Pituitary dysfunction after traumatic brain injury: prevalence and screening strategies

ABSTRACT

Introduction

Pituitary gland is vulnerable to traumatic brain injury (TBI). As a result a series of neuroendocrine changes appear after head injury; in many occasions they reverse with time, while occasionally new late onset changes may develop.

Areas covered

In this review, we focus on the prevalence of anterior and posterior pituitary hormonal changes in the acute and chronic post-TBI period in both children and adults. Moreover, we present evidence supporting the need for evaluating pituitary function along with the current suggestions for the most appropriate screening strategies. We attempted to identify all published literature and we conducted an online search of PubMed, from January 1970 to June 2020.

Expert opinion

Adrenal insufficiency and water metabolism disorders are medical emergencies and should be promptly recognized. Awareness for long-term hormonal derangements is necessary, as they may lead to a series of chronic health issues and compromise quality of life. There is a need for well-designed prospective long-term studies that will estimate pituitary function during the acute and chronic phase after head injury.

KEYWORDS:

• Pituitary dysfunction
• hypopituitarism
• neuroendocrine
• traumatic brain injury

Article highlights

• Epidemiological data suggest that post-TBI pituitary dysfunction (PTPD) is not negligible and it is associated with substantial morbidity and mortality over the whole life span.

• After head injury several neuroendocrine adaptations occur; although the majority will resolve, new late onset may develop.

• Hypoadrenalism and water homeostasis disorders should be early recognized and managed. Awareness for long-term endocrine sequelae is needed as they may lead to a burden of chronic health issues. In particular in children and adolescents follow up of growth and pubertal maturation should be prioritized.

• The most common hormone deficit after 3 months is GH deficiency (GHD), followed by secondary hypoadrenalism and secondary hypogonadism. Secondary hypothyroidism, hyper‐ and hypo‐prolactinaemia and posterior lobe disorders are uncommon.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.