Vascular Blood Supply of the Pituitary Gland
Early investigations of the pituitary gland have shown that the majority of the gland’s blood supply comes from the long hypophyseal vessels (Stanfield 1960). The inferior hypophyseal artery supplies blood to the entire neurohypophysis and to a small section of the adenohypophysis, which is described in the table below (Behan et al. 2008; Sirois 2009).
Table: Vascular Supply of the Pituitary (Sirois, 2009)
|Anterior Pituitary||Posterior Lobe|
a) Superior hypophyseal artery
|a) Supply by inferior hypophyseal artery|
b) Capillary plexus formation with portal vessels
|b) Short portal vessels|
|c) 90% of the anterior lobe is nourished by the portal system||c) 1 capillary plexus|
MECHANISM OF INJURY
An anterior pituitary infarction may be caused by compression of the pituitary gland, the hypothalamus, or interruption of the long hypophyseal vessels. This may be the result of direct trauma (i.e., skull fracture), edema, hemorrhage, elevated intracranial pressure, or hypoxic shock. Direct mechanical injury to the hypothalamus, the pituitary stalk, or the pituitary gland may also result in hypopituitarism. An infarction of the posterior lobe can be avoided if the inferior hypophyseal blood vessels are not transected when the pituitary stalk is ruptured. Diabetes insipidus (DI) often occurs as the result of inflammation and edema around the posterior pituitary gland; however, this has been shown to improve with time (Behan et al. 2008).
Injuries Associated with TBI
Potential lesions associated with TBI are shown in the table below. The types of injuries and respective rates are listed in the table below the previous one.
Table: Hypothalamic-Pituitary-Adrenal Lesions Associated with TBI (Sirois 2009)
|Lesion||Causes of Injury||Location of Injury|
|Primary lesion (direct)||Acceleration-deceleration||Traumatic lesion of the stalk|
|Anterior lobe necrosis|
|Posterior lobe hemorrhage|
|Basal skull fracture||Direct lesion to pituitary, stalk or hypothalamus|
|Secondary lesion (non-direct)||Brain edema|
|Increase intracranial pressure|
Table: Type and Rate of Injury (Benvenga et al. 2000)
|Types of Injury||Percentage|
|Hemorhage of hypothalamus||29%|
|Hemorrhage of posterior lobe||26%|
|Infarction of anterior lobe||25%|
|Infarction of posterior lobe||1%|
In 7% of cases, neuroendocrine disorders are not associated with neuroimaging abnormalities. The gold standard for neuroendocrine dysfunction includes serum tests assessing hormonal function (Benvenga et al. 2000).
Isolated & Combined Hormone Deficiencies
Although early hormonal abnormalities are not necessarily associated with long-term PTHP (Klose et al. 2007), the most common problem following ABI is a single axis or hormonal insufficiency. Research has shown that chronic hormone deficits occur in 30–40% of patients following ABI with more than one deficiency occurring in 10–15% of the population (table below) (Aimaretti et al. 2004; Bondanelli et al. 2004; Kelly et al. 2000; Lieberman et al. 2001). Among individuals with an ABI, growth hormone deficiencies may be seen in 20% of those injured, gonadal hormone deficiencies in 15-30%, prolactin elevation in 30%, and hypothyroidism in 10–30% of the population. Chronic adrenal insufficiency and DI post ABI occurs much more commonly, especially in those with a severe TBI (Bernard et al. 2006; Powner et al. 2006).
Table: Isolated and Multiple Pituitary Axes Affected
|Post Traumatic Phase||1 axis (single deficiency)||2 or more (multiple deficiencies)|