GOUT.

BY W. H. DRAPER, M.D.


DEFINITION.—Gout, as a disease, in the traditional acceptation of the term, is a specific arthritis, characterized by the deposit of the salts of uric acid in the affected joints. Gout, as a diathesis, is a blood crasis in which there is an accumulation in the blood serum of the uric acid salts, the consequence either of the increased formation or of the defective excretion of these products of proteid metamorphosis. The manifold irritations of the different tissues, and the accompanying subjective and objective symptoms provoked by this dyscrasia, are termed gouty.

SYNONYMS.—(a) Eng., Gout; Lat., Gutta; Fr., Goutte; Sp., Gota; Ger., Gicht—derived from the nomenclature of humoral pathology and descriptive of the distillation (goutte à goutte) of the poisonous humor into the joints—arthritis uratica. (b) Gouty diathesis; constitutional gout; irregular gout.

CLASSIFICATION.—(a) Gout as a specific form of articular inflammation is classified according to its location—cheiragra, onagra, podagra, gonagra, etc. (b) Gout as a constitutional disease is classified, 1st, according to the structures affected—e.g. articular gout; tegumentary gout, embracing mucous as well as cutaneous affections of gouty origin; nervous gout; parenchymatous or visceral gout; 2d, according to the degree of the inflammatory process—acute, subacute, and chronic; 3d, according to certain irregularities manifested in the development and progress of gouty lesions as metastatic, retrocedent, and suppressed gout. This classification of constitutional gout is based upon the well-recognized clinical observation in the history of gouty persons and gouty families, that the characteristic lesions of the joint-structures are often correlated with lesions of the skin, mucous and serous membranes, vessels, nerves, and parenchymatous organs, which are marked by the same blood dyscrasia that exists in articular gout, and which are most successfully treated by the same measures which experience has suggested in the management of the arthritic disease.

Musgrave in his work1 treats of a great number of varieties of gout, as follows: De arthritide anomala; de colica arthritica; de diarrhoea arthritica; de dysenteria arthritica; de abscesse intestinorum arthritica; de melancholia arthritica; de syncope arthritica; de calculo renum arthritico; de asthmate arthritico; de catarrho, tussi, et peripneumonia arthritica; de phthise arthritica; de angina arthritica; de capito dolore et vertigine arthritica; de apoplexia arthritica; de paralysi arthritica; de doloribus in corpore vagis, fixis; de ophthalmia, de erysipelate et achoribus arthriticis; etc.

1 De Arthritide Anomala, sive Interna, Dissertatio, Geneva, 1715.

HISTORY.—The records of medicine furnish simple evidence of the prevalence of gout in all ancient as well as in modern civilized communities. Its origin in the perversion of physiological functions was as clearly recognized by the prophets of the old testament of the medical art as it is by the founders of the gospel of modern science. The refined processes of animal chemistry have simply revealed the materies morbi which was foreshadowed in the "peccant matters" of the humoralists, which were supposed to be distilled into the joints and other structures, provoking inflammation and tophous deposits. This is the most notable and interesting fact in the history of gout, that it has from the earliest times been regarded as a specific form of arthritis and dependent upon the circulation in the blood of peccant matter. It was not, however, until the latter part of the eighteenth century, when Murray Forbes, and a few years later Wollaston, called attention to the fact that uric acid was the chief ingredient in urinary calculi and in tophous deposits, that our knowledge of the pathology of gout may be said to have had its beginning. The demonstration by Garrod, in 1848, of the presence of lithate of soda in the blood of gouty persons, also marks an era in the history of the pathology of gout.

While the humoralistic theory of gout has prevailed almost to the exclusion of all others, it is historically interesting to note that the views of the solidists, as represented by Cullen, who maintained that "gout was an affection of the nervous system in which the primary moving powers of the whole system are lodged," have been recently revived and are attracting considerable attention.

ETIOLOGY: PREDISPOSING CAUSES.—Heredity may be regarded as the most prominent of the predisposing causes of gout. Statistics of arthritic gout show this tendency in a varying but always large proportion of cases. Scudamore observed it in nearly 60 per cent. of his cases; Garrod, in 50 per cent. of his hospital cases and, in a much larger proportion, in his private practice; Gairdner found it in 140 out of 156 cases. If all the manifestations of the gouty vice were taken into consideration in determining the influence of heredity, it would doubtless be shown in a still larger percentage of cases.

It is generally supposed that there is a greater frequency of inheritance from the male ancestors and in the male descendants. This may be explained by the fact that men are more exposed to the other predisposing and to the exciting causes of gout. My own experience leads me to suspect that if we took into consideration the irregular manifestations of this morbid inheritance, we should find it as frequently in the female, both in the ascending and descending line; of the greater frequency of acute articular gout, however, in the male, there can be no question. While it is true that acute attacks are comparatively rare in women, both before and after the menopause, it is undeniable that the subacute and chronic forms of gouty arthritis are by no means rare in them, both before and after the cessation of menstruation. The Hippocratic proposition that women enjoy immunity from gout by reason of the menstrual flux can hardly be entitled to much consideration in view of the fact that they are commonly less exposed to the exciting causes of the disease, and that when they subject themselves to the same vicious habits which entail the disease in men they suffer like men.

Statistics as to the age at which articular gout is most often developed show that the larger proportion of cases occurs in the decade from thirty or forty. It is rare before twenty, and the frequency diminishes rapidly after sixty. Some well-authenticated cases have been observed before puberty in children in whom the hereditary taint was strongly developed. Gairdner claims to have seen several cases in infants at the breast. Trousseau saw a case in a boy aged six, and Garrod in a youth of sixteen. At the other extreme Garrod reports a first attack at the age of eighty, and another in the ninetieth year. The cases at the extremes of age are certainly rare, and other causes of arthritic inflammation might easily be invoked to explain them. It is a significant fact that the largest proportion of attacks of acute articular gout occurs after the period of complete development is ended and before the period of degenerative changes has begun, when the necessities of growth have ceased and food is required only for the nutrition of the tissues, the maintenance of vital energies, and the demands of work.

Much stress was laid by the earlier writers on the effect of temperament as a predisposing cause of gout. The vague ideas involved in the classification of mankind according to temperament may be said to have lost their influence in the scientific conceptions of modern pathology. Gout is observed in persons exhibiting the most diverse peculiarities in physical conformation and physical disposition. The true interpretation of the facts in regard to the relations of temperament to gout, so far as those relations exist, would seem to be that the conditions which give rise to gout are responsible also for the physical and moral idiosyncrasies of gouty subjects.

A vicious hygiene may be regarded as one of the chief predisposing causes of gout. The disease is essentially one of advanced civilization, and is alike the product of the luxury and the misery which a high civilization entails. It is a common error to suppose that gout is the consequence only of luxurious living. If the essential cause of the disease is the circulation of imperfectly oxidized plasma, then there are two ways in which this defective oxidation may be brought about: either there is an excess of food ingested beyond the capacity of the individual, under the most favorable conditions, to consume, or the conditions of oxidation may be so impaired that the complete combustion of even a moderate supply of food is impossible. Perfect oxidation requires an even balance between the amount of food ingested and the oxygen inhaled. A consideration of this axiom explains several circumstances in the history of gout. As has been remarked, the disease is rare during the period of growth and development, when the processes of nutrition are active and the consumption of food in excessive quantities is rendered possible by the large demands for the needs of the growing body and for the development of active energy. It is common in adult life when the processes of nutrition are less active, when growth is complete, and when the supply of food must be regulated according to the amount of energy to be developed. It must also be observed that while the disease is most frequently caused by excesses in the consumption of food, it is also often the consequence of an insufficient supply of pure air; hence we find it often among those who cannot be accused of gluttony, but whose occupations or poverty compel them to live and work in a vitiated atmosphere.

The influence of alcoholic liquors in the production of gouty dyscrasia is generally acknowledged. There seems to be a striking difference, however, in the effects of the distilled and fermented preparations of alcohol in this respect. Gout is certainly more prevalent in countries where large amounts of fermented liquors are used than in those where distilled spirits are chiefly consumed. The disease is more prevalent, for example, in England than in Scotland or Ireland, especially among the lower classes; it is said also that it is rare in Russia and Poland, where spirits are more exclusively used. There is a difference also in the predisposing influence of the different varieties of fermented liquors in the production of gouty dyscrasia. The heavier wines, sherry, madeira, and port, are known to be more mischievous in this respect than the lighter wines of France and Germany, though there is abundant clinical evidence of the fact that even these wines, and especially the richer clarets. Burgundies, and Rhine wines, frequently give rise to acute gout and the gouty habit. There can be no question as to the pernicious effects of the malt liquors as gout-producers. The great frequency of gouty diseases particularly among the lower classes who consume these beverages in large quantities is undeniable. This is true especially of the stronger English and Scotch ales, and to a less degree of the lighter English, American, and German beers. The effect of cider and perry as gout-producers is also well recognized. It has been observed in certain districts of England where cider is largely consumed, and, though acute articular gout is said not to be a common disease in New England, where cider has always been much used, there can be no question that it often leads to the development of the irregular forms of gout. As one of the forms of fermented alcoholic beverages containing, in its fresh state especially, a large amount of sugar, it favors the production of the acid dyspepsia which is a common antecedent in the formation of a gouty dyscrasia.

In 1854, Garrod called attention to the fact that a considerable proportion of the gouty patients in hospital practice—at least 30 per cent.—was represented by painters and other workers in lead. This statement has since been confirmed by other observers, and the association of the characteristic symptoms of this form of metallic poisoning, such as the blue line on the gums, colic, and the different forms of paralysis, with both articular and visceral gout, especially the contracted kidney, is certainly frequent. The relation, however, of saturnine poisoning to gout in this association is not easy to determine, Garrod himself pointing out that while the women in the lead-works frequently had the colic, they but rarely had gout. The difference in susceptibility of different individuals to all forms of metallic poisoning is well recognized. It is more strikingly observed perhaps in mercurial and arsenical poisoning than in that of lead. It is well known that the internal use of lead as an astringent in cases of hemorrhage and intestinal catarrh is occasionally, though very rarely, followed by the evidences of lead-poisoning. This difference in susceptibility is perhaps explicable on the theory that persons inclined to gout have less power in eliminating the metal than those who are not gouty, so that it is possible that plumbism is the effect rather than the cause of gout, as has been commonly supposed.

Tanquerel des Planches found none of those changes in the kidneys as the result of plumbism such as are frequently met with in gout, and Rosenstein, who was able to produce saturnine epilepsy in dogs, found no renal changes to have occurred. Charcot and Gombault in recent experiments of feeding guinea-pigs with lead found changes in the kidneys similar to those produced by tying the ureters.

EXCITING CAUSES.—Paroxysms of acute or subacute gouty inflammation of the joints, skin, or mucous membranes, as well as the neuroses of gouty origin, are excited by a variety of causes: errors in diet, both as to quantity and as to specific articles; excesses in the use of fermented liquors—even moderate indulgence, in persons with strong gouty tendencies—are perhaps the most common exciting causes. Sudden changes in temperature, and especially sudden changes in barometrical pressure, sometimes excite and often aggravate the sufferings of gouty persons. Blows, contusions, and mechanical strain frequently determine arthritic attacks; the large proportion of paroxysms affecting the metatarso-phalangeal joint of the great toe is explained by the fact that this joint is more exposed than any other to strain and injury. Finally, nervous exhaustion, from any cause, from overwork or sexual excesses, from grief, anger, or shock, may provoke any of the inflammatory or neurotic consequences of this disease.

PATHOLOGY.—It would be impossible in the limits of this article to review the many theories that have prevailed in regard to the pathology of gout, or even to discuss fully those that may be said to divide professional opinion at the present day. Since the discovery, by Garrod, of the salts of uric acid in the blood-serum of gouty patients, the humoral pathology of gout has certainly had the largest number of adherents.

The lithæmic pathology may be said to be based primarily upon the chemical theory of digestion or food-transformation. This theory proceeds upon the idea that every atom of albuminous or carbonaceous food that enters the body, whether it goes to the construction of tissue or is destined for the direct conversion of potential into active energy, is finally eliminated, for the most part, as urea, carbonic acid, and water. This transformation, of course, is supposed to be effected by a process of oxidation, but neither the exact mode of transformation nor the share which the different organs and tissues take in its accomplishment can be said to be certainly known. Recent investigations seem to indicate that the liver is chiefly concerned, not only in the metamorphosis of the carbohydrates, but also in the formation of urea, so that the arrest in the conversion of starches and sugars which results in glycosuria, and the check in the metabolism of the proteids which give rise to lithæmia, may both have their origin in hepatic derangement. The not infrequent association of glycosuria and lithæmia in the same patient, and the frequent alternation of gout and saccharine diabetes in gouty families, are significant facts in support of the common origin of these diseases.

The purely chemical theory of gout and diabetes, that they are diseases of suboxidation—a theory most ably advocated by Bence Jones2—has much to commend it from the valuable suggestions which it affords in the clinical management of these maladies; but it must be acknowledged that while a defective oxidation seems to be an essential factor in the production of gout and diabetes, it is impossible to reduce the process to the simplicity of a chemical equation. It cannot be claimed that the complex chain of transformations which organic chemistry has demonstrated in the destructive metamorphosis of albumen and starch in the laboratory is represented in the vital chemistry of the body. All that can be said in the present state of knowledge is, that the metabolism of food is in its nature a chemical analysis, modified and regulated by vital force, and resulting in the building up of tissues and in the conversion of potential into active energy. Imperfect blood-elaboration must depend upon much besides a disturbance of the balance between the amount of food ingested and the oxygen inhaled, though this must unquestionably be an important factor in its production. Heredity and the mysterious influence of the nervous system complicate the problem of the malnutrition which leads to gout, in such a way that while the general proposition may be maintained that gout is a disease in which suboxidation occurs, it is not possible to affirm whether suboxidation is the essence of the disease or only one of its phenomena.

2 Lectures on Some of the Applications of Chemistry and Mechanics to Pathology and Therapeutics, H. Bence Jones, London, 1867.

It is probable, however, that the pathogenesis of the gouty dyscrasia involves a much more complex process than the simple accumulation of uric acid salts in the blood. Uric acid, like urea, is one of the normal results of the metamorphosis of the albuminous foods and tissues. In birds and reptiles it takes the place of urea as the final issue of this metabolism. It has been supposed, as one atom of uric acid can be split by oxidation into two atoms of urea and one of mesoxalic acid, that uric acid was the penultimate of urea, the result of a lower degree of oxidation. It is by no means certain, however, that it is a necessary antecedent of urea. In birds, who consume by their rapid breathing an enormous proportion of oxygen, as well as in the slow-breathing reptilia, the nitrogenous excrements are in the form of urates; and under such divergent conditions it is impossible to explain the variations in the proteid metabolism by varying degrees of oxidation. The only reason that can be assigned for the elimination of the nitrogenous waste in some animals in the form of urea and in others in that of urates is the teleological one that the urea is destined for a fluid and the urates for a solid excretion.

But apart from these physiological objections to the theory that uric acid is necessarily the offending substance in gout, it is well known that uric acid salts accumulate in the blood in febrile diseases, in disorders of digestion, and in anæmia—notably in splenic anæmia—and do not produce either the symptoms or lesions of gout. Todd maintained that gout might occur without an excess of uric acid in the blood; and it is certain that in the atonic and irregular forms of the disease uric acid may not be found in excess in the blood or appear in excess in the urine. Another significant circumstance in the history of gouty persons tending to show that uric acid may be, after all, only an epiphenomenon in the disease, and not its exciting cause, is that the power of digesting farinaceous and saccharine foods in this disease is markedly diminished. To such a degree is this true that sufferers from the gouty dyscrasia are most promptly relieved of their symptoms of primary indigestion by restricting their diet very largely to albuminous foods; and not only does such a diet diminish the dyspeptic symptoms, but I am persuaded by a considerable experience that it is one of the surest prophylactics against the recurrence of gouty lesions. It is well known that the fermented preparations of alcohol are among the most frequent exciting causes of acute gout, and cases are by no means infrequent in which indulgence in sweet foods and in fruits will provoke many of the well-recognized local lesions of the disease.

The explanation of this anomaly in the uric acid pathology of gout may possibly be found in the suggestion of Garrod, that the deposition of the urates is caused by their insolubility, and, as this insolubility is increased by the diminished alkalinity of the serum, that the evolution of the acids in the digestion of the carbohydrates so diminishes the normal alkaline state of the blood that the uric acid salts are more readily precipitated. But even if we accept this explanation, the fact remains that as efficient factors in the production of the gouty diathesis the carbonaceous foods may play as large and perhaps a larger part than the albuminous foods. It would seem, therefore, in view of the conflicting evidence in regard to the theory of the uric acid origin of gout, that the chemical pathology of this dyscrasia is still involved in considerable obscurity.

The recent advances in neuropathology have revived of late years the views of Cullen on the pathology of gout. Dyce Duckworth3 has lately advocated the theory that gout is a trophoneurosis. This theory grows out of the recognition of the protean manifestations of this disease, and especially of the neurotic element which is so prominently developed in its evolution. The frequency of purely nervous symptoms in gouty persons is a fact which is daily brought to the notice of those who have much opportunity to study the disease. These symptoms may be said to affect all the functions of the nervous system; among these we may mention psychical disturbances, such as hypochondriasis and hysteria; derangements of sensation, such as neuralgias and dysæsthesias of every variety; and spasms of voluntary and involuntary muscles, such as cramps, grinding of the teeth, asthma, and vesical tenesmus. Another fact which arrests attention in the history of gouty persons is the frequency with which purely nervous influences determine attacks of gout; the effect of nervous exhaustion, whether provoked by overwork or mental anxiety, or the more explosive discharges of nerve-force in rage and great emotional excitement of any kind, is well recognized as a frequent precursor of gouty lesions. The influence of certain diseases of the nervous centres also, such as cerebro-spinal meningitis, Pott's disease, and tabes dorsalis, in determining arthropathies and lesions of the skin and mucous membranes, furnishes a striking analogical argument in favor of the possible nervous origin of the lesions in gout. The recognition of these facts, however, does not necessarily militate against the commonly accepted humoral pathology of gout. The healthy action of the nervous centres must depend primarily upon a normal nutrition, and a normal nutrition depends on healthy blood-elaboration. That perverted innervation may be an important factor in the development of malnutrition through the accident of inheritance is doubtless true, but in the acquired disease it seems more probable that the lithæmic condition is the primary source of disturbed innervation. It may be that gouty lesions are determined as reflex phenomena through the medium of the trophic centres—if such centres there be—rather than by the direct irritation of the affected tissues by the gouty blood; and it is not unreasonable to suppose that nervous exhaustion from any cause may produce in these centres greater reflex excitability.4

3 Brit. Med. Jour., March 26, 1881.

4 Edward Liveing, in his work On Megrim, Sick Headache, and Some Allied Disorders, p. 404, thus expresses his conviction as to the neurotic theory of gout: "The view which is commonly entertained is, that the excessive generation or retention of uric acid in the system, which is regarded as the fundamental fact in the pathology of gout, exerts a toxic influence upon the nervous centres, while the particular character of the disorder is determined by the territory involved. This limited operation of a cause so general in its nature is a real obstacle to this view; on the other hand, there is much in the history of gout—its hereditary character, limitation to particular ages and sexes, periodicity, explosive character, sudden translations, and remarkable metamorphic relations with nervous disorders—which seems to stamp the malady as a pure neurosis; and even the fit itself, with its sudden nocturnal invasion, the late Dr. Todd was accustomed to compare to one of epilepsy or of asthma."

PATHOLOGICAL ANATOMY.—Blood-Changes.—Garrod's demonstration of the excess of uric acid in the blood of gouty persons constitutes the chief recognized hæmic change in this disease. That this is a constant change, and one that is essential to the existence of gout, cannot be said to be proved. The presence of uric acid in the blood is not always productive of gout, since it has often been found in the blood of healthy persons, and its temporary excess during pyrexia, and especially in the fevers and other morbid states in which spleen is congested, has already been noted. The excess of uric acid, however, in gouty blood may reach, according to Garrod, as much as 0.11 grain in 1000 grains of serum. It is probable that other excrementitious substances exist in the blood in gout which bear a closer etiological relation to this disease than uric acid, but they have not been demonstrated. The other blood-changes which are noted by Garrod—the diminished specific gravity of the serum from loss of albumen, the diminished alkalinity, and the increase of the fibrin in the inflammatory forms of the disease—are probably inconstant. In chronic gout the objective signs of anæmia which are often present would indicate a marked diminution in the red blood-corpuscles.

The tissues which are the chief seat of gouty lesions are the connective tissues. In the evolution of the disease the joints, where the connective tissue is most dense and the least vascular, suffer earliest; at a later period the connective tissue of the blood-vessels, nerves, and viscera becomes subject to gouty changes.

According to Garrod, the exudations in articular gout are rich in the urates of soda, lime, magnesia, and ammonia; they also contain some phosphate of lime and traces of organic matter. The watery portion is absorbed and the salts are deposited in crystalline forms. The location of these deposits varies: they are found on the synovial surfaces, in the cartilage-cells, and in the intercellular substance; in the tendons, ligaments, and bursæ, and in the subcutaneous connective tissue. The urate of soda occurs not on the free surface of the cartilage, and replacing the latter, as was formerly generally supposed, but as an infiltration into the substance of that tissue; and Garrod found that there is always a thin layer of unaffected cartilage lying between the deposit and the free articular surface—an observation which has been confirmed by Budd and quite recently by Ebstein.5

5 W. Ebstein, Die Natur und Behandlung der Gicht, Wiesbaden, 1882.

Very important are the recent investigations of the latter. After making numerous observations on the cartilages and other affected tissues of gouty subjects, besides studying the disease artificially produced in fowls, he has shown that those portions of cartilage and other tissues in which the deposit occurs are in a state of necrosis, as is evident from the fact that when the urates are dissolved out by warm water the area in which the deposit occurred, though apparently normal to the eye, refuses to be stained with aniline dyes, and lies plainly visible as a light spot in the midst of stained tissue. Since the work of Weigert we know that this is a sure sign of that peculiar form of death of a tissue to which the name of coagulation necrosis has been given. Ebstein regards this necrosis as primary and the deposition of the uratic salt as secondary. According to him, the urates circulating in the blood give rise to necrosis in parts where the circulation is sluggish (as the articular cartilages, the ears, and the extremities generally), and where, consequently, they remain a greater length of time in contact with the tissues. The necrotic portion has, however, an acid reaction, which causes a deposition, from the soluble neutral salt, of an acid urate in a crystalline form. Ebstein claims that this necrotic area, in which there is deposited a crystalline urate of soda, and around which there is a secondary inflammatory zone, is characteristic solely of gout. "I have never seen," he says, "in gout a crystalline deposit of urates occurring in normal tissue."

In addition to these so-called specific changes we find a hyperplasia of the connective tissue in the fibrous structures of the affected joints. The thickening thus induced, with the contraction of the new tissue and the atrophic changes resulting from pressure and disuse, are the causes of the deformities, subluxations, and impaired movements of gouty joints. Occasionally, the local irritation provoked by the pressure of the tophous deposits results in abscesses from which a mixture of pus and pasty urates may be discharged. These abscesses in feeble and anæmic subjects are sometimes difficult to heal. More frequently the skin undergoes gradual absorption and the chalk-like deposits are exposed.

The frequency with which the metatarso-phalangeal joint of the great toes is affected in gouty persons has always been noted. In Scudamore's tables the proportion of the first attacks in this joint was 72 per cent., and in 66 per cent. one or both great joints were affected to the exclusion of other joints. This frequency is due to the fact that this joint is the most vulnerable one in the body, bearing as it does the weight of the body and being exposed to most frequent shock. The phalangeal joints of the hands and the wrist-joints are also often the seat of acute gout, though these joints are more frequently affected by the subacute form of the disease. The larger joints may also be the seat of true gouty inflammation; indeed, no joint, not even the intervertebral, can be said to enjoy immunity, and the hip and shoulder are occasionally attacked to the exclusion of others. The cartilages of the ear and the arytenoid cartilages are sometimes the seat of gouty deposits.

The great frequency of arterial sclerosis, and the subsequent fatty and chalky metamorphosis in persons who have suffered from chronic gout, are well recognized. Next to syphilis, gout seems to be the most common cause of these arterial changes. The influence of these lesions in the arteries and capillaries in determining cardiac hypertrophy and cerebral hemorrhage is often seen in the accidents which terminate the lives of gouty patients.

In the heart a gouty endocarditis is of not uncommon occurrence, according to Ebstein, who cites Lancereaux as having found uric acid in concretions on the valves. Garrod, however, after examining a number of cases in which cardiac disease existed with gout, states that in his opinion the valvular changes are not due to a gouty deposit, he never having been able to demonstrate the presence of uric acid in them.

Some years ago Sir James Paget called attention to the frequency of adhesive phlebitis as a gouty lesion. This is observed in connection with articular gout, but may also occur independently of joint-lesion. It is observed most frequently in the lower limbs, is generally symmetrical, and shows a disposition to metastasis.

Neuritis and sclerotic lesions of the nerve-centres are not uncommon in the history of acquired and inherited gout. The neuralgias and other temporary dysæsthesias which constitute a considerable category in the symptoms of gouty persons are doubtless due to transient central and peripheral lesions.

The so-called gouty kidney is the most striking illustration of the effect of the gouty dyscrasia in the production of a characteristic visceral lesion. The changes which occur in the kidney as a result of gout are—a contraction of the organ, the result of interstitial inflammatory processes, and a deposition of uratic salts, occurring mainly in the papillary portion. The views as to the exact locality where these deposits occur still differ considerably. Garrod is of opinion that it occurs in the fibrous interstitial tissue. Virchow, on the other hand, regards the lumen of the tubuli as the seat of the deposit, and in this he is supported by Charcot and Cornil and Ranvier, Lancereaux and Wagner. Dickinson inclines to the view of Garrod, and believes that it is the deposition of the urates in the interstitial tissue which gives rise to the chronic inflammation which results in cirrhosis of the kidney—the granular kidney of gout. Ebstein seems to think that the interstitial connective tissue, having previously undergone a state of necrosis, as in cartilage and other connective tissues, is the seat of the deposit. As in cartilage, he regards this necrotic state as typical of gouty deposits. About the necrotic area in which the deposit has occurred a secondary inflammation takes place, leading ultimately to contraction of the new fibrous tissue formed. He calls attention to the fact that (1) the kidneys may be perfectly sound in gout; (2) the kidneys may be the seat of chronic interstitial inflammatory changes, with cirrhosis, without any urate deposits of any kind being demonstrable; (3) there may be chronic interstitial nephritis, with crystallized urates in the urinary tubules.

As regards changes in the liver, few satisfactory accounts exist. Portal originally called attention to the fact that in gout and rheumatism indurations of the liver caused by the deposit of a phosphatic earth occurred, and Charcot has recently referred to the fact. Ebstein cites a case in which in a gouty patient he was able to make a diagnosis of moderate hypertrophic hepatic cirrhosis, but so far he had not been able to confirm it by post-mortem examination.6

6 Gout in Animals.—Of the occurrence of gout in animals not many reliable reports exist; Ebstein has collected a few. Thus, he cites a case where in an old hunting-dog uratic concretions were found in the articular ligaments and in the periosteum of the epiphyses of many joints, but especially those connecting the ribs with their cartilages. In the toes of falcons and of parrots kept in confinement deposits of urates have been observed, and in an alligator dying in captivity deposits were found in the muscles as well as the joints which consisted of free uric acid together with sodium urate.

Experimentally, Ebstein was able to produce gouty lesions having all the characteristics of those occurring spontaneously in man by injecting subcutaneously small quantities of the neutral chromate of potash into the blood of cocks for a considerable period of time. By this method changes in the epithelial elements of the kidney were produced, preventing the elimination of the urates from the blood and causing their consequent accumulation in the system. He obtained in this way typical deposits of urates in the joints, tendons, muscular sheaths, heart, and other organs, while the birds emaciated and finally died. But these experiments, which are extremely valuable and interesting, still need confirmation.

The experiment of tying the ureters of fowls is an old one. Galvani who was perhaps the first to perform it, employed it in his investigations on the kidney, and since then Zalesky, Pawlinoff, Von Schroeder, Colosanti, and others have made use of it in their experimented studies on the site of origin of uric acid. As a result of this operation deposits of urates occur in various organs. Ebstein, however, does not regard them as analogous to the gouty deposit in human beings, as they lack the feature of necrosis, which, as mentioned above, he considers as alone characteristic of the true gouty lesion.

SYMPTOMATOLOGY.—The development of true gouty lesions, whether of the acute or subacute form, is usually preceded by a period, more or less protracted, in which characteristic derangements of the health present themselves. These derangements may be conveniently classified as disturbances of primary digestion and as manifestations of malnutrition.

The disturbances of primary digestion are repeated attacks of flatulent dyspepsia, with pyrosis, colicky pains, alternate constipation and diarrhoea, and a scanty, high-colored, and heavy urine with uratic sediments. This dyspepsia may be accompanied with a variety of reflex nervous symptoms, such as pain in the nape of the neck and occiput, insomnia, palpitation, sighing respiration, singultus, and nausea. These symptoms are commonly described as due to biliousness, and are provoked by excesses in diet, and not unfrequently by moderate indulgence in certain common articles of food, such as sweets, fruits, farinaceous foods, and the fermented preparations of alcohol.

Derangements of nutrition are shown by a disposition to erythematous and catarrhal affections of the skin and mucous membranes, to affections of the sebaceous glands, and to premature falling of the hair. There is often a more or less marked tendency to obesity. Accompanying these derangements there may be a loss of energy, both physical and mental, manifesting itself in indolence and fatigue on slight exertion, in irritability of temper, with diminished intellectual activity and hypochondriasis. Neither the primary indigestion nor the nutritive derangements invariably precede the development of acute gouty lesions, nor are they necessarily followed when they exist by the articular signs of gout; but they are so commonly associated with the evolution of what are regarded as the specific lesions of gout that they may fairly be described as constituting its prodromal period.

ACUTE ARTICULAR GOUT.—A typical attack of acute gout is usually sudden. It seizes its victim without warning, and often rouses him from sleep with a vicious agonizing pain in the joint assailed. Examination will reveal a slight redness, heat, and puffiness of the part affected altogether disproportioned to the intensity of the pain; the tenderness is exquisite, and the torture is often aggravated by the occurrence of reflex spasms of neighboring muscles. There is usually moderate fever, and if the surface be exposed there may be a chill. Sleep is impossible and the restlessness uncontrollable. As the morning advances slight perspiration occurs, and sleep may become possible. With the abatement of pain there is coincident increase in the signs of inflammation: the joint swells, the skin becomes red and oedematous around the joint, and the superficial veins are distended. But, though the pain subsides with the occurrence of swelling, and usually in proportion to its degree, the tenderness and pain on any attempt to move the joint continue to be extreme. The day is passed in comparative ease, but the evening generally brings an exacerbation of pain and fever, and the night another paroxysm of agony—not as severe as the first, but severe enough to make the daylight a benison. The progress of the disease after the second day, provided it is confined to one joint, is usually marked by a steady and regular decline in the severity of the symptoms. If the attack is confined to a single joint, a week may elapse before the inflammatory signs subside, and it may be a fortnight before pressure can be borne or the mobility of the joint is restored. Occasionally the sufferings of an acute attack of gout may be protracted by successive seizures for several weeks. The fever during the attack is distinctly remittent, the evening exacerbation rarely exceeding 103° F.

The urinary symptoms before, during, and after an acute paroxysm of gout are interesting and important in their bearing upon the uric-acid theory of the disease. Garrod's statements upon this point are generally accepted, and have been confirmed by other observers. He says that previous to the attack the amount of uric acid in the urine is below the average—that during the paroxysm the proportion grows smaller, and only rises to the normal standard with the termination of the seizure. The reaction of the urine is strongly acid during the paroxysm. This is due probably to the increased excretion of acid phosphates. The quantity of the urine is generally diminished, the specific gravity increased, and the color deepened.

Attacks of acute gout are generally followed by improved health and capacity for physical and mental work and enjoyment. The blood seems to be purified, the processes of digestion and assimilation are once more normally performed, the equilibrium of the nervous centres is restored, and the evolution of all the vital energies proceeds with ease and vigor. This state of well-being may continue for a year or two years, or even a longer period, after the first attack, the immunity varying according to the intensity of the inheritance or the habits of life. The subsequent attacks are apt to occur at increasingly shorter intervals, and, as a rule, the acuteness of them tends to diminish. Gradually the dyscrasia becomes more profound, and the constitutional symptoms and structural changes which belong to the atonic and irregular forms of the disease are developed.

ATONIC GOUT.—Though subacute, irregular, or atonic gout is often the sequence of repeated attacks of the acute disease, it is not necessarily preceded by them, nor is acute gout invariably followed by a marked gouty dyscrasia. It is not uncommon for a well-characterized gouty habit to exist, manifesting itself by many and varied gouty phenomena, without the occurrence of any acute lesions, and repeated attacks of acute articular gout may occur without the development of the progressive impairment of health and the tissue-changes which distinguish the chronic malady. The recognition of this fact is important, inasmuch as the occurrence of acute gout is commonly regarded as an essential element in the diagnosis of the gouty dyscrasia. Acute articular attacks, as already noted, are very rare in women, in whom the subacute and irregular forms of the disease are by no means infrequent. So far as acute articular gout is of value in the diagnosis of the constitutional vice, it is perhaps as significant if established in the history of a near relative as in the individual in whom the disease is suspected.

The general symptoms of atonic gout—or, as it may more properly be called, the gouty dyscrasia—are similar to those which sometimes precede the development of the acute form. The difference lies in their persistence, in the subacute character of the local lesions, and in the absence of the relief to the constitutional symptoms which follows acute attacks.

The dyspeptic symptoms are perhaps the most pronounced and uniform in the history of the evolution of chronic gout. These symptoms have been already described, but the fact which seems especially to distinguish them is that they are chiefly provoked by the acid fermentation of the carbohydric elements of the food, the sugar and starches, and especially by the fermented preparations of alcohol; the ability to digest these articles of diet appears to be deficient in the gouty dyspeptic.

The changes in the urine in the gouty dyscrasia are especially important. In the formative stages of the gouty vice the amount of urine may not vary much from the normal quantity, but the proportion of solid constituents, especially of the urea, is increased, so that the specific gravity may rise to 1.030 or 1.035. The acid reaction is intensified by the excess of the acid urates and phosphates upon which the normal acidity depends. Sometimes crystalline deposits of uric acid, urates, and oxalates take place in the tubuli of the kidney and in the bladder, and lead to the nephritic and vesical irritations which are often the source of much inconvenience and pain. Where the urine is free from these crystalline constituents as it comes from the bladder it may deposit them within a few hours after its passage. At a later stage in the development of the gouty dyscrasia the quantity and quality of the urine undergo marked changes. The quantity is increased; the color is pale, partly in consequence of dilution and partly through a diminution in the amount of coloring-matter. The quantity may be so considerable as to constitute a polyuria. The reaction is neutral or only feebly acid; crystalline sediments of uric acid and calcium oxalate may occasionally appear, and the specific gravity may be so low as to indicate not only a relative but an absolute diminution in the daily excretion of urinary solids. Traces of albumen and of sugar are not infrequently observed.

The articular symptoms of chronic gout are subacute. They affect the joints, as a rule, which are most exposed to strain and injury, and hence are most common in the hands and feet, but they may involve the knee and the hips, the elbow and the shoulder, and even the intervertebral joints. The pain is less severe, because the tension is never so considerable; the tenderness is often a source of great discomfort; the swelling varies with the acuteness of the inflammatory process, the joints being more or less permanently enlarged by hypertrophic changes affecting the articular structures and by tophous deposits. The deformities are increased by ankylosis, by contractions, by absorption of the cartilages, by partial luxations, and by the atrophy of disused muscles. Crepitations are often observed in the affected joints. Exacerbations of the local symptoms are often provoked by movements, by imprudence in diet, by changes in temperature or in barometric and hygrometric conditions, and not infrequently by psychical disturbances.

The frequency with which tegumentary affections, mucous as well as cutaneous, are observed as correlative phenomena of arthritic lesions in gouty persons and in gouty families justifies the inference that the same lithæmic vice which determines articular inflammations is often responsible for derangements of nutrition in the skin and mucous membranes. The French school of dermatology, which has always maintained the humoral origin of many cutaneous diseases, has long recognized the arthritic nature of a large class of affections of the skin. Bazin7 has given the most precise description of the arthritides, as he terms them. He insists upon certain functional derangements of the skin as characteristic of the gouty diathesis, such as excessive perspiration, especially in certain regions, as the head, the axillæ, the hands and feet, and the sexual organs, and also affections of the sebaceous glands, causing the different forms of seborrhoea and the premature falling of the hair. He notes the liability in gouty persons to certain neurotic affections, such as pruritus, general or localized, about the arms and genital organs. Erythematous affections, especially urticaria, erythema nodosum, and the fugitive erythema which occurs about the face, causing sudden and evanescent swelling of the eyelids, cheeks, lips, and even the tongue and soft palate, are recognized by him and other observers as arthritic in their origin. Among the erythemata which are observed in gouty persons the peliosis rheumatica should be mentioned.

7 Affections génériques de la Peau, Paris, 1862.

The more persistent inflammatory lesions of the skin, such as eczema and psoriasis, which are characterized by long-continued hyperæmia with hyperplasia, are now recognized as among the possible transformations of gout. They are certainly often observed alternating with arthritic lesions, and associated with all the characteristic derangements of nutrition which belong to the gouty habit. The frequency of the various forms of acne, the inflammatory, as well as those which result from excessive function of the glands, in persons having a strong gouty inheritance, is recognized by many dermatologists. I have noticed these lesions especially in young women belonging to gouty families. They are generally accompanied by marked dyspeptic symptoms, and not infrequently by neurotic derangements.

Garrod, in a paper read at the International Medical Congress in 1881 on "Eczema and Albuminuria in Relation to Gout," affirms that each year strengthens his conviction that gout and eczema are most closely allied. Since his attention was first called to this relation in 1860, he has found a gradually increasing percentage of eczema in the cases of gout that have come under his observation. Dividing all the cases from 1860 to 1881 into ten groups, he found the percentage rose from 10 in the first group to 47 in the tenth. He accounts for this rapid increase in the percentage in the fact that in the first few years the eczema was only observed when it was very patent; during the past two or three years he has had made more careful inquiries as to the presence of eczema or other skin eruption in every case of gout, and by these means has frequently discovered its presence when it might otherwise have been overlooked. Garrod believes that eczema is the special skin-lesion of gouty subjects, and does not regard psoriasis as having anything more than an accidental connection with gout. He admits that the latter is often associated with rheumatoid arthritis. It must be remembered, however, that Garrod does not admit that gout ever exists without lithatic deposits.

In regard to the location of gouty eczema, it appears to affect by preference the more tender and vascular regions of the skin. The eyelids, ears, the scalp, and back of the neck, the fingers and toes, particularly the dorsal and lateral surfaces, and in old people the legs, are especially liable to be attacked. The subjective symptoms of gouty eczema are often the source of great suffering; the burning and itching are sometimes intolerable. This is especially true of persons of highly neurotic constitution.

It is not possible to affirm that there are lesions of the mucous membranes which are strictly analogous in their transient character to the erythematous affections of the skin, but it is not unreasonable to suppose that many of the temporary disturbances of indigestion to which gouty patients are subject are caused by an evanescent hyperæmia corresponding to the vaso-motor derangements which are observed in the external integument. In regard, however, to the more persistent catarrhal lesions, there can be no question as to their analogy with those which affect the skin. The continuity of these lesions at the orifices of the mucous tracts, and the frequent association of external eczemas with catarrhs of mucous membranes, are facts of common experience. Greenhow8 of London first called attention to the frequency with which chronic bronchitis is associated with the gouty dyscrasia. In an analysis of 96 cases of chronic bronchitis he elicited the fact that in 34 out of the 96 a distinct gouty history attached either to the patients themselves or to some of their immediate relatives. In 14 of the cases the patients were subject to attacks of acute regular gout as well as to bronchitis. He also noted the association in a number of cases of bronchitis and psoriasis with gravel and gout. My own experience confirms these observations, and also the alternations of catarrhal and parenchymatous tonsillitis, of pharyngeal and laryngeal catarrh, and of asthma and chronic bronchitis, with the more common manifestations of regular and irregular gout.

8 On Chronic Bronchitis, E. Headlam Greenhow, M.D., London, 1869.

The occurrence of subacute gastro-duodenal and intestinal catarrhs with hemorrhoidal complications is even more common that the catarrhal affections of the respiratory tract. The lesion, in fact, which gives rise to the manifold dyspeptic symptoms in gouty subjects is doubtless a catarrhal one.

The genito-urinary tract exhibits also the tendency to catarrhal affections in sufferers from the gouty dyscrasia. It is certain that gouty persons are especially liable to vesical catarrh, and it is generally admitted that rheumatic and gouty persons are particularly susceptible to gonorrhoea. My own experience leads me to suspect that chronic urethral discharge resulting from acute urethritis is more common in rheumatic persons than in those not having this taint. The etiological relations of gonorrhoeal rheumatism and kerato-iritis are still involved in obscurity, though I am inclined to believe that a careful examination of the personal and family history in cases of these diseases would establish the opinion that has been maintained as to their gouty origin.

The presence of albumen in the urine of persons suffering from acute gout is occasionally observed. Under these circumstances it is transient, and has probably no more significance than is usually attached to this symptom in the course of any acute febrile disease. In chronic gout it is by no means infrequently observed as a more or less persistent symptom. It is associated under these circumstances with a copious discharge of urine of pale color and low density, and with the general signs of what Rayer first described as the néphrite goutteuse.

The importance of this symptom is very great when we consider the insidious development of this form of disease and the difficulty of its early diagnosis. Recent investigations point to the value of the changes in the urine in the progress of the gouty dyscrasia as bearing upon this question. It has already been noted that in the early history of gouty persons the urine is often scanty, high-colored, excessively acid, of high specific gravity, occasionally albuminous and saccharine, and frequently depositing sediments of urates and calcium oxalate. McBride of New York9 has recently called attention to this condition of the urine and its association with high arterial tension as the functional stage of the granular kidney—as the stage, that is to say, during which the necessity of eliminating large amounts of imperfectly oxidized nitrogenous material maintains a constant state of renal hyperæmia, which finally induces the changes in the tubular and intertubular structures which constitute the anatomical features of this form of disease.

9 The Early Diagnosis of Chronic Bright's Disease, T. A. McBride, M.D., New York, 1882.

The occasional presence of sugar in the urine of gouty persons has already been noted. I have repeatedly observed this symptom in the urine of gouty dyspepsia. It occurs more commonly in obese subjects, and is usually intermittent and easily controlled by dietetic restrictions. In these cases it is not necessarily associated with a very large amount of urine. In chronic gout and in connection with the granular kidney a more serious form of glycosuria is occasionally observed. Under these circumstances it increases largely the polyuria which is characteristic of gouty nephritis, and is sometimes overlooked because it occurs in a urine of a low density, often not more than 1.010. It is not controlled by diet to the same extent that it is in the cases previously described, and is in my experience a prognostic sign of bad import.

Some of the most distressing symptoms to which gouty persons are especially liable are those connected with the passage of gravel from the kidney to the bladder. Where gravel alone passes, it may cause little uneasiness, and the fact is only recognized through the discovery of blood in the urine in connection with uric acid or calcium oxalate crystals. When, however, the sand forms concretions in the pelvis of the kidney, their dislodgment and passage through the ureter are accompanied by the well-known agonies of renal colic.

Dysuria is a symptom from which gouty persons often experience much inconvenience and suffering. It is usually associated with extremely acid urine of high density containing crystalline sediments. It may manifest itself only in frequent and painful micturition, or it may be associated with such a degree of vesical tenesmus as to cause retention and necessitate the use of the catheter.

DIAGNOSIS.—If the term gout be restricted to that form of arthritis in which an excess of urates is found in the blood with tophous deposits in the affected joints, the cartilages of the ear and nose, and in the subcutaneous connective tissue, then the diagnosis of this disease is a simple one. It is a disease with a pathognomonic sign. But if the pathology of gout consists rather in a more complex morbid condition of the blood, of which an excess of urates in the serum is only one of a number of phenomena, and not necessarily the sole and essential cause of the local lesions, then the question of diagnosis involves a consideration of all the correlated morbid conditions which are so frequently associated in gouty persons and gouty families as to justify the inference that they have a common origin in a perverted nutrition, the essential nature of which is imperfectly understood.

The very existence of the terms gouty rheumatism and rheumatic gout which are in common use shows that what is regarded by many excellent authorities as the confounding of distinct entities must have some foundation in clinical experience. If we consider gout, in its strictest pathological sense, acute inflammatory rheumatism, rheumatoid arthritis, or gouty rheumatism, and senile arthritis or the arthritis deformans and gonorrhoeal rheumatism as separate and distinct diseases, we shall find ourselves compelled to ignore certain common clinical facts which indicate a bond of union between them. Heredity, for example, is common to them all, and more than this, there appears to be a tendency to a differentiation of the taint in families. It is well known, for instance, that the children of gouty parents are especially liable to acute rheumatism, and acute rheumatism in youth is often followed by gout in later years. It is also a fact of common experience that while the men in gouty families are the victims of true gout, the women are apt to be the subjects of rheumatoid arthritis. The arthritis deformans which develops with the degenerations of advancing years is not infrequently associated with a family history of genuine gout. Gonorrhoeal rheumatism also, according to the experience of many trustworthy observers, often recognizes an inheritance to gouty lesions. But it is not alone in heredity and the differentiation of the type of the disease in families that the unity of these affections displays itself. The same disturbances of digestion which characterize the history of true gout are observed in those who are liable to acute rheumatism, to rheumatoid arthritis, and to arthritis deformans. It is true that excesses in food and fermented liquors do not determine, as in gout, attacks of acute rheumatism nor of the chronic forms of arthritis, for these latter diseases are commonly due to causes operating upon the nervous system, as exposure to cold and dampness or to physical or emotional shock of some kind; still, there is in the subjects of these diseases a more or less marked tendency to the same dyspeptic disorders, and especially to the diminished capacity in digesting the carbohydrates, which the subjects of true gout exhibit. In the diagnosis of gout, therefore, it would seem that the question of differentiating this disease from those which simulate it is not one in which we are called upon to distinguish one morbid entity from another, as typhus from typhoid fever or syphilis from cancer, but rather to determine, first, the presence of a recognized constitutional vice; and, secondly, to differentiate the variety of the lesions by which this vice manifests itself.

In the diagnosis of the gouty dyscrasia the first point to determine is that of heredity. This requires a careful inquiry into collateral as well as direct descent, and does not necessarily involve the discovery of arthritic diseases in the ancestors, though these are doubtless the most striking and trustworthy proofs; but the tradition in the family of persistent dyspepsia, or what is commonly called biliousness, of chronic catarrhal affections of the skin and mucous membranes, and of the chronic forms of renal disease, are significant indications of this dyscrasia. In the personal history the evidences of the lithæmic tendency, as indicated by the characteristic dyspeptic symptoms which have been described, and especially by the feeble capacity for the digestion of carbohydrates, are of great diagnostic value.

The diagnosis of gouty joint-lesions, whether acute or chronic, depends partly upon the determination of the gouty dyscrasia, and partly upon the differential distinctions which separate gouty inflammations from acute rheumatism, rheumatoid arthritis, and from the arthropathies which result from traumatism and from lesions of nerves and nerve-centres.

Gouty arthritis may be distinguished from acute rheumatism by the fact that it is more often hereditary—that it occurs in older subjects, attacking generally the smaller joints, and, as a rule, in the acute form, localizing itself in one or two joints. It is also noteworthy that the constitutional symptoms are not as severe as in rheumatism. Gout deforms the joints, while acute rheumatism leaves no traces of the inflammatory process. In addition to these distinctions there is, according to Garrod, the crucial test of an excess of urates in the blood-serum.

From rheumatoid arthritis or rheumatic gout, gout in its acute and regular form is distinguished by the more acute local and constitutional symptoms. Gout is periodical in its attacks, while rheumatoid arthritis is progressive. It attacks the smaller joints or those most exposed to strain, while rheumatoid arthritis occurs in the large as well as the small joints, and appears to be more independent of traumatism as an exciting cause. Gout is more common in men, rheumatoid arthritis in women. According to Garrod and other excellent authorities, deposits of urates are never found in the joints in rheumatoid arthritis, and there is no excess of urates in the blood. This statement is denied by Hutchinson. Ulcerations of cartilages, contractions of tendons, atrophies of muscles with subluxations of joints, are more common in rheumatoid arthritis than in gout.

While these local distinctions are undeniable, it is proper to observe that in rheumatoid arthritis the constitutional symptoms of the gouty dyscrasia, especially the dyspeptic derangements and the nervous disturbances, are often well marked; and it should also be noted that the principal distinction, the absence of urates in the blood and in the diseased joints, is one that is based on the exclusive theory that uric acid is the materies morbi of true gout. If, as is still maintained by some excellent authorities, uric acid is not essential to gout, then it must be confessed that the other distinctions are purely lesional, and that the common constitutional symptoms suggest that these diseases are divergent branches of a single trunk.

Gouty arthritis is not always easily distinguishable from traumatic inflammation of the joints, inasmuch as traumatism plays so important a part as an exciting cause of gouty attacks. The history of previous seizures and the presence of predisposing causes of gout are the points upon which the determination of the gouty nature of the inflammation would depend. A termination in suppuration would exclude the idea of the gouty nature of an arthritis.

With the arthropathies of purely nervous origin, such as occur in paralyzed limbs, in Pott's disease, and in tabes dorsalis, gout can hardly be confounded, although the arthritic complications in these diseases have been used to illustrate the neurotic theory of both gout and rheumatism.

The diagnosis of irregular gout—i.e. of gouty affections of the skin and mucous membranes, of the structures of the eye, and of the parenchymatous organs—must be based more upon the hereditary history and upon the correlated phenomena recognized in the personal history than upon any specific character in the lesions themselves. In the gouty form of nephritis there are, it is true, in the urinary symptoms, in the anæmia, in the arterial fibrosis, and in the cardiac hypertrophy, diagnostic signs of great value.

PROGNOSIS.—Acute, regular, articular gout is probably never a fatal disease where it occurs in a robust person without visceral complications. In rare instances the first attack may never be repeated, or only two or three attacks may occur in the course of a long life. In the majority of instances, however, frequent repetitions are the rule, the intervals between the attacks growing progressively shorter; occasionally repeated seizures go on through a long life, the attacks becoming milder with advancing years, and, save the crippling effects of the disease, the patient may enjoy in the intervals a fair degree of health. This, however, is the exception. With the increased frequency of the arthritic attacks the signs of the constitutional vice become more marked. The dyspeptic disorders become more persistent and rebellious to treatment, various transformations of the disease manifest themselves, and tissue-changes make insidious and inevitable progress. When this stage of the gouty disease is reached, the prognosis becomes more grave because of the complications and accidents to which the sufferer is liable. These complications and accidents are the result of the nervous, vascular, and visceral lesions which have been described. Vaso-motor instability gives rise to a great variety of painful functional derangements resulting from serious cerebral, pulmonary, gastric, and renal congestions. Glycosuria is not an uncommon complication in chronic gout, and seriously affects the question of prognosis. Arterial degenerations may cause thrombotic accidents, and the formation of miliary aneurisms in the brain may determine a fatal issue by softening or hemorrhage. Anginal attacks due to cardiac muscular degeneration may also imperil life.

The principal visceral lesion which leads directly or indirectly to a fatal issue in gout is that of the kidney. This involves danger either through the induction of a hopeless anæmia and its consequences in dropsical effusions, or by determining inflammatory accidents of the gravest nature.

That gout shortens life in the majority of cases is unquestionable—a fact which is sufficiently attested by the care with which life-insurance companies exclude risks in which a well-pronounced inherited tendency or existing manifestation of the disease can be substantiated.

The prognosis varies of course with the rapidity with which the constitutional dyscrasia is developed, and this rapidity will depend on the intensity of the inheritance and the mode of life. Some gouty subjects escape the vascular and visceral complications of the disease for a long period, although crippled and deformed by its articular ravages, and attain advanced age; others may succumb in comparative youth to its most profound lesions. It is a happy circumstance that under wise hygienic management and judicious medication acquired gout may be checked in its progress, and even a strong inherited tendency may be largely controlled.

TREATMENT.—A logical consideration of the treatment of gout embraces, first, the treatment of the constitutional vice, based, as far as possible, on the nature and causes of the disease; and, secondly, the treatment of the lesions which the disease determines. If we regard the accumulation in the blood-serum of the salts of uric acid as the essential cause of the gouty lesions, then the origin of the constitutional vice is in the conditions which bring about this accumulation. As we have urged, none of the theories of the production of the lithæmic state harmonize all its phenomena. It is impossible to represent the complex processes of nutrition by chemical formulæ, and equally impossible to divorce chemical reactions from a share in their production. We can trace the metabolism of the azotized and carbonaceous foods through many changes to their ultimate disintegration into urea, carbonic acid, and water, but we do not know all the steps by which this conversion is effected, nor the organs or tissues in which it is accomplished. We may reasonably assume that the agent through which the potential energy of the food is evolved is oxygen, and that the process of nutrition is hence partly, at least, a process of oxidation. This chemical view of the digestion and assimilation of food may be said to be the rational basis of the treatment of the lithæmic state. To control the accumulation of azotized matters in the blood, and to secure their thorough combustion and conversion into urea, carbonic acid, and water are the recognized aims of the treatment of the vice upon which gout depends.

DIET.—The prevention of the accumulation of azotized matters in the blood involves, first, a consideration of the question of the diet appropriate to the gouty dyscrasia. The almost uniform counsel upon this point of all the authorities from Sydenham to the present time is, that albuminous foods should be sparingly allowed in the diet of the gouty patient, and that vegetable foods, especially the farinaceous, should constitute the principal aliment. This counsel is based upon the theory that uric acid is the offending substance, and, this being the outcome of a nitrogenous diet, the nitrogenous element in diet must be reduced. My own observation has led me to believe that while this may be a legitimate deduction from the uric-acid theory of gout, it is not supported by the results of clinical experience. If there is one signal peculiarity in the digestive derangements of gouty persons, it is their limited power to digest the carbohydrates, the sugars and starches. In whatever form these foods are used, they are more commonly the source of the dyspeptic troubles of sufferers from gout than the albuminous foods. They provoke the acid and flatulent dyspepsia which so generally precedes the explosion of the gouty paroxysm; and it must have attracted the attention of every observer who has studied the dyspeptic disorders of sufferers from inherited gout, who have sought to control their unhappy heritage by abstemious habits, that these disorders are especially provoked by over-indulgence in saccharine and amylaceous foods.

It is not possible to explain satisfactorily why the lithæmic condition should be induced by the carbonaceous aliments, but we believe there can be no question as to the fact. If, as modern physiological investigations tend to show, the liver is the organ in which urea as well as glycogen is formed, it may be that the overtaxing of its functions manifests itself more readily in the conversion of the albuminous than in that of the carbonaceous foods; or it is possible that the carbonaceous foods are destined chiefly for the evolution of mechanical energy, and that when this destiny is not fulfilled through indolence and imperfect oxygen-supply, they escape complete combustion, and so vitiate the blood. But whatever may be the cause of this anomaly, the clinical fact remains that in gouty persons the conversion of the azotized foods is more complete with a minimum of carbohydrates than it is with an excess of them—in other words, that one of the best means of avoiding an accumulation of lithates in the blood is to diminish the carbohydrates rather than the azotized foods.

The diet which a considerable experience has led me to adopt in the treatment of the gouty dyscrasia is very similar to that which glycosuria requires. The exclusion of the carbohydrates is of course not so strict. Abstinence from all the fermented preparations of alcohol is perhaps the most important restriction, on account of the unfermented dextrin and sugar which they contain. This restriction accords with the common experience respecting the part which wine and beer play as predisposing causes of the gouty disease and as occasional exciting causes of gouty lesions.

Next to the fermented liquors, the use of saccharine food in the diet of gouty persons needs to be restricted. This limitation also is one which common experience confirms. Sweet foods cannot be said to be as provocative of the dyspeptic derangements of the lithæmic subjects as wine and beer, but they are certainly often responsible for the formation of the dyscrasia and for perpetuating many most distressing ailments. Their more or less strict prohibition may constitute the essential point of treatment not only in controlling the progress of the constitutional vice, but in subduing some of the most rebellious lesions. It is important to observe that this prohibition sometimes involves abstinence from sweet and subacid fruits, in the raw as well as in the preserved state. Paroxysms of articular gout have been known to follow indulgence in strawberries, apples, watermelons, and grapes, and the cutaneous and mucous irritations which follow even the most moderate use of these fruits in some gouty persons are certainly not uncommon.

Next in order to the saccharine foods as the source of indigestion in gouty persons come the amylaceous aliments. These constitute, necessarily, so large an element in ordinary diet that the limitation of them in the dietary of gouty persons applies, in the majority of cases, only to their excessive use. This excessive use, however, is often observed. There is a popular prejudice in favor of this class of foods, and a corresponding prejudice against the too free indulgence in animal foods. The purely starchy aliments, such as potatoes and the preparations of corn and rice, and even those which contain a considerable portion of gluten, like wheat, oatmeal, and barley, often provoke in gouty subjects a great deal of mischievous and painful indigestion. This feeble capacity for the digestion of farinaceous foods is most frequently observed in the children of gouty parents, and especially in persons inclined to obesity, and in those whose occupations are sedentary and whose lives are passed for the most part in-doors, and they are least common in those whom necessity or pleasure leads to much active muscular exercise in the open air.

The fats are as a rule easily digested by gouty dyspeptics. This is a fortunate circumstance, for the reason that in the anæmia which is frequently one of the consequences of chronic gout the fatty foods are of inestimable value. In cases of persistent and rebellious lithæmia an exclusively milk diet constitutes a precious resource.

The succulent vegetables, such as tomatoes, cucumbers, cauliflower, cabbage, and the different varieties of salads, constitute for the gouty as well as the diabetic subject agreeable and wholesome additions to a diet from which the starchy and saccharine vegetables have to be largely excluded.

The quantity of food proper for gouty persons to consume can only be determined in individual cases by the age, the habits, and the occupation. It is fair to assume that in adults, in whom there is no longer any provision to be made for growth, the daily quantity of food must be regulated according to the amount of energy which is expended. In this energy must be reckoned the amount necessary for the maintenance of animal heat and the other vital functions, and the amount which is necessary for the operation of every variety of nervous force. In other words, the potential energy latent in the food must correspond to the active energy exhibited in the daily evolution of vital, intellectual, and mechanical work. The more nearly this balance is maintained the more closely the physiological standard of health is preserved. That an excess of food is a most frequent cause of the gouty dyscrasia among the well-to-do classes is undeniable, and it is possible that regulation of the quantity according to the rule above mentioned may, after all, be the most important point in the management of many gouty patients. It may be, also, that the reason why the withdrawal of the carbohydrates produces its good effects upon these patients is that we thereby exclude a large amount of force-producing foods which do mischief because they are imperfectly consumed.

EXERCISE.—Next in importance to diet as a hygienic regulation in the management of gouty patients is enforced exercise. The axiom of Abernethy, "to live on a shilling a day, and earn it," comprises the philosophy of the true relations of food to work, and of both to the highest development of physical health. Exercise is to be enforced not simply as a means of securing an active respiration, and thereby an abundant supply of oxygen, but also as a means of converting the potential energy of the food consumed into vital energy. The essential condition, moreover, of healthy nutrition in every organ and in every tissue is the maintenance of a vigorous functional activity. Over-use is not more productive of tissue-degeneration than disuse. Hence the question of exercise in its largest sense involves not only muscular work, but work of all kinds, which tends to promote a healthy activity of the psychical as well as the physical functions. Muscular exercise in the open air has a special value for the victims of this gouty dyscrasia by equalizing the circulation, quickening the respiratory movements, and stimulating the elimination of effete matters from the skin and lungs, but mental work and wholesome diversions are not less important as antagonizing the evil effects of indolence and over-feeding, which are among the common predisposing causes of acquired gout. In persons who are incapacitated by neuræsthenia or by excessive corpulence, the result of long indulgence in indolent and luxurious habits, it may be necessary to resort to passive exercise by rubbing, massage, and electrical excitation in order to secure the good effects of voluntary work.

BATHING.—Another hygienic regulation of great value in the treatment of gouty dyscrasia is the promotion by bathing and friction of the eliminative function of the skin. Daily sponging with cold water, where it is not contraindicated by a feeble circulation and a slow reaction from the shock, is a practice to be commended. Where, for the reasons mentioned, it is not practicable, tepid baths and frictions may be substituted. In cases where the arthritic lesions are progressive and advanced much benefit may be derived from hot baths. It is doubtful whether the thermal alkaline and sulphur spas owe their renown in the treatment of chronic gout so much to the mineral ingredients of their springs as to their high temperature. The Russian and Turkish baths furnish most efficient means for increasing the functional activity of the skin, but they often have a depressing effect on the action of the heart, producing faintness and dyspnoea, and should always be advised with caution.

CLIMATE.—In rebellious forms of the gouty dyscrasia a warm climate is unquestionably a hygienic condition of great value. The geographical distribution of gout, which shows that the disease is much less common in warm than in temperate and cold climates, while it may not perhaps be wholly explained by temperature alone, is very certainly largely due to it. The possibility of out-door life and the increased functional activity of the skin which warm climates favor are circumstances more or less antagonistic to the development of the gouty diathesis.

MEDICINAL TREATMENT.—The objects to be aimed at in medicinal treatment of the gouty dyscrasia are—

1st, the improvement of the primary digestion.

2d, the relief of the gastro-intestinal catarrh, which is the cause of the direct and reflex dyspeptic symptoms which belong to this diathesis.

3d, the augmentation of food-oxidation, so as to secure its thorough combustion.

4th, the promotion of the elimination of the waste products of nutrition.

1. The improvement of primary digestion—or, as it has been aptly called, exterior digestion—often requires very strict attention beyond the proper selection of alimentary substances. The distressing symptoms that indicate primary gastric and intestinal indigestion are certainly often relieved by the rigid exclusion of certain articles of diet, but in many cases it is necessary to assist the preparatory processes which are essential to perfect food-absorption by artificial methods based upon the knowledge derived from physiological experiment. To no one is the knowledge of these methods more largely due than to Roberts of Manchester. Preparations of pepsin and pancreatin, by which the proteids and starches are peptonized and the fats emulsified, are often of inestimable value in the treatment of gouty dyspepsia. Pancreatin, especially, which by means of its trypsin, diastase, and emulsive ferment possesses the threefold property of aiding the digestion of the azotized, amylaceous, and fatty elements of food, is certainly the most valuable of the artificial means for augmenting the efficiency of primary digestion.

2. The relief of the gastro-intestinal catarrh in gouty dyspeptics may often be accomplished solely by dietetic restrictions and by the aid which may be given to primary digestion. It is often necessary, however, to direct some special medication toward the relief of the catarrhal lesion. The circumstances which demand this special medication are the existence of portal congestion, the result of functional derangement, or of chronic atrophy of the liver, or of chronic diffuse or interstitial nephritis, or of cardiac disease. The hydragogues, such as calomel, podophyllin, colocynth, and other vegetable cathartics, with the salts of sodium and magnesium, constitute the most common and efficient means of relieving portal congestion, whether it arise from temporary functional derangement or from organic disease. The renown of some of the more famous mineral springs in relieving the miseries of gouty sufferers is due mainly to the relief of portal congestion and the washing away of the catarrhal mucus which obstructs the process of primary food transformation and absorption. This is especially true of the sulphate of sodium waters, like those of Carlsbad, Marienbad, Friedrichshall, Pullna, and Hunyadi János. While the value of these waters in chronic gout is unquestionable where their use is properly regulated, there is good reason to believe that their long-continued employment is often harmful by relaxing the mucous membrane, and thereby tending to aggravate the condition they are given to relieve. This is markedly true of their use in weak and anæmic persons. For these the milder magnesian waters, such as those of Kissengen, Hombourg, Wiesbaden, and Saratoga, are to be preferred.

3. The augmentation of food-oxidation may be accomplished in a large degree by regulation of the diet and by out-door exercise. The regulation of the diet according to the occupation and habits of life is a point of primary importance in securing proper blood-elaboration. My experience leads me to believe that the evil consequences of in-door occupations and sedentary habits are most common in those who live upon a diet composed largely of starchy and saccharine foods, and that a diet in which animal foods and fats predominate is best suited to indoor workers, whether they be engaged in mechanical or intellectual labor.

The medicines which help to promote the oxidation of the food-elements, especially the carbohydrates, are alkalies and iron. Clinical observation establishes this fact as strongly in the treatment of gout as in that of glycosuria. The relative power of the salts of potassium and sodium in augmenting oxidation is not clearly determined. The salts of sodium appear to be most useful in aiding the process of primary digestion, and the potassium salts in improving the process of sanguification. It is well known that potash predominates in the corpuscles and soda in the serum of the blood. The efficacy of the combinations of iron with the salts of potassium, as in Blaud's pills and in the citrate and tartrate of iron and potassium, in the treatment of anæmia, is well known. In the most renowned ferruginous springs, however, such as those of Schwalbach, Spa, Pyrmont, and St. Moritz, the iron is combined with salts of sodium, calcium, and magnesium. It would appear, therefore, that the increased energy of iron in augmenting hæmatosis, when combined with alkalies, is not relatively greater with potash than with either of the other alkaline bases.

4. The promotion of the elimination of the waste products of nutrition is to be accomplished by remedies which act as solvents of uric acid and as diuretics. As solvents of uric acid the salts of lithia and potash have been shown to be superior to those of soda. The urate of lithia is the most soluble of the uric-acid salts, and the low chemical equivalent of the metal lithium makes the neutralizing power of the oxide much greater than that of equal proportions of the other alkalies. It is used in the forms of carbonate and citrate, and is generally combined with potash and soda. It exists in some of the mineral springs of Europe and of this country, but in such minute proportion as probably to be of little value. In administering the salts of potash and soda it is generally admitted that the carbonates and the neutral salts of the organic acids are to be preferred to solutions of the caustic alkalies. They have less power in neutralizing the acid of the gastric juice, and enter the circulation as neutral salts, where they are decomposed into alkaline carbonates by the oxidation of the organic acids, increasing the alkalinity of the serum and acting as diuretics. The combinations of the alkalies with sulphur, with iodine, and with mineral acids, as in the alkaline springs, are frequently used in the treatment of gouty lesions of the subacute variety. The sulphur salts probably owe their chief value to their alkaline bases when they are used internally; and in sulphuretted baths, as before remarked, the good effects are probably due to the high temperature at which the bath is usually administered.

The salts of iodine are generally supposed to have a special action in removing the consequences of chronic fibrous inflammation in gout and rheumatism. They often disturb the digestion and provoke troublesome irritations of the skin and mucous membranes. In removing the sclerotic effects of gouty inflammation they do not exhibit the same sorbefacient power which they show in their action upon the granulation tissue of syphilitic origin. It must be admitted, however, that in certain catarrhal affections of a gouty nature the iodides of potassium and sodium are almost specific in their good effects. In the pharyngeal, laryngeal, and bronchial catarrhs from which some gouty persons suffer, where there is a dryness and irritability of the mucous membrane, the administration of these salts produces the most prompt and beneficial result. As solvents of uric acid they do not appear to equal the salts of the organic acids.

As to the mode of administering salines in the treatment of the gouty dyscrasia, it is hardly necessary to observe that it must vary with the effect desired. As antacids in acid dyspepsia they should be given soon after meals, and for this purpose the salts of soda are to be preferred, for the reason that they not only neutralize excessive acidity, but they increase the efficiency of the peptonizing process. Where it is desired to introduce these salts into the circulation for their solvent action, as diuretics or to assist the process of sanguification, they should be given three or four hours after meals and largely diluted with water.

Before concluding the consideration of the treatment of the gouty dyscrasia it should be remarked that the ability of water as a solvent, as a means of stimulating tissue-changes and eliminating waste, is not generally estimated at its true value. The use of copious libations of hot water in the treatment of gout, recommended by Cadet de Vaux in 1825, has been revived from time to time, and is at present attracting considerable attention.

TREATMENT OF ACUTE ARTICULAR GOUT.—There are three distinct methods of managing an attack of acute gout—the antiphlogistic, the expectant, and the abortive.

The antiphlogistic method, in the strict application of the term, is practically obsolete. Bloodletting, both general and local, brisk catharsis and diaphoresis, with low diet, were formerly advocated as the natural and imperative antagonists of gout as well as of all other acute inflammatory affections. Carried to its extreme degree, this method was deprecated by Sydenham and his disciples as tending often to prolong the attack and precipitate the manifestations of atonic gout. The natural reaction from the vigorous antiphlogistic practice was what has been termed the expectant method.

The expectant method may be said to be founded upon the aphorism of Mead that "gout is the cure of gout." The discovery of the salts of uric acid in the blood-serum and in the affected tissues gave a scientific basis to the humoral pathology of gout and led to the formulation of definite principles in the application of the expectant method of treatment. These principles are the prevention of the further accumulation of the urates in the blood and the promotion of their oxidation and elimination. The first principle involves restriction to a rigid diet during the attack, excluding albuminous foods and the fermented preparations of alcohol, and allowing only milk and farinaceous gruels. The oxidation of the urates is encouraged by the administration of alkalies and by an abundant supply of air, the inhalation of oxygen even having been recommended. The elimination of the urates is accomplished chiefly by diuretics and moderate catharsis. The local treatment commonly used with this medication consists in the application of alkaline and anodyne fomentations or of dry flannel or cotton. Local bloodletting and blistering are now rarely commended. Under this treatment the intensity of the inflammatory process is abated, the suffering is allayed, but the progress and duration of the disease are not materially modified. The recovery, however, is satisfactory, and it is claimed that the chances of early recurrence of the attack are diminished. This method has many advocates, though it cannot be said to represent the common practice of the present day. It is becoming traditional, and may be said to be gradually giving place to the specific or abortive method.

The abortive method consists in cutting short the attack by the administration of colchicum, veratria, or the salicin compounds.

The value of colchicum in joint affections is a tradition of the earliest records of medicine. It shares its curative effects in acute gout with veratria, and, though the active principle of the meadow saffron and the veratrum album are not isomeric, their effects are similar. They constitute the basis of the famous nostrums so extensively patronized by sufferers from gout. Colchicum is the active agent in the eau médicinale de Husson, in Wilson's and Reynolds's specifics, and in the pills of Lartigue and Blair, while veratria is supposed to be that of Laville's remedy. The action of these substances is not understood. The physiological action of colchicum is that of a local irritant and a cardiac depressant of great energy. It purges violently when given in large doses, causes nausea and vomiting, and may produce collapse. In therapeutical doses in a gouty paroxysm it acts as a diuretic and an antipyretic, and allays, sometimes in a most magical manner, the objective and subjective symptoms of the disease. As simple purging by other cathartics does not abort the gouty seizure, the value of colchicum cannot be ascribed to its purging effect, and, besides, purging is by no means necessary to its efficiency. Nor can its utility be ascribed to its diuretic property. There is some question in regard to its claims as a diuretic, and there seems to be no doubt that it often does good where this effect is not observed. Its influence upon the heart does not explain its marvellous action upon the local process, for the same influence obtained by other drugs has no such result. We are driven, therefore, to the conclusion that colchicum has a specific action in gout as certain and as inexplicable as that of quinia in malarial fever, or iodide of potassium in constitutional syphilis. For those who accept the theory that gout is a tropho-neurosis the therapeutical action of colchicum is a strong confirmation of its neurotic origin, for the reasons that colchicum has no influence upon arthritic lesions which are not gouty, and that its physiological effects point to its action on the nervous system.

It is useless, however, to speculate on the way in which colchicum and allied substances affect gouty inflammation; the practical question to be determined is: Are they the best and safest remedies to control it? Upon this point there is a wide diversity of opinion. The objections to the colchicum treatment are based upon humoral pathology, and upon the idea that the attack is an effort of nature to cast out the poison and purify the blood. Colchicum, it is claimed, arrests this process; the poison is retained, diffuses itself through the tissues, and lays the foundation of vascular and visceral lesions. It shortens the intervals between the attacks, and tempts the patient to continued indulgence in the habits which perpetuate and exaggerate the disease. The advocates of the abortive treatment, on the other hand, claim that these arguments have no real force as applied to its therapeutical value. The cure accomplished is, to all appearances, complete, and the patient is saved the suffering and exhaustion which result from the expectant method. The fact that he is so easily and speedily cured, and that he resumes his vicious habits and suffers recurring attacks in consequence, proves only that the treatment lacks the quality of moral discipline which belongs to prolonged suffering and the penance of vigorous medication. It is an acknowledged fact that the great majority of sufferers from acute gout decide sooner or later in favor of the abortive treatment; and as professional opinion has heretofore generally advocated the expectant or eliminative treatment, they commonly resort to the use of some one of the quack remedies which contain colchicum or veratria.

In view of the present uncertainty of our knowledge of the true pathology of the acute gouty arthritis, as to whether it is a tropho-neurosis or the result of the local irritation caused by the salts of uric acid, the specific treatment seems to be justified by a regard for the comfort of the patient and as a means of protecting him against falling into the reckless use of quack remedies. A speedy relief of the acute symptoms, followed by the treatment appropriate to the gouty habit, would seem to be the most rational and safest mode of managing the acute articular attacks of gout.

The selection of the preparation of colchicum in the treatment of an acute paroxysm is a matter of individual experience and preference. The acetous extract and the wine of the seeds are most commonly used, and many practitioners are not scrupulous in prescribing the proprietary preparations of Reynolds, Laville, and Blair. The wine of colchicum may be given in doses varying from 20 to 40 minims, alone or combined with Epsom salts in drachm doses, with small quantities of opium, every six or eight hours. Under this medication the pain, tenderness, and swelling rapidly abate, and sometimes with an abruptness that is magical. As soon as the acute symptoms subside, the colchicum should be continued in smaller and less frequent doses until the fever and local tenderness subside. The use of quinia with small doses of colocynth after the colchicum has been discontinued helps to re-establish the strength and regulate the digestive functions. The patient should always be warned against the possible demoralizing effects of a speedy recovery from a serious disease. Recurrence after the colchicum treatment is certainly more common than after the expectant method, but this should not be ascribed so much to a defective cure as to the temptation which the antidote offers to trifling with the poison. The accidents which have been ascribed to colchicum through its causing heart-failure are probably to be explained by its injudicious administration in large doses where acute gout is complicated with cardiac or renal degeneration.

Next in importance and value to colchicum in the abortive treatment of gout are salicin, salicylic acid, the sodium salicylate, and the oil of wintergreen. Unlike colchicum, which has no marked effect upon acute rheumatism, these medicines appear to act with similar energy on gout and rheumatism. The rapidity and the almost uniform way with which they allay the inflammatory symptoms in rheumatic fever are well known; their value as specific remedies in both acute and subacute gout is not so generally appreciated. Whether the specific action of colchicum in gout differentiates this disease from rheumatism, or whether the similar action of the salicin compounds indicates that these diseases are allied in their etiology, are questions yet to be solved. The good effects of salicin and the sodium salicylate in many of the forms of irregular gout, and notably in the dyspeptic disorders and the erythematous tegumentary lesions, are especially worthy of notice. In acute attacks of articular gout the salicylic acid or the sodium salicylate, in 15 or 20 grain doses repeated every three or four hours, will often cut short the attack, and will very certainly allay within twenty-four hours the acuteness of the symptoms. As in rheumatism, the medicine should be continued in smaller doses after the acute symptoms have subsided for several days, the tendency to relapse being marked if the drug be discontinued too soon. In subacute articular gout and in the irregular forms of the disease, where the medicine has to be continued for some time, salicin and the oil of wintergreen are to be preferred to salicylic acid and the sodium salicylate. They are less liable to disturb the stomach and to produce toxic effects.

It is unnecessary to describe the treatment of the different forms of irregular gout, inasmuch as the general principles described in the treatment of the gouty dyscrasia involve the most important considerations in the management of these affections.

RACHITIS.1

BY A. JACOBI, M.D.


1 There is a difference of opinion as to the correct spelling of this word, and strong reasons exist to regard the form rhachitis as the proper one. It is true that this spelling of the word has been remarked upon as unorthographical by many, mostly modern, authors. Even Virchow writes "Rachitis," claiming that Glisson took the term from "the then popular rickets." This is a mistake, as H. Rohlffs points out (Deutsches Arch. f. Gesch. d. Med., 1883, p. 294). Rachitis is a Greek word, and was used in the classical time of Hellenism. It has, however, seemed best to preserve here the usual spelling, rachitis, which has become sanctioned by general usage.

DEFINITION.—Rachitis is a general nutritive disorder, almost always of long duration, usually with an introductory stage of weeks or months and a course mostly extending over months or years. Its beginning is mostly gradual, its final recovery slow. It is complicated with or dependent on disorders of the digestive or respiratory apparatuses, which are preceded by a disposition probably created by an undue width of the arteries. It exhibits amongst its prominent symptoms muscular debility; perspiration; anomalies of the subcutaneous tissue, which is either very much infiltrated with fat or deprived of it; disturbances of the intellectual and moral functions, and of those of the large thoracic and abdominal viscera and lymphatic glands; changes in the latter may outlive all others. Its most perceptible symptom, however, consists in an inflammatory disease of the primordial cartilage of the epiphyses, a copious deposit in that region and also under the periosteum of the bones; curvature of the diaphyses, and, while absorption remains intact, softening and retarded ossification of the bone. Without these affections of the osseous system the diagnosis of rachitis is not complete.

ETIOLOGY AND PATHOLOGY.—The nature of rachitis has been considered to be inflammatory by F. A. Walter.2 Renard looked for that inflammation in the periosteum. Guérin emphasizes the vascular increase in periosteum, bone, and marrow; Trousseau and Lasègue the congestive character of the local tumefaction, besides fever and pain. Virchow also3 inclines to the opinion that the rachitical process is of an inflammatory nature, though it be impossible to state the exact cause of the process. Still, he claims that we are no better off in regard to other inflammations of unknown character—for instance, those of the skin—and that we have to look for a future increase of our knowledge of such constitutional predisposition of the organism and of such specific qualities of the blood as will produce the local irritation of the osseous tissue in rachitis. Last, and mainly, it is Kassowitz who seeks the essence of the rachitical process in a chronic inflammation originating in the points of apposition of the growing bones of the foetus or infant. During the chronic inflammation blood-vessels are formed in large numbers, and a morbid congestion takes place in all blood-vessels, but mainly in those of the localities in which new bone is forming; thus in the chondro-epiphyses, in the perichondrium and periosteum, and the sutural substances. Faulty introduction or elimination of lime has nothing to do with this process. It cannot be deposited in the current of a copious circulation; in fact, it is not deposited in the immediate neighborhood of blood-vessels to any extent. Even in otherwise normal bone hyperæmia produced by the experimenter softens the bone, which was fully formed before. If the relative percentage of lime were of any account in the etiology of rachitis, the periosteal and cartilaginous proliferations would find no explanation. But why is it that this peculiar process takes place at an early age only? and in the bone only? Kassowitz urges the fact that the growth of the bone differs in this from the development of all other tissues: that the latter grow uniformly through their whole mass; that the circulation in them is more uniform and carries material through and into every particle simultaneously, while in the bones the only places in which the whole circulation can contribute to their growth—the few blood-vessels distributed in the interior not adding to their growth at all—are the periosteum and the places of apposition between epiphysis and diaphysis. Every morbid irritation, whether resulting from bad air, habitation, and food, or from either chronic or acute ailment, acts on the whole mass of other tissues and organs, but in the bones only on the growing ends or surface.

2 Anatom. Museum, Berlin, 1796, vol. ii.

3 Arch. f. Path. Anat., vol. v.

The results of the pathologists and experimenters are confirmed by chemical analyses. Fat has been generally found somewhat increased in the rachitical bones, and water largely so; chondrin is diminished according to Marchand and Lehmann, but was found unaltered in the later analyses of A. Baginsky. The latter found, after having deprived the bone of fat, the organic and inorganic material to be in a proportion of 100 to 563 in the normal, and of 100 to 160 in the rachitical osseous tissue; and in 100 parts of dry bone, Gorup-Besanez found in the

Ossein.Phosphoric Acid.Lime.Manganese Oxide.
Healthy adult3426340.3
Infant of six months34.927350.5
Rachitical femur72790.3
Rachitical tibia6012.9170.3

Defective calcification of the forming bone is one of the principal characteristics of rachitis. In it lime cannot either enter into the composition of the osseous tissue or remain in it. Its elimination must take place either through the kidneys or the intestinal tract. In the feces Ad. Baginsky, and many before him, have found an abnormal quantity. In regard to the urine, modern investigations do not agree with former analyses. Thus, Baginsky concludes that there is no increase of lime in the urine of rachitical as compared with that of healthy children; Seemann found even a diminution of the percentage of lime. Amongst modern writers only Rehn found an occasional increase of lime in the urine of rachitis.

In regard to the elimination of phosphoric acid, the analyses of different periods do not agree any better. The conclusions of previous researches, pointing to a quadruple elimination of phosphoric acid in the urine of rachitis, are refuted by Seemann, who found no increase, and by Baginsky, according to whose researches the phosphoric acid of the healthy urine compares with that of rachitical urine as 40:12-37.

As far as the elimination of nitrogen is concerned, there appears to be but little difference between normal and rachitical urine. Chlorine was found to be diminished in rachitis by Baginsky. Lehmann and Von Gorup found lactic acid several times. Several times albumen was met with; in a case of Ritchie's, blood; in one of Von Gorup's, fat.4

4 E. Salkowski und W. Leube, Die Lehre vom Harn, 1882, p. 536.

The etiology of rachitis must be studied from two points of view. It has its predisposition and its direct and proximate causes. The former has been studied by F. W. Beneke5 upon an anatomical basis. He finds that the arteries of rachitical patients are large all through the body. This is so particularly in the carotids; it seems probable that the changes taking place in the head are due to this anomaly in the size of the arteries. Three cases in which the width of the arteries of the neck was unusually large terminated fatally—one by hydrocephalus, one with a very large skull, and one suddenly. This width of the arteries is most marked, under ordinary circumstances, from the second to the fourth year; that is, the exact time in which (except the cases of early rachitis) the rachitical process is at its height. It is considered by Beneke to be the cause of the local increase of vascular irritation, particularly in the epiphyses with their retarded circulation; and also of the increase of nutritive development which is so often noticed during recovery from rachitis; and, finally, of the many pulmonary complications of an inflammatory nature.

5 Die Anatomischen Grundlagen der Constitutions Anomalien des Menschen, 1878, p. 75, etc.

There is another interesting consideration in regard to the effect of wide arteries on the relations between the blood and tissues. A great many more blood-cells are required to fill the arteries when wide than when narrow. Now, the formation of blood-cells is hindered by any disease of the digestive and blood-preparing organs, so that the tissues are liable to show the relative increase in the percentage of water, which is uniformly confirmed for rachitis by the biochemists.

The pulmonary artery of the healthy infant is larger than the aorta by not more than four millimeters. In the majority of cases of rachitis examined by Beneke this difference in size was very much more favorable to the pulmonary artery; it is abnormally large in rachitis. This anatomical fact is suggestive of the pathological processes so frequently found in the lungs and in the neighboring lymphatic and large abdominal glands. For, while the amount of blood introduced into the lungs through its wide artery is unusually large, particularly so in a chest which is contracted in consequence of the rachitical process in the bones, the exit from the lungs is relatively impeded. Not only, however, the narrowness of the chest is a cause of this disproportion. For even in rather normal chests the lungs of rachitical children are relatively small.

The liver of almost all rachitical children is large. In but one-half of the cases this enlargement is accompanied with a large heart. In pure cases of scrofula, on the contrary, Beneke found a small heart, rather narrow arteries, and usually a small liver, the size of the lungs offering but few anomalies.

The spleen also is large in the majority of cases. Its size is not dependent on the large size of the liver or the small size of the lungs. For these conditions are found in the majority of cases only, not in all of them, and the large spleen is not always found with a large liver and small lungs. The variability of the anatomical conditions permits of various degrees of combination; so that varying combinations of rachitis with other constitutional disorders may correspond with the different sizes of the principal organs. After all, as there is a great deal of independence of these organs, as to size, of each other, the conclusion is justified that those differences are not the result of the disease, but that they are congenital and stand in some causal relation with it.

The kidneys are large in the majority of cases, like the spleen and liver, while the lungs are small. This disproportion is apt to result in a hyperæmic condition of all the organs of the abdominal cavity, and especially of the kidneys. To what extent this undue amount of volume interferes with, or increases, renal secretion, it is difficult to say. The amount of urine secreted by rachitical children is about normal, though, as already stated, the percentage of lime in it is rather diminished, contrary to the opinions held formerly.

For the direct cause of rachitis Glisson looked to the inequality of nutrition by the arterial blood, and for that of the curvature of the long bones to their superabundant vascularization. He found the disease mainly amongst the well-to-do classes, not unlike a modern American writer, who declares infantile paralysis to be the result of the nervousness of the better classes of the American people! John Mayow (1761) held a disturbance of the innervation responsible; Zeviani (in the same year), improper food in general, and particularly prolonged lactation; and Selle (1791), a peculiar diathesis (acrimonia rachitica). About that time a defective nutrition with abnormal function of the lymph-ducts was looked upon as the cause of rachitis by many—by others, an undue production of acid, and the softening of the osseous tissue thereby. This result was attributed by some to the influence of milk (Veirac, De Krzowitz). Attention was directed at an early time to phosphoric acid and lime, with the view that variations in the elimination of these substances might explain the occurrence of rachitis. A large quantity of both was found in some urines (Malfatti); a superabundance of phosphoric acid was presumed to prevail in the whole system (Wendt, Fourcroy); while symptoms resembling rachitis were found in animals fed upon small doses of phosphoric acid by Caspari (1824). Chossat fed young animals on food deprived of lime, and claimed to produce softening of the bones and death, a result which was denied by Friedleben. Guérin claimed to produce rachitis by feeding young animals on meat in place of their mother's milk, a result equally denied by Tripier, who, like Friedleben, found the bones under such circumstances more liable to fractures, but not rachitical. Wildt and Weiske found the bones uninfluenced by withholding lime from food; Forster, however, and Roloff claimed to notice a marked influence, and the latter stated that animals, after having been rendered sick by depriving them of lime, recovered when they were again supplied with it. Wegner, in his numerous experiments with phosphorus, found that in growing animals it increases the growth and firmness of both long and flat bones; after the growth of the animal has been completed it renders epiphyses and vertebræ denser. There is no change, however, in the relative chemical composition of those parts. He found at the same time that results similar to those caused by the administration of phosphorus were obtained when food deprived of its phosphate of lime was given. But he met with no rachitical changes proper during these several procedures. Teissier having found an increase in the urine of rachitis after the administration of lactic acid, and lactic acid having been frequently found in the urine of rachitical patients by Ragsky, Morehead, Simon, and Lehmann, C. Heitzmann fed with lactic acid both carnivorous and herbivorous animals, found the cortical layer of the bones softened and the medullary substance hyperæmic, and claimed to produce rachitis in the former and osteomalacia in the latter. Both of these assertions were denied by Tripier and Toussaint, who insist upon Heitzmann's having selected animals which have a peculiar disposition to suffer from rachitis. Again, Milne Edwards and Boussaingault found the bones softened when they withdrew both phosphoric acid and lime from the food, without restoring the bone's consistency by administering powdered bone. But, lately, Ad. Baginsky states that he produced rachitis by withholding lime, and increased the effect by introducing lactic acid. By so doing, however, he changed only the relation of the mineral to the organic substances, without interfering with the normal proportions to each other of the constituents of the ashes. Beneke, finding oxalic acid in the urine in many cases of rachitis, attributes to it the want of calcification in rachitis, and Senator suggests that what impedes the deposition of bone might be formic, acetic, and lactic acids, which are also found in the young osseous tissue.6

6 L. Fürth, Path u. Ther. d. Rachitis, Wiener Klinik, 1882.

Of these statements many are uniform, others contradictory. Thus far, they are not convincing except in one way—viz. that both withholding and introducing certain ingredients, mainly lime, influence the growth of the bone considerably. This may prove nothing else but that lime is of paramount importance in the building up of bone, and that bone in the period of rapid development is amenable to a great many influences.

It is in the period of rapid development that rachitis is observed. Thus it occurs in every stage of intra-uterine and infant life. It is met with in the foetus in very early intra-uterine life; it is found as a congenital affection, continuing to develop after birth when it has originated in the latter half of foetal existence; there is, thirdly, the rachitis of early infancy; and, lastly, that of advanced infancy and childhood. Of 624 cases of rachitis enumerated by A. Baginsky, there were 256 less than a year old, 313 in the second, and 63 in the third year. After this time rachitis is rare, as far as the active symptoms of the disease are concerned. But still, a retarded form of rachitis (r. tardiva) has been described by some authors. It is said to occur about puberty, and to exhibit local changes in the bones of genuine rachitical character, but to be wanting in all the other symptoms required for the diagnosis of general rachitis. Such cases have been described by C. Lucas.7 He found it complicated, now and then, with albuminuria. The occurrence of the latter at that time of life had been referred to by Moxon.8 The principal symptoms described by Lucas are scoliosis, talipes valgus, and genu valgum. The epiphyses were slightly thickened; there were pain in the limbs, languor, and pallor. In some of the cases there were also rachitical deformities dating from infancy. He believes rachitis of adolescence to exhibit more symptoms belonging to relaxation of the ligaments than to softening of the bones.

7 Lancet, June 9, 1883.

8 Guy's Hosp. Rep., 1878.

A case of rachitis of undoubtedly congenital nature has been reported by Chiari. There were but twelve teeth. There were no other alveoli, nor was there any intimation of the formation of alveoli in the shape of the jaw, which resembled very much the usual senile form of retrograde metamorphosis.

Twenty years ago I described the lesions in part of a rachitical cranium removed from an infant who lived up to her eleventh day. She was born at full term with hernia of the brain, about one-sixth of which protruded through the small fontanel. Only the cranium could be studied with regard to rachitis, and but small portions of the frontal and the anterior half of the parietal bones surrounding the large fontanel could be removed. In these few square inches of bone there were between twenty-five and thirty openings of the usual craniotabic nature, nothing but a transparent membrane being left. The bony edges of these thin portions were partly sloping off gradually, partly very steeply, and somewhat thickened. They were distributed over the whole part of the skull removed; some were found in the immediate neighborhood of the points of ossification. No recent deposits of soft rachitical bone had taken place under the periosteum. Thus, evidently, the process was of rather an early date of intra-uterine life, and had at birth run the full course of its usual development without having had an opportunity to terminate in the restitution of the normal bone.9

9 Amer. Jour. Obst., Nov., 1870.

In a case reported by Dr. F. A. Burrall10 the infant (female) was cyanosed at birth, and had a small head and feeble general development. The respiration was shrill and piping from birth, as though from congenital laryngismus; in a few days it became raucous. The post-mortem examination proved the larynx normal, with no obstructive growths. She was pigeon-breasted, and the last phalanx of her right finger wanting.

10 Trans. N.Y. Path. Soc., vol. i. p. 81.

In the meeting of June 27, 1883, of the Société de Chirurgie of Paris, Guéniot presented a newly-born baby with well-pronounced rachitis of the extremities which had healed at the time of birth. The bones had recovered their firmness, and the characteristic deformities remained. In the meeting of December 19th he could report that the child had exhibited neither symptoms of rachitis nor of syphilis since. In regard to the latter, a very rigorous examination of the baby's whole family, made by Guéniot and Fournier, resulted in the existence of no trace of syphilis.11

11 Rev. Mens. des Mal. de l'Enfance, Janv., 1884.

Kassowitz has examined many still-born infants, and also children dying at an early age, at the foundling hospital of Vienna. In a large majority of the cases he found rachitical changes in the ends of the bones. In many of those who lived several weeks he found rachitis developed to such an extent that the presumption of its intra-uterine origin became conclusive. Here nothing is left but the conclusion that the cause of congenital rachitis has to be looked for in the condition of the maternal blood.

Thus, the foetal and congenital occurrence of rachitis cannot be doubted. Both forms are represented in literature. Neither requires the presence of rachitis in one or both of the parents. But the cause of the intra-uterine disease has not been found. Perhaps a disease of the mother with considerable nutritive disorders or a defective placentar supply may be found responsible. The foetal form runs its course long before the normal termination of pregnancy; the congenital may have run its full course at birth or complete it afterward. The bones are found of characteristic nature, the diaphyses suffering more than the epiphyses; even a rachitical pelvis has been met with by Fischer. Early foetal rachitis is probably dependent upon a defective development of the very first cartilaginous deposits and the first osseous nuclei; thus, many of the congenital synostoses find a ready explanation. Besides these, abnormal circulation is accounted for. For periosteal proliferation at that early period contracts the foramina carrying the blood-vessels, and, while interfering with the size of the bones, the foramen magnum also. Thus, a certain class of cretinism appears to be due to foetal rachitis, mainly of the base of the cranium, which results in early ossification of the synchondroses, particularly of the sphenoid bone. But lately I have seen a case of this description, which, however, had not terminated at the time of birth. For after birth the rachitical process developed further, and in addition to the rachitical deformity of the base of the cranium there were afterward thickening of the epiphyses, pigeon breast, and thoracic grooving and flattening.

Rachitis is found in city and country, less on mountains than in valleys. Still, it is met with at elevations of two thousand feet. In the tropical regions it is almost unknown. Why it should have been considered quite a new disease in England but a few centuries ago, or whether it did not exist before that time, it is difficult to say. It is certain, however, that deformities have been described in antiquity which we are accustomed to attribute to rachitis.

As the disease is one that occurs during the period of rapid growth, and is a developmental disease, everything that interferes with normal growth and development is apt to change physiological functions into pathological conditions and to produce rachitis. In the pregnant mother her ill-nutrition and the defective cell-material used in the building up of the embryo and foetus, or a defective placenta, may come in for the explanation of foetal and congenital rachitis, although the case of Klein's, who reports twins, of which one was normal and one rachitic, is rather difficult to explain on that basis only. Even rachitis of early infancy is not easily accounted for otherwise, for its first symptoms show themselves at a very early period; thus constipation, adiposity, and afterward craniotabes and thoracic grooving.

The common form, and that which is the usual subject of the text-books and monographs, has, however, in most cases a well-marked preparatory stage in the shape of diseases or ailments reducing sanguification and nutrition. Some cases are ushered in by, or follow the course of, acute exanthems or acute gastric disorders or the presence of entozoa. A larger number appear to result from insufficient oxygenation resulting from lung diseases, with a long chronic ailment following the acute stage. Even acute pneumonia, with its direct influence on general nutrition, stands often for the proximate cause of rachitis. Bad air alone, even swamp air, does not appear to be a sufficient cause. When it seems so, it is complicated with the main cause of rachitis; that is, bad, insufficient, improper food, with its immediate result—viz. intestinal catarrh. Cow's milk, particularly when acid, starchy food administered too early or in too large quantity or too exclusively, early weaning followed by improper artificial food, insufficient mother's milk or such as is either too thin or too caseinous, lactation protracted beyond the normal limit,—may all alike be causes of intestinal disturbances and rachitis.

Is rachitis hereditary? A number of women who were rachitical themselves have been known to have rachitical children. But it has been said that the process runs its full course during infancy, and that therefore a direct inheritance of rachitis from mother to child is an impossibility. Still, we must not forget that the consecutive conditions of the parents may, or will, influence the general condition of the infant and result in similar disturbances. No rule, however, exists. Dyscrasic parents may have healthy children, and healthy parents sickly or dyscrasic ones. But the probability is greater that diseased children should come from dyscrasic parents than from healthy ones. Tuberculosis in the parents has frequently been accused of being the cause of rachitis in the infant—not directly, but in consequence of general impairment of the tissues. Gout has also been accused of being the cause of rachitis, but it is a peculiar fact that the poor have but little gout and a great deal of rachitis. In all of these cases it is better to look upon rachitis as only one of the forms of general mal-nutrition, and to speak of inheritance of the disposition rather than of the disease. Thus it was that about the end of the eighteenth century Portal spoke of scrofulous, syphilitic, scorbutic, rheumatic, arthritic, and exanthematic rachitis. Particularly has syphilis been accused of being the main cause of rachitis by some, and even the only cause by others. Thus it was looked upon by Boerhaave. In modern times Parrot maintained, from 1872 up to the time of his death, which occurred recently, that every case of rachitis is of syphilitic origin. As his proof he relied mainly on the condition of the teeth and the bones. But those appearances in the teeth, the thin and ragged edges, the friability and the grooving, either horizontal or vertical, which have been considered characteristic of syphilis by Hutchinson and others, have no such dignity, and moreover they are not observed in the temporary teeth at all, but in the permanent only; the rachitical softening of the bones also is not found in syphilis at all. Particularly are there no curvatures in syphilis and no infractions. It is true that marasmus is found in both rachitis and syphilis, but it is met with in all sorts of diseases. The changes in the bones of syphilis are found at birth; in rachitis they usually develop in later months. When a baby is syphilitic and rachitic at the same time, the syphilis may last very much longer than the rachitis, which meanwhile has healed. The internal organs in rachitis do not exhibit any such changes as are known to occur in very many cases of syphilis. No gummata are ever found in rachitis, and the interstitial inflammation of the internal organs in syphilis is not met with to the same degree in rachitis. What Parrot claimed as a desquamative syphilide of the tongue—that is, red insulated spots, denuded of their epithelium, small in the beginning, later extending backward and increasing in size—is by no means always syphilitic, but is found in a great many cases where there is no suspicion of syphilis. It is mainly Kassowitz and Bouchut who have taken the stand against Parrot. The former, taking rachitis for a peculiar inflammatory process, admits that syphilis can be one of the causes. The latter directs attention mainly to the fact that by changing food in certain ways rachitis may be produced in dogs, but that they cannot be made syphilitic. There is no doubt, however, that syphilis may give rise to rachitis by its general influence on nutrition, and in this fact lies the key to the connection of great nutritive disorders with each other. Syphilis will undoubtedly change nutrition to such an extent as to result in rachitis. Rachitis will affect the glands; the caseous and suppurative degeneration of the glands will lead to metastatic processes, to acute tuberculosis, and so on.

Malaria been claimed as the main cause of rachitis by Z. Oppenheimer,12 or, rather, rachitis is presumed by him to be the form in which malaria makes its appearance in young infants. After disposing of other alleged causes of rachitis, none of which is proved to give rise to every case, and referring to the anatomical belief that the peculiar hyperæmia and inflammation of rachitical bones is created by the embryonic condition of the growing osseous tissue, he points to the prodromi, amongst which he emphasizes chronic diarrhoea and the nocturnal crying. The latter, with its perspiration and subsequent sleep, he claims as evidence of malaria, and as a substitute for the intermittent neuralgia of adults, the more so as he believes he finds the spleen tumefied. The persistent diarrhoea of these infants is said to be paroxysmal—to take place in the morning, contrary to what is seen in the usual form of intestinal catarrh; the discharges are said to be serous, not tinged with bile; the appetite to be good through the rest of the day; the weight of the body not to be lessened, but anæmia to develop gradually, and fever to occur occasionally. In other cases infants have cold hands and feet and blue lips toward evening; the skin is pale, the spleen enlarged; otherwise there are perhaps no symptoms, but the infants try to get uncovered, and have an increase of temperature of from 1° to nearly 3° F., and a perspiring head in the morning. After a while the rachitical symptoms belonging to the bones and the general system become apparent. After all of the author's ingenious and emphatic assertions and deductions, it becomes evident that malaria—in the severe forms in which it has been found by Arnstein, Browicz, and Henck to cause bone diseases—may give rise to rachitis, but it is also clear that he tries to prove too much. The long series of attempts at proving that every form and case of rachitis depends upon a single and uniform cause have proved futile. The physiological hyperæmia of the bones and the rapid growth of all the infant tissues are shaped into the complex ailment which we call rachitis by more than a single disease or a single nutritive disturbance.

12 D. Arch. f. klin. Med., xxx., 1881.

SYMPTOMS.—Before entering upon a more accurate and elaborate enumeration of the symptoms of rachitis, I mean to dwell upon peculiar differences which take place according to the age in which the disease makes its appearance. Very young babies—that is, infants of a month or two—develop rachitis in such a manner that many cases are overlooked until it is too late to relieve them in time. This occurrence takes place when there are no prominent causes, such as diarrhoea or other nutritive disorders, nor any premonitory symptoms. Such infants appear to be perfectly well; they have the average weight, and even more; they have plenty of adipose tissue, and look well. The only anomaly appears to be an undue degree of paleness. Without pain or flatulency they are constipated. This constipation is not congenital, as it always is when the colon is unusually long even for an infant, and when the sigmoid flexure is of double or even treble length, but makes its first appearance about the end of the first or the beginning of the second month. It is relieved only when the increasing muscular power of the intestine results in more effective peristalsis. The second symptom is the thoracic groove, to which I shall allude later, and a gradual thickening of the costo-cartilaginous junctures, with or without periosteal pain on pressure. About the same time the cranial softening, craniotabes, with its hyperæmia and perspiration of the entire scalp, and baldness, and the first symptoms of maxillary rachitis, become perceptible. During all this time the epiphysial swellings and the diaphysial curvatures develop but very slowly; but at a very early time chronic bronchial catarrh, with a loose cough, begins to be troublesome. When rachitis begins at a late period—say, about the sixth or eighth month—the aspect of the case is different. The infant has suffered before either from bronchitis and broncho-pneumonia, or in most cases from indigestion and intestinal catarrh. There is some degree of emaciation; the skin does not fit the limbs, as it were—is loose, thin, flabby, and rather dry. The tendency to diarrhoea continues to prevail. The epiphyses, particularly of the lower extremities, are thickened at an early time, curvatures of the tibiæ become apparent, and all the rest of the bones participate in the process, with the exception, sometimes, of those of the head.

The head, however, is liable to exhibit symptoms of rachitis at a very early period of life. It is large, or appears to be so,13 mostly for the reason that the face is proportionately small. The forehead is large, the frontal protuberances very prominent, as are also those of the parietal bones. Thus, the head is more or less square. Dilated veins are visible in and through the pale skin; there is but little hair, on the occiput less than on the rest of the head. Sometimes the occiput is quite bald, the hair having been rubbed off on the pillow. The scalp feels warm, except during perspiration. The latter is very copious, particularly on the occiput—to such an extent, indeed, that the pillow is drenched—and will remain so for months. The sebaceous follicles are often still larger and more numerous than they normally are at that age, and seborrhoea is often, though not always, met with. The sutures are wide, sometimes one or two centimeters; the posterior fontanel remains open; the large anterior fontanel is very large, being sometimes several inches long and wide. The pulse is felt very distinctly through it. The systolic cerebral murmur, which was first found by Fisher of Boston in 1833, and considered to be a positive symptom of rachitis (which certainly it is not, as it is found in almost every healthy baby with a patent fontanel), is very audible. The fontanel and sutures remain open for a long period. Instead of closing, as they do normally at the fourteenth or fifteenth month, the former ossifies about the end of the second or third year, or later. Gerhardt reports a case in which it persisted to the ninth year. The cranial bones appear to be thin, and give way under the pressure of the finger. Ordinarily, it is true, the cranial bones of every baby, even if perfectly healthy, are movable under pressure, but they are so only along the sutures, where they may retain this mobility, in some instances, a long time. Indeed, it appears that sometimes about the middle of the first year the occipital bone becomes thinned out in apparently quite healthy children. Moreover, even in the skulls of infants who were taken to be in good health small defects in the bones were found (Friedleben), with no uncomfortable symptoms at all. Therefore it is rather difficult to draw the exact boundary-line between the healthy and the morbid condition; thus it is possible that some of those cases which exhibited apparently morbid local changes without morbid symptoms may not have been diseased after all. In those, however, in which rachitis is really developed in the cranium a peculiar condition is found. In the posterior half or third of the parietal bones, either the right or the left side being more marked, there are in the tissue of the bone distinct spots in which the osseous material is not only thinned out, but has entirely disappeared. In fact, the bone is perforated, the edges of the holes being rather steep, sometimes slightly thickened, and the scalp separated from the brain only by a thin, transparent membrane, the remnant of the periosteum. These holes can be easily found through the integument. The finger, though ever so gently pressing down upon it, moves the cranium, if any be left, before it; the bone feels like paper, and the sensation as if it could be easily broken through is quite distinct and embarrassing. Such perforations are usually quite numerous; from five to twenty or more can often be counted. They are surrounded by normally hard bone, and thereby can be recognized from the flexible part of the cranium extending along the sagittal and lambdoid sutures. Where these results of rachitical softening, craniotabes, are most prominent—that is, on the part on which the infant is mostly reclining—the bone is flattened, and may remain so for life, though in the majority of cases the asymmetry will disappear. The flattening and perforations result from the same causes—viz. softening of the bones and pressure upon the bone between the pillow outside and the brain inside. With it go, hand in hand, thick rachitical deposits under the hyperæmic periosteum of other portions of the skull. Where craniotabes is largely developed on the occipital portion, the frontal and the parietal bones (in their anterior halves) are usually thus thickened. A cross-section with a knife will reveal a diameter of the new osteoid material between the periosteum and bone of one-half to one centimeter in thickness. It is very hyperæmic—even more so than the bone itself, which, when cut into, exhibits an unusual amount of blood. Sometimes the deposits are still larger, and are apt to change the appearance and weight of the skull considerably after recovery has taken place and eburnation and sclerosis have taken the place of the normal osseous tissue.

13 Boötius (1649), quoted by Haller (Bibl. Med. pract., 1779): "Infantibus caput grandescit, reliquum corpus contabescit, ossa in articulis tument, dextrum hypochondrium tumore æquali prominet; hoc malum multis millibus infantum molestum est" ("The infant head grows large, the rest of the body emaciates, the articular bones swell, the right hypochondrium is raised by a uniform tumor; this malady is a sore affection in many thousands of infants").

Such a case of rachitical cranial sclerosis I have described in the Amer. Med. Monthly of 1861. It was, however, by no means a mate of the case related by E. Huschke. The latter skull was that of a girl of seventeen years, and weighed 4117 grammes instead of the normal weight of 600 grammes. The medullary (Havers') canaliculi were large and very numerous on the surface, narrow and very few in the interior of the sclerotic bones, and the osseous canaliculi were more spherical and irregular in site and shape. The chemical composition was also abnormal, phosphate of lime being 65.59, carbonate of lime 11.12, sulphate of magnesia 1.14, cartilage and fat (very little), etc. 22.15 per cent. No fluorate of lime was found. Most of the bones were exceedingly hard, but fragile when tried in small pieces; very white inside, yellowish on the surface, the latter color being the remnant of extravasated blood or other pigmentous matter. Another skull, in Huschke's possession, and moderately sclerotic, weighed (lower jaw excluded) 1075 grammes; a third, in the museum of the University of Jena, is that of a young baboon,14 in which all the bones covering the hemispheres had become sclerotic.

14 Baboons suffer from rachitis very extensively. In the Transactions of the Pathological Society of London (xxxiv., 1883, pp. 310, 312) I. B. Sutton gives the description of two baboons, one of which was six months, the other one year and six months old, when they died. The careful description of the specimens exhibited leaves no doubt as to the rachitical nature of the changes in both the periosteum and the tissue of all the bones of the body.

Of undoubted total cranio-sclerosis Huschke reports but ten cases—those of Malpighi (1697), Cuvier (1822), Ribalt (1828), J. Forster and Bojanus (1826), Ilg (1822), Kilian (1822), Otto (1822), Vrolik (1848), Albers (1851), Huschke (1858). The disease does not affect the auditory bones, the condyles of the maxillary and occipital bones, nor the styloid process of the temporal bone. It is recognizable in the posterior part of the cranium and basis cranii, but affects mostly the bones of the face and the frontal, parietal, and cribroid bones. Thus, the disease takes its origin in the anterior portion of the skull, particularly in the superior maxilla, and proceeds upward and backward, terminating in the basis cranii in the neighborhood of the infundibulum and appendices. But two of all the cases were observed during life. In all the disease was traced back to early life. The chemical composition of the bones was greatly changed in all. Instead of the normal proportion of earthy to organic material = 2.1 (or 1.5):1, it was from 3.5 to 4.4:1. Particularly the carbonate of lime was greatly increased.

The brain and its meninges participate, in many respects, in the changes worked by rachitis, and mainly in the abnormal vascularization of the bones. They are very much congested, and succulent. A section through the brain shows a great many large and small blood-points. This hyperæmia may give rise to over-nutrition, which assumes the character of real hypertrophy of the brain. When that hyperæmia, however, becomes excessive, effusion will take place into the cavities, the tissue of the arachnoid, and the substance of the cerebrum, which latter looks peculiarly brilliant, elastic, and sometimes white, in consequence of the blood-vessels being emptied by the pressure on the part of the enlarged mass of the cerebrum upon the blood-vessels. Thus, instead of cerebral hyperæmia there may be anæmia. Every form of hydrocephalus may follow the rachitical process. Afterward, when the craniotabes has healed, the secondary effusions will generally also disappear, but not a few cases of hydrocephalus may be traced to rachitis occurring during the first half year of life. When that occurs, the intellectual faculties may suffer, while, on the contrary, complete recovery not infrequently exhibits an unusual degree of mental development, for the same reason which improves the chances of the development of the bone. The degrees of physiological and pathological nutrition and over-nutrition are very variable in their nature and results.

This condition of the cranial contents is not the only one brought about by rachitis. The softness of the cranial bones permits a direct pressure on the brain. The side on which the infant for the most part reposes gets flattened, and the brain is also compressed. The skull consequently bulges out in the opposite direction. This anomaly, as stated above, is sometimes visible through life, though in the large majority of cases after recovery from rachitis has taken place this asymmetry will gradually disappear. Before that can occur, however, the infant is liable to suffer from the rachitical changes. Convulsions are by no means rare. Vogel has, however, been able to produce an attack of convulsions by pressing upon the softened spots of the cranium. Permanent or temporary contractures of the fingers and toes I have seen in several instances. Gerhardt looks upon rachitis as one of the causes of tetany.

A frequent symptom of the cerebral changes which take place during, and in consequence of, craniotabes is the crowing inspiration, or laryngismus stridulus, of infants. It may be mild or severe. The mild form is very frequent, and consists in the occurrence of a shrill inspiratory sound while the baby is either quite placid or excited or crying. It is frequently overlooked entirely, is usually overcome after a number of months, and gives rise to serious trouble in but very few instances. The severe form is of a different nature. While the baby is awake or asleep, without any premonitory symptoms, while playing or crying, placid or excited, all at once respiration will cease. This will take place, usually, after expiration. The limbs are hanging down, as it were lifeless, the face turns pale, then purple, and slight convulsive twitching may set in for ten or twenty seconds. There appears to be a complete paralysis, and death from apnoea seems to be imminent. All at once, a long, deep crowing inspiration will be heard, respiration will commence again, and the whole terrible attack is overcome. It may return a number of times every day, or sometimes not for several days, during a period of many weeks or several months. The attacks which set in after inspiration are apt to be more dangerous. In such an one, but also in the other kind which sets in after the expiratory movement, death may occur suddenly, or the attack may be followed by a convulsion which may terminate fatally like any other eclamptic seizure. In this manner it is that the majority of cases of rachitis perish which terminate fatally during the active progress of the morbid process. In this connection, however, it may be well to add that craniotabes is not the only cause of laryngismus, particularly when the latter is found in the second year of life, or even later. But almost every case, without any exception, which is observed during the first eight or nine months is due to that very cause; and a good many cases occurring later, when the craniotabic bones have become normal, arise from the effects, either meningeal or encephalic, of the rachitic process. Still, complications of craniotabes with a large size of the thymus gland may occur, and enlargements of the tracheal and bronchial lymphatic glands are quite frequent, as we shall see below.15

15 Z. Oppenheimer prefers the name rachitic asthma in place of laryngismus, and suggests an explanation of the symptoms from a strictly anatomical point of view. If not correct, it is at all events interesting, as everything this ingenious writer proposes. He points to the ligament situated between the spinæ intrajugulares of the temporal and occipital bones, which, as long as it is of normal consistency, separates the jugular vein from the pneumogastric nerve. As it is covered with periosteum and dura, it is apt to ossify, and forms an osseous partition in the foramen jugulare, which participates in all the changes taking place in the periosteum. As this becomes softened and succulent, so will the ligament, either on both sides or on either. Its influence on the neighborhood depends on its size or succulence (as also on the difference in width of the foramen jugulare or lacerum, which corresponds with the difference in size of the transverse sinuses). The irritation of the pneumogastric is perhaps easily explained thereby, but in very exceptional cases only the accessory nerve would be affected. As, however, the latter controls the sterno-cleido mastoid and trapezius, and also the laryngeal muscles, and is apt to provoke cardiac paralysis during diastole, the occurrence of sudden death would be best accounted for.

While the size of the cranium is normal, or sometimes more than normal, the face undergoes some changes which result in absolute or relative diminution of size. These depend mostly on a reduction in the volume of the jaws. Glisson knew of it, and therefore looked for the cause of rachitis in the process of dentition. Now, both maxillæ are liable to become rachitical at an early date, as early indeed as the bones of the cranium. Rachitical deposits and softening take place in them very generally. The lower maxilla is flat anteriorly, it loses its rounded outline, is shorter in longitudinal direction, while the rami are thick and clumsy; the whole bone is shorter than normal, and sometimes asymmetric. Its changed appearance is greatly due to the effect the muscles, with their powerful insertions, produce on the softened bone; mainly the masseter, also the mylohyoid, which draws the lateral portions inward, and the geniohyoid, which pulls at the central portion. Of the latter, the lower portion is drawn out, the inner and the alveolar part inward. Thus, the teeth, mainly the incisors, of the lower jaw are turned inward to such an extent that, as those of the upper look outward, the two rows of teeth do not touch but cover each other. Besides, the periosteal proliferation around the alveoli is excessive, sometimes so much so as not only to crowd the teeth into irregular positions, but even to absorb and annihilate alveolar processes in the course of the morbid changes. The cases in which the number of teeth are actually diminished by rachitis are not at all rare. In the superior maxilla the last-described anomaly is also observed. Periosteal thickening is mainly noticed about the intermaxillary bone—sometimes to such an extent that above and behind it a considerable impression takes place. The shape of the upper jaw is more spherical than normal, and the cheek-bones become very prominent.

The belief that maxillary rachitis is now and then met without any other symptom of rachitis I do not share. What I said of craniotabes is also valid in regard to this form.

Irregular teething is a constant companion of maxillary rachitis, but is also present where the latter is not well, or not at all, marked. As a rule, the first teeth protrude late, about the ninth or tenth or twelfth month. That the first year and more should elapse without any tooth is of frequent occurrence in rachitis. Cases in which the first teeth do not come before the second year is completed are not very uncommon; in some there are none even when the child is much older. In most cases the retardation of dentition goes hand in hand with very marked retardation in the development of the rest of the bones and in the closure of the cranial fontanel. But not in every case of rachitis is there a retardation in the process of teething. In some a few teeth appear at the regular period (at the completion of the seventh or eighth month), or even at a very early age (in the fourth or fifth month); after which there is an interruption in the protrusion of teeth for an indefinite period. Evidently, the period in which rachitis is developed exerts its influence on the teething process. When it exists at a very early age, it will retard teething until recovery takes place. Still, it is possible that a moderate amount of periosteal and osteal hyperæmia and over-irritation matures the teeth abnormally. In all those cases, however, in which rachitis does not occur before the second half of the first year, the first teeth will appear at the normal time, and a long period will follow in which no teeth at all will make their appearance. Then, again, when the whole process comes to a standstill, and recovery takes place with solidification of the bones, and even eburnation, the teeth will come in rapid succession. Whether they will, as is frequent, decay almost as soon as formed, or whether they will be unusually hard, solid, and yellowish, depends on the stage of the disease in which they made their appearance, and on the complications aggravating the case. Of very grave import in this respect are digestive disorders before and during the course of the disease.

The vertebral column suffers also. In the normal infant it is straight, but in the rachitic it exhibits a kyphotic deformity very soon. When such a baby of three or six months is sitting up, the middle portion of the back is protruding, as in Pott's disease. In almost every case, however, this kyphosis is but apparent and the result of muscular debility. In order to arrive at a diagnosis at once, it is sufficient to place the patient on his face and support the head, and raise the lower extremities and pelvis in the air. If the kyphosis is but functional, the prominence disappears at once. By nothing can the muscular insufficiency of early rachitis be better demonstrated than by this little experiment. But actual deformity is also found in rachitis. It softens both the vertebræ and intervertebral cartilages, and either their anterior or posterior portion may be irregularly developed, and be either too high or too low. Besides, the articulating surfaces are sometimes too convex. Thus the causes of both kyphosis and scoliosis are amply furnished, and complications of the two are quite frequent, and the deformities resulting therefrom quite formidable. Scoliosis is mostly to the left; kyphosis generally complicated with lordosis, and sometimes the vertebral column exhibits a spiral shape.

The ribs of the convex half are prominent and divergent, those of the concave side flattened and parallel. The two halves of the chest are therefore very unequal indeed. Muscular traction, atmospheric pressure, the elastic traction of the lungs, the presence of pulmonary complications, and the pressure from below on the part of the enlarged viscera of the abdominal cavity, come also in for a considerable share in the completion of the deformity.

The ribs and the sternum aggravate it considerably. Even without any affection of the vertebral column they suffer seriously from the general affection. The manubrium is thickened and drawn inward, the ensiform process protuberant, the sternum often swelled and painful to the touch. The ribs are sensitive to the touch on one or both sides. The child cries when taken up or when fearing to be taken up. The costo-cartilaginous junctures are thickened, mainly so from the fourth to the eighth ribs. The insertion of the diaphragm becomes soon perceptible by a deep groove around the chest. The anterior portion of the ribs is flattened, posteriorly they are inserted at acute angles. Thus the intrathoracic space becomes narrow, the sternum with the costal cartilages is pressed forward (pigeon breast, pectus carinatum), the thorax is deprived of its elliptical shape and becomes triangular, the dorsal aspect being flattened, and the distance between the vertebral column and the sternum increased. Below the diaphragmatic groove the thorax expands, the liver and other abdominal organs crowding the ribs outward. All sorts of changes are experienced by the ribs in these conditions. Parts of them are flattened, parts undergo infraction, parts are even concave; they are bent and twisted, now and then to such an extent as to turn the concave side out, the convex surface in. In addition to all this, the scapula is big and clumsy and protuberant, the clavicle considerably bent and frequently infracted, and not rarely covered with genuine callus.

That the respiratory and circulatory organs must suffer from such anomalies, though they be not excessive, is certain. The heart is crowded by the flattening of the ribs and the contraction of the thoracic cavity. Its beat is visible over a large surface, and its percussion dulness is extended over its normal space, though no enlargement have taken place. This, however, is very apt to occur after some time by overexertion. The latter is increased by the condition of the respiratory organs. The ribs being flexible, the chest contracted and compressed, the diaphragm raised, the respiratory muscles feeble, respiration is insufficient, even without the presence of any further complications; thus dyspnoea and a certain amount of cyanosis are frequently met with in consequence of the anatomical changes only. In addition to this, there is from the beginning a tendency to catarrhal and inflammatory conditions. Even without any deformity the rachitical process is accompanied from an early time with bronchial and tracheal catarrh. A chronic cough in an infant, with very little or no fever, disappearing and returning, mostly with copious secretion—which, however, is swallowed as soon as it reaches the pharynx—rouses the suspicion of general rachitis. It is often complicated with extensive dulness over the manubrium sterni, due (to rachitical thickening of this bone and) mostly to the persistence of a large size of the thymus gland; and also with enlargement of the bronchial and tracheal glands, the latter of which are often accessible to recognition by percussion. They are to be looked upon as a frequent occurrence in rachitis, though no associated diseases leading to their enlargement have been noticed. They and the chronic tracheo-bronchial catarrh are closely dependent upon each other. They are each other's both cause and effect. Neither of them, however, remain uncomplicated. Catarrh grows into broncho-pneumonia, with frequent returns. Atelectasis, interstitial pneumonia, dilatation of bronchi, and pulmonary consumption are often traceable to such apparently slight catarrhs, which, when not recognized as depending on their constitutional cause, cannot be removed. Nor are the cases of miliary tuberculosis, resulting from caseous degeneration of rachitical glands, very exceptional.

The anatomical changes in the abdominal viscera may be due to the preparatory diseases or the complications of rachitis; but, at all events, the abdomen yields a number of changes visible through the whole duration of rachitis. It is very large; its size is due to the contraction of the thoracic cavity and the downward pressure of the chest-wall upon the contents of the abdominal cavity. It is also due to the changes wrought by rachitis in the pelvis. Softening of bones and synchondroses, torsion, the weight of the trunk, and the pressure of the femora from below produce the change of the pelvis so well known and much feared in the parturient female. The promontory and sacrum are pushed in, the arcus pubis is large, the pelvis asymmetric; the small pelvis is contracted, the large pelvis broader. Thus, the small pelvis has no room for viscera, which, then, are crowded upward. The digestive disorders which gave rise to, or formed the first stage of, rachitis result in the accumulation of gas; the scrobiculus cordis is greatly expanded. The liver16 is large, congested, and in fatty degeneration. The latter is the more frequent the more a certain degree of fatty condition is a normal attribute of every infant liver. When the liver is found but small in post-mortem examination, it is so because of the general anæmia and emaciation. Sometimes it is amyloid, as are also the spleen (mostly hyperplastic only), the kidneys, and the arteries of the intestines in many instances.

16 Dr. Norman Moore presented a cast and drawing to the Pathological Society of London (Trans., vol. xxxiv., 1883, p. 185) showing how considerable may be the digressions of the diaphragm and local pressure upon the liver in a case of rickets. Three large beads caused as many projections from the under side of the diaphragm, and corresponded with local thickenings of the capsule of the liver, probably produced by the continued pressure through the diaphragm of the beads, which were on the seventh, eighth, and ninth ribs, and the largest of which was equal in size to a hazel-nut.

The alimentary tract is the seat of many changes recognizable during life. The tonsils are often large. The tongue is seldom coated to an unusual degree. On it are found little islands, red, marginated, deprived of epithelium. They will increase in size and number and extend backward. They will heal and reappear. They are by no means syphilitic, as Parrot would have it, and correspond exactly with the erosions near the solitary glands and those of Lieberkühn in the intestinal part, which mean nothing else but a nutritive disorder of the epithelia, and give rise to nothing worse than incompetency of absorption in that locality and abnormal secretion. The stomach is in a condition of chronic catarrh, sometimes dilated. Acid dyspepsia is frequent. Anorexia and bulimia will alternate. Feces contain an abnormally large amount of lime. Diarrhoea and constipation will follow each other in short intervals. The former owes its origin to faulty ingesta or chronic catarrh; the latter, sometimes to improper food, but more generally to muscular insufficiency. This condition has not been estimated at its proper value. Besides myself,17 nobody but Bohn has paid the attention to it which it deserves. Here, again, I have to insist that rachitis is a disease of the whole system, and not exclusively of the bones. Indeed, the muscular system is amongst the first to suffer. In the same way in which the voluntary muscles are not competent to raise and support the head or to allow a baby to sit up without a functional kyphosis, the involuntary muscles of the intestine are too feeble for normal peristalsis. The infant of a month or two months of age may have had normal and sufficiently numerous evacuations; gradually, however, constipation sets in; the feces become dry, but are perhaps not much changed otherwise. If no other cause be apparent, the suspicion of rachitical constipation is justified. Seldom, however, after it has lasted some time—and only after some time has elapsed relief will be sought—it will remain alone. Other symptoms of rachitis will turn up and the case be easily recognized. This constipation is an early symptom, as early as thoracic grooving or craniotabes. Very often it precedes both—is, in fact, the very first symptom—and ought therefore be known and recognized in time.

17 Jour. Obst., etc., Aug., 1869.

The kidneys have been mentioned above. They are often found rather large. Though the fact has been alluded to before, I will here again state that it has always been the general impression that the amount of lime eliminated in the urine of rachitic children is excessive. The reverse of that is true. Seemann and Lander have proved beyond dispute that in most stages of rachitis there is less than the normal amount of lime in the urine. Thus, the theory that lime is eliminated by an excess of acids in the blood is proven to be incorrect. But it is a fact that the rachitical bone contains a proportionately small amount of lime. The conclusion is, then, that its introduction must have been diminished. On the other hand, every article of food contains a large amount of lime, which might be introduced into the circulation if digestion be not at fault. The fact is, that a large amount of lime introduced is not utilized, and is eliminated with the feces.

In connection with these facts the following will be found very interesting. It has been found by Bunge that when potassium, with the exception of chloride of potassium, meets chloride of sodium, the two will exchange their acids, so as to form chloride of potassium and phosphate of sodium. They will be found in the blood also, will be eliminated as such, and result in a comparative absence of chloride of sodium from the serum of the blood. Now, comparative absence of chloride of sodium diminishes the possibility of the development of hydrochloric acid. Thus, it is not a surplus of acid, but a lack of hydrochloric acid, which results from such chemical combinations. If such be the case, calcium salts are not absorbed sufficiently. Thus, they will appear in the feces, and not even be absorbed in the intestines, because of the alkalinity of the intestinal secretion, by which the lime cannot be dissolved. The more lime, then, is introduced under these circumstances, the greater the incumbrance to digestion.

The correct proportion between chlorine, phosphorus, potassium, and sodium is certainly exhibited in woman's milk. There is lime enough in even the poorest article of that kind. But indigestion brought on by woman's milk in a disordered condition or by any other cause will prevent the absorption of lime when a superabundance of phosphorus and potassium disturbs the formation of hydrochloric acid. In these cases not only the development of the bones, but also that of the muscles, is disturbed. The latter is of great importance in regard to circulation, because a large part of the circulation depends on the pressure on the part of the muscular fibres exerted on the small blood-vessels. These facts have been the reason why I insist upon the addition of chloride of sodium to the food of infants and children, particularly those who are fed on cow's milk; for cow's milk and vegetables contain a relative superabundance of potassium compared with sodium. Even adults will find cow's milk very much more digestible by adding table-salt to it.

The extremities begin to suffer at a later period than the ribs and cranium. The opinion of Guérin, that the rachitical process begins in the lower extremities and ascends gradually, is erroneous. It cannot even be stated that the lower extremities are affected sooner than the upper. There is no regularity at all; it is not even necessary that all the osseous tissue should fall sick. But this can be taken as a fact, that hands and feet, and particularly the phalanges, are the latest to undergo the rachitical change. First in the line of morbid alteration of the bones are the epiphyses, mainly of the tibia, fibula, radius, and ulna. Their integument appears to be thin; now and then the cutaneous veins are dilated. The periosteum of the diaphysis becomes thick, softened, and painful to the touch and pressure, its compact layer thin, the medullary space large, the whole bone flexible, at the same time that the ligamentous apparatus of the joint becomes softened and flabby. At this time babies are greatly admired and applauded for the facility with which they introduce their feet into their mouths. For at the same time the bones begin to curve under the influence of the flexor muscles, which are always stronger, as they do in later months under the weight of the body when the child begins to walk. The curvature is not always a mere arching, but sometimes the result of infraction (green-stick fracture), a complete fracture not being accomplished because both of the softness of the osseous tissue and the resistance on the part of the thickened and softened periosteum. Both the legs and forearm bend on the external side, the resulting concavity looking inward. The humerus bends in a direction opposite to that of the forearm; the thigh, usually outward and forward.

The attempts at locomotion are often the causes of quite preposterous anomalies; creeping, sliding, walking, turn the extremities in such unexpected directions that talipes valgus, genu valgum, and now and then double curvatures, are the results. These, however, may not always be very marked, but there is one change in the rachitical bone which is constant—viz. the impairment of longitudinal growth. In every case the diaphyses remain abnormally short, and the proportion of the several parts of the body are thereby disturbed. Chiari measured parts of the skeleton of a rachitical woman of twenty-six years who was nine years old before she could walk. Her height was 116 centimeters, the length of the lower extremities 42, femur 23, tibia 15, fibula 20, humerus 16, right radius 12.5, left radius 11, right ulna 15, left ulna 14 centimeters. In a second case the parts of the skeleton were measured after they had been extended with great care. The right arm from the acromion to the middle finger (incl.) was 39 centimeters, the left 38; the right lower extremity from the trochanter to large toe (incl.) 39, the left 41.

The skin participates in the general nutritive disorder. It is soft and flabby. In those infants who become rachitical gradually while proving their malnutrition by the accumulation of large quantities of fat, it exhibits a certain degree of consistency. When rachitis develops in the second half of the first year or later, with the general emaciation the skin appears very thin, flabby, unelastic. The veins are generally large. Complications with eczema and impetigo are very frequent; where they are found the glandular swellings of the neck and below are still more marked than in uncomplicated cases. Circumscribed alopecia is sometimes found (not to speak of the extensive baldness of the occiput). It is not attended with or depending on the microsporon Audouini, but the result of a tropho-neurosis. In the hair Rindfleisch found fat-globules between its inferior and central third. Then it would break, the axial evolution would cease, and the end become bulbous by the new formation of cells.

Acute Rachitis.

There is a form of rachitis which may be, and has been, called multiple epiphysitis or multiple periostitis of the articular ends of the long bones. The changes which in the usual form of rachitis require months to develop take place in a very short time. Not infrequently the children were quite well before they were taken with this peculiar affection. Cases have been known to occur between the fourth and twenty-fourth months of life, and to last from two to six weeks, or just as many months. They have been known to get well, or a few of them terminate fatally. They are accompanied with fever and rapid pulse, perspiration, now and then with diarrhoea, with eager or reduced appetites. At the same time the epiphyses swell very rapidly, and are painful. The same is true of the diaphyses and the flat bones of the head. Many authors do not recognize this form as an independent variety. Some call it an acute initial stage of certain cases of rachitis, as they are not infrequently found in infants which exhibit a very rapid growth. Some have taken it as an independent disease, developed on the basis of a constitutional disposition; some look upon it as a very intense acute form of rachitis; others, as an intense growth of the osseous tissue only. Others call it an inflammation of the bone. Some refer it to hereditary syphilis, and a few to the influence of malaria. That the disease is epiphysitis and periostitis there is no doubt. I do not hesitate to claim it as rachitis, for epiphysitis and periostitis of early age not of rachitical basis are not apt to run such a favorable course as this form frequently does. The cases complicated with subperiosteal hemorrhages are claimed as scurvy by Th. Barlow.

The differences of opinion would probably not have been so great if every author had seen all the cases of the other observers. It will not do to judge of unobserved cases by the light shed by a single case under one's own observation. I have seen cases of acute rachitis which were the initial stages of general rachitis, and have observed those of local or multiple epiphysitis, mainly after infectious fevers, which were diagnosticated as such. They are, however, very uncommon. But even without a preceding infectious fever, such as scarlatina or more frequently typhoid fever, there are unexplained cases of rachitis and deformity. Thus, R. Barwell had some before the Pathological Society of London,18 which are positive proofs that some forms of ostitis may occur and result in the most formidable deformities without being rachitical. A girl of seventeen years was perfectly well formed up to the age of two and a half or three years. After that time the deformities began to develop, and did not change after she was thirteen, at which time the author saw her the first time.

Herleft humerus measured7¾ inchesfrom shoulder to elbow;distance 6¼
right humerus measured7½ inchesfrom shoulder to elbow;distance 4¼
left tibia measured10 inchesfrom knee to ankle;distance 7¼
right tibia measured9½ inchesfrom knee to ankle;distance 4½

Her bones were always very brittle. When she was between nine and thirteen she broke her arms four times and her lower limbs on several occasions. A male patient of twenty-two years, who was born healthy and well formed, continued thus until five years of age, when he was attacked with a fever, after which his bones became soft and bent. Osteotomy was performed on him, and the femora were found to be mere thin shells of bones surrounding cavities containing great quantities of medulla, which flowed out of the wound as oil; five ounces were discharged at once. In both cases there appeared to be a hypertrophy of the medulla at the expense of the bone-substance—a condition which Barwell proposes to call eccentric atrophy. "While these subjects are still youthful very little bone-earth is deposited, or at least remains in the very thin layer of osseous tissue that subsists. The relationship between infantile ostitis and extreme development of the intraosseous fat, though well known, is still occult; neither should we lose sight of the possibility that the softening process of ostitis may be due to a fatty acid. Now, fatty ostitis usually occurs in epiphyses. In these cases the shafts were affected."

18 Trans., xxxiv., 1883, pp. 203-208.

PROGNOSIS.—The course and the prognosis of rachitis are, as a rule, favorable, but they change according to the degree and locality of the affection and the age of the patient. Generally there is neither fever nor rapid exhaustion. But the process lasts for months and even years. In favorable cases, when recovery takes place the teeth will grow faster, the bones become firmer, the epiphyses will diminish in relative size, the bowels become regular. But the length of the bones is, and remains, reduced, and the head remains large as compared with the length of the body. Not only are the bones of normal firmness, but the compact substance undergoes a process of hardening called eburnation by Guérin. The internal organs also become very active, perhaps because the total amount of blood has to supply only a body less extended in length. Nor does the brain suffer after complete recovery has taken place. On the contrary, it appears that the somewhat more than normal vascular dilatation, which under unfavorable circumstances leads to effusion, is frequently apt to nourish the organ of intellect up to a higher standard. In all cases of rachitis, however, the curvatures of the extremities will not disappear altogether, while mild ones, it is true, are hardly recognizable in advanced age. Curvature of the ribs and of the vertebral column, however, will remain, and interfere with the expansion and the normal functions of the lungs and heart. In regard to the lungs, it appears that in many cases they do not find sufficient space to expand. As far as the heart is concerned, it touches the flattened, no longer elliptic, chest-wall over a larger surface, and is very apt to give rise to the suspicion of enlargement in consequence of extended dulness on percussion. The rachitic pelvis is well known to the obstetrician for the difficulties it gives rise to during parturition.

Thus, the prognosis would, as a general thing, be sufficiently favorable if it were not for the number of complications or severe symptoms. The chronic catarrh of the lungs accompanying rachitis, the enlargement of the tracheal and bronchial glands and the lymphatic glands in general, are apt to lead to inflammatory disease of the lungs, which, after having returned several times, leads to infiltration of the lungs with caseous deposits, and not infrequently results in phthisis. The nervous symptoms accompanying craniotabes may prove very dangerous. Spasm of the larynx and laryngismus stridulus may prove fatal in a single attack by suffocation, or general convulsion may set in during an attack of laryngismus or without it, in which the child may perish. Therefore the prognosis in every case of laryngismus and in every case of craniotabes has to be very guarded. It is my rule to wait from six to eight weeks before giving expression to a decided prognosis, because during that time medicinal and dietetic treatment will probably have resulted in such an improvement of the symptoms and condition as to render the prognosis more favorable. Under no circumstances, however, ought we to lose sight of the fact that, though rachitis may disappear, the causes leading to it may still linger on. Defective nutrition, diseases of the lungs, and intestinal affections which gave rise to or accompanied rachitis will complicate the prognosis, though rachitis itself, as far as the bones were concerned, be no longer in existence.

TREATMENT.—To meet the cause of a disease by preventive measures is the main object and duty of the physician. He thus either obviates a malady or relieves and shortens it. Now, if the original disposition to rachitis, as has been suggested, is to be looked for in early intra-uterine life, when the blood-vessels begin to form and to develop, we know of no treatment directed to the pregnant woman or uterus which promises any favorable result. But the more we recognize an anatomical cause of the chronic disorder, the more we can appreciate the influence upon the child of previous rachitis in the mother, and are justified in emphasizing the necessity on the part of the woman to be healthy when she gets married, and to remain so while she is pregnant. After the child is born the most frequent cause of rachitis is found within the diet or the digestion of the patient. To attend to the former is in almost every instance equal to preventing disorders of the latter; for most of the digestive disturbances during infancy and childhood are the direct consequences of errors in diet. It is, however, impossible to write an essay on infant diet in connection with our subject. I have elaborated the subject in my Infant Diet (2d ed. 1876), in the first volume of Buck's Hygiene, and of C. Gerhardt's Handbuch d. Kinderk. (2d ed. 1882). Still, the importance of the subject requires that some points should be given, be they ever so aphoristic.

The best food for an infant, under ordinary circumstances, is the milk of its mother. The best substitute for the mother is a wet-nurse. Woman's milk ought not to be dispensed with when there is the slightest opportunity to obtain it, particularly when the family history is not good and nutritive disorders are known to exist, or to have existed, in any of its members. When it cannot be had, artificial food must take its place, and it is in the selection of it where most mistakes are constantly made. This much is certain, that without animal's milk no infant can or ought to be brought up; as ass's milk can be had only exceptionally, and dog's milk, which has been said to cure rachitis, is still less available, the milk of either goat or cow must be utilized. The former ought not to be selected if the latter is within reach, mainly for the reason that it contains, besides other objectionable features which it possesses in common with cow's milk, an enormous percentage of fat. Cow's milk differs in this from woman's milk, that it contains more fat, more casein, more potassium, and less sugar than the latter, and that its very casein is not only different in quantity, but also in chemical properties. Even the reaction of the two milks is not the same, woman's milk being always alkaline, cow's milk often either neutral or amphoteric, and liable to acidulate within a short time. Thus, the dilution of cow's milk with water alone yields no equivalent at all of woman's milk, though the dilution be large enough to reduce the amount of casein in the mixture to the requisite percentage of one, and one only, in a hundred. The addition of sugar (loaf-sugar) and of table-salt, and sometimes alkali (bicarbonate of sodium or lime-water, according to special circumstances), is the least that can be insisted upon. Besides, the cow's milk must be boiled to prevent its turning sour too rapidly, and this process may be repeated to advantage several times in the course of the day. Instead of water, some glutinous substance must be used for the purpose of diluting cow's milk. As its casein coagulates in hard, bulky curds, while woman's milk coagulates in small and soft flakes, some substance ought to be selected which keeps its casein in suspension and prevents it from curdling in firm and large masses. Such substances are gum-arabic, gelatin, and the farinacea. Of the latter, all such must be avoided which contain a large percentage of amylum. The younger the baby, the less is it in a fit condition to digest starch; thus arrowroot, rice, and potatoes ought to be shunned. The very best of all farinacea to be used in diluting cow's milk are barley and oatmeal. A thin decoction of either contains a great deal of both nutritious and glutinous elements, the former to be employed under ordinary circumstances, the latter to take its place where there is, on the part of the baby, an unusual tendency to constipation. The decoction may be made of from one to three teaspoonfuls of either in a pint of water; boil with a little salt, and stir, from twelve to twenty minutes, and strain through a coarse cloth. It ought to be thin and transparent. Then mix with cow's milk in different proportions according to the age of the baby. Four parts of the decoction, quite thin, and one of milk (always with loaf-sugar), for a newly-born, equal parts for an infant of six months, and gradual changes between these two periods, will be found satisfactory. Whenever there is a prevalence of curd in the passage the percentage in the food of cow's milk must be reduced, and now and then such medicinal correctives resorted to as will improve a disturbed digestion. Care ought to be taken lest for the newly-born or quite young the preparations of barley offered for sale contain too much starch. The whiter they are, the more unfit for the use of the very young, for the centre of the grain contains the white and soft amylum in preference to the nitrogenous substances which are found near the husk. Thus, it is safest to grind, on one's own coffee-grinder, the whole barley, but little deprived of its husk, and thus secure the most nutritious part of the grain, which is thrown out by the manufacturer of the ornamental and tidy packages offered for sale. But very few cases will ever occur in which the mixtures I recommend will not be tolerated. In a few of them, in very young infants, the composition recommended by Meigs19 has proved successful. It consists of three parts of a solution of milk-sugar (drachm xvij¾ in pint j of water), two parts of cream, two of lime-water, and one part of milk. For each feeding he recommends three tablespoonfuls of the sugar solution, two of lime-water, two of cream, and one of milk: mix and warm. The baby may take all of it, or one-half, or three-fourths.

19 In Med. News, Nov. 28, 1882.

The recommendations given above are based on a long experience, and the simplicity, cheapness, and facility of preparation of the articles. The substitutes offered for sale under the title of infant foods are in part worthless, all of them expensive when compared with the simple articles recommended by me, and not recognizable as to their uniformity and compounds. But no matter how appropriate my mixture may be, it is always for the young infant to be considered as a makeshift. It is to be used as a representative of mother's milk only when this cannot be had. Therefore it is better to alternate with breast-milk when this is secreted in but an insufficient quantity. Some good breast-milk is better than none at all; but with this proviso, that it is good. There are some milks either too watery or too dense and white. The former will produce diarrhoea, the latter hard and dense curd. The former may be improved by feeding and strengthening an anæmic and overworked mother; the latter, by giving the baby, before each nursing, a tablespoonful of a mixture of barley-water and lime-water, or, when it produces constipation, lime-water and thoroughly sweetened oatmeal-water. The cases in which breast-milk, such as can be had, is not digested by the infant are rare, but they will occur. In them the proper substitute will yield a better result than mother's milk; for mother's milk will not always be a boon, and must then be dispensed with. Particularly is this so when it is too old. Weaning ought to take place when the first group or the first two groups of teeth have made their appearance. After that time mother's milk is no longer the proper food, and instead of preventing indigestion and sickness it is a frequent cause of them and of rachitis. Instead of muscle, it will then give fat, and the large fontanels and big head, the paleness of the rotund cheeks, the flabbiness of the soft abdomen and thighs, will tell the story of rachitical disease slowly engendered by the persistent employment of an improper article of food. I cannot insist too often on this, that rachitis may develop with increasing weight, and that the use of the scales alone is no means of ascertaining the healthy condition of a baby. As much harm, therefore, can be done by weaning too late as by so doing too early or too abruptly.

At that early age we treat of here, digestive disorders are more frequently the results of improper diet than of a primary gastric disturbance. But when the latter is once established it furnishes its own indications. A frequent occurrence, together with a general gastric catarrh, is the presence of fat acids in the stomach, such as an improper amount of lactic, acetic, butyric, etc. acids. Before digestion can be anything like normal they must be neutralized. For that purpose calcined magnesia, carbonate and bicarbonate of sodium, prepared chalk, and lime-water have been found useful. The latter, as it contains but a trifle of lime, in order to neutralize must be given in larger doses than is usually done; a tablespoonful contains but a quarter of a grain of lime. And all of the alkalies must not be given in the food only, but also between meals. For when given in the former way alone it neutralizes the abnormal and injurious acids, together with the normal digestive secretion, the lactic and muriatic. Not infrequently, when the infants have suffered for some time, general anæmia will set in, and result in diminishing the normal secretions of the mucous membranes (and glands). In those cases which do not produce their own gastric juice in sufficient quantity or quality pepsin and muriatic acid may be given to advantage. In these cases the plan suggested by me is particularly favorable—viz. to add a fair amount of chloride of sodium (one-half to one drachm daily) to the infant's food. Also that of I. Rudisch referred to by me previously,20 who mixes one part of dilute muriatic acid with two hundred and fifty of water and five hundred of milk, and then boils (one-half teaspoonful of dil. mur. acid, one pint of water, one quart of milk). Again, there are the cases in which wine and the bitter tinctures, which are known to increase the secretion of gastric juice, render valuable service. The addition of bismuth to any of the proposed plans is quite welcome. As a disinfectant and a mild cover on sore and eroded mucous membranes it has an equally good effect.

20 Am. Jour. Obstet., July, 1879.

Under the head of roborants we subsume such substances, either dietetic or remedial, which are known or believed to add to the ingredients of the organism in a form not requiring a great deal of change. Rachitical infants require them at an early period. Meat-soups, mainly of beef, and of mutton in complications with diarrhoea, ought to be given at once when the diagnosis of rachitis becomes clear or probable. Any mode of preparation will prove beneficial; the best way, however, is to utilize the method used by Liebig in making what he called beef-tea. A quarter of a pound of beef or more, tender and lean, cut up finely, is mixed with a cup or a tumbler of water and from five to seven drops of dilute muriatic acid. Allow it to stand two hours and macerate, while stirring up now and then. This beef-tea can be much improved upon by boiling it a few minutes. It may be given by itself or mixed with sweetened and salted barley-water or the usual mess of barley-water and milk which the infant has been taking before. Older infants, particularly those suffering from diarrhoea, take a teaspoonful of raw beef, cut very fine, several times a day. It ought not to be forgotten, however, that the danger of developing tænia medio-canellata from eating raw beef is rather great. Peptonized beef preparations are valuable in urgent cases.

Iron must not be given during any attack of catarrhal or inflammatory fever. The carbonate (cum saccharo) combines very well with bismuth; a grain three times a day, or less, will answer well. The citrate of iron and quinine (a few grains daily) can be given a long time in succession. The syrup of the iodide of iron (three times a day as many drops as the baby has months up to eight or ten), in sweetened water or in sherry or malaga, or in cod-liver oil, acts very favorably when the case is, as so frequently, complicated with glandular swelling.

Cod-liver oil, one-half to one teaspoonful or more, three times a day, is a trusted roborant in rachitis, and will remain so. Animal oils are so much more homogeneous to the animal mucous membrane than vegetable oil that they have but little of the purgative effect observed when the latter are given. The former are readily absorbed, and thus permit the nitrogenous ingesta to remain in store for the formation of new tissue, but still affect the intestinal canal sufficiently to counteract constipation. As the latter is an early symptom in a peculiarly dangerous form of rachitis, cod-liver oil ought to be given in time (in craniotabes). Diarrhoea is but seldom produced by it; if so, the addition of a grain or two of bismuth or a few doses of phosphate of lime (one to four grains each) daily, may suffice to render the movements more normal. There are but few cases which will not tolerate cod-liver oil at all. The pure cod-liver oil—no mixtures, no emulsions—ought to be given; the large quantities of lime added to it in the nostrums of the wholesale apothecaries embarrass digestion and bring on distressing cases of constipation. These mixtures have been prepared and are eulogized on the plea of their furnishing to the bones the wanting phosphate of lime. The bones, however, as we have seen before, are not grateful enough to accept the service offered. But only a certain amount of phosphate of lime is useful in rachitis and in digestive disturbances. In small doses it neutralizes acids like other alkalies; its phosphoric acid combines with sodium very easily, and gives rise to the formation of glyco-phosphoric acid, which is of very great importance in the digestive qualities of the upper portion of the small intestines.

Plain malt extracts will be well tolerated by some older children. The preparations which are mixed with a goodly part of the pharmacopoeia by generous manufacturers are to be condemned.

Craniotabes requires some special care in regard to the head. The pillow ought to be soft, but not hot; no feather pillow is permitted. The copious perspiration of the scalp requires that it should be kept cool, the perspiration wiped off frequently to avoid its condensing into water, and the flattening side of the head may be imbedded in a pillow with a corresponding depression. Copious perspiration indicates the frequent washing with vinegar and water (1:5-6). The muscular debility commands great caution. The baby must not be carried on the arm, but on a pillow which supports both back and head, or in a little carriage. No sitting must be allowed until the back will no longer bend to an unusual degree. No walking must be encouraged at any time. The patients will walk when their time has come. The bones are so fragile that great care is needed sometimes not to fracture or to infract them and to avoid periosteal pain in lifting. The skin must undergo some training by gradually accustoming the little patient to cool water. It can be readily, but gradually, reduced to 70° for a bath at any season. The addition of rock- or table-salt to the bath is a welcome stimulant. And fresh air ought to be granted freely.

Laryngismus stridulus shares the indications for treatment furnished by craniotabes. The general treatment remains the same. Prominent symptoms and complications ought to be treated besides; constipation requires the more attention the more convulsive attacks of any description may arise from reflex action. The general nervous irritability may be relieved by bromide of potassium, sodium, or ammonium. One gramme daily (15 grains) of either, in three doses, is well tolerated for a long period. When there are symptoms of an imminent convulsion, or to soothe the convulsibility which may break out any moment, chloral hydrate, eight or ten grains in from one hour to four hours, two grains in a dose, will be convenient. If the stomach refuses or is to be spared, from four to eight grains may be given in an enema of warm water. A severe attack of convulsions ought to be checked with inhalations of chloroform. When a warm bath is to be had, care should be taken that the child be not tossed about. Hold the baby in a small sheet or a large napkin, and immerge it thus into the water, raising the head and cooling it with cold cloths or an ice-bag. Genuine attacks of laryngismus with well-developed stages—the first paralytic, the second spasmodic—give but little time for any treatment. The proposition to apply the electrical current is well meant, but the attack has passed by, or terminated fatally, or resulted in a general convulsion, before the apparatus can possibly be in operation. I can imagine, however, that a Leyden flask kept ready might be used to advantage during the stage of apnoea for the purpose of bringing on inspiration. Sprinkling with cold water, beating with a wet towel, shaking by the shoulders, may certainly contribute to awake respiratory movements. The advice to wait quietly until the attack has passed by is more easily given than carried out. Marshall Hall's direction to perform tracheotomy will, I hope, soon be forgotten.

Nothing is more gratefully appreciated by the little patients than air. May it never be forgotten that night-air is better than foul air, and that furnace-air means air greatly modified by injurious additions. More than twenty years ago I was in occasional attendance upon a male baby—now a medical man of some promise—with craniotabes and a number of general convulsions. No treatment would remove, or even relieve, the attacks, until, without the physician's advice, the father took the baby into the street in the hardest winter weather. After the first long absence from his furnace the baby was well of his convulsions, and the physicians profited by their involuntary experience.

In the same way that salt-bathing is beneficial, so is sea-air. A summer at the seaside is a great blessing to rachitical children. Sea-baths have been arranged for them in France (Berx-sur-mer), in Italy (San Ilario di Nervi, Viarreggio, Livorno, Volti, Fano), in England (Margate), in Germany (German Sea, by Prof. Beneke), and for some little time past in the neighborhood of our own large cities.

Complications command great attention in rachitis, particularly where there is danger from the affection of the nerve-centres, for the slightest irritation in some distant part of the body may give rise to an outbreak. Thus, in craniotabes it is desirable to watch even the gums. Not sharing the etiological superstition which attributes so many diseases of infancy to dentition, I still know that a slight irritation of the gums may suffice to exhaust the slim resisting power of the infant. If there be local swelling and congestion of the gums over a growing tooth, it may become necessary, or at least advisable, to lance. An otitis which under ordinary circumstances would give rise to no symptoms at all besides some inconvenience or slight pain will prove the source of great danger in a rachitical (craniotabic) infant. The chronic bronchial catarrh and frequent broncho-pneumonia of such patients require early attention, for they and the neighboring lymphatic glands stand too much in the relation of a vicious circle of cause and effect.

Rachitical constipation, depending on incompetency of the intestinal muscle, must not be treated with purgative medicines. Now and then, when a great deal of abnormal acid is formed in the stomach, calcined magnesia, a grain or two given before each meal, will control that disorder and at the same time keep the bowels open. But, as a rule, every purgative after it has taken effect will leave the intestinal muscular layer less fitted to perform its functions than before. Its place may be taken by a daily enema of tepid water. Further indications are—such a change in the food as will contribute to keep the bowels moist and slippery, but principally such a modification of food and such medical treatment as are known to prove beneficial when all the symptoms of rachitis are fully developed. When the cause of the infant's rachitis can be traced back to the mother or to an insufficient quality of her milk, she must give way to a wet-nurse, or the nurse must be changed for similar reasons. When neither mother nor wet-nurse prove competent, or either be dangerous, artificial food will take their place to advantage in the manner I have stated above. Beef-soup or beef-peptone is to be added to the baby's food daily. Of the two best farinacea, barley- and oat-meal, the latter is preferable as an addition to cow's milk, because of its greatly laxative effect. The percentage of cow's milk in the food ought to be more carefully watched than in other conditions. Pure cow's milk or cow's milk mixed with water only is borne worse in no other condition. Half a drachm or more of table-salt and a few drachms of sugar ought to be added to the daily mess. The general indications require the administration of iron, which has no constipating effect in this ailment. Particularly is that the case with the iodide of iron. Cod-liver oil, in three half-teaspoonful or teaspoonful doses daily, acts very satisfactorily both for its general rachitical and for its local effect on the mucous membranes. Now and then massage, repeated many times a day a few minutes each time, practised with the palm of the hand only, or gentle friction, with the dry or oiled hand, of the abdominal surface, will prove effective in bringing about peristalsis and strengthening the intestinal muscle. An obstinate case may also require two daily doses of one one-hundred-and-fiftieth or one one-hundred-and-twentieth of a grain of strychnia for the same purpose, or such other improvements on the above detailed plan as the judgment of the attending physician may direct. At all events, the diagnosis of any case, and the appreciation of the cause of any ailment, are, to a well-balanced and educated mind, of infinitely greater value than any number of specified rules and prescriptions.21

21 Jour. Obstetr., Aug., 1869.

It is not impossible that phosphorus, in substance, not in any of its compounds, may prove of great utility in the treatment of rachitis. Minimal doses of phosphorus render the newly-formed tissue at the points of apposition of the bones more compact in a very brief time. The new formation of blood-vessels in the osteogenous tissue gets retarded by it. Larger doses of phosphorus, however, increase vascularization, and osseous tissue is either less rapidly formed or even softened. When the doses are still larger, vascularization and softening may rise to such a point as to separate the epiphysis from the diaphysis. Thus the administration of the drug results in an irritation which, according to the doses employed, may give rise either to normal condensation or to inflammatory disintegration. This experience, arrived at by Wegner in a great many experiments made on animals, Kassowitz has confirmed. For its therapeutic effect he tried phosphorus in 560 cases of rachitis. Employing doses of one-half milligramme (one one-hundred-and-twentieth of a grain) several times daily (less will suffice), he soon found the skull to become harder, the fontanel smaller, the softening of the bones of the thorax and extremities to disappear, and all the other symptoms of rachitis to improve. This result was obtained though no particular change in the feeding of the patients was resorted to. To what extent this experience will be verified by others we shall soon learn. My own is already sufficiently extensive to base upon it a strong recommendation of the plan of treatment I have detailed. My therapeutical results in other diseases of the bones also encourage me to believe that phosphorus will accomplish much in the treatment of rachitis. Ever since Wegner's publications—viz. these thirteen or fourteen years—I have utilized phosphorus in cases of chronic and subacute inflammations of the bones, mainly of the vertebral column and the ankle-joint and tarsus. After having taught the method for many years in my clinic and otherwise, I made a brief communication on the subject to the Medical Society of the State of New York.22 Since that time, again, I have followed the same plan in many cases of the same description, and feel sure that the prognosis in this serious class of bone diseases has become more favorable and recovery speedier. Infants of a year or more were given a dose of one-eightieth or one one-hundredth of a grain of phosphorus daily. One grain, dissolved in an ounce of oil or cod-liver oil, is a convenient mixture, four or six drops of which may be administered daily in two or three doses.

22 Trans., 1880.

From what I have seen of phosphorus in bone disease, and what is thus far known by experience in rachitis, it appears to me that it will be of decided advantage in that form of acute rachitis which is apt to destroy rapidly with the symptoms of acute epiphysitis, rapid pulse, diarrhoea, rapid diminution of strength, and scorbutic gum. In the few cases I have seen these last years it appeared to me to act satisfactorily, together with immobilization of the whole body.

Rachitical curvatures are very apt to become less marked while growth is increasing and the limbs extending. But many of them are so marked that they remain for life. Many of these might have been benefited by timely orthopædic interference. That the application of Sayre's jacket is indicated in every form and stage of spondylitis, though it be not equally valuable in all forms, goes without saying; and that infractions ought to be straightened and supported by splints when observed and when practicable, is self-evident. But, as a rule, while the chronic rachitical process is developing in the long bones the use of mechanical apparatuses is of doubtful merit; they ought not to be resorted to before the healing has at least commenced. Nor is it advisable to postpone mechanical interference so long that eburnation of the bones has time to take place. Surgical operations for the purpose of removing the curvature are of different nature according to the different types to be treated. Mere straightening of the curvatures is indicated, and successful with children under two years. Osteoklasy—that is, fracturing of the curvature while the periosteum is left intact—is successful in children of three (or four, according to Volkmann) years. The fracture does not injure the periosteum, and is always transverse. In later years osteotomy has proved successful to an almost unexpected degree, and is one of the happiest achievements of modern surgery.

Partly as a preventive, partly as a curative measure, Gramba of Turin and Pini of Milan point to well-directed gymnastics as a requisite in the treatment of rachitis. For older children they have established schools in which systematic exercises are brought to bear on chronic deformities.