Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

Fall of platelet count in children with traumatic brain injury： is it of value？

Objective:Trauma is the leading cause of mortality and morbidity among young age groups in Saudi Arabia and developed countries.This study aimed to evaluate the fall of platelet count in children with traumatic brain injury (TBI) as a potential predictor for clinical severity and outcome.Methods:Totally 74 patients with TBI were admitted to the Pediatric Intensive Care Unit (PICU) of our hospital from the beginning of January 2008 to the end of March 2010 (27months).Baseline enrolling criteria were age ≤ 12 years,admission within 4 hours after trauma event,and abbreviated injury scale (AIS)＜3 for extracranial injuries.Injury severity was classified as mild,moderate and severe according to their Glasgow Coma Scale (GCS) scores.Clinical outcomes at discharge were defined as poor (death,severe neurological morbidity) and favorable (moderate disability and good recovery).Platelet count was taken 2-3 times on the first day after admission and thereafter once daily.The percentage fall of platelet count (PFP) was calculated and taken as an index of change.PFP was considered zero if the platelet count was higher than the initial value.Results:PFP was significantly higher in patients with poor outcomes (mean 56.0％±3.8％,median 55.5％) compared to those with favorable outcomes (mean 25.3％±3.2％,median 20.5％,P＜0.01).PFP was also closely related to the severity of TBI,GCS score,clinical outcome and length of stay for survivors (P＜0.01 for each).The frequency of thrombocytopenia was significantly higher in poor outcome parents than in favorable outcome patients (P＜0.05).The validity of thrombocytopenia as a risk factor to predict poor outcome after TBI was:specificity,77.4％; odd ratio (OR),3.1;relative risk (RR),2.15.Receiver operating characteristic (ROC) curve and Youden index showed that the optimum cutoff point of PFP was at 51.5％.Conclusion:PFP is increased with the severity of TBIand it can be taken as a significant independent predicting factor for its outcome as well.     

Severe traumatic brain injury: is there a gender difference in mortality?

Background

Emerging evidence suggests that male and female nervous systems respond differently to traumatic brain injury (TBI). The objective of this study was to examine outcomes between the sexes after TBI.

Patients and methods

A retrospective review of all severe TBI patients admitted between January and December 2005 was performed. Isolated severe TBI was defined as a head abbreviated injury score greater than 3 with an abbreviated injury score of 3 or less for other anatomic regions. The population was stratified into age subgroups (<14 y, 14-44 y, 45-54 y, and ≥55 y). Logistic regression was used to identify independent predictors of mortality.

Results

A total of 1,807 TBI patients were admitted. The mortality was significantly higher for women (43.2% vs 36.2%, P < .01) with an adjusted odds ratio of 1.4 (95% confidence interval, 1.1-1.9, P < .05). After stratification, only women age 55 and older had a significant difference in mortality (odds ratio, 1.71; 95% confidence interval, 1.11-2.62, P = .02).

Conclusions

Female sex (particularly those age ≥55 y) is associated independently with higher mortality in isolated severe TBI. This increased mortality of postmenopausal women after isolated TBI may suggest a hormonal influence and warrants further investigation.     

Extracorporeal membrane oxygenation and severe traumatic brain injury. Is the ECMO-therapy in traumatic lung failure and severe traumatic brain injury really contraindicated?

Veno-venous extracorporeal membrane oxygenation (ECMO) may be lifesaving in multiple injured patients with acute respiratory distress syndrome (ARDS) due to chest trauma. To prevent circuit thrombosis or thrombembolic complications during ECMO systemic anticoagulation is recommended. Therefore, ECMO treatment is contraindicated in patients with intracranial bleeding. The management of veno-venous ECMO without systemic anticoagulation in a patient suffering from traumatic lung failure and severe traumatic brain injury is reported.     

Aggressive behavior following traumatic brain injury: how common is common?

OBJECTIVE: To assess the prevalence and predictors of aggressive behavior among traumatic brain injury (TBI) survivors at 6, 24, and 60 months postdischarge. DESIGN: Mixed cross-sectional and longitudinal data from a 5-year follow-up study of discharged TBI patients analyzed retrospectively. SETTING: A specialized Brain Injury Rehabilitation Service of a tertiary referral hospital. PATIENTS: Two hundred twenty-eight (228) patients with moderate to severe TBI. MAIN OUTCOME MEASURES: The Overt Aggression Scale; injury-related variables (in particular, Glasgow Coma and Outcome scales and posttraumatic amnesia duration); and a battery of postdischarge questionnaires (Beck Depression Inventory, Trauma Complaints List, General Health Questionnaire, etc). RESULTS: At any given follow-up period, 25% of the participants were classified as aggressive. Aggression, where present, was consistently associated with depression, concurrent traumatic complaints, younger age at injury, and low satisfaction with life rather than with injury, demographic, or premorbid characteristics. Depression was the factor that was most significantly associated with aggressive behavior at all times postinjury, followed by a younger age at the time of injury. CONCLUSIONS: Aggression is a common, fluctuating, and long-term problem following TBI. The underlying association between aggression and psychosocial variables lends support to the provision of ongoing outreach services and psychological and behavioral interventions for all affected TBI survivors.     

Effect of dipeptide of glutamine and alanine on severe traumatic brain injury

OBJECTIVE: To determine the effect of dipeptide of glutamine and alanine on patients with severe traumatic brain injury. METHODS: A total of 46 patients (31 males and 15 females, aged 7-68 years, (47+/-9.6) years on average) with severe traumatic brain injury were randomized into two groups: Group G (n=23) and Group C (n=23). The patients in Group G received nutritional remedy with the dipeptide of glutamine and alanine, whereas the patients in Group C received routine nutritional therapy only. GCS changes, the length of stay in the neurosurgical intensive care unit (NICU), the mortality,the count of lymphocytes, related complications including lung infection and hemorrhage of alimentary tracts, etc, were examined and recorded. RESULTS: The fatality rate and the length of stay in NICU in Group G was lower than these in Group C (P larger than 0.05), but no obvious difference was found in GCS changes of the patients between the two groups (P larger than 0.05). The patients with lung infection and alimentary tract hemorrhage in Group G were less than those in Group C (P larger than 0.05). The count of lymphocytes in Group G was more than that in Group C (P larger than 0.05), but no difference was found in other nutritional data. CONCLUSIONS: Dipeptide of glutamine and alanine can increase the resisting stress and anti-infection ability of patients with severe traumatic brain injury, which can also lower the mortality and shorten the NICU stay.     

Escalation therapy in severe traumatic brain injury: how long is intracranial pressure monitoring necessary?

Neurosurgical Review - Traumatic brain injury frequently causes an elevation of intracranial pressure (ICP) that could lead to reduction of cerebral perfusion pressure and cause brain ischemia....     

Does traumatic brain injury result in accelerated fracture healing?

In patients who have sustained a traumatic brain injury with an associated extremity fracture there is often a clinical perception that the rate of new bone formation around the fracture site is increased. Whether this rapidly forming new bone is fracture callus or a variant of heterotopic ossification, a common complication of traumatic brain injury, is the subject of some debate. This review will provide a comprehensive analysis on this topic and will discuss clinical and physiological evidence as well as potential areas for future research in this field.     

Animal models of traumatic brain injury: Is there an optimal model to reproduce human brain injury in the laboratory?

Compared to other neurological diseases, the research surrounding traumatic brain injury (TBI) has a more recent history. The establishment and use of animal models of TBI remains vital to understand the pathophysiology of this highly complex disease. Such models share the ultimate goals of reproducing patterns of tissue damage observed in humans (thus rendering them clinically relevant), reproducible and highly standardised to allow for the manipulation of individual variables, and to finally explore novel therapeutics for clinical translation. There is no doubt that the similarity of cellular and molecular events observed in human and rodent TBI has reinforced the use of small animals for research. When confronted with the choice of the experimental model it becomes clear that the ideal animal model does not exist. This limitation derives from the fact that most models mimic either focal or diffuse brain injury, whereas the clinical reality suggests that each patient has an individual form of TBI characterised by various combinations of focal and diffuse patterns of tissue damage. This is additionally complicated by the occurrence of secondary insults such as hypotension, hypoxia, ischaemia, extracranial injuries, modalities of traumatic events, age, gender and heterogeneity of medical treatments and pre-existing conditions.This brief review will describe the variety of TBI models available for laboratory research beginning from the most widely used rodent models of focal brain trauma, to complex large species such as the pig. In addition, the models mimicking diffuse brain damage will be discussed in relation to the early primate studies until the use of most common rodent models to elucidate the intriguing and less understood pathology of axonal dysfunction. The most recent establishment of in vitro paradigms has complemented the in vivo modelling studies offering a further cellular and molecular insight of this pathology.     

PTSD and traumatic brain injury: folklore and fact?

A number of controversies and debates have arisen over the years surrounding the dual diagnosis of post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI). Many of these have centred around the around the degree of protection provided by TBI against developing the disorder. The following is brief review of the literature in this area to help resolve some of these issues and to address a number of specific challenges which arise when working with this patient group.