The outcome of scurvy, as we encounter it in peace time in the Temperate Zone, is generally favorable, so that it plays but an insignificant rÔle in our mortality statistics. This results from the fact that we are abundantly provided with a specific remedy, so that if the diagnosis is made early and treatment is prompt and thorough, the patient will rapidly recover and suffer no physical disability. Where antiscorbutic foodstuffs are not procurable, however, this disease constitutes a terrible scourge, causing many deaths and spreading among an army, a ship’s crew, or among the civil population with the rapidity of an epidemic. For example, the ships of the East India Company in their voyages round the Cape often lost nearly one-half of their crews, and in Lord Anson’s famous voyage round the world 380 out of 510 seamen perished from the disease. Moreover, if the antiscorbutic treatment is inadequate or the patient goes untreated for a long period, the cure may be incomplete, a condition of malnutrition and weakness developing, which may persist for years. To appreciate this clinical condition we must refer to the account of physicians who saw thousands of cases of severe and untreated scurvy among the sailors, who were of necessity deprived of aid until they reached land. Lind laid stress on a type of this disease which developed under these circumstances and which he termed “obstinate scurvy.” He writes: “I have met with numerous instances not only among the common seamen, but of officers, with whom it had taken such deep root in the constitution as to prove a lasting affliction to them during a great part of their lives.... Persons are likewise subject in different periods of their life afterwards to habitual rheumatism, pains and stiffness in their joints; and sometimes eruptions on the skin.” In his treatise on scurvy, published in 1685, Harvey refers to this chronic nutritional disorder as “inveterate scurvy.” He pictures patients who had gone untreated for a long time as “molested with vagrant, ambulative, distending, creeping, vellicating or lancinating pains of several parts of the body.... They are often loose and subject to falling into violent fluxes of the belly, diarrhoea and lienteries.”

Infants as well as adults usually recover rapidly and completely from scurvy, the result depending largely upon the early recognition of the disease. We must always bear in mind, however, that from a histologic standpoint the cure is not simultaneous with the magic disappearance of the clinical symptoms, but that months probably elapse before the tissues return to their normal state. It is difficult to give reliable mortality statistics for infantile scurvy, for so many cases are of the rudimentary form that percentages are necessarily misleading. Still writes that in 5 out of 64 cases the disease proved fatal by diarrhoea and exhaustion. The American Pediatric Society reports 29 deaths out of 397 cases, which gives a similar mortality percentage. When infantile scurvy was not so generally recognized by physicians the mortality was much higher, and we find that Barlow encountered 7 deaths in his first series of 31 cases.

Even when the child recovers it may not regain its normal health if it has continued for a prolonged period in a state of chronic scurvy. It may remain pale and fail to gain in weight in spite of a liberal and well-balanced diet. Cases of this kind are not infrequent. In this connection it is worthy of note that 4 of the 41 cases of “coeliac disease,” an interesting intestinal condition described by Still, had scurvy just before or during the onset of the disease. This observation conforms to the experience that chronic bowel disorders often follow in the wake of adult scurvy.

In adults the heart may be weakened by scurvy, and death may result from cardiac failure. Cardiac disturbances occur also in infantile scurvy. This involvement might be expected, in view of the tachycardia (cardiorespiratory phenomenon) which is so frequent a symptom of infantile scurvy. The heart may be rapid for months or even for years after the disorder, and tachycardia may develop on the occasion of even a mild infectious disease. For example, a fever of 101°, due to a common coryza, may cause the heart-beat to rise to perhaps 180 a minute. Children so affected succumb readily to infection, especially to pneumonia, which may lead to sudden collapse followed by death.

An important factor in the prognosis of scurvy, as in that of other disorders due to a lack of vitamines, is the marked susceptibility to infection. Even latent or subacute scurvy causes a peculiar susceptibility to diphtheria (especially the nasal type), to coryza, bronchitis, and pneumonia. A perusal of the literature shows that this susceptibility was noted by the older authors in relation to adults.

The local signs usually disappear quickly without leaving any trace. The hemorrhages are absorbed and the eczema heals within a few days. The fractures unite promptly with the formation of an unusually large callus. The urine, which may have contained red blood-cells or have been markedly hemorrhagic, quickly becomes normal and, in our experience, gives no further evidence of renal damage. Still reports, however, the case of a frail child who had a trace of albumen in the urine two years after an attack of scurvy. A rare local injury, which may lead to death, is cerebral hemorrhage. Recently Sammis reported a case of this kind, which was characterized by convulsions during life, and in which subdural hemorrhage was found at necropsy.

If we acknowledge an individual idiosyncrasy to scurvy we should expect a tendency to a recurrence of the disease. Lind was of this opinion, stating that “by observations made on this disease, it appears that those who are once afflicted with it, especially in so high a degree as that squadron was, are more subject to it afterwards than others.” It is difficult at the present day to express a personal opinion on this matter, as clinical experience is meagre and the scurvy of guinea-pigs is so acute that it cannot be used for comparison. Some of the recurrences have been due probably to the fact that the patient had not been completely cured of his first attack. We have met with two cases of recurrences in infants, one of which is of particular interest as it happened in spite of giving lemon juice in the intervening period. The history was as follows:

In September, 1914, one month after the baby was admitted to the institution, it developed scurvy of a moderate grade. It was then six months of age and weighed 10¼ pounds. It was put on a simple mixture containing from 24 to 30 ounces of pasteurized milk and was given in addition ½ ounce of lemon juice a day. It improved, but during the winter had bronchitis, otitis, enteritis, and later furunculosis. In spite of the fact that it had been receiving an antiscorbutic for almost this entire period, it developed scurvy once more in February, at the age of 11 months, and when it weighed 14½ pounds. It was evident that this baby was peculiarly susceptible to scurvy. It may be added that the second attack was complicated by nasal diphtheria.

In this connection attention should be drawn to a peculiar and puzzling clinical phenomenon, which we have noted several times. Even if the antiscorbutic treatment is carried out incompletely and only for a short period, recrudescences may not take place. We have seen cases where orange juice was given for merely ten days or two weeks—that is, only until all scorbutic signs had disappeared,—and yet the scurvy did not return, the infants thrived for months thereafter, but were merely somewhat pale and undernourished. In the case of two babies which we have in mind, the diet remained absolutely unchanged, with the exception of the short period of antiscorbutic treatment, but this seemed sufficient to bring about a diminished susceptibility.