Introduction
Background
The term scurvy is derived from the Nordic word skyrbjugr, meaning swelling or edema. It has also been suggested that the term is derived from the Old Icelandic words skyrbugr, scarby, or skurvic.
Scurvy is caused by a lack of vitamin C and manifests as collagen defects, hemorrhagic diathesis, abnormalities in bone maturation, epiphyseal disease, lifting of the periosteum, and hemarthroses.1,2,3
Related eMedicine topics:
Scurvy (Endocrinology)
Scurvy (Dermatology)
Frequency
United States
Scurvy is not common in the US, though in one study, vitamin C deficiency was present in up to 23% of respondents.4,5 Young children and older persons are predisposed to scurvy because of their diet or the overpreparation of food (cooking destroys vitamin C). Smokers, non-Hispanic black males, and individuals who do not use vitamin supplements have an increased risk of vitamin C deficiency.4
International
Internationally, scurvy is rare. Young children and older persons are predisposed to scurvy because of their diet or the overpreparation of food (cooking destroys vitamin C).
Mortality/Morbidity
- Scurvy can lead to many other conditions, such as mental status alteration, gum disease and tooth loss, ecchymoses, hemarthrosis, the failure of wounds to heal, the breakdown of healed ulcers, heart and skeletal muscle damage, abruptio placentae, gastrointestinal blood loss, and arrested skeletal development.
- Epiphyseal separation at the epiphyseal plate is a complication.
- Sudden death has been reported.
Sex
Males and females are equally affected.
Age
Those most commonly affected are children aged 6-18 months; however, adults can also be affected. Unless the mother had a deficiency herself, the maternal contribution of vitamin C is generally protective of infants younger than 6 months.
Presentation
Presentation and natural history
Perivascular hemorrhage and lifting of the periosteum caused by hemorrhage are the main anatomic alterations depicted on radiographs. This hemorrhage is due to increased capillary fragility. In scurvy, there is normal mineralization of osteoids; however, the overall amount is decreased. This process is distinct from that in rickets, in which the lack of vitamin D results in defective mineralization of a normal organic matrix.
Scurvy is the direct result of vitamin C deficiency. Vitamin C is required for prolyl and lysyl hydroxylase activity and is essential for collagen synthesis. Defective collagen compromises skin, joint, bone, and vascular integrity. Vitamin C is also required for carnitine synthesis, and it is critical for fatty acid transportation into the mitochondria. This oxidative metabolism is also critical for muscle function.
Scurvy is usually caused by a lack of dietary vitamin C related to inadequate food intake, the destruction of vitamin C in food caused by cooking and canning, or the absence of fresh fruit in the diet. Malabsorption, tobacco use, chronic oxidative stress (eg, HIV infection, inflammatory bowel disease, endotoxemia, diabetes, heat stress), hemodialysis, and therapy with the folic acid antagonist aminopterin all reduce the level of vitamin C in the body. In studies of vitamin C deficiency, the most common associated causes included poor dentition, gastrointestinal disease, food fads, and alcoholism.6,7
The normal total-body pool of vitamin C is 1500 mg. The normal plasma level of vitamin C is 0.7-1.2 mg/dL. Scurvy occurs when the total-body vitamin C level is below 350 mg. The elimination of vitamin C from the diet results in scurvy within 2-3 months. A total vitamin C intake of 10 mg/d maintains the total-body pool above 350 mg and prevents scurvy.Clinical symptoms include the following:
- Lethargy, listlessness, mental confusion, and fatigue
- Pale, bloated complexion and dry, rough skin as a result of defective collagen
- Hair follicle enlargement and plugging; perifollicular congestion; proliferation of blood vessels; formation of lumps in hair follicles; fractured, coiled, or bent hairs; and perifollicular hemorrhage caused by defective collagen
- Swollen and purple gums, putrid and bleeding gums, or loosened teeth as a result of defective collagen
- Ecchymoses due to blood-vessel fragility (Purpura may become palpable.)
- Costochondral junction swelling; hemarthrosis; and pain, stiffness, or swelling of the knees or ankles as a result of bleeding
- Arrested skeletal development caused by defective collagen
- Impaired wound healing and breakdown of previously healed ulcers caused by defective collagen
- Dyspnea, chest pain, abruptio placentae, intraocular hemorrhage, diarrhea, and gastrointestinal blood loss caused by fragile blood vessels and defective collagen
- Femoral nerve compression by hematomas
- Normocytic anemia and macrocytic anemia related to osmotic fragility of the red blood cells
- Hypotension due to blood loss and vascular fragility
- Hematuria
- Subdural hemorrhage
- Sudden death
Individuals with renal complications who are receiving dialysis may be susceptible to vitamin C deficiency. Dietary restrictions associated with dialysis generally limit the amount of potassium that a patient may ingest in order to avoid hyperkalemia. Unfortunately, many foods rich in potassium, such as orange juice, strawberries, and broccoli, are also the best sources of vitamin C. In addition, the dialysis process removes a significant amount of vitamin C from the body. This is further compounded by the fact that the use of vitamin C supplements may lead to oxalosis, which can cause renal and liver problems. Often, physicians have avoided vitamin supplementation in order to safeguard against oxalosis. New research suggests that the benefits of vitamin C supplementation and advances in dialysis techniques may lead to an increased use of vitamin C to control anemia for dialysis patients.8
Treatment
- No radiologic interventions are indicated, although the dietary provision of recommended daily allowances of vitamin C is generally recommended.
Differential Diagnoses
Other Problems to Be Considered
Copper deficiency
Vasculitis
Clotting factor deficiency
Leukemia
Thrombocytopenic purpura
Henoch-Schönlein purpura
Meningococcemia
More on Scurvy |
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References
Bohrer I, Roy M, Nager W, te Wildt B, Emrich HM, Ohlmeier MD. [Scurvy--a wrongly forgotten avitaminosis]. MMW Fortschr Med. Nov 8 2007;149(45):41-3. [Medline].
Léger D. Scurvy: reemergence of nutritional deficiencies. Can Fam Physician. Oct 2008;54(10):1403-6. [Medline].
Sommer A. Vitamin a deficiency and clinical disease: an historical overview. J Nutr. Oct 2008;138(10):1835-9. [Medline].
Hampl JS, Taylor CA, Johnston CS. Vitamin C deficiency and depletion in the United States: the Third National Health and Nutrition Examination Survey, 1988 to 1994. Am J Public Health. May 2004;94(5):870-5. [Medline].
Velandia B, Centor RM, McConnell V, Shah M. Scurvy is still present in developed countries. J Gen Intern Med. Aug 2008;23(8):1281-4. [Medline].
Burk CJ, Molodow R. Infantile scurvy: an old diagnosis revisited with a modern dietary twist. Am J Clin Dermatol. 2007;8(2):103-6. [Medline].
Olmedo JM, Yiannias JA, Windgassen EB, Gornet MK. Scurvy: a disease almost forgotten. Int J Dermatol. Aug 2006;45(8):909-13. [Medline].
Handelman GJ. Vitamin C neglect in hemodialysis: Sailing between Scylla and Charybdis. Blood Purification. 2007;25(1):58-61. [Medline].
Karthiga S, Dubey S, Garber S, Watts R. Scurvy: MRI appearances. Rheumatology (Oxford). Jul 2008;47(7):1109. [Medline].
Francescone MA, Levitt J. Scurvy masquerading as leukocytoclastic vasculitis: a case report and review of the literature. Cutis. Oct 2005;76(4):261-6. [Medline].
Rothschild BM, Martin LD. Paleopathology: Disease in the Fossil Record. London: CRC Press; 1993.
Willmott NS, Bryan RA. Case report: scurvy in an epileptic child on a ketogenic diet with oral complications. Eur Arch Paediatr Dent. Sep 2008;9(3):148-52. [Medline].
Further Reading
Keywords
scurvy, vitamin C deficiency, ascorbutism, scorbutism, Barlow disease, Barlow's disease, subperiosteal hematoma syndrome, hypovitaminosis C, collagen defects, hemorrhagic diathesis, abnormalities in bone maturation, epiphyseal disease, lifting of the periosteum, hemarthroses
