2018年 · 第21卷第03期

Traumatic injury of the central nervous system (CNS) including brain and spinal cord remains a leading cause of morbidity and disability in the world. Delineating the mechanisms underlying the secondary and persistent injury versus the primary and transient injury has been drawing extensive attention for study during the past few decades. The sterile neuroinflammation during the secondary phase of injury has been frequently identified substrate underlying CNS injury, but as of now, no conclusive studies have determined whether this is a beneficial or detrimental role in the context of repair. Recent pioneering studies have demonstrated the key roles for the innate and adaptive immune responses in regulating sterile neuroinflammation and CNS repair. Some promising immunotherapeutic strategies have been recently developed for the treatment of CNS injury. This review updates the recent progress on elucidating the roles of the innate and adaptive immune responses in the context of CNS injury, the development and characterization of potential immunotherapeutics, as well as outstanding questions in this field.

Traumatic brain injury (TBI) remains a major cause of death and disability worldwide. Increasing evidence indicates that TBI is an important risk factor for neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. Despite improved supportive and rehabilitative care of TBI patients, unfortunately, all late phase clinical trials in TBI have yet to yield a safe and effective neuroprotective treatment. The disappointing clinical trials may be attributed to variability in treatment approaches and heterogeneity of the population of TBI patients as well as a race against time to prevent or reduce inexorable cell death. TBI is not just an acute event but a chronic disease. Among many mechanisms involved in secondary injury after TBI, emerging preclinical studies indicate that posttraumatic prolonged and progressive neuroinflammation is associated with neurodegeneration which may be treatable long after the initiating brain injury. This review provides an overview of recent understanding of neuroinflammation in TBI and preclinical cell-based therapies that target neuroinflammation and promote functional recovery after TBI.

Purpose: Early diagnosis of traumatic brain injury (TBI) is important for improving survival and neurologic outcome in trauma victims. The purpose of this study was to assess whether Glasgow Coma Scale (GCS) of 12 or less can predict the presence of TBI and the severity of associated injuries in blunt trauma patients. Methods: A retrospective cohort study including 303,435 blunt trauma patients who were transferred from the scene to hospital from 1998 to 2013. The data was obtained from the records of the National Trauma Registry maintained by Israel's National Center for Trauma and Emergency Medicine Research, in the Gertner Institute for Epidemiology and Health Policy Research. All blunt trauma patients with GCS 12 or less were included in this study. Data collected in the registry include age, gender, mechanism of injury, GCS, initial blood pressure, presence of TBI and incidence of associated injuries. Patients younger than 14 years old and trauma victims with GCS 13-15 were excluded from the study. Statistical analysis was performed by using Statistical Analysis Software Version 9.2. Statistical tests performed included Chi-square tests. A p-value less than 0.05 was considered statistically significant. Results: There were 303,435 blunt trauma patients, 8731 (2.9%) of them with GCS of 3-12 that including 6351 (72%) patients with GCS of 3-8 and 2380 (28%) patient with GCS of 9-12. In these 8731 patients with GCS of 3-12, 5372 (61.5%) patients had TBI. There were total 1404 unstable patients in all the blunt trauma patients with GCS of 3-12, 1256 (89%) patients with GCS 3-8, 148 (11%) patients with GCS 9-12. In the 5095 stable blunt trauma patients with GCS 3-8, 32.4% of them had no TBI. The rate in the 2232 stable blunt trauma patients with GCS 9-12 was 50.1%. In the unstable patients with GCS 3-8, 60.5% of them had TBI, and in subgroup of patients with GCS 9-12, only 37.2% suffered from TBI. Conclusion: The utility of a GCS 12 and less is limited in prediction of brain injury in multiple trauma patients. Significant proportion of trauma victims with low GCS had no TBI and their impaired neurological status is related to severe extra-cranial injuries. The findings of this study showed that using of GCS in initial triage and decision making processes in blunt trauma patients needs to be re-evaluated.

Purpose: "Polytrauma" patients are of a higher risk of complications and death than the summation of expected mortality and morbidity of their individual injuries. The ideal goal in trauma resuscitation care is to identify and treat all injuries. With clinical and technological advanced imaging available for diagnosis and treatment of traumatic patients, point of care-rapid ultrasound in shock and hypotension (RUSH) significantly affects modern trauma services and patient outcomes. This study aims to evaluate the accuracy of RUSH and patient outcomes by early detection of the causes of unstable polytrauma. Methods: This cross-sectional, prospective study included 100 unstable polytrauma patients admitted in Suez Canal University Hospital. Clinical exam, RUSH and pan-computed tomography (pan-CT) were conducted. The result of CT was taken as the standard. Patients were managed according to the advanced trauma life support (ATLS) guidelines and treated of life threatening conditions if present. Patients were followed up for 28 days for a short outcome. Results: The most diagnostic causes of unstability in polytrauma patients by RUSH are hypovolemic shock (64%), followed by obstructive shock (14%), distributive shock (12%) and cardiogenic shock (10%) respectively. RUSH had 94.2% sensitivity in the diagnosis of unstable polytrauma patients; the accuracy of RUSH in shock patients was 95.2%. Conclusion: RUSH is accurate in the diagnosis of unstable polytrauma patients; and 4% of patients were diagnosed during follow-up after admission by RUSH and pan-CT.

Purpose: The incidence of hip fractures is increasing within the aging population. Our objective was to identify and quantify the risk factors and develop a predictive model for the in-hospital mortality among hip fracture patients older than 65 years. Methods: This is a prospective study conducted on 331 hip fracture patients older than 65 years admitted to our hospital from 2011 to 2014. Patients' demographics, prehospitalization residential status, prefracture comorbidity data, anti-aggregant and anticoagulant medication, preoperative hemoglobin value, type of fractures, type of treatments, time to surgery, and complications were recorded. Results: The average age was 83 years, 73% female, and 57% of them sustained a femoral neck fracture. In 62.8% of patients, the number of pre-fracture baseline comorbidities was ≥2. The in-hospital mortality rate was 11.4%. In multivariate analysis, age over 90 years, congestive heart failure, asthma, rheumatologic disease, lung cancer, and not taking antiaggregant medication were independently associated with in-hospital mortality. A formula and risk stratification scoring for predicting the risk for in-hospital mortality was developed. Risk-adjustment model based on these variables had acceptable accuracy for predicting in-hospital mortality (c-statistic 0.77). Conclusion: Advanced age, and five prefracture comorbidities have a strong association with in-hospital mortality in a hip fracture patient older than 65 years old. Our predictive model was specifically designed for the old hip fracture population. It has an accuracy similar to other risk models. The specificity, positive predictive value, and negative predictive value are high. In addition, it could discriminate a high risk patient from a low risk patient for in-hospital mortality.

Purpose: To investigate the mid-term curative effects of the treatment of Pipkin type IV femoral head fractures using a reconstruction plate and bioabsorbable screws and provide the evidence for clinical practice. Methods: From February 2010 to September 2014, 21 patients with Pipkin type IV femoral head fractures were treated surgically. There were 13 males and 8 females with an average age of 41.1 years (range, 20-65 years). The causes of the fractures included traffic accidents (13 cases), falls from a height (four cases), heavy lifting injuries (three cases), and sport injury (one case). All patients were followed up with radiography and three-dimensional reconstruction computed tomography and other checks and any complications were actively managed. Closed reduction of fracture-dislocation of the hip was attempted under general anesthesia using the Kocher-Langenbeck approach. Femoral head fractures were treated with internal fixation or excision based on the size of the fracture fragments, whereas acetabular fractures were fixed with a reconstruction plate and screws following anatomic reduction. Results: The incisions healed by primary intention in all patients after surgery, without any infection, deep venous thrombosis, or other complications. All 21 patients were followed up for 36-76 months, with an average follow-up duration of 49 months. Postoperative imaging data showed that all dislocations and fractures were anatomically reduced, and bony union of the fractures was achieved. Heterotopic ossification was found in four patients, post-traumatic osteoarthritis in three, and avascular necrosis of the femoral head in two. At the final follow-up, the assessment of hip joint function according to the Thompson-Epstein scoring scale was excellent in 10 cases, good in six cases, fair in three cases, and poor in two cases. The rate of excellent and good functional outcomes was 76.1%. Conclusion: The mid-term curative effects of a reconstruction plate and bioabsorbable screws in the treatment of Pipkin type IV femoral head fractures is significant, and such the treatment can significantly improve the patient's joint function and quality of life.

Purpose: Posttraumatic arthritis (PTA) may develop years after acetabular fracture, hindering joint function and causing significant chronic musculoskeletal pain. Given the delayed onset of PTA, few studies have assessed outcomes of delayed total hip arthroplasty (THA) in acetabular fracture patients. This study systematically reviewed the literature for outcomes of THA in patients with PTA and prior acetabular fracture. Methods: Pubmed, EMBASE, SCOPUS, and Cochrane library were searched for articles containing the keywords "acetabular" , "fracture" , "arthroplasty" , and "post traumatic arthritis" published between 1995 and August 2017. Studies with less than 10 patients, less than 2 years of follow-up, conference abstracts, and non-English language articles were excluded. Data on patient demographics, surgical characteristics, and outcomes of delayed THA, including implant survival, complications, need for revision, and functional scores, was collected from eligible studies. Results: With 1830 studies were screened and data from 10 studies with 448 patients were included in this review. The median patient age on date of THA was 51.5 years, ranging from 19 to 90 years. The median time from fracture to THA was 37 months, with a range of 27-74 months. Mean follow-up times ranged from 4 to 20 years. The mean Harris hip scores (HHS) improved from 41.5 pre-operatively, to 87.6 post-operatively. The most prevalent postoperative complications were heterotopic ossification (28% -63%), implant loosening (1%-24%), and infection (0%-16%). The minimum 5-year survival of implants ranged from 70% to 100%. Revision rates ranged from 2% to 32%. Conclusion: Despite the difficulties associated with performing THA in patients with PTA from previous acetabular fracture (including soft tissue scarring, existing hardware, and acetabular bone loss) and the relatively high complication rates, THA in patients with PTA following prior acetabular fracture leads to significant improvement in pain and function at 10-year follow-up. Further high quality randomized controlled studies are needed to confirm the outcomes after delayed THA in these patients.

Septic arthritis of acromioclavicular (AC) joint is a rare entity. It is generally seen in patients who are immunocompromised. Only 15 cases have been reported till now, with only one case series of 6 patients. We report a case of septic arthritis of AC joint in an immunocompetent child. A 9 years old girl presented with history of pain in left shoulder for 4 days associated with fever. No history suggestive of any immunocompromised state was complained. On local examination, a swelling of around 3 cm in diameter was found over left AC joint region with raised local temperature, tenderness on palpation and positive response in fluctuation test. Total leukocyte count was 18.7 × 109/L with 80% of neutrophils. Erythrocyte sedimentation rate (ESR) was 28 mm/1 h. C-reactive protein (CRP) was 12 mg/L. X-ray showed enlarged left AC joint space. Ultrasound revealed hypoechoic collection in the AC joint and the surrounding area. The aspirate was thick and purulent in nature, revealing Gram positive cocci at staining. Arthrotomy and thorough lavage of AC joint was done. Culture of the aspirate showed Methicillin Resistant Staphylococcus Aureus (MRSA) after 48 hours that was sensitive to amikacin, gentamicin, erythromycin and teicoplanin. Patient was symptom-free at 2 months of follow-up with no signs of osteomyelitis on the radiographs. Thus this is the first case of AC joint septic arthritis in healthy individual. Being proximal to the shoulder joint, AC joint septic arthritis can be confused with the shoulder joint septic arthritis. Thus, high index of suspicion is required for accurate diagnosis.