ANAEMIA OF TUBERCULOSIS. By B. K. Rachford, M.D., Newport, Kentucky. Clinician to Children’s Clinic, Medical College of Ohio, Cincinnati, Ohio. Reprinted from Archives of Pediatrics, November, 1892. New York: M. J. Rooney, Printer and Stationer, 1329 Broadway. ANEMIA OF TUBERCULOSIS* B. K. RACHFORD, M.D., Newport, Kentucky. Clinician to Children’s Clinic, Medical College of Ohio, Cincinnati, Ohio. , The following case, with which I introduced my sub- ject, is rather old to appear in pediatric literature. But it was the study of this case which led me to make the investigation of which this paper is a preliminary report, and it is therefore proper that it should serve as an intro- duction to a subject of vast importance to pediatrists, viz., the anaemia of tuberculosis. CASE.+—November 4th, 1891.—Miss A., aet. twenty, came to my office for treatment. All of her family except her father had died of pulmonary tuberculosis. Her mother, her stepmother, two grown brothers and one grown sister died of this disease. Three of these deaths were within the last five years, and she was at home during the sickness of all of them. Her father and herself alone survive, and the father is at present confined * Read before the American Pediatric Society, Boston, May 3, 1892. f This case was one of two which I reported in the N. Y. Medical Journal, May, 1892. It is here reported in greater detail and for another purpose. 2 RACHFORD: Ancemia of Tuberculosis. to his room with pulmonary tuberculosis and she nurses and cares for him. A worse family history, with more constant exposure to the t*ubercular contagion is rarely seen. Personal history.—She has always enjoyed fairly good health ; she remembers that about two years ago, just following the death of her last brother, she was not quite well for a short time and had some “kernels” in her neck; she took some medicine and they disappeared and she has been quite well until within the last three months. During this time she has had more or less dyspnoea and pain in side on exercising, but she thought nothing of these symptoms and continued looking after the sick father and doing the work about the house ; at the pres- ent time these symptoms have increased to such an ex- tent that she can scarcely “keep up.” She comes to-day complaining of great weakness, a tired feeling, considerable dyspnoea, some pain in left side, little appetite, sick stomach and great nervousness. There is no fever and no cough. The menstrual flow during the last few months has been very slight and almost colorless. Last month she had “ no show” at all. Physical examination.—No perceptible disease of the lungs, the heart sounds normal, lymphatic glands not noticeably enlarged; the most pronounced and striking symptom is the extreme anaemia, as manifested in the general pallor of the skin and loss of color in the mucous membrane. Examination of blood.—Only twenty-five per cent, of haemaglobin and 1,680,000 red corpuscles to the cubic millimetre. Treatment.—Three grains of reduced iron and one- fortieth grain arsenious acid three times a day. November 18th.—Haemaglobin thirty per cent. She thinks she is a little better; changed treatment to sac- charated carbonate of iron, ten grains three times a day. November 29th.—Haemaglobin forty per cent. Is much better; can do her housework without much fatigue, but she is still very pale and has some dyspnoea on exercise. On the 23d she had “some show” at her menstrual time last- ing a few hours. December 1st.—Haemaglobin fifty-two per cent. Im- proving in every way; eatsandsleepswell; nervousness and shortness of breath are rapidly disappearing. She is getting Rachford: Ancemia of Tuberculosis. 3 tired of the medicine. Changed treatment to Warner’s compound chalybeate pills, two after each meal. December ioth.—Haemaglobin sixty-five per cent. She says she is well and that itis not necessary for her to continue taking medicine. She was persuaded to continue treat- ment from this time on, because she could see for herself in the haemaglobinometer that her blood had much less color than it ought to have, and as she had noted with me from time to time the gradual increase in the color of her blood, she was the more easily induced to continue the treatment. December 17th.—Haemaglobin seventy per cent. December 29th.—Haemaglobin seventy-eight per cent. Changed treatment to three grains reduced iron, one- twentieth grain ’arsenious acid, three times a day. January 18th.—Haemaglobin ninety per cent. Last monthly time was normal. February 1st.—Haemaglobin ninety per cent. Stopped all medicine after nearly three months of continuous treat- ment. February 17th.—Haemaglobin ninety per cent. Corpus- cles, 4,000,000 to the cubic mm. She is “ perfectly well; ” she “put in” a load of coal during the past week without getting tired. March ioth.—Girl remains well. She is kept closely at home.nursing her father, who is confined to bed with consumption. March 18th.—She has not been taking medicine for about seven weeks ; she says she is well. Examined her blood and was surprised to find only sixty-five per cent, of haemaglobin and 3,200,000 red corpuscles to the cubic mm. She went two weeks over her last monthly time and it was very scanty. She protests that she is not at all sick, but I again prevailed on her to take medicine so as to keep her blood state up as near the normal as possi- ble during the time she was nursing her father. I again gave her iron and arsenious acid. March 30th.—Haemaglobin ninety per cent. Feels well; discontinued medicine and ordered to report in two weeks. In this case I would call special attention to—ist, the very bad tubercular history; 2d, the constant exposure to contagion; 3d, the “kernels” in her neck two years ago ; 4th, no evidence of pulmonary or glandular tuber- culosis at the present time ; 5th, the state of the blood 4 Rachford: Ancemia of Tuberculosis. (twenty-five per cent, of haemaglobin); 6th, the improve- ment of the blood state after treatment (ninety per cent, of haemaglobin); 7th, the rapid diminution in haemaglobin after treatment was discontinued (to sixty-five per cent, in seven weeks); 8th, absence of symptoms when blood contained sixty-five per cent, or more of haemaglobin; 9th, the remarkable fact that this girl has escaped pul- monary tuberculosis for so long a time. The relationship of anaemia to tuberculosis in this case is by no means clear, and it was for the purpose of inquir- ing into this relationship and answering certain other questions suggested by this case that the investigation, of which I here present a preliminary report, was begun. The table below comprehends 166 blood examinations; 164 of these were convent girls ; Nos. 1 and 2 were private cases. The great majority of the girls examined were between the ages of twelve and eighteen. The convent girls were examined at the Convent of Good Shepherd in Cincinnati, Ohio, and Newport, Ky. All except thirty- six of these girls belong to the reform class; this class is made up of young girls who have gone astray and are placed in the convent for reformation. The girls of this class, therefore, do not enter the convent until they are from ten to fifteen years of age. The lives of most of these girls prior to the entering of the convent is one of wretchedness ; many of them no doubt lived in badly ventilated apartments surrounded by sickness, poverty and crime. These facts are of much importance in study- ing the physical condition of these girls. The thirty-six referred to as not belonging to the reform class are in the “preservation class ;” this class is made up of home- less girls who have been taken when quite young, some of them entering the convent at the age of three, four and five years. Most of the girls in this class have, therefore, grown up in the convent, and have had good food and proper hygienic surroundings. In the table these girls are marked with a star (*). The following information is embraced in this table: The name, age, length of time in convent, family history RACHFORD: Ancemia of Tuberculosis. 5 of tuberculosis, exposure to the tubercular contagion, age at first menstruation, regularity or irregularity of the menstrual function, percentage of haemaglobin, number of corpuscles in some of the cases, and points in the per- sonal history in each case. The following table was arranged by Dr. Robert Carothers, who assisted me in this work. The 166 cases recorded below were taken just as they came in the two convents; they were not selected cases. All of them considered themselves fairly well and worked every day, and none of them were under treatment at the time examined. On close examination a few of these girls were found to have a cough, pain in the side and dyspnoea on exer- cise ; but these symptoms were not complained of and they would not have told them unless closely questioned. As one would expect, the family history of many of these girls is absolutely negative, but by careful inquiry and with the kind assistance of the Sisters of the Good Shepherd, I obtained a fairly good family history of many of them. In fifty-eight cases the family history was negative ; in thirty the family history was good, no tuberculosis, and in seventy-eight there was a family history of tuber- culosis. In the seventy-eight cases with tuberculous family histories the average amount of haemaglobin was y8f per cent. In the fifty-eight cases with negative family histories the average amount of haemaglobin was per cent. In the thirty cases with non-tubercular histories the average amount of haemaglobin was eighty-eight per cent. These figures, so far as they go, indicate that family tuberculosis predisposes to anaemia, but they are subject to this criticism, that there may have been sufficient active tuberculosis in Class I. (with tubercular histories) to account for the ten per cent, diminution of haemaglobin in the class. These figures are alone, therefore, of little value in solving the problem of the relationship of the 6 Rachford: Ancemia of Tuberculosis Name. Age. In house. Years. Tubercular History. Expo- sure to conta- First Menstru- ation. Menstrual Function. Per Cent. Hb. No. Corp. per Cm. Personal History. gi°n. i A. L. 20 All family Yes Irregular 25 1,680,000 Kernels in neck 2 yrs. 2 S. P. 20 Mother and aunts ( < << 3° 2,250,000 ago. 3 R- K. 19 4 2 Bros, and 2 sisters 14 Missed 4 mos. 5° 2,650,000 Kernels in neck 2 yrs. ago, dysp., pain in side 4 M. S. 18 12 Negative Neg. 15 Scanty, little col. 60 2,800,000 Dysp., pain in side 5 E. M. 15 i Fath., moth.. 3 bros. Yes Never Never 5° 2,375,0°° 6 M. R. 14 z Father and mother t t !3 Once in 6-7 mos. 55 7 A. W. 8 A. B. 17 4 Half-bro. and uncle < t 14 Regular 45 Scrofulosis, pain in side, dysp. 16 6 Mother and brother t ( 14 Irregular 45 Scrofulosis, pain in side, dysp. 9 L. K. i7 h Sister Neg. 14 j Metrorrhagia j Menorrhagia 35 Scrofulosis 10 A. K. 14 2 Mother No Never Never 60 Small and pale ii S. F. 15 3 Mother and sister Yes 13 Irregular 65 2,533)°°° 12 E. IC. 18 2 Brothers 15 60 13 M. W. 16 \ Mother and sister “ 13 “ 65 2,543,000 Dyspnoea (( 14 R. K. 23 & 2 Brothers No 14 “ 63 4,500,000 15 B. G. 16 M. H.* 18 I Mother Yes 15 Slight and pale 60 Had kernels in neck 2 yrs. ago, pain in side, dysp. i7 2 U No 16 Irregular 65 Dysp., pain in side 17 M. S.* 14 8 Negative Neg. 1.3 Regular 63 Scrofulosis 18 C. L. 16 16 “ Neg. Negative 65 Small and delicate 19 I. R. 14 2 Mother Yes 14 65 Dysp., pain in side 20 M. M.* 14 3 “ “ Never 65 Diarrhoea 2 yrs. 21 M. M.* 10 1 Sister Yes 10 Slightly once 65 Dyspnoea 22 A. M. 28 10 Negative Neg. 18 Irregular 65 Slight cough 23 C. F. 17 2 Good No 15 “ 65 Cough and dysp. 24 A. L. 16 1 6 Negative Neg. Neg. Negative 60 25 A. N. 3i 10 Mother and sister “ 19 Regular 67 Scrofulosis 26 M. A. >9 4 Yes 17 75 Had haemorrhage 27 A. B. 23 2£ Mother and brother “ 15 “ 75 3,460,000 Pain in side 28 M. M. 27 3 3 Aunts and brother No 16 j Metrorrhagia j Menorrhagia 70 3,600,000 Has haemorrhage 29 R. T. 20 6 Mother and sister Yes 14 Irregular 70 2,620,000 Pain in chest, dysp 30 M. R. 19 Negative Neg. 73 3,012,000 Dyspnoea 31 M. E. 17 1 Good No 16 Regular 75 32 B. C.* 33 A. L.* 16 17 10 8 Mother Sister Yes 12 14 Irregular 75 75 7° 34 K. M.* 16 3 Brother and sister “ Regular 35 P- P-* 13 10 Sister No 13 *« 70 36 A. B.* 16 14 Mother Yes 12 Irregular 75 Been taking iron, 37 N. T.* scrofulosis 14 4 Good No Never 70 38 B. E. 22 Moth., bro., sister Yes 15 Regular 75 39 M. N. 18 5 6 Negative Neg. Irregular t ( 75 Dyspncea ( ( 40 C. F. 17 4 Sister Yes 17 70 41 M. B. 21 12 Father “ 13 Regular 70 Cough 42 K. D. 32 11 Mother 14 75 Scrofulosis 43 A. McM. 20 Tf 4 Fath., sister, uncles No? 13 75 70 44 K. H. 37 Father Yes 14 45 c- w- 14 Negative Neg. 11 Irregular 75 46 L. R. H IX Father and mother Yes Never 70 47 A. B, 21 4 Good No 15 Regular 75 48 M. B. 20 5 Negative Neg. 14 70 Scrofulosis 49 M. D. 29 3 Mother and brother Yes 15 7° 50 M. B. 25 6 Mother < ( 16 Irregular 77 51 L. P. 16 Negative Neg. Neg. Regular 75 Rachford; Ancemia of Tuberculosis 7 8 RACHFORD: Ancemia of Tuberculosis Name. Age. In house Years. Tubercular History. Expos- ure to con- tagion. First Menstru- ation. Menstrual Function. Per CentJ Hb. No. Corp. per Cm. Personal History. 52 M. C. 38 18 Negative Neg. 14 Regular 75 53 M. E. 18 *6 Mother and sister Yes 14 44 80 54 U. B. 18 11 Father No 12 4 4 80 56 E. M. 21 3 Mother Yes 13 Metrorrhagia 85 57 K. K.* 17 5 Father l 4 15 Irregular 80 : 58 M. D.* 16 4 Mother and brother 44 14 Regular 80 Pain in side, dysp. 59 L- P-* 16 11 Sister No 15 Irregular 85 44 44 44 60 M. II. 16 11 44 14 44 85 61 C. S. 30 6 Negative Neg. H Regular 85 62 G. P. 22 6 16 Irregular 80 Insane 11 yrs. ago 63 J- J- 17 12 Good No 14 Regular 80 64 C. B. 21 6 Negative 44 Neg. 15 Irregular 80 65 L. R.* 16 5 44 14 Regular 85 66 K. P.* 15 6 “ 4 4 13 80 Exophthalmic goitre 67 A. R. 14 44 C 4 Irregular 85 68 M. D.* 16 4 44 t 4 Regular 85 69 M. T.* 14 4 Good No 13 88 70 N. T. 14 4 (l 4 4 Never 85 71 J- u. 21 3 Mother and sister 4 4 19 Irregular 85 72 M. B. 16 4 Sister Yes 12 85 Pain in side, dysp. 73 R. D. 18 2 Good No 13 Regular 80 74 M. A. 21 2 <1 t l 16 85 75 R. L. 18 5 “ 4 4 12 4 4 85 76 T. W. 16 i “ 4 4 Never 80 Dyspnoea 77 M. I. 19 2 Mother Ys 12 Regular 44 80 78 T. B. 16 4 Father and brother 4 4 13 80 79 M. R. 16 3 Good No 14 “ 80 80 A. H. 16 1 Negative Neg. 12 Irregular 85 RACHFORD: Ancemia of Tuberculosis. 9 81 M. K. 25 12 All family Yes 14 Irregular 85 Cough 82 F. T. 18 J£ Father l « 14 Regular tl 80 Slight cough 83 L. L. 30 16 Good No 14 80 84 M. B. 12 9 “ << Never 85 85 M. W. 14 z Mother and brother Yes l < 77 Well 86 E. F. 14 | Negative Neg. t C 80 87 A. F. 21 4 Good No I2£ Regular 80 88 M. M. 17 4 < ( U 13 Irregular 83 89 M. D. 3° r5£ Negative Neg. t ( 164 Regular 81 90 E. G. 32 18 C ( 18 80 91 K. H. 17 1*2 Bro., sis., moth., aunt Yes Irregular 80 Pain in side 92 E. B. 15 3 Negative Neg. Neg. Regular 85 Well 93 M- T. 16 2£ Mother Yes 15 l ( 100 Dyspnoea 94 S. J. 25 Uncle No 10 “ 100 Pain in side 95 J- S. 15 £ Mother Infancy, Yes Never 95 Pain in side, dysp. 96 J- L. 30 4 Mother and brother No 12 Slight, dark 100 Haemorrhage 97 J- S. 13 £ Mother Infancy, Yes Never 95 Dyspnoea 98 E. O. 28 5 Uncles and aunts No 16 Regular up to 2 months ago 90 3 haemorrhages from stomach 99 B. K. 26 6 Moth., sis., bro. Yes 13 Metrorrhagia 95 Cough, dysp., pain 100 J. M. 16 14 Mother “ 14 Regular 11 100 Well 101 C. T. 16 2£ Mother and sister 13 90 (t 102 M. A. 14 1*2 Mother “ 13 C ( 100 103 L. M. 14 £ Uncles No 124 90 104 L. M. 21 .2 Mother Yes 16 ( ( 90 105 K. Z. 17 Mother and uncle t ( 15 Irregular 100 106 M. T. 24 6 Mother l C Regular ( L 100 107 E. B. 23 9 Mother and brother No 100 108 J. L.* 17 8 Sister Infancy, Yes t i 100 10 Rachford: A nee mi a of Tuberculosis. Name. Age. In house. Years. Tubercular History. Expos- ure to con- tagion. First Menstru- ation. Menstrual Function. Per Cent. Hb. No. Corp. per Cm. Personal History. 109 M. O.* 17 I r Sister No 13 Regular 90 no N. K.* 15 4 Father and sister Yes 13 Irregular 100 Dysp., pain in side hi M. D.* 16 8 Mother and brother No 14 Regular 9° 112 K. C. 25 15 Good 4 ( 16 Metrorrhagia ICO 113 H. G. 22 5 Negative Neg. 16 Regular < t 100 114 M. 35 2 44 14 100 115 K. S. 25 6 “ <4 16 “ 95 Dyspnoea 116 F. M. 18 it Good No 16 Irregular 100 117 J- D- l9 1 Negative Neg. 14 Regular 100 118 A. H. 17 3 Good No 13- 100 119 L. O. 19 2 Negative < 4 Neg. 16 95 120 F. W. 18 10 15 90 121 K. H. 17 44 Good No 16 “ 9° 122 C. R. 17 12 Negative Neg. 13 90 123 K. G. 17 12 “ 13 41 90 124 M. M.* 16 3 Good No 13 4 ‘ 100 123 M. H.* 16 14 Negative Neg. 13 < 4 90 126 A. K.* i7 3 16 44 90 127 M. D.* 16 8 * 1 44 15 90 128 M. G* 21 3 “ 17 4 4 90 129 T. M.* 17 1 44 16 44 100 130 A. P.* 15 10 “ 4 c 12 “ 90 131 M. R.* 13 5 4 4 4 4 Never 100 132 M. E.* 13 2 < 4 4 4 “ 95 133 W. R.* 13 5 “ 90 134 W. E. 14 3 Good No t < 90 Looks delicate 135 G. G. 12 2 Negative Neg. 11 “ 95 136 A. H. 16 3 “ 9 Regular 95 RACHFORD: Ancemia of Tuberculosis. 11 137 M- L. 16 2 Negative Neg. 15 Regular IOO 138 J. C. 19 1 16 44 IOO 139 L. S. 21 3 Brother Yes 20 Metrorrhagia 90 Old scrofulosis 140 M. C. 16 3 Good No 13 Regular IOO 141 A. S. 15 z Negative Neg. 14 Irregular IOO Pain 142 F. E. 17 I Aunts Yes 12 Regular IOO 143 K. W. 23 16 Negative Neg. 13 “ 90 144 E. M. 16 _7L 1 2 Good No H Irregular IOO 145 K. P. 21 4 Negative Neg. 16 “ 93 146 N. K. 15 No 13 Regular IOO 147 C. D. 21 8 Good 44 18 “ IOO 148 F. S. l6 n Brother Yes 14 44 IOO Pain in side, dysp. 149 A. S. l6 4 Good No H Irregular 95 44 44 44 150 M. G. l6 .2. Negative Neg. 14 Regular 95 i.S 1 M- J- l6 2 Father and sister Yes 14 Irregular IOO 152 H. L. 22 5 Mother “ 14 Regular IOO 153 A. Iv. 23 8 Good No 15 44 IOO 154 A. S. 31 7 “ “ 15 Irregular IOO 155 A. R. 21 3 4 4 4 4 15 95 156 A. B. l6 U “ “ 14 Regular 95 157 M. O. 39 ii Negative Neg. Neg. Negative 95 158 L. B. 13 1 I 12 Regular 95 159 A. T. 15 12 “ 4 4 14 Irregular 9° Scrofula ? 160 E. G. 15 l ( t 4 4 Never 95 161 A. C. 37 1 4 4 “ Neg. Negative 9° 162 L. E. 17 4 Father Yes 14 Regular 95 163 T. W. 25 4 Sister No 18 44 90 164 M. M. 3° TO Negative Neg. Neg “ 90 165 A. L. 44 24 20 44 90 166 L. D. 3° 3 Mother . Yes Neg. 44 90 12 RACHFORD: Anosmia of Tuberculosis. anaemia to the tuberculosis. But if we exclude all the cases of tuberculosis and scrofula found in the tables, we find that the above percentages are not materially changed—we then have sixty-nine cases with tubercular family histories, but having no apparent tuberculosis with an average of 80L per cent, of haemaglobin. This per- centage, when compared with the eighty-eight per cent, in the thirty cases with non-tubercular histories, affirms the conclusion arrived at above that there is a relation- ship between tuberculosis and anaemia, apart from the anaemia that is produced by apparent active tubercular disease. By further study of the table we learn that fifty-two of the 166 girls examined were decidedly anaemic, having seventy-five per cent, less of haemaglobin. Of the fifty- two anaemic cases only four, or about seven-and-a-half per cent., have good family histories, no tuberculosis; twelve, or about twenty-three per cent., had negative family histories, and thirty-six, or about seventy per cent., had tubercular family histories. Among the re- maining 114 cases with more than seventy per cent, of haemaglobin there were twenty-six, or twenty-three per cent., with non-tubercular histories; forty-five, or about thirty-nine per cent., with negative histories, and forty- three, or about thirty-seven-and-a-half per cent, with tubercular histories. Here we have two sets of figures worth comparative study, which we may for convenience arrange in the following manner: No tubercular Tubercular Negative family history. family history. family history. 52 cases, anaemia with less than 75% Hb., .... 7i% 70% 23% 114 cases, non-anasmic, with more than 75% Hb. . . 23 % 37% 39% The contrast between these two sets of figures is strik- ing and the percentages are made from a sufficient num- ber of cases to make their study valuable. These figures again show that there is a relationship between family tuberculosis and anaemia; a very small percentage of Rachford: Ancemia of Tuberculosis. 13 anaemia cases have a family history free from tuberculo- sis, and a comparatively large percentage of the non- anaemic cases have good family histories. We conclude, therefore, that girls from tubercular stock are much more likely to be anaemic than girls from non-tubercular stock, or in other words, that family tuberculosis is one of the great sources of anaemia. The following diagram is made from the same group of cases, except that all the cases of apparent pulmonary and glandular tuberculosis have been omitted. It will be seen that this omission does not materially alter the fig- ures given above. No tubercular Tubercular Negative family history. family history. family history. 37 anaemic cases, 75% or less of Hb., with no apparent tu- berculosis, .... rt% 72% 20 \% 100 non-anaemic cases. More than ']<,% of Hb., with no apparent tuberculosis . 25% 4°% 45% The contrast in these two sets of figures is just as striking as in those given above, and these clearly prove that girls from tubercular stock, even though they be apparently free from tuberculosis, are very much more likely—in the ratio of seventy-two to seven-and-three quarters per cent.—to be anaemic than girls with non- tubercular family histories. This gives great importance to the tubercular or non-tubercular family histories in anaemic cases, since family tuberculosis is here shown to be one of the important causes of anaemia. Let us now give attention to the cases of tuberculosis found in the tables. There are eight cases of glandular tuberculosis with no pulmonary disease (Nos. 7, 8, 9, 17, 25, 36, 42, 48). Case 34 is excluded because she had been taking iron for some time. The average amount of haemaglobin in these cases was fifty-seven per cent. There are ten cases of pulmonary tuberculosis with evidence of scrofula (Nos. 22, 24, 26, 28, 41, 81, 82, 96, 98, 99) and the average amount of haemaglobin in these cases was eighty per cent. 14 Rachford: Anosmia of Ttiberculosis. Fifty-seven per cent, of haemaglobin in cases of scrofu- losis and eighty per cent, in the cases of pulmonary-tuber- culosis make indeed a striking contrast and these figures seem to show that it is rather tubercular disease of the lymphatics than tubercular disease of the lungs that pro- duces the most pronounced anaemia. The cases of scrofulosis included in these tables were by no means aggravated ones. They did not complain of being sick and were not under treatment at the time examined. The diagnosis of scrofula was made by the previous history, old scrofulous scars and enlarged glands. The cases of pulmonary tuberculosis were also in a semi-latent stage. They complained of pain in the side and dyspnoea on exercise, all of them had a slight cough and four of them had had haemorrhages. These symptoms and the physical signs sufficient to make a diagnosis. Three of the girls of this class, within a month after the examination, developed a sharp attack of pulmonary tuber- culosis following the influenza. The cases in the two groups are, for the reasons given, fit cases for compari- son. Advanced and active scrofulosis is not here compared with mild and latent pulmonary tuberculosis ; neither is latent scrofulosis compared with a very advanced and active pulmonary tuberculosis. But if there is a difference in degree in these two groups, I think that so far as external symptoms and signs go the pulmonary cases are the more pronounced. But from a critical study of these cases which are not selected, but taken as they come from 166 examina- tions, I see no reason to doubt the correctness of the above figures. I think, therefore, that the table presented, so.far as it goes, seems clearly to show that tubercular disease of the lymphatic tissues causes a great reduction in the amount of haemaglobin in the blood, and that begin- ning tuberculosis of the lungs may cause very little if any reduction at all. Case No. 19, with history of previous haemorrhage, the amount of haemaglobin was normal. Rachford : Ancemia of Tziberculosis. 15 While it is not the purpose of this paper to inquire into all the causes of anaemia, it must be noted that in the group of cases presented, family tuberculosis so over- shadows all other causes that their consideration becomes a matter of secondary importance. If we study the influ- ence of lack of food and bad hygiene in producing anae- mia in these girls before they entered the convent, we find that those that suffered most from these causes before entering the convents, and were the slowest to recover from the effect of these influences after entering the convent, were the girls with tubercular family histories, I am led by this investigation, therefore, to believe that while lack of food and bad hygiene are undoubtedly direct causes of anaemia, it is probable that the most deleterious influence of these factors is exerted in an indirect way by predisposing to and prolonging attacks of This is more evident if we note the fact that anaemic girls with non- tubercular histories ordinarily recover rapidly after enter- ing the convent. In this connection we may call attention to the fact that of the non-tubercular cases with good family histories the lowest percentage of haemaglobin was seventy per cent, and the next lowest seventy-five per cent. Chronic diarrhoea, which is spoken of as one of the causes of anaemia, existed in only one case (No. 20), but this case also had a bad tubercular family history. If there be other factors in producing the anaemia in the group of cases I have here reported I have failed to dis- cover them. Clearly then, we may conclude that the above table establishes a most important relationship between anaemia and family tuberculosis. But we have yet to answer the most important query. How is the anaemia produced in those cases that have no apparent tubercular disease ! Is the anaemia a pre-tubercular con- * | It may be here noted that tuberculosis is probably a much more important factor in producing anaemia among convent girls than it is in the cases one sees in private practice, because of the fact that most convents are notoriously tubercular communities ; but this would not detract from the relative value of the figures given. 16 Rachford : A?icemia of Tuberculosis. dition the result of some mysterious inheritance, or is it due to a secret or hidden tuberculosis of the deep lym- phatics or other blood-forming organs ? We may now intelligently answer this question in the light of the two propositions heretofore established, viz.: 1st. Family tuberculosis is one of the great sources of anaemia. 2d. Tubercular lymphatic disease causes pro- found anaemia, while beginning pulmonary tuberculosis may not produce anaemia. In considering these propositions one is led to the opinion that the anaemia in apparently non-tubercular girls coming from tubercular stock is, when not readily explainable by other causes, very probably due to a deep- seated and hidden glandular tuberculosis. Further light may be thrown on this question by study- ing in the table the cases of anaemia (below seventy per cent.) that have tubercular family histories but are them- selves apparently free from active tuberculosis ; there are eighteen such cases and all of them except four were exposed to the contagion of tuberculosis by living in a house with a person sick of this disease. In the four not exposed§ the average percentage of haemaglobin was 64.5 per cent. In the fourteen exposed the average per- centage of haemaglobin was fifty-seven per cent. These averages, together with the fact that all the cases (5 in number) having fifty-five per cent, and less of haemaglo- bin are in the exposed class seem to indicate that expos- ure to tubercular contagion, as well as the tuberculous family history, plays a role in producing the anaemia. This is strongly confirmatory of the opinion expressed above that anaemia is due to a deep-seated disease of the blood-forming organs. Another very important point bearing on this question is that some of these apparently non-tubercular girls give on close questioning a history of having had, several years ago, “some kernels in the neck.” In such a case, with a history of previous external lymphatic enlarge- § By “ not exposed ” is meant that they did not live for any length of time in the room of one sick of tuberculosis. RACHFORD : A nee mi a of Tuberculosis. 17 ment, it requires no stretch of the imagination to believe that the anaemia is due to some hidden tubercular pro- cess. The case reported at the beginning of this paper is an example of this kind. This girl had the worst pos- sible family history and she had been constantly exposed to the contagion of tuberculosis for years. Notwith- standing these facts, when she presented herself to me for treatment there was no evidence of tubercular disease other than the pronounced anaemia (only twenty-five per cent, of haemaglobin). But this girl two years before “had kernels” in her neck caused no doubt by tubercu- losis of the lymphatic glands, and there is now no doubt in my mind, for the reasons given in this paper, but that her present anaemic condition is due to a tuberculous dis- ease of the deep lymphatics. This view of the case also explains why there is so great a falling off in the amount of haemaglobin in her blood, when the iron is discon- tinued. From all the arguments presented in this paper, I think I am justified in the conclusion that pronounced ance7nia, without apparent cause, is strongly suggestive of concealed tuberculosis. There is another question of great importance which may here be inquired into. Why has this girl, whose history I have recorded, escaped pulmonary tuberculosis? Bearing on this question, Hayem says: “The chlorotic ground,” in some instances, “seems to be unfavorable to the development of the tubercle bacillus.” He here uses the term “chlorotic” as synonymous with the term “ chloro-anaemic,” which he uses to describe the anaemic condition associated with tuberculosis. In some instances he believes that the anaemia occurring in those of tuber- cular stock not only is not caused by tuberculosis but actually protects against this disease by furnishing “ground unfavorable to the development of the tubercle bacilli.” In other instances he believes the anaemia is a pre-tubercular condition which, after the onset of the disease, either may or may not increase in severity with the progress of the disease. In still other instances he 18 Raci-IFORD : A nee mi a of Tuberculosis. looks upon the anaemia as a symptom of active pulmonary or other tuberculosis which progresses with the disease. These various relations between anaemia and tuberculosis, together with the various forms of tubercular chloro-anae- mia (simple anaemia, chlorosis and pernicious anaemia) which Hayem so indefinitely describes, leaves one in as much doubt as ever as to the value and meaning of anaemia in the study of tuberculosis. But it was not to offer a criticism on the work of Hayem that the above references are made, but rather to confirm in a modified form, his observation that “chloro-anaemia” in some instances “seems to protect against tuberculosis.” I also have observed that some of these anaemic girls with tuber- cular family histories, even though they may be repeat- edly exposed to tubercular contagion, escape active pul- monary tuberculosis for a surprisingly long time. The case reported is a striking example. But in the light of the preceding argument I believe that it is not the anae- mia, as Hayem supposes, that gives the protection, but it is the cause of the anaemia, viz., the deep-seated and glandular tuberculosis or hidden scrofula. In this connection may be mentioned an oft-repeated clinical observation that children who have recovered from an attack of scrofulosis seem to have a partial immunity against pulmonary tuberculosis and I may add, by way of parenthesis, that the conferring of immunity from pulmonary tuberculosis by an attack of scrofulosis is not inconsistent with the most rational theories || of immunity as they are taught to-day. The above explanation is given because it offers a sat- isfactory explanation of Hayem’s apparently inconsistent observation, that in certain cases the anaemia protects against tuberculosis; for surely it is difficult to believe that the anaemia itself could in any way protect against the tuberculosis, but it is not difficult to understand that the deep-seated glandular tuberculosis which is the cause |] See my paper “The Mechanism of Immunity,” Philadelphia Medi- cal News, 1892. RACHFORD : Anczmia of Tuberculosis. 19 of the anaemia may, when recovered from, offer some protection against pulmonary tuberculosis. In this paper the term anaemia has been used in a gen- eral sense and refers only to the diminution in the amount of haemaglobin in the blood and has no reference to the number of corpuscles. Although my observations on the classification of the anaemia of tuberculosis are not yet ready for publication, they lead me to believe that the typical anaemia of tuberculosis approaches more nearly simple anaemia than chlorosis, while in many instances the reduction of corpuscles does not correspond to the reduction in haemaglobin, often being less or rarely greater; yet this difference is not so great as to approach either the chlorotic type on the one hand or pernicious anaemia on the other. Cases of chlorosis, however, do occur and they are as a rule of more than ordinary interest and are very sug- gestive of the importance of this field of work ; for exam- ple, one case of simple anaemia was treated with iron until the amount of haemaglobin had reached seventy-five per cent. Under the iron the corpuscles had increased proportionately, the iron was discontinued and arsenic was given for three weeks. At the end of this time the number of corpuscles was 4,500,000 to cm. and the amount of haemaglobin had remained the same, seventy- five per cent. This case had under arsenic passed from simple anaemia to one of chlorosis. Another case IT in which menorrhagia was a prominent symptom was decidedly chlorotic. Another very instructive case IT 01 chlorosis in a colored child nine years of age was one of hip-joint disease, with extensive lymphatic involvement. The long-continued suppuration (three years) in this case had been followed by amyloid disease of the liver and kidneys. The liver in this case is enormously enlarged, occupying almost the entire abdomen. The possible connection in this case between the destruction of the liver function and the chlorotic condition of the blood These cases are not included in the tables. They belong to another group of cases examined later. Rachford: Anaemia of Tuberculosis. 20 SUPPLEMENTAL TABLE. Name. Age. In house. Tubercular History. Expos- ure to con- tagion. First Menses Menstrual Function. Per Cent. Hb. No. of Corpuscles. Personal History. i J. W. 19 6 Mother Yes 15 ( Metrorrhagia j Menorrhagia 30 3,730,000 Pale 2 M. S. 18 6 “ 1t 15 Regular 65 Well 3 A. B. 11 6 Negative Neg. Never 65 Lymph, enlarged 4 B. H. 7 1 Mother Yes “ 65 t t 11 5 K. E. 17 10 Negative Neg. 15 Regular tt 70 Well 6 M. G. 14 A Sister, mother, fath. Yes 13 70 2,200,000 Glands enlarged 7 M. W. !7 8 Father and mother 1t 13 Irregular 70 Pale, heart disease, valvular 8 E. E. 14 9 Negative Neg. 13 Regular 70 Glands enlarged, goi- 9 M. H. 14 8 Mother Yes 13 tt 70 Glands enlarged io E. G. 14 6 “ tt Never 70 No lymph, enlarg. ix L. T. 12 2 Father t1 70 Phthisis 12 C. H. 14 Mother “ “ 70 No lymph, enlarg. 13 R. N. 13 4 Negative Neg. “ 70 Lymph, enlarged 14 A. H. 11 J Mother Yes 70 No lymph, enlarg. 15 K. M. 11 2 Mother, 2 brothers “ “ 75 Decided lymph en- largement 16 R. O’C. 7 4 Father No tt 75 Decided lymph en- largement 17 M. W. 14 6 Mother Yes tt 75 4,400,000 Pain in side, dysp. 18 K. B. 17 3i tt t t 15 Regular 11 75 3,360,000 Scrofula 19 M. G. 18 6 Negative Neg. 14 80 Well Rachford : Anczmia of Tuberculosis. 21 20 M. R. 17 7 Negative C l Neg. 14 Regular 80 Well 21 A. M. 16 7 15 Irregular 80 Pain in side 22 M. F. 16 3i Father Yes 16 Regular 80 Phthisis 23 B. T. 14 3 Brother C1 Never 80 Well 24 E. D. 16 2 Good No Cl 80 “ 25 N. C. 13 i Negative Neg. C t Cl 80 Phthisis 26 M. M. 13 2 CC Cl 80 Lymph, enlarged 27 K. M. 14 10 Father and mother Yes CC 80 CC CC 28 T. M. 12 10 U Cl Cl C l 80 Phthisis 29 A. H. 12 2! Negative Neg. Cl 80 Well 30 E. H. 16 i£ C t Cl 85 c c 31 L. S. 16 7 Father and mother No 14 Regular Cl 85 Lymph, enlarged 32 M. M. 13 2 Mother, 2 brothers Yes 13 85 Phthisis 33 A. O’C. 13 4 Father “ Never 85 Well 34 N. F. 13 6 Good No 13 cc 88 CC 35 K. K. 18 8 Cl “ 14 l c 100 c c 36 J. P. 17 6 “ ( l 15 cc 90 c c 37 M. F. 16 8 1C t i 13 c c 9° Phthisis 38 M. C. 17 2 Brother Neg. 16 cc 90 Well 39 M. L. 17 4 Father and mother Yes 16 “ 100 CC 40 M. M’C. 14 1 Negative CC Neg. 12 cc 90 41 M. B. 15 5 14 c c 95 42 M. S. 16 5 Mother Yes 14 Negative 87 c c 43 A. 0. 14 2 Good No 13 Regular cc 90 Phthisis 44 J. F. 18 2 Father Yes 13 9° Well 45 B. M’C. 16 8 Good No 14 cc 95 CC 46 C. W. 14 6 CC “ 13 c c 90 c c 47 J- W. 14 2 Negative Neg. Never 100 48 N. W. 15 10 It CC 14 Irregular 95 c c 49 A. R. 14 2 “ CC Never 9° cc 50 K. M’C. 15 9 Good No 14 Regular 100 “ 51 M. H. 14 2 14 CC 100 52 M. W. 13 9 Negative Neg. Never 90 “ 53 E. S. 11 2 Good No 11 95 22 RACHFORD : Ancemia of Tuberculosis. offers a tempting field for speculation. These interesting chlorotic cases are, as I have said, the exception and not the rule, and simple anaemia is the characteristic anaemia of tuberculosis. As confirming the conclusions heretofore arrived at, the following points taken from the following table are worthy of note: 25 cases with tubercular family histories have an average of 75! Hb. 17 “ “ negative “ “ “ “ 88J “ 11 “ “ good “ “ “ “ 92J “ Excluding the cases of apparent pulmonary and glandu- lar tuberculosis we have 11 cases with tubercular family histories have an average of 72 %Hb. 12 “ “ negative “ “ “ “ “ H “ “ good “ “ “ “ 92h% “ It is here worthy of note that in none of the children with good family histories was there any evidence of tuberculosis. The following table shows the relationship of the anae- mia to the tubercular or non-tubercular history of these girls. The eighteen cases having less than seventy-five per cent, of haemaglobin are classed as anaemic ; the thirty-five cases having more than seventy-five per cent, of haemaglobin are classed as non-anaemic. No tubercular Tubercular Negative family history. tamily history. family history. 18 anaemic cases, . . None 14 cases, or 77§ % 4 cases, or 22% 35 non-anaemic cases, . 11 cases, or 11 cases, or 13 cases, or 3 ih% 3 '\% 37$% The examinations embraced in the supplemental table on pages 170-171, were made too late to be included in the table upon which this paper was based. An examination of this supplemental table will confirm and strengthen the conclusions arrived at above. These girls belong to the preservation class of the convent of the Good Shep- herd, located at Carthage, Ohio. RACHFORD : Ancemia of Tuberculosis. 23 The following table shows the relationship of the anae- mia to the tubercular family history after all cases of apparent tuberculosis have been excluded. No tubercular Tubercular Negative family history. family history. family history. 8 anaemic cases, with no ap- parent tuberculosis, . None 7 cases, or I case, or 87 i% 12h% 26 non-anaemic cases, with no apparent tuberculosis, 11 cases, or 5 cases, or 10 cases, or 42f % 19} % 3H% This supplemental table also contains thirteen cases of evident tubercular disease of the lymphatics, with an average of seventy-three per cent, of haemaglobin, and six cases of evident tubercular disease of the lungs, with per cent, of haemaglobin. These percentages confirm the conclusion heretofore arrived at, that it is tubercular disease of the lymphatics, rather than tubercular disease of the lungs, that produces the most pronounced anaemia. In short, we may say that a critical study of the second table confirms in every particular the conclusion drawn from a study of the first table and strengthens the deduction that pronounced ance- mia without apparent cause is strongly suggestive of con- cealed tuberculosis. This observation may throw some light on many of the obscure cases of anaemia and chlorosis that are constantly coming under observation. DISCUSSION. Dr. FISCHER.—I would like to state what I said in con- nection with the paper of Dr. Caille. He said amongst other things that he had used ozone in the treatment of tuberculosis with no benefit whatsoever, and had had benefit in connection with chlorosis and anaemia and also in pertussis. I asked Dr. Caille whether he had exam- ined the secretions or excretions of patients afflicted with anaemia or chlorosis for tubercle bacilli. He said he had not. Now I am confident that, as Dr. Rachford has just said, cases of anaemia and chlorosis with nothing else 24 Rachford : Ancemia of Tuberculosis. but anaemia are very often cases of true tuberculosis, because I have examined both secretions and excretions. Especially have I seen one case of a young girl with an obstinate form of chlorosis, who suffered from a severe form of diarrhoea and wherein from the discharges of the bowel I could get distinct tubercle bacilli. She had no cough whatsoever and this case was attended with anae- mia for almost two years until these bacilli were found. It was then proven that she had been in a family as nurse where a young girl had died from tuberculosis. I believe this person was infected and had no other symptoms except the diarrhoea. Dr. Osler.—In how many cases did he find a normal percentage of haemaglobin in the whole group examined ? Dr. Rachford.—I really can’t tell that, but I found a great proportion of the cases above eighty-five per cent. Dr. OSLER—Is it not exceptional to get in young wo- men a normal percentage of haemaglobin ? Dr. Rachford.—Yes. Dr. Osler.—I would like to express my appreciation of the value of this paper. It seems an admirable piece of clinical observation and I think the doctor’s conclu- sions are those which have already been arrived at, that the anaemia of tuberculosis is very commonly a simple anaemia, not chlorotic anaemia, though there are some instances undoubtedly in the early stages of tuberculosis in which the condition is what the French writers describe by the term chloro-anaemia. Dr. Rotch.—I want to express my appreciation of the very large amount of work that must have been done to prepare a paper of that kind. Dr. Rachford.—I that I have besides this, and would have incorporated in this paper, quite a group of younger cases had the time permitted. I have made probably one hundred blood examinations in a convent back of Cincinnati. Th&dA not incorporated in this group and they are very much younger children, fjpbm six to ten years of age. I think nearly all of these cases substantiate the same thing as those in this paper'.