PART V.—MORE OR LESS VOLATILE POISONOUS SUBSTANCES CAPABLE OF BEING SEPARATED BY DISTILLATION FROM NEUTRAL OR ACID LIQUIDS. (continued 3)
Reading edition
§ 262. The very short interval that may thus intervene between the taking of a dose of prussic acid and loss of consciousness, may be utilised by the sufferer in doing various acts, and thus this interval becomes of immense medico-legal importance. The question is simply this:—What can be done by a person in full possession of his faculties in ten seconds? I have found from experiment that, after drinking a liquid from a bottle, the bottle may be corked, the individual can get into bed, and arrange the bedclothes in a suitable manner; he may also throw the bottle away, or out of the window; and, indeed, with practice, in that short time a number of rapid and complicated acts may be performed. This is borne out both by experiments on animals and by recorded cases.
In Mr. Nunneley’s numerous experiments on dogs, one of the animals, after taking poison, “went down three or four steps of the stairs, saw that the door at the bottom was closed, and came back again.” A second went down, came up, and went again down the steps of a long winding staircase, and a third retained sufficient vigour to jump over another dog, and then leap across the top of a staircase.
In a remarkable case related by Dr. Guy,[246] in which a young man, after drinking more wine than usual, was seized by a sudden impulse to take prussic acid, and drank about 2 drachms, producing symptoms which, had it not been for prompt treatment, would, in all probability, have ended fatally—the interval is again noteworthy. After taking the poison in bed, he rose, walked round the foot of a chest of drawers, standing within a few yards of the bedside, placed the stopper firmly in the bottle, and then walked back to bed with the intention of getting into it; but here a giddiness seized him, and he sat down on the edge, and became insensible.
A case related by Taylor is still stronger. A woman, after swallowing a fatal dose of essence of almonds, went to a well in the yard, drew water, and drank a considerable quantity. She then ascended two flights of stairs and called her child, again descended a flight of stairs, fell on her bed, and died within half an hour from the taking of the poison.
Nevertheless, these cases and similar ones are exceptional, and only show what is possible, not what is usual, the rule being that after fatal doses no voluntary act of significance—save, it may be, a cry for assistance—is performed.[247]
§ 263. Chronic poisoning by hydric cyanide is said to occur among photographers, gilders, and those who are engaged daily in the preparation or handling of either hydric or potassic cyanides. The symptoms are those of feeble poisoning, headache, giddiness, noises in the ears, difficult respiration, pain over the heart, a feeling of constriction in the throat, loss of appetite, nausea, obstinate constipation, full pulse, with pallor and offensive breath. Koritschoner[248] has made some observations on patients who were made to breathe at intervals, during many weeks, prussic acid vapour, with the idea that such a treatment would destroy the tubercle bacilli. Twenty-five per cent. of those treated in this way suffered from redness of the pharynx, salivation, headache, nausea, vomiting, slow pulse, and even albuminuria.
§ 264. Post-mortem Appearances.[249]—If we for the moment leave out of consideration any changes which may be seen in the stomach after doses of potassic cyanide, then it may be affirmed that the pathological changes produced by hydric and potassic cyanides mainly coincide with those produced by suffocation. The most striking appearance is the presence of bright red spots; these bright red spots or patches are confined to the surface of the body, the blood in the deeper parts being of the ordinary venous hue, unless, indeed, an enormous dose has been taken; in that case the whole mass of blood may be bright red; this bright colour is due, according to Kobert, to the formation of cyanmethæmoglobin. The lungs and right heart are full of blood, and there is a backward engorgement produced by the pulmonic block. The veins of the neck and the vessels of the head generally are full of blood, and, in like manner, the liver and kidneys are congested. In the mucous membrane of the bronchial tubes there is a bloody foam, the lungs are gorged, and often œdematous in portions; ecchymoses are seen in the pleura and other serous membranes; and everywhere, unless concealed by putrefaction, or some strong-smelling ethereal oil, there is an odour of hydric cyanide.
Casper has rightly recommended the head to be opened and examined first, so as to detect the odour, if present, in the brain. The abdominal and chest cavities usually possess a putrefactive smell, but the brain is longer conserved, so that, if this course be adopted, there is a greater probability of detecting the odour.
The stomach in poisoning by hydric cyanide is not inflamed, but if alcohol has been taken at the same time, or previously, there may be more or less redness.
In poisoning by potassic cyanide, the appearances are mainly the same as those just detailed, with, it may be, the addition of caustic local action. I have, however, seen, in the case of a gentleman who drank accidentally a considerable dose of potassic cyanide just after a full meal, not the slightest trace of any redness, still less of corrosion. Here the contents of the stomach protected the mucous membrane, or possibly the larger amount of acid poured out during digestion sufficiently neutralised the alkali. Potassic cyanide, in very strong solution, may cause erosions of the lips, and the caustic effect may be traced in the mouth, throat, gullet, to the stomach and duodenum; but this is unusual, and the local effects are, as a rule, confined to the stomach and duodenum. The mucous membrane is coloured blood-red, reacts strongly alkaline,[250] is swollen, and it may be even ulcerated. The upper layers of the epithelium are also often dyed with the colouring-matter of the blood, which has been dissolved out by the cyanide. This last change is a post-mortem effect, and can be imitated by digesting the mucous membrane of a healthy stomach in a solution of cyanide. The intensity of these changes are, of course, entirely dependent on the dose and emptiness of the stomach. If the dose is so small as just to destroy life, there may be but little redness or swelling of the stomach, although empty at the time of taking the poison. In those cases in which there has been vomiting, and a part of the vomit has been drawn into the air-passages, there may be also inflammatory changes in the larynx. If essence of almonds has been swallowed, the same slight inflammation may be seen which has been observed with other essential oils, but no erosion, no strong alkaline reaction, nor anything approaching the effects of the caustic cyanide.
In poisoning by bitter almonds no inflammatory change in the mucous membrane of the coats of the stomach would be anticipated, yet in one recorded case there seems to have been an eroded and inflamed patch.
§ 265. Tests for Hydrocyanic Acid and Cyanide of Potassium.—(1.) The addition of silver nitrate to a solution containing prussic acid, or a soluble cyanide,[251] produces a precipitate of argentic cyanide. 100 parts of argentic cyanide are composed of 80·60 Ag and 19·4 CN, equivalent to 20·1 HCN. It is a white anhydrous precipitate, soluble either in ammonia or in a solution of cyanide of potassium. It is soluble in hot dilute nitric acid, but separates on cooling. A particle of silver cyanide, moistened with strong ammonia, develops needles; silver chloride treated similarly, octahedral crystals. It is insoluble in water. Upon ignition it is decomposed into CN and metallic silver, mixed with a little paracyanide of silver.
A very neat process for the identification of cyanide of silver is the following:—Place the perfectly dry cyanide in a closed or sealed tube, containing a few crystals of iodine. On heating slightly, iodide of cyanogen is sublimed in beautiful needles. These crystals again may be dissolved in a dilute solution of potash, a little ferrous sulphate added, and hydrochloric acid, and in this way Prussian blue produced. If the quantity to be tested is small, the vapour of the acid may be evolved in a very short test-tube, the mouth of which is closed by the ordinary thin discs of microscopic glass, the under surface of which is moistened with a solution of nitrate of silver; the resulting crystals of silver cyanide are very characteristic, and readily identified by the microscope.
(2.) If, instead of silver nitrate, the disc be moistened with a solution of sulphate of iron (to which has been added a little potash), and exposed to the vapour a short time, and then some dilute hydrochloric acid added, the moistened surface first becomes yellow, then green, lastly, and permanently, blue. No other blue compound of iron (with the exception of Prussian blue) is insoluble in dilute hydrochloric acid.
(3.) A third, and perhaps the most delicate of all, is the so-called sulphur test. A yellow sulphide of ammonium, containing free sulphur, is prepared by saturating ammonia by SH2, first suspending in the fluid a little finely-precipitated sulphur (or an old, ill-preserved solution of sulphide of ammonium may be used). Two watch-glasses are now taken; in the one the fluid containing prussic acid is put, and the second (previously moistened with the sulphide of ammonium described) is inverted over it. The glasses are conveniently placed for a few minutes in the water-oven; the upper one is then removed, the moist surface evaporated to dryness in the water-bath, a little water added, and then a small drop of solution of chloride of iron. If hydrocyanic acid is present, the sulphocyanide of iron will be formed of a striking blood-red colour.
(4.) The reaction usually called Schönbein’s, or Pagenstecher and Schönbein’s[252] (but long known,[253] and used before the publication of their paper), consists of guaiacum paper, moistened with a very dilute solution of sulphate of copper (1 : 2000). This becomes blue if exposed to the vapour of hydrocyanic acid. Unfortunately, the same reaction is produced by ammonia, ozone, nitric acid, hypochlorous acid, iodine, bromine, chromate of potash, and other oxidising agents, so that its usefulness is greatly restricted.
(5.) A very delicate test for prussic acid is as follows:—About one-half centigrm. of ammonia, ferrous sulphate (or other pure ferrous salt), and the same quantity of uranic nitrate, are dissolved in 50 c.c. of water, and 1 c.c. of this test-liquid is placed in a porcelain dish. On now adding a drop of a liquid containing the smallest quantity of prussic acid, a grey-purple colour, or a distinct purple precipitate is produced.[254]
(6.) A hot solution of potassic cyanide, mixed with picric acid, assumes a blood-red colour, due to the formation of picro-cyanic acid. Free HCN does not give this reaction, and therefore must first be neutralised by an alkali.
(7.) Schönbein’s Test.—To a few drops of defibrinated ox-blood are added a few drops of the carefully-neutralised distillate supposed to contain prussic acid, and then a little neutral peroxide of hydrogen is added. If the distillate contains no prussic acid, then the mixture becomes of a bright pure red and froths strongly; if, on the other hand, a trace of prussic acid be present, the liquid becomes brown and does not froth, or only slightly does so.
(8.) Kobert’s Test.—A 1-4 per cent. solution of blood, to which a trace of ferridcyanide of potassium is added, is prepared, and the neutralised distillate added to this solution. If hydric cyanide be present, then the liquid becomes of a bright red colour, and, examined spectroscopically, instead of the spectrum of methæmoglobin, will be seen the spectrum of cyanmethæmoglobin. Kobert proposes to examine the blood of the poisoned, for the purpose of diagnosis, during life. A drop of blood from a healthy person, and a drop of blood from the patient, are examined side by side, according to the process just given.
§ 266. Separation of Hydric Cyanide or Potassic Cyanide from Organic Matters, such as the Contents of the Stomach, &c.—It is very necessary, before specially searching for hydric cyanide in the contents of the stomach, to be able to say, by careful and methodical examination, whether there are or are not any fragments of bitter almonds, of apples, peaches, or other substance likely to produce hydric cyanide. If potassic cyanide has been taken, simple distillation will always reveal its presence, because it is found partly decomposed into hydric cyanide by the action of the gastric acids. Nevertheless, an acid should always be added, and if, as in the routine process given at p. 48, there is reasonable doubt for suspecting that there will be no cyanide present, it will be best to add tartaric acid (for this organic acid will in no way interfere with subsequent operations), and distil, as recommended, in a vacuum. If, however, from the odour and from the history of the case, it is pretty sure to be a case of poisoning by hydric or potassic cyanide, then the substances, if fluid, are at once placed in a retort or flask, and acidified with a suitable quantity of sulphuric acid, or if the tissues or other solid matters are under examination, they are finely divided, or pulped, and distilled, after acidifying with sulphuric acid as before. It may be well here, as a caution, to remark that the analyst must not commit the unpardonable error of first producing a cyanide by reagents acting on animal matters, and then detecting as a poison the cyanide thus manufactured. If, for example, a healthy liver is carbonised by nitric acid, saturated with potash, and then burnt up, cyanide of potassium is always one of the products; and, indeed, the ashes of a great variety of nitrogenous organic substances may contain cyanides—cyanides not pre-existing, but manufactured by combination. By the action of nitric acid even on sugar,[255] hydric cyanide is produced.
The old method of distillation was to distil by the gentle heat of a water-bath, receiving the distillate in a little weak potash water, and not prolonging the process beyond a few hours. The experiments of Sokoloff, however, throw a grave doubt on the suitability of this simple method for quantitative results.
N. Sokoloff[256] recommends the animal substances to be treated by water strongly acidified with hydric sulphate, and then to be distilled in the water-bath for from two to three days; or to be distilled for twenty-four hours, by the aid of an oil-bath, at a high temperature. He gives the following example of quantitative analysis by the old process of merely distilling for a few hours, and by the new:—
Old Process.—(1.) Body of a hound—age, 2 years; weight, 5180 grms.; dose administered, 57 mgrms. HCN; death in fifteen minutes. After five days there was found in the saliva 0·6 mgrm., stomach 3·2 mgrms., in the rest of the intestines 2·6 mgrms., in the muscles 4·1—total, 10·5.
(2.) Weight of body, 4000 grms.; dose given, 38 mgrms.; death in eleven minutes. After fifteen days, in the saliva 0·8, in the stomach 7·2, in the rest of the intestines 2·2, in the muscles 3·2—total, 13·4.
New Process.—Weight of body, 5700 grams; dose, 57 mgrms.; death in twenty-four minutes. After fifteen days, in the saliva 1·1 mgrm., in the stomach 2·6, in the rest of the intestines 9·6, in the muscles 31·9, and in the whole, 45·2 mgrms. Duration of process, thirteen hours.
From a second hound, weighing 6800 grms.; dose, 67 mgrms.; 25·1 mgrms. were separated three days after death.
From a third hound, weighing 5920 grms.; dose, 98 mgrms.; after forty days, by distillation on a sand-bath, there were separated 2·8 mgrms. from the saliva, 4·8 from the stomach, 16·8 from the intestines, 23·6 from the muscles—total, 48 mgrms.
It would also appear that he has separated 51·2 mgrms. of anhydrous acid from the corpse of a dog which had been poisoned by 57 mgrms. of acid, and buried sixty days.[257]
From another canine corpse, three days laid in an oven, and left for twenty-seven days at the ordinary temperature, 5·1 mgrms. were recovered out of a fatal dose of 38 mgrms.
The estimation was in each case performed by titrating the distillate with argentic nitrate, the sulphur compounds having been previously got rid of by saturating the distillate with KHO, and precipitating by lead acetate.
Venturoli[258] has, on the contrary, got good quantitative results without distillation at all. A current of pure hydrogen gas is passed through the liquid to be tested and the gas finally made to bubble through silver nitrate. He states that the whole of the hydric cyanide present is carried over in an hour. Metallic cyanides must be decomposed by sulphuric acid or tartaric acid. Mercury cyanide must be decomposed with SH2, the solution acidified with tartaric acid, neutralised with freshly precipitated calcic carbonate to fix any ferro- or ferri-cyanides present, and hydrogen passed in and the issuing gases led first through a solution of bismuth nitrate to remove SH2 and then into the silver solution.
§ 267. How long after Death can Hydric or Potassic Cyanides be Detected?—Sokoloff appears to have separated prussic acid from the body of hounds at very long periods after death—in one case sixty days. Dragendorff recognised potassic cyanide in the stomach of a hound after it had been four weeks in his laboratory,[259] and in man eight days after burial. Casper also, in his 211th case, states that more than 18 mgrms. of anhydrous prussic acid were obtained from a corpse eight days after death.[260] Dr. E. Tillner[261] has recognised potassic cyanide in a corpse four months after death. Lastly, Struve[262] put 300 grms. of flesh, 400 of common water, and 2·378 of KCy in a flask, and then opened the flask after 547 days. The detection was easy, and the estimation agreed with the amount placed there at first. So that, even in very advanced stages of putrefaction, and at periods after death extending beyond many months, the detection of prussic acid cannot be pronounced impossible.
§ 268. Estimation of Hydrocyanic Acid or Potassic Cyanide.—In all cases, the readiest method of estimating prussic acid (whether it be in the distillate from organic substances or in aqueous solution) is to saturate it with soda or potash, and titrate the alkaline cyanide thus formed with nitrate of silver. The process is based on the fact that there is first formed a soluble compound (KCy, AgCy), which the slightest excess of silver breaks up, and the insoluble cyanide is at once precipitated. If grains are used, 17 grains of nitrate of silver are dissolved in water, the solution made up to exactly 1000 grain measures, each grain measure equalling ·0054 grain of anhydrous hydrocyanic acid. If grammes are employed, the strength of the nitrate of silver solution should be 1·7 grm. to the litre, each c.c. then = ·0054 hydrocyanic acid, or ·01302 grm. of potassic cyanide.
Essential oil of bitter almonds may also be titrated in this way, provided it is diluted with sufficient spirit to prevent turbidity from separation of the essential oil. If hydrocyanic acid is determined gravimetrically (which is sometimes convenient, when only a single estimation is to be made), it is precipitated as cyanide of silver, the characters of which have been already described.
§ 269. Case of Poisoning by Bitter Almonds.—Instances of poisoning by bitter almonds are very rare. The following interesting case is recorded by Maschka:—
A maid-servant, 31 years of age, after a quarrel with her lover, ate a quantity of bitter almonds. In a few minutes she sighed, complained of being unwell and faint; she vomited twice, and, after about ten minutes more had elapsed, fell senseless and was convulsed. An hour afterwards, a physician found her insensible, the eyes rolled upwards, the thumb clenched within the shut fists, and the breathing rattling, the pulse very slow. She died within an hour-and-a-half from the first symptoms.
The autopsy showed the organs generally healthy, but all, save the liver, exhaling a faint smell of bitter almonds. The right side of the heart was full of fluid dark blood, the left was empty. Both lungs were rich in blood, which smelt of prussic acid. The stomach was not inflamed—it held 250 grms. of a yellow fluid, containing white flocks smelling of bitter almond oil. In the most dependent portion of the stomach there was a swollen patch of mucous membrane, partially denuded of epithelium. The mucous membrane of the duodenum was also swollen and slightly red. The contents of the stomach were acid, and yielded, on distillation, hydride of benzole and hydric cyanide. Residues of the almonds themselves were also found, and the whole quantity taken by the woman from various data was calculated to be 1200 grains of bitter almonds, equal to 43 grains of amygdalin, or 2·5 grains of pure hydric cyanide.
Poisonous Cyanides other than Hydric and Potassic Cyanides.
§ 270. The action of both sodic and ammonic cyanides is precisely similar to that of potassic cyanide. With regard to ammonic cyanide, there are several experiments by Eulenberg,[263] showing that its vapour is intensely poisonous.
A weak stream of ammonic cyanide vapour was passed into glass shades, under which pigeons were confined. After a minute, symptoms of distress commenced, then followed convulsions and speedy death. The post-mortem signs were similar to those produced by prussic acid, and this substance was separated from the liver and lungs.
§ 271. With regard to the double cyanides, all those are poisonous from which hydric cyanide can be separated through dilute acids, while those which, like potassic ferro-cyanide, do not admit of this decomposition, may be often taken with impunity, and are only poisonous under certain conditions.
Sonnenschein records the death of a colourist, after he had taken a dose of potassic ferro-cyanide and then one of tartaric acid; and Volz describes the death of a man, who took potassic ferro-cyanide and afterwards equal parts of nitric and hydrochloric acids. In this latter case, death took place within the hour, with all the symptoms of poisoning by hydric cyanide; so that it is not entirely true, as most text-books declare, that ferro-cyanide is in no degree poisonous. Carbon dioxide will decompose potassic ferro-cyanide at 72°-74°, potass ferrous cyanide being precipitated—K2Fe2(CN)6. A similar action takes place if ferro-cyanide is mixed with a solution of peptone and casein, and digested at blood heat[264] (from 37° to 40° C.), so that it is believed that when ferro-cyanide is swallowed HCN is liberated, but the quantity is usually so small at any given moment that no injury is caused: but there are conditions in which it may kill speedily.[265]
Mercuric cyanide, it has been often said, acts precisely like mercuric chloride (corrosive sublimate), and a poisonous action is attributed to it not traceable to cyanogen; but this is erroneous teaching. Bernard[266] declares that it is decomposed by the gastric juice, and hydric cyanide set free; while Pelikan puts it in the same series as ammonic and potassic cyanides. Lastly, Tolmatscheff,[267] by direct experiment, has found its action to resemble closely that of hydric cyanide.[268]
Silver cyanide acts, according to the experiments of Nunneley, also like hydric cyanide, but very much weaker.
Hydric sulphocyanide in very large doses is poisonous.
Potassic sulphocyanide, according to Dubreuil and Legros,[269] if subcutaneously injected, causes first local paralysis of the muscles, and later, convulsions.
Cyanogen chloride (CNCl) and also the compound (C3N3Cl3)—the one a liquid, boiling at 15°, the other a solid, which may be obtained in crystals—are both poisonous, acting like hydric cyanide.
Methyl cyanide is a liquid obtained by distillation of a mixture of calcic methyl sulphate and potassic cyanide. It boils at 77°, and is intensely poisonous. Eulenberg[270] has made with this substance several experiments on pigeons. An example of one will suffice:—A young pigeon was placed under a glass shade, into which methyl cyanide vapour, developed from calcic methyl sulphate and potassic cyanide, was admitted. The pigeon immediately became restless, and the fæces were expelled. In forty seconds it was slightly convulsed, and was removed after a few minutes’ exposure. The pupils were then observed not to be dilated, but the respiration had ceased; the legs were feebly twitching; the heart still beat, but irregularly; a turbid white fluid dropped out of the beak, and after six minutes life was extinct.
The pathological appearances were as follows:—In the beak much watery fluid; the membranes covering the brain weakly injected; the plexus venosus spinalis strongly injected; in the region of the cervical vertebra a small extravasation between the dura mater and the bone; the right lung of a clear cherry-red colour, and the left lung partly of the same colour, the parenchyma presented the same hue as the surface; on section of the lungs a whitish froth exuded from the cut surface. In the cellular tissue of the trachea, there were extravasations 5 mm. in diameter; the mucous membrane of the air-passages was pale; the right ventricle and the left auricle of the heart were filled with coagulated and fluid dark red blood; liver and kidneys normal; the blood dark red and very fluid, becoming bright cherry-red on exposure to the air; blood corpuscles unchanged. Cyanogen was separated, and identified from the lungs and the liver.
Cyanuric acid (C3O3N3H3), one of the decomposition products obtained from urea, is poisonous, the symptoms and pathological effects closely resembling those due to hydric cyanide. In experiments on animals, there has been no difficulty in detecting prussic acid in the lungs and liver after poisoning by cyanuric acid.
XIII.—Phosphorus.
§ 272. Phosphorus.—Atomic weight 31, specific gravity 1·77 to 1·840. Phosphorus melts at from 44·4° to 44·5° to a pale yellow oily fluid. The boiling-point is about 290°.
The phosphorus of commerce is usually preserved under water in the form of waxy, semi-transparent sticks; if exposed to the air white fumes are given off, luminous in the dark, with a peculiar onion-like odour. On heating phosphorus it readily inflames, burning with a very white flame.
At 0° phosphorus is brittle; the same quality may be imparted to it by a mere trace of sulphur. Phosphorus may be obtained in dodecahedral crystals by slowly cooling large melted masses. It may also be obtained crystalline by evaporating a solution in bisulphide of carbon or hot naphtha in a current of carbon dioxide. It is usually stated to be absolutely insoluble in water, but Julius Hartmann[271] contests this, having found in some experiments that 100 grms. of water digested with phosphorus for sixty-four hours at 38·5° dissolved ·000127 grm. He also investigated the solvent action of bile, and found that 100 grms. of bile under the same conditions, dissolved ·02424 grm., and that the solubility of phosphorus rose both in water and bile when the temperature was increased. Phosphorus is somewhat soluble in alcohol and ether, and also, to some extent, in fatty and ethereal oils; but the best solvent is carbon disulphide.
The following is the order of solubility in certain menstrua, the figures representing the number of parts by weight of the solvent required to dissolve 1 part of phosphorus:—
Carbon Disulphide, 4
Almond Oil, 100
Concentrated Acetic Acid,[272] 100
Ether, 250
Alcohol, specific gravity ·822, 400
Glycerin, 588
Phosphorus exists in, or can be converted into, several allotropic modifications, of which the red or amorphous phosphorus is the most important. This is effected by heating it for some time, in the absence of air, from 230° to 235°. It is not poisonous.[273] Commercial red phosphorus does, however, contain very small quantities of unchanged or ordinary phosphorus—according to Fresenius, from ·6 per cent. downwards; it also contains phosphorous acid, and about 4·6 per cent. of other impurities, among which is graphite.[274]
§ 273. Phosphuretted Hydrogen.—Phosphine (PH3), mol. weight 34, specific gravity 1·178, percentage composition, phosphorus 91·43, hydrogen 8·57 by weight. The absolutely pure gas is not spontaneously inflammable, but that made by the ordinary process is so. It is a colourless, highly poisonous gas, which does not support combustion, but is itself combustible, burning to phosphoric acid (PH3 + 2O2 = PO4H3). Extremely dangerous explosive mixtures may be made by combining phosphine and air or oxygen. Phosphine, when quite dry, burns with a white flame, but if mixed with aqueous vapour, it is green; hence a hydrogen flame containing a mixture of PH3 possesses a green colour.
If sulphur is heated in a stream of phosphine, hydric sulphide and sulphur phosphide are the products. Oxides of the metals, heated with phosphine, yield phosphides with formation of water. Iodine, warmed in phosphine, gives white crystals of iodine phosphonium, and biniodide of phosphorus, 5I + 4PH3 = 3PIH4 + PI2. Chlorine inflames the gas, the final result being hydric chloride and chloride of phosphorus, PH3 + 8Cl = 3ClH + PCl5. One of the most important decompositions for our purpose is the action of phosphine on a solution of nitrate of silver; there is a separation of metallic silver, and nitric and phosphoric acids are found in solution, thus—8AgNO3 + PH3 + 4OH2 = 8Ag + 8HNO3 + PO4H3. This is, however, rather the end reaction; for, at first, there is a separation of a black precipitate composed of phosphor-silver. The excess of silver can be separated by hydric chloride, and the phosphoric acid made evident by the addition of molybdic acid in excess.
§ 274. The medicinal preparations of phosphorus are not numerous; it is usually prescribed in the form of pills, made by manufacturers of coated pills on a large scale. The pills are composed of phosphorus, balsam of Tolu, yellow wax, and curd soap, and 3 grains equal 1⁄30 grain of phosphorus. There is also a phosphorated oil, containing about 1 part of phosphorus in 100; that of the French Pharmacopœia is made with 1 part of dried phosphorus dissolved in 50 parts of warm almond oil; that of the German has 1 part in 80; the strength of the former is therefore 2 per cent., of the latter 1·25 per cent. The medicinal dose of phosphorus is from 1⁄100 to 1⁄30 grain.
§ 275. Matches and Vermin Pastes.—An acquaintance with the percentage of phosphorus in the different pastes and matches of commerce will be found useful. Most of the vermin-destroying pastes contain from 1 to 2 per cent. of phosphorus.
A phosphorus paste that was fatal to a child,[275] and gave rise to serious symptoms in others, was composed as follows:—
Per cent.
Phosphorus, 1 ·4
Flowers of sulphur, 42 ·2
Flour, 42 ·2
Sugar, 14 ·2
100 ·00
Three common receipts give the following proportions:—
Per cent.
Phosphorus, 1 ·5
Lard, 18 ·4
Sugar, 18 ·4
Flour, 61 ·7
100 ·00
Per cent.
Phosphorus, 1 ·2
Warm water, 26 ·7
Rye flour, 26 ·7
Melted butter, 26 ·7
Sugar, 18 ·7
100 ·00
Per cent.
Phosphorus, 1 ·6
Nut oil, 15 ·7
Warm water, 31 ·5
Flour, 31 ·5
Sugar, 19 ·7
100 ·00
A very common phosphorus paste, to be bought everywhere in England, is sold in little pots; the whole amount of phosphorus contained in these varies from ·324 to ·388 grm. (5 to 6 grains), the active constituent being a little over 4 per cent. Matches differ much in composition. Six matchheads, which had been placed in an apple for criminal purposes, and were submitted to Tardieu, were found to contain 20 mgrms. of phosphorus—i.e., ·33 grm. in 100. Mayet found in 100 matches 55 mgrms. of phosphorus. Gonning[276] analysed ten different kinds of phosphorus matches with the following result:—Three English samples contained in 100 matches 34, 33, and 32 mgrms. of phosphorus: a Belgian sample, 38 mgrms.; and 5 others of unknown origin, 12, 17, 28, 32, and 41 mgrms. respectively. Some of the published formularies are as follows:—
(1.) Glue, 6 parts.
Phosphorus, 4 „ or 14·4 per cent.
Nitre, 10 „
Red ochre, 5 „
Blue smalts, 2 „
(2.) Phosphorus, 9 parts, or 16·3 per cent.
Gum, 16 „
Nitre, 14 „
Smalts, 16 „
(3.) Phosphorus, 4 parts, or 14·4 per cent.
Glue, 6 „
Nitre, 10 „
Red lead, 5 „
Smalts, 2 „
(4.) Phosphorus, 17 parts, or 17 per cent.
Glue, 21 „
Nitre, 38 „
Red lead, 24 „
Phosphorus poisoning by matches will, however, shortly become very rare, for those containing the ordinary variety of phosphorus are gradually being superseded by matches of excellent quality, which contain no phosphorus whatever.
§ 276. Statistics.—The following table gives the deaths for ten years from phosphorus poisoning in England and Wales:—
DEATHS FROM PHOSPHORUS IN ENGLAND AND WALES DURING THE TEN YEARS ENDING 1892.
Accident or Negligence.
Ages, 1-5 5-15 15-25 25-65 65 and above Total
Males, 11 1 2 8 ... 22
Females, 15 2 11 5 ... 33
Totals, 26 3 13 13 ... 55
Suicide.
Ages, 5-15 15-25 25-65 65 and above Total
Males, 1 6 20 1 28
Females, 6 33 24 1 64
Totals, 7 39 44 2 92
Phosphorus as a cause of death through accident or negligence occupies the eighth place among poisons, and as a cause of suicide the ninth.
A far greater number of cases of poisoning by phosphorus occur yearly in France and Germany than in England. Phosphorus may be considered as the favourite poison which the common people on the Continent employ for the purpose of self-destruction. It is an agent within the reach of anyone who has 2 sous in his pocket, wherewith to buy a box of matches, but to the educated and those who know the horrible and prolonged torture ensuing from a toxic dose of phosphorus, such a means of exit from life will never be favoured.
Otto Schraube[277] has collected 92 cases from Meischner’s work,[278] and added 16 which had come under his own observation, giving in all 108 cases. Seventy-one (or 65 per cent.) of these were suicidal—of the suicides 24 were males, 47 females (12 of the latter being prostitutes); 21 of the cases were those of murder, 11 were accidental, and in 3 the cause was not ascertained. The number of cases in successive years, and the kind of poison used, is given as follows:—
Number of Cases. In the Years Phosphorus in Substance, or as Paste. Phosphorus Matches.
15 1798-1850 13 2
36 1850-1860 15 21
41 1860-1864 6 35
16 1864-1867 5 11
Of the 108 cases, 18 persons recovered and 90 (or 83·3 per cent.) died.
Falck also has collected 76 cases of poisoning from various sources during eleven years; 55 were suicidal, 5 homicidal[279] (murders), and the rest accidental. Of the latter, 2 were caused by the use of phosphorus as a medicine, 13 by accidents due to phosphorus being in the house; in 1 case phosphorus was taken intentionally to try the effects of an antidote.[280] With regard to the form in which the poison was taken, 2 of the 76, as already mentioned, took it as prescribed by physicians, the remaining 74 were divided between poisonings by phosphorus paste (22) and matches (52) = 70 per cent. Of the 76 cases, 6 were children, 43 adult males, 13 adult females, and 14 adults, sex not given. Of the 76 cases, 42, or 55·3 per cent., died—a much smaller rate of mortality than that shown by Schraube’s collection.
§ 277. Fatal Dose.—The smallest dose on record is that mentioned by Lobenstein Lobel, of Jena, where a lunatic died from taking 7·5 mgrms. (·116 grain). There are other cases clearly indicating that this small quantity may produce dangerous symptoms in a healthy adult.
§ 278. Effects of Phosphorus.—Phosphorus is excessively poisonous, and will destroy life, provided only that it enters the body in a fine state of division, but if taken in coarse pieces no symptoms may follow, for it has been proved that single lumps of phosphorus will go the whole length of a dog’s intestinal canal without causing appreciable loss of weight, and without destroying life.[281] Magendie injected oleum phosphoratum into the veins, and although the animals experimented on exhaled white fumes, and not a few died asphyxiated, yet no symptoms of phosphorus poisoning resulted—an observation confirmed by others—the reason being that the phosphorus particles in a comparatively coarse state of division were arrested in the capillaries of the lung, and may be said to have been, as it were, outside the body. On the other hand, A. Brunner,[282] working in L. Hermann’s laboratory, having injected into the veins phosphorus in such a fine emulsion that the phosphorus could pass the lung capillaries, found that there were no exhalations of white fumes, but that the ordinary symptoms of phosphorus poisoning soon manifested themselves. Phosphorus paste, by the method of manufacture, is in a state of extreme sub-division, and hence all the phosphorus pastes are extremely poisonous.
§ 279. In a few poisons there is a difference, more or less marked, between the general symptoms produced on man, and those noticeable in the different classes of animals; but with phosphorus, the effects on animals appear to agree fairly with those witnessed most frequently in man. Tardieu (who has written perhaps the best and most complete clinical record of phosphorus poisoning extant) divides the cases under three classes, and to use his own words:—“I think it useful to establish that poisoning by phosphorus in its course, sometimes rapid, sometimes slow, exhibits in its symptoms three distinct forms—a common form, a nervous form, and a hæmorrhagic form. I recognise that, in certain cases, these three forms may succeed each other, and may only constitute periods of poisoning; but it is incontestable that each of them may show itself alone, and occupy the whole course of the illness produced by the poison.”[283] Premising that the common form is a blending of irritant, nervous, and hæmorrhagic symptoms, I adopt here in part Tardieu’s division. The name of “hæmorrhagic form” may be given to that in which hæmorrhage is the predominant feature, and the “nervous” to that in which the brain and spinal cord are from the first affected. There yet remain, however, a few cases which have an entirely anomalous course, and do not fall under any of the three classes.
From a study of 121 recorded cases of phosphorus poisoning, I believe the relative frequency of the different forms to be as follows:—The common form 83 per cent., hæmorrhagic 10 per cent., nervous 6 per cent., anomalous 1 per cent. The “anomalous” are probably over-estimated, for the reason that cases presenting ordinary features are not necessarily published, but others are nearly always chronicled in detail.
§ 280. Common Form.—At the moment of swallowing, a disagreeable taste and smell are generally experienced, and there may be immediate and intense pain in the throat, gullet, and stomach, and almost immediate retching and vomiting. The throat and tongue also may become swollen and painful; but in a considerable number of cases the symptoms are not at once apparent, but are delayed from one to six hours—rarely longer. The person’s breath may be phosphorescent before he feels in any way affected, and he may go about his business and perform a number of acts requiring both time and mental integrity. Pain in the stomach (which, in some of the cases, takes the form of violent cramp and vomiting) succeeds; the matters vomited may shine in the dark, and are often tinged with blood. Diarrhœa is sometimes present, sometimes absent; sleeplessness for the first night or two is very common. The pulse is variable, sometimes frequent, sometimes slow; the temperature in the morning is usually from 36·0° to 36·5°, in the evening 37° to 38°.
The next symptom is jaundice. I have notes of the exact occurrence of jaundice in 23 cases, as follows:—In 1 within twenty-four hours, in 3 within thirty-six hours, in 3 within two days, in 11 within three days, in 1 within four days, in 1 within five days, in 1 within nine days, in 1 within eighteen days, and in 1 within twenty-seven days; so that in about 78 per cent. jaundice occurred before the end of the third day. Out of 26 cases, in which the patients lived long enough for the occurrence of jaundice, in 3 (or 11 per cent.) it was entirely absent. In 132 cases recorded by Lewin, Meischner, and Heisler, jaundice occurred in 65, or about 49 per cent., but it must be remembered, that in many of these cases the individual died before it had time to develop. The jaundice having thoroughly pronounced itself, the system may be considered as not only under the influence of the toxic action of phosphorus, but as suffering in addition from all the accidents incidental to the retention of the biliary secretion in the blood; nor is there from this point any special difference between phosphorus poisoning and certain affections of the liver—such, for example, as acute yellow atrophy. There is retention of urine, sleeplessness, headache, frequent vomiting, painful and often involuntary evacuations from the bowels, and occasionally skin affections, such as urticaria or erythema. The case terminates either by acute delirium with fever, followed by fatal coma, or, in a few instances, coma comes on, and the patient passes to death in sleep without delirium. In this common form there is in a few cases, at the end of from twenty-four to thirty hours, a remission of the symptoms, and a non-medical observer might imagine that the patient was about to recover without further discomfort; but then jaundice supervenes, and the course is as described. Infants often do not live long enough for the jaundiced stage to develop, but die within twenty-four hours, the chief symptoms being vomiting and convulsions.
§ 281. Hæmorrhagic Form.—The symptoms set in as just detailed, and jaundice appears, but accompanied by a new and terrible train of events—viz., great effusion of blood. In some cases the blood has been poured out simultaneously from the nose, mouth, bladder, kidneys, and bowels. Among women there is excessive hæmorrhagia. The liver is found to be swollen and painful; the bodily weakness is great. Such cases are usually of long duration, and a person may die months after taking the poison from weakness, anæmia, and general cachexia. In many of its phases the hæmorrhagic form resembles scurvy, and, as in scurvy, there are spots of purpura all over the body.
§ 282. The nervous form is less common than the two forms just described. From the beginning, there are strange creeping sensations about the limbs, followed by painful cramps, repeated faintings, and great somnolence. Jaundice, as usual, sets in, erythematous spots appear on the skin, and, about the fifth day, delirium of an acute character breaks out, and lock-jaw and convulsions close the scene.
The following are one or two brief abstracts of anomalous cases in which symptoms are either wanting, or run a course entirely different from any of the three forms described:—
A woman, aged 20, took about 3 grains of phosphorus in the form of rat-paste. She took the poison at six in the evening, behaved according to her wont, and sat down and wrote a letter to the king. During the night she vomited once, and died the next morning at six o’clock, exactly twelve hours after taking the poison. There appear to have been no symptoms whatever, save the single vomiting, to which may be added that in the course of the evening her breath had a phosphorus odour and was luminous.[284]
A girl swallowed a quantity of phosphorus paste, but there were no marked symptoms until the fifth day, on which there was sickness and purging. She died on the seventh day. A remarkable blueness of the finger nails was observed a little before death, and was noticeable afterwards.[285]
§ 283. Sequelæ.—In several cases in which the patients have recovered from phosphorus poisoning, there have been observed paralytic affections.[286] O. Bollinger has recorded a case in which paralysis of the foot followed;[287] in another, published by Bettelheim,[288] there were peculiar cerebral and spinal symptoms. Most of these cases are to be explained as disturbance or loss of function from small hæmorrhages in the nervous substance.
§ 284. Period at which the first Symptoms commence.—The time when the symptoms commence is occasionally of importance from a forensic point of view. I find that out of 28 cases in which the commencement of evident symptoms—i.e., pain, or vomiting, or illness—is precisely recorded, in 8 the symptoms were described as either immediate or within a few minutes after swallowing the poison; in 6 the symptoms commenced within the hour; in 3 within two hours; in other 3 within four hours; and in 1 within six hours. One was delayed until the lapse of twelve hours, 1 from sixteen to eighteen hours, 1 two, and another five days. We may, therefore, expect that in half the cases which may occur, the symptoms will commence within the hour, and more than 80 per cent. within six hours.
§ 285. Period of Death.—In 129 cases death took place as follows:—In 17 within twenty-four hours, in 30 within two days, in 103 within seven days. Three patients lived eight days, 6 nine days, 13 ten days, 1 eleven days, 1 sixteen days, 1 seventeen days, and 1 survived eight months. It hence follows that 79·8 per cent. of the fatal cases die within the week.
§ 286. Phosphorus Vapour.—There are one or two cases on record of acute poisoning by phosphorus in the form of vapour. The symptoms are somewhat different from the effects produced by the finely-divided solid, and in general terms it may be said that phosphorus vapour is more apt to produce the rarer “nervous” form of poisoning than the solid phosphorus.
Bouchardat[289] mentions the case of a druggist who, while preparing a large quantity of rat-poison in a close room, inhaled phosphorus vapour. He fainted repeatedly, fell into a complete state of prostration, and died within a week.
The following interesting case came under the observation of Professor Magnus Huss:—A man, thirty-nine years old, married, was admitted into the Seraphin-Lazareth, Stockholm, on the 2nd of February 1842. He had been occupied three years in the manufacture of phosphorus matches, and inhabited the room in which the materials were preserved. He had always been well-conducted in every way, and in good health, until a year previously, when a large quantity of the material for the manufacture of the matches accidentally caught fire and exploded. In his endeavours to extinguish the flames, he breathed a large quantity of the vapour, and he fell for a time unconscious. The spine afterwards became so weak that he could not hold himself up, and he lost, in a great measure, power over his legs and arms. On admission, his condition was as follows:—He could make a few uncertain and staggering steps, his knees trembled, his arms shook, and if he attempted to grasp anything when he lay in bed, there were involuntary twitchings of groups of muscles. There was no pain; the sensibility of the skin was unchanged; he had formication in the left arm; the spine was neither sensitive to pressure, nor unusually sensitive to heat (as, e.g., to the application of a hot sponge); the organs of special sense were not affected, but his speech was somewhat thick. He lived to 1845 in the same condition, but the paralysis became worse. There does not seem to have been any autopsy.
The effects of phosphorus vapour may be still further elucidated by one of Eulenberg’s[290] experiments on a rabbit. The vapour of burning phosphorus, mixed with much air, was admitted into a wooden hutch in which a strong rabbit sat. After 5 mgrms. of phosphorus had been in this manner consumed, the only symptoms in half an hour were salivation, and quickened and somewhat laboured respiration. After twenty-four hours had elapsed there was sudden indisposition, the animal fell as if lifeless, with the hind extremities stretched out, and intestinal movements were visible; there was also expulsion of the urine. These epileptiform seizures seem to have continued more or less for twelve days, and then ceased. After fourteen days the experiment was repeated on the same rabbit. The animal remained exposed to the vapour for three-quarters of an hour, when the epilepsy showed itself as before, and, indeed, almost regularly after feeding. Between the attacks the respiration was slowed. Eight weeks afterwards there was an intense icterus, which disappeared at the end of ten weeks.
§ 287. Chronic phosphorus poisoning has frequently been noticed in persons engaged either in the manufacture of phosphorus or in its technical application. Some have held that the symptoms are due to an oxidation product of phosphorus rather than to phosphorus itself; but in one of Eulenberg’s experiments, in which a dove was killed by breathing phosphorus fumes evolved by phosphorus oil, phosphorus was chemically recognised in the free state in the lungs. The most constant and peculiar effect of breathing small quantities of phosphorus vapour is a necrosis of the lower jaw. There is first inflammation of the periosteum of the jaw, which proceeds to suppuration and necrosis of a greater or smaller portion. The effects may develop with great suddenness, and end fatally. Thus Fournier and Olliver[291] relate the case of a girl, fourteen years old, who, after working four years in a phosphorus manufactory, was suddenly affected with periostitis of the upper jaw, and with intense anæmia. An eruption of purpuric spots ensued, and she died comatose. There is now little doubt, that minute doses of phosphorus have a specific action on the bones generally, and more especially on the bones of the jaw. Wegner[292] administered small daily doses to young animals, both in the state of vapour, and as a finely-divided solid. The condition of the bones was found to be more compact than normal, the medullary canals being smaller than in healthy bone, the ossification was quickened. The formation of callus in fractured limbs was also increased.
§ 288. Changes in the Urinary Secretion.—It has been before stated that, at a certain period of the illness, the renal secretion is scantier than in health, the urine diminishing, according to Lebert and Wyss’s[293] researches, to one-half on the third, fourth, or fifth day. It frequently contains albumen, blood, and casts. When jaundice is present, the urine has then all the characters noticed in icterus; leucin and tyrosin, always present in acute yellow atrophy of the liver, have been found in small quantity in jaundice through phosphorus; lactic acid is also present. The urea is much diminished, and, according to Schultzen and Riess,[294] may be towards death entirely absent. Lastly, it is said that there is an exhalation of either phosphorus vapour or phosphine from such urine. In some cases the urine is normal, e.g., in a case recorded by E. H. Starling, M.D., and F. G. Hopkins, B.Sc. (Guy’s Hospital Report, 1890), in which a girl, aged 18, died on the fifth day after taking phosphorus paste, the liver was fatty, and there was jaundice; but the urine contained neither leucin nor tyrosin, and was stated to be generally normal.
§ 289. Changes in the blood during life have been several times observed. In a case attended by M. Romellære of Brussels,[295] in which a man took the paste from 300 matches, and under treatment by turpentine recovered, the blood was frequently examined, and the leucocytes found much increased in number. There is a curious conflict of evidence as to whether phosphorus prevents coagulation of the blood or not. Nasse asserted that phosphorated oil given to a dog fully prevented coagulation; P. I. Liebreck[296] also, in a series of researches, found the blood dark, fluid, and in perfect solution. These observations were also supported by V. Bibra and Schuchardt.[297] Nevertheless, Lebert and Wyss found the blood, whether in the veins or in extravasations, in a normal condition. Phosphorus increases the fatty contents of the blood. Ritter found that phosphorus mixed with starch, and given to a dog, raised the fatty content from the normal 2 per 1000 up to 3·41 and 3·47 per 1000. Eug. Menard[298] saw in the blood from the jugular and portal veins, as well as in extravasations, microscopic fat globules and fine needle-shaped crystals soluble in ether.
§ 290. Antidote—Treatment.—After emptying the stomach by means of emetics or by the stomach-pump, oil of turpentine in full medicinal doses, say 2·5 c.c. (about 40 min.), frequently administered, seems to act as a true antidote, and a large percentage of cases treated early in this way recover.
§ 291. Poisonous Effects of Phosphine (phosphuretted hydrogen).—Experiments on pigeons, on rats, and other animals, and a few very rare cases among men, have shown that phosphine has an exciting action on the respiratory mucous membranes, and a secondary action on the nervous system. Eulenberg[299] exposed a pigeon to an atmosphere containing 1·68 per cent. of phosphine. There was immediate unrest; at the end of three minutes, quickened and laboured breathing (100 a minute); after seven minutes, the bird lay prostrate, with shivering of the body and wide open beak; after eight minutes, there was vomiting; after nine minutes, slow breathing (34 per minute); after twelve minutes, convulsive movements of the wings; and after thirteen minutes, general convulsions and death.
The membranes of the brain were found strongly injected, and there were extravasations. In the mucous membrane of the crop there was also an extravasation. The lungs externally and throughout were of a dirty brown-red colour; the entire heart was filled with coagulated blood, which was weakly acid in reaction.
In a second experiment with another pigeon, there was no striking symptom save that of increased frequency of respiration and loss of appetite; at the end of four days it was found dead. There was much congestion of the cerebral veins and vessels, the mucous membrane of the trachea and bronchi were weakly injected, and the first showed a thin, plastic, diphtheritic-like exudation.
Dr. Henderson’s[300] researches on rats may also be noticed here. He found that an atmosphere consisting entirely of phosphine killed rats within ten minutes, an atmosphere with 1 per cent. in half an hour. The symptoms observed were almost exactly similar to those noticed in the first experiment on the pigeon quoted above, and the post-mortem appearances were not dissimilar. With smaller quantities of the gas, the first symptom was increased frequency of the respiration; then the animals showed signs of suffering intense irritation of the skin, scratching and biting at it incessantly; afterwards they became drowsy, and assumed a very peculiar attitude, sitting down on all-fours, with the back bent forward, and the nose pushed backwards between the forepaws, so as to bring the forehead against the floor of the cage. When in this position, the rat presented the appearance of a curled-up hedgehog. Phosphine, when injected into the rectum, is also fatal; the animals exhale some of the gas from the lungs, and the breath, therefore, reduces solutions of silver nitrate.[301]
Brenner[302] has recorded the case of a man twenty-eight years old, a pharmaceutist, who is supposed to have suffered from illness caused by repeated inhalations of minute quantities of phosphine. He was engaged for two and a half years in the preparation of hypophosphites; his illness commenced with spots before the eyes, and inability to fix the attention. His teeth became very brittle, and healthy as well as carious broke off from very slight causes. Finally, a weakness of the arms and limbs developed in the course of nine months into complete locomotor ataxy.
§ 292. Blood takes up far more phosphine than water. Dybskowsky found that putting the coefficient of solubility of phosphine in pure water at ·1122 at 15°, the coefficient for venous blood was ·13, and for arterial 26·73; hence the richer the blood is in oxygen the more phosphine is absorbed. It seems probable that the poisonous gas reacts on the oxyhæmoglobin of the blood, and phosphorous acid is formed. This is supported by the fact that a watery extract of such blood reduces silver nitrate, and has been also found feebly acid. The dark blood obtained from animals poisoned by phosphine, when examined spectroscopically, has been found to exhibit a band in the violet.
§ 293. Post-mortem Appearances.—There are a few perfectly well authenticated cases showing that phosphorus may cause death, and yet no lesion be discovered afterwards. Thus, Tardieu[303] cites a case in which a woman, aged 45, poisoned herself with phosphorus, and died suddenly the seventh day afterwards. Dr. Mascarel examined the viscera with the greatest care, but could discover absolutely no abnormal conditions; the only symptoms during life were vomiting, and afterwards a little indigestion. It may, however, be remarked that the microscope does not seem to have been employed, and that probably a close examination of the heart would have revealed some alteration of its ultimate structure. The case quoted, by Taylor[304] may also be mentioned, in which a child was caught in the act of sucking phosphorus matches, and died ten days afterwards in convulsions. None of the ordinary post-mortem signs of poisoning by phosphorus were met with, but the intestines were reddened throughout, and there were no less than ten invaginations; but the case is altogether a doubtful one, and no phosphorus may actually have been taken. It is very difficult to give in a limited space anything like a full picture of the different lesions found after death from phosphorus, for they vary according as to whether the death is speedy or prolonged, whether the phosphorus has been taken as a finely-divided solid, or in the form of vapour, &c. It may, however, be shortly said, that the most common changes are fatty infiltration of the liver and kidneys, fatty degeneration of the heart, enlargement of the liver, ecchymoses in the serous membranes, in the muscular, in the fatty, and in the mucous tissues. When death occurs before jaundice supervenes, there may be little in the aspect of the corpse to raise a suspicion of poison; but if intense jaundice has existed during life, the yellow staining of the skin, and it may be, spots of purpura, will suggest to the experienced pathologist the possibility of phosphorus poisoning. In the mouth and throat there will seldom be anything abnormal. In one or two cases of rapid death among infants, some traces of the matches which had been sucked were found clinging to the gums. The stomach may be healthy, but the most common appearance is a swelling of the mucous membrane and superficial erosions. Virchow,[305] who was the first to call attention to this peculiar grey swelling of the intestinal mucous membrane under the name of gastritis glandularis or gastradenitis, shows that it is due to a fatty degeneration of the epithelial cells, and that it is by no means peculiar to phosphorus poisoning. The swelling may be seen in properly-prepared sections to have its essential seat in the glands of the mucous membrane; the glands are enlarged, their openings filled with large cells, and each single cell is finely granular. Little centres of hæmorrhage, often microscopically small, are seen, and may be the centres of small inflammations; their usual situation is on the summit of the rugæ. Very similar changes are witnessed after death from septicæmia, pyæmia, diphtheria, and other diseases. The softening of the stomach, gangrene, and deep erosions, recorded by the earlier authors, have not been observed of late years, and probably were due to post-mortem changes, and not to processes during life. The same changes are to be seen in the intestines, and there are numerous extravasations in the peritoneum.
The liver shows of all the organs the most characteristic signs; a more or less advanced fatty infiltration of its structure takes place, which was first described as caused by phosphorus by Hauff in 1860.[306] It is the most constant pathological evidence both in man and animal, and seems to occur at a very early period, Munk and Leyden having found a fatty degeneration in the liver far advanced in twenty-four hours[307] after poisoning. In rats and mice poisoned with paste, I have found this evident to the naked eye twelve hours after the fatal dose. The liver is mostly large, but in a case[308] recorded in the Lancet, July 14, 1888, the liver was shrunken; it has a pale yellow (or sometimes an intense yellow) colour; on section the cut surface presents a mottled appearance; the serous envelopes, especially along the course of the vessels, exhibit extravasations of blood. The liver itself is more deficient in blood than in the normal condition, and the more bloodless it is, the greater the fatty infiltration.
In the Museum of the Royal College of Surgeons there is a preparation (No. 2737) of the section of a liver derived from a case of phosphorus poisoning.
A girl, aged 18, after two days’ illness, was admitted into Guy’s Hospital. She confessed to having eaten a piece of bread coated with phosphorus paste. She had great abdominal pain, and died on the seventh day after taking the phosphorus. A few hours before her death she was profoundly and suddenly collapsed. The liver weighed 66 ozs. The outlines of the hepatic lobules were very distinct, each central vein being surrounded by an opaque yellowish zone; when fresh the hue was more uniform, and the section was yellowish-white in colour. A microscopical examination of the hepatic cells showed them laden with fat globules, especially in the central parts of the liver.
The microscopic appearances are also characteristic. In a case of suicidal poisoning by phosphorus, in which death took place on the seventh day, the liver was very carefully examined by Dr. G. F. Goodart, who reported as follows:—
“Under a low power the structure of the liver is still readily recognisable, and in this the specimen differs from slides of three cases of acute yellow atrophy that I have in my possession. The hepatic cells are present in large numbers, and have their natural trabecular arrangement. The columns are abnormally separated by dilated blood or lymph-spaces, and the individual cells are cloudy and ill-defined. The portal channels are everywhere characterised by a crowd of small nuclei which stain with logwood deeply. The epithelium of the smaller ducts is cloudy, and blocks the tubes in many cases. Under a high power (one-fifth) it is seen that the hepatic cells are exceedingly ill-defined in outline, and full of granules and even drops of oil. But in many parts, even where the cells themselves are hazy, the nucleus is still fairly visible. It appears to me that, in opposition to what others have described, the nuclei of the cells have in great measure resisted the degenerative process. The change in the cells is uniform throughout each lobule, but some lobules are rather more affected than others. The blood-spaces between the cells are empty, and the liver appears to be very bloodless. The portal canals are uniformly studded with small round nuclei or cells, which are in part, and might be said in great part, due to increase of the connective tissue or to a cirrhotic process. But I am more disposed to favour the view that they are due to migration from the blood-vessels, because they are so uniform in size, and the hepatic cells and connective tissue in their neighbourhood are undergoing no changes in the way of growth whatever. I cannot detect any fatty changes in the vessels, but some of the smaller biliary ducts contain some cloudy albuminous material, and their nucleation is not distinct. No retained biliary pigment is visible.”[309]
Oscar Wyss,[310] in the case of a woman twenty-three years old, who died on the fifth day after taking phosphorus, describes, in addition to the fatty appearance of the cells, a new formation of cells lying between the lobules and in part surrounding the gall-ducts and the branches of the portal vein and hepatic artery.
Salkowsky[311] found in animals, which he killed a few hours after administering to them toxic doses of phosphorus, notable hyperæmia of the throat, intestine, liver, and kidneys—both the latter organs being larger than usual. The liver cells were swollen, and the nuclei very evident, but they contained no fat, fatty drops being formed afterwards.
§ 294. The kidneys exhibit alterations very similar and analogous to those of the liver. They are mostly enlarged, congested, and flabby, with extravasations under the capsule, and show microscopic changes essentially consisting in a fatty degeneration of the epithelium. In cases attended with hæmorrhage, the tubuli may be here and there filled with blood. The fatty epithelium is especially seen in the contorted tubes, and the walls of the vessels, both of the capsule and of the malpighian bodies, also undergo the same fatty change. In cases in which death has occurred rapidly, the kidneys have been found almost healthy, or a little congested only. The pancreas has also been found with its structure in part replaced by fatty elements.
Of great significance are also the fatty changes in the general muscular system, and more especially in the heart. The muscular fibres of the heart quickly lose their transverse striæ, which are replaced by drops of fat. Probably this change is the cause of the sudden death not unfrequently met with in phosphorus poisoning.
In the lungs, when the phosphorus is taken in substance, there is little “naked-eye” change, but Perls,[312] by manometric researches, has shown that the elasticity is always decreased. According to experiments on animals, when the vapour is breathed, the mucous membrane is red, congested, swollen, and has an acid reaction.
In the nervous system no change has been remarked, save occasionally hæmorrhagic points and extravasations.
§ 295. Diagnostic Differences between Acute Yellow Atrophy of the Liver and Fatty Liver produced by Phosphorus.—O. Schultzen and O. L. Riess have collected and compared ten cases of fatty liver from phosphorus poisoning, and four cases of acute yellow atrophy of the liver, and, according to them, the chief points of distinction are as follows:—In phosphorus poisoning the liver is large, doughy, equally yellow, and with the acini well marked; while in acute yellow atrophy the liver is diminished in size, tough, leathery, and of a dirty yellow hue, the acini not being well mapped out. The “phosphorus” liver, again, presents the cells filled with large fat drops, or entirely replaced by them; but in the “atrophy” liver, the cells are replaced by a finely-nucleated detritus and through newly-formed cellular tissue. Yellow atrophy seems to be essentially an inflammation of the intralobular connective tissue, while in phosphorus poisoning the cells become gorged by an infiltration of fat, which presses upon the vessels and lessens the blood supply, and the liver, in consequence, may, after a time, waste.
There is also a clinical distinction during life, not only in the lessening bulk of the liver in yellow atrophy, in opposition to the increase of size in the large phosphorus liver, but also in the composition of the renal secretion. In yellow atrophy the urine contains so much leucine and tyrosin, that the simple addition of acetic acid causes at once a precipitate. Schultzen and Riess also found in the urine, in cases of yellow atrophy, oxymandelic acid (C8H8O4), but in cases of phosphorus poisoning a nitrogenised acid, fusing at 184° to 185°.
According to Maschka, grey-white, knotty, fæcal masses are found in the intestines in yellow atrophy, but never in cases of phosphorus poisoning. In the latter, it is more common to find a slight intestinal catarrh and fluid excreta.
§ 296. The Detection of Phosphorus.—The following are the chief methods in use for the separation and detection of phosphorus:[313]—
1. Mitscherlich’s Process.—The essential feature of this process is simply distillation of free phosphorus, and observation of its luminous properties as the vapour condenses in the condensing tube. The conditions necessary for success are—(1) that the apparatus should be in total darkness;[314] and (2) that there should be no substance present, such as alcohol or ammonia,[315] which, distilling over with the phosphorus-vapour, could destroy its luminosity. A convenient apparatus, and one certain to be in all laboratories, is an ordinary Florence flask, containing the liquid to be tested, fitted to a glass Liebig’s condenser, supported on an iron sand-bath (which may, or may not, have a thin layer of sand), and heated by a Fletcher’s low temperature burner. The distillate is received into a flask. This apparatus, if in darkness, works well; but should the observer wish to work in daylight, the condenser must be enclosed in a box perfectly impervious to light, and having a hole through which the luminosity of the tube may be seen, the head of the operator and the box being covered with a cloth. If there be a stream of water passing continuously through the condenser, a beautiful luminous ring of light appears in the upper part of the tube, where it remains fixed for some time. Should, however, the refrigeration be imperfect, the luminosity travels slowly down the tube into the receiver. In any case, the delicacy of the test is extraordinary.[316] If the organic liquid is alkaline, or even neutral, there will certainly be some evolution of ammonia, which will distil over before the phosphorus, and retard (or, if in sufficient quantity, destroy) the luminosity. In such a case it is well, as a precaution, to add enough sulphuric acid to fix the ammonia, omitting such addition if the liquid to be operated upon is acid.
2. The Production of Phosphine (PH3).—Any method which produces phosphine (phosphuretted hydrogen), enabling that gas to be passed through nitrate of silver solution, may be used for the detection of phosphorus. Thus, Sonnenschein states that he has found phosphorus in extraordinary small amount, mixed with various substances, by heating with potash in a flask, and passing the phosphine into silver nitrate, separating the excess of silver, and recognising the phosphoric acid by the addition of molybdate of ammonia.[317]
The usual way is, however, to produce phosphine by means of the action on free phosphorus of nascent hydrogen evolved on dissolving metallic zinc in dilute sulphuric acid. Phosphine is formed by the action of nascent hydrogen on solid phosphorus, phosphorous acid, and hypophosphorous acid; but no phosphine can be formed in this way by the action of hydrogen on phosphoric acid.
Since it may happen that no free phosphorus is present, but yet the first product (phosphorous acid) of its oxidation, the production of phosphine becomes a necessary test to make on failure of Mitscherlich’s test; if no result follows the proper application of the two processes, the probability is that phosphorus has not been taken.
Blondlot and Dusart evolve hydrogen from zinc and dilute sulphuric acid, and pass the gas into silver nitrate; if the gas is pure, there is of course no reduction; the liquid to be tested is then added to the hydrogen-generating liquid, and if phosphorous or hypophosphorous acids be present, a black precipitate of phosphor-silver will be produced. To prove that this black precipitate is neither that produced by SH2, nor by antimony nor arsenic, the precipitate is collected and placed in the apparatus to be presently described, and the spectroscopic appearances of the phosphine flame observed.
3. Tests Dependent on the Combustion of Phosphine (PH3).—A hydrogen flame, containing only a minute trace of phosphorus, or of the lower products of its oxidation, acquires a beautiful green tint, and possesses a characteristic spectrum. In order to obtain the latter in its best form, the amount of phosphine must not be too large, or the flame will become whitish and livid, and the bands lose their defined character, rendering the spectrum continuous. Again, the orifice of the tube whence the gas escapes must not be too small; and the best result is obtained when the flame is cooled.
M. Salet has proposed two excellent methods for the observation of phosphine by the spectroscope:—
(1) He projects the phosphorus-flame on a plane vertical surface, maintained constantly cold by means of a thin layer of running water; the green colour is especially produced in the neighbourhood of the cool surface.
(2) At the level of the base of the flame, there is an annular space, through which a stream of cold air is continually blown upwards. Thus cooled, the light is very pronounced, and the band δ, which is almost invisible in the ordinary method of examination, is plainly seen.[318]
An apparatus (devised by Blondlot, and improved by Fresenius) for the production of the phosphine flame in medico-legal research, is represented in the following diagram:—
Several of the details of this apparatus may be modified at the convenience of the operator. A is a vessel containing sulphuric acid; B is partly filled with granulated zinc, and hydrogen may be developed at pleasure; c contains a solution of nitrate of silver; d is a tube at which the gas can be lit; e, a flask containing the fluid to be tested, and provided with a tube f, at which also the gas issuing can be ignited. The orifice should be provided with a platinum nozzle. When the hydrogen has displaced the air, both tubes are lit, and the two flames, being side by side, can be compared. Should any phosphorus come over from the zinc (a possibility which the interposed silver nitrate ought to guard against), it is detected; the last flask is now gently warmed, and if the flame is green, or, indeed, in any case, it should be examined by the spectroscope.[319]
§ 297. The spectrum, when fully developed, shows one band in the orange and yellow between C and D, but very close to D, and several bands in the green. But the bands δ, γ, α, and β are the most characteristic. The band δ has its centre about the wave-length 599·4; it is easily distinguished when the slit of the spectroscope is a little wide, but may be invisible if the slit is too narrow. It is best seen by M. Salet’s second process, and, when cooled by a brisk current of air, it broadens, and may extend closer to D. The band γ has a somewhat decided border towards E, while it is nebulous towards D, and it is, therefore, very difficult to say where it begins or where it ends; its centre may, however, be put at very near 109 of Boisbaudran’s scale, corresponding to W. L. 560·5, if the flame is free. This band is more distinct than β, but with a strong current of air the reverse is the case. The middle of the important band α is nearly marked by Fraunhofer’s line E. Boisbaudran gives it as coinciding with 122 of his scale W. L. 526·3. In ordinary conditions (that is, with a free uncooled flame) this is the brightest and most marked of all the bands. The approximate middle of the band β is W. L. 510·6 (Boisbaudran’s scale 129·00).
Lipowitz’s Sulphur Test.—Sulphur has the peculiar property of condensing phosphorus on its surface, and of this Lipowitz proposed to take advantage. Pieces of sulphur are digested some time with the liquid under research, subsequently removed, and slightly dried. When examined in the dark, should phosphorus be present, they gleam strongly if rubbed with the finger, and develop a phosphorus odour. The test is wanting in delicacy, nor can it well be made quantitative; it has, however, an advantage in certain cases, e.g., the detection of phosphorus in an alcoholic liquid.
Scherer’s test, as modified by Hager,[320] is a very delicate and almost decisive test. The substances to be examined are placed in a flask with a little lead acetate (to prevent the possibility of any hydric sulphide being evolved), some ether added, and a strip of filter-paper soaked in a solution of silver nitrate is then suspended in the flask; this is conveniently done by making a slit in the bottom of the cork, and in the slit securing the paper. The closed flask is placed in the dark, and if phosphorus is present, in a few minutes there is a black stain. It may be objected that arsine will cause a similar staining, but then arsine could hardly be developed under the circumstances given. It is scarcely necessary to observe that the paper must be wet.
§ 298. Chemical Examination of the Urine.—It may be desirable, in any case of suspected phosphorus poisoning, to examine the renal secretion for leucin and tyrosin, &c. Leucin may be found as a deposit in the urine. Its general appearance is that of little oval or round discs, looking like drops of fat. It can be recognised by taking up one or more of these little bodies and placing them in the author’s subliming cell (see § 314). By careful heating it will sublime wholly on to the upper cover. On now adding a little nitric acid to the sublimed leucin, and drying, and then to the dried residue adding a droplet of a solution of sodium hydrate, leucin forms an oily drop. Tyrosin also may occur as a sediment of little heaps of fine needles. The best test for tyrosin is to dissolve in hot water, and then add a drop of a solution of mercuric nitrate and mercurous nitrate, when a rose colour is at once developed, if the tyrosin is in very minute quantity; but if in more than traces, there is a distinct crimson precipitate. To separate leucin and tyrosin from the urine, the best process is as follows:—The urine is filtered from any deposit, evaporated to a thin syrup, and decanted from the second deposit that forms. The two deposits are mixed together and treated with dilute ammonia, which will dissolve out any tyrosin and leave it in needles, if the ammonia is spontaneously evaporated on a watch-glass. The urine is then diluted and treated with neutral and basic acetates of lead, filtered, and the lead thrown out of the filtrate by hydric sulphide. The filtrate is evaporated to a syrup, and it then deposits leucin mixed with some tyrosin. If, however, the syrup refuses to crystallise, it is treated with cold absolute alcohol, and filtered, the residue is then boiled up with spirit of wine, which extracts leucin, and deposits it on cooling in a crystalline form. To obtain oxymandelic acid, the mother liquor, from which leucin and tyrosin have been extracted, is precipitated with absolute alcohol, filtered, and then the alcoholic solution evaporated to a syrup. This syrup is acidified by sulphuric acid, and extracted with ether; the ether is filtered off and evaporated to dryness; the dry residue will be in the form of oily drops and crystals. The crystals are collected, dissolved in water, and the solution precipitated by lead acetate to remove colouring-matters; after filtration it is finally precipitated by basic acetate. On decomposition of the basic acetate, by suspending in water and saturating with hydric sulphide, the ultimate filtrate on evaporation deposits colourless, flexible needles of oxymandelic acid. The nitrogenised acid which Schultzen and Riess obtained from urine in a case of phosphorus poisoning, was found in an alcohol and ether extract—warts of rhombic scales separating out of the syrupy residue. These scales gave no precipitate with basic acetate, but formed a compound with silver nitrate. The silver compound was in the form of shining white needles, and contained 33·9 per cent. of silver; the acid was decomposed by heat, and with lime yielded aniline. Its melting-point is given at from 184° to 185°. The occurrence of some volatile substance in phosphorus urine, which blackens nitrate of silver, and which is probably phosphine, was first noticed by Selmi.[321] Pesci and Stroppa have confirmed Selmi’s researches. It is even given off in the cold.
§ 299. The quantitative estimation of phosphorus is best carried out by oxidising it into phosphoric acid, and estimating as ammon. magnesian phosphate. To effect this, the substances are distilled in an atmosphere of CO2 into a flask with water, to which a tube containing silver nitrate is attached; the latter retains all phosphine, the former solid phosphorus. If necessary, the distillate may be again distilled into AgNO3; and in any case the contents of the U-tube and flask are mixed, oxidised with nitromuriatic acid, filtered from silver chloride, and the phosphoric acid determined in the usual way.
In the case of a child poisoned by lucifer matches, Sonnenschein estimated the free phosphorus in the following way:—The contents of the stomach were diluted with water, a measured part filtered, and the phosphoric acid estimated. The other portion was then oxidised by HCl and potassic chlorate, and the phosphoric acid estimated—the difference being calculated as free phosphorus.
§ 300. How long can Phosphorus be recognised after Death?—One of the most important matters for consideration is the time after death in which free phosphorus, or free phosphoric acids, can be detected. Any phosphorus changed into ammon. mag. phosphate, or into any other salt, is for medico-legal purposes entirely lost, since the expert can only take cognisance of the substance either in a free state, as phosphine, or as a free acid.
The question, again, may be asked in court—Does the decomposition of animal substances rich in phosphorus develop phosphine? The answer to this is, that no such reaction has been observed.
A case is related[322] in which phosphorus was recognised, although the body had been buried for several weeks and then exhumed.
The expert of pharmacy of the Provincial Government Board of Breslau has also made some experiments in this direction, which are worthy of note:—Four guinea-pigs were poisoned, each by 0·023 grm. of phosphorus; they died in a few hours, and were buried in sandy-loam soil, 0·5 metre deep. Exhumation of the first took place four weeks after. The putrefying organs—heart, liver, spleen, stomach, and all the intestines—tested by Mitscherlich’s method of distillation, showed characteristic phosphorescence for nearly one hour.
The second animal was exhumed after eight weeks in a highly putrescent state. Its entrails, on distillation, showed the phosphorescent appearance for thirty-five minutes.
The third animal was taken from the earth after twelve weeks, but no free phosphorus could be detected, although there was evidence of the lower form of oxidation (PO3) by Blondlot’s method.
The fourth animal was exhumed after fifteen weeks, but neither free phosphorus nor PO3 could be detected.[323]
A man, as well as a cat, was poisoned by phosphorus. On analysis, twenty-nine days after death, negative results were alone obtained.—Sonnenschein.
It will thus be evident that there is no constant rule, and that, even when decomposition is much advanced, an examination may be successful.