Toxicidade Do Chumbo

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E L S E V I E R

T h e J o u r n a l o 1 ' E m e rg e n c y M e d i c i n e . Vo l 1 6, N o 2 , p p 1 7 1 - 1 7 7 , 1 9 9 8C o p y r i g h t © 1 99 8 E l s e v i e r S c i e n c e I n c .P r i n l e d i n t h e U S A . A l l r i g h t s r e s e r v e d

0736-46 79/98 19 .(X) + .00

PI I S0736-4679 97)00283-7

S e l e c t e d To p ic sT o x i c o l o g y

H E A V Y M E TA L T O X I C I T Y PA R T I1: L E A D A N D M E TA L F U M E F E V E R

K i m b e r l i e A. G r a e m e , M D , * 1a n d C h a r l e s V. P o l l a c k , J r. , M A, M D, FAC EP *

*Department of Emergency Medicine, Maricopa Medical Ce nter. Phoenix, Arizona, and -i-Department of Medical Toxicology,Go od Samaritan Regional Medical Center, Phoenix, Arizona

Reprint Address Charles V. Pollack, J r., MA, MD, FACEP, P.O . Bo x 37936, Phoen ix, AZ 85069-79 36

[ ] A b s t r a c t - - T h i s r e v i e w i s t h e s e co n d o f a tw o - p a r t r e v i e wof heavy me ta l t ox ic i ty. Th i s pa r t w i l l i den t i fy the sa l i en tf ea tu res o f the tox icopa th ophys io log y, c lin i ca l p resen ta t ion ,a n d e m e rg e n c y d e p a r t m e n t m a n a g e m e n t o f le a d t o x i c it yand me ta l fum e feve r. © 1998 E l sev ie r Sc ience Inc .

[ ] K e y w o r d s - - l e a d ; m e t a l f u m e f ev e r : h e a v y m e t a l s ; c h e -l a t ion

L E A D ( P B )

L e a d i s a n A n g l o - S a x o n w o r d f o r t h e e l e m e n t in i ti a ll yk n o w n b y t h e L a t i n w o r dplumbum which s e rves a s t her o o t o f p l u m b i s m , m e a n i n g l e a d p o i s o n i n g ( 1) . H i p -poc ra t e s de sc r ibed l ead co l i c i n a me ta l ex t r ac to r i n370 B .C . By 200 B .C . , l e ad exposu re had been co r r e l a t edwi th pa l lo r, cons t i pa ti on , co l i c , and pa ra ly s i s ( 2 -4 ) . Leadpo i son ing , f rom bo i l i ng g rape j u i ce i n l e ad po t s and f roms to r ing and cu r ing beve rages i n l e ad - l i ned con t a ine r s ,may h ave con t r i bu t ed t o t he f al l o f the Ro man Emp i re .Lead p ipes bea r ing t he i n s ign i a o f Roman empero r s a r es t il l in serv ice today (1 ,4 -7) . In the 18th and 19th cen-tu r ie s , p lum bi sm ma y have l ed to a dec l i ne o f t he Br i t ishuppe r c l a s s , c aused by t he i r heavy consumpt ion o f po r twine (5 ,6 ,8) .

More r ecen t ly, t he r e have been ca se s o f l e ad po i son -ing because o f t he u se o f Mex ican po t scalledjarros andcasuela~ which a r e g l azed w i thgreta ( lead oxide) (4 ,5) .M e x i c a n - A m e r i c a n s i n Te x a s , N e w M e x i c o , A r i z o n a ,Ca l i fo rn i a , and Co lo rado con t inue t o u segreta and az-

arcon ( lead te t roxide) to t rea tempacho ( fo lk i l lness)2 , 5 , 9 , 1 0 ) .

Cl in i ca l l y, man-made con tamina t ion i sof grea t e rquan t i t a t i ve s i gn i f i cance t han na tu ra l l y occu r r ing l ead(11 ). Lead has been u sed heav i ly i n i ndus try. I n t he ea r ly1900s, occup a t iona l l e ad exp osu re by i nha l a t i on o f dus tand fumes was r ecogn ized by Hami l ton , a pa tho log i s t ,who p ionee red i ndus t r i al con t ro l o f occupa t iona l l e ade x p o s u r e . A g a i n s t t h e r e c o m m e n d a t i o n o f H a m i l t o n ,l eaded gaso l ine was i n t roduced in to t he Amer i can mar-

ke t in 1923 , w i th peak consum pt ion i n 1970 . Lead wasemi t t ed f rom veh ic l e exhaus t s a s an o rgano lead vapo r,most ly as ha l ides . In the Uni ted Sta tes , the recent reduc-l i on i n l e aded gaso l ine u sage has r e su l t ed i n a markeddec rease i n t he popu la t i on ' s mean b lood l ead l eve l(11 ,12) .

In 1904 , G ibson co nc luded tha t l e ad pa in t i n the hom ewas r e spons ib l e fo r po i son ing ch i ld r en . Lead w as no tbanned f rom Amer i can househo ld pa in t s un t i l 1977(2 ,4 ) . Pa in t app l i ed be fo re 1950 o f t en con t a ined h ighamou n t s o f le ad ca rbona t e and abou t 74% o f p r iva t e lyowned hous ing bui l t in the Uni ted Sta tes before 1980

con ta in s l e ad -based pa in t ( 13 ) .O the r common sou rces o f l e ad exposu re i nc lude

put ty, indus t r ia l fa l lout , ba t te r ies , Por t land cement , waterf rom l ead p ipe o r l e ad - so lde red j o in t s , impor t ed can nedfoods , l e aded g l a s s a r t work , cosme t i c s , an t i que pewte r,f a rm equ ipmen t , i l l i ci t i n t r avenous d rugs , j ewe l ry , andhome r enova t ion . Lead t ox i c i t y may a l so r e su l t f rom are t a ined bu l l e t o r f rom p ro longed exposu re t o f i r i ng

RECEIVED: 11 M ar ch 1996 ; FINAL SUBMISSIONRECEIVED: 17 Ja nu ar y 1997;

ACCEPTED: 29 Jan ua ry 1997

171



1 7 2 K . A . G r a e m e a n d C . V. P o l la c k J r.

Ta b l e 1 . R i s k F a c t o r s f o r C h i l d h o o d L e a d E x p o s u r e 5 0 )

• S e c o n d y e a r o f li fe• H i s t o r y o f le a d p o i s o n i n g i n a s i b l in g o r p l a y m a t e• His tory of p ica• Liv ing in a house bui l t before 1960

• Paren ts wo rk in a lead indu s t ry• R e s i d e n e a r a n a c t i v e le a d i n d u s t r y

r anges . I ndus t r ia l sou rces o f l e ad expo su re i nc lude l eadsme l t e r s , ba t t e ry r ec l ama t ion p roces so r s , r ad i a to r r epa i rshops , and l ead pa in t f rom sh ips and b r idges when theunde r ly ing me ta l i s cu t w i th an ace ty l ene t o r ch(2 ,4 , l 1 ,14-23 ) .

Toxicopathophysiology

Lead tox i c i t y may be caused by o rgan i c o r i no rgan i c l e adpo i son ing . Lead po i son ing i n humans u sua l ly r e su l t sl ¥om ino rgan i c l e ad , bu t o rgan i c l e ad po i son ing mayoccu r i n t hose who inha l e ga so l ine r ec r ea t i ona l ly. Thep r inc ipa l o rgan i c l e ad com pou nd in ga so l ine i s t e t r ae thy llead , which i s conver ted in the body to t r ie thyl lead andinorganic lead (24 ,25) . Inorganic lead inc ludes sa l t s ofl ead f rom a l l sou rces . Lead fo rms coo rd ina t i on com-plexes wi th su l fur, n i t rogen, and oxygen, and exer ts i t stoxic , e ffec ts by combining wi th su l fhydryl groups inp ro t e in s , t hus i nh ib i t i ng su l fhyd ry l -dependen t enzymes

(26).Lead may be abso rbed t r ansde rma l ly, t h rough inha l a -

tkm, or by inges l ion . Inhala t ion in to the lungs i s the mostco m m on route ~k)r adul t s , how ever, lead par t ic les tend tot r ave l up t he mucoc i l i a ry e sca l a to r and t o be swa l lowedinto r~he gastr ointe st inal tract . In adults , 10 of lead thatpasses through the gas t ro in tes t ina l (G1) t rac t i s absorbed;in ch i l d ren , up t o 50 o f l e ad may be abso rbed . Somesa l t s o f l e ad a r e abso rbed more qu i ck ly and more com-ple te ly, leading to a more rapid , acute d isease . I rondef ic iency increases the r i sk of lead toxic i ty (2 ,4) .

Svmptomatology

The sy mp tom s o f l ead t ox i c i ty a r e o f t en vague and ma ya r i s e acu t e ly, even t hough the po i son ing i s u sua l l ych ron i c . I n t odd l e r s , ano rex i a i s t he ea rl i e s t symp tom o flead poisoning, fo l lowed by vonf i t ing and i r r i tab i l i ty.Hyp e rk ine t i c beh av io r, d i s t rac t i b il i ty, im pu l s ivenes s , andanemia may be s een i n ch ron i c l e ad exposu re s (3 ,27 ) .The r i sk fac tors for ch i ldho od lead exposu re are l i s ted inTab le 1. S igns and sym ptom s o f ch ron i c exposu re i nadu l t s may inc lude ch ron i c r ena l f a i l u r e , hype r t ens ion ,

ar thra lg ias , te ra togenes is , and impotence (2) .

Acu te t ox i c i t y u sua l l y a r i s e s f rom su i c ida l and homi -c ida l exposure to so luble lead sa l t s . Af ter inges t ion orin j ec t i on o f t he se compounds , t he onse t o f symptoms i sr ap id and t he s enso r ium may be dep re s sed w i th in hou r s(28 ) . Acu te exposu re i s a s soc i a t ed w i th hemolys i s andacute hepatorenal fa i lure .

Gaso l ine sn i f f e r s become in tox i ca t ed w i th in 5 r a in o ft ak ing 10 -1 5 d eep i nha l a ti ons and r ema in i n tox i ca ted fo r3 t o 6 h . The i r symptoms a r e l a rge ly due t o t he hyd ro -ca rbon so lven t and p redominan t ly i nvo lve t he cen t r a lne rvous sys t em (CNS) , i nc lud ing euphor i a , r e s t l e s snes s ,d i s inh ib i t i on , and ha l l uc ina t i ons ; GI symptoms , i nc lud -ing nausea , vomi t i ng , and hunge r, and ca rd iovascu l a rsymptoms , i nc lud ing b radyca rd i a and hypo tens ion , maybe s een . Af t e r con t inued exposu re , ev idence o f l e adtox i c i t y i nc lud ing t r emor, weaknes s , con fus ion , cho rea ,man ia , convu l s ions , a t ax i a , musc l e damage , hepa t i c andrena l damage a r e s een . The anemia s een f r equen t ly w i thino rgan i c l e ad t ox i c i t y i s uncommon wi th o rgan i c l e adexposu re (24 ,25 ) .

System Review

The sys t ems p r imar i l y i nvo lved i n l e ad t ox i c i t y i nc ludethe ne rvous , c a rd iovascu l a r (CV) , GI , gen i tou r ina ry(GU) , and hemopo ie t i c sy s t ems (27 ,29 ) .

CNS Ti l e deve lop ing CNS i s t he p r inc ipa l t a rge t o rganfor lead in chi ldren (30) . Lead readi ly enters the bra inand i s s e l ec t i ve ly depos i t ed i n t he h ippocampus andcor tex (12) . I r r i tab i l i ty, dul lness , headache , t remor, fa -t i gue , ha l l uc ina t i ons , and memory l o s s a r e ea r ly symp-toms . A t h igh l ead l eve l s , encepha lopa thy w i th r i sk s o fpe rma nen t men ta l r e t a rda t ion , mo to r def i c it s , and dea thoccu r s . The encepha topa th i c synd rome inc ludes de -pressed sensor ium, vomit ing , i r r i tab i l i ty, a taxia , coma,se izures , and la tera l iz ing neurologic s igns (27 ,31 ,32) .

PNS Weakness and l oca l pa l s i e s , such a s a wr i s t d rop .

a r e s een w i th p lumbi sm. Pe r iphe ra l neu ropa thy i s morecom mo n in adu l ts t han i n ch il d r en . The deg ree o f pe -r i phe ra l neu ropa thy does no t co r r e l a t e w i th t he b loodlead level or wi th the length o f exposu re (2 '7,33) .

CV Chron ic l e ad exposu re m ay cause r enal and sys t emich y p e r t e n s i o n ( 3 4 - 3 6 ) .

GL Abd omina l pa in, ano rex i a , cons t i pa t i on o r d i a rrhea ,nausea and vomi t ing , and a me ta l l i c t a s t e i n t he mou thmay be no t ed . I nges t i on o f r ap id ly abso rbed l ead s a l t scauses an acu t e synd rome o f hepa t ic i n ju ry a s soc i a t ed

wi th hemolys i s (37 ) .



Lead and Metal Fume Fever 73

GU Acute lead toxic i ty a l te rs the renal tubular funct ion ,r e su l t i ng i n aminoac idu r i a , g lycosu r i a , hype rphospha tu -r ia , and prote inur ia (38) . In chronic lead exposure , in ter-s t i tia l nephr i t i s , reduced g lom eru lar f i lt ra t ion ra te , andnonspec i f i c p rox ima l t ubu l a r dys func t ion a r e t yp i ca l ;gou t a l so may be s een (39 ,40 ) .

Hemopoietic Seve ra l enzymes i n t he heme syn the t i cpathway are par t ia l ly inhib i ted by inorganic lead , resul t -i ng i n a mic rocy t i c , hypoch romic anemia (27 ,41 ) . Fu r-the rmore , i nges t i on o f r ap id ly abso rbed s a l t s c auses anacu t e synd rome o f hemolys i s , wh ich i s a s soc i a t ed w i thhepat ic in jury (37 ,42) . Lead a lso in terac ts wi th an en-zym e ac t i ve in the b r eakdow n o f r i bonuc l e i c ac id (RNA ) ,r e su l t i ng i n c lumping o f r i bosoma l RNA, ev idenced bybasoph i l i c s t i pp l ing o f e ry th rocy t e s on pe r iphe ra l b loodsmears (Figure 1) (41) .

Musculoskeletal Lim b and jo in t pa in s a r e ea r ly sym p-toms o f acu t e l e ad t ox i c i t y (43 ) . I n ch ron i c p lumbi sm,l ead is depos i t ed i n te e th and bones , w i th 90% o f bodyburdens ly ing w i th in bone . I n ch i l d ren , l e ad l i ne s canbe r ad iog raph ica l l y v i sua l i zed a s opac i ti e s a t the m e taph -ysea l p la te (Figure 2) . The radiopaci t ies represent toxice ff ec t s o f l e ad on bone g rowth r a the r t han l ead depos i -t ion in bone (44) .

Fetal and teratogenic Lead c ros se s t he p l acen t a andminor congen i t a l anoma l i e s such a s hemang iomas , l ym-

phang io mas , and s t r ab i smus ma y be a s soc ia t ed w i th h ighco rd l ead l eve l s (45 -47 ) . Low b i r t h we igh t s , p r e t e rmde l ive ry, and poo r men ta l deve lopmen t have a l so beenrepo r t ed w i th e l eva t ed ma te rna l and co rd l ead l eve l s .Lead i s t ransfer red in breas t mi lk , but usual ly cont r ibutesl i t t l e t o t he i n f an t ' s body bu rden (4849) .

Figu re 1 . Basoph i l i c s t ipp l ing o f RBCs a s s een i n l e ad tox i c -i ty. Pho tog raph cou r t e sy o f The Reg iona l Drug and Po i son

In fo rma t ion Cen te r fo r New Je r sey. )

F igu re 2 . Lead l i ne s i n t he h and bon es o f a ch i l d w i th ch ron icl ead exposu re . Rep r in t ed w i th pe rmi s s ion , Ma la t ac k J J ,B la t t J , Pench ansky L . Ped i a t r i c hema to log y and onco logy.In: Z i te l l i BJ , Dav i s HW , eds . S l i de a t l a s o f ped i a t r i c phys i ca ld i agnos i s , 2nd ed . London : Gow er M ed ica l P ub l i sh ing ; 1992).

Diagnosis

Both u r ine and b lood l ead l eve l s can be measu red . Tra -d i t i ona l l y, who le b lood l ead l eve l s (BLL) and e ry th ro -cy t e p ro topo rphyr in (EP) l eve l s we re u t i l i z ed . Due t or ecen t l ower ing o f accep t ab l e l e ad l eve l s by t he Cen te r sfo r D i sea se Con t ro l (CDC) , EP a s says a r e no l onge rsu ff i c i en t l y s ens i t i ve fo r s c r een ing (50 ) . Howeve r, EPs tud i e s may r ep re sen t ch ron i c t ox i c i t y and me tabo l i ca l l y

ac t ive lead . With organic lead toxic i ty, EP assays are nota lways e l eva t ed ; BLLs a r e u sua l l y e l eva t ed . The CDCnow r ecom men ds B LLs / 'o r s c r een ing . A B LL o f l e s sthan 10 /xg/dL is cons idered nontoxic (50) . Adul ts to l -e r a t e h ighe r BLLs than young ch i ld r en .

Of t en , t he se l abo ra to ry s tud i e s a r e pe r fo rmed a t c en -t ra l s ta te I t )ca t ions , resul t ing in de layed conf i rmat ion ofthe d i agnos i s; t he r e fo re , examina t ion o f pe r iphe ra l b loodsmea r s fo r ba soph i l i c s t i pp l ing o f e ry th rocy t e s may behe lp fu l . A comple t e b lood coun t , s e rum i ron , i r on -b ind -ing capac i t y, e l ec t ro ly t e s , b lood u rea n i t rogen , c r ea t i -n ine , and u r ina ly s i s a r e he lp fu l i n i den t i fy ing concomi -

t an t i r on de f i c i ency and r ena l damage . Rena l func t ionshou ld be a s se s sed i n l e ad -po i soned pa t i en t s be fo re be -g inn ing che l a t i on w i th e thy l ened i amine t e t r aace t i c ac id( E D TA ) w i t h B A L b e c a u s e 1 6% d e v e l o p a n e p h r o t o x i creaction (51 ) .

Rad iog raphs o f l ong bones and r i b s o f ch ron i ca l l yexposed p re schoo l - aged ch i ld r en may r evea l l e ad l i ne s .Lead l ines in the smal l bones , such as the u lna and f ibula ,i nd i ca t e a l e ad exposu re o f a t l e a s t s eve ra l mon ths 'dura t ion (44) . In acute inges t ions , rad iog raphs o f theabdomen may r evea l r ad iopaque l ead . A compu ted t o -m o g r a p h y ( C T ) s c a n m a y o r m a y n o t d e t e c t c e r e b r a l

edema in pa t i en t s w i th l e ad encepha lopa thy (52 ) . X- r ay





L e a d a n d M e t a l F u m e F e v e r 1 7 5

Table 3 . Lea d Tox ic i ty : C l in i ca l C lues Diagnos t i c Tes t s and Therap ies

Clinical Clues Diagno st ic Tests Therapies

His tory of r isk factors :Ch i ld ren - - see Tab le 1Adu l t s - -wo rk in l ead indus tr i es

re ta ined bul le t /pel le tf i r ing range exposurepaint /gas ol ine sniffing

Com bina t ions o f t he fo l lowing :Unexp la ined anemiaPer ipheral ne uropathies wris t and foot drop)Tremor and a t ax iaMental s ta tus and mood changesGI sym ptom s pain , const ipa t ion, vomit ing)Hepa t ic in jury wi th h emolysis

acute lea d salts)Renal failureHyper tensionArthralgias

Urine levelsB lood l ev e l s - -wh o le b lood l ead level

Erythrocyte protop orphy r in level

Rad iog raphs - -KUB fo r opac i t i e sLong bone and r ibs for lead l ines

CT b ra in - - a s ses s fo r ce reb ra l edem a

X-ray f luo rescence - -a s ses s bo ne bu rden

Periphe ra l b lood sm ear- -baso ph i l i c s t ipp l ing

First l ine of therapy:DMSA if not encep halopa thic)

o r DMPS

Second l ine of therapy:BAL and Na2CaEDTA*if encephalopathic)

* There is l imi ted informat ion on us ing DMSA fo r lead encephalop athy and some rec om me nd using BAL fol lowe d by Na2CaEDTA.

and i s e spec i a l l y common a f t e r exposu re t o z inc ox idefume s 64 ) . W orke r s i n foundr i e s , mar inas , and sh ip -ya rds a r e a t g r ea t e s t r i sk . Worke r s who ga lvan i ze andwe ld h ave t he h ighes t i nc idence o f MFF, bu t t hose whogr ind and b ronze may a l so p re sen t w i th MFF.

The MFF i s a poo r ly unde r s tood in f luenza - l i ke o rma la r i a - l i ke r eac t i on t ha t i s a ccompan ied by an acu t e ,se l f - l imi ted neut rophi l a lveol i t i s . A leukocytos is i s

present dur ing the acute i l lness . The pa thogenes is i spoo r ly unde r s tood ; a l l e rg i c and immuno log i c mecha -n i sms a r e mos t o f t en pos tu l a t ed . One t heo ry ho lds t ha tloca l in jury resul t s in inf lammat ion wi th the re lease of ah i s t amine - l i ke subs t ance , f o l l owed by t he fo rma t ion o fan a l l e rgen complex , r e su lt i ng i n an t i body fo rma t ion andan a l le rg ic resp onse 62 ,64) .

To l e r a n c e t o m e t a l f u m e s d e v e l o p s a n d s y m p t o m sappea r on ly a f t e r exposu re t o me ta l f umes fo l l owing ape r iod o f abs t i nence . A MF F w i ll no t occu r on subse -quen t succes s ive days o f fume exposu re . To le r ance i sd i r ec t l y p ropo r t i ona l t o the l eukocy tos i s 62 ,64 ).

A M F F m a y b e o v e r l o o k e d o r m i s d i a g n o s ed a s as imp le v i r a l in f ec t ion , uppe r r e sp i r a to ry i n f ec t i on , pneu -mon ia , s eps i s, o r even m a la r i a because i t is cha rac t e r i zedby an ab rup t onse t o f f eve r, shak ing ch i l l s , ma la i s e ,excess ive sa l iwt t ion , th i rs t , nausea , myalg ias , headache ,cough , and r e sp i r a to ry d i s tr e s s ; t he cha rac t e r i st i c m e ta l -l i c t a s t e i n t he mou th may a id i n mak ing t he co r r ec td i agnos i s . Leuk ocy tos i s d eve lops 2~ to 5~ h a f t e r exp o -su re. Th i r s t , cough , and a me ta l l i c t a s te deve lop a t 3 -1 0h . Ch i l l s gene ra l l y l a st 20 - 30 r a in , bu t may ex t end up t o3 h . Feve r gene ra l l y peaks a t 5 -12 h a f t e r exposu re andma y pe~ :s is t f o r 4 t o 1 I h . S ym ptom s gen e ra l l y r e so lve

spon taneous ly w i th in 24 -4 8 h 62 ,64 ).

Two other i l lnesses must be cons idered in the d i fferen-t ia l d iagnos is of MFF. Fi rst , a m ore ser ious form o f MF F isassocia ted wi th smoke genera ted by a chemical reac t ion ofburning hexachlore thane , z inc oxide , and a luminum, asoccurs in de tonat ions of smoke bombs. The syndrome iss imi lar to typica l MFF, wi th an acute onse t tha t remi tsear ly ; however, th is more ser ious form is charac ter ized byre lapse and s igni f icant morbid i ty and mor ta l i ty. Exposure

usual ly occurs in a mi l i ta ry envi ronment , but has a lso beenreported in f irefighting training mad in civil defense andter ror is t exerc ises where m i l i ta ry smoke i s used . Sym ptom susua l ly beg in w i th in 2 h o f exposu re and r emi t ove r 6 - 10h. A severe re lapse occurs a f te r 24 -4 8 h . Relapse mayinclude fever, tachycardia , and gray d iscolora t ion of theskin . A dry cough gradual ly becomes product ive . By the2rid to 4th day of i l lness, wheezes and crackles are heard.Pu lmona ry edema and shock may occu r. Symptoms maylas t up to 14 days and m ay be fa ta l 62).

The s econd i l l ne s s t o cons ide r i s c admium pneumo-n i ti s. Acu te i nha l a t ion o f cadm ium ox ide fumes may

cause MFF o r pneum on i t i s . Th ree s t ages o f lung dam agea f t e r c admiu m o x ide i nha l a t ion a r e de sc r ibed i n r a ts : 1 )acu t e pu lmona ry edema , occu r r ing w i th in 24 h and l a s t -ing 3 days ; 2) pro l i fe ra t iv e in ters t it ia l pneu mo ni t i s oc -cu r r ing 3 -10 days a f t e r exposu re ; and u l t ima te ly 3 ) pe r-manen t l ung damage wi th pe r iva scu l a r and pe r ib ronch ia lfibrosis 65).

When eva lua t i ng pa t i en t s w i th su spec t ed MFF, aches t r ad iog raph shou ld be ob t a ined , a l t hough the re a r eusua l ly on ly s l i gh t o r no r ad iog raph ic changes . Leuko-cy tos i s may be de t ec t ed w i th a comple t e b lood coun t .Ur ine s c r eens can con f i rm me ta l exposu re , bu t a r e ex -

pens ive and r a r e ly i nd i ca t ed .



176 K.A . Graem e and C. V. Pollack Jr.

T r e a t m e n t i n c l u d e s r e m o v a l f r o m t h e s o u rc e , a n ti p y r e t-

i t s , h y d r a t i o n , o x y g e n , b r o n c h o d i l a t o r s , a n d r e s t. M o s t p a -

t i en t s c a n b e m a n a g e d a s o u t p a ti e n t s , b u t p a ti e n t s e x p o s e d

t o m i l i t a r y s m o k e s h o u l d b e h o s p i t a l i z e d f o r 4 8 h .

I n t r a v e n o u s s t e r o i d s m a y r e d u c e r e s p i r a t o r y t r a c t

i n j u r y in p a t i e n t s w i t h s e v e re M F F o r c a d m i u m p n e u -

m o n i i t i s . C o r t i c o s t e r o i d s a r e a l s o i n d i c a t e d f o r p a t i e n t s

w i t h a h i s t o r y o f e x p o s u r e t o z i n c c h l o r i d e a n d w i t h

i n t e r s t i t i a l i n f i l t r a t e s o n c h e s t r a d i o g r a p h . C h e l a t i n g

a g e n t s h a v e n o t b e e n s t u d i e d s u f f i c i e n t l y i n t h e m a n -

a g e m e n t o f s e r i o u s M F F .

S U M M A R Y

L e a d p o i s o n i n g a n d M F F a r e i n f r e q u e n t l y e n c o u n t e r e d i n

t h e e m e r g e n c y d e p a r t m e n t ; h o w e v e r , e a r l y r e c o g n i t io n o f

t h e s e p o i s o n i n g s i s e s s e n t i a l f o r e f f i c a c i o u s t r e a t m e n t a n d

e p i d e m i o l o g i c t r a c k i n g o f a c c i d e n t a l e x p o s u r e s . S i g n s

a n d s y m p t o m s a r e n o n s p e c i f i c , m a k i n g a t h o r o u g h h i s -

t o r y a n d p h y s i c a l e x a m i n a t i o n e s s e n t i a l i n a c h i e v i n g a n

a c c u r a t e d i a g n o s i s . H e a v y m e t a l p o i s o n i n g s a r e o p t i -

m a l l y m a n a g e d i n c o n s u l t a t i o n w i t h a t o x i c o l o g i s t o r

r e g i o n a l p o i s o n c e n t e r .

R E F E R E N C E S

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