Post Head Injury Endocrine Complications

Updated: Feb 12, 2016
  • Author: Milton J Klein, DO, MBA; Chief Editor: Consuelo T Lorenzo, MD  more...
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Overview

Background

The greatest challenge associated with endocrine complications in individuals with traumatic brain injury (TBI) is early recognition of these subtle problems. Endocrine complications can produce significant impact on the progress and outcome of TBI rehabilitation. Prompt diagnosis and treatment of endocrine complications following TBI facilitate the rehabilitation process of patients with TBI. [1, 2]

The release of pituitary hormones, orchestrated by the neuropeptide signals from the hypothalamus, provides a tight control of hormone-regulated homeostasis. The pituitary gland is protected well within the sella turcica of the sphenoid bone; however, the pituitary stalk, connected to the anterior pituitary and hypothalamus, is vulnerable to the effects of TBI, especially in patients with associated facial fractures, cranial nerve injuries, and dysautonomia.

Related Medscape Reference topics:

Classification and Complications of Traumatic Brain Injury

Head Trauma [Pediatrics: Cardiac Disease and Critical Care Medicine]

Head Trauma [Trauma]

Post Head Injury Autonomic Complications

Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology

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Pathophysiology

Autopsy studies in fatal traumatic brain injury (TBI) cases demonstrate a fairly high prevalence of hypothalamic and pituitary abnormalities, including anterior lobe necrosis, posterior lobe hemorrhage, and traumatic lesions of the hypothalamic-pituitary stalk. Some variability is noted in studies. Anterior pituitary infarction has been seen to occur in 9-38% of patients; posterior pituitary hemorrhage, in 12-45% of cases; and traumatic lesions of the stalk, in 5-30% of patients.

The traumatic rupture of the pituitary stalk results in anterior lobe infarction because of disruption of the portal blood supply between the hypothalamus and anterior pituitary. Ninety percent of the anterior lobe is nourished by the hypophyseal portal veins, which originate from and follow the pituitary stalk. An alternative explanation is that posttraumatic edema of the pituitary gland within the bony sella turcica compromises the portal blood supply, resulting in anterior lobe ischemia/necrosis. Both mechanisms may contribute to anterior lobe dysfunction following TBI.

Anterior hypothalamic trauma often is observed on postmortem studies and may be associated with pituitary hemorrhage or infarction related to TBI. Anterior pituitary hormones (eg, growth hormone [GH], [3] thyrotropin, corticotropin, gonadotropins) are released by the neuropeptide-releasing hormones from the hypothalamus. The posterior pituitary hormones (eg, vasopressin, oxytocin) are produced by the hypothalamus and are carried by long axonal projections into the posterior pituitary; they are released later. The posterior lobe vascular supply is not affected by pituitary stalk trauma, because it is supplied by the inferior hypophyseal arteries, which arise from the internal carotid artery below the level of the diaphragma sella. Infarction of the posterior lobe is therefore rare, and the mechanism of the development of diabetes insipidus (DI) is by denervation-losing neural integrity with the hypothalamus. [4, 5, 6, 7, 8, 9]

The most common endocrine complication after a TBI is syndrome of inappropriate antidiuretic hormone (SIADH). SIADH causes a dilutional hyponatremia secondary to inappropriate renal water conservation. Relatively less common post-TBI endocrinopathies include anterior hypopituitarism (AH), DI, cerebral salt wasting (CSW), and primary adrenal insufficiency (PAI). [10, 11, 12, 13, 14, 15, 16, 17] The most common endocrinopathies associated with hypopituitarism, in descending order, include hypogonadism, hypothyroidism, adrenal insufficiency, hyperprolactinemia, DI, and GH deficiency. CSW and PAI are peripheral causes of hyponatremia after a TBI. SIADH, AH, and DI have central endocrine etiologies.

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Epidemiology

Frequency

United States

In the United States, the annual incidence of traumatic brain injury (TBI) is 1.5-2 million people. [18] Of that population, 70,000-90,000 persons sustain a chronic, significant disabling condition. A retrospective study demonstrated that 4% of patients with TBI sustained an associated neuroendocrine disorder of the hypothalamic-pituitary axis. This condition is underdiagnosed, [19, 20] as demonstrated by evidence that 40-63% of fatal cases of TBI reveal postmortem pathologic findings of the hypothalamus/anterior pituitary.

Mortality/Morbidity

According to data from the Centers for Disease Control and Prevention, state surveillance projects report the annual incidence of traumatic brain injury (TBI) to be 200 individuals per 100,000 people, with an estimated 52,000 fatalities each year. Estimates of prevalence suggest that a total of 2.5-6.5 million persons are living with the sequelae of TBI. These estimates may be inaccurate, because these data are limited to hospitalized patients with TBI and to prehospital fatalities from TBI.

Race

No known statistical racial predisposition exists in relation to traumatic brain injury (TBI). Approximately 20% of TBI cases are related to violence, especially firearm violence. In general, young African-American males are exposed to violent acts more frequently than other populations are, which may be reflected in a somewhat higher-than-average incidence of TBI in this group.

Sex

The male-to-female ratio for the incidence of traumatic brain injury (TBI) is greater than 2:1. The incidence of neuroendocrine complications following TBI is directly proportional to this ratio.

Age

The populations at greatest risk for traumatic brain injury are young people aged 15-24 years and individuals older than 75 years. Children aged 5 years or younger also are at risk. [3]

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