The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance.

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Term Occurence Count Dictionary
cortisol 24 endocrinologydiseasesdrugs
desmopressin 7 endocrinologydiseasesdrugs
diabetes insipidus 2 endocrinologydiseases
hypogonadism 1 endocrinologydiseases
hypopituitarism 21 endocrinologydiseases
hypothyroidism 2 endocrinologydiseases
testosterone 1 endocrinologydiseasesdrugs
adrenal insufficiency 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
cortisol 13311 the first 10 days after injury, based on early morning (09:00) thresholds for (total) plasma/serum cortisol of <276 nmol/L and <300 nmol/L, respectively.[48] In a cohort of 58 patients admitted to the neurocritical
cortisol 13635 Accepting that the primary endocrine task in acute TBI is to identify those patients with acute hypo cortisol ism who are at risk of developing life-threatening complications (eg, inotrope-resistant hypotension,
cortisol 13958 glucocorticoid therapy. However, it is noteworthy that while there was a clear association between acute hypo cortisol ism and mortality in the study of Hannon and colleagues, those individuals in the lowest quartile for
cortisol 14075 mortality in the study of Hannon and colleagues, those individuals in the lowest quartile for plasma cortisol had the highest mortality despite empirical treatment with hydrocortisone. In addition, no patients
cortisol 14293 study of Olivecrona et al were given glucocorticoids, and yet no association was observed between low cortisol levels and increased mortality or unfavourable outcome.[48] Accordingly, it remains unclear whether
cortisol 15185 al[20]463–150–12 days76–6743328Tanriverdi et al[49]523–1524 hours5620419.86–Agha et al[52]508–13Acute–1880162–*Serum cortisol levels were measured in the morning and in the evening.ACTH, adrenocorticotropic hormone; FSH, follicle-stimulating
cortisol 24216 risk.Anterior pituitary function testing during hospital admissionSome authors advise screening for hypo cortisol ism (relative or absolute) as soon as possible in all patients with clinical features and/or risk factors
cortisol 24410 and/or risk factors for acute adrenal insufficiency.[60] Glynn and Agha have recommended that serum cortisol levels are monitored in the first 7 days post-TBI, so that glucocorticoid replacement can be initiated
cortisol 25534 interpreting the results of endocrine tests in acutely ill patients, and the discordant findings in studies of cortisol replacement therapy based on numerical thresholds, we do not recommend routine testing of pituitary
cortisol 25683 thresholds, we do not recommend routine testing of pituitary function or measurement of serum/plasma cortisol levels in the acute phase after TBI. If there is a clinical suspicion of cortisol insufficiency, for example,
cortisol 25765 measurement of serum/plasma cortisol levels in the acute phase after TBI. If there is a clinical suspicion of cortisol insufficiency, for example, hypotension (especially pressor-resistant) or hyponatraemia, empirical
cortisol 26118 infusion of 4–8mg/hour should be given immediately after taking a serum/plasma sample for random cortisol measurement. A discussion with the endocrinology team should follow within 24–48 hours. We recognise
cortisol 26330 recognise that some patients may be given glucocorticoid therapy for reasons other than suspected classical cortisol deficiency in the acute phase. Most of these patients will wean from therapy uneventfully, but where
cortisol 26901 recommended for the purpose of detecting post-TBI hypopituitarism. (IV, C)Routine measurement of plasma/serum cortisol levels is not indicated in the acute phase following TBI. (IV, C)If there is clinical suspicion of cortisol
cortisol 27009 levels is not indicated in the acute phase following TBI. (IV, C)If there is clinical suspicion of cortisol insufficiency (eg, refractory hypotension, hypoglycaemia, hyponatraemia), immediately start empirical
cortisol 27332 intravenous bolus followed by an infusion of 4-8mg/hour after taking a serum/plasma sample for random cortisol measurement, and discuss with endocrinology. (IV, C)If a patient is started on glucocorticoid therapy
cortisol 27476 endocrinology. (IV, C)If a patient is started on glucocorticoid therapy for reasons other than classical cortisol deficiency, and there is subsequent difficulty in withdrawing treatment, discuss with endocrinology.
cortisol 28924 patients with raised ICP.SIADH may complicate TBI, and in the presence of hyponatraemia, water overload, cortisol insufficiency and hypothyroidism should be considered as potential contributory factors. If there is
cortisol 33791 hypothalamic–pituitary–adrenal axis function.Figure 2Symptoms suggestive of pituitary dysfunction.If cortisol insufficiency (09:00 serum/plasma cortisol <100 nmol/L) is found, the patient should be started on
cortisol 33834 function.Figure 2Symptoms suggestive of pituitary dysfunction.If cortisol insufficiency (09:00 serum/plasma cortisol <100 nmol/L) is found, the patient should be started on oral hydrocortisone immediately (10 mg on
cortisol 34043 on waking, 5 mg at noon, 5 mg at 17:00) and referred to endocrinology on an urgent basis. If the cortisol level is 100–400 nmol/L, a referral for further assessment should be made and the patient advised
cortisol 34387 Referral to endocrinology for assessment of adrenal status is generally not required if the serum/plasma cortisol level is more than 400 nmol/L.Note that while a serum/plasma IGF-I level below the reference range for
cortisol 34665 requires referral to an endocrinologist for dynamic testing to investigate for GHD and coincident ACTH/ cortisol deficiency. Similarly, a serum/plasma IGF-I within the age-related reference range does not exclude
cortisol 36065 as the HAD scale, BDI-II or PHQ-9. (IV, C)The following ‘action limits’ for 09:00 serum/plasma cortisol are advised: <100 nmol/L, start treatment with oral hydrocortisone (10 mg on waking, 5 mg at noon
desmopressin 22059 resuscitation, use of hypertonic fluids, etc). Follow-up data indicate that few patients require long-term desmopressin therapy: Aimaretti et al reassessed 100 patients with TBI at 3 months’ postinjury and found that
desmopressin 27971 hypernatraemia and hypotonic polyuria is important.[1] Tritos et al advise an on-demand approach to desmopressin replacement in this context, with careful monitoring of fluid balance and serum sodium levels, as DI
desmopressin 28306 paired serum/plasma and urine osmolalities should be checked. Treatment with a single stat dose of desmopressin 0.5 μg subcutaneously should be given if there is unexplained polyuria and low urine osmolality.
desmopressin 28463 there is unexplained polyuria and low urine osmolality. Early endocrine review is advised. Regular desmopressin orally or nasally may be required for a period of time. However, it is important to note that in patients
desmopressin 28776 is sometimes used to treat intractable raised ICP, particularly in the intensive care setting. Thus, desmopressin should be used judiciously in patients with raised ICP.SIADH may complicate TBI, and in the presence
desmopressin 29817 creatinine, electrolytes, plasma glucose and paired serum/plasma and urine osmolalities, give a stat dose of desmopressin 0.5 μg subcutaneously, and discuss with endocrinology. (IV, C)Although transient DI is recognised
desmopressin 29998 C)Although transient DI is recognised following TBI, some patients will need to be established on regular desmopressin (either orally or nasally) if there is unexplained polyuria and low urine osmolality, with subsequent
testosterone 33224 thyroid-stimulating hormone (TSH)CortisolLuteinising hormone (LH), follicle-stimulating hormone (FSH), testosterone , sex hormone-binding globulin, albuminWomenUrea, creatinine and electrolytesFree T4 and TSHCortisol†
Select Disease Character Offset Disease Term Instance
adrenal insufficiency 24340 absolute) as soon as possible in all patients with clinical features and/or risk factors for acute adrenal insufficiency .[60] Glynn and Agha have recommended that serum cortisol levels are monitored in the first 7 days
diabetes insipidus 21708 transient (<1 month duration). In the acute phase, the proportion of patients developing cranial diabetes insipidus (DI) again varies markedly between studies, ranging from 2.6% to 51% (table 3),[21] and perhaps reflecting
diabetes insipidus 22583 posterior pituitary dysfunction following TBIStudynGCSTime from injury% of posterior hypopituitarism (cranial diabetes insipidus )<1 monthHannon et al[50]100<14Median 6 days51Hadjizacharia et al[21]4363–15Mean 1.2 days15Agha
hypogonadism 19637 variation in methodologies used and diagnostic tests employed. Nevertheless, GHD and hypogonadotropic hypogonadism remain the two most commonly identified endocrine deficits (similar to the acute phase), while most
hypopituitarism 725 recognised, but potentially underdiagnosed complication of traumatic brain injury (TBI). Post-traumatic hypopituitarism (PTHP) can have major consequences for patients physically, psychologically, emotionally and socially,
hypopituitarism 2430 who, (2) when and (3) how to screen for and manage pituitary dysfunction, including post-traumatic hypopituitarism , in adult patients with TBI, to ensure uniformity of practice across the country. It is primarily targeted
hypopituitarism 5679 independence, unemployment and significantly reduced quality of life.The reported prevalence of post-traumatic hypopituitarism (PTHP) differs significantly between studies. Reasons for this include differences in inclusion/exclusion
hypopituitarism 8491 17 monthsNoLieberman et al[22]70–Median 13 monthsNoGCS, Glasgow Coma Scale; PTHP, post-traumatic hypopituitarism ; TBI, traumatic brain injury.Imaging findingsKelly et al reported that certain imaging findings, such
hypopituitarism 9300 stay.[28] In contrast, possession of apolipoprotein E3/E3 genotype has been linked to a reduced risk of hypopituitarism following TBI.[30]Blast TBI may be a particular risk factor for pituitary dysfunction.[31] Thirty-two
hypopituitarism 14631 life-threatening hypoadrenalism or leads to unnecessary glucocorticoid therapy.Table 2aPrevalence of anterior hypopituitarism following TBI (<1 month)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Alavi
hypopituitarism 14707 2aPrevalence of anterior hypopituitarism following TBI (<1 month)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Alavi et al[51]58<140–7 days10.3––10.3––Hannon
hypopituitarism 15482 hormone; TBI, traumatic brain injury; TSH, thyroid-stimulating hormone.Table 2bPrevalence of anterior hypopituitarism following TBI (<12 months)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Abadi
hypopituitarism 15560 2bPrevalence of anterior hypopituitarism following TBI (<12 months)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Abadi et al[67]759–133 months482416135.3136 months–9.310.742.7–Schneider
hypopituitarism 16398 hormone; TBI, traumatic brain injury; TSH, thyroid-stimulating hormone.Table 2cPrevalence of anterior hypopituitarism following TBI (≥12 months)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Alavi
hypopituitarism 16478 2cPrevalence of anterior hypopituitarism following TBI (≥12 months)StudynGCSTime from injuryAnterior hypopituitarism (axis affected)Total (%)GH (%)FSH/LH (%)ACTH (%)TSH (%)Multiple (%)Alavi et al[51]473–15>6 months*21.3–21.34.3012.8223–15>12 months9.19.1––––Kopczak
hypopituitarism 19116 which resolve on follow-up testing, reflect a normal adaptive endocrine response rather than transient hypopituitarism .Chronic phaseDisturbance of normal pituitary function appears to be transient in many patients, with
hypopituitarism 20655 Recently, Cuesta et al identified symptoms of gonadal dysfunction as being the most reliable predictors of hypopituitarism in patients >6 months post-TBI, while in contrast non-specific symptoms were no more predictive than
hypopituitarism 22558 3Prevalence of posterior pituitary dysfunction following TBIStudynGCSTime from injury% of posterior hypopituitarism (cranial diabetes insipidus)<1 monthHannon et al[50]100<14Median 6 days51Hadjizacharia et al[21]4363–15Mean
hypopituitarism 23972 some patients. However, given the potentially serious clinical consequences of failing to diagnose hypopituitarism (especially hypoadrenalism), there is a pressing need to more reliably identify those patients with
hypopituitarism 24666 glucocorticoid deficiency.[10] For patients with mild TBI, Tanriverdi and colleagues proposed that screening for hypopituitarism (specifically ACTH and TSH deficiency) should be undertaken if (1) the patient is expected to be hospitalised
hypopituitarism 25012 epidural/subdural haematoma, cranial vault fractures); and (3) the patient manifests signs or symptoms of hypopituitarism .[61] Most authors agree that acutely unwell patients with suspected hypoadrenalism should be treated
hypopituitarism 26841 (acute phase) testing for pituitary dysfunction is not recommended for the purpose of detecting post-TBI hypopituitarism . (IV, C)Routine measurement of plasma/serum cortisol levels is not indicated in the acute phase following
hypopituitarism 32096 may require screening for pituitary dysfunction if they experience ongoing symptoms consistent with hypopituitarism . These symptoms can include fatigue, low mood, poor motivation, reduced appetite, loss of libido, sexual
hypopituitarism 36705 temporary. However, patients with a history of TBI who continue to have or develop symptoms of possible hypopituitarism beyond 12 months should be referred to endocrinology for consideration of testing for GHD and other
hypopituitarism 36946 dysfunction.RecommendationPatients with a history of TBI who continue to display or develop symptoms of possible hypopituitarism beyond 12 months should be referred to endocrinology for consideration of testing for GH and other
hypothyroidism 18769 in normal subjects in response to acute intercurrent (non-endocrine) illness (eg, apparent central hypothyroidism due to non-thyroidal illness, for which there is little evidence of a role for thyroid hormone replacement
hypothyroidism 28951 may complicate TBI, and in the presence of hyponatraemia, water overload, cortisol insufficiency and hypothyroidism should be considered as potential contributory factors. If there is suspicion of SIADH, euvolaemia should

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