History.General: scurvy is the clinical state arising from dietary deficiency of vitamin C (ascorbic acid). The Egyptians recorded scurvy as early as 1550 BC. Epidemics were witnessed during the Renaissance era (16th-18th century), at which time scurvy was the scourge of the sea explorers. In 1746, James Lind, a British naval surgeon, established the fact that oranges and lemons were effective in curing scurvy.
Pathophysiology.Vitamin C (ascorbic acid), is a reducing agent, an antioxidant.
It is a cofactor for the enzyme prolyl hydroxylase, most likely by keeping its iron atom in a reduced state. The enzyme prolyl hydroxylase transforms the protein procollagen into collagen by hydroxylation of proline and lysine in procollagen into hydroxyproline and hydroxylysine. This hydroxylation gives the collagen it’s strength, needed for connective tissue, bones and dentine, the major portion of teeth. The lack of collagen produces the symptoms in bones, teeth and bleeding, the symptoms of scurvy.
Curiously, only primates and guinea pigs are unable to manufacture vitamin C on their own, having lost the genetic information necessary for the production of this important cofactor.
Symptoms.Discharge: haemorrhages.
The lack of vitamin C makes the capillaries fragile. Internal haemorrhages cause black-and-blue marks to appear on the skin. At the first visible signs of scurvy, raised red spots appear on the skin around the hair follicles of the legs, buttocks, arms and back. When the tiny capillaries of the hair follicles haemorrhage, the hair-producing cells do not receive the nourishment needed for the hairs to grow normally. Consequently, the skin becomes flecked with small lesions that begin to appear on the body after about five months on a diet deficient in vitamin C.
Haemorrhaging is a hallmark feature of scurvy and can occur in any organ.
Gums and Teeth.The gums have a bluish-purple hue and feel spongy. Gum haemorrhage occurs only if teeth have erupted. Dentin, which lies below the enamel and is part of the root of teeth, breaks down. Teeth loosen and eating becomes difficult and painful. Haemorrhages of the gums usually involve the tissue around the upper incisors.
Bones.Limbs become painful and tender from the haemorrhages under tight periosteum, < touch, < motion. Subperiosteumeal haemorrhage in the tibia and femur cause excruciating pain. It’s often palpable as swelling over the long bones. The limbs adopt the characteristic ‘frog position’ with the thighs abducted and the knees slightly flexed. The excruciating pain can result in pseudo paralysis. Strong joint pain. Calcification of the growth cartilage at the end of the long bones continues, leading to the thickening of the growth plate. The typical invasion of the growth cartilage by the capillaries does not occur. Preexisting bone becomes brittle and undergoes resorption at a normal rate, resulting in microscopic fractures of the spicules between the shaft and calcified cartilage.
Costochondral beading or scorbutic rosary is a common finding. The scorbutic rosary is distinguished from rickety rosary (which is knobby and nodular) by being more angular and having a step-off at the costochondral junction. The sternum typically is depressed.
Roentgen signs.
Trummerfeld scurvy zone: lucent band in metaphysis beneath white line of Frankel.
White line of Frankel: dense zone of provisional calcification at edge of metaphysis, just beneath physis.
Wimberger ringdense: rim of demineralized epiphysis.
Various symptoms.Hair follicles are one of the common sites of coetaneous bleeding.
Energy: weak.
Low-grade fever, anaemia and poor wound healing.
Proptosis of the eyeball secondary to orbital haemorrhage is a sign of scurvy.
Tachypnea.
Sudden death due to cardiac failure is reported in infants and adults.
Loss of appetite; poor weight gain.
Diarrhoea.
Petechial haemorrhage of the skin and mucous membranes can occur. Rarely, haematuria, hematochezia and melaena are noted.
Skin: hyperkeratosis, corkscrew hair and sicca syndrome typically are observed in adult scurvy but rarely occur in infantile scurvy.
MindIrritable.
The infant is apprehensive, anxious and progressively irritable.
Peevishness, Irritability.
= race, sex, age.Causes.
General: scurvy is caused by lack of vitamin C or ascorbic acid. Inadequate intake of fresh fruits and vegetables can lead to this condition, for instance on long sea travels, famines and neglect. The disease is more common in artificially fed infants. Cow’s milk contains less than half the vitamin C found in breast milk. This is reduced further if the milk is boiled or processed.
Scurvy may also occur in older children who are mentally retarded and cannot chew and are consequently fed on sloppy foods.
Treatment.General: scurvy is treated with vitamin C, ascorbic acid. It is found in fresh fruits and vegetables, Indian gooseberry (amla), lemon (bara nimbu) and lime (nmboo), green mangoes, orange, bitter gourd, tomatoes and leafy vegetables such as spinach and cabbage.
The most important factor in the prevention and treatment of scurvy in children is proper feeding. As far as possible, the baby should not be given artificially prepared, patent or tinned milk foods.
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Acute Lymphoblast
Leukemia.
Arthritis, Septic.
Child Abuse & Neglect: Physical Abuse.
Osteomyelitis.
Poliomyelitis.
Retinoblastoma.
Rheumatic Fever.
Thrombocytopenia
Absent Radius Syndrome.
Henoch-Schönlein purpura.
Rheumatoid arthritis.
Acrodynia.