Rohan Wray, 22, and Chana Al-Alas, 19, of London, were accused of abusing baby Jayden but his fractures were later found to have been caused by rickets.
They have both been aquitted,and their other child has been returned to them.
But what is “Rickets”,and why the couple were accused of “Shaken-Baby Syndrom”
Rickets is a softening of bones in children due to deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium, potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries.
The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets (cases of severe diarrhea and vomiting may be the cause of the deficiency).
Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood. Osteomalacia is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.
The origin of the word “rickets” is probably from the Old English dialect word ‘wrickken’, to twist. The Greek derived word “rachitis” meaning “inflammation of the spine” was later adopted as the scientific term for rickets, due chiefly to the words’ similarity in sound.
Signs and symptoms
Bone pain or tenderness
Muscle weakness (rickety myopathy or “floppy baby syndrome” or “slinky baby” (such that the baby is floppy or slinky-like)
Increased tendency for fractures (easily broken bones), especially greenstick fractures
Toddlers: Bowed legs (genu varum)
Older children: Knock-knees (genu valgum) or “windswept knees”
Cranial, pelvic, and spinal deformities (such as lumbar lordosis)
Wrist X ray Showing Changes in Rickets, mainly cupping is seen here.
Chest X ray showing changes consistent with rickets, this changed is usually referred to as Rosary beads of rickets
Hypocalcemia (low level of calcium in the blood)
Tetany (uncontrolled muscle spasms all over the body)
Craniotabes (soft skull)
Costochondral swelling (aka “rickety rosary” or “rachitic rosary”)
Double malleoli sign due to metaphyseal hyperplasia
Widening of wrist
Widening of wrist raises early suspicion, it is due to metaphysial cartilage hyperplasia.
An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive “square headed” appearance. These deformities persist into adult life if not treated. Long-term consequences include permanent bends or disfiguration of the long bones, and a curved back.
The primary cause of rickets is a vitamin D deficiency. Vitamin D is required for proper calcium absorption from the gut. Sunlight, especially ultraviolet light, lets human skin cells convert Vitamin D from an inactive to active state. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcaemia, leading to skeletal and dental deformities and neuromuscular symptoms, e.g. hyperexcitability.
Foods that contain vitamin D include butter, eggs, fish liver oils, margarine, fortified milk and juice, and oily fishes such as tuna, herring, and salmon. A rare X-linked dominant form exists called Vitamin D resistant rickets.
Cases have been reported in Britain in recent years of rickets in children of many social backgrounds caused by inability to make vitamin D because the sun’s ultraviolet light was not reaching the skin because of persistent use of strong sunblock, or too much “covering up” in sunlight, or spending too much time indoors.
Other cases have been reported among the children of some ethnic groups in which mothers avoid exposure to the sun for religious or cultural reasons, leading to a maternal shortage of vitamin D. The British Medical Journal reported in 2010 that doctors in Newcastle on Tyne saw 20 cases of rickets per year
Diet and sunlight
Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet B light (sunshine when the sun is highest in the sky), cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.
A sufficient amount of ultraviolet B light in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned babies need to be exposed longer to the ultraviolet rays. The replacement of vitamin D has been proven to correct rickets using these methods of ultraviolet light therapy and medicine.
Recommendations are for 400 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.
Sufficient vitamin D levels can also be achieved through dietary supplementation and/or exposure to sunlight. Vitamin D3 (cholecalciferol) is the preferred form since it is more readily absorbed than vitamin D2. Most dermatologists recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure. Endogenous production with full body exposure to sunlight is approximately 250 µg (10,000 IU) per day.
According to the American Academy of Pediatrics (AAP), all infants, including those who are exclusively breast-fed, may need Vitamin D supplementation until they start drinking at least 17 US fluid ounces (500 ml) of vitamin D-fortified milk or formula a day.
Infants with rickets often suffer bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation. People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight.