The hypothalamus stimulates production or release of all pituitary hormones other than prolactin, release of which is suppressed by hypothalamus. Post-traumatic hypopituitarism arises from a combination of two processes.
- Anterior pituitary injury arises from ischaemic damage which relates to its dependence on portal circulation within the pituitary stalk, this circulation being damaged by shearing forces.
- Posteriory pituitary receives its blood circulation through a more direct route via inferior hypophyseal artery, and is thus less vulnerable to infarction, but can still be vulnerable to pressure effects associated with haemorrhage.
Due to the longer lasting impact of infarction, anterior pituitary function is more likely to be impaired relative to posterior pituitary function.
Clinical features may be non-specific with gradual insidious onset, but potentially severe if unidentified. For this reason asymptomatic screening programmes are recommended.
Clinical features of anterior pituitary failure may present as deficiencies in the following:
- Growth Hormone (GH): Non-specific features.
- Adrenocorticotropin (ACTH): Lethargy, myopathy, risk of adrenal crisis states.
- Thyroid-stimulating hormone: Lethargy, myopathy, obesity, cognitive slowing.
- Luteinizing hormone (LH)/Follicle-stimulating hormone (FSH): Lethargy, reduced muscle mass, reduced bone density, reduced sexuality.
- Melanocyte Stimulating Hormone (MSH): Non-specific features.
- Prolactin excess which may lead to increased lactation or arousal, but is usually asymptomatic.
Posterior pituitary injury results in loss of hypothalamic control of Antidiuretic Hormone (ADH) release. This can result in:
- Excess release or Syndrome of Inappropriate Antidiuretic Hormone (SIADH) with low sodium levels (hyponatraemia).
- Impaired release leading to Diabetes Insipidus/hypernatraemia (high sodium levels).
Oxytocin deficits or excess are not characteristically associated with any clinical syndromes.