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Childhood Hypopituitarism after Traumatic Brain Injury« Back to Volume 23, Issue 2, June 2007 - Table of Contents The hypothalamus and pituitary are essential for childhood and adolescent development and are vulnerable to injury and dysfunction following brain trauma. Hypothalamic-pituitary dysfunction has been well recognized after traumatic brain injury (TBI) in adults. However, data regarding hypothalamic-pituitary function in brain-injured children and adolescents are scant. It is necessary for physicians as well as patients and family members to know that onset of hypothalamic-pituitary deficits can occur even after several years following brain injury. Acerini et al reviewed the available pediatric data, which showed that after both mild and severe TBI, hypopituitarism may occur; growth hormone (GH) and gonadotropin deficiencies appear to be most common. Precocious puberty has also been documented. Detailed investigations of pituitary function have been reported in 20 patients (12 males, 7 females, and 1 unspecified sex). Subjects ranged in age from infancy to 16 years at the time of injury; they were investigated between 1 and 42 years after the initial episodes of TBI. All patients had multiple anterior pituitary hormone deficiencies, except one, who had isolated GH deficiency. The frequencies of deficient hormones were: GH 85%, LH/FSH 80%, TSH 75%, and ACTH 50%. It was notable that in 6 patients, multiple deficiencies were documented after relatively mild head injury without loss of consciousness. Pituitary stalk transaction was demonstrated on MRI in several cases. The diagnosis of hypothalamic-pituitary deficiency was made during childhood and adolescence in 17 of the 20 patients and during adult life in the remaining 3. The key presenting symptoms were growth failure, delayed or arrested puberty, secondary amenorrhea or reduced libido. Delay in the diagnosis was extreme in many cases and hypopituitarism was clearly not considered as a possible complication of the TBI until defects of growth or reproductive function became obvious. Acerini and colleagues urged pediatric endocrinologists, in collaboration with adult endocrinologists, to perform formal prospective research studies in patients suffering from TBI to clarify prevalence, natural history, and response to hormone replacement. First Editor’s CommentThis is a very interesting report which provides important information for physicians who care for patients with TBI. Traumatic brain injury is a worldwide health problem and a major leading cause of death and disability among young adults. Survivors are often left with significant neuroendocrine dysfunction and adverse physical and/or psychological problems which are perhaps an even greater risk than previously considered. As well, TBI-induced hypopituitarism has been under-recognized, under-investigated, and untreated. Relatively little attention has been paid to the possibility of TBI-induced hypopituitarism, especially in children. As reported by Acerini et al, it became clear that TBI posed substantial risk to hypothalamic-pituitary function in children; the onset of hypopituitarism can evolve over years following injury. Road-traffic accidents, falls, sports injuries, and child abuse are the most common etiological factors for pediatric TBI, although the causes are different among age groups. The perinatal brain injury such as difficult forceps delivery at breech delivery is a well-known cause of hypopituitarism. Infants with TBI have primarily suffered from falls or assaults. Toddlers are more frequently injured as passengers in motor vehicle accidents, although falls still account for the majority of injuries. Children and infants have large, heavy heads with weaker cervical ligaments and muscles compared to adults. Given the same deceleration of the body, head trauma is therefore more likely in infants and younger children than adults. Similarly, the resulting brain injury may be more severe due to the thin, pliable skull and unfused sutures of infants and young children. Possible causes of hypopituitarism include hemorrhage, infarction, ischemia, swelling, stalk transection, or direct trauma to the hypothalamus, stalk, and/or pituitary region. Severity of TBI seems to be an important risk factor for developing hypopituitarism; however, even mild trauma may precede hypopituitarism. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of hypopituitarism, regardless of clinical evidence for pituitary dysfunction. The most common endocrine alterations appear to be GH and gonadotropin, followed by ACTH and TSH deficiency. Hyperprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. The signs and symptoms of TBI-induced hypopituitarism are often nonspecific and can be additionally masked by what has been assumed to be merely the post-traumatic syndrome. These symptoms are likely to be overlooked if endocrine dysfunction is not actively evaluated. Moreover, hormonal deficits may significantly contribute to the chronic disability and the physical, cognitive, health, and social sequel in patients with TBI. Therefore, regular endocrine evaluation and follow-up should be performed throughout life in patients with TBI. In most instances, patients with TBI are first seen and treated by trauma surgeons and neurosurgeons, and subsequently by rehabilitation specialists; all physicians must be informed about the risks of TBI-induced hypopituitarism. It is important to increase awareness among physicians, patients, and family members of the risks of hypopituitarism and the need for appropriate endocrinological assessment and adequate hormonal replacement therapy, if necessary. Thorough assessment may make it possible to improve the quality of life and enhance the rehabilitation prospects. Lack of awareness of this problem may result in long-term adverse consequences of untreated hypopituitarism for these patients. A close collaboration among neurosurgeons, neurologists, rehabilitation specialists, and endocrinologists is essential to achieve a coordinated approach to the care of patients with TBI. Yoshikazu Nishi, MD Second Editor’s CommentThe consensus guidelines on screening for hypopituitarism following TBI for adults1 was published in 2005. These guidelines may also apply to children and adolescents as the data in the paper by Acerni et al on the development of hypopituitarism following TBI are similar to the reported alterations found in adults. A summary of selected studies was presented in a tabular form in the consensus statement. However, the appropriate diagnosis and treatment of the endocrine alterations should always be accompanied by evidence-based cognitive rehabilitation of those patients; these recommendations for clinical practice were published by Cicerone et al.2 Fima Lifshitz, MD References - (linked to
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Volume 24 Number 1
May 2008
www.GGHjournal.com
ISSN 1932-9032
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