Abstract
Pituitary dysfunction following traumatic brain injury (TBI) is significant and rarely considered by clinicians. This topic has received much more attention in the last decade. The incidence of post TBI anterior pituitary dysfunction is around 30% acutely, and declines to around 20% by one year. Growth hormone and gonadotrophic hormones are the most common deficiencies seen after traumatic brain injury, but also the most likely to spontaneously recover. The majority of deficiencies present within the first year, but extreme delayed presentation has been reported. Information on posterior pituitary dysfunction is less reliable ranging from 3%–40% incidence but prospective data suggests a rate around 5%. The mechanism, risk factors, natural history, and long-term effect of treatment are poorly defined in the literature and limited by a lack of standardization. Post TBI pituitary dysfunction is an entity to recognize with significant clinical relevance. Secondary hypoadrenalism, hypothyroidism and central diabetes insipidus should be treated acutely while deficiencies in growth and gonadotrophic hormones should be initially observed.
Highlights
Traumatic brain injury (TBI) is a significant problem in both the developed and undeveloped world.The 2010 Center for Disease Control and Prevention (CDC) estimate of the rate of emergency department visits, hospitalizations, and deaths from TBI in the United States was 823.7 per 100,000, an increase from previous years [1]
There is a significant variability in the timing of presentation with post TBI hypopituitarism ranging from a few days to over forty years, though most cases present within the first year [11,12,13,14,15,16,17,18,19,20,21]
It is recommended that provocative testing be performed to confirm the diagnosis of growth hormone deficiency (GHD) with tests such as the insulin tolerance test (ITT), glucagon stimulation or growth-hormone-releasing hormone (GHRH )+ arginine or secretalogues [86,87,88,89,90,91,92]
Summary
Traumatic brain injury (TBI) is a significant problem in both the developed and undeveloped world. There is a significant variability in the timing of presentation with post TBI hypopituitarism ranging from a few days to over forty years, though most cases present within the first year [11,12,13,14,15,16,17,18,19,20,21]. Ascertaining the rate of pituitary dysfunction following TBI from the literature is difficult given inherent variability in study design and methods [22]. The completeness of evaluation of the hypothalamic-pituitary axis varies among reports with some excluding certain hormones and others only measuring static hormone levels rather than combining static assessments with provocative tests
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