'1

ARSENICAL GAS POISONING.

POISONING;

BY

ARSENIURETTED HYDROGEN OR HYDROGEN ARSENIDE .-:'.'

ITS PROPERTIES, SOURCES, RELATIONS TQ SCIENTIFIC AND INDUSTRIAL OPERATIONS, SYMPTOMS, POST- MORTEM APPEARANCES, TREATMENT, & PREVENTION :

WITH A. RECORD OF ONE HUNDRED AND TWENTY CASES BY DIFFERENT OBSERVERS

BY

Doctor of Medicine of the University of Glasgow

Fellow of the Faculty of Physicians and Surgeons of Glasgow

Licentiate of the Royal College of Physicians and Licentiate of the Royal College

of Surgeons, both of Edinburgh

Diplomale in Public Health of the University of Cambridge

Fellow of the Royal Society of Edinburgh ; Fellow of the Chemical Society

Examiner in Forensic Medicine and Public Health for Diplomas in Medicine and

Surgery, and for Diplomas in Public Health of the Scottish Triple Colleges

Formerly Examiner in the University of Birmingham

Reijius Professor of Forensic Medicine and Public Health in the University of Glasgow

President of the Faculty of Physicians and Surgeons of Glasgow

Medico-legal Examiner in Crown Cases

EDINBURGH

E. & S. LIVINGSTONE 1908

PREFACE.

THE following pages are the outcome of an investigation into the literature of poisoning by Arseniuretted Hydrogen consequent upon two cases which came within the ex- perience of the writer.

Notwithstanding the extremely poisonous character of this gas, it is surprising what little attention, comparatively speaking, has hitherto been paid to it in books devoted to Forensic Medicine and Toxicology, or, indeed, in the literature of medicine generally. From the occurrence of its toxic e fleets among persons engaged in very varied scientific and industrial pursuits, perhaps too little heed has been given to its incidence from the point of view of prevention.

Up till now, so far as we are aware, there has not been any systematic treatment of the subject, if we except a monograph by Geigy which deals with the record of thirty-seven cases, that of Lucas, with only a few, and some of these already recorded by Geigy, an article in one of our English medical periodicals by Dixon Mann and Clegg, which adds twelve additional cases, and some articles relative to the toxic results upon persons especially con- nected with military ballooning.

The remaining recorded cases which find a place in these

vi POISONING

.pages have been found as isolated contributions in the columns of home and foreign medical journals, or as the bases of inaugural theses of graduates for the doctorate degree of Continental universities. They number in all one hundred and twenty cases.

The writer, therefore, has tried in this little book to bring together in collected form all recorded cases from all sources known to him, as well as to consider the original records of the earlier cases, some of which are almost invariably quoted by previous writers. It is quite probable, however, that some cases have been overlooked, because the field of medical literature is now so very wide ; at the same time, an honest endeavour has been made to include in his pages all the known published cases, as well as some that have hitherto not been recorded.

From the very widespread use of arseniferous chemicals, notably of hydrochloric and sulphuric acids and metals, in many departments of chemistry in laboratories and chemical works and other industrial pursuits, it is obvious that cases of fatal poisoning are likely to arise in the future from time to time, and, sometimes, even under circumstances in which their occurrence might not be anticipated.

If .these pages serve no other purpose than to warn still more urgently against the possible risks of using such substances, or to cause precautions of an adequate kind to be taken in the known use of such substances, the book will have fulfilled its intention.

UNIVERSITY OF GLASGOW, 1908.

CONTENTS.

CllAI'. PA(ill

1. Properties and Sources of Arsen hire tted Hydrogen . 1

2. Relation of Incidence of Poisoning to Scientific and

Industrial Operations ...... 9

3. Symptoms . . . . . . . . 19

4. Cause of the Jaundice . . . . ~ . 28

5. Post-Mortem Appearances . . ... . 42

6. Symptoms and Post -Mortem Appearances produced

experimentally on Animals by Administration of the

Gas 56

7. Differential Diagnosis ... 66

8. Treatment . . 77

9. Preventive Measures J . . . . 82

10. Wall-Papers and Arsenical Poisoning ... 90

11. Synoptical Account of Recorded Cases (I. to XIX.) . 100

12. Synoptical Account (Continued) (XX. to XL.) . . 132

13. Cases observed by the Author . . . . .179

14. Cases observed by Author and Additional Cases (XLII.

toXLVII.) : . . . . . .187

15. Analytical Methods for Detection of Arsenic in Animal

Tissues . . . .'•'>.' 205

16. Bibliography. . ~. . . . .. .' 245

viii POISONING

APPENDIX.

TABLK I'AiiK

1. Showing (a) Name of Recorder, (6) Number of Cases,

(c) Occupations of those attacked, (d) Recoveries, (e) Deaths, (/) Time of Death after Exposure to Gas . 252

2. Showing (a) Causes of Poisoning, (6) Time of onset of

Symptoms, (c) Time of Exposure to Gas, (d) Initial Symptoms, (e) Incidence of (I) Hiemoglobinuria, (2) Jaundice, (3) Oliguria, and (4) Anuria . . . 256

3. Showing Post-Mortem Appearances in Brain, Skin,

Lungs, Pleurae, Heart, Liver, Gall-Bladder, Kidneys,

and Stomach ....... 262

4. Showing Conditions of (a) Blood-Corpuscles, (fe) Blood

Spectrum, (c) Urine, and (d) Bowels, during life of

those attacked . . . . . . .265

5. Showing (a) Source of Gas, (6) Source of the Arsenic,

(c) Results of Analyses of Materials for Arsenic, and

(d) Analyses of Organs of Body and of Excretions . 270

Bibliographical References to Cases I. to XLVII. . . 273

ILLUSTRATIONS.

* \'.i.

1. Arseniferous Wall- Paper . . . . . . 92

2. Sheridan Ddlepine's Copper Cone used in Reinsch's

Process 211

3. Apparatus for Marsh's Process . . . . .213

4. Do. do. (Tyrer's) . . . 214

5. Do. do. . . 217

6. Do. do. . . .218

7. Inland Revenue Laboratory Method by Electrolytic

Decomposition of Water . . . . .220

8. Do. do. do. . 221

9. Do. do. do. . 223

10. Do. do. do. . 224

11. M'Gowan and Finlow's Method by generating Hydro-

gen in Kipp Apparatus . . . . .229

12. Thomson's Arrangement for Marsh's Process . . 232

13. Dowzard's Apparatus for Gutzeit's Test . . . 234

14. Another Form for Gutzeit's Test (Kirkby) . . .239

POISONING.

CHAPTER T.

PROPERTIES AND SOURCES OF ARSENIURETTED HYDROGEN.

ARSENIURETTED hydrogen, arsenetted hydrogen, arsine, tri-hydride of arsenic, arseniate of hydrogen, hydride of arsenic, and hydrogen "arsenide are several of the names by which the gaseous compound of arsenic and hydrogen is designated. There is, however, another compound of these two elements. It exists in the solid state, and is commonly known as the hydride of arsenic, having the chemical formula of AsH2 or As2H4. The gaseous form, on the other hand, has the formula of AsH3> and may be produced in a variety of ways, the essential factor in its production being the presence of nascent hydrogen in arseniferous solutions. This gas, therefore, has the same chemical constitution as ammonia, NH3, except that the arsenic takes the place of the nitrogen. While we have but u passing interest in the solid hydride, it will probably be more convenient to dismiss it from further consideration by saying now what needs be said concerning it. In testing for arsenic under certain circumstances, the solid hydride may be formed, and error in the quantitative estimation of the total arsenic present may thereby result ;

B

2 POISONING

for example, in employing Marsh's process it is of the utmost importance that nitric acid, even in the smallest amount, should not be present, else the formation of the gaseous hydride will be prevented to some extent at least, and, instead, the solid hydride will be apt to be deposited as brown -coloured flakes upon the zinc used in the generation of the hydrogen. Again, if the gaseous hydride be passed through strong sulphuric acid (sp. gr. 1,260 to 1,843), the acid first changes into a brown colour, and, if the flow of gas be further continued, a brown flocculent precipitate is thrown down, which, being partly converted into arsenious sulphide, results in the evolution of some hydrogen sulphide gas. After the experiment has been continued for an hour, analysis of the collected precipitate shows that its composition is as follows : Arsenic . . . .95 per cent. Sulphur . . . .4-6 per cent. Hydrogen . . . 0'29 to 0*32 per cent. From which it would appear that the precipitate is composed of a mixture of the solid arsenic hydride, metallic arsenic, and arsenious sulphide.

Moreover, in contact with air, chlorine, nitric acid, and other gases, the gaseous hydride is decomposed into metallic arsenic and the solid hydride.

Since our interest at present, however, is centred upon the gaseous form, it will be well that we should consider some of the ways by which it may be produced, in view of the consideration which is proposed to be given in subsequent pages to cases of poisoning due to its entrance into the human body under diverse circumstances.

The following are some of the principal, viz. :

1. By the solution of arsenides of the metals in water, the solid hydride being formed at the same time.

SOURCES OF ARSENIURETTED HYDROGEN 3

2. By acting upon alloys of zinc, tin, or arsenic, or ores containing these or other metals and arsenic, or upon arseniferous zinc, with hydrochloric acid or sulphuric acid.

3. By the generation of hydrogen from zinc and impure hydrochloric or sulphuric acid, either or both of which contain some proportion of arsenic.

4. By Marsh's process, so-called from Mr. Marsh of Woolwich, who in 1836 was the first to employ the gas test for arsenic.

5. By dissolving zinc, tin, or iron in a solution of arsenic acid, with a dilute acid.

% 6. By electrolysis of arsenious or arsenic acid in solution in water.

Arsenious oxide, or arsenious acid as it is commonly called, has the formula As203, or As4H6, and each molecule of the solid oxide unites with three molecules of water to form two molecules of arsenious acid, thus :

3H2O + As2O3 = 2H3As03.

This arsenious acid, a tribasic acid, has a feebly acid reaction, but up till now has not been obtained in the free condition.

The chemical reactions which happen in Marsh's process, or in the electrolytic process, and generally when arseniferous metals or alloys are mixed with an acid, are as follow :

3Zn + 3H2S04 + H3AsO3 = 3ZnS04 + 3H20 + AsH3 3Zn + 6HC1 + H3As03 = 3ZnCl2 + 3H20 + AsH3

or : As2Zn3 + 6HC1 - 2AsH3 + 3ZnCl2

As2Zn3 + 3H2SO4 = 2AsH3 + 3ZnSO4.

With arsenic acid the equations are as follow :

4Zn + 4H2SO4 + H3As04 = 4ZnS04 + 4H2O + AsH3 4Zn + 8HC1 + H3As04 = 4Zn012 + 4H2O + AsH3.

4 POISONING

The gas which is obtained from any of the foregoing reactions is not pure, but is always mixed with more or less hydrogen. It may be collected over water, but the most scrupulous care must be exercised in any dealings with the gas because of its extremely poisonous action. It is a colourless gas, and "possesses a disagreeable odour, which has been described as " extremely repulsive," but which may be equally well, and more intelligently described as alliaceous or garlicky. It does not redden litmus. Its specific gravity according to Dumas is 2'695, air being reckoned as 1. One volume of the gas contains one and a half volumes of hydrogen and one-quarter volume of vapour of arsenic. It contains 96-15 per cent of arsenic. One cubic centimetre of the gas at a pressure of 760 millimetres and C. contains as much metallic arsenic as is equivalent to 0'0044 gramme of arsenious acid. Two cubic inches of the gas contain 1| grains of arsenic, as arsenicum. It liquefies at - 40° C. according to Stromeyer, but does not solidify even at - 110° C. It is slightly soluble in water, does not combine with acids or bases, and decomposes solutions of many of the metals which are precipitated by sulphuric acid, its hydrogen alone being oxidised and the arsenic precipitated in combination with the metal. At a red heat it is decomposed into free hydrogen and metallic arsenic. It burns in the air with a bluish-white flame, forming water and arsenious acid, which is deposited as a white crust or precipitate upon porcelain held just above the flame. If, however, the porcelain be held in the middle of the flame, the deposit will largely, if not entirely, consist of metallic arsenic.

There is another mode by which this gas, or a kindred gaseous form of arsenic, is evolved, and that is by the

SOURCES OF ARSENIURETTED HYDROGEN 5

growth of certain moulds in substances containing aisenious acids or arsenites, or even arsenic acid and arseniates. It is now well established that during the growth and development of such moulds hydrogen is evolved, and that if this evolution takes place in an arseniferous material a gaseous compound of hydrogen and arsenic is produced. This is a matter of considerable importance relative to arsenical wall-papers which are hung by the agency of paste made with flour or starch and water, because the flour or starch is an agreeable medium for such mould growth, and because of attacks of arsenical poisoning which have arisen, and are apt to arise, in persons living in rooms so decorated. To this we shall allude in more detail later.

By reason of the fact that zinc and other metals and commercial hydrochloric and sulphuric acids are more or less contaminated with arsenical impurities it becomes a matter of urgency that due precautions should be taken whenever operations involving the use of these, or some of them, in combination are engaged in, and it is for this reason that it becomes absolutely essential, whenever it is necessary to employ Marsh's process, where zinc and sulphuric or hydrochloric acid are used, for the detection of arsenic, that the reagents should be arsenic-free and should be proved to be so.

Otto1 emphasises the constancy of the impurity of arsenic in hydrochloric acid ; indeed, he goes the length of saying that " the purity of the hydrochloric acid which, in the process for the detection of arsenic and the metals in general, is often used in considerable quantities, should more especially be attended to. The acid should be treated with sulphuretted hydrogen, for there is no other

1 On the Detection of Poisons, 1857, p. 10.

POISONING

way to remove those traces of arsenic which are, perhaps, never wanting, but which become only evident in operating in large quantities. Four pounds of crude hydrochloric acid which I use in my laboratory for the preparation of the pure acid, and which passes generally for being free from arsenic, afforded, on being diluted with an equal volume of water and treated with sulphuretted hydrogen, a deposit in which the presence of the arsenic could be distinctly shown by Marsh's test."

This is further corroborated by the casual examination of almost any sample of the crude acid of commerce, and, moreover, of samples which make greater claims for purity. If we examine the figures given by Lunge,1 the above statement will be amply verified. The following table will indicate how variable are the proportions of arsenic which are found.

TABLE I.

Name of Observer.

Amount of Arsenic found.

Per cent of As^Os-

Houzeau

O'l gram AsCl3 per kilo.

0-0055

Filhol and Lacassiii

1-02 to 5 -007 ,

0-102 to 0-5007

Glenard

2 -5 grams ,

0-25

H. A. Smith .

6-91

0-691

In pan acid 36° T.

0'66 gram ,

0'066

Hjelt In roaster acid,

0-014 ,,

0-0014

32° T.

The same is true likewise respecting the impurity of sulphuric acid. Commercial acid being. now so largely made by roasting iron pyrites or mixed iron and copper pyrites, both of which contain relatively high proportions of arsenic, it is not difficult to recognise the source of the arsenic. In the sulphuric acid used at Waltham Abbey

1 &Uphuric Acid and Alkali, vol. ii. p. 180.

SOURCES OF ARSENIURETTED HYDROGEN 7

for the purpose of generating hydrogen for lead-burning, the amount of arsenic, as arsenicum, was found to vary from O'OOOll per cent to 0'00022 per cent.1 And since hydrochloric acid is not infrequently made from common salt acted upon by this impure acid, the reason for the impurity of the hydrochloric acid will also become apparent.

The amount of arsenic contained in sulphuric acid is sometimes not small. In 1856 Cameron stated in the Chemical Gazette that he found that about an ounce of crystallised arsenious acid was deposited after long stand- ing from eight pounds of this acid. Since that time, however, the comparative purity of sulphuric acid has improved, and it is now possible to purchase acid guaranteed free from arsenic, which is manufactured from sublimed sulphur. At the same time, most ordinary acids of com- merce are still arseniferous, and as it is from this class of acid that accidental poisonings are most apt to occur, it is essential, in order to avoid risks especially where hydrogen is likely to be evolved, that preliminary trials of purity should be made. It ought to be remembered that even at the present time some acids may be found to contain arsenic in amounts as high as from 0'045 to 0'140 per cent.

The dire results of this contamination or impurity have been brought home to the public by the arseuiferous acid used in the manufacture of glucose, which, in turn, was employed in the brewing of beer, from which, in Manchester especially, and in other parts of England, thousands of cases of arsenical poisoning arose, the most prominent symptom of which probably was peripheral neuritis.

1 Report by Dr. Robertson, 1904.

8

POISONING

In like manner zinc is very frequently contaminated with the same impurity. This is especially true of com- mercial zinc. Otto has compiled the results of analysis of different zincs by different chemists. He states that Jacquelin could not detect any arsenic in French products, that Brett l could not find in any British or foreign zinc any arsenic by a process capable of detecting l-5000th part of that substance, but that Schauffele2 found, on the other hand, the following quantities of arsenic per kilo, of different zincs.

The amount of arsenic, as arsenicum, found in samples of spelter used at Waltham Abbey varied from 0*00004 per cent to O'OOS per cent.3

TABLE II.

Arsenic in terms of a gram.

Villain's Method.

Jacquelin's Method.

French zinc . Silesian zinc . Vielle-Montagnc zinc Corfall zinc .

0-00426 0-00097 0-00062 0-00005

0-019 0-00853 0-0045

From a general survey of the cases recorded, of which a more or less full account is given in succeeding pages, it will be seen that most of the accidental poisonings had their origin in the use of these-or some of these arseniferous acids and metals.

1 London Philosophical Journal, 1842.

2 Journ. de Chimie mtdicale, 3rd series, t. vi.

3 Dr. Robertson, Report, 1904.

CHAPTEIi II.

RELATION . OF POISONING BY HYDROGEN ARSENIDE TO SCIENTIFIC AND INDUSTRIAL OPERATIONS.

IN a succeeding table (V., App.), wherein an attempt has been made to associate with each case of poisoning the source of the gas and the occasion upon which it was generated, the range of risk of poisoning by this gas to industrial and other pursuits will be readily perceived.

Obviously, the hydrogen arsenide was liberated in every case in which nascent hydrogen was being evolved in the presence of arseniferous materials. The occasion for such a chemical reaction as the generation of hydrogen arises in many pursuits ; for example, in physical and chemical experiments, in industrial occupations as far apart as researches in colours from aniliu derivatives, the making of toy balloons, the filling of military balloons, the synthetic manufacture of chemical substances, the making of bleach ing -powder, and the solution of arseniferous metals with hydrochloric and sulphuric acids, or of pure metals with arseniferous acids, such as the manufacture of zinc chloride or iron sulphate. If an analysis of the causes enumerated in the table be made, it will be found that the causes may be grouped under various heads, viz. :

9

10 POISONING

TABLE III.

Gronp Heads.

1. Chemical Operations in Laboratories

(«) Operation with known arseniferous materials = 8

(b) ,, ,, unknown ,, ,, = 14

22

(c) ,, not known ...... 1

2. Trade processes . . . . 4 - . . . .73

3. Military ballooning . . . -" . . . .16

4. Domestic environment (wall-papers) . .6

5. Causes not known ....... 2

Total cases . . . . 120

The laboratory experiments embraced the following, viz. :

(a) Generation of hydrogen for respiration to produce Tyndall's experiment of the " shrill " voice ; Cases IV., VI., X., X1IL, XXI.

(&) Demonstration to students of AsH3 by Marsh's test ; Case V.

(c) Intentional generation of AsH3 for experimental purposes; Cases I., II., III., XXX.

(d) Testing for arsenic in the viscera of a poisoned girl by Marsh's test ; Case VIII.

(e) Other experiments with arsenical compounds ; Cases XXVIII., XXXII.

The trade processes include the following, viz. :

(a) Kesearches in, or manufacture of, anilin colours; Cases VII., XIV., XVII, XXIII., XXIX.

(&) Filling of toy balloons with hydrogen ; Cases XII., XX., XL.

(c) Accidental addition of arsenic acid for sulphuric acid in hydrogen lamp for brazing purposes ; Case IX.

(d~) Extraction and treatment of ores ; Cases XI., XXV., XLVI.

POISONING BY HYDROGEN ARSENIDE 11

(«) Manufacture of zinc chloride and sulphate; Cases XV., XVI, XXVIL, XXXL, XXXIII, XLIV.

(/) Utilisation of galvanisers' zinc flux skimmings ; Case XXII.

(#) Manufacture of bleaching-powder ; Case XLI.

(7t) Bra/ing by the hydrogen flame ; Cases IX, XLIU.

(»') Galvanising; Case XLI I.

(f) In military ballooning, cases have arisen during the inflation and deflation of balloons filled with impure hydrogen; Cases XXIV, XXXIV, XXXVI, XXXVII.

(&) Galvanic processes ; Case XLV.

(/) Tank-cleaning; Case XLVII.

From the foregoing it is evident that cases exhibiting the toxic effects of hydrogen arsenide may arise in a large variety of occupations and enterprises. But if we take the fundamental cause of their occurrence, it is apparent that they arose solely from the presence of arsenical impurities in the reagents employed to generate hydrogen, or from the impure hydrogen liberated in the chemical reaction.

It might have been expected that chemists and scientists would not have been found in the list of victims and sufferers from this form of intoxication, owing to their knowledge of the arsenical impurity which such chemicals contain ; but, as the list indicates, it seems too frequently to have been taken for granted that the chemicals used were pure, and hence mishaps arose. It is very obvious that the observance of the simple precaution of ascertain- ing, before any experiment is made in which hydrogen is to be, or may be, evolved into the atmosphere of a laboratory, that the reagents are arsenic-free, will effectually safeguard against such deplorable occurrences being repeated.

In addition to the foregoing list of causal conditions, there fall to be noticed certain others, and of these the

12 POISONING

first to be noted is the evolution of this arsenical gas in and from electric batteries in which sulphuric acid is employed. M. Grommier de Lyon has recorded ] a certain number of cases of poisoning among persons employed continuously in a confined space in which the electric current was generated by means of bichromate of potash cells. In this instance, as in others, it was found that the cause was arseniferous sulphuric acid. Similar results have followed in a galvanic process for the recovery of copper (Case XLV.), p. 201. Lucas 2 also points out how, for the same reason, like results may arise in the manu- facture of iron sulphate. On one occasion, he states, Professor Layet was making a visit to a chemical work, when he perceived the garlicky odour characteristic of hydrogen arsenide apparently arising from a vat in which, it appeared, ferrous sulphate was being made from scraps of old iron by solution in sulphuric acid. On putting some of the material from the vat into a Marsh apparatus, Layet was able to demonstrate the marked presence of arsenic in the acid by the AsH3 which was liberated.

Eoasting of arseniferous ores is also liable to be attended by similar manifestations of poisoning, but it is not clear in all cases that the cause of the toxic results is this particular gas, although at the same time it seems undoubtedly to be" some gaseous or vaporous form of arsenic. Danger always exists, therefore, in the roasting of those ores which are usually associated with arsenic, such as iron pyrites, iron and copper pyrites, and cobalt ores. Some risk, also, is incurred in the manufacture of cobalt blue, which is a compound of aluminium and the protoxide of cobalt.

1 Acad. de Mid. April 10, 1877. 2 De V Empoisonnement par I'Hydrogene Arsbiie, Paris, 1895.

POISONING BY HYDROGEN ARSENIDE 13

The following table tries to summarise the professions and occupations, the members of which are exposed to risks of poisoning by hydrogen arsenide.

TABLE IV.

I. Professional chemists.

(a) In medico - legal analyses in cases of arsenical

poisoning.

(6) In preparation of AsH3 for demonstration purposes, (c) Researches in anilin colours and in arsenical

compounds. II. Physicists and Physiologists.

(a) Inhalation of arseniferous hydrogen in experiments on

the voice, or as to pulmonary capacity, or other like

experiments.

III. Workers in anilin colours.

(a) Preparation of arsenic acid ; working at retorts ; treatment of raw materials.

IV. Chemical workers.

(a) Manufacture of iron sulphate.

(6) Manufacture of zinc chloride and sulphate.

(c) Zinc-smelting.

(d) Roasting and extraction of mineral ores.

(e) Manufacture of bleaching-powder.

(/) Manufacture of soda sulphate by treatment of soda

lye with arseniferous sulphuric acid. V. Ballooning for military and other purposes, (a) Inflation and deflation of balloons. (6) Leakages during balloon flights. VI. Plumbers. VII. Galvanising.

To this subject of ballooning some detailed attention must be given.

Of late years, probably the most common occupation associated with poisoning by this gas is ballooning, and particularly the operations .of inflating and deflating

14 POISONING

balloons, although it has even been found associated with balloon free ascents. Attention has frequently been called, especially by Continental writers, to this. Among other writers on this aspect of the subject may be named Maljean, Durand, Oulmont, Crone, Granjux, and others. Probably of these the first-named has given most attention to the subject. In a paper on " Intoxication par le gaz hydrogene arse*ni6 chez les ae*rostiers," l he enters very fully into the subject.

He points out that arseniuretted hydrogen is constantly found in the hydrogen employed in filling balloons, because it is manufactured from impure reagents. The accidents to aeronauts and those who work with balloons are often less grave than in other circumstances, although the death-toll among balloonists and those associated with them has not been small.

In military ballooning, hydrogen is exclusively used, because it is the lightest of all the gases, and is the easiest to manufacture. In regular military establish- ments the gas is made in special apparatus from the action of sulphuric acid on iron, but sometimes zinc is used in place of the iron. At a distance from ordinary facilities of manufacture in this way resource is had to the use of compressed hydrogen in steel cylinders, the pressure employed being 120 atmospheres. If the reagents were pure, the hydrogen evolved would be devoid of any foreign gas, and consequently would not be toxic. Besides, as Maljean points out, when pure it possesses the maximum of those qualities which best befit it for ballooning. But owing to the need of manufacturing the gas quickly in large quantities and in a fresh condition, commercial methods have come to be adopted, and from commercial

1 Arch, de mid. et phann. mil. 1900, vol. xxxv. pp. 82-102.

POISONING BY HYDROGEN ARSENIDE 15

products which are always more or less impure. Sulphuric acid made from pyrites contains a relatively large amount of foreign matter, amongst which are arsenious oxide and arsenic oxide. Certain Belgian pyrites, he tells us, contains from 2 per cent to 5 per cent of arsenic in the form of arsenite of iron, and other pyrites contain both arseniciil and selenium compounds. When prepared, however, from sublimed sulphur, the acid may be considered to be free from arsenic, at least in such amounts as to be harmful. The metal used in France in making hydrogen for filling balloons is generally iron in the form of iron turnings or shavings of steel and of castings, which can be bought at a low price as the waste of certain metallurgical industries. All of these contain a certain amount of arsenic associated with carbon, phosphorus, sulphur, and silicon. The source of the arseniuretted hydrogen is not far to seek. Manufactured as above, the gaseous product always has a disagreeable and complex odour, in which, however, the garlicky odour predominates. In view of the elements commonly found in the iron or steel employed, it is not surprising that, in addition to the arsenical gas, other gases as H2S, PHS, SeH3, S02, CO2, and other carbon gases are to be found admixed with the hydrogen. Apart from their poisonous properties, the presence of these adventitious gases is a positive dis- advantage relative to the purpose for which the hydrogen is wanted. Being heavier than hydrogen, they make the product heavier, and consequently cause it to lose some of its ascensional power. Moreover, as experience has proved, some of these gases exert a distinctively destructive effect on the material of which the fabric of the balloon is made, and hence this adds to the danger of ballooning. In one case, for example, when the interior of the fabric

16 POISONING

was examined, it was found covered with a fine brownish- coloured powdery material, which on analysis was found to contain arsenic and selenium.

The apparatus in use in the military establishments in France is the ^invention of Colonel Eenard. It is a circulatory apparatus, in which the gas is generated, washed, dried, and verified as to ascensional power. It consists of the following parts, viz. : (1) the generator, into which the metal and acid are placed, and in which is an arrangement whereby the iron sulphate formed in the reaction is diverted automatically toward the exterior; (2), the washer, into which the liberated gas from the generator passes, and where it is met by a sheet of cold water, which is constantly being renewed, by which it is supposed to be washed or scrubbed free of certain of its contained adventitious gases ; (3), the dryer or desiccator, in whicli is placed caustic lime, or a mixture of caustic lime and of wood sawdust moistened with iron sulphate solution ; and (4) the tester or verifier, by which the contained amount of watery vapour in the gas is ascertained ; and, last of all, an apparatus by which the ascensional power of the gas is estimated.

The question next to be asked is, What is the effect of these united operations on the purity of the gas ? It is known that hydrogen is fourteen times lighter than air, and that, when pure, a cubic metre of the gas should weigh 89 grammes. In practice, however, it has been found that the product obtained from the foregoing process rarely weighs less than 150 to 200 grammes, which fact alone is the proof that other gases than hydrogen are present, and these not in small quantities. The presence of hydrogen arsenide betrays itself in the product by its alliaceous odour; but, in addition, its presence may be

POISONING BY HYDROGEN ARSENIDE 17

demonstrated chemically by the effect of the gas on a piece of filter paper moistened with a strong solution of silver nitrate placed in the stream of the gas. If hydrogen arsenide be present, the paper will show, probably by the end of an hour, certain black* stains due to reduction of the silver to the state of oxide, and certain other brick-red stains of arseniate of silver. Maljean accounts for the presence of the arsenical gas after the foregoing treatment in the following way : The hydrogen and other gases, as they leave the generator, are at a fairly high temperature, and are saturated with watery vapour, besides containing solid and liquid participate matter. When the gases reach the washer, the watery vapour is for the most part condensed and is freed from these solid particles. Some of the contaminating gases are very soluble in water, as C02, H2S, and SO2, and are therefore arrested. Others, however, are less soluble, as, for example, AsH3, which requires five volumes of water for its solution, and resists solution even more than SeH3 ; thus it appears in practice to be little affected in the washer. In the desiccator, the gas gets rid of any remainder of watery vapour, and the lime arrests any C02 and sulphur gases. The iron sulphate in the sawdust arrests the H2S and analogous gases. But the contact of the gases during the circulatory process seems to be too short to have much effect in arresting thoroughly these gases, and besides, the mixture of sawdust and lime is apt to become saturated comparatively quickly : thus the gas is not deprived to any great extent of the arsenical gas.

Of the other papers which deal with this question, the following may be cited, viz. Durand,1 " Intoxication des

1 Annales d'hyy. 1900, 3rd ser., xliv. pp. 35-38.

C

18 POISONING

aerostiers par 1'hydrogene arseiiie," and Granjux l bearing a similar title.

In lead-burning operations, especially those which are being conducted in confined or ill -ventilated places, dangers may arise from the arsenical gas which is present whenever the acid or zinc, or both, used for generating hydrogen for the brazing lamp are arseniferous. Case XLIII. is an example of this kind.

1 IMletin medical, April 14, 1900, p. 354.

CHAPTER III.

SYMPTOMS OF POISONING.

THE symptoms which usher in the poisoning by this gas, while they are indicative of the operation of a profound cause upon the system, cannot be looked upon as character- istic or pathognomonic of this particular form of poisoning, since many or most of them individually or in small groups are common to other conditions with which they may, at first at least, be reasonably confounded. Their incidence and sequence, however, are characteristic, inas- much as they point to the operation of .a poison within the body, and especially to the action of a poisonous gas when the incidence, development, and range of symptoms are fully reviewed.

In not a few cases the interval which elapses between the period of exposure to the gas and the onset of the more definite symptoms is sufficiently long to prevent the causal relationship of the one to the other to be clearly perceived ; at the same time, in several other cases the period of onset is almost coincidental in point of time with the period of exposure, or at most is only separated therefrom by an interval of time which varies from minutes to a few hours.

Period of Onset. The time of onset of symptoms after exposure to the gas, where only hydrogen arsenide is present, depends obviously upon 'two factors, viz. (a)

19

20 POISONING

the percentage volume of the gas in the atmosphere breathed, and (6) the condition of the person at the time of exposure. The latter, however, is probably of minor importance compared with the former, and operates but in a limited way.

To these may be added, in certain very rare instances, the presence in the same atmosphere of other poisonous gases, such as antimoniuretted hydrogen.

From a rapid glance at Table II. App., it will be seen generally that the symptoms begin to appear from a few minutes up to twenty -four hours after exposure, the average period being from three to six hours.

There can be little doubt, moreover, that the time of onset is largely affected and determined by the nature of the operation in which the gas is being evolved, the relation of the workers thereto, and also by the character of the work -place with respect to ventilation. Where the gas has been inhaled as an unknown adulterant, the symptoms are fairly constant as to the time of appearance. While, also, the element of non- ventilation or of im- perfect ventilation of the work-place is operative more or less prejudicially, a careful examination of the recorded cases will reveal that, even where the operation is con- ducted in the open, poisoning equally followed, and sometimes in a very unexpected fashion as to its incidence upon those engaged. Hydrogen arsenide having a greater specific gravity than air, and therefore being more likely in certain conditions of want of ventilation to be found in the lower strata of the atmosphere in the work -place, might be expected to act more constantly and uniformly in such circumstances. Instead of this being the case, however, the gas presents grave anomalies of action, and the factor which evidently determines its action upon a

SYMPTOMS OF POISONING 21

series of individuals so employed at the same operation is the presence or absence of local currents of air which tend to irregular distribution of the gas. This is very apparent in the series of cases recorded on p. 165, which occurred at Accrington. There the men who were working nearest the point of generation of the gas, viz. on the platform, were the least, and those in the well at a lower level were the most seriously affected, while even of those on the platform, one was severely poisoned, one was but slightly attacked, and a third escaped entirely. At the same time, in places where ventilation did not practically exist at all, as in the Wolverhampton cases (p. 141), the Irvine cases (p. 179), and others, the effects upon the workmen were * more disastrous.

Obviously the lethal character of the gas essentially depends upon the precise quantity of it which has been inhaled, and therefore, in general terms, the length of time of exposure to its influence will be indicative of the percentage amount of it in the atmosphere breathed by the person at the time. We must, however, discriminate between those cases in which impure hydrogen had been inhaled intentionally for experimental purposes and those in which it'was inhaled accidentally as part of the ordinary atmospheric environment of the individual worker, because in the former the adventitious arsenical gas, being directly inhaled as an unwitting component of the hydrogen, exercises a more rapid and effective striking action.

Nature and Character of Symptoms. Although in individual cases one particular symptom may be described as being more specially marked and prominent at the outset, and may be specially referable to one organ of the body, the earlier symptoms may be summarised as follows: (1) an indefinable feeling'of illness and of great

22 POISONING

weakness; (2) giddiness; (3)faintness; (4) pains in head and epigastrium ; (5) coldness of body ; (6) sense of oppression of breathing; accompanied, in some cases, by some measure of cyanosis ; and (7) nausea, sickness, and vomiting.

These are quickly followed by (1) continuous vomiting of bilious matters at first, and, later, of bloody material ; (2) jaundice, which may vary in tint from golden yellow to mahogany, ranging through coppery, bronze, and mulatto tints, which extends usually over the whole body, but which, in lighter cases, may be located solely in the conjunctives ; (3) thirst and dryness in the throat, with weakness of voice ; (4) pains in the loins ; (5) pains or sense of fulness over the region of the liver; (6) haemorrhages from one or more different parts of the body ; (7) heemoglobinuria or hasmaturia, oliguria, and, in cases going on to a fatal termination, anuria ; and (8) clear intellectivity, but sometimes, minor degrees of stupor, although generally before death supervenes some measure of unconsciousness, with or without delirium.

In addition to these symptoms, and mostly towards the end, hiccough and subnormal temperature are found, while physical examination of the body of the patient will reveal in most cases enlargement of the area of dul- ness of liver and spleen. Probably the most outstanding symptoms, and those which should lead to a suspicion of poisoning by this gas, especially where there is a history of exposure to gaseous emanations, are the following, viz. (1) severe nervous shock ; (2) bloody urine ; (3) jaundice of a more or less coppery colour which quickly supervenes ; and (4) alterations of the blood, as seen on microscopic examination.

The following detailed description of the symptoms will assist to complete the clinical picture.

SYMPTOMS OF POISONING 23

If those cases be first considered in which hydrogen containing a certain unknown admixture of AsH3 was inhaled for experimental purposes, the time.of onset and the character of the symptoms may be better studied. Nine of the cases hereinafter narrated (IV., VI., X., XIII., and XXI.) had their origin in this way. Of these, two deaths resulted. The symptoms came on immediately after the inhalation. They consisted of giddiness, fainting, general feeling of illness, and unsteadiness of gait, and were succeeded by shiverings and by pains in the loins. More or less quickly after these supervened bloody urine and haemorrhage from the nose or bowel, together with jaundice.

In another series of cases (I. and III., involving three persons) in which AsH3 was being intentionally generated, and in which the effluent tube was sniffed deliberately to discover the precise moment at which the gas began to be evolved, the symptoms also developed with marked rapidity. Moreover, this series is of considerable interest as affording some approximate indication of the very small amount of the gas necessary to produce serious effects. In none of the three cases of this series could much of the gas have been inhaled ; yet, notwithstanding, within an hour thereafter, the symptoms began to exhibit themselves in the form of intense headache, vertigo with buzzing in the ears, vague uneasiness, feeling of great weakness, burning thirst, muscular inco-ordiuation of the lower limbs, shiverings, jaundice, and bloody urine. The reader is referred to Case XXIX. for a graphic description of these symptoms and their incidence.

The remaining cases might be divided in further series, such as those in which the arseniferous gas was being intentionally worked with, and 'those in which it was

24 POISONING

accidentally present in some other chemical operation ; but this would not serve any particularly useful purpose. We therefore confine our observations to the significance of the symptoms themselves.

The keynote of the symptomatology would seem to be the rapid dissolving or haamolytic action of the gas upon the blood corpuscles, and the resulting incapability of the corpuscles to convey sufficient 'oxygen to the different organs of the body, together with the inability of the emunctory organs, liver and kidneys, to cope with the elimination of the dissolved haemoglobin. The symptoms, therefore, have direct relation, first, to the effect upon the organs of this imperfect or disorganised blood -supply, and, second, to the effect upon those organs by which the poison itself and the products of the disintegrated blood- corpuscles are eliminated from the body.

I. Effect upon the Bodily Organs due to Impure and Imperfect Blood-supply.

With reference to the nervous system, it will be evident that the effects on the brain are indicated by the giddiness, pains in the head, inco-ordination of thought or inability to concentrate thought, flashes of light before the eyes, buzzing in the ears, and unusual sensitiveness to jarring sounds, and on the spinal cord, by muscular inco- ordination of the lower limbs and tingling of the limbs ; while on the general nervous system they are indicated by the indefinable feeling of uneasiness, illness, and weak- ness, and by coldness of the body and shiverings.

The effects on the heart are shown by the feeling of faintness and by feebleness of pulse : and on the lungs by the sense of oppression of breathing without any accom- panying physical evidence of lung lesion, due to the increased systemic need for oxygenisatiou of the blood.

SYMPTOMS OF POISONING 25

II. Effect upon Organs by which Poison and Products of Blood-disintegration are eliminated.

The organs mainly involved under this category are the stomach, liver, kidneys, spleen, and, in varying degree, the intestines. The action of the poison circulating in the blood upon the stomach corresponds very closely to the action of the same poison when ingested. Vomiting is a constant feature of all the recorded cases, and it was of a severe, persistent, and continuous character. The vomited matter consists at first of the ordinary contents of the organ, then of bile -tinged fluid, and latterly of bloody matter either of the " coffee-grounds " character, or of more or less pure blood. It would thus appear as if arsenic, by whatever channel it is taken into the body, has an elective action upon the stomach, and the organ may in this light be reckoned as one of the normal emunctories or eliminating organs of the poison from the body.

The action of the gas upon the liver is indicated by the jaundice, that is through its haemolytic action on the blood -corpuscles. It will be noted that jaundice, of varying tints in lighter cases, and of a coppery or bronze hue in severer cases, was present. Indeed, this may be looked upon as one of the chief outstanding symptoms of this form of poisoning.

The cause of the phenomenon is discussed in a separate chapter, therefore it is only now necessary to note the constancy of the phenomenon itself. As a direct result of the importation to the liver of a blood -supply abnormally charged with disintegrated products, enlarge- ment of the organ is usually found to exist, as is indicated by increase of the area of dulness. In this way, also, is accounted for the feeling of fulness or tension in the

26 POISONING

region of the organ, so often complained of by persons attacked.

The kidneys likewise share prominently in the general distress. Early in the history of a case, pains in the loins, sometimes to a marked degree, assert themselves, and accompanying these is a strong desire at first for micturi- tion. The kidneys being among the chief organs by which arsenic in any form is eliminated from the body are always involved to a greater or lesser degree ; and this difficulty in functioning is increased further by the fact that the disintegrated blood - products seek by these channels an outlet from the system. The effect of both is the production of bloody urine and a proliferative nephritis. Blood-coloured urine is an early and constant feature in these cases, and it persists for a variable time after cessation of more serious symptoms. While oliguria is most commonly present, it must not be forgotten that in certain isolated cases it may not be a prominent feature. In most of the cases ending fatally anuria usually is established for some time prior to death. This is in all likelihood due to the nephritis which is set up, from which also undoubtedly originate the symptoms of uraemia which are found in certain of the recorded cases.

The spleen, too, shares in the blood disturbance. In several cases it has been found enlarged during the life of the patient. The intestines exhibit alterations in function which must be reckoned as part of the eliminating pro- cess referable to arsenic. Diarrhosa is not an uncommon symptom, and bloody stools are also by no means rare.

With regard to the occurrence of haemorrhages during the currency of such cases, it ought to be said that they are consequent upon the dissolved condition of the

SYMPTOMS OF POISONING 27

in the blood-stream, and to fatty degenerative changes in the capillary vessels. These haemorrhages may assume the form of meltena, purpuric skin eruptions, epistaxis, or bleeding from the gums, the prepuce, or even the glans penis.

Table II., Appendix, summarises (a) the time of onset of symptoms in the cases recorded, (6) the time of exposure to the gas, (c) the initial symptoms, and (d) the incidence of (1) hamioglobinuria, (2) jaundice, (3) oliguria, and (4) aimria.

CHAPTER IV.

CAUSE OF THE JAUNDICE.

THE intimate cause of the jaundice in this form of poison- ing has long been a vexed question, and much has been written and many experiments on animals have been per- formed to elucidate it. It is not clear, indeed, even now that a uniformity of view has been reached. The crux of the question has always been whether the jaundice originates in the liver or in the blood, or partly in both ; whether, in other words, its source is hepatogenous or hseniatogenous, bilipheic or heemopheic. The interest in this question probably had its origin in the fact that, along with the jaundice which is uniformly present in some measure, this gaseous poison has the power to liberate by its haemolytic action the haemoglobin from the stroma of the red corpuscles, and so to allow it to pass into solution in the blood plasma ; and it was believed that it was because of this fact that the urine which is passed •soon after the onset of toxic symptoms should be highly charged with blood-colouring matters.

For a long time, opinion was sharply divided on the subject, but perhaps only so long as the question was solely or mainly considered from the speculative point of view. This academic discussion did not, however, substantially contribute to the scientific knowledge of the subject. It became clear that two methods only were available by

28

CAUSE OF THE JAUNDICE 29

which the truth could be ascertained regarding the cause, vix. (a) clinical observation, and (6) experimentation on animals. The former, however, could only illustrate the effects of the operation of the poison, and be supplementary to the latter, whereby the mode of action of the poison could be followed stage by stage by preparative methods, such as cutting off the circulation of the liver from the general circulation, or even by the extirpation of the liver itself.

The whole question of the relationship of the blood- pigments to the bile-pigments came thus to be opened up ; and, in addition, the aid of the knowledge of chemical pro- cesses in the bodily economy had to be invoked.

Probably one of the first incentives to the study of the subject arose from the discovery made by Virchow in 1847 that in blood extra vasated into the living tissues a certain metamorphosis of blood-colouring into bile-colour- ing matters took place. From this was suggested the inquiry whether in certain forms of icterus, particularly such as those which occurred where there was no mechanical obstruction to the outflow of bile and by this is meant even catarrhal obstruction, the icterus could be due to such a metamorphosis taking place within the living circulation without the intervention of the liver. The answer at first given to this interrogation was in the affirmative, and thus it came to be assumed that there did exist a hsematogenous form of jaundice as well as a hepato- genous form, the latter arising from a re-absorption of the bile from the liver into the blood. But in respect that the former name committed those who adopted it to a definite theory as to its cause, and thus did not meet the views of those who were not so clear as to its origin, but who at the same time believed that there was a form

30 POISONING

which had not its origin in the liver, Quinke J suggested the name of " anhepatogenous " jaundice, thus getting rid of the view that its production was necessarily due to the blood, while preserving, at the same time, the idea that its source might be other than in the liver.

Then followed the experiments and observations of Kiihne.2 In 1866, however, Ley den in his contributions to the pathology of icterus3 tried' to distinguish clinically between the two forms of jaundice, and he came to the conclusion that the best test whereby to distinguish the anhepatogenous from the hepatogenous form was to determine the presence or absence of bile-acids in the urine. He declared from his experience that the bile- acids could not be demonstrated in the urine of the first- named form, but could be discovered by appropriate tests in the urine of the last-named.

In 1868, Naunyn 4 subjected the question to the crucial test of experiments upon animals. His experiments were made mostly upon rabbits, but were negative in respect of the discovery of bile-acids in the urine.

Clinical experience had, however, in the meanwhile, demonstrated that other conditions and substances than hydrogen arsenide could produce solution of the haemo- globin in the blood-stream ; such, for example, as extensive burning of the body, paroxysmal hsemoglobinuria, haemo- globin uric or " black- water " fever, transfusion of blood, severe infections, and other forms of intoxication, as by potassium chlorate and pyrogallic acid. The general opinion therefrom was that the cause of icterus was to be found in the conversion in the blood-stream itself of the

1 Virchow's Archives, Bd. 94, 1884. 2 Ibid. Bd. 14.

3 Beitrage zur Pathologic des Icterus, 1866.

4 Reichert und Dubois, Archives, 1868.

CAUSE OF THE JAUNDICE 31

blood-pigment into bile-pigment : consequently tbe belief in an anhepatogenous form of jaundice persisted.

Stadeliuann, in an article " Ueber Toluylendiainin und seine Wirkung auf den Thierkb'rper, Beitrag zur Lehre vom Icterus," J gave the results of experiments on dogs as to the poisonous action of toluylendiamin, from which he observed that among the effects produced were icterus of the tissues, hsemoglobinuria, and the presence in the urine of bile -pigment and bile -acids. In the post-mortem examination of these dogs, he found a very marked thickening of the bile and distension of the gall-bladder and ducts with tough, tenacious or inspissated bile, which deposited a considerable amount of amorphous sediment and numerous crystals of bilirubin. He noted, besides, that the more severe the icterus, the more markedly was the bile thickened and the gall-bladder distended. From these facts he concluded that, by reason of the difficulty which such bile experienced in passing through the common duct into the intestine, the resulting engorgement or stasis caused its absorption into the blood, and therefore icterus of the skin and tissues to ensue. This discovery of bile-acids in the urine indicated a jaundice by absorp- tion of bile products from the liver, and proved, for this toxic substance at least, which exercised a hsemolytic action, that the jaundice was not haematogenous but hepatogenous.

The same observer found by further experimentation on dogs poisoned by hydrogen arsenide that the gall- bladder and gall-ducts were likewise filled with tough or inspissated bile, and, further, that the bowel contained a large quantity of that fluid. On a dog in which a biliary fistula had been established, he experimented with this

1 Archiv. fur ejcperimentale Pathologie und Pharmacologie, Bel. xv.

32 POISONING

gas, and he observed that although the total quantity of bile secreted in twelve hours was diminished to about one- third of the average total amount, the relative amount of bilirubin was increased three and a half times above the normal.1 Likewise the bile became dark in colour and thick and tenacious in consistence.

From all these observations, therefore, he reached the conclusion that, although this gas undoubtedly exercised a marked solvent effect upon the haemoglobin of the living blood, the blood itself was not the source of the jaundice, but that the source of the jaundice was the liver, which by reason of the abnormal blood and abnormal nutritive material imported to it, produced an abnormal bile rich in bile-pigment, but poor in bile-acids and water.

Notwithstanding these researches, he approached the solution of the question in another way, viz. by inject- ing into dogs pure crystalline haemoglobin, thus simulating to some extent the condition of the blood after the exhibition of hydrogen arsenide.2

From these experiments, also, he found the same general effects produced, viz. a reduction in the total secretion of bile and the formation of a tough, tenacious bile, rich in bile -pigment. These experiments were followed by other series of experiments by other observers. Stern 3 injected into rabbits varying proportional amounts of haemoglobin. He found that when the amount injected exceeded 0'02 gramme per kilo, of body- weight of animal, the liver of the animal was not able to change the extra blood-pigment into bile-pigment, and consequently that some part of the surplus amount presented itself unchanged

1 Archiv. fur experimentale Patholngie nnd Pharmacolvqie, Bd. xxiii., 1887.-

2 Ibid. 1888. 3 Virchow's Archives, 1888.

CAUSE OF THE JAUNDICE 33

in the bile. If, however, the quantity injected much ex- ceeded the proportion named, ha'iiioglobinuria made its appearance.

Gorodeeki's experiments consisted of injecting into dogs, either subcutaneously or in peritonea, hemoglobin solution, and these showed that the secretion of bile-pigment was increased to the extent of 60 per cent.

Schmidt l has given as his opinion that free haemoglobin under ordinary circumstances is changed by the liver-cells into met-hiumoglobin as a preliminary step in the process by which it is ultimately converted into bile-pigment.

Robert2 is of opinion that between the condition of met-haemoglobin and bile-pigment there is an intermediate state of the colouring matter, which, although it bears a somewhat close resemblance to hamiatin, does not quite correspond to it, since it does not give a spectrum. It has not yet been clearly demonstrated that this inter- mediate colouring matter is bilirubin, but it corresponds to it in the negative fact that, like bilirubin, it yields no spectrum, and therefore is a substance which does not contain iron. It would appear, therefore, that in the liver the iron of the haematin is set free by the action of the hepatic cells, and is probably retained by them, since bilirubin is an iron-free substance. In bilirubin, however, which is eliminated in ordinary bile from the liver, there is a certain percentage of iron present, to the extent, indeed, of T4 to 1-5 per cent, whereas hoematin contains about 9 per cent of that metal.

In order, therefore, to assume the likely production of bilirubin from hrematin, we must suppose that some- where in the animal economy the iron is separated and

1 Biolog. CentralUati, 18&0. 2 JjeJirkuch der /ntoxikationen, 1893.

34 POISONING

stored up for future use. All observations point to the liver as the organ in which this is most likely to take place. On this hypothesis, then, Nencki and Sieber have suggested the following chemical equation as representing the change which occurs, viz. :

C32H32N404Fe + 2H20 = Fe + 2C16H18N203; Hsematin Bilirubin

There can be little or no doubt that the source of bile- pigment is the blood-colouring matter, but whether the precise route which is followed in the process of con- version has yet been unmistakably tracked out is not yet definitely settled.

Hammarsten l discusses at close quarters this definite question, viz. Do the specific constituents of the bile, the bile-acids, and the bile-pigments originate in the liver ; and, if this is the case, do they come from this organ only, or are they also formed elsewhere ? In essaying to. answer these questions, he takes count of experiments made upon animals in whom the liver was either extirpated, or in whom the portal circulation was cut off by ligature from the systemic circulation. Obviously if the bile-pigments and bile-acids are not formed in the liver, or not only in the liver but are simply eliminated from the blood, bile will accumulate in the blood and tissues in such experiments as the foregoing. On the other hand, if these are formed wholly or chiefly in that organ by the action of its cells, then removal of the organ would prevent such a result ; or, again, if the common duct be tied, the bile constituents will collect in the blood and tissues, whether they are formed in the liver or elsewhere in the body.

1 Text-book of Physiological Chemistry, 1893, p. 159.

CAUSE OF THE JAUNDICE 35

Kobner's experiments on frogs point to the fact that bile-acids are produced solely in the liver. After extirpation of that organ, bile-acids could neither be detected in the blood nor tissues, whereas after ligature of the common duct they could be found. The investigations on dogs by Ludwig and Fleisch, conducted on similar lines, corroborated that conclusion. Stern's experiments on pigeons, in which the portal vessels and biliary ducts were ligatured, showed that at the end of twelve hours thereafter, no bile-pigments could be found either in the blood or tissues of these birds, but that at the end of five hours after the bile-ducts were tied, bile-piginents could be found in the blood-serum.

These experiments seem to us to prove that the formation of bile-pigment does not take place in the blood but in the liver. Consensus of opinion on this subject now appears to be that bile-acids are exclusively formed in the liver, and bile-pigment also under usual circum- stances. It ought to be remembered, at the same time, however, that hsematoidin, which is now held to be identical with bilirubin, may be formed in old blood- extravasations. This view is based upon the fact that hscmatoidin, though derived from the blood, shows no absorption bands in the spectrum, thus contrasting with other blood-pigments.

Frerichs experimented upon dogs by injecting pure bile into their blood in order to note the effects of the presence of an abnormal quantity of bile in the blood-stream. Of the twenty-nine experiments which he made, in nineteen did the urine exhibit a larger or smaller quantity of colouring matter than normal, and in these cases the total quantity of urine passed was small in amount, was of a greenish colour, and was neutral or alkaline in reaction.

36 POISONING

After separation of the green flakes by filtration, the filtrate was found to be blood-red in colour, due apparently to dissolved blood-pigment, but no red blood-corpuscles could be found in the sediment. Chemical tests, however, demonstrated the presence of bile-pigment and the absence of bile-acids.

In view of the large number of experiments recorded, and of their results as bearing on the hsematogenous or an- hepatogenous source of jaundice in this form of poisoning, let us return to the consideration of the action of hydrogen arsenide in the causation of icterus and haemoglobin uria.

The experiments of Minskowsky and Naunyu on geese and ducks in which the livers were extirpated, and which afterwards were exposed to atmospheres containing this gas, showed as effects the presence of haemoglobin in the urine, but the absence of biliverdin, whereas in uormal- livered birds after like exposures there was increase of secretion of bile as well as hsemoglobinuria. The former of these observers, collaborating with Basserin, has shown that in the abundant formation of bile-pigments which happens in this form of poisoning, the quantity of iron in the bile is not increased, and does not correspond apparently to that in the decomposing blood-colouring matters. Both observers are of opinion that the iron, for a time at least, is retained in the liver as a pigment rich in iron ; and this view is corroborated by the observations of Minskowsky and Naunyn with respect to the livers of the geese and ducks experimented upon, where such a pigment was found.

On the general question, it would appear as if opinion among French physiologists was not so definitely decided as in Germany. Lucas l discusses the subject of jaundice

1 De V Empoisonnement par V Hydrogene Arsenie, Paris, 1895, p. 87.

CAUSE OF THE JAUNDICE 37

and the cause of its production iii his thesis, and gives the views of the leading writers in France on this point. Lucas himself starts from the position that the pathogenic process of the icterus is singularly obscure. Gubler, he 1>< lints out, admits two kinds of jaundice, the hepatogenous and luematogenous, the latter term, however, being used under some reservation. Dreyfus-Brisac indicates what Gubler exactly means by it. The hemoglobin, says he, coining from the destruction of the corpuscles is trans- formed into biliary pigment, and is eliminated by the bile ; but under the action of a morbid influence, such, for example, as poisoning, the liver becomes powerless to transform into bile the haemoglobin thus set at liberty, and the colouring matter consequently accumulates in the serum, not without undergoing various alterations, how- ever, in the circulation. This type of jaundice is characterised by the presence of urobilin in the urine ; and since in poisoning by the arsenical gas urobilin is found in the urine, the natural conclusion is arrived at that this form of jaundice is of hfeiiiatogenous origin.

Huyem, on the other hand, cannot admit the conclusion, declaring that iKematogcnous jaundice cannot exist, not only because hneniaphein a generic name under which (i abler comprehends together the blood-pigments does not exist as such as a chemically defined body, but because, also, no one has ever succeeded, outwith icterus, in detecting biliary pigments in the blood. Lucas argues that between the luemopheic jaundice and pleiochromic icterus of Stadelmann there is little essential difference, except in the explanations offered by the latter as to its causation ; that in both cases the over-abundance of free haemoglobin in the blood-plasma is the prime cause of the ha-iuoglobiuuria, and likewise of the jaundice; but that

38 POISONING

Stadelmann asserts the jaundice to be a jaundice of resorption, owing to the incapability of the liver to cope with the unusual quantity of haemoglobin sent to it in course of circulation, and that this, in turn, produces a vitiated form of thick, tenacious bile, which being unable, because of these properties and because of the deposition of a sediment, to flow out of the organ by the ordinary channels, is absorbed into the circulation. On a review of the evidence, therefore, Lucas concludes that until the non-existence of the hsematogenous form is more certainly proved, he will provisionally stand by the theory of Gubler. From a careful survey of the whole field of experimental research, from the clinical symptoms which are manifested during life, and from the condition of the organs after death in cases of poisoning by this gas, it seems to us to be clearly proved that the jaundice is a resorption jaundice, and that the conclusions of Stadelmann are nearest the truth which declare that the liver, being suddenly supplied with abnormal blood, that is, blood abnormally charged with free haemoglobin, secretes an abnormal bile which is viscous, tenacious, and difficult to flow, and that this viscosity is the factor which prevents its entrance into the intestine ; hence the abnormal fulness of the gall-bladder and gall-ducts, and the consequent absorption. What, in brief, seems to happen is this : under average conditions of health, the effete blood-products are capable of being converted into bile by the liver, the iron being stored in the economy for further use, but when the liquor sanguinis becomes overcharged with dissolved haemoglobin, as it does in different forms of poisoning, paroxysmal haeino- globinuria, and other affections, the liver ceases to be able to cope adequately with the altered conditions, bile of a tenacious character is formed, and the surplus dissolved,

CAUSE OF THE JAUNDICE 39

haemoglobin finds, or tries to find, a point of discharge by the kidneys, whence it passes to the urine, giving rise to the colour-appearances and constitution of the urine found. As corroboratory of this view, it is a noteworthy fact that, in all of these conditions and affections, the liver is usually found to be enlarged, the bile-ducts and gall-bladder to be distended with bile, and the kidneys to ' be swollen, their tubuli uriniferi being choked with exudation-debris, hence the jaundice, the oliguria, and even the anuria.

But while the conditions in hsemoglobinuric fever, so far as the blood is concerned, are on all fours with those in poisoning by the arsenical gas, there are still those who think with Manson that the jaundice produced in the former may, not improbably, be produced by a hsemo- globinaeniia and not by a cholremia ; in other words, that there are good grounds for believing still the doctrine of an anhepatogenous form of jaundice.

One of the latest writers on the origin of the jaundice arising in poisoning by this gas is Maljean.1 He remarks that the jaundice, considered by itself, is of a distinctive clinical character. The skin and con- - junctivse do not have the yellowish tint of biliary jaundice. The shade of colour is greenish, and recalls, in a more marked degree, the colour of certain chloroses. The condition of the digestive tract differs essentially from that of ordinary jaundice. It is true that at the commencement of the toxic attack there are likely to be sickness, diarrhoea, and, exceptionally, vomiting. But these symptoms supervene suddenly and disappear in some days; they are not simulative of the lingering gastric state which precedes and which follows catarrhal

1 Archives de inM. et depharm. militaires, 1900, vol. xxxv. pp. 82-102.

40 POISONING

jaundice. The tongue conditions differ. There is neither pain nor swelling in the region of the liver. We do not find cutaneous itching, xauthopsy, or yellow sweat. In short, the icterus of these patients resembles jaundice only at first sight. Besides, the conditions of the urine- are contra-indicative of catarrhal jaundice. Although of a coffee-black colour, it gives a reddish colour by reflected light, and not the greenish colour of ordinary jaundice tested in like manner. Moreover, the absence of biliary pigments, together with the presence of haemoglobin in large amount, indicates that something different from ordinary bilious urine exists. Separated from its normal support in the blood-cells and dissolved in the serum, the hiemoglobin becomes a foreign element in the blood- stream, and as such is destined to rapid elimination. But before elimination it circulates in the blood, it impreg- nates all the tissues, and it communicates to them its peculiar coloration. In the skin and conjunctiva it shows itself as a greenish-yellow tint characteristic of hsemato- genous jaundice. The intervention of the liver and bile is in no wise necessary to explain the jaundice. To prove this, he says, the facts of daily observation are more demonstrative of the cause than vivisections practised upon the biliary apparatus of animals at the cost of very intense functional troubles. He draws a parallel between the local results on the tissues of a subcutaneous extra- vasation of blood and the more general effects of the arsenical gas on the blood-stream, and urges that in the gamut of colour-changes which is undergone by the tissues in the local lesion there is reproduced a tint which corre- sponds to that observed in the toxic effects of the gas. Besides, he adduces the fact that after extensive con- tusions, when resorption of large sanguineous effusions

CAUSE OF THE JAUNDICE 41

takes place, a general jaundice sometimes results, which Poncet1 calls traumatic haematic jaundice, and which, Although never very intense, nevertheless exists. Nor does this have its origin in the resorption of biliary matters, because these are absent from the urine. He ranks with this, also, icterus neonatorum, which is found in feeble infants who have suffered during labour, and which, in such cases, he believes to be due to the resorp- tion of the blood from the caput succedaneum or other •• ll'usious of blood of a subcutaneous character, so common during such difficult labours. The urine in these cases does not contain biliary acids, but often crystals of hamiaphein and hsematoidin. From these observations, therefore, it will be apparent that Maljean, like other writers and observers, is inclined to the view that the jaundice of poisoning from arseniuretted hydrogen is luematogenous rather than hepatogenous.

1 De. l"ictere Mmatiqite traumatiijue.

CHAPTER V.

POST-MORTEM APPEARANCES.

OF the 120 cases of poisoning which have been recorded from time to time in various theses, medical journals, and elsewhere, and which form the basis of this monograph, 37 ended fatally. Of this series, therefore, the results of 118 cases being known, the mortality rate was 31 '3 6 per cent. This, however, must not be reckoned as the true mortality of the average hundred cases, because the total number of cases on record is far too small upon which even to base a relatively accurate rate. Of these fatal cases we are only able to present the results of the post-mortem examinations of 19, and some of the records even of these contain but the sparsest particular

Since the post-mortem appearances depend to some extent upon the period of survival of patients after exposure to the gas, it will be well to deal first with these periods in respect of the fatal cases. Table L, Appendix, shows at a glance the periods of survival. From the table it will be seen that the minimum period was two days, and the maximum the thirtieth day. From further examination of the table, it will be found that two deaths occurred on the second day, five on the third day, two on the fifth day, five on the sixth day, five on the seventh day, two on the ninth day, two on the tenth

42

POST-MORTEM APPEARANCES 43

day, and one each on the twenty-fourth and thirtieth day respectively.

Table III., Appendix, summarises the appearances found in the principal organs.

Since one of the most striking post-mortem appearances is the icteric discoloration of the skin and other structures of the body, this will be first considered.

Jaundice. The icteric colour which may be seen at the necropsy of a series of bodies may probably range from a simple yellow tint to a light mahogany or bronxe hue, but in marked cases of poisoning it will be of a bronze or coppery colour. Of course, to some extent the colour will depend upon the length of time the person has been exposed io the gas, and also to the period of survival after exposure. The jaundice is not confined to the skin and conjunctivas, but, as might be expected, is also to be observed in the mucous membranes, and occasionally in the substance of the deeper organs, as liver or brain. The tone of colour observed on the abdominal wall after death differs somewhat from that on the body generally. Various recorders have noted its colour; and from Table II., Appendix.it will be seen that the colour may range from yellow through coppery to greenish or greenish-blue tints.

In some cases a blue line has been observed on the margin of gum and teeth, just as in lead poisoning. Besides the colour seen externally, certain colour-changes h;:ve been observed in some of the internal organs, but these will be discussed later. It only remains to be said that owing to the haemolytic action of the poison, and the liberation of the haemoglobin into the liquor sanguinis, it was to be expected- that colour -changes would be more apparent in some organs than in others,

44 POISONING

while all the organs more or less shared in the general disturbance.

Post- Mortem Appearances in Brain and Membranes. In certain cases the brain and membranes have been found normal, while in those in which any record at all has been made the conditions have varied. Generally speak- ing, however, the meninges are found to be either amemic and cedematous, or the dura mater is amende and the pia mater congested, while the substance of the brain itself is usually pale and anaemic. In individual cases the brain substance has exhibited an icteric coloration.

In Thoracic Viscera. The lungs have generally been found collapsed and congested. The congestion may be confined, however, to the lower lobes, and accompanying the congestion there may be some degree of oedema. It is not surprising to find so little disturbance, compara- tively speaking, of these organs when it is remembered that patients during life have practically no symptoms indicative of lung implication. It is quite true, at the same time, that in certain of the cases cyanosis was a marked symptom, but this was apparently due to the imperfect aeration of the blood consequent upon the destruction of the red blood-corpuscles and their inability to convey the necessary supply of oxygen to the tissues. From the congestion and oedema present during life, it might be expected that exudation-fluid would be found in the pleural cavities. The amount of this fluid varies in different cases, ranging from a few ounces in certain cases up to pints in others. Its colour has been variously described. It has been designated as of a reddish-brown or brownish-red colour, or in colour like bile, or even like blood itself. Its colour is significant of the dissolved state of the haemoglobin, and it resembles nothing so

POST-MORTEM APPEARANCES 45

much as a serous solution containing dissolved haemo- globin.

A similar fluid, in quantities varying from a few drams up to three ounces in amount, may be found in the pericardium.

In respect of the heart there are two important appear- ances, the first being ante-inortein and post-mortem clots, which are constantly found in different cavities, the second being fatty degeneration of the heart-muscle. The latter is of the greater importance, and sometimes plays a significant part in the proximate cause of death. This fatty change not only materially interferes with the ability of the organ to supply sufficient blood to the other organs and parts of the body, but it depreciates the integrity of the function of the heart itself, and tends to lead to sudden death. Indeed the history of some of the cases points to this as the cause of the sudden deatli which occurred. Another point which has been noted of the blood as seen en masse in the heart is its dark colour which may also be said to be characteristic of the blood generally. This is accounted for by the incapacity of the weakened or destroyed corpuscles to act as oxygen- carriers, and also by the reduced state of part of the oxy-ha3inoglobin into rnet-hseinoglobin.

Abdominal Viscera. The most noteworthy pathological changes in the viscera of this region are those which are found in the liver and kidneys, and which are, moreover, constantly found. The reason for this is that these organs have to deal with the unusual amount of dissolved haemoglobin set free in the blood-stream. The rule is to find the liver more or less swollen and enlarged, due to the engorgement of its tissues from the bile stasis which occurs, and to the deposition of blood-pigment which

46 POISONING

takes place in its tissues during the attempt on the part of the organ to cope with the abnormal blood conditions. Microscopic examination of sections of the structure of the organ shows granular deposits of brown -coloured pigment in the hepatic cells, particularly those in the vicinity of the hepatic vein, cloudy swelling of the hepatic cells, the nuclei staining with logwood, and, in addition, areas of fatty degeneration. Tests of the brown pigment for iron do not indicate the presence of that metal.

It may also be here noted that similar pigmentary deposits are to be found in the cellular structures of the heart, kidney, and intestine, as well as in perivascular tissues.

The colour of the liver is also changed in the bulk of cases. Although in rare cases the colour appeared normal, there was mostly some alteration in colour, which in different cases was seen to range from a simple yellow through greyish-brown, yellowish-brown, greenish-yellow, and slaty -blue to a deep indigo. The gall-bladder is found full of dark bile, in some instances to hyper- distension, and the bile itself is of a viscid, tenacious, stringy character.

Marked alterations are usually found in the kidneys, since by these channels the changed blood seeks exit from the body, and also because these organs are chief einunc- tories of the poison itself. The first notable change is that of colour, due in part to the hypersemic state of the organs, and in part, possibly, also to the effects of elimina- tion of the poison. In every case of fatal poisoning in which attention has been given to these organs on post- mortem examination, alteration of colour has been observed. The colours which have been recorded are dark-red, brown, chocolate-brown, brownish-black, violet,

POST-MORTEM APPEARANCES 47

and indigo. The second change is enlargement of the organs, consequent upon the changes which have occurred in the intimate structure of the viscus. On microscopic examination of sections, the glomeruli are found to be swollen, the epithelial lining of Bowman's capsules detached or in a condition of proliferative swelling, the tubules are more or less full of broken-down corpuscles, and to be in a state of desquainative inflammation, forming casts which are either bloody, hyaline, or fatty.

Such conditions as these might, indeed, be expected from the pathological state of the urine, and from these pathological conditions can easily be explained the oliguria, anuria, and also the unernia. The urinary bladder is usually found empty or to contain a very small amount of blood-coloured urine.

Urine. This secretion has to some extent been examined in most of the cases, but in a few with respect only to the presence of blood. In every case hsemo- globinuria was present, and this lasted for variable periods. In the cases which ended fatally, oliguria and anuria usually preceded death. While oliguria was a constant symptom in practically all the cases, usually if the general condition of the patient improved, increase of flow of urine, even to polyuria in some instances, quickly took place. The specific gravity ranged from 1,007 to 1,032. Its reaction was usually weakly acid, but in one case it was found alkaline. The amount of haemoglobin was estimated quantitatively in a single case, and in that, when the urine was at the point of highest colour, it amounted to 5'95 per cent. Albumin was found in every instance ; and where quantitative estimations were made, the amount ranged from O'll to 0"06 per cent. The spectrum given by the blood-colouring matter in the urine

48 POISONING

was commonly that of met-hsemoglobin, but in a few of the cases it was that of mixed oxy-haemoglobin and met- haemoglobin, while in one case it was said to be that of haemoglobin, and in another that of acid heematin. The sedimentary deposit is always considerable in amount. Microscopic examination of it revealed the following as its common constituents, viz. debris of blood-cells ; red blood-corpuscles ; granular matter ; exudation cells ; tube- casts, fatty, hyaline, and bloody ; and, occasionally, amorphous urates or phosphates. Bile-pigment could be detected in some cases, but no bile-acids. In one of the cases it is recorded that hsemin crystals were found in the sediment. We are inclined to doubt the accuracy of the observation ; it appears to us that the crystals were more likely to have been ordinary urinary crystals coloured by the colouring matters of the blood present in the urine.

Spleen. Enlargement of this organ is not so common as is its alteration of colour. In not a few instances the organ was found to be swollen, but in others it was normal in size. Usually its substance is congested and friable, and in some cases soft and easily lacerated. The colour is usually dark, varying in tint from brownish-red to blue.

Stomach and Intestines. Examination indicates changes which point to the direct action of the arsenical poison. As has already been shown, the stomach is one of the organs by which arsenic is eliminated from the body, and in this regard it would appear as if it were of little con- sequence by which channel the poison entered the body. By reason of the more or less constant vomiting which ensues after the inhalation of the gas, and of the great strain on the organ, as is evidenced by the bloody vomit in the later stages, the discovery of pathological changes in the stomach might be anticipated. In addition to a

POST-MORTEM APPEARANCES 49

more or less hypenemic state generally of the mucous membrane, patches of inflammatory action in the greater curvature have been found Submucous luemorrhages, in the form of petechue, are by no means uncommon. The mucous lining of the intestines shares a similar condition.

Diarrho3a is a very common symptom at some stage of the history of cases. In at least sixteen of the recorded cases was diarrhoea present. In some the stools were thin and dark-coloured, in ten there were bloody stools, while in certain others the stools were dark-coloured but did not contain blood. In isolated cases the bowels were normal or constipated, while in one case only a clay- coloured stool was passed, accompanied by a tubular membranous-looking slough, ragged in appearance, and about four inches in length (Case V.).

The chief pathological changes in the intestines may be summarised as follows: Hypenemia of mucous membrane; bluish coloration of the same; and petechial haemorrhages, which are spread more or less extensively over the mucous tract. These petechial haemorrhages are not limited to the intestinal tract, for they have been found in the pericardium and endocardium. The loss of blood from the bowel, nose, gums, and other parts of the body, as well as the petechial haemorrhages, indicate fatty changes in the coats of blood-vessels.

Changes in the Blood. It is only since the haernolytic action of this gaseous poison on the blood has come to be better understood that much attention has been paid to this fluid during life in cases of poisoning by the gas. In Table IV., Appendix, we have tried to show the results of such examinations. Reference, however, to the facts found in the examined cases demonstrates the following general alterations as prevailing : (a) solution of the

E

50 POISONING

blood-colouring matter from the stroma of the corpuscles, and its existence in a dissolved condition in the blood- plasma ; (6) reduction in the hemoglobin value ; (c) altera- tion in shape and colour of the red corpuscles ; and (d) considerable reduction in number of corpuscles per cubic millimetre.

The spectrum in the observed cases has been different in each case : in one it was of oxy-hsemoglobin ; in a second of mixed oxy-haemoglobin and met-hsemoglobin ; and in a third of reduced haemoglobin.

Experiments have many times been made in vitro to discover the exact effects of the gas upon the blood con- stituents when the gas is brought directly in contact with the blood.

Eabuteau l describes the results of passing a current of the gas through defibrinated blood. He found that almost immediately after the gas had been passed for some time the blood became black as ink. On examination by the spectroscope, the blood gave a spectrum of a broad band between Frauenhofer's lines D and E and the intermediate space, which resembled the spectra of seleniuretted hydrogen and of ammonium sulphide, excepting that the centre of the band was less dense. If the blood were diluted with water, and the gas further passed through the mixture, the above band disappeared, the liquid itself became of a greenish -yellow colour, resembling urine, which did not yield a spectrum. If thereafter a current of oxygen were passed through the solution, little or no change was produced. Eabuteau concluded, therefore, that the gas reduced haemoglobin, indeed destroyed it, and that the resulting coloured solution was not changed by the action of oxygen. He maintained further that the

1 Comptes Rendus de la Societe de Biologit, 1873, p. 153.

POST-MORTEM APPEARANCES 51

gas liberated the iron from the blood, as proved by the formation of Turnbull's blue on addition of ferricyanide of potassium. The pigment, which is liberated into the liquor sanguiuis in the above-named circumstances, is peculiar in some respects. It is insoluble in acids, in alkalies, and also in alcohol. By reason of its yellowish colour, it has been called by Kelsch and Kiener " pigment- ochre " or " ochre-pigment." It may be, perhaps, that it is an earlier form of the melanin pigment which is found deposited in the tissues of a patient during life, and found in the liver after death, of persons poisoned by this gas, but it is certain that in this condition it is not identical with melanin. It would appear as if, at first, it was different from its later condition ; for if tests for iron be applied in the earlier stage, they prove negative, whereas when applied later the reactions of ferrous iron are obtained, both with ammonium sulphide and with ferro- cyanide of potassium. In this way, perhaps, is the view probably accounted for that one observer, as Rabuteau, declares that the action of the arsenical gas on the blood is to liberate iron, and another that iron is not liberated.

Mann and Clegg1 repeated these experiments, but passed the gas for varying periods through human blood. After the gas had been passed for about four or five minutes, the blood changed in colour from red to a dirty brown, and showed spectroscopically the additional narrow band of mot-haemoglobin to those of oxy-haemoglobin. If this blood, so changed, were thereafter exposed to the air at about 60° F., for several hours, the former band dis- appeared, but the latter bands remained. If, however, the gas were passed through the blood for half an hour, a considerable portion was permanently converted into

1 Afed. Chron., vol. iii. new series, 1875, p. 168.

52 POISONING

met -haemoglobin, which was quite unaffected by after- exposure to the air. The general effect, therefore, of the arsenical gas upon the blood is similar to that of a, weak- acid, such as boric acid.

Further light has been shed on this subject by the experiments of Joly and Nabias l upon animals with this gas. They constructed an apparatus by which a mixture of gases, oxygen, nitrogen, and hydrogen arsenide in vary- ing proportions might be exhibited to animals. Depending upon the percentage amount of the AsH3 in the gaseous mixture, and the time during which the animals were made to respire it, symptoms of acute or subacute poisoning were produced ; the former terminating in the death of the animal at the end of some minutes or hours, the latter after several days. It is noteworthy that it was only in the latter class of cases that haemoglobinuria was mani- fested. If the blood of an animal so poisoned were examined, it was found that the serum contained more than one-half of the total haemoglobin of the blood, whereas if the death were very slow, the dissolved haemo- globin passed into the serous fluids of the body, pleural, pericardial, and peritoneal, but chiefly into the two first, and also into the urine. It will be observed that in the cases recorded this phenomenon was met with on post- mortem examination in Case XXI. See also Table III., Appendix. These observers also discovered that this was not the only effect of the gas on the blood. They found, in addition, that there was partial transformation of the oxy- haemoglobin into met -haemoglobin, an observation which is corroborated by the experiments of others. Under this double influence, then, arterial blood takes on a colour more or less dark, depending on the degree of

1 Cmnptes Rendus, 1890, vol. ex. p. 626,

POST-MORTEM APPEARANCES 53

intoxication, and is not reddened on after-exposure to the air. I'.y this action, moreover, the respiratory action of tin: blood is seriously depreciated. For example, Joly and Nabias found that the blood of a dog which before inhalation of the mixture of gas and air absorbed 23 c.c. of oxygen per cent, immediately after inhalation absorbed only 7'8 per cent. This fact, they add, is of importance for diagnostic and medico-legal purposes.

Lucas l also made experiments on the blood in vitro by exposing it to the action of the gas. He collected in a preservative solution a litre of the blood of a bull, one halt' of which he left untouched, experimenting only with the other half. This latter half he introduced into a vessel the mouth of which was stoppered with a cork pierced with two holes through which glass tubes were passed for different distances, so that by one tube the gas could be made to pass into and through the blood, and the other to enable the gas to escape from the vessel after it had passed through the blood. The effect was that the superficial layers of blood became black, and the upper part of the vessel became tilled with dark-green coloured bubbles to such an amount that they even forced them- selves out of the exit tube. The lower layers, however, retained their original red colour. But after agitating the whole together, the mass became of a violet colour, just like what he had seen in the blood of animals upon \\hom he had experimented by causing them to inhale the gas. On examining this blood microscopically, he found that the red corpuscles were much changed and deformed in shape, whereas in the untreated blood no such change was apparent. On permitting the treated blood to separate into clot and serum, the latter was found to be of a dark-

1 Op. cit.

54 POISONING

red colour, to contain a few altered red discs, and to give

the spectrum of haemoglobin, whereas the serum of the

untreated blood presented the usual clear straw-yellow

colour. Lucas shares the usual view that hydrogen

arsenide belongs to the class of poisons to which Ponfick

gave the name of cyhsemoly tic poisons, and that consequent

upon this action the residue formed by the destruction of

the red corpuscles accumulates in the different organs,

and operates to produce the intense congestion of these

organs which is found in necropsies. He thinks that for

the most part the colouring matter is eliminated by the

urine, but that a certain proportion of it remains in the

body, as shown by Ponfick, Lebedeff, and Litten, who are

of opinion that it is possible to have hsemoglobinaernia

without hseinoglobinuria. Lucas also believes from his

observations that some part of this dissolved haemoglobin

is utilised by the liver to form biliary pigments.

From the foregoing experiments, therefore, there cannot remain the least doubt that hydrogen arsenide produces rapidly a profound change in the blood, and it is hardly possible to believe that accompanying this physical destruction of the red corpuscles there is not, at the same time, and probably as the result of that destruction, some change also in its chemical composition. This is indicated by the fact that in experiments which have been made free hydrogen arsenide has not been found in the blood of those who have been exposed to its influence. In one of the cases recorded by Dixon Mann and Clegg,1 attempts were made by distilling the blood in vacuo to discover whether or not the arsenical gas existed in a free state, but without success. The inference is further strengthened by the diminution in the oxygen-absorbing capacity of the

1 Op. dt.

POST-MORTEM APPEARANCES 55

blood after exposure to the gas. Without appearing to be too dogmatic on this point, it seems to us that the chemical change which the gas undergoes takes the form of an oxidation process, and that this probably occurs at the expense of the oxygen of the blood in the conversion of the AsH3 into As203, the hydrogen also uniting with the oxygen to form water.

Table IV., Appendix, summarises in the cases recorded : (a) the condition of the blood corpuscles ; (5) the blood spectra ; (c) the condition of the urine ; and (d) the state of the bowels : so far as these have been observed and noted.

CHAPTER VI.

SYMPTOMS AND POST-MORTEM APPEARANCES PRODUCED EXPERIMENTALLY UPON ANIMALS.

LuCAS,1 under the head of pathological anatomy in his brochure, gives an account of experiments which lie made upon dogs with this gas. The apparatus used was as follows : Into an ordinary hydrogen-generating apparatus containing some zinc and acid they put 8 grammes of arsenious acid. Before adding the acid, the apparatus was connected with a gas-holder filled with water, into which the gas-effluent tube from the hydrogen apparatus was fitted. This precaution was adopted to prevent any of the gas being diffused into the surrounding atmosphere. By the foregoing method they obtained hydrogen con- taining AsH3 in considerable proportion, but not pure AsHr Since the bulk of accidental poisonings ordinarily occur from the gas in like impure or mixed condition, it was not deemed necessary to have the gas absolutely pure. The box in which the animals were confined during the experiments had a communication with the gas-holder by means of a rubber-tube furnished with a tap. The object of the experiments was to study the lesions of the principal organs produced by the inhalation of the gas, and especially those of the liver and kidneys.

Six dogs in all were the subjects of experiment. Four of

1 Op. cit. 56

SYMPTOMS PRODUCED ON ANIMALS 57

them succumbed within thirty-two hours after exposure to the gas, the fifth died at the end of five days, and the last, which was subjected to the repeated operations of small doses of the gas, was killed at the end of thirty-five days. The first four died of sub-acute poisoning. The symptoms which they exhibited were as follows : Obstinate vomiting of a distressing kind in all ; paresis of the hind-quarters in all ; haemoglobin uri a in three ; and jaundice in two. In the others, death was too rapid for these latter symptoms to have time to develop. Hannoglobimemia, however, was found in all the six subjects of experiment.

The following are the leading details of the experi- ments :

I. A young dog weighing about 8 kilogrammes was made to respire the gas for eight minutes. When it left the experimental box, it was observed that it had already vomited on two occasions, that it was dull and walked with its head down, and that its hind-quarters were enfeebled. It made incessant efforts to vomit, at first rejecting undigested food, and later, stringy, bilious mucous matter. The pulse was regular and numbered 140 per minute. The breathing was short and quickened. Half an hour later, after severe efforts to defecate, it passed with difficulty some drops of a greenish liquid. The breathing became more oppressed, and the animal became cold. Still later, its respirations numbered only ten per minute, the pulse fell to 60, it lay upon its side, and its tongue, bluish in colour, hung out of its mouth. It died five minutes later.

A few minutes before its death it was bled from the saphenous vein. The blood was found to have a dark- violet colour. Microscopically, it- showed among the healthy red corpuscles a large number of discs with various

58 POISONING

deformities. Some of these were crenated, others were of diverse polyhedric forms, and others appeared to be nucleated. The serum, separated from the clot and diluted with water, showed the spectrum of oxy-hpenioglobin.

Post-Mortem Examination. In almost all the organs no lesion other than intense congestion was found. The lungs were extremely congested, red, and swollen, they did not crepitate, and their surfaces presented large ecchymotic patches. On section, an abundant rose-coloured mucous liquid exuded. The organs, however, floated freely in water. The heart was filled with clots, and there were two small blackish patches under the endocardium, one on the posterior wall of the left ventricle, the other at the base of the mitral valve. The liver was dark-red in colour. The gall-bladder contained about 10 grammes of bile, which was dark in colour. The spleen was practically normal. The stomach was contracted, very congested, and contained a considerable amount of bilious and mucous liquid. The first part of the intestine was filled with bile, and was also much congested. The kidneys were smooth on the surface, the capsules stripped easily, and on section the organs presented a uniformly red colour. The urinary bladder contained about 20 grammes of normal urine.

Histological Examination. In the lungs the alveolar epithelial cells were found to be swollen, and some of the cells had become detached from the walls and had fallen into the alveolar cavities. In the interior of the lobules were collected masses of red corpuscles, white corpuscles, and epithelial elements. The vessels were filled with coagulated blood, their walls were thickened, and the capillaries dilated. In the liver, the arteries and veins were found full of blood, and their walls thickened ; the biliary channels had thickened walls, the epithelial lining

SYMPTOMS PRODUCED ON ANIMALS 59

was swollen and granular, and the nuclei of the cells were much coloured. The hepatic cells were also swollen, their nuclei being very apparent. In some of the sub-hepatic veins some endophlebitis was found. In the kidneys, the glomeruli were normal for the most part, some presented a granular zone more or less extensive, the epithelial cells of the cortical tubules were swollen, their protoplasm cloudy and granular, and their nuclei very apparent but less coloured than normal The lumen of the tubes was obstructed by granular debris. The vessels were engorged with blood and their walls thickened.

II. A dog weighing 10 kilogrammes respired the gas on two separate occasions with an interval of a quarter of an hour. Vomiting occurred as in the former animal, and its gait was staggering. An hour later its respirations were 33 per minute. The pulse was regular and numbered 110 per minute. There was gradually increasing feebleness of the hind-quarters, and, generally, the animal bore the appearance of being profoundly affected. It was bled at the last, and showed no sensibility whatever during the operation. The blood had like appearances as in the former case. Half an hour later, the respirations had increased to 53 per minute, but the pulse had fallen to 95, though still regular. Its tongue was violet in colour. It died three hours after the experiment.

Post-Mortem Examination. The lungs were as in the former case. The heart showed only one black patch near the mitral valve. The liver was enlarged and was violet in colour. There was little bile in the gall-bladder. The spleen was very large, very congested, and its tissue very soft. In the stomach, near the pyloric orifice, was a red patch about the size of a two-franc piece. The organ contained a large quantity of bile, as did also the first

60 POISONING

part of the intestine. But for being congested the kidneys were fairly normal. The gall-bladder was absolutely empty. Histological examination of liver, lungs, and heart gave practically the same results as in the previous case, but the kidneys were less affected, as only in a few of the glomeruli was any granular zone detected.

III. A dog weighing about 15 kilogrammes respired the gas for Jive minutes. On leaving the experimental chamber it passed some urine of normal appearance which, however, was not collected. The animal looked ill, was sick, and from time to time made efforts to vomit. Its gait was staggering. These were the only symptoms evident to the eye at first glance. Four and a half hours later, it took a meal with apparently good appetite, and it being thought that its symptoms were of a very light character, it was left overnight with the intention of exposing it to the gas on the following day. Next day, however, it was found lying very stricken, having in the interval passed no urine. Fibrillary contractions of the muscles of the shoulder were seen, but there had not been any vomiting. Its respiration was good, as was also its heart's action, its rectal temperature being 36'5° C. The eyes were injected, the sclerotics having a decided icteric coloration. Five hours later it became cold, its temperature now being 36'2° C. It was bled from the saphenous vein, and the blood was collected in an artificial serum composed as follows:

Distilled Water . . . 800 grammes.

Glycerine . 200 Sodium Chloride ... 10

Sulphate . 10

Corrosive Sublimate 0'5

SYMPTOMS PRODUCED ON ANIMALS 61

K\ niiination of the blood gave identical results to those already recorded in the first case. The animal died three hours later.

Post-Mortem Examination. The lungs, heart, and spleen were normal. The liver was very jaundiced and was markedly congested. The gall-bladder was distended by thick bile, very dark in colour, but with no sediment. The kidneys were extremely congested and of a dark-violet colour. On section, they presented a uniform reddish- black colour. The urinary bladder contained 200 grammes of black urine, blood-colon red, and very albuminous. The urine contained no corpuscles, no biliary pigments, no bile-acids, but after dilution with water gave the spectrum of oxy-hsemoglobin. The stomach was full of bile, as was also the h'rst part of the intestine.

Histological Examination. There was nothing found abnormal in the structure of lungs or heart. In the liver the large biliary channels were dilated and obstructed with bile, their walls were thickened, and the epithelial cells lining their walls showed coloured nuclei. The hepatic cells were large and showed granular deposit. The kidney conditions were much the same as in the previous case, but perhaps more severe. In the tubuli uriniferi the nuclei were imperceptible in the greater number of the epithelial cells. Numerous crystals of an undetermined kind were observed in the cortical substance. These had a rose-colour, were disposed in bundles, but were without any very characteristic crystalline form.

IV. A young, vigorous dog weighing 12 kilogrammes, which had on previous occasions respired the gas for two minutes at a time, was made on this occasion to inhale the gas for four minutes. On coming out of the chamber

62 POISONING

it did not appear to have vomited, or, indeed, to have been much disturbed by its exposure ; but at the end of five minutes it fell on the floor as if suddenly struck down, in a condition of absolute muscular helplessness. Respira- tion was at first rapid, then slowed down little by little, the movements of the chest grew less distinct, and then disappeared, although diaphragmatic breathing continued for a little longer. It then b'ecame cold, and died at the end of twenty minutes.

At the autopsy the lungs were found to be pale and retracted ; the heart contained the usual clots ; the urinary bladder was quite empty; and there was nothing note- worthy in the other organs. Owing to an accident, the parts were not histologically examined.

V. A dog weighing 8| kilogrammes respired the gas for one and a half minutes. Next day it passed blood-coloured urine in abundance, which contained no red discs, but was very albuminous. Nevertheless it did not seem to be ill. On the following day it again respired the gas for one minute, which was followed the day after by the voidance of urine more black in colour than before, and which now contained a large number of misshapen red discs. It also contained abundant urea, as shown by the formation of nitrate of urea on the addition of nitric acid. The following day the dog seemed better. The urine became lighter in colour and gave the reactions for bile-pigments and bile-acids, although jaundice was not apparent externally. The urine, how- ever, still contained red discs and crystals of ammonio- magnesia phosphate.

The same evening it was made to respire the gas for half-a-minute. Next day feebleness of hind-quarters appeared. It refused all food. Albumin and red

SYMPTOMS PRODUCED ON ANIMALS 63

corpuscles, together with the ingredients already named, were still present in the urine, but there was no trace of haemoglobin. The same day it was made to respire the gas for two minutes. It died on the day following.

At the autopsy the heart was found normal, the lungs a little congested, but the liver was icteric, and the gall- bladder full of somewhat thick bile, but sufficiently fluid to How through the excretory ducts. The stomach and first part of the intestine contained much bile. The kidneys on section were red in colour and congested. The urinary bladder held some drops of urine together with a blackish mass, resembling the marc of coffee, which was found to be composed of altered blood-corpuscles.

Histoloyical Examination. There was nothing unusual found in tissues of lungs or heart except congestion of vessels. In the liver the large biliary canals contained a certain amount of bile, but they were neither dilated nor obstructed by that secretion. The hepatic cells were swollen and enlarged, and their nuclei much coloured. The condition of kidneys was as in the previous cases.

VI. A dog weighing 8 kilogrammes respired the gas for one minute. Next day, early in the morning, the act was repeated for one and a half minutes. Nothing unusual appeared until the afternoon, when the animal voided urine of a blood-red colour and containing albumin. The day following it seemed ill, had vomited all the food it had taken, and had passed no more urine. Later in the day, however, it voided about 300 grammes, which contained no red discs. Having been put at liberty in the laboratory it disappeared, and was not again seen until two days later, when it was found in the neighbour- hood of the building. In the meanwhile it had aborted a foetus of five months. That night it was found that

64 POISONING

the urine was only a little coloured, but contained still some albumin. By next day, the 19th of the month, it was visibly improving, and on the 20th every morbid symptom had disappeared. From the 21st till the 25th it was exposed to the gas daily for half a minute, but no unusual symptom meanwhile developed. From the 25th till the 29th the exposure was increased to one minute daily, and on the latter date the albumin re- appeared in the urine. From the 29th October till the 2nd November the minute period was continued daily, and the albumin increased in amount, and much urea appeared. From the 3rd till the 6th November the daily period of inhalation was increased to two minutes, and the albumin became intense. The inhalations were now definitely stopped. From the 5th till the 7th, the dog seemed almost completely paralysed in its hind- quarters, and it did not pass a drop of urine. By the 9th, however, the urine again became abundant although very albuminous. It was killed on the 18th.

Post-Mortem Examination. The kidneys were very pale-yellowish in colour, and manifestly had undergone granular fatty degeneration. The capsules peeled easily. Section disclosed a very pale surface, and the cortical substance, which was thin, showed parallel streaks directed perpendicularly to the surface of the organ. The ureters were very large, as thick as the finger, and were even more swollen in some places; their walls were much thickened. On making a cross section, their interior lumen was much constricted by a thickened layer, greyish generally in colour but black in places, which was granular in character, and could easily be broken down by scraping with the finger-nail. Histological examina- tion showed fatty degeneration in many of the liver-cells,

SYMPTOMS PRODUCED ON ANIMALS 65

and, in addition to the signs of parenchymatous nephritis, the renal tissues showed the same fatty degeneration.

From these experiments Lucas concluded that the most constant lesion produced hy exposure to the gas was epithelial nephritis. During the period of intense haerno- globinuria, besides, the tubes of the kidney are obstructed by crystals, the precise nature of which is not yet known, but which, according to this observer, are not those of haemoglobin, because they are not soluble in ether, nor are they urates, because they do not respond to the reaction for murexine. In all probability these crystals are the same as those observed by Lit ten, and which he believed to be, mistakenly in our view, haemoglobin crystals.

CHAPTER VII.

DIFFERENTIAL DIAGNOSIS.

FROM the clinical account of symptoms exhibited in poisoning by hydrogen arsenide, while it may not be a question of very great difficulty to decide as to the cause when the precise circumstances under which they have arisen and developed are fully known, the line of symptoms is not, in several respects, singular to poisoning by this gas, and therefore might be confounded with other diseases and affections. Respecting this form of poisoning, let us recall the following facts regarding the symptoms, viz. (a) that in both early and late stages they observe a marked constancy and order of onset ; (6) that their gravity and lethal character vary within certain limits, depending mostly upon the amount of gas inspired ; and (c) that they are indicative of a profound constitutional disturbance.

Some observers, more especially Lucas, are inclined to separate these cases of poisoning into two groups because of the prominence of certain symptoms, but this seems to us not to serve any useful purpose. Lucas divided cases into two groups, his differentiating line being the urinary function, viz. (1) that class characterised by serious symptoms and anuria ; and (2) that characterised by less severe symptoms and normal diuresis. It is quite clear, however, that for practical purposes such a kind of

66

DIFFERENTIAL DIAGNOSIS 67

cleavage cannot be sustained, since there must be an intermediate class of cases which refuse reasonably to be grouped in either of the foregoing. As matter of fact, since the effects produced are in direct ratio to the intensity of action of the cause, we may expect to find varieties in gravity of symptoms and difference in results.

Before contrasting and comparing the symptoms in this form of poisoning with other conditions, it may be well to keep them before us. They are as follows: (a) an indefinable feeling of illness and weakness ; (6) giddi- ness ; (c) faintness ; (rf) pains in head and epigastrium ; (0) coldness of body and extremities ; (/) sense of op- pression of breathing, with, perhaps, some cyanosis ; (g) nausea, sickness, and vomiting. These are followed by (a) continuous vomiting of bilious matters, and sometimes of blood ; (&) jaundice, which varies in tint from golden- yellow to mahogany, but which is more usually of a coppery or bronze hue ; (c) thirst and dryness in mouth and throat ; (d) pains in loins, sometimes very severe, and constant in all cases ; (e) luemoglobinuria, oliguria, and, in serious cases, anuria ; (/) pain or sense of fulness or distension over liver region ; (</) hiccough ; (h) subnormal temperature ; and (t), accompanying the foregoing, clear intellectivity as a rule, but in certain cases there may be minor degrees of stupor, and, generally before death, unconsciousness or coma.

The diseases and conditions which most closely simulate the above are the following, viz. :

I. Haemoglobin uric or Black water fever. II. Paroxysmal htemoglobinuria.

III. Weil's disease.

IV. Poisoning by potassium chlorate. V. Poisoning by pyrogallic acid.

68 POISONING

I. Ifccmoylobinuric or Elackwater Fever. This disease, which is peculiarly a disease of tropical climates, is but very rarely seen in this country. Sir Patrick Maiison states that he knows of but five cases which occurred in this country four in England, and one in Scotland. Its general line of symptoms bears a striking resemblance to that of poisoning by hydrogen arsenide. Rigors, bilious vomiting, jaundice, hsemoglobinuria, oliguria, and occasion- ally anuria, are its most prominent symptoms ; and if we add fever, we complete the picture. Perhaps the existence of hypernormal temperatures is the feature which most differentiates it from poisoning by this gas. At the same time, careful perusal of the recorded cases reveals the fact that in the latter, also, fever has to be noted as occasion- ally present, although, as a rule, the temperature is either practically normal, or in some cases subnormal.

Blackwater fever being, therefore, a disease notably of tropical climates, there would probably be a history of residence in some such part of the world which would help to clear up the diagnosis. Microscopic examination of the blood of the patient, however, does not always indicate the cause of the origin of the disease. It is true, in some cases, that plasmodia malarice have been found both in the blood and organs of such patients, but the parasitology of the disease for it is believed by most observers to be due to a parasite has not yet been worked out to determine its precise character, if, indeed, it be due to a single parasite. There are some, however, who are inclined to attribute its origin to over-dosing with quinine. In the blood, however, very considerable destruction of red corpuscles is found. Sir Patrick Manson, describing the blood of a person suffering from this affection, says, "There did not seem to be a sound

DIFFERENTIAL DIAGNOSIS 69

corpuscle in the patient's body ; nearly all were mis- shapen, tailed, buckled, shrivelled, or otherwise deformed; inicrocytes, megalocytes, and pallid ghost-like corpuscles wmi present in abundance in every case."

Accompanying the fore-named symptoms are others which contribute to further confusion. These are aching, or even severe pain in the loins, pains over the region of the liver, and pains in the urinary apparatus, the last being accompanied by a strong desire to pass urine, and there may be hiccough.

The urine, when passed, is dark-bloody in colour, some- times almost black. If it be allowed to stand in a sediment glass, it separates into two distinct layers, the upper being of a clear or dark port- wine colour, the lower of a brownish-grey deposit, amounting to between one- half and one-third the depth of the upper, which deposit on microscopic examination is seen to contain considerable numbers of hyaline and blood tube-casts, much granular material, and epithelium. In addition, there are usually some red discs to be seen. Spectroscopically, the urine gives the spectrum either of haemoglobin or of met- hfemoglobin.

Jaundice becomes, as in arsenical gas poisoning, an early and prominent symptom. The skin and sclerotics develop a deep saffron colour, which may even be darker than that in some individual cases. In fatal cases, the termination is almost identical with that in poisoning by the gas, viz. either suddenly from syncope or by unemia.

Post-morteui examination of bodies of victims of this affection shows that the appearances of the kidneys and liver are closely alike to those found in the same organs in gas poisoning. The kidneys are enlarged and hypersernic, the tubules are blocked with htemorrhagic

70 POISONING

infarcts and blood debris, the cells are filled with pigment, and the capillaries with melanic granular particles. In the liver, which is also enlarged, there is cloudy swelling of the hepatic cells, with deposition of yellow, and, it may be, melanic pigment.

Taking the differential diagnosis of this affection and arsenical gas poisoning from a broad point of view, it would seem, therefore, as if former residence in a tropical climate and fever were the chief features of difference.

II. Paroxysmal Hcemoglobinuria. Attention was first called in this country to this affection by the late Dr. George Harley,1 although Dessler - was probably the first observer of all to describe it fully.

The illness begins with a feeling of cold and shivering, not unlike the cold stage of ague, is succeeded by a rise of temperature, and terminates in the passage of bloody urine. These attacks are intermittent or paroxysmal in their character, hence part of the designation of the affection. The general opinion which seems to prevail concerning it is that, while in the case of some of those affected it is undoubtedly associated with a history of malaria, no such history is obtainable in others. How- ever, whether or not we take the following fact as evidence of its malarial identity, it is, nevertheless, a striking fact that the very same drugs which prove of most benefit in malaria act equally beneficially in the treatment of this affection. Drs. Bristowe and Copeman 3 have recorded a case which may be taken to be typical of the affection, in which the blood of the patient was subjected to careful and exact examination. This man was an omnibus-driver who had contracted syphilis twenty years before, but who

1 Med.-Chirurg. Trans. 1865. 2 Virchow's Archiv, 1854.

3 The Lancet, vol. ii., 1889, p. 256 et seq.

DIFFERENTIAL DIAGNOSIS 71

had never had rheumatism or ague. He had been, and was subject to absolute bloodlessness of the fingers during cold weather and to fits of shivering, followed by the discharge of a porter-coloured urine. He had often been told by his friends that he became jaundiced during the currency of these attacks. An attack came readily upon him even when in hospital on exposure to cold, and thus the precise conditions prior to and succeeding each attack could be closely studied. After such exposure, his temperature was for a short time thereafter subnormal, and then within a few hours later would rise to between 101° F. and 103° F., but again, after the voidance of bloody urine, would fall back to normal.

The average urine passed under those circumstances had the following characteristics, viz. a specific gravity of from 1,020 to 1,025, a colour ranging from dark reddish- brown to a dark-brown sherry, an abundant sediment, acid reaction, and contained haemoglobin. On examination spectroscopically, it showed the spectrum of acid htematin along with that of lueinoglobin, and microscopically, amorphous pigment, white corpuscles, but no red corpuscles. After a variable time the urine resumed its normal appearance. Examination of the blood proved that during an attack there was rapid and marked destruction of red corpuscles. On a certain day before exposure the corpuscles numbered 3,665,000 per cubic millimetre ; after exposure, there being the usual rise of temperature and voidance of bloody urine, the number fell to 2,970,000. On other days, prior to the exposure to cold, they numbered 3,612,000, 3,270,000, and 3,433,000 respectively, and after the exposure they fell to 2,930,000, 2,870,000, and 2,984,000 respectively. Moreover, the blood discs did not at all or not readily form rouleaux,

72 POISONING

and they were found to have lost more or less their normal shape, some being fused together, and many being de- colorised, looking like shadows or phantom corpuscles. The haemoglobin value, besides, had fallen. In the blood on certain occasions minute crystals of hfemoglobin, amorphous hoematin, and small colourless crystals re- sembling the proteid crystals of Charcot were found.

Quite apart from the sallott state of the skin which always follows a considerable loss of blood or blood-colour- ing matter from the body, distinct icteric tints were observed in this case, as have been also observed in other cases of this affection, but never to the degree prevalent in arsenical gas poisoning. It does not seem clear that the true pathology of this affection has as yet been discovered. It is difficult, indeed, to believe that the mere action of cold should be able to induce such grave changes in the blood-stream as are here demonstrated, notwithstanding that the history of the foregoing case points to this. But in a case observed by us, which after several severe attacks spread over some months ended fatally, no such history as the above could be recorded. In view, moreover, of more recent researches into the cytology and parasitology of the blood, and of the discoveries therein, it would, perhaps, be well to suspend judgment meanwhile regarding the exact cause or causes of this affection.

III. Weil's Disease. More or less closely allied in symptomatology and to the mode of onset and progress of the symptoms of poisoning by this arsenical gas, is the affection denominated as above, of which typical cases present the following history and appearances, viz. a history of shivering, severe headache, aching pains in limbs, great debility, gradual onset of drowsiness and

DIFFERENTIAL DIAGNOSIS 73

stupor, increasing even to incoherency of thought, un- consciousness, delirium, coloration of skin ranging from simple duskiness to deep jaundice, pain in stomach and over region of liver, both initially and on pressure, oliguria, mclsena, and sometimes diarrluea. In fatal cases the stupor gradually increases up till time of death. In cases which go on to recovery, the urine increases in quantity and improves in general appearance, the jaundice lightens, and the stupor disappears. Tost-mortem examina- tion reveals enlargement of the liver,1 but no jaundice of liver substance, the gall-bladder empty and collapsed, and the bile-ducts also empty. The kidneys are swollen and hyperaemic, the epithelial cells granular, the tubules filled with exudation, mostly translucent, but in some tubules piemen ted and of a dark granular appearance.

IV. Poisoning by Potassium Chlorate. -- This is relatively of very rare occurrence when we consider its common use as an internal drug or in gargles. Cases have, however, been reported from time to time, and the symptoms are so like in some respects to those produced by the gas in question that careful notice must be given to them. The following two cases may be deemed to be fairly typical.-

One was that of a young woman, aged twenty, who took by mistake for Rochelle salts two tablespoonfuls of this salt. About twenty hours thereafter, her symptoms were as follows : She was profoundly prostrated ; her temperature was 99° F. ; her pulse numbered 36, and her respirations 32 per minute ; the body surface was cyanotic ; the breathing rapid but not laboured ; the pulse rapid though not feeble. She had vomited freely,

1 The Lancet, vol. ii., 1888', p. 42. 2 New York Med. Record, July 21, 188*. -

74 POISONING

and was still vomiting after admission into hospital. Two hours after admission the temperature had risen to 104° F. Three dark-brown motions had been passed, and dark-coloured urine was voided involuntarily. The urine contained many blood - cells, large masses of altered haemoglobin, and much albumin. ' Next day there was a slight improvement, which, however, soon passed away. Her skin, conjunctive, and lips' showed an extraordinary colour, something between cyanosis in an anaemic person and a sepia or brown-chocolate tint. She died thirty- seven hours after the poison had been taken, having been in a state of stupor up till her death.

The necropsy showed that in addition to the chocolate colour of the body there was a slight icteric tinge. The blood of all the great vessels was liquid and of a very dark chocolate colour. The heart was soft and flabby ; the lungs were normal, but on section were very brown in colour ; the spleen was large, firm, and of a very distinct chocolate colour, and the kidneys were large, containing chocolate-coloured blood, the capsules being non-adherent. The bladder contained three ounces of urine of a dark- brown colour. Spectroscopic examination of the blood showed distinctly the spectrum of met-haemoglobin. Microscopic examination of the tissues of various organs revealed, among others, a very extensive fatty degeneration of the heart muscle, and that the tubules of the kidney were filled to distension with broken-down corpuscles and blood-pigment.

The second case was that of a man of the age of fifty- three years, who had taken, for a couple of years at least, this drug very freely for a chronic throat affection. The immediate cause of his condition was an overdose of the chlorate. His symptoms were practically those just

DIFFERENTIAL DIAGNOSIS 75

described. He became aiuemic, ariuric, and jaundiced, and lie died comatose. At the autopsy, the heart and kidneys were in the conditions above described, the bladder contained urine which was almost black in colour, and the gall-1 (ladder was full of thick and very dark-green bile. The spleen was six times larger than normal, and of a very dark chocolate colour, the kidneys also sharing this colour. Other cases will be found under the following references.1

V. Poisoning &// PyrogoMic Acid. This acid, like the previous salt, when swallowed or absorbed into the body, produces symptoms very much alike to those from arseniur- etted hydrogen. They do not usually come on, however, until from one to fifteen days have elapsed, depending upon whether the acid has been swallowed or has been absorbed. They consist of nausea, vomiting, diarrho3a, threat weakness, haemoglobinuria, bloodlessness, and great difficulty of breathing. The acid, like the salt, acts as a htemolytic poison, setting free the corpuscular haemoglobin into the blood-plasma, hence the hremoglobinuria. It will be remembered that in gas analysis pyrogallate of potassium is used as an absorbent of oxygen. When, therefore, the acid is taken into the body, it is likely to unite with alkalies to form salts, and thus produce in a limited way the same effects upon the tissues and blood. Used by those who practise the photographic art, and thus being comparatively easily procured, it is being more frequently employed for suicidal purposes.

Keviewing, then, the conditions and affections which simulate by their symptoms poisoning by the arsenical gas, it will be apparent that care and discrimination must

1 Jacob, Bci-tiiifi- /.-fin. Wochf-nschr. 1897 ; Brit. Mcd. Journ.vo\. i., 1907, . 116.

76 POISONING

be employed in the differential diagnosis of the last-named. If such be used, however, and if, in addition, the inquirer have some knowledge of chemistry, the circumstances attendant upon the sudden illness will ordinarily assist in arriving at an accurate conclusion as between the operation of diseases and the effects of poisoning. At the same time it has to be borne in mind that poisoning by the arsenical gas sometimes arises in the most unexpected circumstances.

CHAPTEK VIII.

TREATMENT IN ARSENITJRETTED HYDROGEN POISONING.

THERE is probably no class of cases of poisoning more difficult to treat satisfactorily than those in which the poison has entered the body in the gaseous form, because the poison is at once absorbed into the blood, through which it more or less seriously interferes with the integrity of the functions of all of the various important organs. This is particularly true of such gases as carbon monoxide, phosphuretted hydrogen, seleniuretted hydrogen, the gas at present under consideration, and some others, as sulphuretted hydrogen, which either form compounds with the haemoglobin, or exercise a direct destructive action on the blood corpuscles. No matter the precise effect they produce, however, the general effect is to cripple in a greater or lesser degree the capacity of the red corpuscles to convey oxygen to the tissues ; consequently it becomes a most difficult problem to devise measures to counteract such action, and to tide the patient over the period of critical illness. So long as the integrity of the red corpuscles is not involved, there is some chance in being able to do this, because in the poisonous action resulting, for example, from inhalation of carbon dioxide or other carbon gases except the monoxide, time will quickly tell whether or not the efforts employed are likely to prove

77

78 POISONING

availing. But the case is entirely different when the corpuscles are themselves attacked by the gas, when they are broken-down, altered in shape, and, in short, destroyed in large part, and particularly when the haemoglobin is dissolved out of the corpuscular plasma into the liquor sanguinis ; for then we have to deal not only with an imminent menace to life, but we are confronted with a series of difficulties even after the patient has survived the primary effects of the profound shock to the system, difficulties, besides, which are experienced from interfer- ence with the physiological functions of important organs, and also from histological changes which the tissues of some of these organs undergo. It is not difficult to compre- hend why the functional integrity of so many organs is involved when we remember that the nutritive fluid which is conveyed to them is in such a disorganised con- dition, and is thus incapable of supplying them with properly oxygenated blood, not to speak of the action of the toxic substance which is also held therein.

If we consider for a moment the symptoms which are exhibited in poisoning by this arsenical gas, the foregoing statements will be fully borne out. The pains in the head, the sense of profound depression, the incapacity to think, and the sleeplessness all point to serious disturb- ance in the brain circulation ; the nausea, sickness, and vomiting, which are continuous and severe, to distinct irritant action on the stomach ; the oppression in breath- ing and the cyanosis, to interference with the oxygenation of the blood ; the weakness in the lower limbs and the staggering gait, to functional disturbance of the spinal cord ; and the appearance of jaundice, to functional mis- chief in the liver, due to the large import to the organ of abnormal blood. Moreover, the onset of bloody urine, the

ARSENIURETTED HYDROGEN POISONING 79

partial, and, it may even be, the total suppression of urine, together with its unusual constituents, indicate hut too truly that the kidneys are experiencing not only great difficulty in functioning, but also that this is accompanied by structural changes in the organs themselves. As has already been incidentally remarked, it is somewhat remark- able that, in this gaseous form of arsenical poisoning, the very organs which are mainly attacked when the poison has been ingested or absorbed by some other channel should also be elected for special injury ; indeed, there can be little doubt that arsenic, no matter the form or manner in which it has been administered or exhibited, exercises a selective action upon the stomach and kidneys, more especially perhaps upon the latter organs, by reason of their being the principal emunctories of the poison from the body.

The treatment of arsenical gas poisoning must resolve itself into three main lines, viz. (a) to provide in some artificial manner oxygen to the blood which, by reason of its disorganised state, is incapable of being sufficiently aerated in the lungs, and is therefore unable to supply to the various organs the needed oxygenated blood ; (&) to enable the body to rid itself of the poison which it con- .tains, and which it is trying to effect mainly by the kidneys ; and (c) to treat urgent symptoms, give comfort to the patient by affording sleep, and, if possible, to allay the stomach irritation.

Some are inclined to add to the above the administra- tion of certain neutralising drugs, such as magnesia in some form or other. But this, in our opinion, would be futile if the patient is constantly vomiting, as he is likely to be, and would only tend toward -increased discomfort. I'.ut even supposing that the patient were able to retain

80 POISONING

such medicines, it is impossible to expect that they could in any effective way be operative upon a poison which is no more present in the stomach than in any other organ of the body ; hence they cannot exercise any essential antidotal effect.

The urgent requirement in such cases, particularly where the case is severe, is the administration of oxygen, and what promises to be the most effective method of administering it is by inhalation. But this mode of supplying the system with oxygen is not quite so effective as at first sight it would appear to be, for it is but reason- able to suppose that if the blood, on account of its dis- organised state, is incapable of being oxygenated in the natural way, it will equally be incapable of utilising it if presented artificially in more abundant form. Notwith- standing these objections, however, it is undoubtedly the remedy which ought to be offered to a patient in this condition, in the hope that some benefit may result, and all the more because all the red corpuscles are not destroyed, and are therefore still able to exercise their duty as oxygen- carriers. From the history of the cases which were treated by oxygen inhalation, and by reason of the apparent benefit which the patients experienced, we are encouraged to expect some measure of relief, if even temporary, from its use ; in any case, it appears to be the best remedy at our disposal to overcome the primary effects of the poison. Where oxygen may not readily be procured there may be substituted some medicinal agent which contains available oxygen, such as hydrogen peroxide, in small but frequently repeated doses.

To enable the system to rid itself of the poison, that end is likely to be best achieved by assisting the skin and kidneys to act as freely as possible, the former by the use

ARSENIURETTEI) HYDROGEN POISONIN7G 81

of dilueiit diuretic drinks, and the latter by the use of hot packs or baths. There can be no doubt of the efficacy of hot or vapour baths in setting up free ])erspiration, but should the patient be too weak to be lifted with safety into a bath, hot wet packs may be applied in bed. The establishment of free action of the skin affords much relief to such patients, and it has the e fleet of warding off the onset of unumic complications, which, in certain cases, Mvm to have hastened the end. It is necessary during the treatment, after some recovery from the primary effects has been attained, to keep strictly in mind the tendency to fatty degeneration which the heart muscle undergoes. Any sudden exertion on the part of the patient, or even the lifting of the patient from his bed, may be followed by serious consequences, such as heart failure. In some of the recorded cases, heart failure seems to have caused death some days after the primary eH'ects had been survived.

The last line of treatment must be determined by the circumstances of each individual case, and, therefore, need not be considered in detail. And the same is true of the adequate alimentation of the patient throughout the currency of the attack ; indeed, by the administration of stimulants and small quantities of non-nitrogenous foods at short intervals, after the skin has commenced to show signs of more active function and the stomach to retain food stuffs, not a little may be done to expedite recovery.

CHAPTER IX.

PREVENTIVE MEASURES.

As has already been incidentally remarked, if care were exercised to test the purity of reagents necessary for the generation of the hydrogen used in physiological experi- ments, poisoning by this gas would never occur under such circumstances. It is only too clear, however, that in the cases recorded in this connection, either suspicion was not entertained respecting the likely contamination or impurity with arsenic of the chemicals employed, or that the users were lulled into a sense of false security by these chemicals having been purchased as pure, since in no instance do the reagents seem to have been tested as to purity. It should be a standing rule, however, when hydrogen is required for laboratory physiological purposes, that the reagents should be submitted to a preliminary trial with respect to their possible arsenical content. There is no hardship or sacrifice involved in this for scientific persons, and, moreover, it would secure absolute safety.

Circumstances are different, however, with respect to trade processes. It would be impracticable to expect, as a rule, in chemical works where products are manufactured on a commercial scale, that the chemicals employed should be absolutely pure and arsenic-free ; at the same time, workers therein have a right to expect that provisions shall lie made for their reasonable protection, especially

82

83

when it is known that they are engaged in working with and among arseniferous materials. Such occupations must be looked upon as dangerous, and, therefore, such necessary precautions should be enforced as the Legislature is entitled to exact.

In the Report of the Departmental Committee on Compensation for Industrial Diseases, 1907,1 before which ('oiumittee we were invited to give evidence, the Com- missioners say "it is unnecessary to add this form of poisoning to the list, as it is already included under the heading of ' Arsenic Poisoning or its SequeUe.' As the symptoms described, however, differ so markedly from the cutaneous and gastric symptoms of arsenic poisoning, as ordinarily understood, we are glad to have the opportunity of calling attention to the point."

What provisions ought to be made to prevent the occurrence of poisoning by this deadly gas ? From a review of the circumstances of the cases hereinafter described, it will be found that in the bulk of them the operations which gave rise to attacks were being commonly conducted in confined spaces, or under conditions in which the evolved gas was impeded in its movement. In view of these facts, therefore, the preventive measures generally must consist of arrangements whereby the noxious gases evolved may be removed from the place of generation as rapidly as possible, in order by free dilution with the air that they may be rendered relatively as innocuous as possible. It is obvious that any provision in the way of muzzle- wearing on the part of employees would bei of little actual practical value. Generally speaking, therefore, in all such works ventilating arrangements must be provided lor the purpose of drawing away the fumes into_a Hue, if

1 j>. 5.

84 POISONING

possible. It would, indeed, be better in every case if, before passing the gases into the flue, they should be made to pass through the furnace. Particularly ought this to be insisted upon in works in which enormous quantities of hydrochloric or sulphuric acid are used for dissolving metals, such as iron or zinc, to manufacture zinc chloride or iron sulphate. We agree fully with the views ex- pressed by Dixon Mann and jClegg,1 where they say " it ought to be a standing rule at all works where zinc is dissolved on a large scale in sulphuric or hydrochloric acid, or where any similar operations are performed in which hydrogen is largely evolved from crude materials, that the process should be carried out in a closed vat, furnished with a sufficiently wide earthenware tube, so as to conduct the gases evolved directly into the tall chimney of the works. In this way, dangerous fumes are carried away by the powerful upcast of the shaft even when it is necessary to open the trap-door in the cover of the vat ; the workmen are thus enabled to fulfil their duties without incurring any risk." Ordinarily such ventilation by extraction can be secured where there are a furnace and a flue, but where such operations have to be conducted in a building without a flue, or at some distance from one, ventilation by a fan, actuated by electrical, gas, or water motor, could easily be substituted. It ought to be borne in mind, besides, that in such operations it is not enough to secure that they are performed in the open air as far as possible, because, as will be shown in the Accrington cases (p. 165), the arsenical gas, being heavier than air, is apt in still, warm weather, and especially owing to the absence of movement of air, to fall earthwards and to be irregularly distributed or dispersed over unlikely as well

1 Op. tit.

PREVENTIVE MEASURES 85

as likely areas. It is necessary, in short, that the scheme of ventilation for removal of gases, whatever it be, should operate directly upon the gas as it is evolved from the vat or retort in which the chemical action is proceeding. In Case X X X I II., in which the zinc was being dissolved by crude hydrochloric acid, arrangements existed in the works whereby the acid was poured down a trough entering into a covered cistern, and provisions likewise existed in con- nection therewith for carrying away the generated gases to the works chimney by means of a draught apparatus, lint on the occasion in which the man was poisoned, he himself had entirely neglected to avail himself of these arrangements. While it is impossible, therefore, to suggest or devise measures of this kind which would be applicable to every work, it will probably be sufficient to establish the principle that in every work such essential measures ought to be instituted as will secure the efficient carrying away of the gases from the point of generation.

In certain trade processes in which fatal issues have occurred, the gaseous poison did not exist in esse but only in posse. In the Wolverhainpton cases, and in those we ourselves record, the gas was generated by the action of the workmen themselves ; action, however, which was not only reasonable since it was usual and unavoidable under ordinary circumstances, but which proved to be entirely inapplicable under the peculiar conditions. In the former case, it will l>e seen that in a large boiler used as a mortar, in which paddle-arms were rotated by machinery, xinc- skimmings were being treated by water from an adjacent canal, the water of which had an acid reaction ; that the machinery became jammed by the material, and that the first workman entered the boiler to disengage the jammed material by means of an iron crowbar. In the latter

86 . POISONING

cases the workmen descended by means of a man-hole into a Welldon retort to clear out the debris which had collected on the floor of the retort after three weeks' continuous working in the generation of chlorine, the implements used for the purpose being an ordinary iron shovel and a zinc-galvanised iron pail. While it is likely in the former case, by reason of the acidity of the canal water, that a certain amount of arseniuretteU gas was already present in the atmosphere of the boiler at the time the workman entered, there cannot be the least doubt that by his use of the iron crow-bar he generated sufficiently more gas to produce poisoning. In the latter cases, none of this gas existed in the atmosphere of the retort at the time of entrance of the first workman, but it began to be evolved the moment the workman commenced to shovel the acid debris with his iron shovel into the zinc pail ; and, bending over his work as he had to do, besides working in a confined space devoid of any distinct air-movement, the amount of gas generated was sufficient to cause rapid and marked poisonous effects almost immediately, from which he ultimately died. Case XLVII. is a case in many respects similar to the foregoing. In such contingencies as these, while active free ventilation would probably have pre- vented both accidents, it is evident from the known chemical action which takes place between iron and zinc and either hydrochloric or sulphuric acid in presence of arsenic, that if implements other than those of iron and zinc, as, for example, wood, had been used, the arsenical gas would not have been generated, and the toxic effects would not have been produced ; hence the two preventives, viz. active ventilation and the use of wooden implements, are calculated in the future to protect from risk workmen under such or similar conditions.

I'liKVENTIVK MEASUliKS 87

I >r. RnliortBon, chemist at Walthum Abbey, has reported (1904) certain experiments conducted by him for the purpose of freeing hydrogen used in lead-burning from arseuiuretted hydrogen. The danger arises when the hytlm-rn is evolved from zinc and sulphuric acid, either or both of which contain arsenic. He finds from experi- mentation that the danger may be entirely prevented by passing the gas through an efficient gas-washing apparatus or scrubber containing potassium permanganate in solution.1

With special reference to ballooning and the operations connected with the inflation and deflation of balloons, probably no writer has devoted so much attention to the preventive measures connected therewith as Maljean.2 The- measures which he recommends divide themselves into two classes, viz. («) general, and (&) particular.

Of the former is the use of pure hydrogen, and, failing that, better purification of the gas produced by the use of more efficient absorbents or of destructive reagents, and of the latter, more care in the operation of filling and empty- ing of the balloons on the part of those so employed, particularly with reference to keeping clear of the filling or deflating parts, and especially the cessation of the habit of sniffing the afferent gas-pipe to discover the arrival of the gas, together with certain modifications of the official instructions contained in the regulations for aeronauts relative to inflating and deflating balloons.

Up till recently (and even largely at present) supplies of hydrogen were exclusively obtained by the methods described in a previous chapter. Maljean, like many others, has realised that the ideal method of production

1 Dr. Rotertson, Report, 1904.

2 Arch, de w&lecine et <(e phann. militairex, 1900, vol. xxxv. pp. 82-102.

88 POISONING

would be the electrolytic decomposition of water. Such a method has been invented, but" whether the increased cost of production over the older method will not be more or less prohibitive, and is likely, therefore, to retard its adoption, is a question for the future to determine. In any case, it can only have a limited use. Till that time, however, when the electrolytic method comes to be more generally adopted, he suggests t£e use in the circulatory apparatus of such substances as copper sulphate and mercuric chloride, which will decompose the arsenical gas, and, by forming new compounds with its arsenical content, render its passage with the hydrogen impossible. As an alternative, he thinks the sulphuric acid used should be made from sublimed sulphur and not from arsenical pyrites in order to minimise the risks, if not, indeed, to prevent them.

There can be no doubt, as he and others have pointed out, from accidents which have already happened, that so long as the present method of making hydrogen from arseni- ferous materials continues, those who follow the official instructions contained in the regulations for aeronauts will be exposed to considerable risks of poisoning. He draws special attention to the risks to which civilians are exposed during the bringing to earth of a balloon, and, afterwards, during its deflation, if they are not forewarned against placing themselves within the range of inhalation of the escaping gas. Not infrequently, a balloon conies to earth in an open field in the country, and persons are soon attracted through curiosity to the spot owing to the occur- rence of this somewhat unusual experience. Such persons are ordinarily very willing to render any help they can give to the aeronauts. In the army official instructions to balloonists the following is to be found : " The aeronaut

PREVENTIVE MEASURES 89

places at the [orifice of the balloon] three or four willing persons, recommending them not to be disquieted by the odour of the escaping gas, and not to leave their posts : he proceeds in the same way at the appendix" 1

Since persons placed in the above positions are bound to be within the range of leaks and escapes of gas, they are liable to sutler from the effects of the inhalation of the impure gas. At least one fatal case of a willing helper falls to be recorded. Oulmont relates the case of a peasant who, while assisting to bring a balloon to earth, respired the gas which escaped from the valve, and died from the effects of the arsenical gas contained. Maljean recom- mends, therefore, that the instruction above quoted should be altered so as to contain a warning of the. risks to which such persons are exposing themselves. In short, he advises that aeronauts and assistants, military or civil, should be forewarned of the possible risks, and to keep clear of leaks and escapes of gas from afferent pipes or balloon valves, and especially of the dangers attendant upon the common habit of sniffing the former. He points out at the same time that the act of compression at 120 atmospheres of the gas in steel cylinders makes the con- tained gas less dangerous in respect that the compression tends to decompose the arsenical gas.

1 Instruction pratique sur leu aerostats wilitaires, Paris, 1887.

CHAPTER X.

WALL-PAPERS AND ARSENICAL POISONING.

IT has been for a long time a well-established fact that persons who lived for any lengthened consecutive periods in rooms, the walls of which were covered with decorative coloured papers which contained arsenical pigments, were liable to be seized with symptoms of ill-health. Gmelin was the first to draw attention to the relationship between these wall-coverings and the development of the symptoms. He gave particulars of the case of two married persons who, sleeping in a bedroom the walls of which were covered with a green wall-paper, developed unexpected symptoms. The husband awoke each morning with intense headache, dryuess of the mouth, and a feeling of general tiredness, which gradually disappeared during the day, only, however, to return the next morning. The wife developed an irritating cough. When the true cause was suspected, and after vacating the room, the symptoms disappeared almost at once. Basedow, also, drew attention to the same facts, and instanced cases in which such symptoms as emaciation, general weakness, especially in the lower limbs, and diarrhcea developed in individuals who lived in apartments decorated with green wall-papers. Two of the cases falling within his observations are of peculiar interest. The first was that of a woman who developed pains throughout her body to such an extent

90

WALM'Al'KKS AND ARSENICAL POISONING 91

that tor tho best part of three years she became practically bed -ridden because of the symptoms which indicated s-.me leaiou of the spinal cord. When, however, she changed her abode, the symptoms disappeared, and she was cured spontaneously and quickly. The second was that of a young married lady who suffered from symptoms of amesthesia referable to the spinal cord. Becoming more and more feeble, she left to spend the summer in the country, when she recovered her health and became pregnant. Returning home, however, the symptoms returned, and she aborted. She recovered rapidly when the true cause of her illness was discovered. Others have recorded like cases.

The symptoms to which the above circumstances are apt to give rise are as follow, viz. coryza and conjunctivitis, a red or silvery -coated tongue, gradual loss of flesh, gastro- intestinal catarrh, indicated by gastric irritability and diarrhoea, and certain not very well - defined nervous symptoms. Most of the cases of poisoning happening under the above circumstances have been associated with wall- papers of a green colour. Such colours are produced by the use of Scheele's green and Schweinfurth's green. We reproduce from our text-book l an illustration of a piece of tlock wall-paper, dull -green in colour, which measures 23'5 centimetres in length and 15 centimetres in breadth (Fig. 1). From a disc of this, measuring 11*5 centimetres in diameter, crystals of arsenic in the form of arsenious acid were obtained on analysis. The crystals enclosed within the disc were obtained by Reinsch's process, were drawn by the camera lucida, and are magnified exactly 100 diameters.

1 Text-book of Forensic Medicine, Toxicology, and Public 1/ailflt, 1902, p. 400.

92

POISONING

While such wall-papers are not now so much manu- factured as formerly, it is believed that they are not

FIG. 1. This figure represents a piece of dark-green flock wall-paper measur- ing 23 '5 centimetres in length and 15 centimetres in breadth. From a disc of the paper measuring 1 1 '5 centimetres in diameter, the amount of arsenic present was estimated. The crystals of arsenious oxide enclosed in the disc were obtained by Reinsch's process, were drawn by the aid of the camera lucida, and are magnified exactly 100 diameters. (Author.)

wholly excluded from the market. Besides, wall-papers containing arsenical pigments of light colours are not

\\ ALL-PAPERS AND ARSENICAL POISONING 93

unknown. Therefore because such wall coverings are not present in rooms inhabited by persons who develop the above train of symptoms, the absence of green colour must not be permitted to lead the observer away from the true clue ; indeed, the observer should not rest content until analysis of the wall-paper has been made.

Basedow narrates as one of his cases that of an entire family living under the influence of a room wall-papered with a covering tinted with an arsenical pigment, all of whom suffered from a similar train of symptoms. By reference to Case XIX. in the series of cases embraced in these pages (p. 129), it will be seen that several children of a family were attacked similarly. But it ought to be noted of this family outbreak that there was one symptom, common to them all, which is not noted as having characterised Basedow's family outbreak, viz. jaundice. This jaundice seems, indeed, to have been the most prominent symptom, and it is a sign of some importance as indicating the form in which the arsenic was exhibited in the atmosphere breathed by the children. Probably icterus is the most outstanding differential sign between the action of arsenic exhibited in the form of arsenious acid and exhibited as arseniuretted hydrogen. Indeed, on this point Lucas (op. cit. p. 19) goes the length of declaring that jaundice is the chief sign by which poisoning by this arsenical gas may be differ- entiated from that by arsenious oxide. In this opinion we are inclined to share.

The causal relationship of arseniferous wall-papers to the train of symptoms above enumerated is now so well founded that the matter need not be discussed further.

Differences of opinion, however, have arisen from time to time as to the exact manner in which the arsenic is

94 POISONING

disengaged from such papers, and also as to the precise chemical composition of the liberated material. Some have entertained the view that the pigment as it existed in the paper was merely disengaged by attrition, and that the fine product thrown into the room atmosphere was thus inhaled by the occupants ; others have affirmed the belief that the arsenic is volatilised by heat in the upper levels of the apartment and is disengaged in the form of arsenious oxide ; and others, again, have been forced to the con- clusion that the arsenic is liberated in the form of a gaseous compound. While it cannot, perhaps, be asserted with certainty that attrition alone is not a probable mode of disengaging the poison, the results of modern research have made it abundantly clear that the cause in the large percentage of cases is very different. It has been proved beyond doubt that microscopic organisms or moulds are not only capable of growing and thriving in the adhesive starch-paste by which the wall-papers are hung, but that they are also capable of maintaining an active existence in arsenical media, in which during their growth they split up the arsenic and liberate it in the form of a volatile or gaseous substance. At an early stage of the investigation, it was believed that this gaseous form was arseniuretted hydrogen, but later researches have shown that it is not so composed. It may now be taken for certain, therefore, that this gaseous or volatile arsenical compound liberated by these moulds is the source of the poisonous consequences.

There has been a great and fruitful investigation in this field by many observers. Among these may be named Bujwid,1 Morpurgo and Brunner,2 Gosio,3 Abel and

1 L Union Pharnuiceutique, vol. xvi. p. 293.

2 Oesterr. Apoth.-Zeiiuwj, i. 167. 3 L'Orosi, 1900, vol. xxiii. pp. 361-377 ; Berichte, 1897, 30, 1024.

\\AU.P.\PKRS AND ARSENICAL POISONING 95

Butteuberg,1 Biginulli,2 Abba,3 Selnii,4 Gigliotti,6 Maast-n: and others.

The microscopic moulds or fungi which have been found to exercise this liberating action are Penicillium, Mucor, and Aspergillus. Their development is very little, if at all, hindered or retarded by the presence of arsenic in the medium which affords them food for their growth. Of over forty different moulds with which definite experi- ments have been made, it has been found that at least ten of these are not only capable of living and growing freely in arseuicated media, but that they are also able to decompose arsenical compounds, and to form gaseous or volatile compounds therefrom. Of these ten, Penicillium brevicaule was found to give the most marked transforming results. Biginelli found that on growing pure cultures of this mould in presence of sodium arsenite rapid decom- position of this sodium salt took place and a gaseous substance was evolved, which, when passed into a hydro- chloric acid solution of mercuric chloride, caused colourless tabular, triclinic crystals to separate out which had the following composition, viz. AsHEt, + 2HgCl2 ; or, AsHEt2, AsHEt2 + 4HgCl2. These, on standing exposed to the air, gave off an odour of garlic, and became darkened in colour. Further, if the gas was passed into a solu- tion of mercuric nitrate, an infusible, insoluble, yellow amorphous powder was formed, which had the composition of AsHEt22HgN03. From these and other results,

I Zeit. llyy. 1899, vol. xxxii. pp. 449-490.

<2 Atti Real Accad. Lined. 1900, vol. ix. ii. 210-214, and 242-249.

' nlri. Kakt. Par. ii. 4, 806. 4 /i<-ri<-li(,- </<•/• <li ntsfln-ii chfmischen (jes. 7, 1642. •"' //-/(/. 14, 'J29").

II Arl>. Kais. G'esellsch. A. 1902, 18, 475-489. Vide also Scholtz, Berl. 1:1 in. \Vin-h. .\.\.\vi. pp. 913-91/i ; Marpmaui*, Pharm. I'entr. Halle, vol. lii. 6M-072.

96 POISONING

Biginelli reached the conclusion that the gas which is evolved from arsenical wall-paper, and which gives rise to the symptoms of poisoning, is di-ethyl-arsine.

It will be apparent, therefore, that while we are not strictly justified, from the chemical point of view, in including cases of arsenical poisoning which arise from arsenical wall-papers under the head of poisoning by arseniuretted hydrogen, the relation of that gas to di- ethyl-arsine is sufficiently close to justify their inclusion in our list of cases.

So definite and so conclusive is the reaction which takes place by the growth of P. brevicaule in suitable media to which have been added arsenical compounds that Gosio has initiated a test, known now by his name, or by that of Abba, whereby this action is utilised to detect in various substances minute amounts of arsenic. Scholtz affirms the value of this test in the detection of arsenic in skin perspiration, hairs, urine, etc., and declares the process to be much more delicate than that of Marsh, stating that amounts of arsenic of ^^th to -g^th of a milligramme may thus be detected. The test has also been employed for the purpose of demonstrating the presence of arsenic in natural waters, coloured fabrics, beer, sugar, and other materials, with satisfactory results. The food medium which is used for the growth of the mould is sterilised bread crumbs, to which the sterilised substance to be tested is added after the medium is inoculated with the mould.

The value of the test chiefly, if not, indeed, entirely, depends upon the detection by the sense of smell of the observer of the garlicky or alliaceous odour which is evolved when arseniuretted gas is present. It is so far, therefore, dependent upon the acuteness of the olfactory sense of the

WALL-PAPERS AND ARSENICAL POISONING 97

individual observer, in which respect it is not completely satisfactory. Doubtless, however, the gas may be chemic- ally demonstrated by utilising along with the foregoing procedure Gut/eit's test, in such a manner that its presence may be made visually apparent by the yellow stain which forms upon the spot of mercuric chloride on the test paper. Moreover, it would be unwise to depend upon the test of smell alone as an incontestable sign of the presence of the arsenical gas, because other chemical substances which are capable of being generated in the same precise way have also this garlicky odour. For example, if a soluble salt of tellurium be substituted for an arsenical salt in the mould-tube, a gas, telliuretted hydrogen, will be given off which has a distinctly garlicky odour, not to be distinguished by the sense of smell from that of the arsenical gas. This has been pointed out by several observers. Maasen (op. cit.} has shown that not only the soluble compounds of tellurium but also the soluble salts of selenium are capable of being dissociated, with formation of volatile substances, by P. brevicaule, that the volatile substance of the former, like that of arsenic, has an alliaceous odour, while that of the latter has a distinct f«3cal odour, probably of the nature of, or allied to, skatol or mercaptan. He shows, however, that while the sulphides and insoluble salts of tellurium and selenium are not attacked by P. brevicaule, or at most only very limitedly and after a long time, those of arsenic are freely and rapidly decomposed. This serves as a means of differentiation of these chemical substances. Further, Maasen has found that, by passing the hydrogen gases of tellurium and selenium through solutions of the same composition as those used by Biginelli for hydrogen arsenide, the products formed were of similar

H

98 POISONING

composition as respects their character: that is to say, ethyl or methyl derivatives of these elements are formed depending on the source of their production. Rosenheim l has also pointed out that pure tellurium and selenium, unlike arsenic, are not attacked by this mould, and Maasen, that the compounds of these non-metals are capable of being attacked by several moulds which do not act upon arsenic. Such behaviour affords a clue to a method, when more fully investigated, of differentiating these substances from each other.

Rosenheim in an article " Concerning the Influence of Selenium on certain Tests for Arsenic"2 has pointed out the effects of that substance on the recovery of arsenic by certain tests commonly employed for that purpose. The importance of a knowledge of this inhibit- ing effect of the former on the latter is all the greater in respect that selenium and arsenic may co-exist in the same material. During the Manchester beer -poisoning outbreak, he and Tunnicliffe 3 showed that selenium com- pounds were present in the beer as well as arsenic, and they were inclined to attribute the evil effects which were produced more to these than to the arsenic. He shows by experiment that selenium compounds when present with arsenic exhibit a marked inhibitory effect on the magnitude or extent of formation of the arsenical mirror in Marsh's process, and on the deposit upon the copper foil in Reinsch's process. To these, however, we shall return in our consideration of the methods of analysis for the detection of small amounts of arsenic in inorganic and orgauic substances.

1 Journ. Chem. Soc. 1902, P. ii. p. 138.

2 Chem. News, 1901, vol. Ixxxiii. p. 277.

3 The Lancet, Feb. 2, 9, and March 30, 1901.

WALL-PAPERS AND ARSENICAL POISONING 99

In the Annual Report of Inspector of Factories for 1900, an investigation was reported by the Factory Department of the Home Office regarding wall-papers. The results were to the general effect that British-made papers might be deemed to be practically arsenic-free, if infinitesimal amounts are left out of count, and that bronze colour contains relatively more arsenic than others.

In 1904 the Department of Agriculture of the United States 1 published a report which contains the results of investigations into (1) cases of poisoning by arsenical wall-papers and fabrics, (2) the arsenical ingredients of those sold in America, and (3) the laws governing the sale of these. Among other valuable information, it is reported that the State Legislature of Massachusetts enacted in 1900 that in wall-papers the amount of contained arsenic must be limited to O'lO grain per square yard. Of 537 samples of wall-papers analysed, four were found to contain more than the above limit. Two of these four samples were imported from England. Five samples contained between 0'0077 and O'lO grain per square yard, and 90 per cent of the above total samples less than 0'046 grain per square yard.

1 Bulletin No. 86, Washington, 1904.

CHAPTEE XI.

SYNOPTICAL ACCOUNT O*F RECORDED CASES, ARRANGED CHRONOLOGICALLY.

1815. CASE I.1 M. Gehlen, a professor of chemistry, was working with his colleague Euhland in the chemical laboratory at Munich at an investigation of the reactions arising from the interaction of arsenic and potassium oxide or potash. The solutions used being somewhat dilute, the odour of the gas was tardy in manifesting itself, and Gehlen, trying to judge the moment when the hydrogen began to combine with the arsenic, sniffed about the apparatus, and thus involuntarily inhaled the gas. Hardly an hour had elapsed, when he was seized with continuous vomiting, shivering, and alarming feebleness, and, later, he passed bloody urine. After considerable suffering, he died on the ninth day.

Ruhland, writing to his friend Guyton de Morveau on 1st April 1815, gives an account of the occurrence as follows: "My colleague, whom you knew through the Journal which he published for many years, has died in the saddest way. We were preparing together, five days ago, AsH3 gas. The solution with which we were working being somewhat dilute, the gas was slow to manifest its

1 Halle'sche Allgemeitie Literaturzeitung, No. 15, 1815 ; Buclmer's Toxicologie, p. 476 ; Brit, and For. Med.-Chir. Review, vol. xx., 1857, p. 521 ; Geigy, Beitrag zur Kenntniss tier Arsenuwssersto/vergiftinni ili-s Menschen, Basel, 1890.

100

SYNOPTICAL ACCOUNT OF RECORDED CASES 101

particular odour. With the intention to h'll successively small bottles with the gas, M. Gehlen sought to judge by the odour when the hydrogen gas began to combine with the arsenic, and it was in this way that he was poisoned. Hardly an hour had elapsed when he was attacked with constant vomiting, shivering, and alarming weakness. He died in my arms after nine days of unheard-of suffering, a victim of his zeal for the progress of science."

1836. CASE II.1 R. Schindler, a pharmacist, began to evolve AsH3 gas from a Woulffs bottle at 5.30 P.M. of the 14th April 1836, and thereafter for about two hours respired the gas in the air of his laboratory. Four hours later, he was seized with pains in the loins, shiverings, coldness of the extremities, pain in the epigastrium, vomiting, and bloody urine. These symptoms persisted on following days. In addition, there was dark-brownish discoloration of the skin of his body and a yellow icteric tint of the conjunctives. On the sixth day the blood in the urine ceased. On the seventh, there was improve- ment in his condition generally, which continued. By the end of the seventh week, he was fairly well again. It was reckoned by his brother that he had inhaled gas equal to not more than one-eighth of a grain of metallic arsenic. Curiously enough, Lucas 2 says of this man that " la niort survint le huitienie jour et ne fut pas suivie d'autopsie."

1836. CASE III. In December 1836, a young chemist generated the gas from a mixture of arsenic, zinc, and

1 Repertorium fur die Fharniacie, Bd. 69, p. 271 ; Von Graefe und Walther, Journal de Ckirurgie, Bd. xxvi. S. 624, 1838 ; Eulenberg, Die Lehre von den schddliclien mid giftigen (Jasen, 1865 ; Christison, On Poisons, p. 326.

2 Op. cit.

102 POISONING

sulphuric acid. He died twenty-four days after. Taylor,1 who mentions his case, gives no particulars as to the symptoms, although he remarks " but a very small portion of the gas could have entered his lungs."

1841. CASE IV. Mr. Brittan, aged thirty -one, a chemist and druggist, on 23rd October 1841, while in good health, inhaled on two separate occasions about 150 cubic inches of hydrogen gas for the 'purpose of producing the shrill voice of Tyndall's experiment. He was at this period engaged in writing a manual of chemistry. Immediately after the second inhalation, he was seized with giddiness and fainting, which were succeeded later by shivering and the passage of two ounces of bloody urine. Shortly afterwards, he was seized with pain in the lower extremities, accompanied by numbness and tingling in these as well as in the upper limbs. These symptoms lasted for about two hours. Then he complained of slight pains in his loins, and was attacked by vomiting which was violent, constant, and continuous for four hours. When he was seen by Dr. O'Reilly,2 who records the case, his pulse was 90, and feeble, the temperature of the body-surface was lowered, his voice was like a whisper, a condition, however, which came on while inhaling the hydrogen, and he had dull pain in the epigastrium on pressure. The vomited matter was copious in amount and greenish in colour.

Oct. 24. Vomiting had occurred every hour during the night. The face presented a "copper-colour, or rather a dark reddish-yellow " colour, the rest of the body a greenish-yellow colour, and the conjunctivse bore a like

1 On Poisons, 3rd edit. 1875, p. 358.

2 Dublin Journal of Medical Science, vol. xx. p. 422 ; Brit, and For. Med.-Chir. Review, vol. xx., 1857, p. 521.

SYNOPTICAL ACCOUNT OF RECORDED CASES 103

colour to that of the body. There was, however, no xanthopsy. In the evening, he passed about halt' an ounce of urine, which was still bloody.

Oct. 25. The pulse was 76, there was occasional hiccough, he had no pain, but he had not passed any more urine.

Oct. 26. The stomach now retains fluids. Patient had only vomited three times. The jaundice was beginning to disappear. The bowels were freely evacuated, the motions being loaded with bile. No more urine, however, had been passed.

Oct. 27. The jaundice had nearly disappeared. Patient had only vomited once. No urine had yet been passed. The pulse was 80. The face was somewhat oedomatous.

Oct. 28. Patient had had a restless night. His tongue seemed somewhat large, showing a deep, irregular ulcer on its right side. His breath had an ammoniacal odour. He had not passed any urine, and none was found in bladder on catheterisation. In the evening he appeared to become increasingly drowsy, although there was no loss of memory.

Oct. 29. Patient had passed seven stools. He had also voided an exceedingly small quantity of urine, which, on standing, deposited a little blood. The pulse numbered 102. By mid-day, there was great weakness, the pulse having fallen to 76. The oedema had increased. He began to sink at 4 P.M., and died at 7 P.M.

Autopsy was held thirty-six hours after death. The following conditions were found: there was general anasarca of the body ; the abdominal integuments were of a slightly greenish colour ; and the abdomen itself was greatly distended with gas.

The lungs were completely collapsed, but were natural

104 POISONING

in structure. Two pints of a reddish-brown fluid were present in the pleural cavities. The heart was pale and flabby, and its cavities contained no blood. There was a little fluid in the pericardium.

The liver was of a deep-indigo colour, but was normal in size ; the gall-bladder was distended with bile. The kidneys were of the same colour as the liver, the left being larger than normal. The.«tomach was empty, and two inflammatory patches were discovered on the greater curvature. The urinary bladder was empty. The brain and membranes were practically normal.

Dr. O'Eeilly found arsenic in the sulphuric acid and zinc used in the experiment, and by further research was able to affirm that the acid was the immediate source of the arsenic. He also found arsenic in the fluid taken from the pleural cavities of deceased. He concluded that the amount of arsenic inhaled as arseniuretted hydrogen was about 1 2 grains, since he found 6 grains of orpiment (arsenious sulphide) in 200 grains of the acid used, and calculated the equivalents of the sulphide and the arsine as practically the same.

1850. CASE V. Professor Eobertson, aged fifty-seven years, professor of chemistry in the Calcutta Medical College, was engaged in demonstrating to his class the method of performing Marsh's test for arsenic. The apparatus, properly charged, was abundantly evolving the arsenical gas, he meanwhile standing between an open door and the apparatus. During the currency of the experiment, a student opened one of the windows of the room, which caused a draught of air to blow the gas about the operator. This he unwittingly inhaled for a short time, but very soon becoming aware of a sense of burning and constriction in his throat, he had abruptly

SYNOPTICAL ACCOUNT OF RECORDED CASES 105

to leave the class-room. He began to vomit almost i in mediately thereafter, and continued to do so for some time, the exact time not being stated, at the end of which period, the vomited matter consisted of material having the "coffee-grounds" character. He had severe pains in his loins, and passed three or four pints of bloody urine, which he locked up for the purpose of submitting later to chemical examination.

Sixteen hours after the above occurrence he was seen by Dr. Mouat, who noted in him the following symptoms, viz. considerable fever, the skin being hot and dry, the pulse hard; burning pain in the whole course of the alimentary canal ; deep-seated pain in the lumbar region ; intense restlessness, anxiety, and general uneasiness ; pallor of countenance ; and general prostration. On the third day, there was tenderness along with a sense of dragging in the left iliac region, and on administration of castor-oil, a copious clay -coloured evacuation, with a tubular, membranous-looking slough, which was ragged in appearance and about four inches in length, was passed. This slough was found on more minute examination to consist of the lining membrane of the rectum with added fibriuous exudation. On the seventh day, he had pain in the right hypochondriac region, and at the end of eighteen hours thereafter, he became jaundiced. By the end of the twenty-second day, all the distressing symptoms had disappeared, although he was left in a weakly condition. The urine, which had been preserved, was examined by Reinsch's process and was found to contain minute traces of arsenic.1

1854. CASE VI. A teacher inhaled hydrogen which had been generated from zinc and sulphuric acid for the

1 Mouat, Indian Annals of Medical Science, April 1857, p. 657.

106 POISONING

purpose of an experiment, presumably that of Tyndall on the voice. Immediately thereafter, he perceived a sensation of heat in his eyes, weakness of the limbs, with an inclination to faintness and shivering. The symptoms of weakness and faintness, however, passed away later. Next day he voided black urine. When he was examined, his pulse was found to be quiet, his lungs showed no signs of irritation, and his intelligence was quite clear. The urine, which was still black in colour, amounted in quantity to about 200 c.c., and gave on being boiled a plentiful brownish -red coagulum, which was almost identical to that which is formed when blood diluted with water is boiled. No red corpuscles, however, were found in the urine on microscopic examination. At the end of a day and a half, the urine began to get lighter in colour. Examination of the gases evolved from the zinc and sulphuric acid used indicated the presence of arsine gas.

An experiment was made on a dog with the gas produced in the same way as that inhaled by this patient, and the animal exhibited the same general signs of poisoning, and, like the patient, voided bloody urine.1

1863. CASE VII. A young chemist, named C. B., aged twenty-two years, employed in a chemical manufactory, was engaged in researches on the production of colouring matters from anilin, and on the morning of 3rd March 1863, at 7 A.M., he set free a considerable amount of arseniuretted hydrogen gas. An hour later, he was seized with violent pain in the head, but he opened his window only and continued his work for two more hours.

1 Vogel, Arch, des Vereins fiir Arbeiten zur Forderung d. wissenschuft- lichen Heilkunde, 1854, vol. i. Part ii. p. 209 ; Brit, ami For. Med.-Chir. Review, Jan. 1854, p. 279 ; Neubauer uud Vogel, Anleituny zur Analyse des Harns, 7th edit. 1876, p. 310.

SYNOPTICAL ACCOUNT OF RECORDED CASES 107

At 10.30 A.M., he took a hearty meal. One hour later, the headache began to become more severe, pain set in in the epigastrium, and he vomited all the food of which he had partaken. He was now taken to La Charitu Hospital, and placed under the charge of M. Piorry. During his journey to the hospital he vomited three times. On admission, he was pallid, complained of frontal headache, of pain in the loins, and of a sense of constric- tion in the lower part of the chest. There were accelerated respiration, little cough, great thirst, and cold extremities, but he was quite intelligent. The pulse was 110, and was full and strong. There was then no abdominal pain, either spontaneous or provoked on pressure. The liver, however, was tender to palpation. Measures were at once adopted to aid the restoration of the body-heat, and these were successful at the end of an hour. About 5 P.M., he passed two foul and copious stools, and about 220 c.c. of red-coloured urine, the latter, however, not showing on microscopic examination any red corpuscles. He vomited much greenish -coloured matter. Acute pain in the head still persisted at night. The conjunctivse were injected. About 10.30 P.M., his speech became embarrassed, and his replies to questions slow. He was bled to the extent of 500 grammes, which seemed to be followed by almost immediate relief. At 1 A.M., M. Piorry found him in the following state, viz. his face was slightly icteric in colour ; the skin hot ; the pulse regular and good, numbering 100 ; his intelligence active, and his responses to answers clear. The vomiting had ceased. The bowel was then washed out, and he was given a bath, after which measures he felt himself better.

March 4. The face had developed an earthy-yellow colour ; the skin was dry ; pulse 104 ; respirations 40 ;

108 POISONING

he had great thirst ; he had now a listless air ; there was some congestion of the lungs posteriorly; and he had passed no urine.

March 5. There was complete anuria. The tongue and lips were covered with a smoky-looking fur. The skin of body was now of a bronze colour. The pulse during the day became weaker, and latterly almost imperceptible. The breathing- ' became quickened and embarrassed. He gradually became unconscious, and died in the evening.

Autopsy. This was performed twenty-four hours after death. There was no congestion of any organ except of the liver, in which, however, there was no alteration of the hepatic cells. The spleen was softened. The kidneys were augmented in volume, the organs being injected throughout, but especially in the tubular substance. They were of a violet colour. Both ventricles of the heart contained voluminous clot, partly fibrinous and partly of black clotted blood. On microscopic examination, the red corpuscles showed no change.1

1863. CASE VIII.— On the 2nd December 1863, the apothecary Mettrier was making, with two of his colleagues, an examination chemically of the intestines of a girl who had been poisoned. On testing with Marsh's apparatus, he found abundant traces of arsenic, so much so, indeed, that the twelfth porcelain cup-head and cup used to receive the arsenical deposit were quite covered with the deposit. During the experiment, he perceived a marked odour of garlic. By the early evening the work was finished. Mettrier took his food that night as usual, and,

1 OHivier, Gaz. des HbpUaux, 1863, p. 128 ; Comptes Rendus des Afdmoires de la Socittd de Biologic, Hi. series, vol. v., 1863 ; Chemical News, vol. viii., 1863, p. 307.

SYNOPTICAL ACCOUNT OF RECORDED CASES 109

except that he felt a little out of sorts, went to bed at 10 P.M. Early in the morning he awoke with a violent headache and symptoms of disordered digestion, coldness in his extremities, shiverings, and a general feeling of dejection. Inability to sleep prevailed for a few nights after. After some days he recovered.1

1870. CASE IX.— On 12th January 1870, a working mechanic named C., and aged thirty years, was called to do some repairs of apparatus in a chemical work in Lyons. The repair consisted in welding a piece of metal apparatus, and he undertook the work under the supervision and with the assistance of a chemist of the chemical work named L., aged twenty-nine years. Both were at the time in robust health. To accomplish the repair the metal was heated by a flame composed of a mixture of hydrogen and air, the former gas being generated in a suitable apparatus in the form of a brazing-lamp. The machine, of which the part in question was under repair, stood in a large workshop open to the air on all sides. During the operations, the flame in the brazing-lamp became unsatisfactory, and L., believing it due to a want of hydrogen, added more zinc and, what at the time he believed to be, more sulphuric acid. Still the flame was not satisfactory. He thereupon opened up the apparatus to ascertain the cause. Both of them then noticed that the gas which was coming off was nauseating and possessed a garlic odour, but neither of them realised its import. A few minutes afterwards L. was called away to speak with the manager, leaving the other to continue the work as best he could. The manager during his conversation with L., observed that L. was changed in appearance, and asked him if he felt well enough. To

1 Chevallier, Journ. de Chimic tiutdicale, iv. series, 1864.

110 POISONING

this L. replied that he was sick, that he thought his breakfast had disagreed with him. Soon after, L. began to vomit freely. Meanwhile C., the mechanic, continuing the work which was proceeding poorly, tried by himself to discover the cause of the failure of the hydrogen brazing-lamp. But soon after, he also began to feel ill, had to leave the workshop to vomit, and, having at the same time a strong desire to mjcturate, he discovered, to his surprise, that he was passing bloody urine. He returned to the workshop and spoke to some of the workmen of what had occurred, and these, having in the interval heard of the illness of L., at once declared that he had been poisoned. They then rolled him in blankets and hurriedly took him to a pharmacy in the town, where 25 grammes of magnesia hydrate were given him. He was thereafter taken home. When seen by Dr. Valette an hour after, his condition was as follows : his face was choleraic in aspect, the conjunctives were jaundiced, his body was cold, and his pulse numbered 90. He had very painful and constant vomiting, had passed two stools, complained of pains in his lower limbs, but withal was quite clear in mind. He was given a vapour bath.

Jan. 13. His condition was about the same as before. His feebleness was very marked ; the acts of vomiting were as frequent and as painful ; and he had only passed about an ounce of blackish bloody urine. His eyes were now distinctly icteric in hue. He was prescribed hydrated peroxide of iron, of which in all he got that day about 15 grammes. The urine was tested by a chemist, who obtained indications of arsenic by Marsh's process.

Jan. 14. The vomiting still continued, but was not so frequent. He had perspired nmch because of the vapour baths which had been prescribed.

SYNOPTICAL ACCOUNT OF RECORDED CASES 111

Jan. 15. Improvement was observable. He had vomited only once since yesterday. The jaundice of conjunctiva} had disappeared. He had passed urine to the amount of 250 c.c., which, however, was still strongly blood-coloured. His pulse numbered 96, and his temperature was 37'250 C.

Jan. 16. Vomiting had ceased. Urine had been passed of similar amount to last, and was now of a saffron colour.

Jan. 17. Vomiting had returned, as also had pain in the head and epigastrium. He had great thirst. Con- juuctival jaundice likewise had returned. The pulse was 76, and the temperature 37° 0. One and a half litres of urine had been passed, which was of less high colour than formerly, and contained less sediment on standing. By the 25th January he seemed to be quite recovered, except for weakness in the limbs.

L. was also seen on 12th January, and was found to have like symptoms to those of the previous patient, although, perhaps, less severe. The sclerotics were injected with blood, and were jaundiced. The pulse was small and frequent, the skin cold, vomiting was almost constant, and there was great feebleness, but no pain.

Jan. 13. He had vomited but once. No urine had been passed during the previous twenty-four hours.

Jan. 14-15. His condition generally was as the day before, but on the 15th he had passed about half an ounce of urine, dark-red, indeed almost black in colour. The pulse was 84, and the temperature 37'35° C.

Jan. 16. Vomiting was at longer intervals. Drinks were swallowed, but with pain. He was thirsty. Other- wise, he was as before.

Jan. 17. He had vomited once only since the day

112 POISONING

before, and had passed about one ounce of dark-coloured urine.

Jan. 18. Condition much the same. Urine in amount and colour had been passed as on day previous. This was his condition generally until 21st January, when he passed a bloody stool. Besides, an eruption of blood- tinged papules appeared on this date on the abdomen, thighs, and loins, not unlike purpuric measles. There was no fever, but there was almost complete suppression of urine, half an ounce only having been voided. This state of the urinary organs continued up till the 24-25th January, when he passed about 100 c.c. of urine per twenty - four hours. This quantity was voided daily during the next three succeeding days. During these three days also he had three bloody stools. During this period, moreover, he seemed entirely indifferent to all that passed around him, although he answered all questions put to him.

Feb. 1. Eestlessness became more marked, and acts of vomiting more frequent. He had great thirst and much difficulty in swallowing. He suffered from epistaxis, which was oozing in character. His gums, up till now anaemic, became bloody and began to ooze of blood, as did also the mucous membrane of the mouth. There was a disagreeable odour from the mouth. The skin eruption now assumed a violet tint.

Feb. 2. The bleeding from gums continued, and ooz- ing of blood from the prepuce and glans penis had also set in. The urine, however, had now become abundant and clear. It was estimated that from the time the bleeding had commenced he had lost in all about 300 to 400 grammes of blood.

Inhalations of oxygen were tried during the two

SYNOPTICAL ACCOUNT OF RECORDED CASES 113

following days, the only apparent effect, however, being a reduction in the loss of blood. The temperature had now fallen to 36'35° C. This was his condition till the 8th of February, when he began to exhibit a somnolent tendency, although he could be awakened easily, and was then quite clear in intellect. The skin of his face had now a brownish tint.

Feb. 9. On this date he vomited blood, and fainted twice in the early part of the day. He died in the course of the day while in the act of conveying some fluid to his mouth.

The cause of the accident consisted in the fact that when L. replenished the hydrogen lamp, he added by mis- take, the label of the bottle having become partly torn and therefore illegible, a solution of arsenic acid instead of sulphuric acid.1

1872. CASE X.— On 22nd May 1872, a professor of physics was making an experiment on himself by inhaling hydrogen gas, which he generated from zinc and sulphuric acid. The object of the experiment was to demonstrate the shrill voice of Tyndall's experiment. He inhaled the gas for the first time at 11 A.M., and again a second time the same day at 4 P.M. He estimated the amount of gas evolved to be between 14 and 15 litres. He felt, however, no active discomfort thereafter, but he perceived that the urine passed by him afterwards was bloody. For days after, the urine was of a high -yellow or saffron colour. His skin became jaundiced of a highly-yellow colour. By the 25th, however, the jaundice began to lighten in colour, and by the 10th of June, it had entirely dis- appeared. The reddish -yellow urine vanished with the

1 Valette, Lyon Medicate, March 27, 1870, p.- 440 ; Woodman and Tidy, Handy-Book of Forensic Medicine, p. 166.

I

114 POISONING

icterus. On one day only did he have a bloody stool, and on one occasion only, epistaxis.

His assistant, a much younger man, had inhaled from 16 to 18 litres of the gas, and twenty-four hours later he was jaundiced, and passed bloody urine like his chief. Both recovered.1

1873. CASE XI. Nine men were engaged in a lead work in the process of extracting silver from lead and zinc ores by using hydrochloric acid which was heated. All the materials, including the acid, were afterwards found to be arsenical, indeed, to contain 0'027 per cent of arsenic. The men worked the process by what was essentially a large Marsh apparatus. Symptoms of illness began to show themselves in the workmen on the day of operation, the 1st of September, and on the 2nd all of them were ill.

1. H. K., aged twenty-two years, felt ill at mid-day, his symptoms being want of appetite, sickness, giddiness, eructations, depression, and oppression of breathing. That night he slept only for one and a half hours. Next day, however, he went back to work, but he felt unable for it. He passed some bloody urine, the act being accom- panied by pain. The following day he was jaundiced. He had difficulty in breathing, headache, dryness of mouth, thirst, pains in his joints, had again passed bloody urine, and had had one blood-coloured stool. His pulse numbered 100. There was no arsenic, however, found in the urine on chemical examination.

2. J. Z., aged nineteen years, had observed while engaged in the above process that the fumes given off had a garlicky odour. Five hours later, he was seized with headache, giddiness, vomiting, and at night, he passed

1 Ollivier, Comptes Rendus de Biologit, 1873,

SYNOPTICAL ACCOUNT OF RECORDED CASES 115

some bloody urine. Next day, he had marked jaundice of the conjunctiva}, his pulse was frequent, and he had voided a little bloody urine, but had passed no further stools. By 5th September, his urine was normal. He recovered.

3. C. B., director, was ill one day only. He was, how- ever, only a short time near the apparatus.

4. L. M., aged thirty-seven years, was found on the evening of 2nd September to be suffering from depression, headache, dragging sensation in abdomen, and from vomiting. He had passed a liquid stool and some bloody urine. Later in the evening, he became delirious and somnolent. Next day the conjunctive were jaundiced, his extremities were cold, he had hiccough, and, later, sweating supervened. His pulse was small, numbering between 150 and 160. For a number of days afterwards, the urine continued to be bloody, and his general condi- tion serious. He died.

5. T. S. supervised the work for two days. On the evening of the second day he had abdominal pain, vomit- ing, headache, and depression. On the following day he grew worse. He had pain in the loins, thirst, and his conjunctivte had become yellow in colour. The urine was scanty and bloody. He had had a dark-brown stool. Anuria then developed. His morning pulse was 110, and that of the evening 130. Next day the anuria continued, his pulse being 130, and his temperature 38'5° C. Next day, he became delirious, and by the day following, comatose, the pulse being 160. He died on the succeeding day.

6. M. R., aged thirty -six years, took ill on 1st September with symptoms exactly like those of the previous patient. He died on 3rd September,

116 POISONING

7. J. J., aged fifty-two years ; (8) M. S., aged nineteen years ; and (9) C. S., aged forty-three years, sickened on 2nd September and exhibited similar symptoms, but they all recovered, although they were only able to return to work after some months.

Another workman, who worked in the vicinity of the apparatus, complained for some hours of headache and nausea, which, however, quickly 'passed away.

Post-mortem examinations were made of the bodies of the men who died. In the case of L. M., it was performed thirty-six hours after death. The following were the main features of the examination : The skin was of a dirty- yellow colour. Brain. The dura mater was anaemic, and the pia mater congested. Chest. The mucous membrane of trachea, larynx, and mouth was of a greenish-yellow colour, and that of the gullet of a dirty-yellow tint. Heart. The left ventricle was empty, but the right auricle contained a little blood. Abdomen. The liver was moderately enlarged but not congested, its colour being greenish-yellow; the gall-bladder was half-full of bile. The small intestine was empty ; the spleen was normal in size, firm, and not congested ; the kidneys were much congested, but firm, their colour being dark-red.

The body of T. S. was examined twenty-eight hours after death. The skin was yellowish in colour. Brain. Dura mater was anaemic, the pia mater hypergemic. The brain substance was neither hypersemic nor yellow in colour. Chest. The heart conditions were the same as in previous case. Abdomen. The liver was normal in size, its tissue compact, not congested, its colour being yellowish- brown. The small intestine was brownish-red in colour. The spleen was normal in size, firm in texture, and brownish-black in colour. The kidneys were normal

SYNOPTICAL ACCOUNT OF RECORDED CASES 117

in size, very hyperaemic, and dark -red in colour; on section, they were brownish-black in colour.

The body of M. R. was examined sixty hours after death. The skin was bluish-green in colour. The brain and meninges were similar to the previous cases, as were also the conditions of the heart. The liver was enlarged, anaemic, softer in texture than normal, and slaty -blue in colour. The gall-bladder was very full of bile. The spleen was much enlarged, hypersemie, soft in consistence, and dark-red in colour. The kidneys were normal in size, very hypenernic, and also dark-red in colour.1 Arsenic was found by analysis in the organs of the deceased.

1878. CASE XII.— On 16th July 1878, four Italian pedlars were employed for about five hours in filling toy rubber-balloons with hydrogen gas which they generated from zinc and sulphuric acid. The room in which the operation was being conducted contained about 700 cubic feet of space only, and was ventilated solely by a broken window-frame. During the filling process they perceived no garlicky odour from the gas. About an hour later, they showed the following signs of illness, viz. tiredness, trembling of limbs, giddiness, headache, nausea, and, still later, vomiting and sleeplessness. In the morning, there was jaundice of the skin, with bloody urine and painful micturition. They were taken to hospital, when their condition was found to be, generally, as follows :

1. A. B., aged twenty-five years, who had inhaled the gas for half an hour, had jaundice, a pulse strong and full, numbering 100, temperature 38'6° C., respirations 30, and his urine, though free as to amount, was dark-yellow in

1 Trost, Viertdjahrsschrift fur gerichtliche und S/etUl.iche Medicin, vol. xviii., 1873, p. 369 ; Layet, LHygUne hulUstrielle, Paris, 1897, pp. 493- 497 ; Sonnenscheiu, Ilandbuch der gerichtliclie Medicin.

118 POISONING

colour, but contained no blood. The internal organs were found to be normal.

On 20th July the jaundice was disappearing, and although the urine still appeared slightly bilious-looking, it contained no blood. Some of the red blood-corpuscles taken from the blood-stream were found on microscopic examination to be shrivelled.

July 21. The spleen was now felt to be enlarged. By the end of July he was convalescent.

2. C. A. had inhaled the gas for two hours. On 18th July, his skin was of a citron-yellow colour. The liver area seemed rather smaller than normal. Spleen was normal. He was passing painlessly very bloody urine. His pulse was 108, temperature 38° C., and respirations 36. Next day, the liver area still appeared diminished. He had voided 2200 c.c. of urine during the past twenty- four hours, of a sp. gr. of 1,016, which, however, was less bloody than before, but which now showed much sediment, which microscopically was found to consist mainly of epithelial cells and isolated red and white blood- corpuscles. This state of urine steadily improved, and by 2nd August, he was convalescent.

3. B. St., aged thirty years, had worked for three hours at the process. On 18th July, he was found to have very dark jaundice of skin. His pulse numbered 120, his heart was feeble in action, respirations were 36, and his tempera- ture 38'2° C. He complained of pain in the stomach and chest, and of a feeling of oppression over the regions of liver and kidneys. He was passing bloody urine, accompanied by strangury. Next day his skin had assumed a dirty greyish -yellow colour. The liver area was diminished. There was no vomiting, but he had a burning sensation in the mouth. He had voided a stool which

SYNOPTICAL ACCOUNT OF RECORDED CASES 119

contained both blood and bile. He was still passing bloody urine, its total amount during previous twenty-four hours being 1800 c.c., of a sp. gr. of 1,015, and of weakly acid reaction. It deposited a sediment consisting of epithelium and red corpuscles.

July 20. Urine was now of a dirty brownish-red colour. The spleen had become enlarged.

July 25. The urine still contained a little blood and albumin. The spleen was still enlarged. He was con- valescent by 4th August.

4. C. G., aged thirty-three years, had worked with the gas for three hours. His first symptoms showed bilious vomiting, and a sense of oppression over liver and kidneys. He was voiding bloody urine in drops, the act being accompanied by tenesmus and strangury. He had, how- ever, no headache.

July 19.— The bilious vomiting continued. The liver area was less than normal. He had had no motion of the bowels, but had much desire for micturition. He had only passed during the previous twenty-four hours 150 c.c. of urine, which showed much bloody sediment, in which were found red corpuscles. The urine had a sp. gr. of 1,007, and it contained haemoglobin.

July 20. He complained now of dragging pain in liver and kidneys. The jaundice was beginning to dis- appear. There was complete anuria, the bladder being found to be empty.

July 23. He passed to-day for the first time since the 20th urine amounting in quantity to 40 c.c., which was of a brownish-red colour. Next day, he complained of pain in the head. Amount of urine voided, 50 c.c., dirty-red in colour.

July 25. He had much pain over liver, and on

120 POISONING

examination that organ was found to be enlarged. No further urine had been voided.

July 26. Urine was passed to amount of 50 c.c. He died at 5 P.M.1 Arsenic was found in the blood, bile, brain, and urine of deceased.

1879. CASE XIIL— Dr. X. turned ill unexpectedly at 5 P.M. of the 1st November 1879, with severe shivering and general feeling of illness. He became feverish as night advanced, with troubled sleep. He began to perspire toward morning. His urine at bedtime was copious in quantity, but was blood-red in colour and without sediment. It contained hsematin. There were great weakness and loss of appetite. Next day, the fever had gone. There was a distinctly jaundiced condition of the sclerotics, of the forehead, and of the skin of the body generally. His tongue was furred. The urine was still red in colour, but acid in reaction.

Nov. 3. He had had a better night, and himself felt better. The urine was now clear, and non-albuminous. He had a slight shivering in the evening. Next day, the urine had become reddish -brown in colour, was acid in reaction, contained much albumin, and microscopically showed red corpuscles. The diagnosis up till this time was periodic hsemoglobinuria.

Nov. 5. Urine had now become clear and straw- coloured, and did not now contain albumin. He felt well enough to resume his duties.

On 6th November he discovered for the first time that another lecturer and two pupils had been attacked as well as himself with like symptoms on the same day and under precisely similar conditions. It appeared that all of them

1 Wachter, Vierteljahrsschrift fur gerichtliche Medici n, vol. xxviii. Part ii. 1878 ; Layet, op. cit.

SYNOPTICAL ACCOUNT OF RECORDED CASES 121

were engaged on that day in experimenting onjtheir voices with hydrogen gas, which was generated from zinc and sulphuric acid.

The three others were more or less affected like himself with bloody urine and other symptoms, and one of the pupils had jaundice. By the 7th November, however, their symptoms having mostly vanished, and a likely common source of the trouble having been discovered, the acid used in generating the gas was analysed, and was found, relatively speaking, to contain much arsenic.1

1884. CASE XIV. A workman in an anilin manufac- tory, aged forty-three years, took ill on the evening of the 15th November 1883. During the day he had been work- ing in the vicinity of an apparatus from which gases were being evolved freely, and some of which he respired. Soon after going home from work, he began to take rigors, whicli were followed by pain in the head and loins, and by much vomiting. He passed a fair night, but voided only about 150 c.c. of black urine. Dr. Coester, who was called to see him, was inclined at first to look upon his illness as a case of anilin poisoning, but after inquiry at the work, was compelled to conclude that it was one of poisoning by AsH3 gas, possibly by reason of impurities in the hydrochloric acid and zinc which were being employed in the process. This diagnosis was confirmed during the course of the illness.

The condition of the patient, as noted by Dr. Coester on the morning of the 16th, when he first saw him, was briefly as follows : He complained of pain in the head and of lumbar pains, and he was and had been vomiting. He passed in presence of the doctor about 50 c.c. of blackish urine. His temperature was 38'5° C., and the pulse 88 and

1 Eitner, Berliner Idinische Wochenschrift, vol. xiii., 1880, p. 256.

122 POISONING

regular. On examination of the internal organs nothing was found amiss. Analysis of the urine showed that it contained haemoglobin but no blood corpuscles. Next day the patient felt a little better, but a very marked jaundice had now developed. He had no pain, and he had vomited once only. He had voided a very small quantity of urine. He had still a dragging feeling at the loins. The liver was found to be distinctly enlarged, as was also the spleen. He had occasional stupor accompanied by slight delirium. During the following days there was almost complete anuria ; indeed, it was estimated that he had only passed on the average about 5 c.c. of urine per hour during the twenty-four hours.

Nov. 21. Convulsive contractions of the muscles of the forearm had now appeared, and by the following day these had extended to the eye muscles. Although he was perspiring freely from the warm baths which had been given him since the 21st, anuria was still practically present.

Nov. 25. He died suddenly in the morning while in the act of trying to raise himself in bed.

Post-mortem examination was made of his body sixty hours after his death by Dr. Pfeiffer, in the interests of justice. It gave, however, almost negative results owing to the advanced state of decomposition of the body. The liver was found to be firm in consistence, and not to be enlarged. The kidneys and spleen were both enlarged, but were black and decomposed. Analysis of the liver proved that it contained arsenic.1

1886. CASE XV. In a chemical work at Basle, five workmen took ill on 2nd February 1886, while engaged in the manufacture of zinc chloride from zinc and hydro-

1 Coester, Berliner klinische Wodienschrift, vol. xxi., 1884, p. 209.

SYNOPTICAL ACCOUNT OF RECORDED CASES 123

chloric acid. They had the same symptoms in common, which were evidently those of poisoning.

1. J. P., aged forty-eight years, gave the following infor- mation on 10th February concerning the circumstances of the 2nd. On the afternoon of that day, he was seized with marked indisposition, vomiting, headache, smarting in the eyes, and dryness in the throat. In spite of these feelings, however, and although he did not feel much better, he went out next morning to resume his work, but feeling quite unfit and gradually becoming worse, he was compelled to return home after mid-day. To the foregoing symptoms were added bloody urine, jaundice, and particu- larly, great weakness and shaking of the limbs. After treatment, these began to improve : the urine to become clearer ; the appetite to return ; and the jaundice and weakness to disappear.

Feb. 10. The eyes were still discoloured, of a light- yellow colour. The blood-colouring matter had now dis- appeared entirely from the urine, but the patient was still ansemic.

2. J. R., aged fifty-eight, was seized with the first symptoms of poisoning on the early morning of 2nd Feb- ruary, in the form of bloody urine. The urine remained quite black until the evening, and his general state of health was bad. From the 3rd February he was confined to bed by reason of the jaundice. The other symptoms, as well as their course, were like to those of the preceding patient. He eventually recovered.

3. F. K., aged forty-five years, was engaged for two days at the same employment as the others. On 2nd February at 8.30 A.M., he was suddenly seized with much giddiness, violent pain in the stomach^ and an inclination to vomit. At 2.30 P.M., blood appeared in the urine. At

124 POISONING

5 P.M., there was a little improvement in his condition after a bath. On his way home, however, he experienced great weakness. The next day there was jaundice. After that, his case was like the former cases.

Cases 4 and 5 of this series were identical generally to the rest, both as to symptoms and progress. Analysis of the hydrochloric acid used proved it to be contaminated with arsenic.1

' 1887. CASE XVI. This case was treated in the Basle Town Hospital by Dr. Geigy, who records the particulars of the symptoms.2 In the Correspondenzblatt fiir Schweizer Aertze, 1887, p. 727, Professor Immermann had already given an account of the case under the title of " A Case of Acute Blood-Solution."