Early endocrine alterations reflect prolonged stress and relate to one year functional outcome in patients with severe brain injury (original) (raw)
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Acute and long-term pituitary insufficiency in traumatic brain injury: a prospective cohort study
2007
Objective To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early posttraumatic hormone alterations. Design A 12-month prospective study. Patients Forty-six consecutive patients with TBI (mild: N = 22; moderate: N = 9; severe: N = 15). Measurements Baseline and stimulated hormone concentrations were assessed in the early phase (0-12 days post-traumatically), and at 3, 6 and 12 months postinjury. Pituitary tests included the Synacthen-test (acute +6 months) and the insulin tolerance test (ITT) or the GHRH + arginine test if the ITT was contraindicated (3 + 12 months). Insufficiencies were confirmed by retesting. Results Early post-traumatic hormone alterations mimicking central hypogonadism or hypothyroidism were present in 35 of the 46 (76%) patients. Three months post-traumatically, 6 of the 46 patients failed anterior pituitary testing. At 12 months, one patient had recovered, whereas none developed new insufficiencies. All insufficient patients had GH deficiency (5 out of 46), followed by ACTH-(3 out of 46), TSH-(1 out of 46), LH/FSH-(1 out of 46) and ADH deficiency (1 out of 46). Hypopituitary patients had more frequently been exposed to severe TBI (4 out of 15) than to mild or moderate TBI (1 out of 31) ( P = 0·02). Early endocrine alterations including lowered thyroid and gonadal hormones, and increased total cortisol, free cortisol and copeptin were positively associated to TBI severity ( P < 0·05), but not to long-term development of hypopituitarism ( P > 0·1), although it was indicative in some. Conclusion Long-term hypopituitarism was frequent only in severe TBI. During the 3-12 months follow-up, recovery but no new insufficiencies were recorded, indicating manifest hypothalamic or pituitary damage already a few months postinjury. Very early hormone alterations were not associated to long-term posttraumatic hypopituitarism. Clinicians should, nonetheless, be aware of potential ACTH deficiency in the early post-traumatic period.
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.
Clinical Endocrinology, 2007
Objective To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early posttraumatic hormone alterations. Design A 12-month prospective study. Patients Forty-six consecutive patients with TBI (mild: N = 22; moderate: N = 9; severe: N = 15). Measurements Baseline and stimulated hormone concentrations were assessed in the early phase (0-12 days post-traumatically), and at 3, 6 and 12 months postinjury. Pituitary tests included the Synacthen-test (acute +6 months) and the insulin tolerance test (ITT) or the GHRH + arginine test if the ITT was contraindicated (3 + 12 months). Insufficiencies were confirmed by retesting. Results Early post-traumatic hormone alterations mimicking central hypogonadism or hypothyroidism were present in 35 of the 46 (76%) patients. Three months post-traumatically, 6 of the 46 patients failed anterior pituitary testing. At 12 months, one patient had recovered, whereas none developed new insufficiencies. All insufficient patients had GH deficiency (5 out of 46), followed by ACTH-(3 out of 46), TSH-(1 out of 46), LH/FSH-(1 out of 46) and ADH deficiency (1 out of 46). Hypopituitary patients had more frequently been exposed to severe TBI (4 out of 15) than to mild or moderate TBI (1 out of 31) ( P = 0·02). Early endocrine alterations including lowered thyroid and gonadal hormones, and increased total cortisol, free cortisol and copeptin were positively associated to TBI severity ( P < 0·05), but not to long-term development of hypopituitarism ( P > 0·1), although it was indicative in some. Conclusion Long-term hypopituitarism was frequent only in severe TBI. During the 3-12 months follow-up, recovery but no new insufficiencies were recorded, indicating manifest hypothalamic or pituitary damage already a few months postinjury. Very early hormone alterations were not associated to long-term posttraumatic hypopituitarism. Clinicians should, nonetheless, be aware of potential ACTH deficiency in the early post-traumatic period.
Brain Injury, 2007
Primary objective: There are only limited data regarding pituitary functions in the acute phase of traumatic brain injury (TBI) and previous studies have been conducted in only small cohorts of subjects. Therefore we have investigated the pituitary functions in the early acute phase, within 24 hours of trauma, in 104 patients with TBI. Additionally, the relationships between basal pituitary hormones, severity of the trauma and mortality due to trauma were also investigated. Methods and procedures: One hundred and four TBI patients were included in the study consecutively. All patients underwent basal hormonal evaluation within the first 24 hours of admission. Twenty of 104 patients died during the acute phase. Main outcomes: Prolactin levels were negatively correlated with the Glasgow coma scale (GCS), cortisol levels were positively correlated with the GCS and cortisol levels were positively correlated with ACTH levels. Additionally there was a significant positive correlation between the total testosterone levels and the GCS in males. Logistic regression analysis revealed that mortality after TBI was unrelated to basal pituitary hormone levels. However age and GCS were significantly related to the mortality. The percentages of pituitary hormone deficiencies were as follows: 3.8% had TSH deficiency, 40.0% had gonadotrophin deficiency, 8.8% had ACTH deficiency and 20.0% had GH deficiency. Conclusions: Present data clearly demonstrate that pituitary function is disturbed in TBI and the most frequently deficient pituitary hormones were gonadotrophins in the early acute phase of TBI. Basal hormone levels including cortisol, prolactin and total testosterone were related to the severity of the trauma. However there was no relation between basal hormones and mortality due to TBI. Age and GCS were significantly related to mortality.
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.
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.
Pituitary, 2008
Several studies have reported a close association between traumatic brain injury (TBI) and pituitary dysfunction, and expert panels have recently proposed recommendations for hormone assessment and replacement for pituitary insufficiency after TBI. Given the high incidence of TBI, identification of reliable predictors is of utmost importance in order to secure a cost-effective screening strategy. It has not yet been possible to identify early hormone alterations as a useful tool for the prediction of longterm post-traumatic hypopituitarism, whereas indicators of increased trauma severity have been reported as predictive in an increasing number of studies. Outcome studies have moreover indicated that post-traumatic hypopituitarism is of clinical significance, which may justify introduction of neuroendocrine screening in TBI. Much larger cohorts are, however, still needed for further evaluation and confirmation of reliable screening markers, and future studies should be designed to ensure a high diagnostic robustness for proper identification of reliable predictors, as the results may be highly dependent on diagnostic pitfalls.
Prevalence of hypothalamo pituitary dysfunction in patients of traumatic brain injury
Indian journal of endocrinology and metabolism
Traumatic brain injury (TBI) is common in young soldiers of armed forces leading to significant morbidity and mortality. We studied the prevalence of hypopituitarism following TBI and its association with trauma severity. We conducted a 12-month prospective study of 56 TBI patients for the presence of hormonal dysfunction. Hormonal parameters were estimated during the early phase (0-10 days posttraumatically) and after 6 and 12 months. Dynamic testing was done when required, and the results were analyzed by appropriate statistical methods. Hormonal dysfunction was seen in 39 of the 56 (70%) patients at initial assessment. Persisting pituitary deficiencies are seen in 7 and 8 patients at the end of 6 months and 12 months, respectively. Hypogonadotropic hypogonadism, hypothyroidism, and growth hormone deficiency are the most common diagnoses. Initial severe TBI and plurihormonal involvement predicted the long-term hypopituitarism. Early hypopituitarism was common in severe TBI, but re...