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Study Of Adrenal Insufficiency After Traumatic Brain Injury

Posted on:2014-08-14Degree:DoctorType:Dissertation
Country:ChinaCandidate:M LiFull Text:PDF
GTID:1264330428483262Subject:Neurosurgical intensive
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ObjectiveGlucocorticoid was unable to release encephaledema and anti-inflammation reaction in acute phase after traumatic brain injury (TBI). Because Hypothalamic-Pituitary-Adrenal axis (HPA axis) might be directly damaged and indirectly inhibited function by severe TBI, Adrenal insufficiency (AI) in the acute phase has been increasingly recognized as an important complication after traumatic brain injury. Homodynamic disorder and life threatening were so serious that hormone replacement therapy in patients with AI. Correct evaluation of HPA axis function is to guide the cortical hormone replacement therapy premise, but nerve endocrine function is affected by many factors in acute phase after traumatic brain injury and the best method for HPA axis function evaluation was non-existent. So the results of adrenal insufficiency evaluation were not the same after traumatic brain injury. To explore the relative risk for AI and clear association between adrenal insufficiency and severity of TBI, we conducted a series of clinical study and laboratory investigation in patients with TBI.MethodFirstly, after strict selection of isolated craniocerebral injury patients with different severity of injury, we used low dose short synacthen test (LDSST) to assessment of adrenal insufficiency. According to the result of the judgment of AI, all basic information and clinical data of the selected patient introduced into the statistical model, multivariable logistic regression models based univariable were performed for risk factors of AI. Secondly a case control study based on determining the risk factors was conducted for determining non traumatic factors inhibit the function of HPA axis. Thirdly out than the non traumatic brain injury factors, the relation between incidence of AI and severity of TBI was investigated by packet control study in patients, and the change trends of the HPA axis hormone level were continuously researched within6days after the injury. Lastly, we measurement serum free cortisol level by High Performance Liquid Chromatography to assessment adrenal insufficiency after TBI, and contrasted of two kinds of evaluation methods.ResultWe performed66patients with brain trauma injury cohort study, Our multivariable logistic regression models Analysis showed severe traumatic brain injury(OR:6.69, CI:1.04-43.26), sedation(OR:10.71, CI:1.15-78.89) and prolonged mechanical ventilation (OR:4.75, CI:1.20-18.81) were relation with occurrence of adrenal insufficiency in early stage after TBI. However, control study on34cases of traumatic brain injury showed that45%of patients with propofol sedation had incidence of AI and non sedating patients only7.1%(P=0.024).The incidence of AI was no significant differences between patients with mechanical ventilation>4days and<4days (38.9%vs18.8%, P=0.27). Basal cortisol and stimulated peak cortisol post LDSST levels decreased significantly with cumulative dose of propofol(r=-0.819, p=0.001and r=-0.683, p=0.001), but ACTH levels were not this change trend (r=-0.418, p=0.056). In27patients without sedation, incidence of AI was18.8%, all patients with AI existed severe TBI group which had the lowest baseline cortisol and ACTH level at72hours after injury settle. Non-responders to the LDSST having stimulated peak free cortisol concentrations<52.5nmol/L were defined as adrenal insufficiency. However, this new evaluation method for AI had a good consistency results with LDSST of total serum cortisol (kappa value=0.842,p<0.001)ConclusionIt was prolonged sedation time but not prolonged mechanical ventilation is highly correlated with the risk of AI for patients with TBI. We proposed that large doses of propofol sedation should avoid as assessing the relation of severity of brain injury and HPA axis damage. The severe TBI was associated with risk of AI in acute phase of traumatic brain injury. Incidence of AI was focus on72hours after injury settle. AI was secondary to decreased levels of ACTH and serum free cortisol level was decline in patients with severe TBI. Serum free cortisol directly testing should assess adrenal insufficiency, but the measurement of free serum cortisol was not more accurate than assessment of adrenal insufficiency than LDSST in early stage after TBI...
Keywords/Search Tags:traumatic brain injury, sedation, adrenal insufficiency and free serumcortisol
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