Clinical Study Of HPA Axis Injury And Stress Disorders During Brain Trauma Subacute Phase

Objective: Hypothalamic-pituitary-adrenal(HPA) axis damage after traumatic brain injury(TBI) is widespread concerned. However, it is little knowledge about the characteristics of HPA axis injury after TBI, like the difference with othe causes to HPA axis injury, the diagnostic criteria, the prognosis, and treatment strategies. Therefore, we hypothesis that: 1, dexamethasone suppression test(DST) can objectively diagnose injury of HPA axis in TBI, which has important implications for the diagnosis of TBI patients prognosis. 2 there is a significant difference of the function of the HPA axis between non-TBI patients(acute nosocomial pneumonia) function and TBI patients with secondary pneumonia.Methods: Case inclusion criteria: 1 open or closed TBI patients survived more than two weeks; TBI with pneumonia(based on the image-CT or chest X-rays, blood test and body temperature), the survival of patients is more than two weeks; 2 non-TBI pneumonia patients: patients with community-acquired pneumonia, no head injuries and other diseases; without metabolic diseases and endocrine disorders(including diabetes). Case Exclusion criteria: 1.patients had pneumonia before TBI, wiht large organ damage, especially primary lung injury, hemorrhagic shock and diabetes. Glucocorticoid was used; 2. patients with non-TBI pneumonia: nosocomial lung infection, expected to survive less than two weeks, the application of corticosteroids after admission; GCS was administrated at the 5th day after injury, cortisol levels were detected at 8am, and DST was used with a small dose dexamethasone(0.75mg) at 12 am, cortisol levels were tested 8h later. Patients were divided into DST(-) and DST(+).GOS was used to assess the prognosis after 3 months following. Mechanical ventilation and the time, pneumonia infection duration, leukocyte, breathing, heart rate and other changes had been recorded.Results: 136 cases of TBI patients from Oct. 2010 – Oct. 2013, light(GCS 13~15) 35 cases, medium(GCS 9~12) 31 cases, severe(GCS 6~8) 50 cases, particularly severe(GCS 3-5) 20 cases; 53 cases of pneumonia among TBI; non-TBI with pneumonia, 42 cases. The overall incidence of HPA axis dysfunction in patients with TBI is 19.1%, light 2.9%, meduim 9.7%, severe 22%, particulary severe 55%. Incidence in pneumonia after TBI is 39.0%. HPA axis dysfunction correlated with GCS score, hernia or diffuse axonal injury(p <0.05). Two Logistic regression analysis showed admission GCS score is independent risk factor of the HPA axis, with GCS score lower and HPA axis dysfunction higher. Also HPA axis function can determine the neurological prognosis. Serum cortisol concentraion of non-TBI patients with pneumonia was 403.8 ± 310.18 nmmol / l, TBI with pneumonia was of 331.09 ± 149.31 nmmol / l, DST(-) TBI with pneumonia was 163.55 ± 47.48 nmmol / l, DST(+)TBI with pneumonia was 416.31 ± 103.80 nmmol / l. serum cortisol levels was higher in patients of non-TBI with pneumonia than DST(-) TBI with pneumonia(p = 0.002). Cortisol level from patients of DST(+) TBI with pneumonia was 422.85 ± 108.33 nmmol / L, while 668.55 ± 256.83 nmmol/L in TBI with pneumonia, there is significant difference between these two(p = 0.001). Base on receiver operator characteristic curve(ROC) analysis, the threshold of cortisol level is 526.93 nmmol/L in non-TBI pneumonia, while it’s 286 nmmol/L in TBI with pneumonia, there is a difference between these two(p <0.05).Conclusion: Low-dose DST can be used as a diagnostic criteria for HPA axis dysfunction in TBI patients; and which was associated to GCS, hernia, injury mechanisms. DST can be used to determine the prognosis of patients with TBI; Prognosis of DST+ group is better than DST- from the patients of TBI with pneumonia. Also the cortisol levels from good inflammation prognosis in patients with non-TBI pneumonia is higher than TBI with pneumonia. It is no necessary to have a high cortisol level of patients from TBI with pneumonia to get a good prognosis, which support the viewpoint that high-dose corticosteroids after TBI is not conducive to supplement treatment of patients with complications.