Pathophysiology of Hypopituitarism

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

  • Branch of internal carotid 
a) Supply by inferior hypophyseal artery

b) Capillary plexus formation with portal vessels

  •  Primary and secondary
  •  Run down in the stalk with two long 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
Hypoxia
Increase intracranial pressure
Hemorrhage
Inflammatory mediators

 

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%
Stalk resection 3%

 

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)
Acute 48% 28%
3 months 6.5% 6.5%
12 months 4.3% 6.5%