Acute angulation at the thoracolumbar junction
with segmental subluxation of the spine occurring at the level above
an anteriorly hypoplastic vertebra in otherwise normal children
is a rare condition described as infantile developmental thoracolumbar
kyphosis. Three patient series with total of 18 children have been
reported in the literature. We report five children who presented
with thoracolumbar kyphosis and discuss the treatment algorithm. We
reviewed the medical records and spinal imaging at initial clinical
presentation and at minimum two-year follow-up. The mean age at
presentation was eight months (two to 12). All five children had
L2 anterior vertebral body hypoplasia. The kyphosis improved spontaneously
in three children kept under monitoring. In contrast, the deformity
was progressive in two patients who were treated with bracing. The
kyphosis and segmental subluxation corrected at latest follow-up
(mean age 52 months; 48 to 60) in all patients with near complete
reconstitution of the anomalous vertebra. The deformity and radiological
imaging on a young child can cause anxiety to both parents and treating
physicians. Diagnostic workup and treatment algorithm in the management
of infantile developmental thoracolumbar kyphosis is proposed. Observation
is indicated for non-progressive kyphosis and bracing if there is evidence
of kyphosis and segmental subluxation deterioration beyond walking
age. Surgical stabilisation of the spine can be reserved for severe
progressive deformities unresponsive to conservative treatment. Cite this article:
The scoliosis observed in chickens after pinealectomy resembles that seen in humans with an adolescent idiopathic scoliosis, suggesting that melatonin deficiency may be responsible. However, to date there have been no studies of pineal gland glucose metabolism in patients with adolescent idiopathic scoliosis that might support this hypothesis. We examined the excretion of urinary 6-sulfatoxyl-melatonin as well as the glucose metabolism of the pineal gland in 14 patients with an adolescent idiopathic scoliosis and compared them with those of 13 gender-matched healthy controls using F-18 fluorodeoxyglucose brain positron emission tomography. There was no significant difference in the level of urinary 6-sulfatoxyl-melatonin or pineal gland metabolism between the study and the control group. We conclude that permanent melatonin deficiency is not a causative factor in the aetiology of adolescent idiopathic scoliosis.
We studied 70 consecutive patients with adolescent idiopathic scoliosis who underwent corrective surgery. They were divided into two groups. In the study group of 38 patients one or more modern blood-conservation measures was used peri-operatively. The 32 patients in the control group did not have these measures. Both groups were similar in regard to age, body-weight, the number of levels fused and the type of surgery. Only two patients in the study group were transfused with homologous blood and these transfusions were ‘off-protocol’. Wastage of autologous pre-donated units was minimal (6 of 83 units). By contrast, all patients in the control group were transfused with homologous blood. In the study group there was a significant decrease (p = 0.005) in the estimated blood loss when all the blood-conservation methods were used. The use of blood-conservation measures, the lowering of the haemoglobin trigger for transfusion and the education of the entire team involved in the care of the patient can prevent the need for homologous blood transfusion in patients undergoing surgery for adolescent idiopathic scoliosis.
