A vitamin C deficiency characterized by tooth and gum
bleeding and decay, hemorrhages, and increased susceptibility to infection.
Hypoascorbemia; Vitamin C Deficiency.
Not known. Uncommon in developed countries but
increasing incidence in certain populations, including alcoholics,
institutionalized elderly, and those with postsurgical malabsorption
Scurvy arises from the deficiency of ascorbic acid
(vitamin C), which is often the result of prolonged lack of fresh fruit or
vegetables in diet, historically common among the sailors on long sea
voyages. Humans, unlike most other animals, do not possess the enzyme l-gulonolactone oxidase and thus are unable to synthesize ascorbic acid
from the glucuronic acid or galactonic acid derived from glucose.
Recommended daily allowance for ascorbic acid is 35 mg in infants, 45 to 50
mg for children, and 60 mg for adults. Ascorbic acid accelerates the
hydroxylation reactions in a number of biosynthetic pathways. If ascorbic
acid is replaced by other reductants, most of the enzymes in these pathways
are still functional but not at optimal activity. It is best known for its
essential role in the hydroxylation of proline and lysine to enable
cross-linking and stabilization of collagen.
Clinical features and laboratory evaluation. Plasma
ascorbate level is absent in clinical significant cases. Blood count usually
shows anemia, which may be as a result of poor iron and/or folate
absorption. Coagulation and biochemistry may also show abnormalities in
association with poor nutritional status, including prolonged activated
partial thromboplastin time (aPTT) and international normalized ratio (INR),
low albumin, low protein, low cholesterol, and low sodium and potassium
levels. Skin biopsy may show the characteristic hyperkeratosis of hair
follicles and rule out vasculitis.
“The four Hs” are the classical manifestations
of scurvy: hemorrhagic signs, hyperkeratosis of hair follicles,
hypochondriasis, and hematologic abnormalities. The earliest sign is usually
petechial hemorrhages, usually in hyperketotic areas such as the anterior
forearms. Next to occur are ecchymoses and purpura, usually at sites of
pressures, trauma, or irritation. Further depletion brings coiled
(corkscrew) and fragmented hair with hyperkeratosis and hemorrhagic
gingivitis. In severe cases, other symptoms include lower extremity edema,
muscle tenderness, conjunctival and ocular hemorrhages, arthralgias,
hemarthroses, gastrointestinal hemorrhage, sicca (dry eye) syndrome, poor wound healing, and
peripheral neuropathy. Generalized symptoms are weakness, fatigue, and
weight loss. Psychological symptoms include hypochondriasis, emotional
lability, depression, and hysteria. Sudden death for unknown reasons has
been reported. Treatment is simple, by replacing body stores of vitamin C by
oral or intravenous route in severe case.
Establish diagnosis from history,
examination, and laboratory results. Ensure that treatment is adequate from
clinical and biochemical status. Make sure that all hematologic disorders are
corrected before elective surgery.
Few reports have considered anesthesia
in cases of scurvy because of its rarity in the last 50 years in developed
countries. In principle, no surgery or anesthesia should be considered in
cases with clinically significant scurvy because of the systemic