By Homer I. Ostrom, M.D., New York.
Surgical technique, by which I understand the mechanical details of operative surgery, is based upon such sound principles, and has at present attained such a degree of perfection, that we must turn our attention in other directions to account for the casualties that occasionally follow operations in which technically no flaw can be detected, and which have been conducted in accordance with the most approved tenets of our art.
Sepsis is eliminated, and we are positively able to do this when the case is clean, and should be almost as positively able to exclude infection when the case is dirty. Environment is favorable, that is, there is good light, and good air, and the food is all that can be desired. The conditions of the operation we feel satisfied make for success, and notwithstanding our patient becomes intoxicated, and her convalescence is interrupted with symptoms of toxaemia, the overpowering dose of which may lead to a fatal termination. Confronted with such propositions we may well ask ourselves the cause, that happily we may avert the effect.
By the process of exclusion we deduce, that the toxine is generated within the individual; in other words, we turn to nature’s laboratory. To metabolism, to the processes by which cells are nourished and maintained, and the effete matter eliminated for other uses.
For us as surgeons this question of faulty metabolism possesses an especial interest, for together with the imperfect assimilation of food, and hence “vital decrease,” there are manufactured, and thrown into the circulation, very definite substances that poison the system, and cause what may be more specifically called “acid intoxication.” This toxaemia is quite distinct from septicaemia, though may be associated with it, such an association having frequently led to a confusion of the two clinical pictures, and in consequence erroneous treatment.
Broadly stated, looking to the etiology, we may say; that septic intoxication is always caused by actively developing bacteria, in contradistinction to “acid intoxication,” which is in no manner dependent upon the presence of micro-organisms, but is due to a ferment, generated in the chemical laboratory of the system. What this ferment is we cannot at present say, but its presence is always noted by an excess of acetone, and diacetic acid in the blood, and in the urine. This condition was formerly thought to belong exclusively to diabetes, but it is now known to occur independently of that organic lesion, and to be very frequently associated with acute yellow atrophy of the liver. Certain it is, that when acetone and diacetic acid exist in any considerable quantity in the urine, such subjects are not favorable ones for operations. They early develop symptoms of intoxication, which, though not necessarily fatal, retard convalescence, and give rise to much anxiety on the part of the surgeon.
The metabolic changes that give rise to “acetonuria” may exist without a traumatic cause, and mask the true nature of the case, raising the suspicion of septicaemia; of some deep-seated focus of suppuration. To operate in such instances would be not only useless, but possibly fatal, the true cause lying in an increased destruction of proteid matter and not in anything removable by operation. We, therefore, eliminate very positive dangers from operative surgery by making ourselves familiar with the metabolism of our patients, and this knowledge will be acquired by a thorough examination of the blood and urine. Not the routine examination of the renal secretion for albumen, and sugar, for urates and solids, all of which are important, but the more extended examination for acetone, and diacetic acid, for urea, and indicin. The chief object of this paper is to urge the necessity for such examinations and to bring to your notice the dangers that may be avoided by familiarity with the processes of reconstruction that are going on within the organism of the subject that is brought to us for operation.
Such examinations should always be made by the specialist when one can be reached, but in case the surgeon must depend upon his own laboratory, the presence of acetone in the urine is easily detected by adding to one drachma of urine a small crystal of sodium nitro-prussiate, and then enough sodium hydrate to make the solution strongly alkaline. After thoroughly shaking, the addition of glacial acetic acid gives a purple color to the foam. By adding a strongly aqueous solution of ferric chloride to the urine it turns a deep Burgundy red color if diacetic acid is present.
Aside from the chemical tests of blood and urine, how are we to recognize the faulty metabolism that gives rise to acid intoxication, and what are the surgical casualties that attend “acetonuria;” in other words, what is the clinical picture of this disease, that presents itself?
We have two groups to study, the anti-operative and the post-operative cases, for acetone and diacetic acid may exist without traumatic cause, or its development may depend upon the depressing effect of shock upon metabolism. The symptoms are much the same in both cases, and resemble in many particulars profound septic intoxication. There is a peculiar apathy, frequently thee first symptom to attract attention, but probably the most characteristic and constant symptom is the odor of the breath. This is a sweetish, pungent odor that resembles Chloroform, and continues in varying degree during all stages of the intoxication. It is unlike the sweetish sickening odor of sepsis, which has none of the pungent quality of the “acetonuria” breath.
Vomiting, or rather quick rejection of anything taken into the stomach is liable to be present, the fluid vomited having a most foul odor. The toxine attacks the heart also, as shown by the rapid pulse, with low tension. The temperature does not rise, save in very severe cases, but usually continues normal or subnormal. The tongue is usually dry and red.
Alternately with apathy is cases reaching a state of stupor, there may be great restlessness and low delirium. The face and mucous membranes are usually congested, and “air hunger” is usually a prominent symptom of fatal cases, showing that the toxine affects also the metabolism of the blood, causing an excessive oxidation, with resulting deficient oxygen.
Such a clinical picture following an injury, or occurring independently of an operation, may mask the diagnosis, but with acetone and diacetic acid in the urine and blood, and in the absence of any positive evidence of suppuration, the doubt should be in favor of acetonuria, as against sepsis, and operative treatment deferred. Undoubtedly many cases of appendicitis presenting this group of symptoms have been operated upon with the expectation of finding pus, no pus or exudate being found in the abdomen. While I would not regret the removal of the appendix under such conditions, believing that a diseased appendix never quite recovers itself, and while in situ remains a menace to the health, thee state is regarded too seriously, and an operation performed with unnecessary haste, when delay would give an opportunity to improve metabolism, and so place the patient in a better condition to withstand surgical shock.
This group of symptoms, the result of faulty metabolism, occurring after an operation, may well be regarded as among the serious casualties of surgery, for though we have not septic intoxication to combat, or to remove the focus of its generation, we must deal with the springs of life, with the processes by which waste and repair are equalized, and at the same time overcome the toxine that will continue to be thrown out as the product of the imperfect manner in which that process is carried on. The “vital decrease,” That is a necessary part of faulty metabolism, looms up as an additional very certain menace to success, for we realize most forcibly that there is a direct relation between nature’s resisting power, her phagocytism, and the invasion of disease, and if we would avoid some of the most fatal casualties of surgery we will see to it that faulty metabolism is corrected as quickly as possible.
The etiology and history of “acetonuria” indicate the lines along which successful treatment must be pursued. Whatever will improve general health, either in the direction of dietetics, or remedies, must be given. The tissue salts, Kali phosphoricum, Kali sulphuricum, etc., will be thought of. Well developed post-operative cases will require active treatment, much upon the lines followed in septicaemia, save that an operation is not to be thought of, there being no pus focus as a factor to consider. The heart must be sustained, and here Adrenalin is of great value. Intravenous saline transfusions of 500 cubic centimeters of a 1-50,000 solution of Adrenalin are followed by excellent results. The cyanosis is modified, the mental condition improved. And the heart strengthened. The kidneys are also excited to action, and a reduction in the quantity of acetone and diacetic acid follows.
All food will, of course, be withheld from the stomach as long as vomiting continues, and the patient nourished by the rectum.
I know of no remedy more exquisitely similar to this stage of the disease than Gelseminum. The congested face and mental apathy with dull delirium, are perfectly covered by Thais drug. Veratum vidide is a rival, but I more frequently use Gelseminum.
Inasmuch as the liver has been found to suffer fatty degeneration in cases of acid intoxication, we may conclude that this organ is functionally at fault, and therefore our treatment should include such remedies as will restore its function. Of these nothing I believe equals Merc. dulc., and this I administer until I am satisfied that its action is well demonstrated.
