The Impact of Traumatic Brain Injury on Pituitary Function

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Key points

  • The pituitary gland is vulnerable to both mechanical and ischemic injury, accounting for the estimated 27.5% prevalence of anterior hypopituitarism after traumatic brain injury (TBI).

  • Although patients with severe TBI may be at increased risk of hypopituitarism, patients with mild TBI remain at significant risk, and overall there is a lack of reliable predictors.

  • Somatotropin and gonadotropin deficiencies occur more commonly than thyrotropin and corticotrophin deficiencies.

  • There is generally

Background

The Centers for Disease Control and Prevention (CDC) estimate that each year 1.7 million Americans are seen in a hospital for a traumatic brain injury (TBI).1 Of these patients, 52,000 die, 275,000 are hospitalized, and 1.365 million are treated and released from an emergency department. The number of people who sustain a TBI and do not seek medical care is unknown. Sports-related concussions are routinely underreported, and it has been estimated that there are 1.6 to 3.8 million cases each

Prevalence of posttraumatic hypopituitarism

Hypopituitarism following TBI was first reported in 1918.15 Since this report almost a century ago, the phenomenon of both anterior and posterior pituitary deficiencies after TBI has been widely reported in case reports16, 17, 18, 19, 20 and literature reviews.21, 22, 23 However, this clinical entity remains largely underdiagnosed, with understanding of this condition improving only in recent years.

The prevalence of hypopituitarism following TBI has been reported to range from 15% to 68%.24, 25

Pathophysiology of hypopituitarism after TBI

The underlying mechanism of posttraumatic hypopituitarism remains unclear. It is likely that several factors are involved, most significantly the primary brain injury and the ischemic injury that can be caused by this primary event or by secondary events such as hypotension, increased intracranial pressure, hypoxia, or anemia.44

The pituitary gland is located within the bony sella turcica at the base of the skull and is covered by the dural diaphragma sellae, through which the stalk connects to

Clinical impact of posttraumatic hypopituitarism

Untreated hypopituitarism is associated with increased morbidity and mortality, providing a compelling reason to improve awareness of this clinical entity. Arguably of greatest clinical significance is the identification of the relationship between posttraumatic hypopituitarism and the neurocognitive impairments that affect patients with TBI. As previously mentioned, patients with moderate to severe TBI experience a variety neuropsychiatric complaints including impairments of memory,

Screening for posttraumatic hypopituitarism

As previously mentioned, the natural history of posttraumatic hypopituitarism varies such that deficiencies that are present immediately following the initial injury may resolve and new hormonal deficits may develop over time, necessitating periodic monitoring of pituitary function. Any patient with life-threatening signs or symptoms of hypopituitarism, such as adrenal insufficiency or diabetes insipidus, should be immediately tested for these deficiencies, the specifics of which are discussed

Diagnostic testing of posttraumatic hypopituitarism

The diagnostic tools used in posttraumatic hypopituitarism are the same as those used to diagnose hypopituitarism from any other cause. In the acute setting, adrenal insufficiency should be suspected in patients with hypotension, hyponatremia, and/or hypoglycemia. Dynamic testing is generally not performed in the acute phase of illness. A morning serum cortisol level less than 3.5 μg/dL strongly indicates adrenal insufficiency, whereas a level greater than 18 μg/dL makes the diagnosis less

Initiation of treatment of posttraumatic hypopituitarism

The decision to initiate hormone replacement in the first 3 to 6 months after injury depends on the specific deficiency present. Hormone replacement should be initiated for isolated deficiencies of posterior pituitary, thyrotroph, and corticotroph function at the time of diagnosis, because of the critical roles of these hormones. Isolated gonadotropin and somatotropin deficiencies that occur 3 to 6 months after the initial trauma are often transient; therefore, some suggest that pituitary

Clinical benefits of treatment of hypopituitarism and potential impact on outcomes

Appropriate hormone replacement for hypopituitarism in general has known clinical benefits as summarized in Table 3. In addition to resolution of symptoms that are caused by each hormonal deficiency, treatment has a significant impact on long-term outcomes, which is especially important given the young age of most patients with TBI.81

The effect that hormone replacement has on quality of life and neurocognitive impairments is of particular interest in this patient population. Treatment of each

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    Disclosure statement: The authors have no disclosures or conflicts of interest to declare.

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