Traumatic brain injury: initial resuscitation and transfer

Traumatic brain injury (TBI) is common and carries a high morbidity and mortality. Initial management of the traumatic brain injury patient is directed toward preventing and limiting secondary brain injury while facilitating rapid transport to an appropriate facility capable of providing definitive neurocritical care. During resuscitation of the TBI patient, management is directed at correcting and maintaining mean arterial pressure (MAP), blood glucose, PaO₂ and PaCO₂ within their normal ranges. After the initial resuscitation, management is directed at limiting secondary damage to the brain that occurs in response to inflammatory changes, expanding haematomas, cellular swelling, seizures, and systemic complications such as haemodynamic or pulmonary changes, fever and pain. The transport of critically ill brain injured patients carries inherent risks. Although both intrahospital and interhospital transport must comply with regulations, patient safety is enhanced during transport by establishing an organised, efficient process supported by appropriate equipment and personnel. This review examines the evidence base for the initial resuscitation and transfer of head-injured patients.     

Traumatic brain injury: initial resuscitation and transfer

Traumatic brain injury continues to be a leading cause of injury-related death worldwide. The immediate post-injury phase is a time of high-risk for impaired cerebral oxygen delivery and raised intracranial pressure. Initial resuscitation is therefore focused on interventions that can limit subsequent secondary brain injury. Prioritization is the main feature in this approach with rapid assessment, guided by established protocols, performed in parallel with early resuscitation. This review examines the best-practice principles involved in the initial resuscitation of traumatic brain injury in a clinically relevant systems-based approach, while recognizing the lack of strong evidence for some treatment recommendations. Patients with traumatic brain injury will often require transfer across trauma networks for definitive neurosurgical intervention and specialized neurocritical care. The precision and planning required for the transfer of brain-injured patients is also described here, alongside practical recommendations aimed at mitigating the risks involved.     

Traumatic brain injury: initial resuscitation and transfer

Traumatic brain injury (TBI) is common and is associated with significant morbidity and mortality. The initial resuscitation and management of patients with traumatic brain injury is focused on limiting secondary brain injury and this may be complex in patients with significant injuries to other organ systems. The transport of critically ill brain injured patients for definitive treatment also carries significant risks which must be managed. This review describes the initial resuscitation and transfer of patients with traumatic brain injuries.     

Traumatic brain injury: initial resuscitation and transfer

Traumatic brain injury (TBI) is common and is associated with significant morbidity and mortality. The initial resuscitation and management of patients with TBI is focused on limiting secondary brain injury and this may be complex in patients with significant injuries to other organ systems. The transport of critically ill brain-injured patients for definitive treatment also carries significant risks which must be managed. This review describes the initial resuscitation and transfer of head-injured patients.     

Traumatic brain injury: initial resuscitation and transfer

Traumatic brain injury (TBI) is a major cause of mortality and morbidity in the young adult population. Targeted resuscitation with the aim of avoiding hypoxia and hypotension – two of the most important determinants of secondary brain injury – can produce significant improvements in outcome. Guidelines exist to aid the structured conduct of this resuscitation and then to aid the planning and execution of safe transfer for definitive management. However, there remains recurring problems with both the initial resuscitation and the transfer. This article addresses these common problems, and in conjunction with the referenced guidelines provides the basis for local treatment and transfer algorithms to deliver adequately resuscitated TBI patients, safely, to a neurosurgical centre for definitive care.     

The protective effects of dexmedetomidine on ischemic brain injury: A meta-analysis

BackgroundIntracranial lesions, trauma or surgery-related damage activate immune inflammation and neuroendocrine responses, causing ischemic brain injury. Studies have shown that inflammatory cascade mediated by neuroendocrine hormones and proinflammatory mediators is implicated in the pathophysiology of ischemic brain injury. Alpha2-adrenoceptor agonists, dexmedetomidine, is widely used as neuroprotectants in anesthesia practice. However, it is still lack of a comprehensive meta-analysis to evaluate the neuroprotection of dexmedetomidine against ischemic brain injury via suppressing these two physiological responses.MethodSearched the Cochrane Library, Pub-Med, EMBASE, EBSCO, Ovid, Chinese biological and medical database (CBM). Related literatures published in English or Chinese before January 2017 were enrolled. We assessed the quality of eligible studies and synthesized predefined outcomes with a random-effects model or fixed-effects model.ResultNineteen Randomized Controlled Trials including 879 patients were included. Findings for meta-analysis of various outcomes were summarised. Primary results shown that compared with placebo, dexmedetomidine reduced a surge of TNF-α [SMD = − 2.34, 95%CI (− 3.25, − 1.44)], IL-6 [SMD = − 2.44, 95%CI (− 3.40, − 1.47)], S100-β [SMD = − 2.73, 95%CI (− 3.65, − 1.82)], NSE [SMD = − 1.69, 95%CI (− 2.77, − 0.61)], cortisol [SMD = − 2.48, 95%CI (− 3.38, − 1.58)] and glucose [SMD = − 1.44, 95%CI (− 1.85, − 1.04)]; maintained the level of SOD [SMD = 1.36, 95%CI (0.62, 2.10)]; decreased the rise in CRP level at postoperative one day. In response to stress reaction, dexmedetomidine attenuated the stress-related increasing of MAP, HR and intracranial pressure without significant effects on cerebral oxygen metabolism.ConclusionAlpha2-adrenoceptor agonists, dexmedetomidine, could reduce the release of inflammatory mediators and neuroendocrine hormones as well as maintain intracranial homoeostasis, alleviating ischemic brain injury and exerting an effect on brain protection.     

谷氨酸转运体与缺血性脑损伤

背景 缺血性脑损伤严重威胁人类的生命健康,谷氨酸损伤在缺血性脑损伤的疾病进展中起重要作用,调控谷氨酸浓度对缺血性脑损伤的治疗具有重要意义.目的 探讨缺血性脑损伤与谷氨酸转运体的关系及多种预处理方法对谷氨酸转运体的影响,寻找一种缺血性脑损伤的治疗方法.内容 综述谷氨酸转运体的亚型、分布、结构和功能以及谷氨酸转运体与缺血性...     

线粒体Ca2+超载与缺血性脑损伤

人们致力于脑缺血的研究已有数十年,然而其予后仍然较差。溶栓治疗仅对部分病人有效,但2/3以上的病人即使在中风发病3 h内开始溶栓治疗其治疗效果仍不理想[1]。缺血和再灌注时间是决定脑损伤程度的重要因素。缺血后神经细胞的死亡常延迟到缺血后数小时直到数日,临床实验表明,缺     

Quantitation of ischemic events after severe traumatic brain injury in humans: a simple scoring system

BACKGROUND: Cerebral ischemia is recognized as one of the most important mechanisms responsible for secondary brain damage following severe traumatic brain injury (TBI), contributing to an increased mortality and a worse neurologic outcome. METHOD: A simple 5-item scoring system, taking into account the occurrence of specific potentially brain-damaging events (hypoxemia, hypotension, low cerebral blood flow, herniation, and low cerebral perfusion pressure) has been tested in a large population of severe TBI patients. Aims of this retrospective study were to validate the ability of the proposed ischemic score to predict neurologic outcome and to correlate the ischemic score with the results of microdialysis-based neurochemical monitoring and brain tissue oxygen monitoring. FINDINGS: In a population of 172 severe TBI patients, a significant correlation was found between ischemic score and neurologic outcome, both at 3 months (r = -0.32; P < 0.01) and at 6 months (r = -0.31; P < 0.01). Significant correlations were also found with the most important neurochemical analytes. CONCLUSIONS: The ischemic score proposed here, may be determined during the acute intensive care unit period, and correlates closely with outcome, which can only be determined 3 to 6 months, after injury. It also shows a correlation with neurochemical analytes.     

A novel technique designed to minimize the morbidity of failure of arteriovenous access in hemodialysis patients

The failure of dialysis access grafts leads to significant morbidity rates in patients with end-stage renal disease. We describe a novel technique for the insertion of new polytetrafluoroethylene graft segments designed to reduce this morbidity rate. Patients found to have significant intragraft deterioration at thrombectomy undergo insertion of a new nonanastamosed graft parallel to the existing graft. At the next failure of the existing graft, the nonanastamosed segment is anastamosed and used immediately for dialysis, obviating the need for a temporary catheter. Thirty patients have undergone this technique, and 89% of those who returned to surgery have had successful anastamosis of their new segments. Two patients were found to have inadequate incorporation of their new segments into the subcutaneous tissue, and one became frankly infected.     

Potential effect of lidocaine on ischemic myocardial injury: Experimental and clinical observations

The effect of lidocaine on ischemic myocardial injury was studied in acute myocardial infarction (AMI). In 20 anesthetized dogs coronary artery ligation (CAL) was performed. Dogs were divided into three groups. Group I (n = 8) had CAL only, Group II (n = 6) received 3 mg/kg of lidocaine (L) 30 min post-CAL, Group III (n = 6) received the same bolus injection of L and an L infusion of 2 mg/min for 120 min. In Group I the sum of ST segment elevation (Σ ST) and the number of sites showing >1 mV ST elevation (NST), as measured from epicardial mapping, were unchanged between 30 and 150 min post-CAL, the mean R magnitude decreased significantly, and 12 new Q waves were recorded. In Groups II and III, 15 min after L administration, Σ ST and NST decreased significantly (P < 0.05) and remained unchanged until the end of the study. There was no difference in Σ ST and NST changes between Groups II and III. No R wave magnitude changes or Q waves were observed between 30 and 150 min post-CAL in Groups II and III. Coronary sinus CPK at 150 min post-CAL increased more in Group II than in Group I (23 ± 3 vs 49.7 ± 9, P < 0.05). A negative inotropic effect was demonstrated by decreases in peak dp/dt (510 ± 50 mm Hg/sec, P < 0.05) and dQ/dt (28 ± 2%, P < 0.05) 5 min after the L bolus.This effect of lidocaine on Σ ST and NST was studied in six patients with anterior AMI. L decreased significantly both Σ ST and NST in the patients studied.These data suggest that lidocaine has a beneficial effect, decreasing ischemic injury and/or delaying the process of ischemic necrosis. This appears to be caused by a negative inotropic effect, which may be beneficial in the early post-open-heart surgery period and in patients with acute myocardial infarction.     

A new blade for the bookwalter retractor system

The table-fixed Bookwalter retractor system has been widely adopted in abdominal surgery, and during the past 15 or more years, we have succeeded in using the retractor system for thousands of cases operated on at the Taipei Veterans General Hospital, Taiwan. However, for some surgical procedures, such as gastrectomy, the blades that are currently available do not adequately hold deeper organs or tissue, such as the liver. We have successfully designed and fabricated a blade for grasping deeper tissue or organs, which is reusable and cost-effective. The shape of this new blade is described.     

Evaluation in an anaesthetic simulator of a prototype of a new drug administration system designed to reduce error

Ten anaesthetists were observed while providing anaesthesia for two simulated surgical procedures, twice using conventional methods and twice using a prototype of a new drug administration system designed to reduce error. Aspects of each method were rated by users on 10-cm visual analogue scales (10 being best) and comments were invited. Median safety scores were 7.7 cm (range 4.3-8.9) for the new system and 4.6 cm (1.3-8.2) for conventional methods (p = 0.009). The new system was compared favourably with conventional methods in respect of safety (p = 0.005), clinical acceptability (p = 0.008), organisation and layout (p = 0.047), and acceptability for use on patients (p = 0.005). The new system saved time in the preparation of drugs both before anaesthesia (105 vs. 346 s; p < 0.001) and during anaesthesia (20 vs. 104 s; p < 0.001). Comments facilitated development of the system and the evaluation endorsed proceeding to a clinical trial.     

短暂缺血预处理减轻缺血性脑损伤的研究

目的 观察缺血预处理对再次脑缺血损伤的保护作用。方法 将SD大鼠分为3组，分别给予生理盐水右侧颈内动脉灌注（SI）、双侧颈总动脉夹闭（BCAO）和双侧颈总动脉夹闭并生理盐水右侧颈内动脉灌注（BS）。每次持续3min，间隔7min，反复3次，24h后作经插线右大脑中动脉栓塞（MCAO），观察MCAO后脑组织含水量、血脑屏障通透性（以脑伊文思蓝含量表示）后梗死体积。结果 BS组MCAO后24h和48h脑伊文思蓝（EB）含量和脑含水量明显较其他两组低（P＜0.01）；MCAO72hBS组脑梗死低于其它两组（P＜0.05）。结论 双侧颈总动脉夹闭并生理盐水右侧颈内动脉灌注对脑再次缺血有明显的保护作用。     

Modified liver-hanging maneuver designed to minimize blood loss during hepatic parenchymal transection in hemihepatectomy

Purpose  

We evaluated the efficiency of a modified liver-hanging technique for minimizing intraoperative blood loss during right and left hemihepatectomy.     

Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats

Purpose  Dexmedetomidine has been used for purposes of anesthesia and sedation, and experimental studies have demonstrated its neuroprotective effects. However, it has also been shown that the constriction of cerebral vessels in response to high doses of dexmedetomidine decreases cerebral blood flow. We tested the hypothesis that dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic cerebral injury. Methods  The effects of dexmedetomidine on cerebral blood flow and mean arterial blood pressure were studied first. Six rats received intravenous infusions of dexmedetomidine in doses ranging from 0.01 to 10 μg·kg⁻¹·min⁻¹. At the end of this phase of treatment, the alpha-2 adrenergic antagonist yohimbine was administered (3 mg·kg⁻¹ ip). Cerebral blood flow and mean arterial blood pressure were recorded continuously. A second series of experiments was then performed using a rat model of transient middle cerebral artery occlusion. Forty-two rats received 1μg·kg⁻¹·min⁻¹ or 10 μg·kg⁻¹·min⁻¹ dexmedetomidine with or without pretreatment with either of the alpha-2 adrenergic antagonists yohimbine or rauwolscine. Five days after middle cerebral artery occlusion and reperfusion, the rat brains were removed and the infarct volumes were measured. Results  In the first protocol, increasing the dose of dexmedetomidine significantly decreased cerebral blood flow. Mean arterial blood pressure decreased to 79.9% relative to baseline with a dose of 0.01 μg·kg⁻¹·min⁻¹ dexmedetomidine, and increased to 119.9% relative to baseline with a dose of 10 μg·kg⁻¹·min⁻¹ dexmedetomidine. In the second protocol, the infarct volume in the control group was 9.5% of the total brain volume; the infarct volume increased to 11.3% in rats treated with 1 μg·kg⁻¹·min⁻¹ dexmedetomidine and the volume increased to 24.5% in rats treated with 10 μg·kg⁻¹·min⁻¹ dexmedetomidine. Pretreatment with an alpha-2 adrenergic antagonist, either yohimbine or rauwolscine, reduced the size of these high-dose dexmedetomidine-induced infarct volumes. Conclusion  Hypertension following the administration of high-dose dexmedetomidine is associated with cerebral hypoperfusion and the exacerbation of ischemic brain injury, possibly through alpha-2-induced cerebral vasoconstriction.     

酸敏感离子通道在缺血性脑损伤中的作用

背景 酸敏感离子通道(acid sensing ion channels,ASICs)属于阿米洛利敏感的上皮钠通道/退变素(epithelial Na+ channels/degenerin,ENaC/DEG)超家族中的一员,该通道广泛分布在周围和中枢神经系统.最新研究表明Ca2+敏感的ASIC1a的激活在酸中毒介导、谷氨酸受体非依赖的脑缺血性神经损伤中起重要作用.目的 综述ASICs在缺血性脑损伤中的作用.内容从ASICs的结构、分布、功能特点及其在缺血性脑损伤中的作用进行综述.趋向 ASICs可能为阐述缺血性脑损伤的潜在机制提供依据,并为其临床治疗提供方向和思路.