§ 688. Oxalic acid is widely distributed both in the free state and in combination with bases throughout the vegetable kingdom, and it also occurs in the animal kingdom. In combination with potash it is found in the Geranium acetosum (L.), Spinacia oleracea (L.), Phytolacca decandra (L.), Rheum palmatum (L.), Rumex acetosa, Atropa belladonna, and several others; in combination with soda in different species of Salsola and Salicornia; and in combination with lime in most plants, especially in the roots and bark. Many lichens contain half their weight of calcic oxalate, and oxalic acid, either free or combined, is (according to the observations of Hamlet and Plowright[679]) present in all mature non-microscopic fungi. Crystals of oxalate of lime may be frequently seen by the aid of the microscope in the cells of plants. According to Schmidt,[680] this crystallisation only takes place in the fully mature cell, for in actively growing cells the oxalate of lime is entirely dissolved by the albumen of the plant.

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In the animal kingdom oxalic acid is always present in the intestinal contents of the caterpillar. In combination with lime, it is constantly found in the allantois liquor of the cow, the urine of man, swine, horses, and cats. With regard to human urine, the presence or absence of oxalate of lime greatly depends upon the diet, and also upon the individual, some persons almost invariably secreting oxalates, whatever their food may be.§ 689. Oxalic Acid, H₂C₂O₄2H₂O (90 + 36), specific gravity 1·64, occurs in commerce in prismatic crystals, very similar to, and liable to be mistaken for, either magnesic or zincic sulphates. The crystals are intensely acid, easily soluble in water (1 part requiring at 14·5° 10·46 parts of water); they are also soluble in parts of cold, and readily in boiling, alcohol. Oxalic acid is slightly soluble in cold absolute ether; but ether, although extracting most organic acids from an aqueous solution, will not extract oxalic acid.

Oxalic acid sublimes slowly at 100°, but rapidly and completely at 150°; the best means of obtaining the pure anhydride is to put a sufficient quantity of the acid into a strong flask, clamp it by suitable connections to a mercury pump, and sublime in a vacuum; in this way a sufficient quantity may be sublimed a little above 100°. It is well to remember, not only its low subliming temperature, but also that an aqueous solution, if kept at 100°, loses acid; hence all evaporating or heating operations must not exceed 98°, or there will be some loss. The effect of heat is first to drive off water, then, if continued up to about 190°, there is decomposition into carbon monoxide, carbon dioxide, water, and formic acid; the two reactions occurring simultaneously—

C₂H₂O₄ = CO₂ + CO + H₂O.

C₂H₂O₄ = CO₂ + CH₂O₂.

Heated with sulphuric acid to 110°, the following decomposition takes place:—

H₂C₂O₄ = H₂O + CO₂ + CO.

Oxalic acid decomposes fluor spar, the phosphates of iron, silver, zinc, copper, and the arseniates of iron, silver, and copper. It may be used to separate the sulphides of iron and manganese from the sulphides of zinc, cadmium, uranium, cobalt, mercury, and copper—dissolving the former, not the latter. Many minerals and other substances are also attacked by this acid.

If a solution of oxalic acid in water is boiled with ammonio or sodio terchloride of gold (avoiding direct exposure to light) the gold is precipitated—

2AuCl₃ + 3H₂C₂O₄ = 6CO₂ + 6HCl + Au₂.

When black oxide of manganese (free from carbonate) is mixed with an oxalate, and treated with dilute sulphuric acid, the oxalic acid is decomposed, and carbon dioxide evolved—

MnO₂ + H₂C₂O₄ + H₂SO₄ = MnSO₄ + 2H₂O + 2CO₂.

A similar reaction occurs with permanganate of potash.

If to a solution of oxalic acid, which may be neutralised with an alkali, or may contain free acetic acid, a solution of acetate of lime be added, oxalate of lime is thrown down. This salt, important in an analytical point of view, it will be well to describe.§ 690. Oxalate of Lime (CaC₂O₄H₂O), 1 part ·863 crystallised oxalic acid. This is the salt which the analyst obtains for the quantitative estimation of lime or oxalic acid; it is not identical with that occurring in the vegetable kingdom, the latter containing 3H₂O. Oxalate of lime cannot be precipitated for quantitative purposes from solutions containing chromium, aluminium, or ferric iron, since somewhat soluble salts are formed. It dissolves in solutions of magnesium and manganese,[681] and citrate of soda, and is also decomposed by boiling with solutions of copper, silver, lead, cadmium, zinc, nickel, cobalt, strontium, or barium. It is insoluble in solutions of chlorides of the alkalies and alkaline earths, and in water, in alkaline solutions, or in acetic acid; and is soluble in mineral acid only when the acid is strong and in considerable excess. It is unalterable in the air, and at 100°. When carefully and slowly ignited it may be wholly converted into carbonate of lime; if the heat is not properly managed (that is, if excessive), caustic lime may be formed in greater or smaller quantity.

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§ 691. Use in the Arts.—Oxalic acid is chiefly used by dyers and calico-printers, but also by curriers and harness-makers for cleaning leather, by marble masons for removing iron stains, by workers in straw for bleaching, and it is applied to various household purposes,[682] such as the whitening of boards, the removing of iron-mould from linen, &c. The hydropotassic oxalate (binoxalate of potash), under the popular names of “essential salt of lemons” and salts of sorrel, is used for scouring metals and for removing ink-stains from linen.

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§ 692. Hydropotassic Oxalate, Binoxalate of Potash, KHC₂O₄(H₂O), is a white salt, acid in reaction, soluble in water, and insoluble in alcohol. Heated on platinum foil it leaves potassic carbonate, which may be recognised by the usual tests. Its aqueous solution gives, with a solution of acetate or sulphate of lime, a precipitate of calcic oxalate insoluble in acetic acid.§ 693. Statistics.—Poisoning by oxalic acid is more frequent in England than in any other European country. In the ten years 1883-92, there were registered in England and Wales 222 deaths from oxalic acid—of these 199, or 89·6 per cent., were suicidal, the remainder accidental. The age and sex distribution of these cases is set out in the following table:—

POISONING BY OXALIC ACID IN ENGLAND AND WALES DURING THE TEN YEARS 1883-1892.

Accident or Negligence.
Ages,	0-1	1-5	5-15	15-25	25-65	65 and above	Total
Males,	1	...	...	2	...	14	17
Females,	...	...	...	1	5	...	6
Total,	1	...	...	3	5	14	23
Suicide.
Ages,				15-25	25-65	65 and above	Total
Males,				9	102	3	114
Females,				21	62	2	85
Total,				30	164	5	199

§ 694. Fatal Dose.—The smallest dose of oxalic acid known to have destroyed life is, according to Dr. Taylor, 3·88 grms. (60 grains); but recovery has taken place, on prompt administration of remedies, after eight times this quantity has been swallowed.

With regard to oxalate of soda, or binoxalate of potash, 14·2 grms. (half an ounce) have been taken without fatal result, although the symptoms were very serious; and it may be held that about that quantity would usually cause death. Oxalic acid is not used in medicine, save as a salt, e.g., oxalate of cerium.§ 695. Effects of Oxalic Acid and Oxalates on Animals.—The first cases of poisoning by oxalic acid occurred early in the nineteenth century, a little more than fifty years after its discovery. Thompson[683] was the first who attempted, by experiment on animal life, to elucidate the action of the poison; he noted the caustic action on the stomach, and the effects on the heart and nervous system, which he attributed simply to the local injury through the sympathetic nerves. Orfila[684] was the next who took the matter up, and he made several experiments; but it was Robert Christison[685] who distinctly recognised the important fact that oxalic acid was toxic, quite apart from any local effects, and that the soluble oxalates, such as sodic and potassic oxalates, were violent poisons.

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§ 696. Kobert and KÜssner[686] have made some extended researches on the effects of sodic oxalate on rabbits, cats, dogs, guinea-pigs, hedgehogs, frogs, &c.—the chief results of which are as follows:—On injection of sodic oxalate solution in moderate doses into the circulation, the heart’s action, and, therefore, the pulse, become arhythmic; and a dicrotic or tricrotic condition of the pulse may last even half a day, while at the same time the frequency may be uninfluenced. The blood-pressure also with moderate doses is normal, and with small atoxic doses there is no slowing of the respiration. On the other hand, toxic doses paralyse the respiratory apparatus, and the animal dies asphyxiated. With chronic and subacute poisoning the respiration becomes slower and slower, and then ceases from paralysis of the respiratory muscles. The first sign of poisoning, whether acute or chronic, is a sleepy condition; dogs lie quiet, making now and then a noise as if dreaming, mechanical irritations are responded to with dulness. The hind extremities become weak, and then the fore. This paresis of the hind extremities, deepening into complete paralysis, was very constant and striking. Take, for example, from the paper (op. cit.) the experiment in which a large cat received in six days five subcutaneous injections of 5 c.c. of a solution of sodic oxalate (strength 1: 30), equalling ·16 grm.; the cat died, as it were, gradually from behind forwards, so that on the sixth day the hinder extremities were fully motionless and without feeling. The heart beat strongly. The temperature of the poisoned animal always sinks below the normal condition. Convulsions in acute poisoning are common, in chronic quite absent; when present in acute poisoning, they are tetanic or strychnic-like. In all the experiments of Kobert and KÜssner, lethal doses of soluble oxalates caused the appearance of sugar in the urine.

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J. Uppmann[687] made forty-nine experiments on dogs, in which he administered relatively large doses by the stomach; no poisonous effect followed. Emil Pfeiffer[688] gave a dog in three successive days ·2, ·5, and lastly 1 grm. oxalic acid with meat, but no symptoms resulted. Yet that oxalic acid, as sodic oxalate, is poisonous to dogs, if it once gets into the circulation, cannot be disputed. The accepted explanation is that the large amount of lime phosphates in the digestive canal of dogs is decomposed by oxalic acid, and the harmless lime oxalate formed.

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Oxalic acid is absorbed into the blood, and leeches have been known to die after their application to a person who had taken a large dose. Thus Christison[689] quotes a case related by Dr. Arrowsmith, in which this occurred:—“They were healthy, and fastened immediately; on looking at them a few minutes after, I remarked that they did not seem to fill, and on touching one it felt hard, and instantly fell off motionless and dead; the others were in the same state. They had all bitten, and the marks were conspicuous, but they had drawn scarcely any blood. They were applied about six hours after the acid had been taken.”

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§ 697. Effects of Vaporised Oxalic Acid.—Eulenberg has experimented on pigeons on the action of oxalic acid when breathed. In one of his experiments, ·75 grm. of the acid was volatilised into a glass shade, in which a pigeon had been placed; after this had been done five times in two minutes, there was uneasiness, shaking of the head, and cough, with increased mucous secretion of the nasal membrane. On continuing the transmission of the vapour, after eight minutes there was again restlessness, shaking of the head, and cough; after eleven minutes the bird fell and was convulsed. On discontinuing the sublimation, it got up and moved freely, but showed respiratory irritation. On the second day after the experiment, it was observed that the bird’s note was hoarse, on the fourth day there was slowness of the heart’s action and refusal of food, and on the sixth day the bird was found dead. Examination after death showed slight injection of the cerebral membranes; the cellular tissue in the neighbourhood of the trachea contained in certain places extravasations of blood, varying from the size of a pea to that of a penny; the mucous membrane of the larynx and trachea was swollen and covered with a thick croupous layer; the lungs were partially hepatised, and the pleura thickened; the crop as well as the true intestines still contained some food.[690]

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§ 698. The Effects of Oxalic Acid and Hydropotassic Oxalate on Man.—The cases of oxalic poisoning have been invariably due to either oxalic acid or hydropotassic oxalate, the neutral sodic or potassic oxalates having hitherto in no instance been taken. The symptoms, and even the locally destructive action of oxalic acid and the acid oxalate, are so similar that neither from clinical nor post-mortem signs could they be differentiated by anyone not having a previous knowledge of the case.

The external application of oxalic acid does not appear to cause illness; workmen engaged in trades requiring the constant use of the acid often have the nails white, opaque, and brittle; but no direct injury to health is on record.

A large dose of either causes a local and a remote effect; the local is very similar to that already described as belonging to the mineral acids, i.e., more or less destructive of the mucous membranes with which the acid comes in contact. The remote effects may only be developed after a little; they consist essentially of a profound influence on the nervous system. Though more than 120 cases of oxalic acid poisoning have occurred since Christison wrote his treatise, his graphic description still holds good. “If,” says he, “a person immediately after swallowing a solution of a crystalline salt, which tasted purely and strongly acid, is attacked with burning in the throat, then with burning in the stomach, vomiting, particularly of bloody matter, imperceptible pulse, and excessive languor, and dies in half an hour, or still more, in twenty, fifteen, or ten minutes, I do not know any fallacy which can interfere with the conclusion that oxalic acid was the cause of death. No parallel disease begins so abruptly, and terminates so soon; and no other crystalline poison has the same effect.” The local action is that of a solvent on the mucous tissues. If from 10 to 30 grms. are swallowed, dissolved in water, there is an immediate sour taste, pain, burning in the stomach, and vomiting. The vomit may be colourless, greenish, or black, and very acid; but there is a considerable variety in the symptoms. The variations may be partly explained by saying that, in one class of cases, the remote or true toxic effects of the poison predominate; in a second, the local and the nervous are equally divided; while in a third, the local effects seem alone to give rise to symptoms.

In a case at Guy’s Hospital, in 1842, there was no pain, but vomiting and collapse. In another case which occurred in 1870, a male (aged 48) took 10·4 grms. (162 grains); he had threatening collapse, cold sweats, white and red patches on the tongue and pharynx, difficulty in swallowing, and contracted pupils. Blood was effused from the mouth and anus; on the following day there were convulsions, coma, and death thirty-six hours after taking the poison. In another case, there was rapid loss of consciousness and coma, followed by death in five hours. Death may be very rapid, e.g., in one case (Med. Times and Gaz., 1868) it took place in ten minutes; there was bleeding from the stomach, which doubtless accelerated the fatal result. Orfila has recorded a death almost as rapid from the acid oxalate of potash; a woman took 15 grms.; there was no vomiting, but she suffered from fearful cramps, and death ensued in fifteen minutes. In another case, also recorded by Orfila, there was marked slowing of the pulse, and soporific tendencies. With both oxalic acid and the acid oxalate of potash, certain nervous and other sequelÆ are more or less constant, always provided time is given for their development. From the experiments already detailed on animals, one would expect some paresis of the lower extremities, but this has not been observed in man. There is more or less inflammation of the stomach, and often peritonitis; in one case (Brit. Med. Journal, 1873) there were cystitis and acute congestion of the kidneys with albuminuria.

In two cases quoted by Taylor, there was a temporary loss or enfeeblement of voice; in one of the two, the aphonia lasted for eight days. In the other, that of a man who had swallowed about 7 grms. (¹/₄ oz.) of oxalic acid, his voice, naturally deep, became in nine hours low and feeble, and continued so for more than a month, during the whole of which time he suffered in addition from numbness and tingling of the legs. As a case of extreme rarity may be mentioned that of a young woman,[691] who took 12 grms. (185 grains) of the acid oxalate of potash, and on the third day died; before death exhibiting delirium so active and intense that it was described as “madness.”

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§ 699. Physiological Action.—Putting on one side the local effects of oxalic acid, and regarding only its true toxic effects, there is some difference of opinion as to its action. L. Hermann considers it one of the heart poisons, having seen the frog’s heart arrested by subcutaneous doses of sodic oxalate, an observation which is borne out by the experiments of Cyon,[692] and not negatived by those of Kobert and KÜssner. The poison is believed to act on the extracardial ganglia. Onsum[693] held at one time a peculiar theory of the action of oxalic acid, believing that it precipitated as oxalate of lime in the lung capillaries, causing embolic obstruction; but this view is not now accepted—there are too many obvious objections to it. Kobert and KÜssner do not consider oxalic acid a heart poison, but believe that its action is directed to the central nervous system, as attested by sinking of the blood-pressure, the arhythm and retardation of the pulse, the slow breathing, the paralytic symptoms, and the fibrillary muscular contraction; but, with regard to the latter, Locke[694] has observed that a frog’s sartorius, immersed in 0·75 sodium oxalate solution, becomes in a few seconds violently active, much more so than in Biederman’s normal saline solution. After thirty to forty-five minutes it loses its irritability, which, however, it partially recovers by immersion in 0·6 sodium chloride solution. He thinks this may explain the symptoms of fibrillary muscular contraction observed by Kobert and KÜssner, which they ascribe to an action on the central nervous system.

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§ 700. Pathological Changes.—Kobert and KÜssner observed that when oxalate of soda was subcutaneously injected into animals, there was often abscess, and even gangrene, at the seat of the injection. If the poison were injected into the peritoneal cavity, death was so rapid as to leave little time for any coarse lesions to manifest themselves. They were not able to observe a cherry-red colour of the blood, nor did they find oxalate of lime crystals in the lung capillaries; there were often embolic processes in the lung, but nothing typical. They came, therefore, to the conclusion that the state of the kidneys and the urine was the only typical sign. The kidneys were dark, full of blood, but did not show any microscopic hÆmorrhages. Twelve hours after taking the poison there is observed in the cortical substance a fine striping corresponding to the canaliculi; in certain cases the whole boundary layer is coloured white. If the poisoning lasts a longer time, the kidneys become less blood-rich, and show the described white striping very beautifully; this change persists several weeks. The cause of this strange appearance is at once revealed by a microscopical examination; it is due to a deposition of oxalate of lime; no crystals are met with in the glomerules. Both by the microscope and by chemical means it may be shown that the content of the kidney in oxalates is large.[695] So far as the tissues generally are concerned, free oxalic acid is not likely to be met with; there is always present sufficient lime to form lime oxalate. The urine was always albuminous and contained a reducing substance, which vanished about the second day after the dose. Hyaline casts and deposits of oxalates in the urine never failed.[696]

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§ 701. Observations of the pathological effects of the oxalates on man have been confined to cases of death from the corrosive substances mentioned, and hence the intestinal tract has been profoundly affected.

In the museum of St. Thomas’ Hospital is a good example of the effects produced. The case was that of a woman who had taken a large, unknown quantity of oxalic acid, and was brought to the hospital dead. The mucous membrane of the gullet is much corrugated and divided into numerous parallel grooves, these again by little transverse grooves, so that the intersection of the two systems makes a sort of raised pattern. It is noted that in the recent state the mucous membrane could be removed in flakes; in the upper part it was whitish, in the lower slate-coloured. The stomach has a large perforation, but placing the specimen beside another in the same museum which illustrates the effect of the gastric juice, in causing an after-death solution of a portion of the stomach, I was unable to differentiate between the two. The mucous membrane had the same shreddy flocculent appearance, and is soft and pale. The pyloric end is said to have been of a blackish colour, and no lymph was exuded.§ 702. The pathological changes by the acid oxalate of potash are identical with those of oxalic acid, in both the gullet and stomach being nearly always more or less inflamed or corroded; the inflammation in a few cases has extended right through into the intestinal canal; there are venous hyperÆmia, hÆmorrhages, and swelling of the mucous membrane of the stomach. The hÆmorrhages are often punctiform, but occasionally larger, arranged in rows on the summits of the rugÆ; sometimes there is considerable bleeding. In the greater number of cases there is no actual erosion of the stomach, but the inner layer appears abnormally transparent. On examining the mucous membrane under the microscope, Lesser[697] has described it as covered with a layer which strongly reflects light, and is to be considered as caused by a fine precipitate of calcic oxalate. Lesser was unable to find in any case oxalic acid crystals, or those of the acid oxalate of potash. There are many cases of perforation on record, but it is questionable whether they are not all to be regarded as post-mortem effects, and not life-changes; at all events, there is little clinical evidence to support the view that these perforations occur during life. In the case (mentioned ante) in which death took place by coma, the brain was hyperÆmic. The kidneys, as in the case of animals, show the white zone, and are congested, and can be proved by microscopical and chemical means to be rich in oxalates.

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§ 703. Separation of Oxalic Acid from Organic Substances, the Tissues of the Body, &c.—From what has been stated, no investigation as to the cause of poison, when oxalic acid is suspected, can be considered complete unless the analyst has an opportunity of examining both the urine and the kidneys; for although, in most cases—when the acid itself, or the acid potassic salt has been taken—there may be ample evidence, both chemical and pathological, it is entirely different if a case of poisoning with the neutral sodic salt should occur. In this event, there may be no congested appearance of any portion of the intestinal canal, and the evidence must mainly rest on the urine and kidneys.

Oxalic acid being so widely distributed in the vegetable kingdom, the expert must expect, in any criminal case, to be cross-examined by ingenious counsel as to whether or not it was possible that the acid could have entered the body in a rhubarb-pie, or accidentally through sorrel mixed with greens, &c. To meet these and similar questions it is important to identify, if possible, any green matters found in the stomach. In any case, it must be remembered, that although rhubarb has been eaten for centuries, and every schoolboy has occasionally chewed small portions of sorrel, no poisoning has resulted from these practices. When oxalic acid has been taken into the stomach, it will invariably be found partly in combination with lime, soda, ammonia, &c., and partly free; or if such antidotes as chalk has been administered, it may be wholly combined. Vomiting is nearly always present, and valuable evidence of oxalic acid may be obtained from stains on sheets, carpets, &c. In a recent case of probably suicidal poisoning, the writer found no oxalic acid in the contents of the stomach, but some was detected in the copious vomit which had stained the bed-clothes. The urine also contained a great excess of oxalate of lime—a circumstance of little value taken by itself, but confirmatory with other evidence. If a liquid is strongly acid, oxalic acid may be separated by dialysis from organic matters, and the clear fluid thus obtained precipitated by sulphate of lime, the oxalate of lime being identified by its microscopic form and other characters.

The usual general method for the separation of oxalic acid from organic substances or mixtures is the following:—Extract with boiling water, filter (which in some cases must be difficult or even impossible), and then precipitate with acetate of lead. The lead precipitate may contain, besides oxalate of lead, phosphate, chloride, sulphate, and various organic substances and acids. This is to be decomposed by sulphuretted hydrogen, and on filtering off the sulphide of lead, oxalic acid is to be tested for in the filtrate. This process can only be adopted with advantage in a few cases, and is by no means to be recommended as generally applicable. The best general method, and one which insures the separation of oxalic acid, whether present as a free acid, as an alkaline, or a calcic oxalate, is perhaps the following:—The substance or fluid under examination is digested with hydrochloric acid until a fluid capable of filtration is obtained; the free acid is neutralised by ammonia in very slight excess, and permitted to deposit, and the fluid is then carefully decanted, and the deposit thrown on a filter. The filtrate is added to the decanted fluid, and precipitated with a slight excess of acetate of lime—this precipitate, like the first, being collected on a filter. The first precipitate contains all the oxalic acid which was in combination with lime; the second, all that which was in the free condition. Both precipitates should be washed with acetic acid. The next step is to identify the precipitate which is supposed to be oxalate of lime. The precipitate is washed into a beaker, and dissolved with the aid of heat by adding, drop by drop, pure hydrochloric acid; it is then reprecipitated by ammonia, and allowed to subside completely, which may take some time. The supernatant fluid is decanted, and the precipitate washed by subsidence; it is lastly dried over the water-bath in a tared porcelain dish, and its weight taken. The substance is then identified by testing the dried powder as follows:—

(a) It is whitish in colour, and on ignition in a platinum dish leaves a grey carbonate of lime. All other organic salts of lime—viz., citrate, tartrate, &c.—on ignition become coal-black.

(b) A portion suspended in water, to which is added some sulphuric acid, destroys the colour of permanganate of potash—the reaction being similar to that on p. 511—a reaction by which, as is well known, oxalic acid or an oxalate may be conveniently titrated. This reaction is so peculiar to oxalic acid, that there is no substance with which it can be confounded. It is true that uric acid in an acid solution equally decolorises permanganate, but it does so in a different way; the reaction between oxalic acid and permanganate being at first slow, and afterwards rapid, while the reaction with uric acid is just the reverse—at first quick, and towards the end of the process extremely slow.

(c) A portion placed in a test-tube, and warmed with concentrated sulphuric acid, develops on warming carbon oxide and carbon dioxide; the presence of the latter is easily shown by adapting a cork and bent tube to the test-tube, and leading the evolved gases through baryta water.

Alexander Gunn[698] has described a new method of both detecting and estimating oxalic acid; it is based on the fact that a small trace of oxalic acid, added to an acid solution of ferrous phosphate, strikes a persistent lemon-yellow colour; the depth of colour being proportionate to the amount of oxalic acid.

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The reagents necessary for both quantitative and qualitative testing are as follows:—A standard solution of oxalic acid, of which 100 c.c. equal 1 grm., and a solution of ferrous phosphate, containing about 12·5 per cent. of Fe₃2PO₄, with excess of phosphoric acid.

Into each of two Nessler graduated glasses 7·5 c.c. of the ferrous phosphate solution are run and made up to 50 c.c. with distilled water; both solutions should be colourless; 1, 2, or more c.c. of the solution to be tested are then run into one of the Nessler glasses; if oxalic acid be present, a more or less deep tint is produced; this must be imitated by running the standard solution of oxalic acid into the second Nessler cylinder—the calculation is the same as in other colorimetric estimations. It does not appear to be reliable quantitatively, if alum is present; and it is self-evident that the solution to be tested must be fairly free from colour.§ 704. Oxalate of Lime in the Urine.—This well-known urinary sediment occurs chiefly as octahedra, but hour-glass, contracted or dumbbell-like bodies, compound octahedra, and small, flattened, bright discs, not unlike blood discs, are frequently seen. It may be usually identified under the field of the microscope by its insolubility in acetic acid, whilst the ammonio mag. phosphate, as well as the carbonate of lime, are both soluble in that acid. From urates it is distinguished by its insolubility in warm water. A chemical method of separation is as follows:—The deposit is freed by subsidence as much as possible from urine, washed with hot water, and then dissolved in hydrochloric acid and filtered; to the filtrate ammonia is added in excess. The precipitate may contain phosphates of iron, magnesia, lime, and oxalate of lime. On treatment of the precipitate by acetic acid, the phosphates of the alkaline earths (if present) dissolve; the insoluble portion will be either phosphate of iron, or oxalate of lime, or both. On igniting the residue in a platinum dish, any oxalate will be changed to carbonate, and the carbonate of lime may be titrated with d. n. HCl acid and cochineal solution, and from the data thus obtained the oxalate estimated. The iron can be tested qualitatively in the acid solution by ferrocyanide of potassium, or it can be determined by the ordinary methods. If the qualitative detection of oxalate of lime in the deposit is alone required, it is quite sufficient evidence should the portion insoluble in acetic acid, on ignition in a platinum dish, give a residue effervescing on the addition of an acid.§ 705. Estimation of Oxalic Acid.—Oxalic acid is estimated in the free state by direct weighing, or by titration either with alkali or by potassic permanganate, the latter being standardised by oxalic acid. If (as is commonly the case) oxalic acid is precipitated as oxalate of lime, the oxalate may be—

(a) Dried at 100° and weighed directly, having the properties already described.

(b) Titrated with dilate sulphuric acid and permanganate.

(c) Ignited, and the resulting carbonate of lime weighed; or dissolved in standard acid and titrated back—one part of calcic carbonate corresponds to 1·26 part of crystallised oxalic acid, or 0·90 part of H₂C₂O₄; similarly, 1 c.c. of standard acid equals ·05 of calcic carbonate (or ·063 of crystallised oxalic acid).

(d) The oxalate may be dissolved in the smallest possible amount of hydrochloric acid, and boiled with ammonio chloride of gold, avoiding exposure to light; every part of gold precipitated corresponds to ·961 part of crystallised oxalic acid.

(e) The oxalate may be placed in Geissler’s carbonic acid apparatus, with peroxide of manganese and diluted sulphuric acid. The weight of the gas which at the end of the operation has escaped, will have a definite relation to that of the oxalate, and if multiplied by 1·4318 will give the amount of crystallised oxalic acid.

CERTAIN OXALIC BASES—OXALMETHYLINE—OXALPROPYLINE.

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FROGS.
Chlorine-Holding Bases.	Chlorine-Free Bases.
Notable narcosis; no heightened reflex action, muscular cramps, nor spontaneous convulsions.	Narcosis occurs late, and is little pronounced; a notable increase of reflex excitability; more and more muscular paralysis; between times, muscular cramps.
CATS.
Notable narcosis and salivation; no mydriasis; convulsions and paralysis; no change in the respirations.	Great excitement; general shivering, rising to pure clonic convulsions; paralysis of the hind legs; notable mydriasis, jerking, and superficial respiration; weak narcosis.
DOGS.
Notable narcosis; occasional vomiting; the rest as in cats.	Narcosis evident; the rest as in cats.