Document 5LEwqmObXDzBmJ1zoOD9XGOxR

't American Medical Association November 30, 1963 EDITORIAL BOARD KATHARINE R. BOUCOT, M.D., Chief Editor Woman's Medical College of Pennsylvania 3300 Henry Avenue Philadelphia, Penn. 19129 Wil l ia m F. As h e , M.D., Columbus, Ohio An n a M. Ba e t JER, Sc.D., Baltimore He n r y J. Ba k s t , M.D., Boston Ro n a l d F. Bu c h a n , M.D., Boston Jo h n H. Fo u l GER, M.D., Wilmington, Del. Jo h n R. Go l d s mit h , M.D., Berkeley, Calif. Da v id E. Go l d s t e in , M.D., New York Th e o d o r e H. In g a l l s , M.D., Philadelphia Ru t h e r f o r d T. Jo h n s t o n e, M.D., Los Angeles Ca r l A. Na u , M.D., Oklahoma City Sh e r ma n S. Pin t o , M.D., Tacoma Da v id M. Sp a in , M.D., Brooklyn He r b e r t E. St o k in g er , Ph .D., Cincinnati Le o Wa d e , M.D., New York Jo h n H. Ta l b o t t , M.D., Director DIVISION o f s c ie n t if ic p u bl ic a t io n s Gil b er t S. Co o p e r , Managing Editor T. F. RlCH, Assistant Managing Editor Robert A. Kehoe, M.D. The Kettering Laboratory University of Cincinnati College of Medicine Eden Avenue Cincinnati 19, Ohio Dear Bob, Is this anything new and important? If so, will you please abstract it, write an editorial, or do whatever you think should be done? With many thanks and kind regards, Cordially, Katharine R. Boucot, M. D. KRBrcrt Enc.: Sonkin, N.: Stippling of the Retina. A New Physical Sign in the Early Diagnosis of Lead Poisoning, New England J. Msd. 269:779 (Oct. 10) 1963. I^ET 0010460 Vol. 269 No. 15 STIPPLING OF THE RETINA -- SONKIN 779 STIPPLING OF THE RETINA A New Physical Sign in the Early Diagnosis of Lead Poisoning Na t h a n So n k in , M.D.* PAWTUCKET, RHODE ISLAND T EAD poisoning was a subject of major im- portance during the first four decades of this century because of the absorption of lead from paint, especially among children and painters. Intoxication with lead products was also common among battery workers and those unfortunate enough to ingest it from the insecticide residues on fruits and vegetables. It is no longer as prevalent because of the safeguards that have been introduced in lead-free paints and the greater sophistication of industrial users of lead. Nevertheless, it is still an important problem in the wire and battery industries. The classic physical findings and laboratory data such as a lead line in the mouth, chronic gastritis, encephalopathy and extensive basophilic stippling of erythrocytes are manifestations of advanced stages of heavy-metal intoxication. An early diagnostic sign would have merit from both an individual and a public-health standpoint. A physical finding of this nature has been observed in a small series of cases. A grayish stippling of lead pigment that is circum ferential around the optic disk has been observed in persons exposed to several lead compounds. Visual ized through the ophthalmoscope, particles of lead appear as glistening, discrete, gray pigment concen trated in the retinal area around the optic disk. It should be noted that this pigment differs distinctly visually from that observed in the elderly and those of olive or swarthy complexions and in the Negro race. This sign is shown in Figure 1. Deposition of lead pigment is not mentioned in ophthalmologic textbooks, which consider other eye manifestations in lead poisoning.1'2 Optic neuritis, edema of the disk, ocular-muscle paralysis, ptosis and central-vision disturbance are described. These path ologic conditions are relatively rare and usually occur in association with generalized systemic disturbance ifi"advanced plumbism. Several textbooks do not even mention eye changes in lead intoxication.3'6 A review of the literature did not disclose any recent periodicals dealing with this subject. There were, however, several articles in past decades on ocular changes in advanced lead intoxication.7-13 These described findings of amblyo pia, retinal edema, retrobulbar neuritis, scotomas, cataracts, extraocular-muscle paralysis, choked disks and either partial or total blindness. The present study was made during a period of Physician, Veterans Administration Regional Office Outpatient Clinic, Providence; physician. Memorial Hospital, Pawtucket; member, Medical Staff, Miriam Hospital, Providence. approximately a year. A total of 25 persons were exposed to lead compounds in their work for an in dustrial wire-manufacturing company through man ual handling of bulk lead compounds and by inhala tion of whatever lead dust contaminated the atmo sphere of the working area. Seventeen members of this group worked for intervals of three months or less and did not give any clinical or laboratory evi dence of lead absorption. The remaining group of 8 men worked for intervals of six months to a year, and were followed medically. Their work consisted of mixing various industrial lead compounds in an enclosed area for the manufacture of wire insulation on a basis of forty hours a week.f Several safeguards were instituted to protect these men. A large exhaust fan was installed in the mixing room to minimize inhalation of the powders. All employees were required to wear masks, gloves and coveralls during various phases of their work. Prior to leaving the work area they were also required to wash their hands. Despite these precautions lead intoxication occurred due to carelessness and pro longed exposure. Fig u r e 1. Drawing, Showing Deposition of Lead Pigment in an Area Surrounding the Optic Disk. These workers were followed by blood counts, urinary lead determination and physical evaluations with especial attention to funduscopic and mouth examinations. Those who excreted abnormal amounts of lead in the urine frequently exhibited ILead compounds (lead vinyl stabilizers) were as follows: basic lead silicate sulfate, 68.0 per cent total lead; dibasic lead phosphite, 90.8 per cent total lead; dibasic lead phthalate, 79.8 per cent total lead; lead chlorosilicate complex, 47.5 per cent lead; and dibasic lead stearate, 55.3 per cent total lead. HE 0010461 N 25031.01 780 THE NEW ENGLAND JOURNAL OF MEDICINE Oc 11, 1963 Ta b l e 1. Summary of Findings. No. 1 2 3 5 7 8 Ex p o s u r e t o Le a d f o r >6 Mo. Yes Yes Yes Yes Yes Yes Yes Yes Er y t h r o c y t e St ip p l in g Le a d i n Ur in e * Le a d Lin e o n Gu ms Mo u t h Hy g ie n e Le a d -Pig me n t De p - OSITiON IN Re t in a ON INITIAL 4 MO. AFTER EXAMINA- REMOVAL TION FROM EX- POSURE Rare Occasional No Rare Rare Yes No No No No No No No No No No o n INITIAL 4 MO. AFTER EXAMINA- REMOVAL TION FROM EX- POSURE mg./liter mg./liter 0.12+ 0.16+ O.I6f 0.241 0.08** 1.5611 0.12++ 0.12** 0.04 0.08 0.08 0.04 0.04 0.08 0.08 0.08 ON INITIAL 4 MO. AFTER EXAMINA- REMOVAL TION FROM EX- POSURE None None None None None None None None None None None None None None None None ON INITIAL 4 MO. AFTER EXAMINA- REMOVAL TION FROM EX- POSURE Poor Poor Poor Good Poor Good Poor Poor Poor Poor Poor Good Poor Good Poor Poor ON INITIAL 4 MO. AFTER F.XAMINA- REMOVAL TION FROM EX- POSURE Yes No Yes No Yes No Yes No Yes Decreased Yes No Yes No Yes Decreased "Single sample; normal range, 0-0.15 mg./liter (determinations through courtesy of R. I. State Dept, of Public Health, Providence). f7 mo. after exposure. {6 mo. after exposure. 8 mo. after exposure. ^Largest exposures in group -- 12 mo. ; 12 mo. after exposure. **11 mo. after exposure, ft11^2 mo. after exposure. rare basophilic erythrocyte stippling. No one had any evidence of a lead line. However, an abnormal urinary lead concentration showed some correlation with the retinal findings of grayish lead pigmentary deposits in the area peripheral to the disk margins. I was able to predict with good reliability which workers would excrete abnormal amounts of urinary lead by prior ophthalmoscopic examination. Table 1 summarizes the findings in the series. Statistical analysis by application of the binomial test yields probability values equal to or less than 0.016, with one-tailed hypotheses that retinal pig mentation is a reliable sign.* Dis c u s s io n Deposition of pigment in the retina appears to be a reliable early sign of lead intoxication. Although the retinal stippling in this small series of cases could possibly have come from some other source, the most likely assumption would be that it was due to lead or to a lead compound. Retinal pigmentation is reversible within a period of months if the environ mental exposure is eliminated. Positive laboratory data correlate somewhat with eye findings. There appears to be a relation between absorption of lead and cleanliness when oral hygiene is used as an index. Poor personal hygiene apparently serves as a predis posing factor in lead absorption. Retinal changes *Statistical analysis performed by Arthur Tamkin, Ph.D., of Cranston, Rhode Island, are visualized as a glistening deposition - of, grayish lead pigment surrounding the optic disk. This may be present before there is laboratory evidence of lead toxicity. Su mma r y a n d Co n c l u s io n s A previously unrecorded physical sign in the diag nosis of incipient lead poisoning is described. Pig ment deposition in the retinal area circumscribing the optic disk can be readily seen by any physician with an ophthalmoscope and a discerning eye. 353 Armistice Boulevard Re f er e n c e s 1. Duke-Elder, W. S. Textbook of Ophthalmology. Seventh edition. 5G0 pp. Philadelphia; Saunders, 1947. 2. Tassman, I. S. The Eye Manifestations of Internal Diseases. 542 pp. St. Louis: Mosby, 1942. P. 393. 3. Adler. F. H. Textbook of Ophthalmology. Seventh edition. 560 pp. Philadelphia: Saunders. 1962. 4. Kuhn, H. Industrial Ophthalmology. 294 pp. St. Louis: Mosby, 1944. 5. May, C. H. May's Manual of the Diseases of the Eye for Students and General Practitioners. Nineteenth edition. Edited by C. A. Pereira. 521 pp. Baltimore: Williams & Wilkins, 1947. 6. Hughes, W. F. The Year Book of Ophthalmology: (1961-1962 Year Book series). 382 pp. Chicago: Year Book Publishers, 1962. 7. Williams, C. Review of lead amblyopia and presentation of case of left homonymous lateral hemianopsia due to lead poisoning. Ann. Ophth. 20:719-723, 1911. 8. Shcrer, J. W. Lead amblyopia with cataract from same source: report of case. Missouri State M. A. 32:275-277, 1935. 9. Alexander, E. Eye changes in chronic lead poisoning with report of case. Ophthalmologica 5:634-636, 1909. 10. Good, P. Choked discs in lead encephalopathy. Am. J. Ophth. 24:794-797, 1941. 11. Brosc, L. D. Ophthalmoplegia interna: result of lead poisoning. Arch. Ophth. 44:26-28, 1915. 12. Sautter, A. C. Encephalopathy with ocular complications probably due to lead poisoning. Am. J. Ojthth. 5:468-470, 1922- 13. Locwe, O. Case of transient lead amaurosis. Arch. Ophth. 35:164* 171, 1906. tfE" 0010462