Endocrine failure after traumatic brain injury in adults
To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation. A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publication...
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| Veröffentlicht in: | Neurocritical care 2006-01, Vol.5 (1), p.61-70 |
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| creator | Powner, David J Boccalandro, Cristina Alp, M Serdar Vollmer, Dennis G |
| description | To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.
A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.
Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary 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.
Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, 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. |
| doi_str_mv | 10.1385/NCC:5:1:61 |
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A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.
Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary 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.
Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, 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.</description><identifier>ISSN: 1541-6933</identifier><identifier>EISSN: 1541-6933</identifier><identifier>EISSN: 1556-0961</identifier><identifier>DOI: 10.1385/NCC:5:1:61</identifier><identifier>PMID: 16960299</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Adrenal Insufficiency - epidemiology ; Adrenal Insufficiency - etiology ; Adult ; Brain Injuries - complications ; Diagnosis, Differential ; Euthyroid Sick Syndromes - epidemiology ; Euthyroid Sick Syndromes - etiology ; Growth hormones ; Humans ; Hyperprolactinemia - epidemiology ; Hyperprolactinemia - etiology ; Hypopituitarism - epidemiology ; Hypopituitarism - etiology ; Hypopituitarism - physiopathology ; Hypotension ; Hypothalamo-Hypophyseal System - physiopathology ; Hypothyroidism ; Inappropriate ADH Syndrome - epidemiology ; Inappropriate ADH Syndrome - etiology ; Pituitary-Adrenal System - physiopathology ; Traumatic brain injury</subject><ispartof>Neurocritical care, 2006-01, Vol.5 (1), p.61-70</ispartof><rights>Humana Press Inc 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-401c58d8db3a3e41a6353d12160a53a4474c5c3c9e94577a588ff248e02221073</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2919981590?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,776,780,21367,27901,27902,33721,33722,43781</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16960299$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Powner, David J</creatorcontrib><creatorcontrib>Boccalandro, Cristina</creatorcontrib><creatorcontrib>Alp, M Serdar</creatorcontrib><creatorcontrib>Vollmer, Dennis G</creatorcontrib><title>Endocrine failure after traumatic brain injury in adults</title><title>Neurocritical care</title><addtitle>Neurocrit Care</addtitle><description>To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.
A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.
Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary 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.
Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, 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.</description><subject>Adrenal Insufficiency - epidemiology</subject><subject>Adrenal Insufficiency - etiology</subject><subject>Adult</subject><subject>Brain Injuries - complications</subject><subject>Diagnosis, Differential</subject><subject>Euthyroid Sick Syndromes - epidemiology</subject><subject>Euthyroid Sick Syndromes - etiology</subject><subject>Growth hormones</subject><subject>Humans</subject><subject>Hyperprolactinemia - epidemiology</subject><subject>Hyperprolactinemia - etiology</subject><subject>Hypopituitarism - epidemiology</subject><subject>Hypopituitarism - etiology</subject><subject>Hypopituitarism - physiopathology</subject><subject>Hypotension</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Hypothyroidism</subject><subject>Inappropriate ADH Syndrome - epidemiology</subject><subject>Inappropriate ADH Syndrome - etiology</subject><subject>Pituitary-Adrenal System - physiopathology</subject><subject>Traumatic brain injury</subject><issn>1541-6933</issn><issn>1541-6933</issn><issn>1556-0961</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0EtLAzEUBeAgiq3VjT9ABgQXwmhuXpPMTob6gKIbXYc0k4GUedRksui_d6QFxY2rcxcfB-5B6BLwHVDJ71-rquQllAKO0Bw4g1woSo9_3TN0FuMGY1Kogp-iGQglMFFqjuSyrwcbfO-yxvg2BZeZZnQhG4NJnRm9zdbB-D7z_SaF3RSZqVM7xnN00pg2uotDLtDH4_K9es5Xb08v1cMqt1TiMWcYLJe1rNfUUMfACMppDQQENpwaxgpmuaVWOcV4URguZdMQJh0mhAAu6ALd7Hu3YfhMLo6689G6tjW9G1LUQkrGKJX_QgJAGON8gtd_4GZIoZ-e0ESBUhK4wpO63SsbhhiDa_Q2-M6EnQasv2fX0-yaa9ACJnx1qEzrztU_9LAz_QImsHpM</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>Powner, David J</creator><creator>Boccalandro, Cristina</creator><creator>Alp, M Serdar</creator><creator>Vollmer, Dennis G</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20060101</creationdate><title>Endocrine failure after traumatic brain injury in adults</title><author>Powner, David J ; Boccalandro, Cristina ; Alp, M Serdar ; Vollmer, Dennis G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-401c58d8db3a3e41a6353d12160a53a4474c5c3c9e94577a588ff248e02221073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adrenal Insufficiency - epidemiology</topic><topic>Adrenal Insufficiency - etiology</topic><topic>Adult</topic><topic>Brain Injuries - complications</topic><topic>Diagnosis, Differential</topic><topic>Euthyroid Sick Syndromes - epidemiology</topic><topic>Euthyroid Sick Syndromes - etiology</topic><topic>Growth hormones</topic><topic>Humans</topic><topic>Hyperprolactinemia - epidemiology</topic><topic>Hyperprolactinemia - etiology</topic><topic>Hypopituitarism - epidemiology</topic><topic>Hypopituitarism - etiology</topic><topic>Hypopituitarism - physiopathology</topic><topic>Hypotension</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Hypothyroidism</topic><topic>Inappropriate ADH Syndrome - epidemiology</topic><topic>Inappropriate ADH Syndrome - etiology</topic><topic>Pituitary-Adrenal System - physiopathology</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Powner, David J</creatorcontrib><creatorcontrib>Boccalandro, Cristina</creatorcontrib><creatorcontrib>Alp, M Serdar</creatorcontrib><creatorcontrib>Vollmer, Dennis G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurocritical care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Powner, David J</au><au>Boccalandro, Cristina</au><au>Alp, M Serdar</au><au>Vollmer, Dennis G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endocrine failure after traumatic brain injury in adults</atitle><jtitle>Neurocritical care</jtitle><addtitle>Neurocrit Care</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>5</volume><issue>1</issue><spage>61</spage><epage>70</epage><pages>61-70</pages><issn>1541-6933</issn><eissn>1541-6933</eissn><eissn>1556-0961</eissn><abstract>To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.
A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.
Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary 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.
Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, 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.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>16960299</pmid><doi>10.1385/NCC:5:1:61</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenal Insufficiency - epidemiology Adrenal Insufficiency - etiology Adult Brain Injuries - complications Diagnosis, Differential Euthyroid Sick Syndromes - epidemiology Euthyroid Sick Syndromes - etiology Growth hormones Humans Hyperprolactinemia - epidemiology Hyperprolactinemia - etiology Hypopituitarism - epidemiology Hypopituitarism - etiology Hypopituitarism - physiopathology Hypotension Hypothalamo-Hypophyseal System - physiopathology Hypothyroidism Inappropriate ADH Syndrome - epidemiology Inappropriate ADH Syndrome - etiology Pituitary-Adrenal System - physiopathology Traumatic brain injury |
| title | Endocrine failure after traumatic brain injury in adults |
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