Lead poisoning

General: Now rare and mostly of industrial 242c23c origin; cumulative poisoning; excreted slowly; absorption slow by any route; prolonged exposure required for development of symptoms; acute poisoning virtually nonexistent.

Ocular: Sclerosis and obliteration of choroidal vessels; retinal arterial spasms; retrobulbar neuritis; papilledema; optic atrophy; cortical blindness; divergence palsy; papillary paralysis; bilateral abducens paralysis; accommodative palsy; mechanism of ocular pathology with this condition is not well defined, although there is evidence pointing to the level of cyclic adenosine monophosphate.

Clinical: Loss of appetite; weight loss; colic; constipation; insomnia; headache; dizziness; irritability; moderate hypertension; albuminuria; anemia; blue line edge of gum; encephalopathy; peripheral neuropathy leading to paralysis; convulsions; mania; coma.

Kasper DL, et al., eds. Harrisons Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 2005.

Chisolm JJ. Treatment of lead poisoning. Mod Treatment 1967; 4:710.

Citirik M, Acaroglu G, Mutlway AH, et al. Lead poisoning : report of a case. Ann Ophthalmol 2004; 36: 32-3

Fox DA. Lead-induced alterations in rod-mediated visual functions and cGMP metabolism: new insights. Neurotoxicology 1994; 15:503-512.