Hypothalamic-pituitary-adrenal axis dysfunction in critically ill patients with traumatic brain injury: Incidence, pathophysiology, and relationship to vasopressor dependence and peripheral interleukin-6 levels*

Dimopoulou, Ioanna; Tsagarakis, Stylianos; Kouyialis, Andreas T.; Roussou, Paraskevi; Assithianakis, G; Christoforaki, M; Ilias, Ιoannis; Sakas, Damianos E.; Thalassinos, Nikolaos; Roussos, Charis

doi:10.1097/01.ccm.0000108885.37811.ca

Cited by 127 publications

(66 citation statements)

References 45 publications

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“…A recent evaluation of 50 patients in the acute phase post-TBI showed central hypothyroidism in 1 case (5%) (49). Central hypothyroidism was also demonstrated in 15% of critical care patients with moderate to severe TBI (54).…”

Section: Consequences Of Tbimentioning

confidence: 99%

“…On the contrary, adrenal insufficiency has been found in 16% of patients during the early phase post-TBI, suggesting post-traumatic damage at the hypothalamic -pituitary level (49). Primary or secondary adrenal insufficiency has been shown in 15% of patients with moderate to severe TBI, 7-60 days after injury, by using the low-dose ACTH test and corticotropin-releasing hormone (CRH) test (54). These data highlight the importance of an early recognition of adrenal insufficiency that may lead to a worse outcome.…”

Section: Consequences Of Tbimentioning

confidence: 99%

“…Gonadotropin levels also decrease, but their response to gonadotropin-releasing hormone (GnRH) administration may be normal (57) or increased (55), indicating a hypothalamic mechanism. In the early recovery period post-TBI or during rehabilitation hypogonadism has been demonstrated in 25 -67% of cases (48,54,59). A more recent study performed in 50 patients in the early, acute phase of moderate-tosevere TBI has detected central hypogonadism in 80% of cases, including 18 patients with hyperprolactinemia (49).…”

Section: Consequences Of Tbimentioning

confidence: 99%

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Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

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Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

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Section: Consequences Of Tbimentioning

confidence: 99%

Section: Consequences Of Tbimentioning

confidence: 99%

Section: Consequences Of Tbimentioning

confidence: 99%

See 1 more Smart Citation

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

View full text Add to dashboard Cite

show abstract

“…Kaynaklar mevcuttur. TBH'nın erken dönemi sırasında prolaktin salgısının yüksek olması kötü prognozun habercisi olabilir 17,29,30 . Çalışmamızda ise GKS ile PRL düzeyleri arasında pozitif bir ilişki bulunmuştur yani kafa travması ağır olan hastaların PRL düzeyleri dü-şük çıkmıştır (p<0,01).…”

Section: șEkil 3 Hastaların Gkssi Ile Yatıș Süreleri Arasındaki Ilișkiunclassified

“…Genellikle TSH normal kalmasına rağmen, dolaşımdaki T4 düzeyi azalabilir veya normal kalabilir 29,30 . Hastalar iyileştikçe tiroid hormonları da birkaç hafta içinde yavaşça normale döner.…”

Section: șEkil 3 Hastaların Gkssi Ile Yatıș Süreleri Arasındaki Ilișkiunclassified

Evaluation of pituitary functions during acute phase of head trauma

Dogan¹,

Seyithanoğlu²,

Özkan³

et al. 2012

Kafkas J Med Sci

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AIM: To evaluate the functional outcome of the pituitary gland after the traumatic brain injury and to present the pituitary functional changes during the acute phase of the trauma in order to identify the possible factors. METHODS: The study included records of 30 patients (22 male and GirișKafa travması, saçlı deri yaralanmasından, yaygın beyin hasarına kadar geniş bir spektrumda yer alan birçok patolojiyi içine alan klinik bir durumdur. Kafa travmalarının insidansı ve buna bağlı mortalite ve morbidite riski giderek artmaktadır 1,2 . Travma sonucunda merkezi sinir sisteminde primer doku hasarı meydana gelmektedir. Ancak, kafa travması sonucu oluşan hasardan sadece primer hasar sorumlu değil-dir. Primer doku hasarını takiben ortaya çıkan birçok karmaşık fi zyopatolojik olaya bağlı olarak sekonder hasar da oluşmaktadır [3][4][5] . Beyin hasarında rol oynayan

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Hydrocortisone therapy in a cat with vasopressor‐refractory septic shock and suspected critical illness‐related corticosteroid insufficiency

Pisano

Howard

Posthaus

et al. 2017

Clinical Case Reports

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Key Clinical MessageA 27‐month‐old female cat was presented with septic peritonitis secondary to a ruptured pyometra and subsequent pyothorax. Vasopressor‐refractory septic shock led to a suspicion of critical illness‐related corticosteroid insufficiency, successfully treated with intravenous hydrocortisone. Previous megestrol acetate administration may have played a role in the development of adrenocortical dysfunction.

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Hypothalamic-pituitary-adrenal axis dysfunction in critically ill patients with traumatic brain injury: Incidence, pathophysiology, and relationship to vasopressor dependence and peripheral interleukin-6 levels*

Abstract: Adrenal cortisol secretion after dynamic stimulation is deficient in a subset of critically ill patients with moderate to severe head injury. This disorder is associated with prior vasopressor dependency and higher interleukin-6 levels.

Cited by 127 publications

References 45 publications

Hypopituitarism after traumatic brain injury

Hypopituitarism after traumatic brain injury

Evaluation of pituitary functions during acute phase of head trauma

Hydrocortisone therapy in a cat with vasopressor‐refractory septic shock and suspected critical illness‐related corticosteroid insufficiency

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