Berlin, 1889; _Sep.-Abdr. aus Ztschr. f. klin. Med._, Bd. xv.
At the same time the protoplasm of the tissues is paralysed, and unable
to take up the loosely bound oxygen presented. This explains a striking
symptom which has been noticed by many observers, that is, if
hydrocyanic acid be injected into an animal, the venous blood becomes of
a bright red colour; in warm-blooded animals this bright colour is
transitory, but in cold-blooded animals, in which the oxidation process
is slower, the blood remains bright red.
§ 259. =Symptoms observed in Animals.=--The main differences between the
symptoms induced in cold-blooded and warm-blooded animals, by a fatal
dose of hydric cyanide, are as follows:--
The respiration in frogs is at first somewhat dyspnœic, then much
slowed, and at length it ceases. The heart, at first slowed, later
contracts irregularly, and at length gradually stops; but it may
continue to beat for several minutes after the respiration has ceased.
But all these progressive symptoms are without convulsion. Among
warm-blooded animals, on the contrary, convulsions are constant, and the
sequence of the symptoms appears to be--dyspnœa, slowing of the pulse,
giddiness, falling down, then convulsions with expulsion of the urine
and fæces; dilatation of the pupils, exophthalmus, and finally cessation
of the pulse and breathing. The convulsions also frequently pass into
general paralysis, with loss of reflex movements, weak, infrequent
breathing, irregular, quick, and very frequent pulse, and considerable
diminution of temperature.
The commencement of the symptoms in animals is extremely rapid, the
rapidity varying according to the dose and the concentration of the
acid. It was formerly thought that the death from a large dose of the
concentrated acid followed far more quickly than could be accounted for
by the blood carrying the poison to the nervous centres; but Blake was
among the first to point out that this doubt was not supported by facts
carefully observed, since there is always a sufficient interval between
the entry of the poison into the body and the first symptoms, to support
the theory that the poison is absorbed in the usual manner. Even when
Preyer injected a cubic centimetre of 60 per cent. acid into the jugular
vein of a rabbit, twenty-nine seconds elapsed before the symptoms
commenced. Besides, we have direct experiments showing that the
acid--when applied to wounds in limbs, the vessels of which are tied,
while the free nervous communication is left open--only acts when the
ligature is removed. Magendie describes, in his usual graphic manner,
how he killed a dog by injecting into the jugular vein prussic acid, and
“_the dog died instantly, as if struck by a cannon ball_,” but it is
probable that the interval of time was not accurately noted. A few
seconds pass very rapidly, and might be occupied even by slowly pressing
the piston of the syringe down, and in the absence of accurate
measurements, it is surprising how comparatively long intervals of time
are unconsciously shortened by the mind. In any case, this observation
by Magendie has not been confirmed by the accurate tests of the more
recent experimenters; and it is universally acknowledged that, although
with strong doses of hydric cyanide injected into the circulation--or,
in other words, introduced into the system--in the most favourable
conditions for its speediest action, death occurs with appalling
suddenness, yet that it takes a time sufficiently long to admit of
explanation in the manner suggested. This has forensic importance, which
will be again alluded to. Experiments on animals show that a large dose
of a dilute acid kills quite as quickly as an equivalent dose of a
stronger acid, and in some cases it even seems to act more rapidly. If
the death does not take place within a few minutes, life may be
prolonged for hours, and even, in rare cases, days, and yet the result
be death. Coullon poisoned a dog with prussic acid; it lived for
nineteen days, and then died; but this is quite an exceptional case, and
when the fatal issue is prolonged beyond an hour, the chance of recovery
is considerable.
§ 260. The length of time dogs poisoned by fatal doses survive,
generally varies from two to fifteen minutes. The symptoms are
convulsions, insensibility of the cornea, cessation of respiration, and,
finally, the heart stops--the heart continuing to beat several minutes
after the cessation of the respirations.[244] When the dose is short of
a fatal one, the symptoms are as follows:--Evident giddiness and
distress; the tongue is protruded, the breath is taken in short, hurried
gasps, there is salivation, and convulsions rapidly set in, preceded, it
may be, by a cry. The convulsions pass into paralysis and insensibility.
After remaining in this state some time, the animal again wakes up, as
it were, very often howls, and is again convulsed; finally, it sinks
into a deep sleep, and wakes up well.
[244] N. Gréhant, _Compt. rend._, t. 109, pp. 502, 503.
Preyer noticed a striking difference in the symptoms after section of
the vagus in animals, which varied according to whether the poison was
administered by the lungs, or subcutaneously. In the first case, if the
dose is small, the respirations are diminished in frequency; then this
is followed by normal breathing; if the dose is larger, there is an
increase in the frequency of the respirations. Lastly, if a very large
quantity is introduced into the lungs, death quickly follows, with
respirations diminished in frequency. On the other hand, when the poison
is injected subcutaneously, small doses have no influence on the
breathing; but with large doses, there is an increase in the frequency
of the respirations, which sink again below the normal standard.
§ 261. =Symptoms in Man.=--When a fatal but not excessive dose of either
potassic or hydric cyanide is taken, the sequence of symptoms is as
follows:--Salivation, with a feeling of constriction in the throat,
nausea, and occasionally vomiting. After a few minutes a peculiar
constricting pain in the chest is felt, and the breathing is distinctly
affected. Giddiness and confusion of sight rapidly set in, and the
person falls to the ground in convulsions similar to those of epilepsy.
The convulsions are either general, or attacking only certain groups of
muscles; there is often true trismus, and the jaws are so firmly closed
that nothing will part them. The respiration is peculiar, the
inspiration is short, the expiration prolonged,[245] and between the two
there is a long interval ever becoming more protracted as death is
imminent. The skin is pale, or blue, or greyish-blue; the eyes are
glassy and staring, with dilated pupils; the mouth is covered with foam,
and the breath smells of the poison; the pulse, at first quick and
small, sinks in a little while in frequency, and at length cannot be
felt. Involuntary evacuation of fæces, urine, and semen is often
observed, and occasionally there has been vomiting, and a portion of the
vomit has been aspirated into the air-passages. Finally, the convulsions
pass into paralysis, abolition of reflex sensibility, and gradual
ceasing of the respiration. With large doses these different stages may
occur, but the course is so rapid that they are merged the one into the
other, and are undistinguishable. The shortest time between the taking
of the acid and the commencement of the symptoms may be put at about ten
seconds. If, however, a large amount of the vapour is inhaled at once,
this period may be rather lessened. The interval of time is so short
that any witnesses generally unintentionally exaggerate, and aver that
the effects were witnessed _before_ the swallowing of the liquid--“As
the cup was at his lips”--“He had hardly drunk it,” &c. There is
probably a short interval of consciousness, then come giddiness, and, it
may be, a cry for assistance; and lastly, there is a falling down in
convulsions, and a speedy death. Convulsions are not always present, the
victim occasionally appears to sink lifeless at once. Thus, in a case
related by Hufeland, a man was seen to swallow a quantity of acid,
equivalent to 40 grains of the pure acid--that is, about forty times
more than sufficient to kill him. He staggered a few paces, and then
fell dead, without sound or convulsion.
[245] In a case quoted by Seidel (Maschka’s _Handbuch_, p. 321), a man,
36 years of age, four or five minutes after swallowing 150 mgrms.
anhydrous HCN in spirits, lay apparently lifeless, without pulse or
breathing. After a few minutes was noticed an extraordinary deep
expiration, by which the ribs were drawn in almost to the spine, and the
chest made quite hollow.
§ 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.
[246] _Forensic Medicine_, 4th ed., p. 615.
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]
[247] Dr. J. Autal, a Hungarian chemist, states that cobalt nitrate is
an efficacious antidote to poisoning by either HCN or KCN. The brief
interval between the taking of a fatal dose and death can, however, be
rarely utilised.--_Lancet_, Jan. 16, 1894.
§ 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.
[248] _Wiener klin. Woch._, 1891.
§ 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.
[249] Hydric cyanide has, according to C. Brame, a remarkable antiseptic
action, and if administered in sufficient quantity to animals, preserves
them after death for a month. He considers that there is some more or
less definite combination with the tissues.
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.
[250] The following case came under my own observation:--A stout woman,
35 years of age, the wife of a French polisher, drank, in a fit of rage,
a solution of cyanide of potassium. It was estimated that about 15
grains of the solid substance were swallowed. She died within an hour.
The face was flushed, the body not decomposed; the mouth smelt strongly
of cyanide; the stomach had about an ounce of bloody fluid in it, and
was in a most intense state of congestion. There was commencing fatty
degeneration of the liver, the kidneys were flabby, and the capsule
adherent. The contents of the stomach showed cyanide of potassium, and
the blood was very fluid. The woman was known to be of intemperate
habits.
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.
[251] In the case of testing in this way for the alkaline cyanides, the
solution must contain a little free nitric acid.
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.
[252] _Neues Repert. de Pharm._, 18, 356.
[253] This reaction (with tincture of guaiacum and copper) has been long
known. “I remember a pharmaceutist, who attended my father’s laboratory,
showing me this test in 1828 or 1829.”--Mohr’s _Toxicologie_, p. 92.
(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]
[254] M. Carey Lea, _Amer. Journ. of Science_ [3], ix. pp. 121-123; _J.
C. Society_, 1876, vol. i. p. 112.
(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.
[255] _Chemical News_, 68, p. 75.
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:--
[256] _Ber. d. deutsch. chem. Gesellsch._, Berlin, ix. p. 1023.
=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]
[257] Without wishing to discredit the statements of M. Sokoloff, we may
point out that a loss of half-a-dozen mgrms. only appears rather
extraordinary.
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.
[258] L’Orosi. xv. 85-88.
§ 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.
[259] Dragendorff, G., _Beitr. zur gericht. Chem._, p. 59.
[260] Casper’s _Pract. Handbuch der gerichtlichen Medicin_, p. 561.
[261] _Vierteljahr. f. gerichtl. Med._, Berlin, 1881, p. 193.
[262] _Zeitschrift f. anal. Chemie_, von Fresenius, 1873, xii. p. 4.
§ 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.
[263] _Gewerbe Hygiene_, p. 385.
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]
[264] Autenrieth, _Arch. Pharm._, 231, 99-109.
[265] The presence of ferro-cyanide is easily detected. The liquid is,
if necessary, filtered and then acidified with hydrochloric acid and a
few drops of ferric chloride added; if the liquid contains
ferro-cyanide, there is immediate production of Prussian blue. It may
happen that potassic or sodic cyanide has been taken as well as
ferro-cyanide, and it will be necessary then to devise a process by
which only the prussic acid from the simple cyanide is distilled over.
According to Autenrieth, if sodium hydrocarbonate is added to the liquid
in sufficient quantity and the liquid distilled, the hydric cyanide that
comes over is derived wholly from the sodium or potassium cyanide.
Should mercury cyanide and ferro-cyanide be taken together, then this
process requires modification; bicarbonate of soda is added as before,
and then a few c.c. of water saturated with hydric sulphide; under these
circumstances, only the hydric cyanide derived from the mercury cyanide
distils over. If the bicarbonate of soda is omitted, the distillate
contains hydric cyanide derived from the ferro-cyanide.
=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]
[266] _Substances Toxiques_, pp. 66-103.
[267] “_Einige Bemerkungen über die Wirkung von Cyanquecksilber_,” in
Hoppe-Seyler’s _Med. Chem. Untersuchungen_, 2 Heft, p. 279.
[268] Mercury cyanide may be detected in a liquid after acidifying with
tartaric acid, and adding a few c.c. of SH₂ water and then distilling.
S. Lopes suggests another process: the liquid is acidified with tartaric
acid, ammonium chloride added in excess, and the liquid is distilled. A
double chloride of ammonium and mercury is formed, and HCN distils over
with the steam.--_J. Pharm._, xxvii. 550-553.
=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.
[269] _Compt. rend._, t. 64, 1867, p. 561.
=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.
[270] _Gewerbe Hygiene_, p. 392.
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.
[271] _Zur acuten Phosphor-Vergiftung_, Dorpat, 1866.
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
[272] Phosphorus is very little soluble in cold acetic acid, and the
solubility given is only correct when the boiling acid acts for some
time on the phosphorus.
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] A hound took 200 grms. of red phosphorus in twelve days, and
remained healthy.--Sonnenschein.
[274] Schrotter, _Chem. News_, vol. xxxvi. p. 198.
§ 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:--
[275] Casper’s 204th case.
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:--
[276] _Nederlandsch Tijdschr. voor Geneesk._, Afl. i., 1866.
(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 Total
above
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 Total
above
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:--
[277] Schmidt’s _Jahrbuch der ger. Med._, 1867, Bd. 186, S. 209-248.
[278] _Die acute Phosphorose und einige Reflexionen über die acute gelbe
Leberatrophie, &c., Inaug. Diss._, Leipzig, 1864.
Phosphorus in Phosphorus
Number of Cases. In the Years Substance, Matches.
or as Paste.
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.
[279] Dr. Dannenberg has shown by direct experiment that a poisonous
dose of phosphorus may be introduced into spirits or coffee, and the
mixture have but little odour or taste of phosphorus.--Schuchardt in
Maschka’s _Handbuch_.
[280] Géry, “_Ueber Terpentinessenz als Gegenmittel gegen Phosphor_,” in
_Gaz. Hebd. de Méd._, 2 sér., x. 2, 1873.
§ 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.
[281] Reveil, _Ann. d’Hygiène Publ._ (3), xii. p. 370.
[282] _Arch. f. d. Ges. Physiologie_, iii. p. 1.
§ 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.
[283] _Étude Médico-Légale et Clinique sur l’Empoisonnement_, Paris,
1875, p. 483.
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]
[284] Casper’s 205th case.
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]
[285] Taylor on _Poisons_, p. 277.
§ 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.
[286] See Gallavardin, _Les Paralyses Phosphoriques_, Paris, 1865.
[287] _Deutsches Archiv f. klin. Med._, Bd. 6, Hft. 1, S. 94, 1869.
[288] _Wiener Med. Presse_, 1868, No. 41.
§ 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.
[289] _Annuaire de Thérap._, 1874, p. 109; Schuchardt in Maschka’s
_Handbuch_; also Schmidt’s _Jahrbuch_, 1846, Bd. 51, S. 101.
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.
[290] _Gewerbe Hygiene_, p. 255.
§ 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.
[291] _Gaz. hebd. de Méd._, 29, p. 461, 1868.
[292] Virchow’s _Arch. f. path. Anat._, lv. 11.
§ 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.
[293] _Archiv Générale de Méd._, 6 Sér., Tom. 12, 1868, p. 709.
[294] _Annalen der Charité_, Berlin.
§ 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.
[295] Tardieu, _op. cit._, Case 31.
[296] _Diss. de Venefico Phosphoreo Acuto_, Upsal, 1845.
[297] V. Bibra u. Geist, _Die Krankheiten der Arbeiter in den
Phosphorzundholz Fabriken_, 1847, S. 59, &c.; Henle u. v. Pfeuffer’s
_Zeitschr. f. ration. Med._, N. F., Bd. 7, Hft. 3, 1857.
[298] _Étude Expérimentale sur quelques lésions de l’Empoisonnement aigu
par le Phosphore (Thèse)_, Strasbourg, 1869.
§ 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.
[299] _Gewerbe Hygiene_, p. 273.
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]
[300] _Journ. Anat. and Physiol._, vol. xiii. p. 19.
[301] Dybskowsky, _Med. Chem. Untersuchungen aus Hoppe-Seyler’s Labor.
in Tübingen_, p. 57.
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.
[302] _St. Petersburg Med. Zeitschr._, 4 Hft., 1865.
§ 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.
[303] _L’Empoisonnement_, p. 520.
[304] _Poisons_, 3rd ed., p. 276.
[305] Virchow’s _Archiv. f. path. Anat._, Bd. 31, Hft. 3, 399.
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.
[306] Hauff collected 12 cases, and found a fatty liver in
11.--_Würtemb. Med. Corresp. Bl._, 1860, No. 34.
[307] _Die acute Phosphor-Vergiftung_, Berlin, 1865.
[308] This case, from the similarity of the pathological appearances to
those produced by yellow atrophy, deserves fuller notice:--“Frances A.
Cowley, aged 20, on her own admission, took some rat paste on Tuesday,
June 19th. Death ensued eleven days later. The initial symptoms were not
very marked. Nausea and vomiting continued with moderate severity for a
few days and then ceased. There ensued a feeling of depression. Towards
the end insensibility, icterus, and somewhat profuse metrorrhagia
supervened. At the necropsy the skin and conjunctivæ were observed of a
bright yellow colour. There was no organic disease save of a recent
nature, and entirely attributable to the action of the poison ingested.
The stomach contained about three-quarters of a pint of dark
claret-coloured fluid, consisting largely of blood derived from
capillary hæmorrhage from the mucous membrane. There was no solution of
continuity of the mucous membrane, which showed traces of recent
irritation. The whole surface presented a yellow icteric tint, except
the summits of some of the rugæ, which were of a bright pink colour.
There was also faint wrinkling of the mucous membrane. The upper part of
the small intestine was affected in much the same manner as the stomach.
The large intestine contained a quantity of almost colourless fæces. The
liver was shrunken, weighing only 26 ozs., and both on its outer and
sectional surface exactly resembled the appearances produced by acute
yellow atrophy, except that there were greater congestion and
interstitial hæmorrhage in patches. The lobules of the liver were in
many places unrecognisable; in others they stood in bold relief as
brilliant canary-yellow patches, standing in strong contrast to the deep
dark-red areas of congestion and extravasation. The gall-bladder
contained about 2 drachms of thin greyish fluid, apparently all but
devoid of bile. The urinary bladder was empty; the kidneys were
enlarged; the cortex was very pale and bile-stained, of greater depth
than natural, and of softer consistence. The spleen was not enlarged,
nor was it in the least degree softened. In addition to the bleeding
from the uterus noticed during life, there was capillary hæmorrhage into
the right lung and pleura, into the pericardium, and, as already
mentioned, into the stomach. The brain was healthy.”
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]
[309] “A Recent Case of Suicide,” by Herbert J. Capon, M.D.--_Lancet_,
March 18, 1882.
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.
[310] Virchow’s _Archiv. f. path. Anat._, Bd. 33, Hft. 3, S. 432, 1865.
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.
[311] _Ibid._, Bd. 34, Hft. 1 u. 2, S. 73, 1865.
§ 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.
[312] Deutsch. _Archiv f. klin. Med._, vi. Hft. 1, S. 1, 1869.
=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]--
[313] It has been recommended to dissolve the phosphorus out from
organic matters by carbon disulphide. On evaporation of the latter the
phosphorus is recognised by its physical properties. Such a method is of
but limited application, although it may sometimes be found useful. I
have successfully employed it in the extraction of phosphorus from the
crop of a fowl; but on this occasion it happened to be present in large
quantity.
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.
[314] Any considerable amount of phosphorescence can, however, be
observed in twilight.
[315] Many volatile substances destroy the luminous appearance of
phosphorus vapour, _e.g._, chlorine, hydric sulphide, sulphur dioxide,
carbon disulphide, ether, alcohol, petroleum, turpentine, creasote, and
most essential oils. On the other hand, bromine, hydrochloric acid,
camphor, and carbonate of ammonia do not seem to interfere much with the
phosphorescence.
[316] Fresenius states that he and Neubauer, with 1 mgrm. of phosphorus
in 200,000, recognised the light, which lasted for half an
hour.--_Zeitschr. f. anal. Chem._, i. p. 336.
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]
[317] Sonnenschein, _Handbuch der gerichtlichen Chemie_, Berlin, 1869.
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]
[318] Consult _Spectres Lumineux_, par M. Lecoq de Boisbaudran, Paris,
1874. See also Christofle and Beilstrom’s “Abhandlung,” in _Fresenius’
Zeitschr. f. anal. Chem._, B. 2, p. 465, and B. 3, p. 147.
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:--
[Illustration]
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]
[319] F. Selmi has proposed the simple dipping of a platinum loop into a
liquid containing phosphoric acid, and then inserting it into the tip of
a hydrogen flame.
§ 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.
[320] _Pharm. Central-halle_, 20, 353.
§ 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.
[321] _Giornale Internaz. della Scienza Med._, 1879, Nro. 5, p. 645.
§ 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.
[322] _Pharm. Zeitsch. f. Russl._, Jahrg. 2, p. 87.
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]
[323] _Vierteljahrsschrift für gerichtliche Medicin_, Jan. 7, 1876; see
also _Zeitschr. f. anal. Chemie_, 1872.
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.