Ghrelin decreases motor deficits after traumatic brain injury

Background

Pharmacologic therapy for traumatic brain injury (TBI) has remained relatively unchanged for decades. Ghrelin, an endogenously produced peptide, has been shown to prevent apoptosis and blood-brain barrier dysfunction after TBI. We hypothesize that ghrelin treatment will prevent neuronal degeneration and improve motor coordination after TBI.

Materials and methods

A weight drop model created severe TBI in three groups of BALB/c mice: Sham, TBI, and TBI + ghrelin (20 μg intraperitoneal ghrelin). Brain tissue was examined by hematoxylin and eosin and Fluoro-Jade B (FJB) staining to evaluate histologic signs of injury, cortical volume loss, and neuronal degeneration. Additionally, motor coordination was assessed.

Results

Ghrelin treatment prevented volume loss after TBI (19.4 ± 9.8 mm³versus 71.4 ± 31.4 mm³; P < 0.05). Similarly, although TBI increased FJB–positive neuronal degeneration, ghrelin treatment decreased FJB staining in TBI resulting in immunohistologic patterns similar to sham. Compared with sham, TBI animals had a significant increase in foot faults at d 1, 3, and 7 (2.75 ± 0.42; 2.67 ± 0.94; 3.33 ± 0.69 versus 0.0 ± 0.0; 0.17 ± 0.19; 0.0 ± 0.0; P < 0.001). TBI + ghrelin animals had significantly decreased foot faults compared with TBI at d 1, 3, and 7 (0.42 ± 0.63; 0.5 ± 0.43; 1.33 ± 0.58; P versus TBI <0.001; P versus sham = NS).

Conclusions

Ghrelin treatment prevented post-TBI cortical volume loss and neurodegeneration. Furthermore, ghrelin improved post-TBI motor deficits. The mechanisms of these effects are unclear; however, a combination of the anti-apoptotic and inflammatory modulatory effects of ghrelin may play a role. Further studies delineating the mechanism of these observed effects are warranted.     

Puerarin ameliorates oxidative stress in a rodent model of traumatic brain injury

Background

A wealth of evidence has suggested that oxidative stress is involved in the secondary brain injury after traumatic brain injury (TBI). Recently, numerous in vivo and in vitro studies were reported that puerarin could inhibit oxidative stress through the activation of phosphatidylinositol 3-kinase (PI3K)-Akt pathway. It is unknown, however, whether puerarin can provide neuroprotection and reduce oxidative stress after TBI. The present study investigated the effects of puerarin on the TBI-induced neurodegeneration, oxidative stress, and the possible role of PI3K-Akt pathway in the neuroprotection of puerarin, in a rat model of TBI.

Materials and methods

Rats were randomly distributed into various subgroups undergoing the sham surgery or TBI procedures. Puerarin (200 mg/kg) was given intraperitoneally at 10 min before injury and PI3K-Akt pathway inhibitor LY294002 was also administered intracerebroventricular in one subgroup. All rats were killed at 24 h after TBI for examination.

Results

Our data indicated that puerarin could significantly reduce TBI-induced neuronal degeneration, accompanied by the partial restoration of the redox disturbance and enhanced expression of phospho-Akt in the pericontusional cortex after TBI. Moreover, PI3K-Akt pathway inhibitor LY294002 could partially abrogate the neuroprotection of puerarin in rats with TBI.

Conclusions

These results indicate that puerarin can ameliorate oxidative neurodegeneration after TBI, at least in part, through the activation of PI3K-Akt pathway.     

Extracellular signal–regulated kinase 1/2 is involved in a tamoxifen neuroprotective effect in a lateral fluid percussion injury rat model

Background

The aim of the present study was to determine whether tamoxifen (TMX) causes attenuation of traumatic brain injury (TBI) induced by fluid percussion injury.

Materials and methods

Immediately after the onset of fluid percussion TBI, anesthetized male Sprague-Dawley rats were divided into three major groups and intraperitoneally administered the vehicle solution (1 mL/kg), TMX (1 mg/kg), or TMX (1 mg/kg) plus the extracellular signal–regulated kinase 1/2 antagonist SL327 (30 mg/kg). Another group of rats were used as sham-operated controls. The functional outcomes, such as motor outcomes, were evaluated using an incline plane. The cellular infarction volume was evaluated by triphenyltetrazolium chloride staining. Neuronal loss, apoptosis, and p-ERK1/2 and Bcl2 expression in neuronal cortex cells were evaluated by immunofluorescence methods. All the parameters were assessed on day 4 after injury.

Results

Compared with the sham-operated controls, the TBI-induced motor deficits and cerebral infarction after TBI were significantly attenuated by TMX therapy. The TBI-induced neuronal loss and apoptosis were also significantly reduced by TMX therapy. The numbers of Bcl2- and phospho-ERK1/2-positive neuronal cells in the ischemic cortex after TBI were significantly increased by TMX therapy. These TMX effects were significantly blocked by SL327 administration.

Conclusions

Our results suggest that intravenous injection of TMX may ameliorate TBI in rats by increasing neuronal p-ERK1/2 expression, which might lead to an increase in neuronal Bcl2 expression and a decrease in neuronal apoptosis and cell infarction volume, and it might represent one mechanism by which functional recovery occurred. TMX may be a promising TBI treatment strategy.     

Neuroprotective effect of tadalafil,a PDE-5 inhibitor,and its modulation by L-NAME in mouse model of ischemia-reperfusion injury

Background

The present study investigates the neuroprotective effect of tadalafil, a selective phosphodiesterase-5 inhibitor, in a mouse model of ischemia-reperfusion injury.

Materials and methods

Bilateral carotid artery occlusion for 12 min followed by reperfusion for 24 h was employed to produce ischemia-reperfusion-induced cerebral injury in male Swiss mice. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Memory was assessed using Morris water maze test. Degree of motor incoordination was evaluated using inclined beam walk test, rota-rod test, and lateral push test. Brain nitrite/nitrate, brain acetylcholinesterase activity, brain thiobarbituric acid reactive species, and glutathione levels were also estimated.

Results

Bilateral carotid artery occlusion, followed by reperfusion, produced a significant rise in cerebral infarct size, brain nitrite/nitrate levels, acetylcholinesterase activity, and thiobarbituric acid reactive species level along with a fall in glutathione. A significant impairment of memory and motor coordination was also noted. Pretreatment of tadalafil significantly attenuated the above effects of ischemia-reperfusion injury. Tadalafil-induced neuroprotective effects were significantly attenuated by administration of L-NAME, a nonselective nitric oxide synthase inhibitor.

Conclusions

Results indicate that tadalafil exerts neuroprotective effects, probably through nitric oxide–dependent pathways. Therefore, phosphodiesterase-5 can be explored as an important target to contain ischemia-reperfusion injury.     

Hypernatremia severity and the risk of death after traumatic brain injury

Purpose

To investigate the relationship between severity of hypernatremia and the risk of death for patients with traumatic brain injury (TBI) who have been admitted to the neurosurgical intensive care unit (NICU).

Methods

A total of 1044 patients with TBI were admitted to our NICU from January 2005 to January 2010. Of these patients, 881 were included in this study. Based on blood serum sodium level in the NICU the 881 patients were divided into four groups: 614 had normal serum sodium (Na < 150 mmol/L), 34 had mild hypernatremia (Na 150–<155 mmol/L), 66 had moderate hypernatremia (Na 155–160 mmol/L) and 167 had severe hypernatremia (Na ≥ 160 mmol/L).

Results

The mortality rates for the mild, moderate, and severe hypernatremia groups were 20.6%, 42.4%, and 86.8%, respectively; the mortality rate for the normal group was 2.0%. In multivariable analysis, mild, moderate, and severe hypernatremia were independent risk factors for mortality; compared with the normal group the odds ratios of mild, moderate, and severe hypernatremia were 9.50, 4.34, and 29.35, respectively.

Conclusions

Severe hypernatremia is an independent risk factor with extremely high odds ratio for death in patients with TBI who are admitted to the NICU.     

Neuroprotective effects of progesterone in traumatic brain injury: blunted in vivo neutrophil activation at the blood-brain barrier

Background

Progesterone (PRO) may confer a survival advantage in traumatic brain injury (TBI) by reducing cerebral edema. We hypothesized that PRO reduces edema by blocking polymorphonuclear (PMN) interactions with endothelium (EC) in the blood-brain barrier (BBB).

Methods

CD1 mice received repeated PRO (16 mg/kg intraperitoneally) or vehicle (cyclodextrin) for 36 hours after TBI. Sham animals underwent craniotomy without TBI. The modified Neurological Severity Score graded neurologic recovery. A second craniotomy allowed in vivo observation of pial EC/PMN interactions and vascular macromolecule leakage. Wet/dry ratios assessed cerebral edema.

Results

Compared with the vehicle, PRO reduced subjective cerebral swelling (2.9 ± .1 vs 1.2 ± .1, P < .001), PMN rolling (95 ± 1.8 vs 57 ± 2.0 cells/100 μm/min, P < .001), total EC/PMN adhesion (2.0 ± .4 vs .8 ± .1 PMN/100 μm, P < .01), and vascular permeability (51.8% ± 4.9% vs 27.1% ± 4.6%, P < .01). TBI groups had similar a Neurological Severity Score and cerebral wet/dry ratios (P > .05).

Conclusions

PRO reduces live pericontusional EC/PMN and BBB macromolecular leakage after TBI. Direct PRO effects on the microcirculation warrant further investigation.     

In vivo leukocyte-mediated brain microcirculatory inflammation: a comparison of osmotherapies and progesterone in severe traumatic brain injury

Background

Mannitol, hypertonic saline, and progesterone may blunt leukocyte recruitment after traumatic brain injury (TBI). We hypothesized that progesterone reduces pericontusional recruitment of leukocytes to a greater extent than either osmotherapy a day after TBI.

Methods

CD1 mice underwent controlled cortical impact and were treated with osmotherapy (mannitol and hypertonic saline) or progesterone. Thirty-two hours after TBI, live pial microscopy was used to evaluate leukocyte–endothelial interactions and immunohistochemistry was used for the detection of pericontusional tissue polymorphonuclear neutrophils. Neurologic recovery was assessed before sacrifice.

Results

Mannitol resulted in the lowest in vivo leukocyte recruitment compared with progesterone (795 ± 282 vs 1,636 ± 434 LEU/100 μm/minutes, P < .05). Mannitol also displayed lower tissue accumulation of leukocytes as compared with progesterone (5.7 ± 1.7 vs 15.2 ± .1 LEU/mm², P = .03). However, progesterone resulted in better neurologic recovery than either osmotherapy.

Conclusions

Leukocyte recruitment to injured brain is lowest with mannitol administration. How different agents alter progression of secondary brain injury will require further evaluation in humans.     

Use of neuron-specific enolase to predict mild brain injury in motorcycle crash patients with maxillofacial fractures: A pilot study

Purpose

Mild traumatic brain injury (TBI) is common but accurate diagnosis and its clinical consequences have been a problem. Maxillofacial trauma does have an association with TBI. Neuron-specific enolase (NSE) has been developed to evaluate neuronal damage. The objective of this study was to investigate the accuracy of NSE serum levels to detect mild brain injury of patients with sustained maxillofacial fractures during motor vehicle accidents.

The neuronal protective effects of local brain cooling at the craniectomy site after lateral fluid percussion injury in a rat model

Background

The aim of the present study is to investigate whether local brain cooling at the craniectomy site causes attenuation of traumatic brain injury (TBI) induced by fluid percussion injury (FPI).

Methods

Anesthetized male Sprague–Dawley rats were divided into two major treatment groups. Immediately after the onset of fluid percussion TBI, a craniectomy window of 6 × 8 mm was made at the right parietal, and a cold water bag (0°C–1°C or 5°C–6°C) was applied locally for 30 min. Additional groups of rats were used as craniectomy and craniectomy + FPI controls. Physiological parameters, such as brain and colonic temperature, mean arterial pressure, and heart rate, were monitored during FPI. Functional motor outcomes were evaluated using the inclined plane test (maximal grasp angle). Cellular infarction volume was calculated using triphenyltetrazolium chloride staining. Apoptosis and neuronal marker–positive cells in the cortex were measured by immunofluorescence staining. All functional and morphologic parameters were assessed 72 h after injury.

Results

Compared with the craniectomy + FPI control groups, the groups treated with 5°C–6°C local cold water therapy showed significant attenuation of the FPI-induced motor deficits, weight loss, and cerebral infarction but no effect on colonic temperature. The FPI-induced apoptosis and neuronal loss were also significantly reduced by local cooling.

Conclusions

Our results suggest that local cooling with 5°C–6°C cold water therapy may ameliorate TBI in rats by reducing infarction volume, neuronal cell loss, and apoptosis, resulting in improved functional outcome. We propose that the use of local cooling at the craniectomy site after FPI might have clinical benefits in the future.     

Expression of intestinal CD40 after experimental traumatic brain injury in rats

Background

Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI. Hence, we designed the current study to explore the intestinal expression pattern of CD40 after TBI in rats. We hypothesized that CD40 could mediate inflammation and ultimately contribute to acute intestinal mucosal injury after TBI.

Methods

We randomly divided rats into control and TBI groups at 3, 6, 12, 24, and 72 h, respectively. We assessed the expression of CD40 by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical study, and detected the levels of tumor necrosis factor-α (TNF-α), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by enzyme-linked immunosorbent assay.

Results

The mRNA and protein levels of -CD40 increased by 3 and 6 h, peaked at 6 and 12 h, and remained elevated until 24 and 72 h post-injury, respectively. Levels of TNF-α, VCAM-1, and ICAM-1 also markedly increased in jejunum tissue after TBI. Interestingly, there was a positive relationship between the expression of CD40 and that of TNF-α, VCAM-1, and ICAM-1.

Conclusions

CD40 could be markedly elevated in intestine after TBI in rats, and it might have an important role in the pathogenesis of acute intestinal mucosal injury mediated by inflammatory response.     

Increased risk of pneumonia among ventilated patients with traumatic brain injury: every day counts!

Background

Patients with traumatic brain injury (TBI) frequently require mechanical ventilation (MV). The objective of this study was to examine the association between time spent on MV and the development of pneumonia among patients with TBI.

Materials and methods

Patients older than 18 y with head abbreviated injury scale (AIS) scores coded 1–6 requiring MV in the National Trauma Data Bank 2007–2010 data set were included. The study was limited to hospitals reporting pneumonia cases. AIS scores were calculated using ICDMAP-90 software. Patients with injuries in any other region with AIS score >3, significant burns, or a hospital length of stay >30 d were excluded. A generalized linear model was used to determine the approximate relative risk of developing all-cause pneumonia (aspiration pneumonia, ventilator-associated pneumonia [VAP], and infectious pneumonia identified by the International Classification of Disease, Ninth Revision, diagnosis code) for each day of MV, controlling for age, gender, Glasgow coma scale motor score, comorbidity (Charlson comorbidity index) score, insurance status, and injury type and severity.

Results

Among the 24,525 patients with TBI who required MV included in this study, 1593 (6.5%) developed all-cause pneumonia. After controlling for demographic and injury factors, each additional day on the ventilator was associated with a 7% increase in the risk of pneumonia (risk ratio 1.07, 95% confidence interval 1.07–1.08).

Conclusions

Patients who have sustained TBIs and require MV are at higher risk for VAP than individuals extubated earlier; therefore, shortening MV exposure will likely reduce the risk of VAP. As patients with TBI frequently require MV because of neurologic impairment, it is key to develop aggressive strategies to expedite ventilator independence.     

The role of neuropeptide Y and aquaporin 4 in the pathogenesis of intestinal dysfunction caused by traumatic brain injury

Background

Although the exact incidence is unknown, traumatic brain injury (TBI) can lead to intestinal dysfunction. It has important influence on the early nutrition and prognosis of TBI patients. Experiments were designed to study the roles of neuropeptide Y (NPY) and aquaporin 4 (AQP4) in the pathogenesis of intestinal dysfunction caused by TBI and to find some new solutions for the treatment of intestinal dysfunction after TBI.

Methods

Forty adult male Wistar rats were randomly divided into control, mild trauma, moderate trauma, and severe trauma groups. TBI was induced by Feeney's impact method. Control animals were sham operated but not subjected to the impact test. All rats were killed 24 h after surgery. Blood samples were obtained from the abdominal aorta for enzyme-linked immunosorbent assay measurement of NPY concentrations. Jejunum segments 15 cm distal to the Treitz ligament were taken for analysis of NPY and AQP4 expression by polymerase chain reaction, Western blot, and immunohistochemistry. Pathologic changes in intestinal cell structure and ultrastructure were studied by light microscopy and transmission electron microscopy.

Results

The specimens from different groups showed different degrees of structural changes, ranging from swelling and degeneration of villous epithelial cells to extensive denudation and collapse of the villi. The more severe the trauma, the more serious the degree of intestinal mucosal injury. Intestinal smooth muscle also showed varying degrees of edema and structural disorder. Electron microscopy showed that intestinal mitochondria had varying degrees of swelling and the structure of mitochondrial crista was disordered and even fractured. Plasma concentrations of NPY and jejunal gene and protein expressions of NPY and AQP4 increased significantly following TBI (P < 0.05), with greater increases at higher levels of injury. Moreover, there were positive correlations between NPY and AQP4 (P < 0.05).

Conclusions

Increasing grades of TBI caused increasing degrees of intestinal ischemia and edema, and thus caused increasingly severe intestinal dysfunction. AQP4 and NPY may be involved in the pathogenesis of intestinal dysfunction after TBI. Increased NPY levels may be responsible for intestinal ischemia and hypoxia, and AQP4 may play an important role in intestinal edema. Increased NPY levels may be one of the main causes for the increase in AQP4 after TBI.     

Protective effects of hydrogen sulfide in a rat model of traumatic brain injury via activation of mitochondrial adenosine triphosphate–sensitive potassium channels and reduction of oxidative stress

Background

Hydrogen sulfide (H₂S) is considered an important neuromodulator in the central nervous system. We designed the present study to investigate the effects of exogenous H₂S in a rat model of traumatic brain injury (TBI) and the mechanism(s) that underlie this effect.

Methods

We induced a TBI model by controlled cortical impact injury. We intraperitoneally administered sodium hydrosulfide (NaHS) (an H₂S donor) (3 mg/kg) or vehicle alone at 5 min after a TBI operation. We then measured the H₂S level, brain edema, blood-brain barrier integrity, neurologic dysfunction, and lesion volume in all animals. Moreover, we assessed the role of mitochondrial adenosine triphosphate–sensitive potassium (mitoK_ATP)channels by intraperitoneal injection of the selective blocker 5-hydroxydecanoate before NaHS administration. In addition, we detected the levels of oxidative products and the activities of antioxidant enzymes in brain tissue.

Results

Administration of NaHS significantly increased the H₂S level of brain tissue in TBI-challenged rats. The TBI-challenged animals exhibited significant brain injuries, characterized by an increase of blood-brain barrier permeability, brain edema, and lesion volume, as well as neurologic dysfunction, which were significantly ameliorated by NaHS treatment. However, the protective effects of H₂S in TBI could be abolished by the mitoK_ATPchannel blocker 5-hydroxydecanoate. Moreover, we found that NaHS treatment increased endogenous antioxidant enzymatic activities and decreased oxidative product levels in brain tissue of TBI-challenged rats.

Conclusions

Exogenous H₂S administered at an appropriate dose can exert a protective effect against TBI via activation of mitoK_ATP channels and reduction of oxidative stress.     

Interhospital transfer of blunt multiply injured patients to a level 1 trauma center does not adversely affect outcome

Background

Stops at nontrauma centers for severely injured patients are thought to increase deaths and costs, potentially because of unnecessary imaging and indecisive/delayed care of traumatic brain injuries (TBIs).

Methods

We studied 754 consecutive blunt trauma patients with an Injury Severity Score greater than 20 with an emphasis on 212 patients who received care at other sites en route to our level 1 trauma center.

Results

Referred patients were older, more often women, and had more severe TBI (all P < .05). After correction for age, sex, and injury pattern, there was no difference in the type of TBI, Glasgow Coma Scale (GCS) upon arrival at the trauma center, or overall mortality between referred and directly admitted patients. GCS at the outside institution did not influence promptness of transfer.

Conclusions

Interhospital transfer does not affect the outcome of blunt trauma patients. However, the unnecessarily prolonged stay of low GCS patients in hospitals lacking neurosurgical care is inappropriate.     

Infant car safety seats and risk of head injury

Background/Purpose

We observed a high incidence of traumatic brain injuries (TBI) in properly restrained infants involved in higher speed motor vehicle crashes (MVCs). We hypothesized that car safety seats are inadequately protecting infants from TBI.

Methods

We retrospectively queried scene crash data from our State Department of Transportation (2007–2011) and State Department of Public Health data (2000–2011) regarding infants who presented to a trauma center after MVC.

Results

Department of Transportation data revealed 94% of infants in MVCs were properly restrained (782/833) with average speed of 44.6 miles/h when there was concern for injury. Department of Public Health data showed only 67/119 (56.3%) of infants who presented to a trauma center after MVC were properly restrained. Properly restrained infants were 12.7 times less likely to present to a trauma center after an MVC (OR = 12.7, CI 95% 5.6–28.8, p < 0.001). TBI was diagnosed in 73/119 (61.3%) infants; 42/73 (57.5%) properly restrained, and 31/73 (42.5%) improperly/unrestrained (p = 0.34). Average head abbreviated injury scale was similar for properly restrained (3.2 ± 0.2) and improperly/unrestrained infants (3.5 ± 0.2, p = 0.37).

Conclusion

Car safety seats prevent injuries. However, TBI is similar among properly restrained and improperly/unrestrained infants involved in higher speed MVCs who present to a trauma center.     

Patterns of healthcare service utilisation following severe traumatic brain injury: An idiographic analysis of injury compensation claims data

Background

The rate and extent of recovery after severe traumatic brain injury (TBI) is heterogeneous making prediction of likely healthcare service utilisation (HSU) difficult. Patterns of HSU derived from nomothetic samples do not represent the diverse range of outcomes possible within this patient group. Group-based trajectory model is a semi-parametric statistical technique that seeks to identify clusters of individuals whose outcome (however measured) follows a similar pattern of change over time.

Aim

To identify and characterise patterns of HSU in the 5-year period following severe TBI.

Methods

Detailed healthcare treatment payments data in 316 adults with severe TBI (Glasgow Coma Scale score 3–8) from the transport accident compensation system in the state of Victoria, Australia was accessed for this analysis. A semi-parametric group-based trajectory analytical technique for longitudinal data was applied to monthly observation counts of HSU data to identify distinct clusters of participants’ trajectories. Comparison between trajectory groups on demographic, injury, disability and compensation relevant outcomes was undertaken.

Results

Four distinct patterns (trajectories) of HSU were identified in the sample. The first trajectory group comprised 27% of participants and displayed a rapid decrease in HSU in the first year post-injury. The second group comprised 24% of participants and showed a sharp peak in HSU during the first 12 months post-injury followed by a decline over time. The third group comprised 32% of participants and showed a slight peak in HSU in the first few months post-injury and then a slow decline over time. The fourth group comprised 17% of participants and displayed a steady rise in HSU up to 30 months post-injury, followed by a gradual decline to a level consistent with that received in the first months post-injury. Significant differences were observed between groups on factors such as age, injury severity, and use of disability services.

Conclusions

There is substantial variation in patterns of HSU following severe TBI. Idiographic analysis can provide rich information for describing and understanding the resources required to help people with TBI.     

A second look at the utility of serial routine repeat computed tomographic scans in patients with traumatic brain injury

Background

The practice of a routine repeat head computed tomographic scans in patients with traumatic brain injury (TBI) is under question. The aim of our study was to evaluate the utility of a more than 1 repeat head computed tomography (M1CT) scans in patients with TBI.

Methods

We performed a 3-year analysis of a prospectively collected database of all TBI patients presenting to our level I trauma center. Patients who received M1CT scans were included. Findings and reason (without neurologic decline vs after neurologic decline) for M1CT were recorded. Primary outcome measure was neurosurgical intervention.

Results

A total of 296 patients that underwent M1CT were included. Of those, 291 patients (98.6%) had M1CT without a neurologic decline, and neurosurgical intervention was performed in 1 patient (.3%) who was inexaminable (Glasgow coma scale score = 6). The remaining (n = 5) had M1CT due to a neurologic decline; 4 patients (80%) of the 5 had worsening of ICH; and neurosurgical intervention was performed in 3 (75%) of the 4 patients.

Conclusions

The practice of multiple repeat head computed tomographic scans should be limited to inexaminable patients or patients with neurological deterioration.     

Decompressive craniectomy for severe traumatic brain injury: The relationship between surgical complications and the prediction of an unfavourable outcome

Object

To assess the impact that injury severity has on complications in patients who have had a decompressive craniectomy for severe traumatic brain injury (TBI).

Methods

This prospective observational cohort study included all patients who underwent a decompressive craniectomy following severe TBI at the two major trauma hospitals in Western Australia from 2004 to 2012. All complications were recorded during this period. The clinical and radiological data of the patients on initial presentation were entered into a web-based model prognostic model, the CRASH (Corticosteroid Randomization After Significant Head injury) collaborators prediction model, to obtain the predicted risk of an unfavourable outcome which was used as a measure of injury severity.

Results

Complications after decompressive craniectomy for severe TBI were common. The predicted risk of unfavourable outcome was strongly associated with the development of neurological complications such as herniation of the brain outside the skull bone defects (median predicted risk of unfavourable outcome for herniation 72% vs. 57% without herniation, p = 0.001), subdural effusion (median predicted risk of unfavourable outcome 67% with an effusion vs. 57% for those without an effusion, p = 0.03), hydrocephalus requiring ventriculo-peritoneal shunt (median predicted risk of unfavourable outcome 86% for those with hydrocephalus vs. 59% for those without hydrocephalus, p = 0.001), but not infection (p = 0.251) or resorption of bone flap (p = 0.697) and seizures (0.987). We did not observe any associations between timing of cranioplasty and risk of infection or resorption of bone flap after cranioplasty.

Conclusions

Mechanical complications after decompressive craniectomy including herniation of the brain outside the skull bone defects, subdural effusion, and hydrocephalus requiring ventriculo-peritoneal shunt were more common in patients with a more severe form of TBI when quantified by the CRASH predicted risk of unfavourable outcome. The CRASH predicted risk of unfavourable outcome represents a useful baseline characteristic of patients in observational and interventional trials involving patients with severe TBI requiring decompressive craniectomy.     

Effect of alcohol in traumatic brain injury: is it really protective?

Background

Studies have proposed a neuroprotective role for alcohol (ETOH) in traumatic brain injury (TBI). We hypothesized that ETOH intoxication is associated with mortality in patients with severe TBI.

Methods

Version 7.2 of the National Trauma Data Bank (2007–2010) was queried for all patients with isolated blunt severe TBI (Head Abbreviated Injury Score ≥4) and blood ETOH levels recorded on admission. Primary outcome measure was mortality. Multivariate logistic regression analysis was performed to assess factors predicting mortality and in-hospital complications.

Results

A total of 23,983 patients with severe TBI were evaluated of which 22.8% (n = 5461) patients tested positive for ETOH intoxication. ETOH-positive patients were more likely to have in-hospital complications (P = 0.001) and have a higher mortality rate (P = 0.01). ETOH intoxication was an independent predictor for mortality (odds ratio: 1.2, 95% confidence interval: 1.1–2.1, P = 0.01) and development of in-hospital complications (odds ratio: 1.3, 95% confidence interval: 1.1–2.8, P = 0.009) in patients with isolated severe TBI.

Conclusions

ETOH intoxication is an independent predictor for mortality in patients with severe TBI patients and is associated with higher complication rates. Our results from the National Trauma Data Standards differ from those previously reported. The proposed neuroprotective role of ETOH needs further clarification.