Although scurvy is more a deficiency disease than one of the haemopoietic system, it has two points of resemblance: marked capillary bleeding and progressive anemia. Scurvy is due to a prolonged deficiency of vitamin C in the diet and takes about 4 to 8 months to develop clinical signs. Habitation in an unhealthy surrounding predisposes.

Vitamin C is required for the activity of prolyl hydroxylase, which is responsible for the extensive hydroxylation of prolines in collagens. Deficiencies in proline hydroxylation interfere with the assembly of the procollagen triple-helix, resulting in degradation of the collagen. An understanding of the cause and remedy for scurvy grew out of the experience of British sailors in the 18th century. It occupies an interesting place in the history of the world when English sailors became progressively ill after long voyages at sea. It was only with the observation that the consumption of fruit helped to ward off the devastating effects of scurvy did the sailors begin to transport limes with them.

Scurvy has been known since ancient times, but the discovery of the link between the dietary deficiency of ascorbic acid and scurvy has dramatically reduced its incidence over the past half-century. Sporadic reports of scurvy still occur, primarily in elderly, isolated individuals with alcoholism. The incidence of scurvy in the pediatric population is very uncommon, and it is usually seen in children with severely restricted diets attributable to psychiatric or developmental problems. The condition is characterized by perifollicular petechiae and bruising, gingival inflammation and bleeding, and, in children, bone disease.

Scurvy was in some ways a more serious, certainly a more widespread problem. Relatively few men actually died of scurvy except on very long ocean passages, but it effectively limited the time a squadron could stay at sea, and thus directly affected the efficiency of the Service. No strategy of blockade, or any other which depended on keeping squadrons at sea for long periods, was possible in the face of endemic scurvy. The difficulty was to find a cure.

Much has been made by medical historians of the work of Dr. James Lind, the great naval physician who first provided experimental proof of the antiscorbutic properties of oranges and lemons, and the Admiralty has been freely castigated for not adopting this remedy at once. In fact Lind's celebrated controlled trial may have occurred by accident, and he does not appear to have appreciated its importance himself, or to have made it very clear to his readers.

The value of lemons against scurvy was a commonplace known amongst seafarers for generations, but the fruit was only one of many remedies, good or bad, which neither the naval nor the medical world had any scientific method of sifting. Moreover, lemons were scarce and expensive in northern Europe, and the obvious method of preserving them incidentally destroyed the vitamin.

Patients may present with hyperkeratotic papules centered in follicles. Hair may grow in a corkscrew-like pattern and may be associated with hemorrhage, often with minor trauma. In chronic disease, ecchymoses, usually over pressure points such as the shins, may occur. The mouth may show gingival hypertrophy. Hemorrhage may occur in any mucosal surface including conjunctiva, sublingual, and skin. In addition, hemorrhage in the skeletal muscle, intra-articular sites, and subperiosteal region of the epiphyses of the long bones may occur.

What are the causes of scurvy?

Fortunately, there was a general understanding among sea officers that scurvy was a dietary disease, caused either by the presence of something harmful in the sailor's diet, or by the absence of something essential, and in either case curable by fresh victuals.

Scurvy is due to a prolonged deficiency of vitamin C in the diet and takes about 4 to 8 months to develop clinical signs.

Habitation in an unhealthy surrounding predisposes.

What are the signs and symptoms of scurvy?

In scurvy, the body stores are markedly depleted; plasma concentration is nearly nil and none in the urine. The white blood cells and the platelets normally have a concentration of about thirty times of blood plasma.

The chief deficiency sign is an inability of producing and maintaining the intercellular ground substance as collagen of all fibrous tissues: the matrix of bones, cartilages and dentine and all non-epithelial cement substances especially of vascular endothelium. As a result there is an increased permeability of the capillaries to the red blood corpuscles causing hemorrhages, new bone formation stops but as bone absorption still goes on, the bones become friable at the growing ends, interference with timely collagen formation causes delay in healing of wounds.

Some other important symptoms of scurvy are gradual weakening, pale skin, sunken eyes, tender gums, muscle pain, loss of teeth, internal bleeding, and the opening of wounds such as sword cuts that had healed many years before.

Exhaustion, fainting, diarrhea, and lung and kidney trouble followed.

There is massive periosteal reaction with increase in the distance between tibia and fibula.

This deficiency disease usually shows epidermal pallor in the upper part of the epidermis.

Psoraisiform hyperplasia with pallor of the lower half of the epidermis.

Numerous extravasated rbcs with lymphocytic infiltrate in the upper dermis are also present.

The diagnosis of scurvy is made on clinical and radiographic grounds, and may be supported by finding reduced levels of vitamin C in serum or buffy-coat leukocytes. The response to vitamin C is dramatic. Clinicians should be aware of this potentially fatal but easily curable condition that is still occasionally encountered among children.

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