Treatment in the Inter-paroxysmal Period
Despite the fact that heredity plays so dominant a rôle in the genesis of gout, how relatively scanty the attention paid to prophylactic measures! It is the second, never the initial, attack of gout that we endeavour to avert. Surely to inhibit the development rather than to prevent the recurrence of the malady is the better part. The idea is not wholly utopian, for such shrewd observers as Scudamore, Austin Flint, and others, were convinced that by timely and judicious intervention a threatened outbreak might be averted or at least its severity mitigated.
It was to this end that in a preceding chapter I urged the desirability of more attention being paid to the prodromal symptoms of gout and the clarifying light that might be thrown on otherwise inexplicable derangements by the disclosure of a hereditary tendency thereto. The failure to elicit such familial predisposition is but too common, and so those who may be led to expect the gout by inheritance are bereft of all the benefit that might accrue from a prophylactic regimen.
The indications may, indeed, be more explicit, for, apart from hereditary proneness, some subjects, even though they may never have experienced an articular outbreak, yet exhibit tophi, and therewith frequently suffer from gastric or hepatic disturbance. Obviously, is not this the opportune time for prophylaxis—the institution of hygienic and dietetic rules conjoined with the occasional use of medicines? For the “potentially” gouty, as Scudamore said, cannot “too early be taught to pay the most careful regard to their constitution, nor too surely confirm the best habits by long practice.” We hear much nowadays of the “beginnings” of disease, and who can doubt that this is a fruitful sphere for their study?
Unfortunately it is, as a rule, only when the disease has made its invasion that we wake up to our responsibilities in this respect; but happily even then we may do much to prevent consolidation of its tyranny, for even in those who have experienced regular gout there are derangements to correct, warnings to note, if we do but take heed. Of these the more common are dyspepsia and costiveness, signs of portal congestion, etc., not to mention local symptoms, i.e., the onset of pricking and tenderness in already existing tophi, twinges in the toes, etc.
We see therefore that in regard to the prophylaxis of gout the victims fall into two main groups, i.e., firstly, the “potentially” gouty, who as yet have not experienced arthritic outbreaks, and, secondly, those who have, and wish to obviate their recurrence. Happily the premonitory gastric symptoms, though varied in character, are in both instances more or less similar; nor need I say that in either alike medicinal measures are but the smallest part of the prophylaxis, whose chief stay and strength must be the golden rule of temperance in eating and drinking conjoined with adequate exercise. For, whatever our views as to the proximate origin of gout, there is every reason to suppose that the principal exciting cause resides in the alimentary canal. As Sydenham long since said, “The more closely I have thought upon gout, the more have I referred it to indigestion or to the impaired concoction of matters both in the parts and the juices of the body.” Even so to-day do medical men suffering from gout tell me that they, like Sydenham, have found by experience that almost invariably dyspeptic symptoms are the forerunners of attacks, and that their avoidance or timely correction is the best means wherewith to avert paroxysms.
As to the nature of the “indigestion,” it is of subacute or chronic type, and only very exceptionally is it acute. As to symptomatology, there is nothing distinctive about the “dyspepsias” of the “gouty,” save perhaps their marked tendency to recurrence, the facility with which they are occasioned by trivial causes, their frequent obduracy to ordinary measures, and their response to such as take cognisance of the constitutional factor.
Nevertheless such is the frequency and persistence often of gastric derangements in the “gouty” that it may safely be affirmed that the treatment of these subjects in their inter-paroxysmal periods is essentially that of the “dyspeptic.” It is, in truth, the basal indication in their therapy, for correction of the “gouty” man’s digestive disabilities is the surest way to prevent articular outbreaks, or, failing this, to postpone their recurrence or mitigate their severity.
The primary object of medicinal treatment is the restoration to functional efficiency of the alimentary tract and its accessory glands and maintenance of the action of the kidneys and skin. While diet and general hygienic regulations are all essential, we often have to fight the vicious inclination of the victim who is desirous that some medicine may be found which will avert the threatened gout without his being obliged to forego his accustomed indulgence.
He must be promptly and firmly disabused of this fallacy. Indiscriminate drugging is the bane of these cases. They fly from one remedy to another rather than give up this or that excess, and so frequently superimpose a “drug dyspepsia” upon the original disorder.
The most common form of indigestion in the “gouty” is atonic dyspepsia. The primary indication is, of course, to correct the dietetic errors, i.e., to remove the cause, and, secondly, to stimulate the secretory and motor power of the stomach. To this end, the alkalies and alkaline carbonates should be administered shortly before meals in combination with nux vomica, bitters, and carminatives.
| ℞ | Mag. carb. | gr. 10 |
| Sodæ bicarb. | gr. 15 | |
| Tinct. nucis vomicæ | ♏︎ 7 | |
| Spts. chloroformi | ♏︎ 10 | |
| Infus. calumbæ ad unciam, ter in die sumenda ante cibos. | ||
In the milder type of case the above may suffice, supplemented, if necessary, by some gentle aperient. Unfortunately in many instances the condition is apt to become complicated by fermentation with excessive formation of organic acids. It is to these that the “acid risings” are due, and not to excess of HCL. Indeed, the reverse is the case, viz., a deficiency of HCL. It is this that is responsible for the fermentation with the production of butyric, lactic, and acetic acids. Moreover, in middle-aged “gouty” subjects of sedentary habits there is often superadded motor defect, which may end in dilatation.
For treatment of this condition careful dieting alone may suffice. Indeed, attention to general health often succeeds where stomachic therapy alone conspicuously fails. The medicinal indications in these cases will vary according to the stage at which they are seen. In the milder forms we may stimulate the flow of gastric juice by alkalies and bitters before meals, or hydrochloric acid after food may be taken to replace the defect.
Now, theoretically speaking, this may sound very simple, but in practice it is often not so. Moreover, the less the attention paid to correction of diet and faulty habits, the more bewildering and disappointing the effect of drugs. Conversely, the more care expended on the selection of food and hygienic measures, the less need for drugs and the clearer the indications for such as may be helpful.
Thus simply under a revised diet the acid eructations may wholly disappear and the subject suffer only with languor, discomfort, or drowsiness after meals. Here dilute hydrochloric acid combined with strychnine and pepsine after food will be found useful.
On the other hand, many of these patients are impatient of dietetic control, yet nevertheless clamour for relief of their “acid” eructations. In such cases alkalies must be given an hour or so after meals to correct the excess of organic acids. The same may be combined with antiseptics—carbolic, B. naphthol, creosote, etc.—or some artificial digestive, such as papain, pancretin, or taka-diastase.
| ℞ | Bismuth carb. | gr. 15 |
| Calcii carb. | gr. 5 | |
| Acid. carbol. pur. | ♏︎ ½ | |
| Oleum cajeput | ♏︎ 2 | |
| Fiat cachet, 1 or 2 an hour or more after meals. | ||
The calcium and bismuth carbonates are best, inasmuch as, though they act slowly, they give rise to no secondary hypersecretion. Of digestive adjuvants in these cases, Luff speaks highly of taka-diastase (gr. 2½) immediately before meals in addition to bismuth and alkalies. The taka-diastase assists the digestion of carbohydrate foodstuffs, and so lessens or inhibits the formation of organic acids. But as a digestive adjuvant in these cases of “dyspepsia” with acid eructations papain is most useful, acting in acid, alkaline, or neutral media. This indifference on its part enables us to combine it with alkalies, and so attain the dual effect of reinforcing the digestive capacity and neutralising hyperacidity.
| ℞ | Mag. carb. pond. | gr. 15 |
| Sodii bicarb. | gr. 10 | |
| Papain | gr. 3 | |
| Oleum caryophylli | ♏︎ ½ | |
| Fiat cachet, 1 or 2 after meals when acidity is at its height. | ||
Our forefathers in such cases thought highly of rhubarb and magnesia, and certainly in hospital patients some such combination as the following is invaluable in so-called “gouty dyspepsia”:—
| ℞ | Mag. carb. | gr. 10 |
| Sodii bicarb. | gr. 15 | |
| Acid. carbol. pur. | ♏︎ 1 | |
| Tinct. rhei co. | ♏︎ 15 | |
| Spts. chloroformi | ♏︎ 15 | |
| Inf. caryophylli ad unciam, ter in die post in cibos. | ||
Almost always in these cases more or less constipation prevails, which must be corrected. To this end, of course, the magnesia contained in one of the above cachets may be all that is necessary; but often it is not so, especially if the subject be taking bismuth. Moreover, inasmuch as we have to take cognisance of the constitutional taint in these individuals, we may with advantage give an occasional aloetic pill containing colchicum or a nightly dose of guaiacum and sulphur. Again, if the urine be scanty, we may substitute a morning draught of phosphate of soda (¼-½ ounce), which not only stimulates the liver, but exercises also an antacid and diuretic effect.
| ℞ | Ext. colchici | gr. ¼ |
| Aloin | gr. ¼ | |
| Menthol | gr. ½ | |
| Ext. rhei | gr. 1 | |
| Fiat pil., 1 alternis noctibus sumenda. | ||
As soon as the symptoms of fermentation and organic acidity relent to the above or similar measures we should, if possible, dispense with drugs and rely wholly on diet and general hygienic regulations; but unfortunately a case of atonic “dyspepsia,” if of prolonged duration, gradually merges into one of chronic gastritis. Especially in those given to alcoholic indulgence do we meet with a condition of mucous catarrh, with its associated deficiency of hydrochloric acid. Indeed, apart from alcoholic excess, such is the frequency in “gouty” subjects of this form of “dyspepsia,” i.e., fermentation with excess of organic acids, that I am inclined to think that the subacidity which permits of such developing is, if I may say so, the inherent digestive disability in “gouty” subjects. Unquestionably hyperacidity—i.e., excess of organic acids due to hypochlorhydria—is in their instance infinitely more common than hyperchlorhydria, or excess of HCL, that is, much more frequent than the latter as differentiated from organic acidity by the only possible means, viz., an examination of the stomach contents.
Again, accepting the view that infections are the chief excitants of gouty paroxysms, the desirability of reinforcing the antiseptic action of the gastric juice is obvious. In other words, the defensive powers of the stomach against intruding microbes must be raised by prescribing hydrochloric acid. For this purpose it is well to use strong or fuming hydrochloric acid in doses of from 5-10 minims, freshly mixed at the time of administration with 6-8 ounces of water, and the same taken at every meal. The hydrochloric acid may with convenience be placed in a drop bottle, and beginning with 5 minims, an extra minim may be added every few days until 10 or 15 minims are taken at each meal.
Some years ago Armstrong, of Buxton, spoke highly of its value in alimentary toxæmia, which is precisely the condition we are confronted with in gout. Falkenstein, again, highly eulogises it in the latter disorder. He gives from 40-60 drops of pure hydrochloric acid in a large quantity of effervescing water each day. It is taken during meals, and the dilution with water is arranged so that the patient is struck by the acid taste. The diet taken was an ordinary one, and yet Falkenstein noted that the dyspeptic symptoms disappeared and the attacks of gout grew more rare and much less severe. As an alternative to water, either still or effervescing, the hydrochloric acid in from 5-15 drops may be given in mucilage, or, if preferred, we may give the dilute hydrochloric acid in some such form as the following:—
| ℞ | Acid. hydrochlor. dil. | ♏︎ 10-15 |
| Glycerin pepsinæ | dr. 1 | |
| Liq. strych. hyd. | ♏︎ 3 | |
| Tinct. capsici | ♏︎ 1 | |
| Inf. aurantii co. ad unciam, ter die sumenda statim post cibos. | ||
Sometimes it so happens that while taking the above acid mixture the subjects an hour or more after meals complain of acidity. If so, it is due to fermentation, and at the time of its occurrence must be met by an adequate dose of an alkali with or without some antiseptic preparation. It goes without saying that if such can be referred to dietetic errors—food-bolting, etc.—these also must be corrected.
In these cases, too, the liver is frequently inactive, though often their attacks of “biliousness” signify nothing but constipation; but when there are definite signs of hepatic torpor we may substitute for the hydrochloric acid in the above mixture the dilute nitro-muriatic acid. Simultaneously we may occasionally at night give a pill containing calomel, iridin, or podophyllin combined with aloes and belladonna, or we may instead invoke colchicum as a cholagogue, following it up in either case the morning after by a saline purge. As a substitute we may in suitable cases order every morning for some days a full dose of Rubinat, Hunyadi Janos, or other bitter water.
So much for the more common derangements of the inter-paroxysmal period and the measures wherewith to combat them. Collectively their aim is the restoration to functional efficiency of the alimentary canal and its accessory glands, this to the end that, as far as possible, a condition of intestinal asepsis may be attained, with its correlated diminution of the excitants most fertile of outbreaks.
Nevertheless, from time to time, either from failure of the patient’s co-operation or other mischances, our best efforts at prophylaxis fail, and it becomes clear that an attack is imminent. What then, save brisk purgation, can be done to avert the threatened outbreak? Our forefathers, in cases in which the fits recurred periodically and might be forecast with tolerable accuracy, were accustomed some time before the threatened attack to place the subject on a rigorous diet, this in combination with a course of alkalies, those of soda being given the preference in dyspeptic or hepatic disturbance and those of potash when the urine was scanty.
That this was sound treatment and abundantly justified by the results is well acknowledged, and all I would suggest is that this is yet another juncture at which atophan is indicated, viz., immediately before a paroxysm. At this particular time the urinary output of uric acid is often diminished, a clear indication for enlistment of atophan, which increases uric acid elimination. I note that both Retzlaff and Brugsch consider it an especially advantageous time for its exhibition. As a prophylactic measure the former gives 30-45 grains daily for three days at intervals of a fortnight, and if cardialgia or heartburn ensues, adds ¼-½ teaspoonful of bicarbonate of soda to each gramme of the drug.
Lastly, we have to recollect, too, that colchicum is credited with some prophylactic powers. Some, it is true, discountenance its employment in the inter-paroxysmal period, on the plea that it tends to favour recurrence and chronicity of attacks. While I think it is better to reserve it for acute or subacute attacks, still I have not found that colchicum, given in what Sir Thomas Watson called alterative doses, is anything but beneficial, provided that it be taken intermittently, not continuously, for long periods. As to special indications for its employment, I think it is more effectual in aborting a threatened attack when, in addition to dyspeptic phenomena, the imminence of a fit is betokened by what may be termed specific harbingers thereof, i.e., pricking and tenderness in existing tophi, twinges in the toes, etc.
In conclusion, are we not in this matter of the prophylaxis of gout somewhat too prone to resort, both in and out of season, to what we are pleased to term special medication? Almost every week some new and of course infallible “uric acid solvent” is lauded ad nauseam in the press. Are not we ourselves, too, somewhat overanxious to go with the tide in prescribing these vaunted “gout specifics”?
The true aim of prophylaxis is rather to prevent the incidence of those functional derangements that in some subtle way determine the disturbances in nuclein metabolism, with secondary accumulation of uric acid in the organism. That drugs, such as atophan, which diminish the uric acid content of the blood and increase its urinary output, fulfil an invaluable rôle in ridding the system of excessive amounts of this chemical outcast, I fully admit.
Albeit, this achievement does but deal with the consequences or sequels, not the exciting causes, of gout. In truth, there is no short cut to the cure of gout. Only under suitable treatment, applied to meet all the necessities of individual cases, will any long immunity from its onslaughts be secured or their intensity attenuated.