Moderate to Severe Traumatic Brain Injury
Conditions
Keywords
Traumatic brain injury, Paediatrics, Hypopituitarism
Brief summary
Annual incidence of severe traumatic brain injuries (TBI) varies from 180 to 300 out of 100.000. Mortality or severe sequelae risk is increased 8 fold after a TBI. Studies in adults showed an ante-hypophyseal deficit in 28 to 68 % of patients with a TBI. The most common deficit is Growth Hormone Deficit (GHD); followed by gonadotropic and corticotropic (AdrenoCorticoTropic Hormone (ACTH)) insufficiencies. Thyrotropic deficits (Thyroid-Stimulating Hormone (TSH)) are less frequent. From a pathophysiological point of view, the lesional mechanism responsible for hypopituitarisms would be a damage of hypophyseal vessels or hypothalamic-pituitary vessels. The frequency of pituitary deficits and the potential beneficial effects of replacement therapy on quality of life, tiredness, loss of energy and productivity, justify the systematic detection of the deficits in patients with moderate to severe TBI. Study hypotheses : At the present time, the lack of data in children does not give us the opportunity to affirm that one part of the symptoms showed by children with post-TBI neuropsychological sequelae, are linked to pituitary deficiency and that they can be improved with a replacement therapy. Firstly, it is essential to better understand the natural history of post-TBI pituitary deficiencies, studying the connexion between observed deficiencies in acute and late phase of sequelae.
Interventions
OTHERBiological and behavioral explorations
Blood dosages: * biochemistry * pituitary gland * somatotropic axis * corticotropic axis * gonadotropic axis * thyrotropic axis * antidiuretic axis Questionnaires and scales (quality of life, Vineland Adaptive Behavior Scales (VABS)-II)
Sponsors
Hospices Civils de Lyon
Study design
Allocation
NA
Intervention model
SINGLE_GROUP
Primary purpose
PREVENTION
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
2 Months to 16 Years
Healthy volunteers
No
Inclusion criteria
* children from 2 months to 16 years * in the intensive care unit * TBI : moderate (Glasgow Coma Scale (GCS) between 9 and 12) to severe (GCS \<9), whatever the mechanism involved * informed consent form signed by parents
Exclusion criteria
* obesity (Body Mass Index (BMI) \> 97th percentile for the age) * patient already under replacement therapy. * patient taking AntiEpileptic Drugs (AEDs) * patient with long-term systemic corticotherapy * history of neurological disease or learning difficulties * no covered by a national health insurance
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Study the link between pituitary deficiencies highlighted at the acute phase and one year after moderate to severe TBI. | 12 months after inclusion |
Secondary
| Measure | Time frame |
|---|---|
| Study the association between pituitary deficiencies highlighted at the acute phase, 3 months and 1 year after moderate to severe TBI, globally and per deficiency category. | day0, when leaving intensive care unit, month3 and month12 |
| Identify the other risk factors of deficiency, during the acute phase and the tardive phase i.e. signs of gravity of the TBI, type of cerebral lesion, age, lesional mechanism. | day0, when leaving intensive care unit, month3 and month12 |
| Study the correlation between corticotropic deficiencies and post-hypophysis insufficiencies during the acute phase and the hemodynamic instability over the first 3 days after the TBI | day0 to day3 |
| Compare the level and the type of behavioural and neuropsychological sequelae in children suffering from a TBI, with and without hypopituitarism. | day0, when leaving intensive care unit, month3 and month12 |
Countries
France
Outcome results
None listed