• Talc particles embolize to other organs, including the eye.
• After many talc particles become lodged in the small arterioles of the retinal vasculature, an ischemic retinopathy develops.
ETIOLOGY
Intravenous drugs that contain talc particles
COMMONLY ASSOCIATED CONDITIONS
Intravenous drug abuse
DIAGNOSIS
HISTORY
Chronic intravenous drug abuse, especially with crushed tablets or powder such as methylphenidate (Ritalin)
PHYSICAL EXAM
• Small, white, glistening crystals concentrated at end arterioles (intravascular space) throughout the retina, most prominent in the posterior pole.
• Ischemic retinopathy with capillary nonperfusion, including microaneurysms, cotton wool spots, and venous loops
• Severe cases can have optic disc and peripheral retinal neovascularization with vitreous hemorrhage (2).
• Inspection of skin may reveal evidence of intravenous drug abuse.
DIAGNOSTIC TESTS & INTERPRETATION
Imaging
Fluorescein angiography is used to assess capillary nonperfusion and retinal neovascularization.
DIFFERENTIAL DIAGNOSIS
• Crystalline retinopathy
– Cholesterol emboli (Hollenhorst plaque)
– Canthaxanthin ingestion (oral tanning agent)
– Tamoxifen (history of breast cancer)
– Methoxyflurane anesthesia
– Cystinosis
– Parafoveal telangiectasia
– Calcified drusen
– Bietti’s crystalline dystrophy
– West African crystalline retinopathy
– Intraretinal lipid exudates
TREATMENT
ADDITIONAL TREATMENT
General Measures
• Patients should stop intravenous drug abuse.
• In the absence of retinal or optic nerve neovascularization, observation is appropriate.
SURGERY/OTHER PROCEDURES
• In the presence of peripheral nonperfusion and neovascularization, panretinal photocoagulation should be considered.
• Pars plana vitrectomy for non-clearing vitreous hemorrhage or visually significant tractional retinal detachment can be beneficial.
ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Yearly exam for asymptomatic talc retinopathy, more frequent if there is significant non-perfusion
PATIENT EDUCATION
Systemic and ocular risks of intravenous drug abuse
PROGNOSIS
• Visual prognosis is variable
• Visual acuity can be decreased because of macular ischemia, vitreous hemorrhage, macular fibrosis, and tractional retinal detachment (3).
• In the absence of ongoing intravenous drug abuse, talc retinopathy has been shown to be static and nonprogressive (4).
COMPLICATIONS
• Ischemic retinopathy
• Retinal and optic nerve neovascularization
• Vitreous hemorrhage
• Preretinal fibrosis/tractional retinal detachment
REFERENCES
1. Murphy SB, Jackson WB, Pare JA. Talc retinopathy. Can J Ophthalmol 1978;13:152–156.
2. Tse DT, Ober RR. Talc retinopathy. Am J Ophthalmol 1980;90:624–640.
3. Sharma MC, Ho AC. Macular fibrosis associated with talc retinopathy. Am J Ophthalmol 1999;128:517–519.
4. Martidis A, Yung CW, Ciulla TA. Talc embolism: a static retinopathy. Am J Ophthalmol 1997;124:841–843.
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