MEDICINAL AND OTHER MODES OF THERAPY (_continued_)—INTER-PAROXYSMAL PERIOD
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.