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[Post-traumatic hypopituitarism after skull injury: apropos of 3 cases]
R Mariani1, M N Bortoluzzi, C Richelme
1Service de pédiatrie, hôpital de Cimiez, Nice, France.
Insights
Cranial trauma can cause delayed hypopituitarism, including growth disorders and hypogonadism, years after the initial injury. Early recognition and dynamic MRI are crucial for identifying these subtle pituitary lesions.
Area of Science:
- Pediatric Endocrinology
- Neurotraumatology
- Radiology
Background:
- Hypopituitarism is a rare complication of cranial trauma.
- Delayed diagnosis is common due to progressive symptoms and lack of overt diabetes insipidus.
Observation:
- Three children with cranial trauma developed pituitary hormone deficiencies.
- Two patients presented with diabetes insipidus, one later developing growth hormone deficiency, hypothyroidism, and hypogonadism.
- The third patient exhibited hypothalamic/pituitary deficiencies without diabetes insipidus.
Findings:
- MRI revealed complete pituitary stalk severance in two patients.
- Absence of posterior pituitary signal was noted in one patient with diabetes insipidus.
- Symptoms of hypopituitarism manifested years after trauma, including growth disorders and hypogonadism.
Implications:
- Growth disorders and hypogonadism can manifest years after cranial trauma, even if initially forgotten.
- Dynamic MRI is essential for diagnosing heterogeneous pituitary lesions.
- Prompt evaluation for hypopituitarism is necessary in children with a history of cranial trauma.
Background:
Hypopituitarism is a rare but well-known complication of cranial trauma. In the absence of overt diabetes insipidus, its recognition is difficult as the onset of clinical symptoms can be very progressive, up to several years.
Case Reports:
Three children, aged 8, 9 and 2 years, respectively, were admitted after a cranial trauma. Manifestations of diabetes insipidus occurred a few days later in two patients; one of them developed secondary growth hormone deficiency, hypothyroidism and hypogonadism, only evidenced at the age of 14 years. The third patient also developed manifestations of hypothalamic and/or pituitary hormone deficiencies without diabetes insipidus at the age of 12 years-6 months. MRI showed complete severance of the pituitary stalk in two patients and absence of posterior pituitary signal in one of the two patients with diabetes insipidus.
Conclusion:
Growth disorders and/or hypogonadism may occur many years after a trauma that may have been forgetten. Search for such an etiology and dynamic MRI are necessary in identifying heterogenous hypophyseal lesions.