Endocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome? (original) (raw)
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Endocrine consequences of traumatic brain injury. Literature review
Romanian Journal of Legal Medicine, 2016
Traumatic brain injury (TBI) is associated with increased mortality and morbidity, as well as high rates of longterm disability in survivors. TBI-related deficiencies of both anterior pituitary (posttraumatic hypopituitarism, PTHP) and posterior pituitary (diabetes insipidus PTDI or syndrome of inappropriate antidiuretic secretion, SIADH) are much more frequent than previously known and associated with an unfavourable outcome. The pathophysiology of pituitary dysfunction after TBI is not entirely clear. The traumatic event can induce skull base fractures, hemorrhages or infarction affecting the hypothalamic and pituitary region with consequent endocrine dysfunction. In addition, metabolic and vascular brain changes, frequent in a critically ill patient also aggravate the neuroendocrine dysfunction. In the first days after trauma, the deficiency of adrenocorticotropic hormone and PTDI or SIADH are the main concern because if undiagnosed and untreated are associated with severe dyselectrolitemia and hypotension with increased mortality rate. Posterior pituitary dysfunction occurs in the first days after injury; SIADH usually resolves completely, PTDI can persist in a minority of cases. In contrast, PTHP can occur after a long time interval after TBI. Some degree of PTHP is present in 30-40% of TBI survivors. Early recognition and endocrinological treatment are essential to optimize the outcome of the intensive care management and of the rehabilitation process.
Assessment of endocrine abnormalities in severe traumatic brain injury: a prospective study
Acta Neurochirurgica, 2009
Objective The frequency and pattern of endocrine abnormalities among patients with traumatic brain injury have been the subject matter of very few studies. This study was intended to assess the pattern of endocrine dysfunction following severe head injury. Methods Severe head injury patients admitted to the Sciences, New Delhi, from January to December in 1 year formed the study group. Apart from clinical assessment, NCCT of the head was performed on all patients on admission. A complete anterior pituitary hormone analysis was performed within 24 h of injury and was repeated at 2 weeks, 3 months and 6 months amongst patients who survived. Results A total of 99 patients were included in the study. Forty of our patients succumbed in the hospital. Rest of the patients were followed up for 6 months. Elevations of cortisol followed by prolactin were the most common hormonal derangements at admission. Midline shift on CT scans was inversely related to cortisol elevation and directly related to GH elevation. Infarct on CT scans was inversely related to cortisol and LH elevation. A significant alteration was found in the decreasing trend of the mean T4 values and normalisation or a decreasing trend from initially elevated mean cortisol and GH levels during follow-up (p<0.05). Conclusions This study reveals that abnormalities in hormonal profiles appear to be relatively common in severe traumatic brain injury and fluctuate significantly over at least 6 months; there is a correlation with age and radiological findings. Performance of hormonal analysis evaluation should be considered in patients with severe brain injury so that appropriate hormonal replacement can be done to optimise the clinical outcome.
Endocrine Failure After Traumatic Brain Injury in Adults
Neurocritical Care, 2006
Objective: To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation. Methods: A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications. Results: Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamicpituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5-15%, growth hormone 18%, vasopressin 3-37%, and gonadal (25-80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30-40% of selected patients after TBI, more than one deficiency in 10-15%, growth hormone in 15-20%, gonadal hormones in 15%, and hypothyroidism in 10-30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy. Conclusions: Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unres ponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.
Neuroendocrine dysfunction in the acute phase of traumatic brain injury
Clinical Endocrinology, 2004
BACKGROUND Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury ( TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post-TBI period is unknown. AIM To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI. SUBJECTS Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3 -13], and 31 matched healthy control volunteers were studied. METHODS The glucagon stimulation test (GST) was performed at a median of 12 days (range 7-20) following TBI. Baseline thyroid function, PRL, IGF-1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges. RESULTS Control data indicated that peak serum GH of > 5 ng / ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response < 5 ng/ml (12 mU/l). Eight patients (16%) had peak cortisol responses < 450 nmol/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses ( P < 0·05). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF-1 values ( P > 0·05). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS ( r = 0·32, P = 0·04). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score ( r = − − − − 0·36, P = 0·011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion. CONCLUSION Our data show that post-traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.
Journal of Neurotrauma, 2009
Neuroendocrine dysfunction following traumatic brain injury (TBI) has been described extensively. However, few studies are longitudinal and most lack subtle radiological, clinical, and repetitive endocrine assessment in the acute phase. Accordingly, we prospectively assessed neuroendocrine function in 71 patients after TBI. Injury was documented by a computed tomography (CT). During the first week, critical clinical data (Glasgow Coma Score, APACHE score), treatment variables such as duration of analgosedation for mechanical ventilation, were related to basal pituitary function. More than 2 years later, a subgroup of patients was re-evaluated using dynamic testing with ACTH and GHRH-arginine tests. The Pearson's correlation analysis and Mann-Whitney rank sum test for group differences were used for statistical analysis. None of the CT findings predicted neuroendocrine dysfunction following TBI. The adaptive response to critical illness with significantly elevated cortisol levels on admission and decreased levels thereafter in patients ventilated for more than 24 h ( p < 0.05) was attenuated following severe TBI ( p < 0.05). However, the coincidence of low serum cortisol and increased urinary excretion of glucocorticoid metabolites in about 80% of patients challenges the relevance of basal hormone measurements. In ventilated patients, total T3 and free T4 were decreased ( p < 0.05), TSH was low on day 3 ( p < 0.05), and a gonadotropic insufficiency was present ( p < 0.05). The thyrotropic and gonadotropic system recovered completely within the follow-up period. With regard to the somatotropic system, neither brain injury severity nor mechanical ventilation was associated with an insufficiency during the acute phase post-injury. However, initially low GH levels predicted a persistent deficiency (r ¼ 0.731, p < 0.001). We conclude that both severe TBI and prolonged mechanical ventilation result in hormonal disturbances early after injury, suggesting a pathophysiological response to brain injury and subsequent intensive care treatment rather than morphological damage.
Neuroendocrine Disturbances after Brain Damage: An Important and Often Undiagnosed Disorder
Journal of Clinical Medicine, 2015
Traumatic brain injury (TBI) is a common and significant public health problem all over the world. Until recently, TBI has been recognized as an uncommon cause of hypopituitarism. The studies conducted during the last 15 years revealed that TBI is a serious cause of hypopituitarism. Although the underlying pathophysiology has not yet been fully clarified, new data indicate that genetic predisposition, autoimmunity and neuroinflammatory changes may play a role in the development of hypopituitarism. Combative sports, including boxing and kickboxing, both of which are characterized by chronic repetitive head trauma, have been shown as new causes of neuroendocrine abnormalities, mainly hypopituitarism, for the first time during the last 10 years. Most patients with TBI-induced pituitary dysfunction remain undiagnosed and untreated because of the non-specific and subtle clinical manifestations of hypopituitarism. Replacement of the deficient hormones, of which GH is the commonest hormone lost, may not only reverse the clinical manifestations and neurocognitive dysfunction, but may also help posttraumatic disabled patients resistant to classical treatment who have undiagnosed hypopituitarism and GH deficiency in particular. Therefore, early diagnosis, which depends on the awareness of TBI as a cause of neuroendocrine abnormalities among the medical community, is crucially important.
Acute neuro-endocrine profile and prediction of outcome after severe brain injury
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 2013
Object: The aim of the study was to evaluate the early changes in pituitary hormone levels after severe traumatic brain injury (sTBI) and compare hormone levels to basic neuro-intensive care data, a systematic scoring of the CT-findings and to evaluate whether hormone changes are related to outcome.
Frontiers in Endocrinology, 2018
Neuropsychiatric symptoms following traumatic brain injury (TBI) are common and contribute negatively to TBI outcomes by reducing overall quality of life. The development of neurobehavioral sequelae, such as concentration deficits, depression, anxiety, fatigue, and loss of emotional well-being has historically been attributed to an ambiguous "post-concussive syndrome," considered secondary to frank structural injury and axonal damage. However, recent research suggests that neuroendocrine dysfunction, specifically hypopituitarism, plays an important role in the etiology of these symptoms. This post-head trauma hypopituitarism (PHTH) has been shown in the past two decades to be a clinically prevalent phenomenon, and given the parallels between neuropsychiatric symptoms associated with non-TBI-induced hypopituitarism and those following TBI, it is now acknowledged that PHTH is likely a substantial contributor to these impairments. The current paper seeks to provide an overview of hypothesized pathophysiological mechanisms underlying neuroendocrine abnormalities after TBI, and to emphasize the significance of this phenomenon in the development of the neurobehavioral problems frequently seen after head trauma.
Endocrine Sequelae of Traumatic Brain Injury in Childhood
Hormone Research, 2007
childhood, early detection of hormone abnormalities is vital. A multidisciplinary approach to follow-up and endocrine assessment is required for the long-term management and rehabilitation of children and adolescents who survive moderate to severe head injury.