In an earlier study we identified severe Vitamin D deficiency as a problem in institutionalised children with cerebral palsy (CP), which resulted in rickets and a high incidence of fractures. The purpose of this study was to establish whether a cohort of non-ambulatory children with CP, living at home, presented with Vitamin D deficiency. The participants were a consecutive sample (N=100) of non-ambulatory children with CP attending a CP outpatient clinic. Their ages ranged from 2 to 15 years (mean 5.8, SD 3.3 years). There were 57 males and 43 females. Nineteen were on Level IV of the Gross Motor Function Classification System (GMFCS), and 81 were on Level V. 66% were on anticonvulsant therapy (ACT). Basic demographic data was collected, and measurements included blood sample analysis and wrist radiographs. There was radiographic evidence of osteopenia and delayed ossification of the carpal bones.Aim
Method
This study was to determine the outcome of 5 years of vitamin D supplementation in children and adults with spastic quadriplegia living in a long-term care facility where a high incidence of pathological fractures had been noted. Twenty of 88 patients with spastic quadriplegia had sustained 56 atraumatic fractures in the 4 years before this study. The median age was 17.5 years (6 to 29). An earlier study showed that rickets and osteomalacia were more severe in the patients with fractures. There was a significant relationship (p =0.002) between the number of fractures and the use of anticonvulsant therapy (ACT). The fractures were treated conservatively. ACT was continued. The patients were initially given 5000 IU of calciferol a day for 3 months, followed by a maintenance dose of 50 000 IU (one capsule) a month. Vitamin D supplementation was extended to all non-ambulatory patients, who spent most of their time indoors and had little exposure to sunlight. Two of the 20 patients with fractures died of respiratory complications in the first year of the study and one was discharged. At 5-year follow-up, when 17 were assessed, none had pain on movement of the previously fractured limbs. In 14 patients, the fractures had healed in acceptable alignment. Three patients who had sustained multiple fractures had severe bowing deformities of the affected limbs. Since the implementation of the intervention, no non-ambulatory patient in the facility has sustained a fracture. We recommend vitamin D supplementation for children and adults with cerebral palsy if exposure to sunlight cannot be guaranteed.
The purpose of this study was to determine factors contributing to the high incidence of fractures in patients with spastic quadriplegic cerebral palsy in residential care, and to assess the effect of vitamin D therapy. Over a period of four years, 20 patients in a cohort of 88 had sustained 56 long bone fractures. We compared them to an age-matched group from the same cohort with no history of fractures. The mobility of patients, who spent their time indoors, was severely restricted in both groups. There was radiological and biochemical evidence of rickets and osteomalacia in both groups, but the disease was more severe in the fracture group. There was a significant relationship between the number of fractures and the use of anticonvulsant therapy. Administration of vitamin D (5 000 IU per day) to both the fracture and control group over three months resulted in a marked increase in mean serum calcium (p =0.01), and a dramatic decrease (p <
0.003) in mean alkaline phosphatase to a level just above normal. All non-ambulatory residents with cerebral palsy now receive a maintenance dose of 50 000 IU of calciferol a month. No further fractures have occurred since vitamin D administration. We recommend vitamin D supplementation for all non-ambulatory children with cerebral palsy in residential care who do not get regular exposure to sunlight.
