SCURVY SIGNS (BARLOW'S DISEASE-INFANTILE SCURVY)

Scurvy Signs (Barlow's disease--Infantile Scurvy)

http://www.emedicine.com/ped/byname/scurvy.htm

In 1914, Alfred Hess, a pediatrician practicing at the Hebrew Asylum in New York,
observed an increase in scurvy among the infants at the asylum. This increase
in scurvy coincided with the introduction of pasteurized milk and exclusion of
orange juice from the infants’ diet. Modifying the infants’ diet, with the provision of
raw milk or orange juice or potatoes, Hess reversed the scurvy and effected a cure.
Hess had demonstrated that pasteurization results in the loss of vitamin C.
He recommended the provision of fresh fruit or vegetable juice for the prevention of scurvy in infants fed on heated formulas. This practice of supplementing the diet of infants receiving heated formulas with fresh fruit or vegetable juices eventually led to the eradication of infantile scurvy in the United States.

The human body lacks the ability to synthesize and make vitamin C and therefore depends on exogenous dietary sources to meet vitamin C needs. Consumption of fruits and vegetables or diets fortified with vitamin C are essential to avoid ascorbic acid deficiency. Even though scurvy is uncommon, it still occurs and can affect adults and children who have chronic dietary vitamin C deficiency.

http://www.emedicine.com/derm/topic521.htm
Pathophysiology: Scurvy is caused by a prolonged deficiency of vitamin C intake that results in defective collagen synthesis, tissue repair, and synthesis of lipids and proteins. It functions both as a reducing agent and as an antioxidant and is required for many physiologic functions, including metabolism of iron and folic acid, resistance to infection, and integrity of blood vessels.

The clinical manifestations of scurvy are primarily due to abnormal collagen synthesis resulting from a lack of vitamin C. Vitamin C is a cofactor required for the function of several hydroxylases. The absence of vitamin C reduces the function of prolyl hydroxylase, which is required to form hydroxyproline, an amino acid found in collagen but rarely found in other proteins. The presence of hydroxyproline in collagen stabilizes the collagen triple-helix structure by forming interstrand hydrogen bonds. Collagen lacking hydroxyproline is more fragile and contributes to the clinical manifestations of scurvy, including purpura due to vessel wall fragility. In addition, osteoid matrix formation is defective and bone resorption is increased in persons with vitamin C deficiency.

History:

* Symptoms of scurvy develop after 3 months of severe or total vitamin C deficiency.

(Infection or vaccination-induced accelerated infantile scurvy, particularly with chronic subclinical scurvy at birth can manifest much more quickly.)

* Patients may complain of weakness, fatigue, shortness of breath, and aching limbs. Left untreated scurvy progresses, with potentially fatal complications, including cerebral hemorrhage or hemopericardium.

* Infantile scurvy is uncommon before age 7 months, and clinical and radiographic manifestations rarely occur in infants younger than 3 months. Early clinical manifestations consist of pallor, irritability, and poor weight gain.

* In advanced infantile scurvy, the major clinical manifestation is extreme pain and tenderness of the arms and, particularly, the legs. The baby is miserable and tends to remain in a characteristic immobilized posture from subperiosteal pain, with semiflexion of the hips and the knees (frogleg posture), as described by Thomas Barlow in 1884. The body is both wasted and edematous, and petechiae* and ecchymoses are commonly present.

petechiae*A small purplish spot on a body surface, such as the skin or a mucous membrane, caused by a minute hemorrhage and often seen in typhus.

Physical:

* Symptoms and signs of scurvy may be remembered by the 4 Hs: hemorrhage, hyperkeratosis, hypochondriasis, and hematologic abnormalities. Patients may be miserable, irritable, depressed, resentful, and full of aches and pains.

* The earliest signs are found on the skin, often on the shins, after 3 months of severe or total vitamin C deprivation. Perifollicular hyperkeratotic papules are surrounded by hemorrhagic halos. The central hairs are twisted like corkscrews, and they may become fragmented. The posterior parts of the legs develop purpura that may coalesce.

* Soft, spongy swelling of the gums and gingival interdental papillae is followed by gingival hemorrhage, which is accentuated by coexistent poor oral hygiene and periodontal disease. Disrupted tooth formation and loosening of teeth may result in permanent defects of dentition. (Only where teeth are present.)

* Ocular features include those of Sjögren's syndrome, subconjunctival hemorrhage, and bleeding within the optic nerve sheath. Funduscopic changes include cotton wool spots and flame-shaped hemorrhages.

* Bleeding into the joints causes exquisitely painful hemarthroses. Subperiosteal hemorrhage may be palpable, especially along the distal portions of the femurs and the proximal parts of the tibias of infants. In advanced cases, clinically detectable beading may be present at the costochondral junctions of the ribs. This finding is known as the scorbutic rosary (Costochondral beading). Bleeding into the femoral sheaths may cause femoral neuropathies, and bleeding into the muscles of the arms and the legs may cause woody edema.

* Heart complications include cardiac enlargement, ECG changes (reversible ST-segment and T-wave changes), hemopericardium, and sudden death.

* Anemia develops in 75% of patients, resulting from blood loss into tissue, coexistent dietary deficiencies (folate deficiency), altered absorption and metabolism of iron and folate, gastrointestinal blood loss, and intravascular hemolysis. The anemia is most often characterized as normochromic and normocytic. Vitamin C enhances iron absorption by reducing dietary iron from the ferric form to the ferrous form. Thus, vitamin C deficiency may reduce the availability of intracellular iron. Vitamin C is also necessary to convert folic acid to its active metabolite, folinic acid.

* Other problems include increased redness and swelling in recently healed wounds and the failure of new wounds to heal.

Causes:

* Scurvy is caused by a prolonged deficiency of vitamin C intake.

* Most animals can convert gluconate into ascorbate. Primates, including humans, and guinea pigs as well as a few other species cannot convert gluconate into ascorbate and, therefore, require exogenous ascorbic acid, otherwise known as vitamin C. Humans obtain 90% of their intake of vitamin C from fruits and vegetables, and cooking these sources decreases vitamin C content 20-40%. The US Food and Drug Administration recommends a daily dietary allowance of vitamin C of 75 mg for women and 90 mg for men.

* The total body pool of vitamin C is approximately 1500 mg. The absorbed vitamin is found ubiquitously in body tissues, with the highest concentrations in glandular tissue and the lowest concentrations in muscle and stored fat. Ascorbic acid is metabolized in the liver by oxidation and sulfation. The renal threshold for excretion by the kidney in urine is approximately 1.4 mg/100 mL plasma. Excess amounts of ascorbic acid are excreted unchanged or as metabolites. When body tissue or plasma concentrations of vitamin C are low, excretion of the vitamin is decreased. Scurvy occurs after vitamin C has been eliminated from the diet for at least 3 months and when the body pool falls below 350 mg. (Can occur prenatally.)

http://www.emedicine.com/ped/topic2073.htm
History:

* Initial symptoms are nonspecific and include the following:

o Loss of appetite

o Peevishness

o Poor weight gain

o Diarrhea

o Tachypnea (Rapid breathing.)

o Fever ?

* Specific symptoms include the following:

o Irritability

o Pain and tenderness of the legs

o Pseudoparalysis

o Swelling over the long bones

o Hemorrhage

Physical:

* The infant is apprehensive, anxious, and progressively irritable. Upon handling and changing of diapers, severe tenderness over the thighs is present. The excruciating pain results in pseudoparalysis. The infant assumes the frog leg posture (ie, keeping hips and knees slightly flexed and externally rotated) for comfort.

* Hemorrhages of the gums usually involve the tissue around the upper incisors. The gums have a bluish-purple hue and feel spongy. Gum hemorrhage occurs only if teeth have erupted.

* Subperiosteal hemorrhage is a typical finding of infantile scurvy. The lower ends of the femur and tibia are the most frequently involved sites. The subperiosteal hemorrhage is often palpable and tender in the acute phase.

* Petechial hemorrhage of the skin and mucous membranes can occur. Rarely, hematuria, hematochezia, and melena are noted.

* Proptosis of the eyeball secondary to orbital hemorrhage is a sign of scurvy.

* 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 is typically depressed.

* Low-grade fever, anemia, and poor wound healing are signs of scurvy.

* Hyperkeratosis, corkscrew hair, and sicca syndrome are typically observed in adult scurvy but rarely occur in infantile scurvy.

http://www.itg.be/itg/DistanceLearning/LectureNotes
VandenEndenE/50_Vitamin_deficienciesp4.htm

4.6 Scurvy, clinical aspects

A pronounced lack of vitamin C results in a clinical disease known as scurvy. Haemorrhagic problems and bone abnormalities are the most characteristic and recognizable features of this disease. When a diet is chronically deficient in vitamin C (less than 10 mg/day) the first signs may be expected to appear after 3 to 6 months (half life of vitamin C is about 18 days). This explain why scurvy only appeared on board ships during long sea voyages. The patient first complains of general debility of slow onset, irritability, weight loss and vague muscular and joint pain. Sometimes the first symptom is stiffness in the calves, due to local haemorrhages. Because of the pain in the legs, children may present with pseudoparalysis. In many cases they spontaneously adopt an antalgic posture, with endorotation and bent knees and hips. This is usually seen in babies born prematurely when they reach about 6-12 months of age if they have been fed deficient artificial food. Splinter haemorrhages beneath the fingernails may occur, as in endocarditis. Haemorrhages around the eyes, ears, neck and on the roof of the mouth may occur and are very suggestive of scurvy. Spontaneous bleeding may occur anywhere in the body, including bleeding leading to palpable subperiosteal haemorrhages. Hyperkeratotic hair follicles and perifollicular petechiae (scorbutic purpura) are quasi pathognomonic. Old scars break open. New wounds do not heal or heal poorly. The gums become swollen, purple and spongy and bleed easily. Often there will be secondary infection. In advanced scurvy, teeth fall out spontaneously. Endochondral bone development ceases because osteoblasts no longer produce osteoid. A fibrous area is formed between diaphysis and epiphysis. The costochondral junctions enlarge. This is clinically palpable as a scorbutic rosary (not to be confused with rachitic rosary). Other symptoms include femoral neuropathy and oedema of the legs. Microcytic hypochromic anaemia may develop, which only improves after administration of vitamin C. If other deficiencies are simultaneously present (e.g. folic acid), the anaemia may be macrocytic.

4.8 Scurvy, diagnosis

The vitamin C content in peripheral blood can be measured in specialized laboratories. A level of less than 11 µmol/litre is diagnostic for scurvy. Measurement in leukocytes is more precise. The urinary excretion after administration of a test dose of vitamin C can also be measured. A capillary fragility test will be positive. When this is measured using the sphygmomanometer, it is called the Hess capillary test. The regular haemostasis parameters (platelets, coagulation times) are normal. On X-rays of the legs, a ‘ground-glass’ appearance of the epiphysis is often described.

http://www.medal.org/visitor/www%5CActive%5C
ch12%5Cch12.01%5Cch12.01.10.aspx
Scurvy is the term for clinical deficiency of vitamin C (ascorbic acid). Although encountered less often today than in the past, it still occurs and mild cases may go unrecognized.

Patients at risk for vitamin C deficiency:

(1) infants

(2) adults > 55 years of age, especially males

(3) refugees or displaced persons

(4) malnutrition

(5) heavy cigarette smokers

(6) abnormal diets devoid of vegetables and vitamins

Clinical features of scurvy - bleeding tendency:

(1) petechiae

(2) purpura

(3) ecchymoses

(4) subperiosteal hemorrhage

(5) bleeding gums (when teeth are present)

(6) intracranial hemorrhage, which may be fatal

(7) conjunctival hemorrhages

Clinical features of scurvy - oral:

(1) gingival swelling and gingivitis

(2) loose or missing teeth

(3) scurvy buds on the gingiva

Clinical features of scurvy - skeletal changes in children:

(1) bowing of long bones in the lower extremities

(2) scorbutic rosary (depression of sternum with projection of the ends of the ribs)

(3) tender or aching limbs

Clinical features of scurvy - other:

(1) anemia?

(2) hyperkeratosis?

(3) abnormal wound healing

(4) poor localization of bacterial infections?

(5) fatigue or weakness

The diagnosis of scurvy involves both of the following:

(1) the presence of clinical features in a person with a risk factor for vitamin C deficiency

(2) low blood levels of vitamin C, or clinical response to ascorbic acid replacement

References:

Cotran RS, Kumar V, et al (editors). Robbins Pathologic Basis of Disease, 5th Edition. WB Saunders Company. 1994. pages 423-425.

Sauberlich HE. Laboratory Tests for the Assessment of Nutritional Status, Second Edition. CRC Press. 1999. pages 12-13.

Pediatrics International
Vol. 46 Issue 6 Page 753 December 2004
Could Vitamin C deficiency have a role in shaken baby syndrome?
Eva Lai-Wah Fung, Edmund Anthony Severn Nelson
Department of Paediatrics, The Chinese University of Hong Kong, China

Correspondence: ELW Fung, MBChB, MRCP, Department of Paediatrics, The Chinese University of Hong Kong, 6/F, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong, China. Email: b300875@mailserv.cuhk.edu.hk

http://tinyurl.com/2gc3fm

Scurvy in a 10-month-old boy.

Case report
International Journal of Dermatology. 46(2):194-198, February 2007.
Larralde, Margarita PhD, MD; Munoz, Andrea Santos MD; Boggio, Paula MD; Di Gruccio, Vanesa MD; Weis, Isaac MD; Schygiel, Adolfo MD

Abstract:
We report a 10-month-old boy with inflammatory and necrotic gingival lesions, fever, irritability, and pseudoparalysis of the legs. Laboratory examinations revealed moderate anemia and skeletal X-rays showed osteopenia, scorbutic rosary at the costochondral junctions, and "corner sign" on the proximal metaphyses of the femora. The boy had been fed only with diluted cow's milk. He had never taken solid food, vitamin C, or iron complement. Seventy-two hours after starting oral vitamin C supplementation, there was significant improvement in the patient's gingival lesions and general health. The clinical presentation and laboratory and imaging findings, together with the dramatic response to ascorbic acid intake, allowed us to confirm the diagnosis of infantile scurvy.

Scurvy, a dietary disease due to the deficient intake of vitamin C, is uncommon in the pediatric population. In an infant who has never received vitamin C, the combination of gingival lesions, pseudoparalysis, and irritability strongly suggests a diagnosis of scurvy. The clinical picture, together with the laboratory data, radiological studies, and therapeutic response to vitamin C administration, confirmed the diagnosis.

http://www.itg.be/itg/DistanceLearning/LectureNotesVandenEndenE/50_Vitamin_deficienciesp4.htm
4 Scurvy
* 4.1 Scurvy, summary
* 4.2 Scurvy, general
* 4.3 Scurvy, ascorbic acid
* 4.4 Scurvy, collagen
* 4.5 Scurvy, aetiology
* 4.6 Scurvy, clinical aspects
* 4.7 Scurvy, differential diagnosis
* 4.8 Scurvy, diagnosis
* 4.9 Scurvy, treatment
* 4.10 Scurvy, prophylaxis

4.1 Scurvy, summary

* A deficiency of ascorbic acid leads to poor quality collagen

* Haemorrhages and bone abnormalities dominate the clinical picture

* Rapid improvement with vitamin C tablets or fresh fruit and vegetables

4.2 Scurvy, general

Scurvy is a disease caused by lack of vitamin C. The condition was a common ailment aboard European seagoing ships in the early days of world exploration and was a serious problem on long voyages. In 1498, Vasco da Gama lost no fewer than 100 of his original crew of 160 to scurvy. In Magellan’s expedition to the Philippines (1519) he lost 200 of his original crew of 218. On board the ships there was a systematic lack of fresh fruit and vegetables. Nowadays, scurvy only occurs in the event of an unbalanced diet with nutritional deficiency, as in some elderly people and alcoholics. Scurvy is sometimes seen in persistent problematical situations in the tropics (refugees, starvation), certainly in warm and dry regions where there is a lack of fresh fruit and vegetables. In the general population living in stable conditions, scurvy is rare.

4.3 Scurvy, ascorbic acid

For a long time the origin of scurvy was a mystery. Before vitamin C was identified, however, a form of empirical treatment and prophylaxis had been discovered, but the nature of the compound that cured scurvy was not clear. A breakthrough came with the discovery that guinea pigs could develop scurvy (guinea pigs, primates and humans – unlike most mammals – are unable to synthesize ascorbic acid). Scientists now had an animal model and an in vivo assay for measuring the antiscorbutic activity of different food products. It was demonstrated that drying, cooking and prolonged exposure to air destroyed the active ingredient. During his research at Cambridge University in 1928, the Hungarian biochemist Szent-Gyorgyi isolated vitamin C. He isolated the compound from adrenal cortex, oranges and cabbage. He received the Nobel Prize for Medicine in 1937. Subsequently it became evident that vitamin C occurs in numerous food products. Vegetables such as broccoli and tomatoes, but also potatoes and citrus fruit have large concentrations of vitamin C. Sir Walter Norman Haworth discovered an efficient synthesis method for the preparation of vitamin C based on a carbohydrate precursor. Sir Norman Haworth and Paul Karrer (Switzerland) were jointly awarded the Nobel Prize for Chemistry for their work in 1937.

Vitamin C is also known as ascorbic acid. This name refers to ‘antiscorbutic’ (from the Low German term for scurvy: schorbock). Vitamin C is essential for the production of collagen. It is a highly reducing compound and is capable of undergoing reversible oxidation. In consequence, it fulfils a role in redox reactions in the body. Vitamin C promotes the uptake of iron in the intestine and protects folic acid reductase. Vitamin C regenerates antioxidants such as vitamin E, flavonoids and glutathione. It plays a role in the synthesis of steroids and the production of carnitine. The highest concentrations are found in white blood cells, the lens and the brain. The total body pool of vitamin C is approximately 1500 mg. The excess is excreted. There is a turnover of 3% per day, which gives a half-life of approximately 18 days. This explains the latency period for symptoms to occur after starting a diet without vitamin C.

4.4 Scurvy, collagen

The symptoms of scurvy can be traced back to defective collagen. Collagen is the commonest protein in the animal kingdom. Large amounts of unusual amino acids are found in collagen: hydroxylysine and hydroxyproline. These are essential for the chemical stability of collagen. The conversion of proline into hydroxyproline is stimulated by the enzyme proline hydroxylase. For this purpose it uses a Fe2+ion, which is converted during the reaction into Fe3+. This inactivates the enzyme. Enzyme regeneration takes place by an interaction with ascorbate, in which vitamin C is converted into dehydroascorbic acid. For a better understanding of scurvy, we briefly sketch the normal production of the commonest form of collagen. Individual collagen polypeptide chains are synthesized on the ribosomes of the rough endoplasmatic reticulum. The strands are released in the lumen of the endoplasmic reticulum as large precursor molecules, the so-called pro-alpha chains. Signal peptides are still present at front and rear. In the lumen, selected proline and lysine residues are hydroxylized to hydroxyproline and hydroxylysine. Every pro-alpha chain subsequently combines with two other chains to form a triple-strand helix via hydrogen bridges, the fibrillar procollagen. This is subsequently secreted. Procollagen is converted extracellularly into tropocollagen by enzymatic cleavage (with the exception of collagen IV in the basal lamina). Tropocollagen subsequently develops further into mature collagen. Normal collagen is broken down slowly by extracellular collagenases. In scurvy, defective pro-alpha chains are formed (the formation of hydroxy-amino acids is disrupted). They do not form a triple helix and are quickly degraded. The consequences are first noticed first in the tissues where collagen turnover is fastest, such as blood vessels. Owing to the gradual loss of the existing collagen, the blood vessels become progressively fragile.

The hydroxylation of lysine in collagen has a different function than the hydroxylation of proline. It is needed for an unusual form of lysine-crosslinking (covalent intra- and intermolecular crosslinks between modified lysine sidechains). Lysine and hydroxylysine are first deaminated by lysyl oxidase, thereby creating highly reactive aldehyde groups. These groups spontaneously form covalent bonds with one another. Compare this with the pathology in osteolathyrism.

Collagen structure. This is disturbed in osteolathyrism and in scurvy (vitamin C deficiency). Drawing by JP Wenseleers, copyright ITM.

4.5 Scurvy, aetiology

Primary deficiency is due to an unbalanced diet, i.e. a diet containing less than 10 mg vitamin C per day. Pregnancy, lactation, smoking, surgical procedures, thyrotoxicosis, burns and chronic inflammation increase the body’s requirements up to 70-90 mg/day. In achlorhydria and chronic diarrhoea, less vitamin C is absorbed. Ascorbic acid is unstable in the presence of heat and prolonged cooking of food considerably reduces the quantity of active vitamin C.

4.6 Scurvy, clinical aspects

A pronounced lack of vitamin C results in a clinical disease known as scurvy. Haemorrhagic problems and bone abnormalities are the most characteristic and recognizable features of this disease. When a diet is chronically deficient in vitamin C (less than 10 mg/day) the first signs may be expected to appear after 3 to 6 months (half life of vitamin C is about 18 days). This explain why scurvy only appeared on board ships during long sea voyages. The patient first complains of general debility of slow onset, irritability, weight loss and vague muscular and joint pain. Sometimes the first symptom is stiffness in the calves, due to local haemorrhages. Because of the pain in the legs, children may present with pseudoparalysis. In many cases they spontaneously adopt an antalgic posture, with endorotation and bent knees and hips. This is usually seen in babies born prematurely when they reach about 6-12 months of age if they have been fed deficient artificial food. Splinter haemorrhages beneath the fingernails may occur, as in endocarditis. Haemorrhages around the eyes, ears, neck and on the roof of the mouth may occur. are very suggestive of scurvy. Spontaneous bleeding may occur anywhere in the body, including bleeding leading to palpable subperiosteal haemorrhages. Hyperkeratotic hair follicles and perifollicular petechiae (scorbutic purpura) are quasi pathognomonic. Old scars break open. New wounds do not heal or heal poorly. The gums become swollen, purple and spongy and bleed easily. Often there will be secondary infection. In advanced scurvy, teeth fall out spontaneously. Endochondral bone development ceases because osteoblasts no longer produce osteoid. A fibrous area is formed between diaphysis and epiphysis. The costochondral junctions enlarge. This is clinically palpable as a scorbutic rosary (not to be confused with rachitic rosary). Other symptoms include femoral neuropathy and oedema of the legs. Microcytic hypochromic anaemia may develop, which only improves after administration of vitamin C. If other deficiencies are simultaneously present (e.g. folic acid), the anaemia may be macrocytic.

4.7 Scurvy, differential diagnosis

Scorbutic rosary on the thorax and bone abnormalities must be distinguished from rachitic rosary (vitamin D deficiency). Scorbutic gingivitis must be distinguished from other causes, such as candidiasis, herpes, trench mouth, syphilis, pemphigus and Behçet’s syndrome. Scorbutic haemorrhages must be distinguished from other bleeding diatheses. Subperiostal haemorrhage with periost elevation should be distinguished from congenital syphilis.

4.8 Scurvy, diagnosis

http://www.fao.org/DOCREP/W0073e/w0073e05.htm#P4193_489043
Infantile scurvy (Barlow's disease)

Scurvy sometimes occurs in infants, usually aged two to 12 months, who are bottle-fed with inferior brands of processed milk. During the processing of the milk, the vitamin C is frequently destroyed by heat. Good brands of processed milk are fortified with vita`min C to prevent scurvy.

The first sign of infantile scurvy is usually painful limbs. The infant cries when the limbs are moved or even touched. The child usually lies with the legs bent at the knees and hips, widely separated from each other and externally rotated, in what has been termed the "frog-leg position". Bruising of the body may be seen, although it is difficult to detect in darkly pigmented African skin. Swellings may be felt, especially in the legs. Haemorrhages may occur from any of the sites mentioned above, but bleeding does not take place from the gums unless the child has teeth.

Diagnosis and laboratory tests

The capillary fragility test is not specific for scurvy but may be useful. It is simple to perform in any health facility. The cuff of a blood pressure machine or sphygmomanometer is placed around the upper arm. It is inflated to a pressure approximately midway between the subject's systolic and diastolic pressure (perhaps 100 mm Hg) and left in place for four to six minutes. In a positive test, numerous small red spots appear in the skin below the cuff; these are petechial haemorrhages arising from capillary fragility. The test is a little more difficult in very dark-skinned people, but usually the anterior surface of the lower arm is pale enough for recognition of petechial haemorrhages.

Ascorbic acid levels can be determined in blood plasma or in white blood cells. These levels provide evidence of body reserves of vitamin C. If the level of ascorbic acid in either the blood plasma or the white blood cells is within the normal range, the condition almost certainly is not scurvy.

In infantile scurvy X-ray examination will reveal periosteal haemorrhages, which together with clinical signs provide the diagnosis.

Treatment

Because of the risk of sudden death, it is inadvisable to treat scurvy with only a vitamin C-rich diet. It is advisable rather to give 250 mg ascorbic acid by mouth four times a day as well as to put the patient on a diet with plenty of fresh fruit and vegetables. It is only necessary to inject ascorbic acid if the patient is vomiting.

Increased intake of vitamin C with meals can have a manifest effect on the absorption of iron. In many iron-deficient populations, increasing vitamin C intake will help reduce the incidence and severity of iron deficiency anaemia.

http://books.google.com/books?id=4AkgAAAAIAAJ&pg=PA285&dq=infantile+scurvy#PPA285,M1

A few other pages:
hemorrhaged lids
bone callus appearing like healing fractures
swollen cheeks
animal models
ocular lesions
scurvy signs
shaken baby or scurvy?

Dianne Jacobs Thompson Est. 2007
Also http://truthquest2.com (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"