Scurvy, Past and Present

by Alfred F. Hess

The identity of scurvy in the infant, in the young child and in the adult is thoroughly established and requires no further substantiation. There are, however, sufficient differences between the symptoms of adult scurvy and those of Barlow’s disease to render it advisable to consider them separately. These distinctions are due largely to the fact that the former disorder affects mature tissues, whereas the latter is engrafted upon tissues which are in the process of rapid growth and development. The symptomatology is influenced also by the striking differences in environment—the passive, shielded existence of the infant, contrasted with the active and exposed life of the adult. Although we shall, therefore, treat adult and infantile scurvy separately, it should be borne in mind that, from an etiologic and pathologic viewpoint, such a division is artificial and is resorted to merely for purposes of clarity.

Adult Scurvy.—The earliest sign of scurvy is usually a change in the complexion of the individual. His color becomes sallow or muddy, an aspect difficult to describe, but one which is characteristic, and constitutes an important danger signal to the eye of the experienced physician. About the same time the patient loses his accustomed vigor, seemingly becomes indolent and complains of tiring quickly, and of breathlessness. He may experience fleeting pains in the joints and limbs, especially in the legs, symptoms which are frequently attributed to rheumatism. At this early stage the appetite may still be normal, there is usually no loss in weight, but merely a general malaise which is significant, although in no way distinctive. Very soon the gums become sore, bleed readily, and are found to be congested, spongy, and somewhat hemorrhagic at their edges. Absolute reliance must not, however, be placed on this sign for early diagnosis, as at times it does not appear until later. Careful examination at this stage will disclose petechial spots on the body, more especially on the legs, at the site of the hair follicles, or even larger ecchymoses, depending upon the hemorrhagic tendency of the individual, his exposure to bruising, the adequacy of his diet, and secondary infection. Less frequently bleeding from the nose occurs early, or the eyelid suddenly becomes swollen and purple, or the urine shows the presence of blood.

These signs progress steadily with a varying degree of rapidity. The complexion becomes more dingy and somewhat brownish, the weakness increases so that the slightest exertion causes breathlessness and palpitation, and the gums become spongy and even fungous. If there is infection of the gums and the teeth are carious, the breath is extremely foul—a sign long associated with scurvy. Later the teeth become loose and may fall out, and the alveolar process undergoes necrosis. The surface hemorrhages increase in severity, large effusions appearing on the trunk, on the extremities, and less often beneath the mucous membrane of the mouth. A bloody diarrhœa may take the place of the constipation which is generally noted earlier in the disease. There are at this time hemorrhages into the muscles and deeper tissues, especially into the calves of the legs, giving rise to hard, brawny, tender swellings which have been termed “scurvy sclerosis.” This is sometimes the earliest sign noted by the patient and may puzzle the physician who has not met with it before. The swelling may be found in the popliteal space or at the site of the tendo Achilles, and result in lameness and contracture of the neighboring joint. Frequently there is slight edema of the ankles associated with a glossiness of the extensor surfaces of the legs. This infiltration differs from ordinary edema in being firm and not pitting on pressure. The skin is dry and rough, the follicles being unusually elevated;[46] the hair likewise is dry and loses its lustre. Not infrequently subperiosteal hemorrhages occur, giving rise to exquisitely tender swellings, especially of the tibia or of the femur, or of the ramus of the lower jaw, as has been noted in connection with guinea-pig scurvy. If there are wounds or ulcers they assume a hemorrhagic aspect, the edges becoming bluish or livid and showing no tendency to heal; even scars which have existed for many years change in color and show an altered state of nutrition, and ulcers long healed break out afresh.

Nowadays, the disease usually does not reach this stage, and rarely progresses further. If, however, the patient remains untreated, he becomes progressively weaker and more lethargic; there is frequent palpitation, shortness of breath, and increasing loss of weight. The pains in the limbs render him helpless and an object of pity. Marked edema may be added to the picture as the result of starvation, so that the legs become swollen, and even the face becomes bloated. Hemorrhages into the skin as large as the palm of the hand appear on different parts of the body. The gums swell to such an extent that they overlap and may even hide the teeth and protrude from the mouth as foul fungoid growth. Death comes about in various ways. Frequently sudden and fatal syncope occurs, due to heart weakness or to the pouring out of fluid into the pleural or the pericardial cavities. Another frequent cause of death is secondary infection, resulting in pneumonia, which finally ends the suffering of the patient. The fatal outcome is thus described in the narrative of Lord Anson’s voyage:

“Many of our people, though confined to their hammocks, ate and drank heartily, were cheerful, and talked with much seeming vigor, and in a loud, strong tone of voice; and yet, on their being the least moved, though it was only from one part of the ship to another, and that in their hammocks, they have immediately expired; and others, who have confided in their seeming strength, and have resolved to get out of their hammocks, have died before they could well reach the deck. And it was no uncommon thing for those who could do some kind of duty, and walk the deck, to drop down dead in an instant, on any endeavor to act with their utmost vigor; many of our people having perished in this manner during the course of this voyage.”

The disease may develop and progress in various ways. It may remain latent for a long period and be cured by some accidental change of diet, or, as more frequently occurs, it runs a moderately acute course, and is promptly cured by means of antiscorbutics. In the days when scurvy was common and widespread it sometimes became chronic, developing into the “inveterate scurvy” of the older authors, which was notably resistant to treatment. Harvey, in his treatise published in 1685, states that “a mild scurvy may continue or be protracted to ten, twenty, or thirty years.”

In addition to the general picture of the disease which we have presented, mention should be made of other less common symptoms. As is well known, one of the characteristic signs of scurvy is hemorrhage. Indeed, in many of the systematic treatises of medicine it is classified as a hemorrhagic disease. Besides the bleeding into the gums, skin and bones, hemorrhage into the stomach may take place, giving rise to hæmatemesis, or there may be hemorrhage into the eye, under the conjunctiva or into the anterior chamber, leading to the destruction of the eyeball. A very unusual form is meningeal bleeding, giving rise to symptoms of apoplexy. It may be stated in general that hemorrhage dominates the picture of scurvy. Eruptions which in normal individuals are simply macular or papular, assume a hemorrhagic character when occurring in a scorbutic individual. This phenomenon was noted in the recent war in connection with the eruption of typhus fever, and has been observed by military and naval surgeons in numerous expeditions.

Scurvy reduces the nutritional state of probably all the cells and tissues of the body. If the resistance is still further lowered by exposure, nutritional disturbances will result more readily than where the tissues are normal and well nourished. For this reason we believe that scurvy may predispose to frostbite. Reports of congelations occurring in the trenches in the course of the World War tend to confirm our opinion that scurvy was a predisposing factor in many of these cases. This has been true in other wars. For example, Munson writes that “during the Crimean War the temperature was never very low and a report of the times suggests that the large number of congelations observed among the soldiers might well be regarded as gangrene owing to a scorbutic tendency exaggerated by the cold.”

In connection with the involvement of the gums, another typical symptom of scurvy, it should be remembered that this sign may appear late and therefore fail to be of value for early diagnosis, and that it occurs also in purpura and thus may lead to error. This is especially the case if there is pyorrhœa. As is well known, hemorrhages of the gums appear only where teeth are present, and are absent in the edentulous gums of old people as well as in babies who have no teeth. Immerman is probably correct in believing that an injury is always necessary to produce a hemorrhagic lesion in scurvy, and that this explains the early involvement of the gums and also their non-implication in the absence of teeth.

It is a common belief that separation of the epiphyses occurs only in infants and young children, and not in the scurvy of adults. This, however, is not correct, as in severe adult scurvy there is frequently a separation of the epiphyses of the long bones of the lower extremities or of the ribs, the latter resulting in a sinking of the sternum.