scholarly journals Hypothalamo-Pituitary Dysfunction in Patients With Chronic Subdural Hematoma

2012 ◽  
pp. 161-167 ◽  
Author(s):  
V. HÁNA ◽  
M. KOSÁK ◽  
V. MASOPUST ◽  
D. NETUKA ◽  
Z. LACINOVÁ ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Diabetes Insipidus ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Clinical Severity ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Pituitary Dysfunction ◽  
One Year

Relatively frequent pituitary hormone deficiencies are observed after traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) and according to the published studies the neuroendocrine consequenses of traumatic brain injury are underdiagnosed. In a cohort of 59 patients (49 males, mean age 68.3 years, 36-88 years) after evacuation of subdural hematoma (SDH) were evaluated hypothalamo-pituitary functions one week after surgery, after three months and after one year. Hypogonadism was present in 26 % of patients in an acute phase, but in the majority had a transient character. Less than half of patients was GH deficient (GHD) according to the GHRH+arginine test. We did not find any serious case of hypocortisolism, hypothyroidism, diabetes insipidus centralis nor syndrome of inappropriate secretion of ADH (SIADH). Transient partial hypocortisolism was present in two cases, but resolved. We did not find relation between extension of SDH or clinical severity and development of hypopituitarism. In conclusion, in some patients with SDH growth hormone deficiency or hypogonadism was present. No serious hypocortisolism, hypothyroidism, diabetes insipidus nor SIADH was observed. The possibility of neuroendocrine dysfunction should be considered in patients with SDH, although the deficits are less frequent than in patients after TBI or SAH.

scholarly journals Experience of a Pituitary Clinic for US Military Veterans With Traumatic Brain Injury

2021 ◽  
Vol 5 (4) ◽  
Author(s):  
Jonathan Lee ◽  
Lindsey J Anderson ◽  
Dorota Migula ◽  
Kevin C J Yuen ◽  
Lisa McPeak ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Care Center ◽  
Hormone Replacement ◽  
Tertiary Care ◽  
Puget Sound ◽  
Symptom Burden ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Pituitary Dysfunction

Abstract Context Traumatic brain injury (TBI) is considered the “signature” injury of veterans returning from wartime conflicts in Iraq and Afghanistan. While moderate/severe TBI is associated with pituitary dysfunction, this association has not been well established in the military setting and in mild TBI (mTBI). Screening for pituitary dysfunction resulting from TBI in veteran populations is inconsistent across Veterans Affairs (VA) institutions, and such dysfunction often goes unrecognized and untreated. Objective This work aims to report the experience of a pituitary clinic in screening for and diagnosis of pituitary dysfunction. Methods A retrospective analysis was conducted in a US tertiary care center of veterans referred to the VA Puget Sound Healthcare System pituitary clinic with a history of TBI at least 12 months prior. Main outcome measures included demographics, medical history, symptom burden, baseline hormonal evaluation, brain imaging, and provocative testing for adrenal insufficiency (AI) and adult-onset growth hormone deficiency (AGHD). Results Fatigue, cognitive/memory problems, insomnia, and posttraumatic stress disorder were reported in at least two-thirds of the 58 patients evaluated. Twenty-two (37.9%) were diagnosed with at least one pituitary hormone deficiency, including 13 (22.4%) AI, 12 (20.7%) AGHD, 2 (3.4%) secondary hypogonadism, and 5 (8.6%) hyperprolactinemia diagnoses; there were no cases of thyrotropin deficiency. Conclusion A high prevalence of chronic AI and AGHD was observed among veterans with TBI. Prospective, larger studies are needed to confirm these results and determine the effects of hormone replacement on long-term outcomes in this setting.

Lasting Pituitary Hormone Deficiency after Traumatic Brain Injury

2012 ◽  
Vol 29 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Odile Kozlowski Moreau ◽  
Edwige Yollin ◽  
Emilie Merlen ◽  
Walter Daveluy ◽  
Marc Rousseaux
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Pituitary Hormone Deficiency

scholarly journals Acute and Chronic Posterior Pituitary Insufficiency Among Traumatic Brain Injury Patients at a Tertiary Care Center

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A623-A623
Author(s):  
Imtiyaz Ahmad Bhat ◽  
Moomin Hussain Bhat ◽  
Shariq Rashid Masoodi ◽  
Javid Ahmad Bhat ◽  
Zafar A Shah ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Diabetes Insipidus ◽  
Hospital Stay ◽  
Tertiary Care ◽  
Posterior Pituitary ◽  
Urinary Osmolality ◽  
Pituitary Dysfunction

Abstract Background: Traumatic brain injury (TBI) is the leading cause of death and disability in young adults. Disorders of salt and water balance are the most commonly recognized medical complications in the immediate post-TBI period and contribute to early morbidity and mortality. Objective: We aimed to evaluate the prevalence of acute (during hospital stay) and chronic posterior pituitary dysfunction in patients of head injury admitted at our tertiary care hospital. Study Design: Prospective, Observational study. Participants: 136 patients, attending tertiary care in North India with TBI with radiological evidence of head injury. Methodology: The severity of brain injury was assessed by the Glasgow Coma Scale (GCS), and Modified Rankin Scale (MRS) score at the time of admission. Lab measurements, apart from routine CBC and biochemical tests, included tests of serum and urinary osmolality, serum sodium, cortisol, and thyroid function test during the hospital stay. All patients were monitored closely during the hospital stay. Surviving patients were evaluated at 3, 6, and 12 months of follow-up. Urinary output and water deprivation tests were done to determine chronic posterior pituitary dysfunction. The results were compared against normative data obtained from 25 matched, healthy controls. Serum & urinary osmolality was measure by the freezing point method. Diabetes insipidus (DI) and Syndrome of inappropriate ADH secretion (SIADH) were diagnosed according to standard criteria. Results: Of 136 patients admitted, 61 (44.85%) had a mild head injury (GCS, ≤8), 47 (35.55%) had a moderate injury (GCS, 9-12), and 27 (19.85%) had a severe injury (GCS, 13-15). DI occurred in 10 patients (7.4%), while SIADH was observed in 4 patients in the immediate TBI period. Risk factors for diabetes insipidus were GCS of ≤ 8 at admission, midline shift, and surgical intervention. DI was an independent risk factor for death. There was a negative correlation between the presence of DI and GCS score (r, -0.367). Most of the patients with DI (8 out of 10) died during the hospital stay. One patient persisted to have partial diabetes insipidus and another one SIADH at three months post-TBI; both patients had recovered at six months of follow-up. No new case of DI or SIADH occurred on the follow up to 12 months. Conclusion: The incidence of acute DI in severe head injury (GCS ≤ 8) could be an indicator of the severity of TBI, and associated with increased mortality as most of our patients died during the hospital stay.

scholarly journals Growth Hormone Deficiency Following Traumatic Brain Injury

2019 ◽  
Vol 20 (13) ◽  
pp. 3323 ◽  
Author(s):  
Oratile Kgosidialwa ◽  
Osamah Hakami ◽  
Hafiz Muhammad Zia-Ul-Hussnain ◽  
Amar Agha
Keyword(s):  
Traumatic Brain Injury ◽  
Growth Hormone ◽  
Brain Injury ◽  
Growth Hormone Deficiency ◽  
Dynamic Testing ◽  
Recombinant Human Growth Hormone ◽  
Chronic Phase ◽  
Hormone Deficiency ◽  
Pituitary Hormone

Traumatic brain injury (TBI) is fairly common and annually affects millions of people worldwide. Post traumatic hypopituitarism (PTHP) has been increasingly recognized as an important and prevalent clinical entity. Growth hormone deficiency (GHD) is the most common pituitary hormone deficit in long-term survivors of TBI. The pathophysiology of GHD post TBI is thought to be multifactorial including primary and secondary mechanisms. An interplay of ischemia, cytotoxicity, and inflammation post TBI have been suggested, resulting in pituitary hormone deficits. Signs and symptoms of GHD can overlap with those of TBI and may delay rehabilitation/recovery if not recognized and treated. Screening for GHD is recommended in the chronic phase, at least six months to a year after TBI as GH may recover in those with GHD in the acute phase; conversely, it may manifest in those with a previously intact GH axis. Dynamic testing is the standard method to diagnose GHD in this population. GHD is associated with long-term poor medical outcomes. Treatment with recombinant human growth hormone (rhGH) seems to ameliorate some of these features. This review will discuss the frequency and pathophysiology of GHD post TBI, its clinical consequences, and the outcomes of treatment with GH replacement.

scholarly journals Neuroendocrine dysfunctions and their consequences following traumatic brain injury

2012 ◽  
Vol 153 (24) ◽  
pp. 927-933 ◽  
Author(s):  
Sándor Czirják ◽  
Károly Rácz ◽  
Miklós Góth
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Ice Hockey ◽  
Hormone Deficiency ◽  
Public Health Importance ◽  
Morning Serum Cortisol ◽  
Life Threatening ◽  
One Year

Posttraumatic hypopituitarism is of major public health importance because it is more prevalent than previously thought. The prevalence of hypopituitarism in children with traumatic brain injury is unknown. Most cases of posttraumatic hypopituitarism remain undiagnosed and untreated in the clinical practice, and it may contribute to the severe morbidity seen in patients with traumatic brain injury. In the acute phase of brain injury, the diagnosis of adrenal insufficiency should not be missed. Determination of morning serum cortisol concentration is mandatory, because adrenal insufficiency can be life threatening. Morning serum cortisol lower than 200 nmol/L strongly suggests adrenal insufficiency. A complete hormonal investigation should be performed after one year of the trauma. Isolated growth hormone deficiency is the most common deficiency after traumatic brain injury. Sports-related chronic repetitive head trauma (because of boxing, kickboxing, football and ice hockey) may also result in hypopituitarism. Close co-operation between neurosurgeons, endocrinologists, rehabilitation physicians and representatives of other disciplines is important to provide better care for these patients. Orv. Hetil., 2012, 153, 927–933.

scholarly journals SAT-235 Young Male with Persistent Central Diabetes Insipidus After a Car Accident

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Liudmila Yesaulava ◽  
Caroline Houston ◽  
Sanjeda Sultana
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Specific Gravity ◽  
Diabetes Insipidus ◽  
Intracranial Hypertension ◽  
Serum Sodium ◽  
Mass Effect ◽  
Midline Shift ◽  
Pituitary Dysfunction ◽  
Ct Head

Abstract BACKGROUND: Central diabetes insipidus (CDI) occurs in 20% of cases of traumatic brain injury (TBI). Most cases of post-TBI CDI resolve within 2–5 days. Only 6% of long-term survivors of TBI have evidence of persistent CDI.1 We report a patient with persistent CDI after TBI. Clinical Case: A 27 year old male was referred for polyuria. Three months prior he was in a rollover motor vehicle accident. At that time, CT head revealed frontal and occipital contusions with scattered subarachnoid, subdural, and intraventricular blood. There was no evidence of skull fracture, mass-effect, or midline shift. On hospital day 4, his urine output increased to > 3L/day, with serum sodium of 146 mEq/L (n 135–145) and urine specific gravity of 1.015 (n 1.005–1.030). Repeat head CT revealed bilateral subdural hematomas causing mild mass effect. During the rest of his 2-month hospitalization, he continued to have polyuria with specific gravity as low as 1.005, and occasional hypernatremia, with a peak serum sodium of 149 mEq/L. Serum sodium on discharge was 144 mEq/L. On presentation to our clinic, his family and caretakers reported polydipsia, polyuria and nocturia. He had no history of diabetes mellitus or lithium use. On exam he was tachycardic but normotensive with no signs of dehydration. Neurologic exam was normal except for distractibility and impaired long- and short-term memory. After 3 hours of water deprivation, laboratory testing revealed serum sodium 150 mEq/L, serum osmolality 307 mOsmol/kg (n 270–295), urine osmolality 119 mOsmol/kg (n 300–900), and ADH 3 pmol/L (n </= 14); consistent with CDI. Oral desmopressin led to resolution of polydipsia and polyuria. Evaluation of anterior pituitary function was normal. Six months post TBI, CT head revealed increased left frontal subdural hematoma with effacement of the right lateral ventricle and 1cm left-to-right midline shift. A burr hole procedure was performed but CDI persisted. Conclusion: Animal studies have shown that neurohypophyseal apoptosis occurs by inducing intracranial hypertension lasting 12 hours or more.2 Persistent DI may herald rising intracranial pressure (ICP), as reflected by our patient’s case.1 Clinicians should be aware of the reciprocal association between increased ICP and persistent CDI following TBI. References: (1) Tudor R. M., Thompson C. J. Posterior pituitary dysfunction following traumatic brain injury: review. Pituitary. 2019 Jun; 22(3):296–304. (2) Tan H., et al. Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI. Sci Rep. 2017 Jun; 7(1):3805.

scholarly journals SUN-067 Pituitary Dysfunction in Children with Ectopic Posterior Pituitary

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Ghada Naji ◽  
Erica Poletto ◽  
Rita Ann Kubicky
Keyword(s):  
Diabetes Insipidus ◽  
Median Eminence ◽  
Third Ventricle ◽  
Retrospective Chart Review ◽  
Pituitary Stalk ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Posterior Pituitary ◽  
Pituitary Dysfunction ◽  
Ectopic Posterior Pituitary

Abstract Background: Imaging studies aid in the detection of structural abnormalities that may be associated with pituitary dysfunction, such as ectopic posterior pituitary (EPP). The location of the ectopic lobe can vary, but it is most commonly located along the median eminence in the floor of the third ventricle. An EPP could result from complete or partial defective neural migration during embryogenesis, which could explain the different loci of EPP. Affected individuals have either severe isolated growth hormone deficiency (IGHD) or combined pituitary hormone deficiencies (CPHD); diabetes insipidus is not a feature, indicating that the EPP is functioning normally. Aim: To detect the prevalence of IGHD or CPHD in children with EPP. In addition, to evaluate the association between the location of EPP and pituitary dysfunction. Methods: A retrospective chart review of MRI reports at St. Christopher’s Hospital for Children (SCHC) from 2006-2018 that were found to have EPP. Pituitary hormone function was evaluated in the majority of the patient population. Results: Of the 26 patients with EPP, [16 males (M) and 10 females (F)], mean chronologic age was 5.98+5.18 yrs, only 20 patients had an endocrine evaluation at SCHC. Of the 20 children, 14 had CPHD and 4 had IGHD. Patients were classified into 3 groups (upper, middle & lower) according to EPP location along the pituitary stalk. Of the 21 patients with upper EPP, 17 had pituitary dysfunction (14 with CPHD, 3 with IGHD). Of the 4 children with middle EPP, only 1 had pituitary dysfunction which was IGHD. One patient had lower EPP with hyperprolactinemia. Diabetes insipidus was not identified in any of the children. Conclusion: Our study supports previous reports that CPHD and IGHD are frequent in patients with EPP. Similarly, our data further demonstrate that no cases of diabetes insipidus have been reported in children with EPP. In our study, EPP is most commonly located along the upper third of pituitary stalk at the median eminence level, with a higher prevalence of CPHD and IGHD, a finding similar to prior studies. No CPHD was reported in middle/lower but IGHD was found in the middle EPP group.

scholarly journals Hypogonadism after traumatic brain injury

2009 ◽  
Vol 53 (8) ◽  
pp. 908-914 ◽  
Author(s):  
Alexandre Hohl ◽  
Tânia Longo Mazzuco ◽  
Marisa Helena César Coral ◽  
Marcelo Schwarzbold ◽  
Roger Walz
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Life Quality ◽  
Hormone Deficiency ◽  
Common Finding ◽  
Pituitary Hormone ◽  
Potential Contribution ◽  
Negative Consequences ◽  
Cranial Trauma

Traumatic brain injury (TBI) is the most common cause of death and disability in young adults. Post-TBI neuroendocrine disorders have been increasingly acknowledged in recent years due to their potential contribution to morbidity and, probably, to mortality after trauma. Marked alterations of the hypothalamic-pituitary axis during the post-TBI acute and chronic phases have been reported. Prospective and longitudinal studies have shown that some abnormalities are transitory. On the other hand, there is a high frequency (15% to 68%) of pituitary hormone deficiency among TBI survivors in a long term setting. Post-TBI hypogonadism is a common finding after cranial trauma, and it is predicted to develop in 16% of the survivors in the long term. Post-TBI hypogonadism has been associated with adverse results in the acute and chronic phases after injury. These data reinforce the need for identification of hormonal deficiencies and their proper treatment, in order to optimize patient recovery, improve their life quality, and avoid the negative consequences of non-treated hypogonadism in the long term.

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