Document NN2Nd6EyGy6K0OJ1b74J9D65R

F CARDIAC M E C H 4N IS JI - th at it is impossible now to say : cardiac mechanism to normal of nodal extrasystoles added to very short P -R intervals (0.10 ne of the two necessary requirebeats arising in Tawara's node,3 ventricle should contract simulme should be distinctly shortened 0.17 second). The other requirelar activity, should be of altered in the second beat of each pair nervous condition of the patient me to obtain records free from literature a rhythm made up of one of each of these records has spite of the fact th a t Lewis and arising at an appreciable distance ity or inversion of the P wave. A esbyterian Hospital of New York1 cases of apparent nodal rhythm to a prolonged P -R interval equal iiac cycle, so th a t P of one cycle Whether true nodal rhythm can the form of P is a point th a t is well he gradual lengthening of the P-R gitalis without change in the form short P-R interval of both cycles , arising in Tawara's node, but to ulses arising in the sinus node and actively. As the chief factor in the the delay caused by' the passage of )undle,s one must assume th a t the was due to positive dromotropic th a t these influences disappeared iers, as did the bathmotropie influextrasy'stoles. About the possible nductivity, however, there is pracler clinical or experimental, arrhythmia is described in which a z in different parts of Tawara's node onduction time (P -R interval) with ; (pulsus bigeminus). liectrocardiography, p. 50__ >m D r. S tro n g . :ts. Phy3., 1909-1910, cxxxsi, 572. a LEAD POISONING IN CHILDREN WITH ESPECIAL REFERENCE TO LEAD AS A CAUSE OF CONVULSIONS.1 \ B y K e n n e t h D. B la c k f a n , M .D ., BALTIMORE, W *RTLAND .:: W e are indebted to the Australian writers Gibson, Love, Turner, - Breinl and Young and others for much of the recent literature regarding lead poisoning in children- They have had an unusually ; good opportunity to study this condition. Thus, in the Brisbane Children's Hospital, 76 cases were seen in five .years and Gibson himself observed 24 cases in six years. A w '- v - I shall not attempt to give a complete review of th e literature .on the subject, as the chief object of this communication is to :draw attention to lead as a cause of convulsions in children and to report 4 cases seen in Dr. Howland's clime at the Harriet Lane Home, the Johns Hopkins Hospital. For the more important articles, the reader is referred to those from which I have freely quoted.12 - ' The symptoms of lead poisoning vary' according to the suscepti bility of the child and to the duration of the infection. The degree of susceptibility is variable. Breinl and Young refer to many instances - in which only one child in a family was affected, although the other children were exposed to the same influences. In other instances, one child reacted with pronounced symiptoms while the .only evidence of infection in the others was a blue line on the gums. Gibson3 considers the ingestion of lead as the most likely source of infection, although he appreciates th at it may occur from the inhalation of dust containing lead. H e points out th a t children of 1PFerdoimatritchse, JHoharnrsieHt oLpakninesHUonmivee. rJsoithyn.* Hopkin-s Hospital, and the D---epartment - Gibson, Love, Hardie, P. Bancroft, Jefrris Turner: Notes on Lead Poisoning as Observed in Children in Brisbane, Intercolonial Medical Congress of Australasia, Sydney, 1S92, p. 76. Gibson, Lockhart: Ocular Neuritis Simulating Basal Menin gitis Plumbism, Australasian Med. Gaz., October 20, 1897, p. 479. A Plea for Painted Railings and Painted Walls of Rooms as the Source of Lead Poisoning Among Queensland Children, Australasian Med- Gaz., 1904, xriii, 149. The Import ance of Lumbar Puncture in the Plumbar Ocular Neuritis of Children. Tr. Austral asian Med. Congress, 1911, ii, 750. Breinl and Young: The Occurrence of Lead Poisoning Among North Queensland Children. Ann. Trop. Med. and Parasitol.," 1914-15, viii, 475. Turner, JeSris: Lead Poisoning Among Queensland Children, Australasian Med. Gaz., 1897, October 20, p. 475. 3A Plea for Painted Railings and Painted Walls of Rooms as the Source of Load Poisoning Among Queensland Children. Australasian Med. Gaz., 1904, xxiii, 149. blackfan: T.E4D poisoning in children who bite their fingernails and suck their fingers are much more frequently affected, and believes th at their hands became contamin- ated with dried paint from porch railings and houses. T h at poisoning may occur through inhalation has been shown by the expert- VSiments of Goadby and Goodbody* and by Legge and Goadby.5' f-f They conclude th a t the danger from inhalation is far greater than from the ingestion of lead. While this, no doubt, is true among .'if workers in lead, the swallowing of lead in some form is probably ; the more common source of the poisoning in children... In the early cases a change in disposition is often the first. symp--T tom which is noticed. The child becomes fretful, peevish, and often ^ very restless at nights The appetite becomes poor, the breath foul, and frequently hemorrhages occur from the gums. The child may .complain of pain in the epigastrium and legs. V t's'llsSP* r v In the cases of longer duration the pains in the abdomen become--? continuous and more severe. Constipation is present, as a rule. :.i Vomiting rarely occurs. The muscles are often so painful as not to 'permit of. the weight of the bed-clothing. The gait of the patients is Tj ^described as being characteristic. I t is a waddling gait; they walk - on the outside of the feet, the toes are dragged, and with each step the legs are swung sideways before the feet are put to the ground. Yt, Occasionally the parents' attention may be attracted by one o n r^ "` more of the many indefinite signs enumerated above, but not^H infrequently nothing abnormal is noticed until the development oEy cerebral disturbances. The cerebral manifestations will be referred.-;-0' to later. - V * . : Very few of the cases reported by Breinl and Young showed the characteristic wrist-drop so common in adults. This has been-Y ' the experience of others, and generally the paralysis first affects the- gl,. legs in children. A paralysis much like that of the Aran-Duchenney* tvpe_ occurring in muscular dystrophy has been reported in 2 cases.y .Paralysis of the cranial nerves is very' common; the facial and theE motor oculi nerves, either entire or in part, are those most frequently^ involved. Gibson6 has reported a most interesting group of eye symptoms which he refers to as a " plumbic ocular neuritis." The neuritis^ usually occurs in children below the age of eight years. There mayyp be an optic neuritis, with retinal hemorrhages, or an optic atrophy^ IThere is an accompanying weakness of one or both extemalnecf" . muscles. He has seen as many as 9 such cases in a year, but firth 22 cases reported by Breinl and Young only 1 patient-was?! affected. ' > - 1 -- "v h v ; V-A c/.-Yv/. - ' 4Seventh International Congress of Applied Chemistry, 1909, Section v i ll a . A * Poisoning and Lead Absorption, London, 1912, p. 122. 1 Ocular Neuritis Simulating Basal Meningitis' Plumbism, Austral. Med^CIa**^ . October 20, 1S97, p. 479. The Importance of Lumbar Puncture in thePIumblcgs Ocular Neuritis of Children,. Tr. Austral. Med. Congress, 1911, ii, ToO- VVVAhY BLACKFAN: I.PU i The temperature is, as a rule elevated. In the fatal cases, disturbances, it may be high, i Very often the clinical symi diagnosis of lead poisoning, cases. However, when there dences of the condition are ust the blue line on the gums and : granulations are present i n a s in the majority of the cases, characteristic, although there i apparently is determined by tl Direct evidence of lead poison of lead in the urine or feces. Ir tions of Breinl and Young are eight children with early signs of epigastrium and legs, but withe lead line, and found appreciabL They found there was always a the urine, and th a t it was often not be demonstrated in the u: quantities of lead present in th. have made this observation, anc in the urine is not so common nc From the foregoing summary seen in lead poisoning in children fication of the cases into different has to be based on the severity of instance, one patient may presen disease, one m ay show only irrifc abdomen, whereas another may b with convulsions while in apparent attendant upon establishing a < Jeffris Turner3 speaks of four mar 1. Paralytic cases showing symi spasm of the calf muscles, and as talipes equinus; (2) cases character limbs, concomitant with habitual blue line on the gums, the child irritable and neurotic; (3) childre a neuritis involving the optic, at motor nerves; (4) eclamptic cases sistent convulsions which often ei ' In the cases reported from Aust 7Forensic M edicine and Toxicology, Loud *Lead Poisoning Among Queensland Chi 20, 1S97, p. 475- USWfiWf..-=e A Si:/ ''-- IN CHILDREN ir fingers are much more r hands became contaminand houses. T h at poisonteen shown by the experi- by Legge and Goadby.* lalation is far greater than no doubt, is true among in some form is probably ig in children. don is often the first symps fretful, peevish, and often :omes poor, the breath foul, the gums. The child may id legs. tins in the abdomen become ation is present, as a rule, re often so painful as not to ;. The gait of the patients is . a waddling gait; they walk dragged, and with each step : feet are put to the ground, lay be attracted by one or enumerated above, but not red until the development of lanifestations will be referred / Breinl and Young showed ion in adults. This has been the paralysis first affects the re th at of the Aran-Duchenne has been reported in 2 cases. / common; the facial and the part, are those most frequently isting group of eye symptoms ;ular neuritis" The neuritis ige of eight years. There may icrrhages, or an optic atrophy. ; of one or both external recti such cases in a year, but in the ifoung only 1 patient was so d Chemistry, 1909, Section V illa , 306. , 1912, p. 122. ngitis Plumbism, Austral. Med. Gar.. of Lumbar Puncture in the Plumbic Med. Congress, 1911, ii, 750. . 1 - BLACKFAN: LEAD POISONING' IN The temperature is, as a rule, normal, though it may be i r r e g u l a r ly ^ ^ ^ ^ elevated. In the fatal cases, and especially those with cerebral Jg| disturbances,"it may be high, reaching 105 or 106 before death." Very often the clinical symptoms are not sufficient to warrant a diagnosis ,of lead poisoning. This is especially true in the early cases. However, when there are suggestive symptoms other evi- dences of the condition are usually to be found. Among these are the blue line on the gums and stippling of the red cells. Basophilic granulations are present in a small number of red blood corpuscles in the majority of the cases. The blood otherwise shows nothing characteristic, although there may be a secondary anemia. This * apparently is determined by the duration of the tx)isonmg.~%.2ri:-A-r^:-uy%^ p jp: Direct evidence of lead poisoning is obtained by the demonstration; of lead in the urine or feces. In this connection the recent observa-y^rii .3~*|prjf tions of Breinl and Young are most interesting. They examined eight children with early signs of the disease, i. e., slight pains in the epigastrium and legs, but without basophilic granulations and the lead line, and found appreciable quantities of lead in the e x c re ta .^ y > 1 ^ J ^ 1 fc They found there was always a larger amount in. the feces than in -* the mine, and th at it was often present in the feces when it could yYC'- not be demonstrated in the urine. Dixon M ann7 found larger. : quantities of lead present in the feces than in the urine. Others v -y ; -r.. have made this observation, and Legge and Goadby say that lead in the mine Is not so common nor definite a symptom as supposed. From the foregoing summary of the more common clinical signs 'Qrj. seen in lead poisoning in children it is evident that a definite dassi-'^S fication of the cases into different groups is difficult, and when made has to be based on the severity of the predominating symptom. For 1 instance, one patient may present the characteristic picture of the ' disease, one may show only irritability and indefinite pains in the yy abdomen, whereas another may become paralyzed or may be seized with convulsions while in apparent health. In spite of the difficulties - attendant upon establishing a classification for lead poisoning, Jeffris Turner8 speaks of fom main groups as follows: - ' *>$> 1. Paralytic cases showing symmetrical wrist-drop and foot-drop; spasm of the calf muscles, and as a secondary lesion, a persistent . talipes equinus; (2) cases characterized by pains in the abdomen and - limbs, concomitant with habitual constipation, and an occasional blue line on the gums, the children becoming a t the same time irritable and neurotic; (3) children suffering from ocular neuritis, '. a neuritis involving the optic, and a t the same time the oculo motor nerves; (4) eclamptic cases suffering from severe and per sistent convulsions which often end fatally. In the cases reported from Australia, convulsions were observed TForensic Medicine and Toxicology. London, 1908, p. 4S7 (C. Giffim & Co.). 8Lead Poisoning Among Queensland Children, Australasian Med. Gaz., October 20, 1897, p. 475. BLACKFAN : LEAD POISONING IN CHILDREN very infrequently, though mild cerebral disturbances were frequently present. T hat convulsions may occur in the course of lead poisoning, has been recognized since the observations of Stockhausen9 in the seventeenth century. The first careful investigation of the cerebral disorders due to lead was made by Tanquerel.10 He grouped them under the term Encephalopathia Satumina. .Though his researches were published in 1SS2, but little attention has been paid to the'. lead encephalopathies except as they are found in adults and in particular among workers in lead. Lead as a cause of convulsions in children has been ignored almost entirely, and especially among observers in this country. : ; . .-'' An interesting and extensive series of cases with convulsions has - been reported by Stewart,11' They occurred among 64-cases, of lead poisoning which he investigated in Philadelphia, due to eating buns colored with chrome yellow. Seven of the 16 eases in which con- avulsions occurred were in children between one and a half years and. 'twelve years-of age. Stewart believed that of the various forms ' of cerebral disorders produced by lead, the convulsive was by far ; the most common--th at it formed two-thirds, if not more, of all the . cerebral manifestations, and that it had the highest mortality. He- i (Stewart) thought it impossible to make, any clinically exact sys-- ktematic grouping of the different'forms of the lead encephalopathies t as Tanquerdf2 did, as one form merges into the other.. kp'. Stewart cites 2 cases of so-called idiopathic epilepsy which were s.secondary to convulsions, symptomatic of lead poisoning, and sug-\ t gested th a t epilepsy of lead origin may be of much more frequent - ^occurrence than is generally supposed-. LT'The macroscopic changes most frequently found in the brain a re : pan edema and anemia,, with flattening of the convolutions.- -The.' kbrain-m ay, however, be markedly congested. There is often a. . thickening-of the pia--it may be adherent to the cortex. There m ay ~ be hemorrhages into the pia and between the pia and the cortex.. v There is also a round-cell infiltration within the pia, and the neuroglia.- ' cells of the cortex are found to be increased. Spiller13 observed a - proliferation of the endothelial cells upon the surface of the cerebral: 2pia. Such pathological findings may occur in other conditions, and' - similar lesions may be found in patients with lead poisoning who: '.' have not manifested cerebral symptoms.: . yv. There is no way by which the convulsive seizures per se~in-lead; l poisoning can be distinguished from those due to other causes.-.fAlL-i 1types of_convulsions are- seen. They may be local or generals i f * Quoted by Stewart (see note 11). * iv Lead Diseased (translation by Dana, 1848), p. 263. v- ^ 11Lead ConvnLnona, A it. Joub-. M ed . Sc., 1895, cix, 2S8. * ' y* r 12Tanquerel established the following divisions: (1) delirious forms; (2):comatOf form; (3) convulsive forms; (4) above forms combined. V* " Jour. Med. Research, 1903, x. No. 1. * .xiiev may De mild or severe, do, however)'have certain pec acteristic of the disease. They a tendency to recur, and they are The persistence of the convul Enormous doses of bromides, c tered to each patient without ca I t was only by the continued us controlled, and when this was c anew. In one patient (Case I) t a period of seven and a half n after a period of eighteen days L each recurrent attack they wen with chloroform. One patient (C attack. The convulsions in one ing. only one day. He was deliri after which he was comatose for s patient serves to support Stewart xjac mgii morranty ot convx Stewart's cases. The terminatin' A series of most remarkable case the fatality of the condition equa . who lived day and night in an fumes, the father suffered from th alopathy.. Seven children died frequent cerebral disorders and Several of the grandchildren diec cases 3 of the 4 patients died. T shown any evidences of a recurre: convulsions during the third atta second attack, and the other (Cas The temperature, which was no (Case I I and Case i n ) , preceding respectively. Such a hyperpvre death from lead convulsions in m Evidences of cerebral involven present. In one patient (Case I) a positive-Kernig sign. He had a rectus muscle of the eye. . Anothi of the neck and a temporary para ; Mosny and Malloizel15 and Plat that there is very generally evident u B erl. klin. W chnschr., 1S74. 15 L a m eningite sa tu rn in e , 1907, xxvii, 5( u U eber einen F ail von M eningitis satu Is, 2343. V_ "V OKING TN CHILDREN ;bral disturbances were frequently ;ur in the course of lead poisoning, nervations of Stockhausen9 in the reful investigation of the cerebral y Tanquerel.10 He grouped them iaturnina. Though his researches e attention has been paid to the they are found in adults and in Lead as a cause of convulsions ost entirely, and especially among ries of cases with convulsions has v occurred among 64 cases of lead a Philadelphia, due to eating buns ren of the 16 cases in which coni between one and a half years and elieved that of the various forms y lead, the convulsive was by far d two-thirds, if not more, of all the it had the highest mortality. He to make any clinically exact sysforms of the lead encephalopathies aerges into the other, led idiopathic epilepsy which were omatic of lead poisoning, and sugin may be of much more frequent Dposed. t frequently found in the brain are ttening of the convolutions. The edly congested. There is often a adherent to the cortex. There may d between the pia and the cortex, don within the pia, and the neuroglia be increased. Spiller13 observed a ells upon the surface of the cerebral may occur in other conditions, and a patients with lead poisoning who mptoms. ie convulsive seizures per se in lead Tom those due to other causes. All They may be local or general. i, 1848), p. 263. ' >. Sc., 1895, cix, 288. ' ; divisions: (1) delirious forms; (2) coms'c^e forms combined. 1. blackfak: head poisoning in cm thnw y ggpA-Aj They may. be mild or severe. :.The convulsions in lead- poisoning 5, do, however, have certain peculiarities which appear to be char-T; acteristic of the disease. They are very persistent, they show a great' 4 tendency to recur, and they are attended by a high mortality.-' -"yyT The persistence of the convulsions is shown in Cases H and IH . A Enormous doses of bromides, chloral, and morphin were adminis- j . tered to each .patient without causing an y effect on the convulsions.^ I t was only by the continued use of chloroform that they could be ty controlled, and when this was discontinued the convulsions began?; anew. In one patient (Case I) there were two recurrent attacks in Af a period of seven and a half months. '-:The convulsions recurred A after a period of eighteen days in another patient (Case II). W ith-y each recurrent attack they were severe, and were controlled only r. with chloroform. One patient (Case H I) died in the first convulsive attack. The convulsions in one patient (Case IV) were mild, last- A ing only one day. . He was delirious a t first, then had convulsions, A; after which he was comatose for several days.' The behavior of this ' patient serves to support Stewart's contention th a t it is not possible y to define sharply the encephalopathies into definite groups.-yddy The high mortality of convulsions due to lead is shown by Stewart's cases. The termination was fatal in 6 of the 7 children. ` A series of most remarkable cases reported by Berger14emphasizes the fatality of the condition equally welL In a pot-glazier's family, ? . who lived day and night in an atmosphere saturated with lead Z fumes, the father suffered from the comatose variety of lead enceph-tf alopathy. . Seven children died in convulsions, Tour others had frequent cerebral disorders and suffered from peripheral neuritis. Several of the grandchildren died in convulsions. In my series of cases 3 of the 4 patients died. The patient who recovered has shown any evidences of a recurrence. One patient (Case I) died convulsions during the third attack, another (Case H ) during the second attack, and the other (Case IH ) during the first attack. . A: The temperature, which was normal on admission in two patients (Case II and Case H I), preceding death rose to 107.5 and 105.5 respectively. Such a hyperpyrexia has been present preceding death from lead convulsions in most of the reported cases. Evidences of cerebral involvement other than convulsions were present. In one patient (Case I) there was rigidity of the neck and a positive Kernig sign. He had also a paralysis of the left external rectus muscle of the eye. Another patient (Case IV) had rigidity of the neck and a temporary paralysis of the facial nerve. Y-- - . Mosny and MalloizeH and Plate 16 and others have pointed out that there is very generally evidence of involvement of the meninges, MBerl. Min. Wcimscbr., 1874. 15La meningite saturnine, 1907, xxvii, 506. ; . ' : 15 Ueber einen Fall von Meningitis satum ina, Munchem med. TVchnschr., 1913, lx, 2343. as shown by the fact that the cerebrospinal fluid contains an ; increased number of cellular, elements. In chronic lead poisoning ' they rarely found any change in the cerebrospinal fluid. In this ? series the spinal fluid from all the patients was examined and changes V .were found in three of them. In these three patients the spinal '! fluid was clear, not under increased pressure, and a fibrin clot did A not form on standing. In two patients (Case I I and Case III) the'' 1 cellular elements were not increased, but there was a marked J globulin reaction (Ross-Jones). In one patient (Case I) there were ... thirty cells per cubic millimeter, mainly lymphocytes, and a markedd globulin reaction. The spinal fluid from this patient was examined"on several occasions over a period of eight months, and on each.-e examination there was an increase in cells and a positive globulin, 'a In the fourth patient (Case TV) the spinal fluid was not examined^? until four weeks after he had recovered, and at this time it showed 1 . no changes other than twelve cells per cubic millimeter; Such arc ; slight increase in cells does not signify a pathological change. ,. .r~l ft-E y e changes during the course of lead encephalopathies have')* -been noted by a number of different observers. Wilbrand andSS Sanger,17who have collected reports of most of the cases, believe thafcp (optic neuritis may occur primarily through the direct toxic action??; - of lead on the nervous system or by the production of interstitial * >neuritis or through the alterations of the bloodvessels in the retina:-! land optic nerves. I t also may occur secondarily through intra-% - cranial changes or changes in the kidney. Gibson, as mentioned;? (previously, has written extensively on the eye changes in children^ and believes that, they frequently occur without other symptoms?! of lead poisoning. In two of my patients (Case I and Case II )A there were extensive hemorrhages into the retina and optic neuritistil In one (Case I) th e condition gradually subsided and the eye grounds'^ became normal after a month. At the time of his second admission^ -there were retinal hemorrhages and a choked disk. The eye grounds^ were normal in the other two patients (Cases III and IV). > As a rule there are certain symptoms which precede the develop-^ ment of the convulsions. These may be the common symptoms of. plumbism or they may be so slight as to escape notice.. Colic hatiS been more frequently observed than paralysis or arthralgia, but more^ common are irritability, restlessness, and a blue line on the. gumsiti '-Vomiting and constipation are not infrequent, and many p a tie n t^ r complain bitterly of pain in the head. In two patients (Case I andEj (Case IV) of this series there was an interval of several days beforeg| -'the convulsions, when the children were irritable during the' daySI ' and restless, a t night. ; One of them complained of headache? and^i they both had attacks of vomiting. In one instance (Case III) the^ - indefinite symptoms covered a period of about three months. gTheres| ENG IN CHILDREN ebrospinal fluid contains an s.' In chronic lead poisoning : cerebrospinal fluid. In this mts was examined and changes iese three patients the spinal pressure, and a fibrin clot did its (Case II and Case III) the ;d, but there was a marked _ ne patient (Case I) there were alv lymphocytes, and a marked rom this patient was examined of eight months, and on each n cells and a positive globulin. spinal fluid was not examined red, and at this time it showed per cubic millimeter. Such a ify a pathological change, of lead encephalopathies have rent observers. Wilbrand and of most of the cases, believe that through the direct toxic action by the production of interstitial of the bloodvessels in the retina iccur secondarily through intra- , kidney. Gibson, as mentioned on the eye changes in children, occur without other symptoms r patients (Case I and Case II) into the retina and optic neuritis, rally subsided and the eye grounds t the time of his second admission i a choked disk. The eye grounds tients (Cases III and IV). atoms which precede the developmay be the common symptoms of ;ht as to escape notice. Colic has an paralysis oarthralgia, but more less, and a blue line on the gums, lot infrequent, and many patients head. In two patients (Case I and ; an interval of several days before iren were irritable during the day hem complained of headache, and ng. In one instance (Case H I) the eriod of about three months. There des A uges, 1913, vol. v. d t T;-! - " : '. blackfak: lead po iso n in g i n c h il d e e n ^ ^ ^ 8 ^ 3 ^ was evident impairment of general health with frequent attacks of2? vomiting and colic. At times the onset of convulsions is suddenA?^ The duration of the period between the first exposure to lead and S the development of cerebral symptoms is variable The exact time / of the exposure in the patients of this series could not be determined with certainty. Three of them (Cases I, I I and n i ) had been exposedis for many months, as the source of the infection was found to be from' s eating paint. In one patient (Case IV) the source of lead was notT ascertained. - . : In addition to the symptoms preceding the convulsions the (I patients in this series showed other evidences of lead poisoning."-''.' The blood picture was that of a moderate secondary anemia, and :/ in all a few red blood corpuscles showed basophilic degeneration. _ In the four patients there was a leukocytosis of about 20,000, withi-r-.-.^.--^ ^ a moderate increase in the polymorphonuclear cells. The blue line on the gums was present in three of the four patients (Cases I, H I//-) IV).. It should be remembered that a continuous lead line is seldom found.-. The characteristic appearance is the presence of black dots in the margin of the mucous membrane around teeth which-are covered with tartar. I t is difficult to see and without the aid of a hand lens may readily be overlooked.' Efforts made to determine lead in the urine of two patients (Cases I jfcVjfMW- I and II) were unsuccessful. The feces were not examined- The following are brief histories of the 4 cases which form the basis for this-report: % ~ . C a se I.--The patient, W . M .," aged five and one-half y e a r s ^ ^ S ^ ^ ^ S complained first of pain in his head, and was very restless at n i g h t . ' ^ ^ ^ ^ ^ The following day he vomited several times, and it was noticed that his neck was stiff. He appeared very ill,_became rapidly and on the fourth day of his illness severe generalized convulsions began. On the fifth day, August 22, 1913, he was brought to the ? hospital in a comatose state. He continued to have recurrent generalized convulsions, his neck was retracted, and there was an y- internal strabismus of the left eye. There was an optic neuritis, and a hemorrhagic retinitis on the right. The left optic nerve was normal. The temperature was normal The leukocytes were 27,600. The spinal fluid obtained ' on four occasions was - ./tNri-ggy clear and sterile. It was under slightly increased pressure at the first spinal puncture, but subsequently the pressure was normal..; There were from twenty to forty cells per cubic centimeter (mostly'/ mononuclears). The Noguchi globulin reaction was positive. The Wassermann (blood) was negative. The convulsions ceased after the first lumbar puncture, but he remained in coma for the next two days. He gradually improved and after a week seemed nearly well. The convulsions did not recur and he was discharged 18 T h is case w as rep o rted b y T h o m as a n d BLackfan: A m . J o u r . DLs. C h ild ., 1914. viii, 377. BLACKFANt LEAD POISONING IN CHILDREN . . . September 20, 1913. The abnormal changes in the right optic nerve gradually subsided, but the spinal fluid contained an increase . in cells and a positive globulin reaction. With the exception of an occasional attack of vomiting and abdominal pain, he remained in - excellent condition for five months. - S-Y-7 /_ On March 1, 1914, he complained of headache and he vomited. . The convulsions recurred, and on March 3 he was again admitted c to the hospital. His condition was almost identical with that at ` the time of the first admission. There were generalized and per-- sistent convulsions,' a definite rigidity of the neck, and an optic_5| r neuritis and hemorrhagic retinitis of the right eye. At this examina--- -'?3r?4:;;tion the characteristic lead ,line was seen on the gums. The redti blood corpuscles were 4,480,000, the white blood corpuscles 23,000, r-jpyry and the hemoglobin 55 per cent. There was well-marked, stippling ,f the red blood corpuscles (Grawitz granules).. No lead could be_ > ...demonstrated in the urine. The convulsions subsided after lumbar- , puncture. Two or three days after admission an internal strabismus. T-efgry: of the right eye developed;. The patient made an uneventful recovery; 'TivtirN. and was discharged on M ay 1. . . . . . . remained in apparently good health for three weeks, when 51 v.i^feV-'on May 25 he had a-severe-convulsion and died. No postmortem Tkj N-examination was obtained. The source of the lead was determined r- when his lips were found covered with white lead paint which hew --had nibbled from the .railings of his crib. On investigation a t the " NSgS'JrN orphanage where he lived it was found that the white paint on his.J yzjt&j&g* bedstead had been entirely gnawed off. - Case EL--EL B. (7094). This patient was aged two and one--! ; tS lw L .b alf years. On March 8, 1915, he had a convulsion which lasted^ - about two hours. From then until March 12 he seemed.weIL_ li ; t `=7- ; On the morning of March 12 convulsions began about 7.30. .He5j was brought to the hospital at noon the same day in convulsions^ r'jN-v - which continued for about twenty-four hours. These convulsions) v v f involved the eyes, the left side of the face, and the left arm. He had- no fever. There was a' leukocytosis of 19,000. The red blood cells: .; :d ~~ 4,000,090. Hemoglobin, 50 per cent. There was well-marked: NylL-y.;.''stippling of the red cells. - - -N Yv - - . On examination the positive findings were a lead line about the! i E x \ ; ' upper and lower teeth and an enlarged spleen. He was entirely;? i i y k relaxed between the convulsions, the reflexes were not exaggerated^ and Kernig's sign was absent.. The eye grounds were normal.. Thelpl spinal fluid was clear and not under pressure. There were seven < per cubic millimeter and a positive globulin reaction. Examination of the urine for lead was negative. -v -L The child had no convulsions in the hospital, and was disc 011 March 25. He was brought back to the hospital on March 26j rw'Sgf-c*- twelve hours after discharge, in a convulsion which involved the face?; jxryG y' and the left arm. He continued to have convulsions for twenty-fou blackfan: l e a d p t hours in spite of energetic trea bromides. " By the administrat could be checked, but they recu The temperature rose to 107.5 Source of Lead. The father st. painted article, and that he and set of parlor furniture by eating Case EH.--(9182) H. B ., age - Case No. H ) died in the Johns I March 27, 1915. The patient was a normal child: at sixteen months. Shortly after abdomen and was operated on 1 (February, 1915). The append! months preceding the onset of his often vomited and complained a j vomited more than usual on Oct. a convulsion. The convulsions c. the hospital the following day, Oc tose on admission and was having . The convulsions were general in involvement of the right than the was not rigid; there was no Kerni obtained. Examination of the m failed to show a lead line. Ophthalmoscopic Examination. was obscured. The vessels were fi retinal hemorrhages. Left: The i by a large retinal hemorrhage, a: areas throughout. The leukocyt cells were 3,600,000 and the hem stippled red cells were present. T under increased pressure. There w and the reaction for globulin was p Course in Hospital. The coi enormous doses of chloral and m u control them by the use of chlo: temporary benefit, as the convuL was discontinued. The patient die temperature, which was 97.6 on just before death reached 105.5 Source of Lead. Same as in Ca Case IY (8491).--J. N., aged thi of two children, was of normal de tion of pertussis a t two years, hac no history of convulsions. The p July 30, 1915, with drowsiness. K OKING IK CHILDREN aaal changes in the right optic spinal fluid contained an increase ction. With the exception of an abdominal pain, he remained in s. " '' ed of headache and he vomited. March 3 he was again admitted as almost identical with that at There were generalized and peridity of the neck, and an optic f the right eye. At this examinaas seen on the gums. The red ae white blood corpuscles 23,000, There was well-marked stippling itz granules). No lead could be onvulsions subsided after lumbar admission an internal strabismus 'lent made an uneventful recovery ad health for three weeks, when tlsion and died. No postmortem ource of the lead was determined with white lead paint which he lis crib. On investigation at the ound that the white paint on his ed off. patient was aged two and onee had a convulsion which lasted intil March 12 he seemed well, avulsions began about 7.30. He oon the same day in convulsions, y-four hours. These convulsions he face, and the left arm. He had sis of 19,000. The red blood cells per cent. There was well-marked ndings were a lead line about the nlarged spleen. He was entirely the reflexes were not exaggerated, he eye grounds were normal. The er pressure. There were seven cells e globulin reaction. Examination v*e. n the hospital, and was discharged oack to the hospital on March 26, convulsion which involved the face ,o have convulsions for twenty-four nours m spite ot energetic treatm ent with morphia, chloral, and bromides. By the administration of chloroform the convulsions could be checked, but they recurred as soon as it was discontinued. The temperature rose to 107.5 just before death. ; -t-T; Source of Lead. The father stated th at the child would gnaw any painted article, and that he and his brother had recently ruined a set.of parlor furniture by eating the paint from it.--r.v-r.v^^:~v~. Case III.--(9182) H. B., aged two years. A brother (R. B., Case No. H) died in the Johns Hopkins Hospital of lead poisoning March 27, 1915. ') -') ;v-CfAw -: : - A The patient was a normal child, and was well until he had varicella at sixteen months. Shortly after this he complained of pain in the abdomen and was operated on by an orthopedist for appendicitis (February, 1915). The appendix was normal; For two or three months preceding the onset of his acute illness he was not well. He often vomited and complained a great deal of abdominal pain. He vomited more than usual on October 15, 1915, and a t 11 p .m. had a convulsion. The convulsions continued, and he was admitted to the hospital the following day, October 16. -The patient was coma tose on admission and was having repeated and severe convulsions. The convulsions were general in character, with possibly greater involvement of the right than the left side of the body. The neck was not rigid; there was no Kemig's sign. The knee-kicks were not obtained. Examination of the mucous membrane about the teeth failed to show a lead line. ' A . ' . N - r A . Ophthalmoscopic Examination. Right: The margin of the disk obscured. The Vessels were full and tortuous; there were small retinal hemorrhages. Left: The margin of the disk was obscured by a large retinal hemorrhage, and there were other hemorrhagic' areas throughout. The leukocytes were 20,000. The red blood cells were 3,600,000 and the hemoglobin was 55 per cent. Many stippled red cells were present- The spinal fluid was d ear and not under increased pressure. There were nine cells per cubic millimeter and the reaction for globulin was positive. yfyA Course in Hospital. The convulsions persisted in spite of enormous doses of chloral and morphia. I t was only possible to control them by the use of chloroform. This, however, was of temporary benefit, as the convulsions commenced again when it was discontinued. The patient did not regain consciousness. The temperature, which was 97.6 on admission, gradually rose, and just before death reached 105.5 (fifteen hours after admission).; Source of Lead. Same as in Case H. ' Case IV (8491).--J. N., aged three years. The patient, the older of two children, was of normal development and, with the excep tion of pertussis at two years, had always been well. There was no history of convulsions. The present illness began acutely on July 30, 1915, with drowsiness. He slept the greater part of that day, was very weak, refused his food, and vomited. At night he ,'% was delirious. He jumped out of bed, cried out several times, and .A threw his bead back as though in pain. The next day, July 31, he appeared better, though still weak and drowsy. Again, at night, he . became delirious and had several attacks of crying and throwing his head back. On August 1 he was comatose, and he had several con- | vulsions. He did not improve, and was admitted to the hospital August 2. . ;"'v - - The temperahire on admission was 101, pulse 124, respirations 20. He lay quiedy in bed, with his eyes closed, and made no effort to '^! speak. He was well-nourished and did not appear very ill. The-p^p neck musdes were slightly rigid and attempts to flex the- neckiSf||| caused pain. The reflexes were active ;but not increased. The.Jr jp examination of the heart and lungs was negative. The spleen wasj* || palpable. There was a well-marked lead line present in the mucous!jJ| membrane about several of the upper teethe- I t was especially well defined about the upper lateral incisors. The optic discs w erey || normal. ' '.cut;':'.;-,- 4: .A'-.-- .' .The red blood corpuscles showed stippling in a few cells. -T h eg ig l white blood corpuscles were 7500 pen cu.mm. The differential count:fj|| *7 The Wassermarm p>Iood) was negative. . . . 7iSH p||| A Course in the EosvitaL - The child lay in a semistupor for most of-g the day after his admission. He was easily aroused, and at times=fi appeared conscious but would not speak. The respirations were fulEg and deep, varying between eighteen and twenty-four. They were*, irregular, and a few periods of apnea were observed. There wasa^i well-marked tache cerebrale, and Kemig's sign was suggestive^ The neck was rigid. The condition remained the same for the n ex tj two or three days. There were no convulsions. On August 5 the| patient seemed much better. He sat up in bed and could walkgj when placed on his feet. On this day an incomplete paralysis of theA right facial nerve was observed. Improvement in his condition^ continued- The temperature gradually became normal, andlsnEg days after (August 8) admission he appeared quite well, except.thatSi he was very weak. The facial paralysis slowly became less m arked^ and it disappeared after about ten days. When he was discharg^^ on August 12 (ten days after admission) h e was apparently w elE||3 "~"A lumbar puncture was made several times during his stav~5|| the hospital, but blood was obtained each time, and for this reasong a cytological examination was not made. Four weeks after theonsetjjl when the child was apparently imder increased-pressure, and millimeter. The globulin reactic source of lead was not determint Onset of con vulsions : : L eukocytes . Spinal fluid; ' Cells .. Globcifin Temperature. on admi^ion Lead line Stippling red blood ceils Eye - - , Hemorrhagic re- trnitis; cboked Same Cas External rectus Convt palsy; convul- .com t: sions; coma; - r rigidity of neck 1. Eating paint Eating Died Died C o x clchio ns. In conclusion, phylactic measures be taken w painted articles in order to guard' poisoning. Since my attention ha I have found a number of childrer enameled cribs. In all patients with convulsior is not clear, lead should be suspe mined, as in the majority of ins of the condition, e. g., the lead the presence of lead in the feces. The examination of the spinalJ to the seriousness of the affection the four patients changes were changes ware present in the spins patient eventually succumbed. 1 has recovered, and in whom the spinal fhndcould not be examine N`G IN -CHILDREN r .- i, and vomited. At night he , cried out several times, and a. The next day, July 31, he 1 drowsy. Again, at night, he i s of crying and throwing his atose, and he had several conwas admitted to the hospital 101, pulse 124, respirations 20. closed, and made no effort to did not appear very ilL The id attempts to flex the neck tive but not increased. The vas negative. The spleen was ead line present in the mucous iper teeth. I t was especially incisors. The optic discs were stippling in a few cells. The cu.mm. The differential count egative.-' ' i lay in a semistupor for most of as easily aroused, and at times >eak. The respirations were full a and twenty-four. They were ea were observed. There was a Xemig's sign was suggestive. remained the same for the next convulsions. On August 5 the sat up in bed and could walk ay an incomplete paralysis of the Improvement in his condition dually becajne normal, and six appeared quite well, except that ilysis slowly became less marked, days. When he wss discharged ission) he was apparently well, several times during his stay in .ed each time, and for this reason nade. Four weeks after the onset, BLACKFAX: LEAD POISONING D f when the child was apparently well, the spinal fluid was clear, not under increased pressure, and contained twelve cells per cubic millimeter. The globulin reaction a t this time was positive. The source of lead was not -Caae. Onset of-con-*r^: vulsions Xeukocytes Spinal fluid Cells ~Z' Globulin T emperature,V./" on admission ^.i.; Leadline _ tV.^T-7 Stippling red - - blood cells : W - .Eye ; H< N eurological. External Negative. Delirium Result CoNCLrsioxs. In cooeliision, I would urge th a t energetic pro phylactic measures be taken with children who habitually eat painted articles in order to guard against the development of lead poisoning. 'Since my attention has been directed to lead poisoning I have found a number of children who nibble the white paint from enameled cribs. .... :&*-4'ty.# In all patients with convulsions in which the etiological factor is not clear, lead should be suspected. This can be readily deter mined, as in the majority of instances there are other evidences of---th--e---c-o--n-d-itiofni, e.' g., the *lead l--ine, basophilic degeneration, and globulin reaction was normal.