Document wrBqp2OrZM7Zg8KYODypyp1KD

' who ja w s tliaf excessive or pathologic contraction. induced by solution ot pituitary, is potentially 0f pathologic sates. There is an obvious reason ''-olrsuoa oi pituitary, given immediately after the delivery i '^ b y , does not frequently cause trouble. It requires from ? ja twenty minutes to produce a hard contraction of the lj by this means, and in the majority of instances the gga will have been delivered before the expiration of that ^ It seems unnecessary to give solution of pituitary imme- (jfy after delivery of the baby, when 700 out of 1,000 (2 are delivered with less than ZOO cc. of blood loss, and ( sasoe 2 per cent develop hemorrhage. I hope that Dr. Ijdl wm substantiate his routine by presenting his figures 5*j of blood. ?; lhe leaa maustry aim ll IV. uiu...- and toys, informed of the danger to small children from the ingestion of lead paint, have cooperated by sub stituting other types of pigments for the lead pigments formerly used. New cribs are seldom painted with lead paint, and the better grades of toys are largely free from lead pigment.1 Painted woodwork and painted furniture continue to present sources of lead available to the child. Intoxication following the ingestion or inhalation of lead appears to be dependent on a number of factors. Of primary importance are the amount of lead ingested and the period of time over which it is taken in. The absorption of small amounts of lead by all persons, TtEA D POISONING IN CHILDREN whether in urban or in rural populations,- seems to be l CHARLES F. McKHANN, M.D. of normal occurrence and is said to be unaccompanied by danger.* An increase in the amount of lead ingested, AND <4. ft.- EDWARD C VOGT.' M.D. BOSTON x 54. or the continuation of absorption over a period of time, may lead to intoxication. Age is a third factor of importance. Children appear more susceptible to severe Jie continued occurrence of lead poisoning in intoxication than adults. A similar observation is made h jr e n , despite the efforts of physicians, health paes. and insurance companies to disseminate gjjBxadan concerning this preventable disease, warcS-the presentation of a review of certain phases of Sssadition and a further report of the cases observed -rfaa clinic. in experimental animals, for likewise the young animals seem more susceptible to lead poisoning than do the adults of the same species. In addition to the influence of age on susceptibility to lead, there is observed con siderable individual variation in tolerance to the metaL Some children, after the ingestion of moderate - ' amounts of the metal, rapidly develop encephalitis. SOURCES OF LEAD Others are capable of tolerating quite large amounts poisoning in infants may follow the prolonged with the minimal development of symptoms but with, lead nipple shields; *1*567in Japan poisoning has however, the deposition of abnormal amounts of lead jturred frequently from-the use by the mother of face in the body, a condition which we designate latent lead pfjigg containing lead.* In infants and older children @ iagestion, over a fieriod o f time, of water containing Ta u 1.-- A g e Incidence o f Lead P oisoning in In fa n t? and fei small amounts of lead, may result in intoxication, C hildren's H ospitals, Boston, 1924-1933 gssatly there was reportedpan.extensive series of cases Tfed poisoning following the inHalation of fumes in ' ... S o . C l M where storage- battery casings were used as y>j However, most frequently the ingestion of'lead bt result of the habit observed in small children, of unusual substances.*. ................................... ... * 4 to 6 y e a x a ...^ . .. s ^Perversions of appetite, designated pica, leading to T o ta l .................. >iagestion of foreign substances such as sand, coal, hair or piaint are observed in mentally defective S3 neurotic children, in those suffering from anemia ip . in those harboring intestinal parasites. In the sHjority of cases of lead poisoning due tb ingestion of the'pica has apparently been merely a pernicious unrelated to any underlying abnormal condition, incidence of lead poisoning (table I) is highest in slants and small children in whom teeth are erupting sad in whom there is a great tendency to put things i the mouth. poisoning, for under certain circumstances s u c h : .".' patients may mobilize the lead deposited in apparently inert form and thereafter develop serious manifestAr- tions. ' sy m ptom s 1 Usually the ingestion of lead in small amounts has taken place over a period of weeks or months before * symptoms are noted-' The early manifestations are- ., traceable to disturbed- function of the gastro-intestinal v tract. Anorexia, constipation, vomiting and abdominal l?ro*a. th e D e p a rtm e n t of P ediatric*, H a rv a rd M edical School. a n d th e [feeac' t t \A C h ild re n '* H o spital*. before the Section oo Pediatrics a t the Eirirty-Fottrth A nneal CTaa cd rise A m erican M edical A aeobarioa, M ilw aukee, Jtm a 15, 1933. 1 &o W ilcox, i L B ., an d C ailcy. J . P . : L e a d P oiaom nf in N u rsin g . R eport of Tw o C ases iSue to U se- of Lead N ippia Slbekia^ U, A . M x 1514 (M ay 15) 192A. '.&! (e) H ira i, I . : M eningiam ia Sockirac* in J a p a n from L ead Pot*ow , Arch, P ediat. 4 4 : )37, 1927. ( b) Fukuabim a, M ., and U a tn n o t s , Statistics of Taro H undred and N inety-Eight Cases of Infantile Lead . O rient. J . D rv In fan ts 3 t 27, 1928. (c) Kata. K atsa/i: Lead t tat I n f a n ta : R esu m e oi Jap an ese C ontributions on. the D i*r* i of T P oiso n in g in Nuralxna*, A n . J . Eh*. C hild. 4 - 4 : 56$ t) IfJ2. '$. W J K , - H .; S c h u lte . W . H .; R otbchild, H . B .; B row n, A . P ^ Sezstkv V. R ., J r . : L ead Poisoning fro m tb e B urn in g of B attery _ iaca, J . A . M . A . 1<MM 1485 (M ay 13) 1933. Z 4. T&oama. H . M .. Blackfan, K. D .: R ecurrent M eningitia D an i Lead in a C hild of F ir e Y ear*, A n . J. Di*. Child. 8 x 3 7 7 (N ov.) 1914. C. F .: L ead P o iso o m f in C hildren, ibid. 3 3 x 384 (S ep t.) Stroue, R. A .: M eningitis Caused by Lead Poiaoning in a Cnild N ia e m e a iio n th a , A rch. P ediat. 3 7 : 532. 1920. Ruddock. T. C .: L ead w in Children with Special Reference to Pica, J. A. M. A. 8 3 s (M ay 24) 1924. cramps are commonly, observed,' associated with; a variable degree of anemia. More serious symptoms---'' are those referable to the central nervous system. Peripheral neuritis, the usual accompaniment of lead-' intoxication in adults," is observed, infrequently, in.^ children, particularly in-the younger age groups where-rt t-h--e---d-e-v--e-l-o-p-m---e-n-t---o--f--e-n--c-e-p-h--a-l-i-ti-s---i-s-'--m--o--r-e---c-o--m--m--o-n--.* "~?t, 5. P ersonal m m m u n |P ip n to tbe author* o i a ru rv ry of c rib tojr* *.*' m an u factu re r* m ade by tb e L end In d u strie * Associa tio n , accrcxary, F . EUf - . 6. R e bo*. IL A .: E d g a r, G rah am } T h a m e s * , F red , a n d . S a n d e r* L ester: T b* E x c retio n o f L e n d by N orm al Persona. J . A . M . A* I T f - - 2081 (Dec. 18) 1926. Keboe, R. A .; T h amann . F ., and Cbolak, - On the Normal Absorption and Excretion of Lead: L Lend Absorption ' - . and Excretion in Prim itive L ife; II. Lead A bsorption and Excretion in T . . M odern American L ife; IV . Lead Absorption and E xcretion ur-G nidre*. J. In d iu t. H yg., to be published. 7. M cK h in n , C. F . : L ead P oisoning in C h ild ren : T he C erebral M aw . - feetationa. A rch . N curoi. Sc PfycfaiaL 3 7 t 2 9 4 - (F e b .) 1932. -- E v i d e n c e s of the o*'set of encephalitis are a change in s h e mental state of the child and more persistent vomit ing. frermently of projectile character. Visual distur b a n c e s . alteration in rates of pulse and respiration, delirium. stu|H>r. coma or convulsions may ensue. These manifestations often are accompanied by an elevation of the blood pressure, choking of the optic disks and. in extreme cases, separation of the cranial sutures. W hen death occurs it follows a period of T able 2.--Additional D it on Lead Poisoning from the Infants' iaid Children's Hos*it,ils. 1V24-19.13 S u m te r o f p a tie n t? w ith lead in to x ic a tio n ..................................................... 77 S u m te r of p a t e n t s w ith encvpholitic s y m p to m s ............................. .. 4*. D eatho fro m lead e n c rp h a lltl* ......................................................................... 11 S u m t e r o f p a tie n ts w ith ncurltl* w ith o u t r n r r p h a li tl f ......................... 4 X V ra a n fn t w u i r l a e in 12 p a tie n ts , a s follow*: C o n ru te io n s persisted In .............................................................. 4 C ere b ra l a tr o p h y ............................................................................ 4 T rem o ro ............................................................................................... 2 M ental re ta r d a tio n ......................................................................... 6 M uscular w eakness ......................................................................... 2 Blindsepfl ............................................................................................. .1 Steeefa d efec t .................................................................................... t K um te? of p atien ts with roentgen eridenc** of lend. Inn with m inim al s y m p to m s, la ten t !cal p o is o n in g " ............................................................... 12 Total number of eases of plumhlsm c o m a o r convulsions and appears to be clue to central r e s p i r a t o r y failure, as the heart continues to beat for s o m e t i m e after respirations cease. Although localized lesions such as minute hemor r h a g e s and cellular infiltrations have been found in the b r a i n s of patients who have succumbed to lead encepha litis.98 it is possible to attribute the train of symptoms observed in the disease to the rapid development of generalized, in e rte d intracranial tension due >n intense c e r e b r a l edema. Cerebral edema in a child with lead poisoning present ing cerebral symptoms \ms observed by Chvostek in 1 8 9 7 . A young girl with lead poisoning developed headache, vomiting, a slow pulse rate, coma, choked disks a n d vasomotor disturbances. At necropsy the meninges w e r e clear.. The whole b*ain appeared swollen, the c o n v o l u t i o n s were flattened, the medulla was pressed i n t o the foramen magnum, and the ventricles were very small. This description of the gross appearance of the brain in children succumbing to lead encephalitis has b e e n c o n f i r m e d repeatedly. W e l l e r 8 studied the pathology of lead encephalitis in experimental animals and observed a similar intense c e r e b r a l edema. We also have produced lead encepha litis in animals and in the course of our experiments h a v e confirmed Weller's observations. I f a c h i l d survives severe lead encephalitis there f r e q u e n t l y remain sequelae indicating cerebral injury o f a p e r m a n e n t nature. Cerebral atrophy or degenera t i o n m a y become manifest in cerebral palsy, epilepti f o r m seizures or mental deficiency. By encephalography t h e extensive nature of the injury may be demonstrated. A l t h o u g h lead is known to be deposited in the brain a n d may directly injure or kill the nerve cells, the destruction of brain tissue which is observed need not be e x p l a i n e d by a specific action of the metal but may be attributed to degenerative processes resulting from 8. Okubo, A - and Tanaka. H .: flisto-Pathological Changes in Lead Poisoning. J . P ediat. (T okyo), no. 304. p. 1325. 1925. 9. W elle?. C. V .. and C hristensen. A. D .: The C erebrospinal Fluid in Lead Poisoning, Arch. N eurol. & Psychiat. 1 4 : 327 (S ept.) 1925; T h e C erebrospinal Fluid in Lead Poisoning, chap. 29 in T he H um an Cerebrospinal F luid. The Association for Research in N ervous and M ental D isease, New Y ork, P au l D. H oeber, In c., 1924. impaired circulation to the brain during the prolrjn state of intense cerebral edema. `^ While an encephalopathy is the usual form of ] poisoning seen in infants and children, milder tvi*^-1 intoxication are encountered which, although not ,| '* gerous to life, are of great ini|>ortance in that ti"!!!" recognition may result in the prevention of the Ml,"r serious and frequently fatal encephalitis. Xeuriti, |'fe been mentioned. (Jastro-intestinal disturbances a*' present in almost all cases. In addition to those svn rt toms and ~igns which have been mentioned, the tion suddenly oi large amounts of lead may. by |f)CaJ irritation, induce bleeding into the lower intestinal tr^ with the passage of fresh or changed blood in n,1 stools. Occasionally also the kidneys arc irritated that a transient albuminuria or hematuria is observed Glycosuria was seen frequently in our more severe cases, especially those with encephalitis. There considerable doubt as to whether the elevated blood sugar level and glycosuria were due to injury to the pancreas, or whether they were of the type designated as cerebral and observed in other forms of encephalitis The incidence of lead encephalitis in the series oi cases of lead poisoning observed since 1924 in this clinic is shown in table 2. The relatively high fatality rate and the frequency of permanent sequelae are to be noted. D IA G N O S IS Lead encephalitis must he distinguished from other types of disease with cerebral involvement, notably various forms of encephalitis and meningitis. The his tory of ingestion of lead and the presence of symptoms of gastro-intestinal disturbance preceding the develop ment of cerebral manifestations suggest lead poisoning. In our opinion the cerebral manifestations are evi dences only of the cerebral edema and are not pathog nomonic of lead intoxication. Xor are the changes in the cerebrospinal fluid of diagnostic importance in dis tinguishing lead intoxication from other forms of T able 3.--Determination} of Lead and Calcium in the Cortex of the Shaft of the fem ur and in the Lead Line at the Growing End of the Femur * Calcium. Mr. ter Grn. of Boot Cortex of shaft......... ....... Lead line................... ....... coo.o 83J Lead, Mr. per Ora. of Bone 0.114 0.602 Lftd. Jtf. Calcium, Gau 0.546 7,210 * By Themlc*l examination the lead line waa found In this eaae ta contain over Arc times as much lead per cram of bone aa did the cortex of the shaft, uirile the Icad/calelum ratio (column 3) waa thirteen times aa creat In the lead line aa In the shaft. Chemical examinations im made through tha courtesy of Dr. L. T. fairhalL encephalitis. In cases of lead encephalitis the spinal fluid escapes under increased pressure, oftentimes as high as from 600 to 700 mm. of water pressure. The fluid is clear and colorless, contains usually a trace of globulin and shows an elevation of the total protein. Occasionally a slight pleocytosis is observed. Examination of the. blood for basophilic stippling of the red cells is of diagnostic aid. Stippling of the red blood cells is not, however, pteculiar to lead poisoning, nor is it found even with constancy in cases of the disease. Particularly it is likely to be absent in cases of so-called latent lead poisoning,, and it may be absent even in children showing definite symptoms of intoxi cation. In ptatients and experimental animals the num bers of stippled cells in the circulating blood vary front ai.rt L E A D P 0 1 S 0 X 1 S G -- M c K H A X S AMD i>UL l ami reflect perhaps more accurately the level troscopic examination.13 This determination is said to ,jt ot lead in the blood than the total amount permit an exact diagnosis of the presence of lead within lv or the amount deposited in certain organs twenty-four hours after blood is withdrawn from the icing svinptoms referable to these organs, vein of the patient. ul line observed in the gums of adults suffer The demonstration of lead in the excreta of children e d intoxication is found rarely in children. by chemical examination is not adequate evidence nt ;\v of our patients had a lead line in the mar- intoxication, as it has been shown by Kelioe 1 and con he g u m s . When present the lead line is a firmed in this clinic that normal children excrete small ijirn' although it must be distinguished from amounts of lead in the urine and stools. However, ncs produced bv other heavy metals, notably patients with lead poisoning excrete much larger amounts of the metal than do normal children, so that , the most useful aids in the diagnosis of quantitative determinations of lead in the excreta, prop i in children are the recently recognized erly appraised, may be accepted as satisfactory evidence in the bones demonstrable by roentgenogram, of plumbism. hanges. recognized independently by Park.10* TREATMENT and one of us (E. C. V .)13 in this country Although it is impossible within the scope of this arious foreign investigators,13 consist of zones paper to discuss the chemistry of lead in the body, a ised density at the growing ends of the long brief statement may aid in the understanding of the d at the margins of the flat bones. The devel- suggested methods of treatment. of these changes appears to be dependent on Aub and his co-workers 10 have pointed out that lead ;ased deposition of lead in place of calcium in in the body is absorbed, transported, deposited and .ving ends of the long bones, as well as on a excreted much as is calcium, so that, in general, factors abnormality in the microscopic structure of s formation. The results of chemical analysis tone substance of the dense band as compared it of similar material taken from the shaft are ia table 3 and indicate that there is a definite : in lead in the dense bands observed at tbe yseal margins of the long bones. Microscopic ation shows further that in cases of plumbism beculae in these rapidly growing parts of the ire more numerous and are more closely packed* r than in normal bone. change in the bones has proved to be one of constant observations in lead poisoning in n, and has led to the discovery of numerous vith minimal symptoms or with unustial clinical stations. Rarely has the lead line in the bones bsent. In one patient, 20 months of age, a diag- jf lead encephalitis was made and confirmed by ral analysis of the excreta for lead, but the diag- lead line in the bones was absent. The child ved gradually and within a few weeks had devel- the definite dense band found in lead poisoning. / lines in the ends of the long bones are not a r to lead poisoning, as the ingestion of phos- F ig . 1.-- A , d en se tra n sv e rs e band* at th e grow ing en d s of th e lo n g bone* observed in a child with lead poisoning. B , roentgenogram of the long bones of the same patient four month* later. Note the greater b read th oi the band*. s and other substances may produce similar * Narrow lines of sufficient density to be con- with a lead line may be found at the ends of the bones in healing rickets and in infants with u'n A deficiency. Occasionally in the normally ing child there may be a zone of increased density e metaphyseal margins of the long bones, owing to a heavy deposit of calcium. These lines should confused with the lines observed in lead poisonwhich are of greater density and width (fig. 1). which influence calcium metabolism might be expected to have an influence on lead. Lead is absorbed through the lungs or intestinal tract and, in rare instances, through the skin. It is carried in the blood stream presumably as the phosphate and is deposited in various organs, especially the brain, liver, pancreas and bones. Lead deposited in the organs of the body may induce the symptoms referable to the various systems, but lead deposited in the bones is in an inert form. Thus in irther confirmation of the presence of lead in the relieving lead poisoning measures are usually recom irospinal fluid or blood may be obtained by spec mended which tend to hasten the removal of lead from the circulation and the deposition of the metal in the Park, E. A , in discussion of M cLean. Stafford: T he Bone Lesion* ejenital Syphili*. Am. J. D is. Child. 3 9 : 899 (A p ril) 1930. P ark. bones. To this end calcium salts1* or phosphates11 ; Jackson. D eborah, and K ajdi. Laslo: Shadow* Produced by Lead e X-Ray P ictu res of the G row ing Skeleton, ibid. 4 1 : 485 (M arch) Caffey, J . P .: Clinical and Experim ental Lead Poisoning: Some are administered to diminish the solubility of lead in the blood, and viosterol is given to hasten the growth eenologic a n d A natom ic Changes in Growing Bones, Radiology 1 7 x 19J1. Vogt, E . C .: A R oentgen Sign of P lurabiira, A m . J. Roentgenol. 350, 1930; R oentgenologic D ia g n o sii of L ead P o iso n in g in In fa n t* C hildren. J . A . M . A 9 8 : 125 (J a n . 9) 1932. Koga, S ato an d K ashahara. cited by K ato. K ., and K ra ft. E .: ifeubefunde bei B le iv e rg iftu n g e n ira K in d esalter, F o rts c h r. a. d. Geb. ontgenstrablen 4 6 : 249, 1932. Phem ister. D. B .: The Effect of Phosphorus on G rowing, Normal Diseased B ones, J . A. M. A 7 0 : 1737 (Ju n e 8) 1918. 15. K im u r* * n d LTchida, cited by K ato .14 S h ip ley , P . G .: S co tt, T . F . M ., and Blum berg, H .: T he S pcctrograpbic Detection of Lead in the Blood as an A id to the C lin ical D iagnose* of Plum bi*m , BulL John* Hopkin* Hosp. 5 1 : 327, 1932. 16. A u b . J . C .; F a irh a ll, L. T . ; M inot. A . J .. an d R cxnikoff, P .: L e a d P oisoning, M edicine 4 : 1, 1925 (a co m prehensive d iscu ssio n o f tb o chem istry, physiology and other aspect* of lead poisoning). )7. Shelling. D. H .: Effect of D ietary C alcium an d Pbo*phoro* a T oxicity of Lead in the R at: R ationale of Phosphate T herapy, P roc. Soc. E x p e r. BioL & M ed. 3 0 : 2 4 8 . 1932. ni' Imhic. Tlie efficacy nt tlioe therapeutic measures i> difficult to evaluate, as the milder eases of itituxicatinu show prompt improvement it the ingestion of lead is prohibited ami if the child remains tree from infec tion and in a good state of nutrition. Removal of lead from the Ixxly. or deleading, may !>e accomplished by inducing an acidosis or an alka losis. by deprivation of calcium or by the administra tion of parathyroid cxtract-Collipri' In view of the fact that acute infection or the development of acidosis may induce symptoms in a child who harbors lead in the bones but who has been symptom-free for a period of time, and furthermore because efforts at deleading have resulted in the recurrence of cerebral symptoms, we have given up the attempt to delead our patients. effects. It would appear [hat life can lie prolonged or maintained by the use of drugs which control the con vulsive seizures, hut the unfortunate sequelae cannot he prevented by these substances. In the more severe cases separation of the sutures of the skull |Us occurred, resulting in relief to the patient through spontaneous cerebral decompression. The pressure required to accomplish this decompression is great and may account for the permanent cerebral injury that is so common among the children who survive the acute encephalitic stage. The following case illustrates the course of severe hut nonfatal lead encephalitis: REPORT OF A CASE R. M,, a girl, aged 2'A years, was admitted to the hospital because of anorexia, drowsiness and tremors of three days' duration. For three months she had vomited, suffered frocs abdominal cramps and been constipated. The history revealed that for four and a half months she had been chewing paint from the woodwork and furniture of the house. After admission to the hospital she remained in a stuporous state, refused food, continued to vomit almost everything taken, had constant tremors of the extremities and periodically suffered from generalized convulsions. Examination of the blood showed a moderately severe anemia, with numerous stippled cells present in the smears. Roent. genograms of the long bones showed definite lead lines. The blood pressure was elevated. Severe papilledema developed rapidly, and over a period of three weeks the sutures of the skull gradually separated (fig. 2 A and B ). The spinal fluid was found to be under greatly increased pressure; globulin was present, the sugar content was normal and the cell count was elevated, ranging in various examinations from 19 to 31 mononuclear cells. Therapy directed toward hastening the deposition of lead in the bones as well as measures designed to relieve increased intracranial tension were apparently without effect on the course of the disease. An operative procedure, in the nature of a widespread flap decompression, was contemplated but was not performed. Following the spontaneous* decompression, whether or not because of it we cannot say, she began gradually to improve. The tremors subsided and the vomiting ceased. As she became less stuporous it was apparent that she had become mentally defeetive and that she was almost totally blind. With the dis appearance of papilledema the optic disks became very pale. Encephalograms made seven weeks after admission and three weeks after the subsidence of symptoms of increased intra cranial pressure showed considerable cerebral atrophy as evidenced by markedly enlarged lateral ventricles and an exersa of air over the cortex (fig. 2 C). Further observation of the child over a period of several months indicated that her mental condition gradually improved and fortunately her visioa returned at least in part, but she remained obviously and probably permanently retarded mentally. , : | J j 1 i * i j ! I [ > F if . 2.-- A , roeB tfw jofrm m o f tb* tk u ll of R . M . cm h er adm iM ioo to be hoapitaL No abnorm ality is noted. B , roentgm ofram of the tirull three weeks a fte r adm ission, showing the su tu res widely separated. C. encephalogram sere* w eeks after the onset and three weeks after the baidence of sym ptom s of lead en c ep h alitia . C ere b ra l atro p h y is evi d e n c e d in th e m a rk e d ly e n la rg e d v e n tric le s a n d th e ex cess o f a ir o v e r the cortex of the brain. Although danger of return of the symptoms of lead poisoning persists for some time, it gradually subsides owing to the spontaneous elimination of the metal. The treatment of children who have already devel oped lead encephalitis is not satisfactory. Lead deposited in the brain appears to induce intense cerebril edema which is highly resistant to the ordinary methods of combating cerebral edema. Intravenous injections of magnesium sulphate or of hypertonic solutions of salt or dextrose have had only temporary 18. A ub, J. C .. an d H u n te r. D .: L ead S tu d ie s : X V . T h e E ffect o f th e P arath y ro id H orm one on the E xcretion of Lead an d of Calcium in Patients Suffering from Lead Poisoning, Q uart. J. M ed. 2 0 1 12J, 1927. In view of the failure of therapy in children with cerebral manifestations of lead poisoning, we have been prompted to undertake the experimental investigation of lead encephalitis. By means of organic lead salts given by mouth it was found to be possible to induce with great regularity a fatal type of lead encephalitis in rats, guinea-pigs and rabbits. After a few days the animals developed tremors which were followed by generalized clonic convulsions. After a variable period of convulsions death ensued from respiratory failure. . .Measurements of the blood pressure of guinea-pigs in ; the stage of tremors or convulsions of lead encephalitis showed an elevation almost" 50 per cent above the normal level established by similar determinations in control animals of the same ages and weights. The brains of animals succumbing to lead encephalitis showed the intense edema described by Weller. Thus lead encephalitis induced experimentally in guinea-pigs resembled in many aspects the disease as a^rv-,1 111 ini:int> ami children. A lter priKlucinj; and uJviuiI the m:imie>tatinit> o f lead etteeplialitis in iic.ard o f tMC.tv t;uinea-|iivis. w e undertm ik to test i'e etticicy o f varimi? il.era iv n tic agents. T im s far 1 n a -eric* o f over titty anim als we have been m .ahle to ntluence the course <>f the d isease if treatm ent has ^ei. delayed until the anim al is in a state o f con vu l- i,,ns. Control o f the con vu lsive seizures has been ^co.nplished hv the use o f m agnesium sulphate, pheno- varbital. pentoharhital-sotlium . autytal or paraldehyde, .cull considerable prolongation o f life but w ithout effect in the final outcom e. T he parenteral adm inistration o f aJciutn salts, sodium salts, including phosphates, iodide, thiosulphate, ferricyanide and thiocyanate, and other Irugs which theoretically m ight have som e effect on the .olubility o f lead in the blood or the deposition o f the metal in the body, has been tried w ithout influence on :he course o f the disease. O ther m eans o f com bating lead encephalitis in experim ental anim als are now- under investigation. -------- SUMMARY A diagnosis of plumbism can be made in children in the early stages of intoxication by the correlation of the history, physical signs and laboratory data in con junction with the roentgenologic findings. Cerebral manifestations seldom occur in patients who receive, at this stage of the disease, treatment directed toward hastening the deposition of lead in the bones. Although, progress has been made and is being made in the underhanding of lead encephalitis, the treatment of patients with lead encephalitis remains in an unsatisfactory state. TThe attack on lead poisoning in childrey must be made largely through prophylactic measures. Realiza tion by physicians of the dangers to ctt.ldren of the continued ingestion of lead and the dissemination to mothers of information on the subject should result .in prevention of the disease. ABSTRACT OF DISCUSSION Dr. R. A. K e h o e . Cincinnati: I shall emphasize a few coasts made by the authors and speak briefly on lead excretion. Although lead encephalitis occurs in adults, it is relatively rare? treat ring only when massive doses of lead have been absorbed, la children, on the other hand, it is not infrequent. It is of articular interest and importance that in children with lead jmsoning there is a striking tendency for symptoms of the teatial. nervous system to develop, indicating the fundamental lifference in the disease in children and adults. Encephalitis in children, as in adults, has a bad prognosis. From available figure* one concludes that the prognosis in children and the outlook for complete recovery are even somewhat worse than in adults. The preventive as{*ct oi this problem should therey fore be greatly stressed. Since the authors' figures have shown that this condition occurs at the period when children are most likebAto eat abnormal things and to chew various objects in diei^kvironment. pediatricians should be alert to note abnormal appJBfe and behavior. Pica being the most frequent cause of lead poisoning in children, strenuous efforts must be devoted t'eliminatin*TH3<i from their environment. This situation is rery serious in Queensland. A targe number of cases have been reported, presumably because children play on weathered, lead-painted verandas where the lead pigments have dusted out to the. surface. The contributions of the roentgenologist to the diagnosis of lead poisbning are among the most significant in V our day. and it is an unfortunate limitation that they are appli cable only to children. This sign oi the line in the bones is extremely important. Recognizing, however, that it may not ; always be possible to differentiate this line from certain other densities that occur on the epiphyseal end, it is of some conse quence to stress the diagnostic importance of lead in the excreta. It ha> been siiuun nevuiia w% ivas>>><uic uouui mat normally in the excreta of children, as of adults. The quantity oi lead that may lie found under normal conditions is small. 1 he levels ui lead m the excreta that can he demonstrated to have clinical siumhcance are comparatively well defined. It is thus possible, with accurate analytic methods, to recognize the probable existence nut only of lead poisoning but also of lead exposure in unusual amounts, both in children and in adults. This method, as an adjunct to the much quicker and much more convenient x-ray method, will aid materially the correct diagnosis of lead poisoning in children. D r. Robert A. S trong. New Orleans: In 1914 I reported a case oi lead encephalitis in a child 18 months old and at the time I could find only six other reports in young children, although the literature at the time seemed to indicate that it prevailed extensively among adult workers in the lead industry in France. As the authors have stated, physicians must be lead conscious in order to tie able to elicit lead poisoning. A considerable amount oi lead poisoning has been overlooked in these little patients. Since hearing papers such as Drs. McKhann and Vogt have presented, I have been more alert. I have seen three cases in New Orleans during the past winter in which the lead line was demonstrable. Unfortunately, the cases had advanced until the central nervous system was involved and consequently the cases were not amenable to treat ment. The authors have called attention to the fact that stip pling of the cells is by no means common to lead. Dr. Foster Johns, of the department of clinical medicine at Tulane. had his attention called to a widespread mortality among wild ducks around the hunting grounds on the Gulf Coast of Louisiana. An examination of the blood of these ducks revealed the cause of the mortality. His observations were similar to those made by Dr. McGrath of the Mayo Clinic a few years ago. When the gizzards of the ducks were opened, it was found that they were filled with lead shots such as are used in hunting ducks. The shot removed from the gizzards were about one-third the size of shot that have never been used. These ducks died from lead poisoning as a result of mistaking the shot in the bottom of the lagoons for the small stones they usually ingest. The authors have informed me that they have received the coopera tion of some of the manufacturers of toys and other articles which find their way into the hands of children and have received reasonable assurance that they will use something other than lead in the paints used in coloring these articles. Dr. K a t s c j i K a t o , Chicago: This presentation on lead poisoning reminds me of conditions in Japan. It is rather unusual in this country to see so many cases as Drs. McKhann and Vogt have experienced in Boston in a period of nine or ten years, for even in Japan there is an average annual figure of about ten cases of lead poisoning in the larger pediatric clinics. I am anxious to point out that among various forms of lead poisoning there is one particular type to which but little attention has been paid in the past; namely, congenital saturnism, or lead poisoning. In Japan the source of lead has been chiefly in the form of face powders. At present the government requires the use of titanium instead of lead in the manufacture of cosmetics. In spite of this, lead is still being used in a certain percentage of face powders, because lead seems to give a better spreading effect on the skin. The authors informed me that the pregnant mother has a greater tolerance for lead, owing to the fact that the metal is taken up in the rapidly growing bones of the fetus. The Japanese mothers continuously use lead-containing cosmetics on their necks, faces, shoulders and breasts during pregnancy, often to the extent of veritably white washing the exposed parts of ihe body. This would strongly suggest the possibility of congenital origin of lead poisoning in new-born infants. In certain* cases of congenital hydro cephalus. may it not be reasonable to suspect intra-uterine lead poisoning as its cause? Again, in some cases of spastic paral ysis of the limbs, with or without convulsive seizures, which are usually thought to be due to intracranial hemorrhage, con genital lead poisoning may be a possibly cause. This suggests at once that the so-catlcd lead lines at the metaphyses of long bones in the new-born infant presenting suggestive symptoms should be looked lor by making roentgenograms. This is impor tant both in diagnosis ^nd in treatment