Document NEE07J9M9KQQxvvZVaV5Z6NYV

St a t e o f Oh io B u r e a u o f W o r k m e n 's C o m p e n s a t i o n Claim No. 00-10*319 Claimant . Address Dat of Examination...... .M ^.y.. .f.i?59;.... Ohio SPECIALIST'S REPORT ..Age.:.. .31 years ., ' NOTE: Submit report under following headings:, (1) History. (2) Complaints. (3) Examinations, . including X-ray and laboratory work. (4) Discussion. (5) Opinion. Sign and mail,THREE ` copies to the MEDICAL SECTION--Retain one for your file. " ' ... - r , ; , REPORT OF EXAMINATION TO BE RETURNED WITHIN TWO WEEKS r- : j JFOLLOWING REQUEST. ' ; . f" HISTORY W .^ -t y; rvftifl-'snij, M P i n i w c . ' i,c, - f.O 'll i , The opinion rendered herein Is based upon the examination o f t h e record asr provided to the undersigned In accordance with a letter of A.L, Kefauver,M.D., dated JTu.tMne* 2Q5C* Tmhue. claimant was not exaalnad, nor was Uhe. requested Ato. appear <3 for examination, in as much as the, lapse of tiae since the onset o f his dis- = ; ability .had been such as to render futile, the application at this tiae o f `j!- procedures which, at an earlier inforaation concerning the.role date, would probably have elicited precise played by occupational exposure to, and ;,, ...m, absorption.of, lead in his illness and disability. Such c o n c l u s i o n a a h a s 1' been, or can be, arrived at at this tiae, aust depend upon the Interpretation;. of the facts set. forth in the record, since these could; not be clarified or/7 - extended by inforaation gained froa.the elalaant at this tiae... ' `- Summary of Case _______ ^ :C;o Briefly to restate the facts, M r ^ m p f c developed certain visual.!disturbances - which were first interpreted by a physician as a toxic central optic peurltis - in May 1957. Prior.to this he had'suffered froa.nervousness, dizziness a n d headaches and he continued to be disturbed by these syaptpas, which appear;... to have been augaented somewhat jby anxiety. The claimant's loss of vision progressed,' and he was referred to various, physicians and specialists, froa r tiae to t^Lae, over a period.which caae to an end, so far as the results of examinations have been recorded here,' with the oopfithalaologic. examination, of Or. C. Wilbur Rucker of the Mayo Clinic on January 6, 1958,' the .neurological.' exaalnatlon by Dr. H,P.Ooldsteln of the Mayo Clinic oh January 9, 1958, and t a general consideration of his problem froa the viewpoint of causation by ,, I Dr. M.M. Hargraves of rthe Havo Clinic, just after the examination, of D r s . Rucker and Goldstein. Mr, ^ ^ w a s seen early in his illness/ and was followed up,to and after h i T w x S x t to the Mayo Clinic, by Dr. J.C. Daaitz of Akron, a specialist In diseases o f the eye, ear, nose and throat. The record does not show the precise degree of visual loss now (July 1959), althoug..h..i.t..i.s'sa..i.d..i.n'..t.h.e..r.e.p.or't..o.f an i'nvest'i'gat'or -(-H-e-l-t-on ~5-2`22--58) t'hat all v l s l o n l n both eyes'has,been lost, but the report of Dr.; Rucker indicated that, In January of 1958, .the visual acuity had1been reduced $,0,1/60 in each ^ eye, and that there were ,,"large dense central scotomas" . . All in all, the - records available are entirely satisfactory in deaonstratlng the clinical '' entity, froa which' this claimant has buffered and is still suffering. He now has a very. Berlous (perhaps total) loss of vision, in association with a ,, bilateral optic neuritis of a type said b y the ophthalmologists to be of , ~'!` toxic, origin; without other evidence of disease of the central or peripheral nervous system that would explain (or help, by association, to explain) the optio Involvement# ` ...... ; Discussion*of the Case v ,,,, ... ......................... . There is no evidence in the. reedrd b y Which to establish reasonably or probably the cause of the injury to theoptic nerves. One of the ophthal- aologists strongly advised the patient against the further use of tobacco, obviously on the grounds that the effects of nicotine dn the vascular supply to the optic nerves might well be the toxic mechanism# Multiple sclerosis was suggested as the.basis for the optic lesions# Arsenic was thought of - and. evidently dlsalssed, but not on evidential grounds. Lead, almost `- inevitably,' caae under, scrutiny, and a.case w s& ja a d e vigorouslv by i w (S ig n atu red Examiner) -M.D. (CONTINUE REPORT DOWN FROM HERE) of the ephttebrologists (Drs, Kyriakides and Damitz) for the significance . or tne patient1a occupational exposure to lead. Several points are noteworthy In connantlpn with the hypothetical incrimination,of lead in the etiology of I f r . f l P H ^ o o n d i t i o n t r , .; ; Cl) It does not appear that this factor was. even taken seriously by any one, including the physicians'tit the Cleveland Clinic .or the Crile Veteran's Hospital, at the tine of onset and development. It seems evident that the, occupational aspect of the case, in relation to lead absorption, was n o t ; - regarded as a sufficient justification for the analytical determinations of the lead content of the urine or blood, despite the fact that this has come to be the normal or expected procedure when it la suspected that lead is a factor It is unlikely that this.was merely ignored (our analytical facilities have been called upon by Cleveland Clinic physicians for years in asuspected eases of lead intoxication); rather it was not believed that this patient had sustained significant exposure to lead. The only indication in tiie record that either lead .or arsenic was under serious consideration, initially, even for the purposes of diagnostic exclusion, is the eommunicatioi of Dr, Hargraves of the Kayo Clinic, who reported the finding of O.Ol mg. of lead per liter of urine (approximate date January 9 or 10, 1958). The r finding with respect to arsenic was not even reported, .and It is evident that it was regarded as insignificant. This single instance of finding an in- , significant concentration of lead (and arsenic) in the urine was not followed up with further analysis, a n d ,it is evident that the analysis was done merely as a part of a "fishing expedition". The result was not considered to he of any consequence, and even its negative value, as evidence, has been Ignored by all.of the physicians*.. . ........ > . ., .; . ( 2 ) l n the foregoing connection, while the finding of a low normal -,'0 concentration of lead in one sample of urine (volume not stated)!has.little diagnostic usefulness, requiring as .it does confirmation in other ways, and.liifi especially by the determination of the concentration'b lead In the blood, in relation to the lead content of the body, it cannot" he ignored utterly. f1ok The onset of this man's illness appears to have been in the spring (April i/ or Ray) of 1957. If he had lead poisoning at this time'of sufficient ' V ' severity to g i v e `rise to encephalopathy (in retrospect), in association ` % with a distruotlve 'lesion of. the optic,nerves, he must have .been subjected ,, to severe (not borderline) exposure to lead, and he must have absorbed a r large quantity of load* (Neither encephalopathy nor neuropathy is known to. , have occurred except, ini consequence of the absorption of unusually large ,, ^ quantities of vlead.^ These are the most severe forms of saturnism known, '*' and they are growing rare because industrial exposure to lead, while common, - occurs .to a less severe degree than it did formerly. It is necessary to -.- -.i establish that an unusual degree of absorption has actually occurred,.in order to substantiate either of these diagnoses.) If Mr; Austin had large quantity of lead in his body in the spring of 1957, he would not have eliminated them so completely.fr his body by January 1958 as to have low normal,levels of _ lead concentration in his blood and .urine* Relatively high'levels,persist ,, for much longer periods of time. The blood was not examined, and .the one piece of (inadequate) evidence available to us is .the low normal concentr&fcioi of lead In the urine. As such, it suggests, .without proof, that .Sr.'Austin, did not have abnormal quantities of lead in his body,. If anyone had r e a l l y .', believed that lead was the responsible agent, this was,the time to establish the facts by further'investigation. This was not done, and in vieW'of the eminence of the physicians who examined Mr. Austin, during the period when this might well have been done, it seems highly improbable that they consider ed lead to be the likely cause of his tragic condition; 5 (5) Such evidence (inadequate) as is available supports the probability that lead was not the toxic agent in this instance. . , . ~ lead* (a) There is no plausible history of occupational exposure to The work in which this man engaged could* perhaps, have provided f' '' ; V ' - : (DO NOT W R IT E 'B E L O W T H IS L IN E )________________________________ ' ' i'/v ; . ' .... i' ' __ ' vj ' OV .:S C- 0000207 0000208 Optic neuritis due to lend is a severe manifestation of load poisoning and is associated, only lit* the absorption of large quantities of lead* it is also associated with some of the other clinical manifestations of extensive lead absorption* such as -characteristic digestive disturbances* typical nmiromsaeular abnormalities and hematologic chafes of more or leas, characteristic type* fho failure in the appearance of any of these necessary diagnostic criteria* tends to eliminate lead from consideration in this case* and leaves 'the ease* as described at the Voteram Hospital in Cleveland m one l,cf unknown etiology1*# . Signed: Robert A . Kdho, M.D. x :