Hypopituitarism Following Traumatic Brain Injury and Subarachnoid Hemorrhage

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The hypothalamus and pituitary are vulnerable to injury and dysfunction following traumatic brain trauma (TBI) and subarachnoid hemorrhage (SAH). These constitute worldwide public health problems and leading causes of death and disability in young adults. Survivors of both TBI and SAH are at a great risk of significant neuroendocrine dysfunction, adverse physical and/or psychological problems, depression, and sleep disturbances that result in disturbed quality of life (QOL).

Schneider et al searched the MEDLINE database for articles published between 2000 and 2007 pertaining to TBI and SAH. They identified 19 studies including 1137 patients (1015 TBI patients and SAH 122 patients). Only 2 of these studies (with 74 patients) reported on pediatric populations. The authors investigated 13 studies (with 809 TBI patients and 102 SAH patients) that were performed at least 5 months following the injury (chronic phase). They excluded studies in the early phase after injury to avoid the confounding effect of acute critical illness on neuroendocrine function and the pediatric populations for reasons of homogeneity. The pooled prevalence of anterior hypopituitarism in the chronic phase after TBI and SAH was 27.5% (95% CI, 22.8%-28.9%) and 47% (95% CI, 37.4%-56.8%), respectively. The pooled prevalence of hypopituitarism was greater in patients with severe TBI, as compared with those with mild or moderate TBI (as defined by the Glasgow Coma Scale). On the contrary, clinical severity of SAH did not help discriminate between patients at high and low risk of developing hypopituitarism. Early neuroendocrine abnormalities were transient in some patients while hypopituitarism evolved over time in others.

The authors considered that hypopituitarism appears to be a common occurrence following TBI and SAH and might contribute to morbidity and poor recovery after brain injury although most cases remained unrecognized and untreated. All patients hospitalized for TBI or SAH should be evaluated for endocrine alterations long-term.

Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, Stalla GK, Agha A. Hypothalamopituitary dysfunction following traumatic brain injury and aneurismal subarachnoid hemorrhage. A systemic review. JAMA. 2007;26:1429-38.

Editor’s Comment

Another article regarding TBI published in the recent literature was reviewed in GGH last year.1 The current paper by Schneider et al provides specific information regarding patients with SAH. Considering the large number of individuals who have TBI and SAH each year, post-traumatic hypopituitarism is an important public health issue. TBI and SAH pose substantial risks to hypothalamopituitary dysfunction. Hypopituitarism after TBI and SAH might contribute to a delayed or hampered recovery during rehabilitation. However, in both adults and children, a large number of patients with hypopituitarism after TBI or SAH remain undiagnosed and untreated.
Possible causes of hypopituitarism include hemorrhage, infarction, ischemia, necrosis, fibrosis, swelling, stalk transaction, or direct trauma to the hypothalamus, stalk, and/or pituitary region. The severity of TBI seems to be an important risk factor for developing hypopituitarism, however, post-traumatic hypopituitarism can also manifest after even mild TBI. Whereas hypothalamopituitary dysfunction occurred without regard to the severity of SAH.

The signs and symptoms associated with hypopituitarism are often nonspecific and mimic the sequelae of TBI and SAH such as depression, neuropsychological deficits, or personality changes. They are likely to be overlooked if endocrine dysfunction is not actively assessed. Moreover, hormonal deficits may contribute to the chronic disability and the physical, cognitive, health, and social sequelae in patients with TBI and SAH. Therefore, accurate endocrine evaluation and long-term follow-up of TBI and SAH patients are necessary in order to detect the occurrence of hypopituitarism, regardless of clinical evidence for hypothalamopituitary dysfunction. In order to improve outcome and quality of life of TBI and SAH patients, adequate hormone replacement therapy may be necessary in those who develop hypopituitarism. It is necessary for physicians as well as patients and family members to know that hypothalamopituitary dysfunction following TBI and SAH may occur long after the initial trauma. A close collaboration among neurosurgeons, neurologists, rehabilitation specialists, internists, pediatricians, and endocrinologists is essential to achieve a coordinated approach to the care of patients with TBI and SAH. The consensus guidelines for assessment and for clinical practice of such patients have been published.2,3

Yoshikazu Nishi, MD

References - (linked to )

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Last Updated: 04/30/2008