Treatise on Poisons by Sir Robert Christison

15. The last are _colic_, _iliac passion_, and _obstructed intestine_.

5878 words  |  Chapter 62

As the symptoms of some poisons are the same with those of colic, it is of course sometimes impossible to distinguish the natural disease from the effects of poison by attending to the abdominal symptoms only. But the distinction in severe cases of poisoning may almost always be drawn from collateral symptoms and extraneous circumstances.—The iliac passion is distinguished by a complete reversion of the vermicular motion of the intestines in consequence of which the fæces are often discharged by vomiting. I am not aware that stercoraceous vomiting is ever caused by poisoning.—A case has been recorded in Corvisart’s journal, in which iliac passion, originating in obstruction of the ileum by hardened fæces, and proving fatal in twenty-six hours, gave rise to a judicial inquiry into the possibility of poisoning.[193] Another instance, that led to a strong suspicion of poisoning, has been lately published by M. Rostan, in which there was continued vomiting and pain of abdomen, proving fatal in two days, and arising from the small intestines being obstructed by an adventitious band.[194] In this case the first inspectors failed to observe the true cause of the symptoms; but Rostan and Orfila, who were appointed to examine the body a second time, discovered the constriction, and were unable to find any poison in the stomach by analysis. Stercoraceous vomiting occurred during life; which might have been held sufficient to settle the real nature of the case.—Obstruction of the intestines arising from twisting of the gut, intussusception, foreign bodies, or strangulated hernia, is easily known by the seat where the pain begins, by the obstinate constipation, and also by the excessive enlargement of the belly,—which last, however, is rather an equivocal symptom. The preceding observations will enable the medical jurist to determine, how far a diagnosis may be drawn from the symptoms between poisoning with the irritant and the diseases which resemble it. It will be remarked that the most embarrassing disease, on account of its frequency, and peculiar symptoms, is cholera. Cholera, however, may be recognised in some instances even considered in regard to the irritants as a class; and we shall presently find that it may be distinguished still better from the effects of some individual poisons. SECTION II.—_Of the Morbid Appearances caused by Irritant Poisons, compared with those of certain natural diseases._ The next subject for consideration is the morbid appearances produced by the irritants as a class, together with those of a similar nature, which arise from natural causes. The powerful irritants, which are not corrosives, produce simply the appearances characteristic of inflammation of the alimentary canal in its various stages,—in the mouth, throat, and gullet vascularity, and also, if the case has lasted long enough, ulceration;—in the stomach, vascularity, extravasation of blood under and in the substance of the villous coat and likewise into the cavity of the organ, abundant secretion of tough mucus, deposition of coagulable lymph in a fine network, ulceration of the membranes, occasionally perforation, preternatural softness of the whole or of part of the villous coat, and on the other hand sometimes uncommon hardness and shrivelling of that coat; in the intestines vascularity, extravasation, and ulceration.—Sometimes several of these appearances are to be seen in the whole alimentary canal at once. In poisoning with arsenic or corrosive sublimate it is no unusual thing to meet with redness or ulceration of the throat, great disease in the stomach, vascularity of the small intestines, ulcers in the great intestines, and excoriation of the anus.—When the poison is an active corrosive much more extensive ravages are sometimes caused, particularly in the stomach. After poisoning by the mineral acids, for example, the whole mucous membrane of the stomach is at times found wanting; nay, large patches of the whole coats may be wanting, and the deficiency supplied by the adhesion of the margin of the aperture to the adjoining viscera, and the conversion of the outer membrane of these viscera into an inner membrane for the stomach. Of the appearances here briefly enumerated the particulars will be related partly under what is now to be said of the appearances arising from natural causes, which are liable to be confounded with the effects of poisons, partly under the head of individual poisons. _Of redness of the stomach and intestines from natural causes, and its distinction from the redness caused by poisons._ Simple redness of the alimentary mucous membrane in all its forms, whether of mere vascularity, or actual extravasation, not only does not distinguish poisoning from inflammatory disorders of natural origin, but will even seldom distinguish the effects of poison from those of processes that occur independently of disease, and subsequent to death. On the subject of real inflammation, as distinguished from redness originating after death, or pseudo-morbid redness, as it is commonly termed,—a subject of great consequence to the medical jurist,—the reader may consult with advantage a paper by Dr. Yelloly,[195] an essay by MM. Rigot and Trousseau,[196] or that of M. Billard.[197] The former authors proved by experiment, that various kinds of pseudo-morbid redness may be formed, which cannot be distinguished from the parallel varieties caused by inflammation; that these appearances are formed after death, and not till three, five, or eight hours after it; that they are to be found chiefly in the most depending turns of intestines, and in the most depending parts of each turn, or of the stomach; and that after they have been formed, they may be made to shift their place, and appear where the membrane was previously healthy, by simply altering the position of the gut. M. Billard, on the other hand, has laid down their characters, and made a minute arrangement of the several kinds. He has divided them into ramiform, capilliform, punctated, striated, laminated, and diffuse redness,—terms which need hardly be explained. I must be content with merely referring to these sources of information for a particular account of the appearances in question. But it may be right at the same time to quote an instance of the most aggravated form of pseudo-morbid redness, in order to convince the reader that all forms may equally arise from the same causes. Among other example, then, which have been related of laminated redness, or redness in patches from extravasation, M. Billard mentions the case of a man who hanged himself, and in whose body was found, on the mucous membrane of the small intestine where it lay in the right flank, “a large, amaranth-red patch, six finger-breadths wide, covered with bloody exudation, and not removable by washing:” and in the lower pelvis there was a similar patch of even larger dimensions.[198] Although morbid and pseudo-morbid redness of the inner coat of the alimentary canal cannot be distinguished from one another by any intrinsic character, M. Billard thinks this may be done by attending to collateral circumstances. According to his researches, redness is to be accounted inflammatory only when it occurs in parts not depending in position, or is not limited to such parts: when the mesenteric veins supplying the parts are not distended, nor the great abdominal veins obstructed at the time of death; when the reddened membrane is covered with much mucus, particularly if thick, tenacious, and adhering; when the mucous membrane itself is opaque, so that when dissected off and stretched over the finger, the finger is not visible; when the cellular tissue which connects that membrane with the subjacent coat is brittle, so that the former is easily scratched off with the nail. Some observations may be here also made on another appearance, allied to the present group, but which there is strong reason to believe always indicates some violent irritation at least, if not even irritation from poison only, in the organ where it is found. It is an effusion under the villous coat of the stomach, and incorporation with its substance, of dark brownish-black, or as it were charred, blood; which is thus altered either by the chemical action of the poison, or by a vital process. In many cases of poisoning with the mineral acids, oxalic acid, arsenic, corrosive sublimate, and the like, there are found on the villous coat of the stomach little knots and larger irregular patches and streaks, not of a reddish-brown, reddish-black, or violaceous hue, like pseudo-morbid redness, but dark-grayish-black, or brownish-black, like the colour of coal or melanosis,—accompanied too with elevation of the membrane, frequently with abrasion on the middle of the patches, and surrounded by vascularity. This conjunction of appearances I have never seen in the stomach, unless it had been violently irritated; and several experienced pathologists of my acquaintance agree with me in this statement. It bears a pretty close resemblance to melanosis of the stomach;[199] but is distinguished by melanotic blackness being arranged in regular abruptly-defined spots, and still better by melanosis not being preceded by symptoms of irritation in the stomach. Referring to what was already said under the head of the symptoms of gastritis [p. 102], I must again express my doubts whether the appearances now described ever arise in this country from natural disease. In the intestines they are sufficiently familiar to the physician, as arising from idiopathic enteritis, and from dysentery. But in the stomach their existence as the effect of natural disease is very doubtful. Another kind of coloration of the inner membrane of the stomach, which may be shortly alluded to, because it has actually been mistaken for the effect of irritation from poison, although by no means like it,—is staining of the membrane with a reddish, brownish, yellowish, or greenish tint, observed in bodies that have been kept some time, and produced by the proximity of the liver, spleen, or colon if it contains fæces. No unprejudiced and skilful inspector could possibly mistake this appearance for inflammation. But under the impulse of prejudice it has been considered such, and imputed to poison. On the occurrence of such stains an attempt was made by the French to ascribe to poison the death of the republican general Hoche. He died rather suddenly on his way from Frankfort to join his troops; and as poisoning was suspected, the body was opened in the presence of three French army-surgeons, and a French and two German physicians. The only appearance of note in the alimentary canal was two darkish spots on the villous coat of the stomach. The surgeons drew up a report which imputed his death to poison; but the physicians refused to sign it; and other medical people who were subsequently added to the commission decided with the latter.[200] The surgeons probably would not have been so hasty, if they had not known that the result of their complaisance would have been the levying of a heavy fine on the inhabitants. The last kind of discoloration of the inner coat which requires mention is dyeing from the presence of coloured fluids in the contents. A remarkable instance has been recorded where redness of this nature was mistaken for inflammation, and the death of the individual in consequence ascribed at first to poison. A person long in delicate health died suddenly after taking a laxative draught; and the stomach, as well as the gullet, being found on dissection red and livid in various places, it was hastily inferred by his medical attendants, that these appearances were the effect of poison, and that the apothecary had committed some fatal error in compounding the draught. But another physician, who was acquainted with the deceased, although he did not attend him professionally, strongly suspected he had died a natural death; and happening to know he was in the practice of taking a strong infusion of corn-poppy, inferred that the supposed signs of inflammation were merely stains arising from the habitual use of this substance. Accordingly, on making the experiment, he found that in dogs to which a similar infusion was given, appearances were produced identically the same.[201] _Of the effusion of mucus and lymph from natural causes._—The abundant secretion of tough mucus in the stomach is a sign of that organ having been irritated. But the effusion of lymph is more characteristic. This may be produced by natural inflammation as well as by irritating poisons. As arising from either cause, however, it is rare; and certainly by no means so common as would be supposed from what is said in systematic works; for tough mucus has been often mistaken for it. Reticulated lymph adhering to the villous coat, and accompanied with corresponding reticulated redness of that coat, such as I have seen in animals poisoned with arsenic or oxalic acid, is an unequivocal sign of inflammation. _Of idiopathic ulcers and perforation of the stomach and intestines, and their distinction from those caused by poison._—Both ulceration and perforation may be produced by natural disease. In the ulceration produced by poisons there is generally speaking nothing to distinguish it from natural ulcers; but that caused by some poisons, such as iodine, is said to differ by the surrounding coloration of the membrane; and when the ulcer is caused by a sparingly soluble poison in a state of powder, such as arsenic, the cavity of the ulcer is sometimes filled with the powder. Perforation is a rare effect of the simple irritant poisons; but it is often caused by corrosives. It is imitated by two of the varieties of perforation from natural disease. The form of natural perforation caused by a common ulcer is precisely the same as that caused by the simple irritants, and is incapable of being distinguished, except when it is attended with scirrhus. By far the most remarkable variety, however, of spontaneous perforation is that which takes place, without proper inflammatory action, from simple gelatinizing of the coats. It is very apt to be mistaken, and in a celebrated trial, which will be immediately noticed, was actually mistaken for the effect of corrosive poison. It may be situated on any part of the stomach, but is oftenest seen on the posterior surface. It is sometimes small, more often as big as a half-crown, frequently of the size of the palm, and occasionally so great as to involve an entire half of the stomach. Sometimes there is more than one aperture. The margin is of all shapes, commonly fringed, and almost always formed of the peritoneum, the other coats being more extensively dissolved. In one instance, however, the peritonæal surface was on the contrary the most extensively destroyed;[202] and in a case which occurred in the infirmary here, and was pointed out to me by the late Dr. W. Cullen, the peritonæum alone was extensively softened, and partly dissolved, so as to lay the muscular coat bare on its outer surface. The gelatinization therefore sometimes, though very rarely, begins on the outside of the stomach. Internally the whole is surrounded by pulpiness of the mucous coat, generally white, occasionally bluish or blackish, never granulated like an ulcer, very rarely vascular; and when vascular, the blood may be squeezed out of the loaded and open vessels. The organs in contact with the hole are also frequently softened. Thus an excavation is sometimes found in the liver or spleen; or the diaphragm is pierced through and through. The margins of the latter holes are without any sign of vascular action, but are generally besmeared with a dark pulpy mass, the remains of the softened tissue. The pulp never smells of gangrene; with which, indeed, this species of softening is wholly unconnected. The edge of the hole in the stomach never adheres to the adjoining organ; yet, even when the hole is very large, the contents of the stomach have not always made their escape. Often the dissolution of the coats is incomplete. John Hunter and others, indeed, have said that a stomach is rarely seen without more or less solution of the mucous coat.[203] The best account of the appearances in this state is given by Jaeger of Stuttgardt.[204] The circumstances under which this extraordinary appearance occurs are singularly various. Professor Chaussier and the French pathologists conceive it to be always a morbid process constituting a peculiar disease; and doubtless cases have occurred in which death appears to have arisen from the stomach being perforated during life by gelatinization.[205] But it has been found much more frequently, when death was clearly the consequence of a different disease, and when there did not exist during life a single sign of disorder in the stomach. Thus it has been found in women who died of convulsions after delivery,—in children who died convulsed or of hydrocephalus,—after death from suppuration of the brain, both natural and the result of violence,—from coma following an old ulcer of the back, which communicated with the spinal canal,—from diseased mesenteric glands,—from phthisis,—from nervous fever,—and after sudden death from fracture of the skull or hanging:[206] and in all of these circumstances it has occurred without any previous symptom referrible to a disorder in the stomach. The opinions of pathologists are divided as to its nature. The French conceive it arises from a morbid corrosive action, which, however, may extend after death, in consequence of the fluids acquiring a solvent power. Hunter ascribed it entirely to the solvent power of the gastric juice after death. There are difficulties in the way of both doctrines. A full examination of the whole inquiry, which is one of much interest and considerable complexity, would be misplaced in this work; but some remarks are called for, by reason of the important medico-legal relations of the subject, and the uncertainty in which it is at present involved. In the first place, then, it appears difficult, if not impossible, to comprehend how a vital erosive action can account for the perforations observed after death from diseases wholly unconnected with the stomach, and unattended during life by any symptom of disorder in that organ. For, not to dwell on other less weighty arguments,—on the one hand, there is during life no symptom of perforation, an accident which if deep stupor be not present at the same time is always attended with violent symptoms when it arises from any cause but gelatinization,—and on the other hand, there is frequently no escape of the contents of the stomach into the cavity of the abdomen, though the hole is of enormous size, and its edge not adherent to the adjoining organs.—All such perforations, however, are perfectly well accounted for, on the other theory, by what is now known of the properties of the gastric juice. This will appear from the following exposition. The power of the gastric juice to dissolve the stomach and other soft animal textures was long thought to be fully proved by the well-known researches of Spallanzani,[207] Stevens,[208] and Gosse.[209] In later times doubts were entertained on the subject in consequence of negative results having been obtained by other experimentalists, more especially by Montégre.[210] But these apparently discrepant facts and opinions have been reconciled by the ulterior experiments of Tiedemann and Gmelin on digestion;[211] who found that the nature and quality of the fluid secreted by the stomach vary much in different circumstances,—that, when its villous coat is not subjected to some stimulus, the fluid which lines it is not acid, and does not possess any particular solvent action,—but that when the membrane is stimulated by the presence of food or other sources of excitement, the quality of the secretion is materially changed, for it becomes strongly acid and is capable of dissolving alimentary substances both in and out of the body. And still more lately the solvent power of the proper gastric juice over the stomach, and its capability of producing perforation in animals after death, have been established in the most satisfactory manner by Dr. Carswell,[212] who has shown by a series of incontrovertible facts,—that in the rabbit when killed during the digestion of a meal, and left for some hours afterwards in particular positions, all the phenomena of spontaneous gelatinized perforations observed at times in man, may be easily produced at will,—that acidity of the gastric juice is an invariable circumstance when such perforations are remarked,—and that the appearances in question as they occur in the rabbit are the result of chemical action alone, and occur only after death. Thus, then, the physiological experiments of Tiedemann and Gmelin, together with the investigations of Carswell, not merely establish positively the fact, that the stomach may be perforated after death by the gastric juice, but likewise account clearly for the negative results obtained by other experimentalists. For example, passing over earlier experiments, they explain sufficiently the negative results obtained by Dr. Pommer of Heilbronn,[213] an experimentalist of some reputation in Germany; for, falling into the error of some of the less recent experimentalists on this subject, he made his observations on animals killed slowly by starving,—in which circumstance there is no proper gastric juice in the stomach, and consequently no solvent action can exist. These statements relative to the causes and phenomena of gelatinized perforation in the stomach supply the strongest possible presumption which analogy can furnish, that a great proportion of spontaneous gelatinized perforations in the human subject are owing to the action of the gastric juice after death. And this presumption is increased to something not far removed from demonstration by the circumstance, that in man the process of softening has actually been traced extending in the dead body. This interesting fact was first noticed by Mr. Allan Burns.[214] In the body of a girl who died of diseased mesenteric glands he found an aperture in the fore part of the stomach with the usual pulpy margin, and the liver in contact with the hole uninjured. In two days more the liver opposite the hole had become pulpy, and its peritonæal coat quite dissolved; and the back part of the stomach opposite the hole was also dissolved, so that only its peritonæal coat remained. Dr. Sharpey has communicated to me a similar observation. On finding in the body of a child the stomach perforated and gelatinized, but the adjoining organs uninjured, he sewed up the body, to show the appearances to some of his friends next day. By that time the peritonæal surfaces of the spleen and left kidney were found much softened and pulpy where they lay in contact with the hole in the stomach. I have since met with a similar occurrence where the perforation affected the duodenum (p. 120). It must be admitted, then, that the action of the gastric juice after death is quite sufficient to account for the greater number of gelatiniform perforations in the human stomach. But in the second place, it seems scarcely possible to explain every perforation of the kind in this way. The solvent action of the gastric juice for example, affords no explanation of a singular case related by M. Récamier,[215] where, after death in the secondary stage of small-pox, the stomach was transparent and brittle, and perforated in the splenic region by a gelatinized hole large enough to admit the fist,—although the fluid in the stomach was subsequently found incapable of dissolving another stomach, and almost destitute of free acid. And still less will the solvent action of the gastric juice account for such cases as those of Laisné and Gastellier, quoted in pp. 107–8, or the French medico-legal case to be mentioned in p. 118,—where death is preceded by a short illness, indicating a violent disorder of the stomach, and sometimes even characterized by all the marked symptoms of perforation. In the last description of cases, which are comparatively very rare, it seems necessary to admit that the gelatinization takes place during life; unless, indeed, it be supposed that the stomach is first perforated during life by ordinary ulcerative absorption, and then gelatinized after death, in consequence of the irritation existing before death having given rise to an unusual secretion of gastric juice. Passing now to the differences between these gelatinized perforations, and the perforations caused by corrosive poisons, it may in the first instance be observed, that the margin of a corroded aperture is sometimes of a peculiar colour,—for example, yellow with nitric acid, brown with sulphuric acid or the alkalis, orange with iodine. But a much better, perhaps indeed an infallible criterion, and one of universal application, is the following. Either the person dies very soon after the poison is introduced, in which case vital action may not be excited in the stomach: or he lives long enough for the ordinary consequences of violent irritation to ensue. In the former case, as a large quantity of poison must have been taken, and much vomiting cannot have occurred, part of the poison will be found in the stomach: In the latter case, the poison may have been all ejected; but in consequence of the longer duration of life, deep vascularity, or black extravasation must be produced round the hole, and sometimes too in other parts of the stomach; changes which will at once distinguish the appearance from a gelatinized aperture. There is no doubt that the stomach may be perforated by the strong corrosives, and yet hardly any of the poison be found in the stomach after death. Thus in a case related by Mertzdorff of poisoning with sulphuric acid, where life was prolonged for twelve hours, he could detect by minute analysis only 4½ grains of the acid in the contents and tissue of the stomach. But then the hole was surrounded by signs of vital reaction, and so was the spleen upon which the aperture opened.[216] Judging from what I have often seen in animals killed with oxalic acid, which is the most rapidly fatal of all corrosives, so that little time is allowed for vital action, and also several times in persons who had died quickly from the action of sulphuric acid, I believe no poison can dissolve the stomach, without such unequivocal signs of violent irritation of the undissolved parts of the villous coat, as will secure an attentive observer from the mistake of confounding with these appearances the effects of spontaneous erosion. Spontaneous erosion is very generally united with unusual whiteness of the stomach, and there is never any material vascularity. Resting on the description now given of the spontaneous and poisonous varieties of corrosion, it is an easy matter to decide a controversy, which at the time it occurred made a great deal of noise, and upon which the opinions of toxicologists have been unnecessarily divided. It is the question regarding death by poison which occurred in the trial of Mr. Angus at Liverpool in 1808 for the murder of his housekeeper Miss Burns. The poison suspected was corrosive sublimate. The symptoms were those of irritation in the alimentary canal,—vomiting, purging, and pain. In the dead body there was not any particular redness either of the intestines or of the stomach. But on the fore part of the stomach an aperture was found between the size of a crown piece and the palm of the hand; it had a ragged, pulpy margin; and the dissolution of the inner coat extended two inches from it all round the hole. No mention is made of adhesion or coloration of the margin. This description, it will be remarked, answers exactly that given above of spontaneous gelatinized perforation; and the absence of the signs of vital action around the hole and in the rest of the stomach is incompatible with the effects of a strong corrosive poison, unless death had occurred very soon after it was swallowed. This, however, was out of the question; for then the poison would have been found in the stomach,—which it was not.[217] The case of Angus is not the only instance in recent times of spontaneous perforation having given rise to an opinion by medical men in favour of poisoning, and consequently to a criminal trial. Six years afterwards a similar incident occurred in France. A young woman near Montargis having died of a short illness, and a large erosion having been found in the stomach after death, six practitioners, on a view of the parts, and without referring to the antecedent symptoms or attempting an analysis of the contents of the stomach, declared that she died of the effects of some corrosive poison. The husband and mother-in-law, against whom there does not appear to have been a shadow of general evidence, were therefore imprisoned and subsequently tried for their lives. Luckily, however, an intelligent physician of the town saw the error of the reporters, and after vainly endeavouring to persuade them to revise their opinion, was the means of the case being remitted to the medical faculty of Paris. That distinguished body, with Professor Chaussier at its head, gave a unanimous and decided opinion, not only that there was not any proof of poisoning, but likewise that the woman could have died of nothing else than spontaneous perforation. The leading features of the medical evidence will at once show how indefensible the conduct and opinion of the original reporters were. The last meal taken by the woman before she became ill, and the only one at which poison could have been administered by the prisoners, was her supper; her illness did not begin till past six next morning; the symptoms were mortal coldness, fainting, general pains, headache, pain in the stomach, purging and colic, without vomiting, and she died after twenty-four hours’ illness; the morbid appearances were general redness of the stomach, softening and pulpy destruction of a third part of its posterior parietes, and nevertheless the presence in the stomach of a pint and a half of fluid matter, containing evidently the remains of soup taken by the woman after she felt unwell. On the decision of the Parisian faculty the prisoners were discharged; and the original reporters were deservedly handled with great severity in several publications that appeared not long after.[218] _Of perforations of the Gullet and Intestines from natural causes, and their distinctions from those produced by poisons._—The intestines, and sometimes even the gullet, may be perforated by the same erosive or solvent process as the stomach. Thus Mr. Allan Burns observes, that in four plump children, whose previous history he could not learn, he found every part of the alimentary canal, from the termination of the gullet down to the beginning of the rectum, reduced to a gluey, transparent pulp, like thick starch. The bodies were quite free from putrefaction; but the abdomen exhaled a very sour smell when opened. No other organic derangement could be detected.[219] The particulars of a similar case, with an account of the symptoms, have been lately published by Mr. Smith, a London surgeon. In the body of a child who died of protracted diarrhœa subsequent to weaning, the whole intestines, from the duodenum to the sigmoid flexure of the colon, were found fourteen hours after death gelatinous, semitransparent, and so soft and brittle that they could not bear their own weight, but tore when lifted between the fingers. The stomach and rectum were healthy.[220] I lately met with the following instance, where the erosion clearly took place after death. In the body of a girl who died within twelve hours of poisoning with red-precipitate, the stomach and duodenum were found much inflamed, but quite entire and firm three days after death. Eighteen days afterwards, when I had an opportunity of examining these organs, their textures remained firm everywhere, except a few inches below the pylorus, where I found two apertures in the duodenum, each as big as a crown, and surrounded by extensive jelly-like softening. The following case from Laisné’s treatise shows that the gullet may be also dissolved in the same way. A woman three days after delivery was attacked with puerperal peritonitis, and died in four days. In the belly were found the usual morbid appearances of peritonitis: but in addition there was in the lower part of the gullet a large oval aperture two inches long, which penetrated through the posterior mediastinum into the lungs.[221] Another singular instance of the same kind has already been mentioned under the head of the symptoms (see p. 107). Another has been described by Dr. Marshall Hall. In a child who died of bronchitis, an opening was found in the gullet about the size of a pea, so that the canal of the gullet communicated with the sac of the pleura; and several veins appeared also to have been opened.[222] The stomach was likewise perforated. It is not difficult to draw the distinction between these perforations and the effects of poison. The throat and gullet may be partially disorganized or corroded by the strong corrosives; but they are very rarely penetrated, since the greater part of the poison must pass into the stomach or be rejected by vomiting. Destruction of the mucous coat is a common consequence, and stricture occasionally follows; but I have hitherto met with only one instance among the innumerable published cases of poisoning with the mineral acids, alkalis, and other corrosives, where the gullet was perforated. In that case the perforation was the result of slow ulceration from poisoning with sulphuric acid, where life was prolonged for two months.[223] Perforation from simple corrosion never occurs. The intestines are never perforated by chemical corrosion from within, for either the poison is in a great measure expelled from the stomach by vomiting, or the pylorus contracts and prevents the passage of every poison that is sufficiently concentrated to corrode. Both the small and great intestines might be corroded from without, in consequence of the poison escaping through a hole in the stomach. I am not acquainted, however, with any case of the kind where, intestinal perforation has occurred. When the intestines are pierced by true ulceration, it is impossible to tell whether it arose from natural disease or an irritant poison. The mode of forming a diagnosis between the symptoms and appearances of irritant poisoning and those of natural disease being thus explained, the different species of poisons which have been arranged in the class of irritants will now be considered in their order. The irritant class of poisons may be divided into five orders: the acids and their bases; the alkalies and their salts; the metallic compounds; the vegetable and animal irritants; the mechanical irritants. In a short appendix some substances will be mentioned which are not usually considered poisonous, but are capable of causing violent symptoms when taken in large doses. The greater number of poisons included in the first order have a very powerful local action. Most of them possess true corrosive properties when they are sufficiently concentrated. Most of them likewise act remotely. One of them, oxalic acid, is evidently not so much an irritant as a narcotico-acrid; but since its most frequent action as seen in man is irritation, it seems inexpedient to break the natural arrangement for the sake of logical accuracy. This is far from being the only instance where the toxicologist is compelled to violate the principles of philosophical classification. In the present Order are included four of the mineral acids, the sulphuric, nitric, muriatic and phosphoric, with their bases, phosphorus, sulphur, and chlorine: To these may be added iodine and bromine, with their compounds, and also oxalic and acetic acid, two of the vegetable acids.

Chapters

1. Chapter 1 2. PART II.—OF INDIVIDUAL POISONS. 3. CHAPTER I. 4. 1. _On the Action of Poisons through Sympathy._ In the infancy of 5. 2. _Of the Action of Poisons through Absorption._—If doubts may be 6. 1. _Quantity_ affects their action materially. Not only do they produce 7. 2. _As to state of aggregation_,—poisons act the more energetically the 8. 3. The next modifying cause is _chemical combination_. This is sometimes 9. 4. The effect of _mixture_ depends partly on the poisons being diluted. 10. 5. _Difference of tissue_ is an interesting modifying power in a 11. 6. With respect to differences arising from _difference of organ_, these 12. 7. _Habit and Idiosyncrasy._—The remarks to be made under the present 13. 8. The last modifying cause to be mentioned comprehends certain 14. CHAPTER II. 15. 1. The first characteristic is the _suddenness of their appearance and 16. 2. The next general characteristic of the symptoms of poisoning is 17. 3. Another characteristic is _uniformity in the nature of the symptoms_ 18. 4. The fourth characteristic is, that _the symptoms begin soon after a 19. 5. Lastly, _the symptoms appear during a state of perfect health_. This 20. 1. As to the _suddenness of their invasion and rapidity of their 21. 2. As to the uniformity or _uninterrupted increase of the symptoms_, it 22. 3. It was stated above, that the third character, _uniformity in kind_ 23. 4. In the next place, it was observed that some reliance may be placed 24. 5. Little need be said with regard to _the symptoms beginning, while the 25. 1. It may have been discharged by vomiting and purging. Thus on the 26. 2. The poison may have disappeared, because it has been all absorbed. It 27. 3. Poisons may not be found, because the excess has been decomposed. 28. 4. Lastly, the poison which has been absorbed into the system, and may 29. 1. The evidence derived from _the effects of suspected food, drink, or 30. 2. In the case of _the vomited matter_ or _contents of the stomach_ 31. 3. The effects of _the flesh of poisoned animals_, eaten by other 32. 3. The next article, which relates to the proof of the administration of 33. 4. The next article in the moral evidence relates to the intent of the 34. 5. The next article among the moral circumstances,—the simultaneous 35. 6. The next article of the moral evidence relates to suspicious conduct 36. CHAPTER III. 37. CHAPTER I. 38. 1. _Arsenical_ White arsenic 185 39. 2. _Acids_ Sulphuric acid 32 40. 3. _Mercurials_ Corrosive sublimate 12 41. 4. _Other mineral irritants_ Tartar-emetic 2 42. 5. _Veget. irritants_ Colchicum 3 43. 7. _Opium_ Opium or Laudan. 180 44. 8. _Hydrocyanic acid_ Med. Hydroc. acid 27 45. 9. _Other veget. Narcotics_ Nux-vomica 3 46. 11. Unascertained 22 47. CHAPTER II. 48. 1. _Distension of the Stomach._—Mere distension of the stomach from 49. 2. _Rupture of the Stomach_ is not a common occurrence; but it sometimes 50. 3. _Rupture of the Duodenum_ is a very rare accident from internal 51. 4. Under the next head may be classed rupture of the other organs of the 52. 5. The next accident which may be noticed on account of its being liable 53. 6. _Of Bilious Vomiting and Simple Cholera._—Of all the diseases which 54. 7. _Of Malignant Cholera._—The history of this disease affords a fair 55. 8. _Of Inflammation of the Stomach._—Chronic inflammation of the stomach 56. 9. _Inflammation of the Intestines_ in its acute form is more common 57. 10. _Inflammation of the Peritonæum_, or lining membrane of the belly, 58. 11. The subject of _Spontaneous Perforation of the Stomach_ is an 59. 12. The _gullet_ may be perforated in a similar manner either with or 60. 13. _Perforation of the alimentary canal by worms_ may here also be 61. 14. The next diseases to be mentioned are melæna and hæmatemesis, or 62. 15. The last are _colic_, _iliac passion_, and _obstructed intestine_. 63. CHAPTER III. 64. 1. _When concentrated_ it is oily-looking, colourless, or brownish from 65. 2. _When diluted_, it may be distinguished from all ordinary acids by 66. 3. It is seldom that the medical jurist is called on to search for 67. 1. The most ordinary symptoms are those of the first variety,—namely, 68. 2. The second variety of symptoms belong to a peculiar modification of 69. 3. The third variety includes cases of imperfect recovery. These are 70. 4. The last variety comprehends cases of perfect recovery, which are 71. 1. _When concentrated_, nitric acid is easily known by the odour of its 72. 2. _In a diluted state_ this acid is not so easily recognised as the 73. 3. _When in a state of compound mixture_, nitric acid, like sulphuric 74. 1. Hydrochloric acid, _in its concentrated state_, is colourless, if 75. 2. _When diluted_, it is recognised with facility, first by 76. 3. In the last edition of this work I proposed for the detection of 77. CHAPTER IV. 78. CHAPTER V. 79. CHAPTER VI. 80. 1. In the form of a pure solution, its nature may be satisfactorily 81. 2. The only important modifications in the analysis rendered necessary 82. CHAPTER VII. 83. CHAPTER VIII. 84. CHAPTER IX. 85. CHAPTER X. 86. CHAPTER XI. 87. CHAPTER XII. 88. CHAPTER XIII. 89. 3. The arsenite of copper, or _mineral green_. 4. The arsenite of potass 90. 2. _Of the Tests for Arsenious Acid._ 91. 7. After the precipitate has thoroughly subsided, the supernatant liquid 92. introduction as a poison into the body. This topic, one of paramount 93. 1. _Arsenic may exist as an adulteration in some reagents._—It must be 94. 2. _Arsenic may be present in some articles of chemical 95. 3. _Arsenic may have existed in antidotes administered during life._—It 96. 4. _Arsenic sometimes exists naturally in the human body._—This 97. 5. _Arsenic may exist in the soil of churchyards._—This proposition too 98. 3. _Arsenite of Copper_. 99. 4. _Arsenite of Potass_. 100. 5. _Arseniate of Potass._ 101. 6. _The Sulphurets of Arsenic._ 102. 7. _Arseniuretted-Hydrogen._ 103. 1. In one order of cases, then, arsenic produces symptoms of irritation 104. 2. The second variety of poisoning with arsenic includes a few cases in 105. 3. The third variety of poisoning with arsenic places in a clear point 106. CHAPTER XIV. 107. 1. _Of Red Precipitate._ 108. 2. _Of Cinnabar._ 109. 3. _Of Turbith Mineral._ 110. 4. _Of Calomel._ 111. 5. _Of Corrosive Sublimate._ 112. 1. _Hydrosulphuric acid gas_ transmitted in a stream through a solution 113. 1. _Lime-Water_ throws down the binoxide of mercury in the form of a 114. 6. _Of Bicyanide of Mercury._ 115. 7. _Of the Nitrates of Mercury._ 116. 1. The symptoms in the first variety are very like what occur in the 117. 2. The second variety of poisoning with mercury comprehends the cases, 118. 3. The third variety of poisoning with mercury comprehends all the forms 119. introduction of corrosive sublimate into the stomach. The poison then 120. CHAPTER XV. 121. 1. _Mineral Green._ 122. 2. _Natural Verdigris._ 123. 3. _Blue Vitriol._ 124. 1. _Ammonia_ causes a pale azure precipitate, which is redissolved by an 125. 2. _Sulphuretted hydrogen gas_ causes a dark brownish-black precipitate, 126. 3. _Ferro-cyanate of potass_ causes a fine hair-brown precipitate, the 127. 4. A polished rod or plate of _metallic iron_, held in a solution of 128. 4. _Artificial Verdigris._ 129. 1. Should the subject of analysis not be a liquid, render it such by 130. 2. If the copper be extremely minute in quantity, sulphuretted hydrogen 131. CHAPTER XVI. 132. 1. _Caustic potass_ precipitates a white sesquioxide, but only if the 133. 2. _Nitric acid_ throws down a white precipitate, and takes it up again 134. 3. The _Infusion of Galls_ causes a dirty, yellowish-white precipitate; 135. 4. The best liquid reagent is _Hydrosulphuric acid_. In a solution 136. 5. When the solution is put into Marsh’s apparatus for detecting arsenic 137. 1. Subject a small portion of the liquid to a stream of hydrosulphuric 138. 2. If hydrosulphuric acid do not distinctly affect the liquid, or if no 139. 3. If antimony be not indicated in either of these ways in the fluid 140. CHAPTER XVII. 141. CHAPTER XVIII. 142. 1. _Of Litharge and Red Lead._ 143. 2. _Of White Lead._ 144. 3. _Of Sugar of Lead._ 145. 1. _Hydrosulphuric acid_ causes a black precipitate, the sulphuret of 146. 2. _Chromate of potass_, both in the state of proto-chromate and 147. 3. _Hydriodate of potass_ causes also a lively gamboge-yellow 148. 4. _A rod of zinc_ held for some time in the solution displaces the 149. 4. _Goulard’s Extract._ 150. introduction of lead into the body; and in the last the whole course of 151. introduction of lead into the body may be presumed to be the real cause. 152. introduction of lead into the system. Dr. Burton thinks it will when the 153. CHAPTER XIX. 154. CHAPTER XX. 155. CHAPTER XXI. 156. CHAPTER XXII. 157. CHAPTER XXIII. 158. CHAPTER XXIV. 159. CHAPTER XXV. 160. CHAPTER XXIV. 161. 1. Apoplexy is sometimes preceded at considerable intervals by warning 162. 2. Apoplexy attacks chiefly the old. It is not, however, confined to the 163. 3. The next criterion is, that apoplexy occurs chiefly among fat people. 164. 4. A fourth criterion is drawn from the relation which the appearance of 165. 5. Another criterion relates to the progress of the symptoms. The 166. 6. Although there is a great resemblance between the symptoms of 167. 7. In the last place, a useful criterion may be derived from the 168. 1. The epileptic fit _is sometimes preceded by certain warnings_, such 169. 2. The symptoms of the epileptic fit _almost always begin violently and 170. 3. As in apoplexy, so in epilepsy the patient _in general cannot be 171. 4. When a person dies in a fit of epilepsy, _the paroxysm generally 172. 5. M. Esquirol, a writer of high authority, says that epilepsy _very 173. CHAPTER XXVII. 174. 1. If there be any solid matter, it is to be cut into small fragments, 175. 2. Add now the solution of acetate of lead as long as it causes 176. 3. The fluid part is to be treated with hydrosulphuric acid gas, to 177. 4. It is useful, however, to separate the meconic acid also; because, as 178. 5. If there be a sufficiency of the original material, Merck’s process 179. 546. There is little doubt that poisoning with opium may cause 180. CHAPTER XXVIII. 181. CHAPTER XXIX. 182. CHAPTER XXX. 183. CHAPTER XXXI. 184. 1. M. Chomel of Paris has related a case of poisoning with the gas 185. 2. The fumes of burning charcoal have been long known to be deleterious. 186. 3. It is probable that in some circumstances a very small quantity of 187. 4. The vapours from burning coal are the most noxious of all kinds of 188. 5. Somewhat analogous to the symptoms now described are the effects of 189. CHAPTER XXXII. 190. CHAPTER XXXIII. 191. CHAPTER XXXIV. 192. CHAPTER XXXV. 193. CHAPTER XXXVI. 194. CHAPTER XXXVII. 195. CHAPTER XXXVIII. 196. CHAPTER XXXIX. 197. CHAPTER XL. 198. CHAPTER XLI. 199. 1. When the dose is small, much excitement and little subsequent 200. 2. When the effect is sufficiently great to receive the designation of 201. 160. In twenty-four hours more the breathing became laborious and 202. 3. The third degree of poisoning is not so often witnessed, because, in 203. CHAPTER XLII. 204. 1. _Poisoning with Arsenic and Alcohol._—A man, after taking twelve 205. 3. _Poisoning with Tartar-Emetic and Charcoal Fumes._—Under the head of 206. 4. _Poisoning with Alcohol and with Laudanum._—Under the head of 207. 5. _Poisoning with Laudanum and Corrosive Sublimate._—Of all the cases 208. 6. _Poisoning with Opium and Belladonna._—A lady, who used a compound 209. 7. In the following cases, the active poisons to which the individuals 210. 2. Apparatus for the distillation of fluids suspected to contain 211. 3. Tube for reducing very small portions of arsenic or mercury. The 212. 4. A small glass funnel for introducing the material into the tube 213. 5. The ordinary apparatus for disengaging sulphuretted-hydrogen. The 214. 6. Instrument for washing down scanty precipitates on filters. It is a 215. 7. Tubes of natural size for collecting small portions of mercury by 216. 8. Pipette, one-fourth the natural size, for removing by suction 217. 9. Apparatus for reducing the sulphurets of some metals by a stream of 218. 36. Quoted by Marx, die Lehre von den Giften, I. ii. 163. 219. 92. Vicarius, Ibidem, Obs. 100. Riselius, Ibidem, Dec. i. An. v. Obs. 220. 1762. See Marx, i. ii. 29. 221. 1. P. 476, changed “exasperated by the use of oil” to “exacerbated by 222. 2. P. 513, changed “I may here add a very opposite instance of 223. 6. Enclosed italics font in _underscores_.

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