Acidum Carbolicum

Carbolic Acid

Carbolic acid. Phénique acide, Fr.; Car-bolsäure, Ger. A product of the distillation of coal-tar. Is either in acicular crystals or in crystalline masses; white or colorless when perfectly pure, but, even when slightly impure, either reddish or becoming so on exposure; deliquescent and readily assuming the liquid state in the presence of a little water, yet not dissolving; of a strong odor and taste, recalling those of creosote, but distinct; fusible at from 93° to 106°, forming an oily liquid. It is soluble in from twenty to thirty-three parts of water, the purest being most soluble. Alcohol, ether, chloroform, glycerin, and the essential oils, dissolve it freely. It combines with alkalies and other salifiable bases, but its compounds have still an alkaline reaction and are decomposed by the feeblest acids, even by carbonic acid. Dose, gr. 1/4—gr. j.

Acidum Carbolicum Crudum

Impure carbolic acid. Is either colorless or has a brown shade. It consists of carbolic and cresylic acids, in variable proportion, with impurities derived from coal-tar, which vary from ten to thirty per cent.

Glyceritum Acidi Garbolici

Glycerite of carbolic acid. (Twenty grm. of carbolic acid; 80 grm. of glycerin.)

Aqua Acidi Carbolici

Carbolic-acid water (not official). (Glycerite of carbolic acid, 3 x; water, one pint.) Dose, a teaspoonful to a half ounce.

Unguentum Acidi Carbolici

Ointment of carbolic acid. (Carbolic acid, 5 grm.; ointment, 95 grm.)

Antagonists and Incompatibles

Combination with alkalies diminishes, but does not entirely check, the physiological activity of carbolic acid. Saccharate of lime, or lime, is probably the most efficient antagonist from the chemical point of view (Th. Husemann). In cases of poisoning, this substance should be given freely. The mucous membrane should be protected as far as possible by the administration of vegetable demulcents, but not by oils and glycerin, which favor absorption. I am indebted to Dr. A. C. Post, of New York, in a verbal communication, for the important fact that atropine is a physiological antagonist to the systemic symptoms induced by carbolic acid. He was induced to administer atropine in a case of poisoning by carbolic acid, on observing the minutely contracted pupils and the failing circulation. The result was successful. Similar success has attended the same practice in other cases. Experiments on animals have also demonstrated the existence of this antagonism, which may now be regarded as an established fact. The rules for guidance in the administration of atropine are the same as in other cases: a sufficient quantity of the antagonist is administered to maintain dilatation of the pupil and to overcome the depression of the circulation and respiration. Elimination should also be promoted by the free use of diluents.

Synergists

All of the phenols, the antiseptics, the motor depressants, etc., increase the effects of carbolic acid.

Physiological Actions

Applied to the integument or to the mucous membrane, carbolic acid produces a burning sensation of short duration, and there is formed a whitish, superficial eschar, which subsequently becomes brownish. The taste of carbolic acid is sweetish, cooling, and then pungent and hot. When swallowed by accident or design, the mucous membrane appears as if brushed over with a strong solution of nitrate of silver, and becomes hard and dry like leather. This appearance is observable about the lips, fauces, the aesophagus, the cardiac and pyloric extremities of the stomach, and the summits of the folds of the mucous membrane in the organ generally. This change in the condition of the membrane is due to the power of carbolic acid to coagulate the albumen of the tissues. Vomiting is not constant, even when toxic doses are swallowed, and the vomited matters smell of the poison. From medicinal doses, a cooling, rather grateful sedative effect is experienced in the stomach. It diffuses into the blood with great facility, from the stomach, from the external integument, and from wounded surfaces. Cases of poisoning have resulted from application to a patch of psoriasis (Toel), to scabies (Hoppe-Seyler, Machin), to the uterine cavity, after the enucleation of a fibroid (Rheinstädter), to abscesses (Köhler, Wallace, White), to the rectum for the relief of ascarides (Pinkham, Mi-chaelis), and to the integument and wounds, in cases of antiseptic surgery. Diffusion takes place with such rapidity, from these various sources, that formidable symptoms arise in a few minutes. The amount necessary to produce distinct effects varies; besides the difference due to age, there are variations in susceptibility. A one-per-cent solution has caused serious symptoms when injected into an abscess and into the rectum. Six drops of the pure acid have caused dangerous symptoms, and a teaspoonful has terminated fatally, but one case is reported in which this amount was recovered from when taken by a child two and a half years old (Dessau). A tablespoonful has caused death in several instances (Cowling, Packer, and others). In Hoppe-Seyler's cases, while the two apprentices were rubbing each other's backs, both were seized suddenly with giddiness, vertigo, and tension of the head, and quickly passed into unconsciousness. These effects are also experienced when the poison is taken into the stomach. The warnings of danger, which may be expected when the remedy is brought in contact with the tissues at any point, are, besides the local irritation, sudden vertigo, contracted pupils, pallor of the face, embarrassed respiration, and feeble circulation. When the dose is a fatal One, unconsciousness quickly supervenes, the breathing becomes stertorous, the surface grows cold, the action of the heart gets more and more feeble, and death finally occurs from failure of respiration. Convulsions occur in animals, but in man this symptom is wanting, or at most fibrillary trembling, and some trismus of the jaws, are present.

The changes in the blood induced by carbolic acid have been much disputed. That it enters the blood as carbolic acid seems positively established, although, having acid properties, it may become a carbolate. The acid has been discovered in the blood by Hoppe-Seyler. That it appropriates oxygen and thus undergoes some change in the blood is highly probable. Husemann maintains that the blood in carbolic-acid poisoning is very much altered in character, becoming dark in color and coagulating with difficulty, but in the reports of various post-mortem examinations it is remarked that the blood was coagulated in the heart and great venous trunks. Outside of the body the blood is quickly changed on the addition of carbolic acid, but these changes do not correspond to those which occur within the body. The action of the heart is at first slowed, but toward the end it becomes rapid. The blood-pressure falls considerably below the normal, due, Hoppe-Seyler says, to vaso-motor paresis. The first slowing of the heart is caused by stimulation of the end-organs of the vagus, and is prevented by division of the trunk of the nerve. The subsequent rapid action is due to the removal of the inhibition from paralysis of the vagus. Respiration is at first stimulated and the respiratory acts are more frequent, but they are also more shallow. Division of the pneumogastrics does not entirely prevent this stimulation, although it lessens the effect, whence it is concluded that carbolic acid also stimulates the respiratory center in the medulla (Salkowsky). This conclusion is strengthened by the fact that, if the vagi are previously divided, the administration of carbolic acid will still increase the respiratory acts for a time, showing that the stimulation of respiration must be effected by an action on the end-organs of the vagi in the lungs as well (Salkowsky). Lowering of the temperature has been constantly observed in the experiments on animals, and in the cases of poisoning of man. The surface of the body is cool, and more or less livid. There are several factors concerned, doubtless, in the reduction of temperature. The diminution in the blood-pressure and the arrested oxidation are the chief. The power of carbolic acid to reduce the temperature of fever is also clear, but in this respect it is inferior to salicylic acid (Eisenstein). In cases of poisoning the reduction of temperature reaches several degrees, but in the normal condition in man ordinary medicinal doses have but little effect in this direction.

A more or less minutely contracted pupil is a nearly constant phenomenon in carbolic-acid poisoning. It can hardly be doubtful that this effect is due to paralysis of the radiating fibers, leaving the circular fibers unopposed. Carbolic acid unquestionably acts on the cerebral lobes—on the centers of conscious impressions—and suspends their functions. Vertigo and singing in the ears occur, and then consciousness is lost, the reflexes are suspended, and complete muscular resolution ensues. In warm-blooded animals clonic convulsions are produced, succeeded by paralysis. By direct application, as Bill was the first to demonstrate, carbolic acid suspends the irritability of the sensory nerves. If a tract of the integument be painted over with pure carbolic acid, an incision may be made into the part without the least pain being experienced. The peripheral nerves, sensory and motor, are not affected by the systemic action. The muscles after poisoning respond energetically to the usual forms of stimulation. It follows, then, that the action of the poison is centric and not peripheral (Sal-kowsky, Lemaire, Rothe).

The elimination of carbolic acid takes place by various channels of excretion, chiefly by the urine. It may be detected by the odor in the breath of poisoned animals (Lemaire). It has been found in the saliva by Hoppe-Seyler, but Bill could not detect it in the perspiration or in the faeces. Hoffmann maintains that carbolic acid undergoes oxidation in the blood, but, as a part of it may be separated unchanged from the urine, this statement is not wholly true. That much of the carbolic acid taken is oxidized before being excreted is proved by the character of a secondary product which appears in the urine. One of the earliest indications of the toxic action of carbolic acid, especially when applied locally, is a dark-greenish, blackish, or smoky hue of the urine. Although this appearance does not actually prove that danger to life is imminent, it is a warning to be heeded. One of the results of the oxidation of carbolic acid is the formation of oxalic acid. The same process takes place in animals, in whom carbolic acid is excreted as oxalic. Doubt has been thrown on the methods by which carbolic acid is detected in the urine of those taking it, through the experiments of Städeler, who has discovered that carbolic acid is present in normal urine. Hoppe-Seyler, however, has proved that, by Städeler's process, carbolic acid is made from the indican of the urine (Hermann). The elimination of carbolic acid taking place through so many channels is readily effected, and probably the whole amount is thrown out in twenty-four hours. When death occurs very quickly in fatal cases of poisoning, the tissues and organs will smell distinctly of the poison (Ogston). Death has occurred in a few minutes—in a great majority of the fatal cases within two hours (Jeffreys), and is rarely postponed to two days. The amount of carbolic acid present will therefore vary.

There are no characteristic post-mortem appearances, except the changes wrought at the points of contact with the acid. The mucous membrane of the mouth, fauces, aesophagus, and stomach, where acted on, appears corrugated, tough, and discolored—whitish changing to brownish discoloration, surrounded by a zone of hyperemia, or capillary haemorrhages here and there sloughing off. Congestion of the viscera generally, especially of the brain and the meninges, is a constant phenomenon. The lungs are aedematous as well as congested. The heart may be distended with loose clots, and relaxed, or empty and contracted. By some observers changes akin to those of phosphorus-poisoning have been uniformly discovered (Neumann), i. e., acute fatty degeneration of liver, heart, kidneys, and other organs, notably the renal epithelium. Husemann, Salkowsky, and others, deny the reality of these observations, so that further examinations are necessary to determine this point.