Prolonged disruption of plasma beta-endorphin dynamics after trauma in the nonhuman primate

Recent evidence has suggested that a circadian rhythm exists for plasma beta-endorphin-like immunoreactivity. The purpose of the present study was to examine the long term effects of surgical trauma on plasma beta-endorphin dynamics. Blood samples for RIA were obtained from female baboons every 4 h for three 48-h periods: one beginning 1 week before surgical trauma, the second 30 min after surgical trauma, and the third 1 week after surgical trauma. Animals were subjected to laparotomy and 30-min anesthesia (n = 8), 5-min surgical trauma under 30-min anesthesia (low trauma; n = 8), or 20-min surgical trauma under 30-min anesthesia (high trauma; n = 8). Computer analysis of beta-endorphin levels as a function of clock time demonstrated a true preoperative circadian rhythm for all animals, with a mean of 87.9 pg/ml. In the immediate 48-h postoperative period, a postoperative alteration in circadian beta-endorphin dynamics occurred that was correlated with the severity of trauma. A disruption of circadian rhythms of plasma beta-endorphin occurred in the high trauma group only, in which it persisted for longer than 1 week after trauma. These studies establish a relationship between the alteration of circadian rhythmicity of plasma beta-endorphin-like immunoreactivity and the magnitude of trauma and injury.     

Ventricular tachycardia in an ice-hockey player after a blunt chest trauma

A case of a professional ice-hockey with a blunt chest trauma is presented. A year after the first cardiac evaluation, he experienced sustained ventricular tachycardia after another slight chest trauma. An implantable cardioverter-defibrillator was implanted. The pathophysiological background of tachycardias after a blunt chest trauma and its management are discussed.     

Effect of voluntary exercise on urinary excretion of catecholamines after traumatic shock in rats

Thirteen rats were kept in cages equipped with running wheels for 10 months (exercise group), and 12 rats were kept in cages without running wheels during the same period (control group). Rats in both groups were subjected to a Noble-Collip drum trauma (40 rpm, 350 revolutions in total) after the 10-month conditioning period. Urine output, urinary epinephrine (E), and norepinephrine (NE) were measured until the seventh day after the trauma. Urine output decreased after the trauma in both groups to the same extent, but the recovery of urine output after trauma was accomplished faster in the exercise group than in the control group, and diuresis after trauma was seen only in the exercise group. Urinary E increased in both groups within 24 hours after trauma, but the increase in the exercise group was significantly less than in the control group. The amount of NE excreted depended somewhat on the urine volume, but there was no significant difference in changes in urinary NE after trauma between the groups. These results suggest that rats bred in an active condition suffered less severe traumatic shock accompanied by a reduced sympathoadrenal activity as compared with rats bred in a relatively sedentary condition.     

不同切肝量大鼠血清HSP70水平变化及其意义

目的观察不同切肝量大鼠血清HSP70水平的变化,并探讨其意义。方法将310只大鼠随机分为正常对照组10只、切肝组150只和谷氨酰胺（Gln）干预组150只。后两组又分为轻度、中度、重度切亚组各50只,分别建立不同切肝量手术创伤模型,干预组造模前经大鼠尾静脉注入Gln 0.75 g/kg。对照组只给予麻醉处理。检测对照组及其他两组术后2、8、12、24、48 h大鼠血清HSP70和肝功能指标。结果与正常对照组比较,切肝组和干预组血清HSP70于术后2 h开始升高,12 h达高峰,48 h仍较高;中、重度切肝组术后ALT、TB均增高,经Gln干预后均降低。结论手术创伤可导致大鼠血清HSP70水平明显升高;检测血清HSP70表达有助于诊断及预测手术创伤程度,术前诱导HSP表达对机体有保护作用。     

Prior blunt chest trauma may be a cause of single vessel coronary disease; hypothesis and review

Prompted by a case where a patient (with no risk factors, and single vessel disease) developed angina pectoris after previous blunt chest trauma, we searched Medline for blunt chest trauma and myocardial ischaemia. We found 77 cases describing AMI after blunt chest trauma, but only one reporting angina pectoris. We focused on the age and sex distribution, type of trauma, the angiography findings and the time interval between the trauma and the angiography. The age distribution was atypical, compared to AMI in general; 82% of the patients with AMI after blunt chest trauma were less than 45 years old, and only 2.5% more than 60 years old. The most common trauma was a road traffic accident, and the LAD was the vessel most often affected. Angiography revealed 12 cases with completely normal vessels, which might be due to spasm or recanalisation; 31 cases showed occlusion but no atherosclerosis, which strongly suggested a causal relation between the trauma and subsequent occlusion. AMI should therefore be considered in patients suffering from chest pain after blunt chest trauma. Because traumatic AMI might often be the result of an intimal tear or dissection, thrombolytic therapy might worsen the situation and acute PCI must be considered preferable. It seems likely that lesser damage could lead to longer-term stenosis we suspect that this sequence is grossly under-reported. This could have medico-legal implications.     

Pattern of trauma determines the threshold for epileptic activity in a model of cortical deafferentation

Epileptic activity often occurs in the cortex after a latent period after head trauma; this delay has been attributed to the destabilizing influence of homeostatic synaptic scaling and changes in intrinsic properties. However, the impact of the spatial organization of cortical trauma on epileptogenesis is poorly understood. We addressed this question by analyzing the dynamics of a large-scale biophysically realistic cortical network model subjected to different patterns of trauma. Our results suggest that the spatial pattern of trauma can greatly affect the propensity for developing posttraumatic epileptic activity. For the same fraction of lesioned neurons, spatially compact trauma resulted in stronger posttraumatic elevation of paroxysmal activity than spatially diffuse trauma. In the case of very severe trauma, diffuse distribution of a small number of surviving intact neurons alleviated posttraumatic epileptogenesis. We suggest that clinical evaluation of the severity of brain trauma should take into account the spatial pattern of the injured cortex.     

Acute myocardial infarction caused by coronary artery dissection after a blunt chest trauma

Acute myocardial infarction is a life-threatening condition. Coronary dissection after blunt chest trauma is a rare event. Chest pain is a common symptom after chest trauma, which may relate to chest contusion without cardiac injury or myocardial infarction. Differentiation between minor cardiac contusion and significant cardiac injury is difficult and it is a challenge for physicians to diagnose traumatic cardiac injury early. We report a case of a 40-year-old man suffering from coronary artery dissection after a blunt chest trauma and intracranial hemorrhage after percutaneous coronary intervention.     

Delayed cardiac tamponade in a patient with previous minor blunt chest trauma

Hemopericardium with cardiac tamponade after non-penetrating chest trauma is a very rare but life-threatening condition. If this complication develops after an interval of several weeks following the non-penetrating chest trauma, the causal relation with the traumatic event is less evident, which may delay proper diagnosis and adequate treatment. We describe diagnosing and therapeutic management of a patient in shock who suffered from cardiac tamponade four weeks after a minor blunt chest trauma.     

Outcome of patients with blunt trauma transferred after diagnostic or treatment procedures or four-hour delay.

STUDY OBJECTIVE: This study was conducted to assess the outcome of patients suffering multiple injuries from blunt trauma who were transferred to a Level I trauma center for definitive care after special diagnostic or treatment procedures (DTPs) or after a simple delay of four hours at a primary receiving hospital. DESIGN: Retrospective review of aeromedical registry data and clinical chart review. MEASUREMENTS: Aeromedical trauma transfers made during a four-year period were studied. The TRISS method was used to determine predicted survivals for DTP patients, patients transferred after a four-hour delay, and patients transferred promptly. RESULTS: The observed survival for 469 aeromedically transferred patients with blunt trauma was the same as that predicted by TRISS analysis (394 vs 392.5). Survival for 86 patients with DTP was also the same as predicted (62 vs 61.6). Outcomes for nonDTP patients and for 92 patients experiencing a delay in transport of four hours or more were also the same as predicted. CONCLUSION: Early versus delayed decision to transfer patients with blunt trauma did not appear to influence overall outcome. These data suggest that minor delays in recognizing the need to transfer patients with blunt injuries to a trauma center for definitive care may be offset by rapid, skilled transfer and highly specialized trauma care and support the hypothesis that regional trauma center care after initial evaluation and resuscitation elsewhere can be effective even when the timing of transfer is not ideal.     

Interferon-gamma counteracts reduced endotoxin responsiveness of whole blood following trauma and cardiopulmonary bypass

Accidental as well as surgical trauma has been reported to cause reduced endotoxin responsiveness of blood in terms of cytokine production. In this study, the effect of interferon-gamma (IFN-gamma) on tumour necrosis factor-alpha (TNF-alpha)-producing capacity of whole blood after severe trauma and cardiac surgery was investigated. Blood samples of severely injured patients were collected at the first day after trauma and of cardiac surgery patients before, 4 h and 2 days after cardiopulmonary bypass (CPB). The blood samples were incubated with INF-gamma (0-100 U/ml) for 20 h and subsequently lipopolysaccharide (LPS)-induced TNF-alpha production was determined. Compared to healthy donors, LPS-induced TNF-alpha production was significantly reduced in blood cultures of trauma patients on day 1 after trauma and 4 h after CPB. Pre-incubation with IFN-gamma in vitro increased endotoxin-induced TNF-alpha production in volunteers' and all patients' blood specimens in a dose-dependent manner. IFN-gamma prompted an elevation of cytokine synthesis in CPB patients' blood which equalled that of volunteers, whereas it caused a lower rise in TNF-alpha production in blood of multiply injured patients, reaching levels of untreated donors only after incubation with 100 U/ml IFN-gamma. These experiments show that hyporesponsiveness of whole blood induced by trauma or cardiac surgery with CPB is not irreversible, but can be counteracted by the immunostimulant IFN-gamma. IFN-gamma, therefore, could be applied clinically in trauma patients or after cardiac surgery to prevent or to resolve infection complications.     

硫化氢对截肢创伤后心肌线粒体功能的保护作用

目的 探讨外源性H2S对截肢创伤应激后心肌线粒体功能的影响，以及截肢创伤应激后，心肌线粒体损伤与H2S对心肌线粒体功能的保护作用。方法 建立截肢创伤应激模型。雄性SD大鼠48只（平均体质量260～300 g），分为正常对照组、创伤组（截肢后6 h）、NaHS组（截肢后立即腹腔注射NaHS 28 μmol/kg，6 h后处死）和炔丙基甘氨酸（PPG）组（截肢后立即给予腹腔注射PPG 50 mg/kg，6 h后处死），每组8只。提取心肌线粒体，用strathkelvin氧电极法测定线粒体的呼吸功能。用罗丹明123(Rh123)荧光测定线粒体的膜电位，用微量ATP酶试剂盒检测线粒体总ATP的变化。结果 与正常对照组比，创伤后心肌线粒体的呼吸功能受损［呼吸控制率(RCR)及磷氧比(P/O)降低，P<0.05］，膜电位下降（P<0.05），总ATP酶的含量降低（P<0.05）。与创伤组比，NaHS组心肌线粒体的呼吸功能改善（RCR、P/O升高，P<0.05），膜电位升高（P<0.05），总ATP酶的含量增加（P<0.05）。PPG组心肌线粒体的呼吸功能进一步受损（RCR、P/O降低，P<0.05），总ATP酶的含量减少（P<0.05）。结论 截肢创伤应激可使心肌线粒体的呼吸功能受损，膜电位下降，能量代谢障碍，硫化氢对截肢创伤后心肌线粒体的损伤具有保护作用。     

Effects of L-arginine on cerebral blood flow, microvascular permeability, number of perfused capillaries, and brain water content in the traumatized mouse brain

It is has been suggested that decreased production of the vasodilatory and anti-aggregative substance NO (nitric oxide) may result in lower cerebral blood flow (CBF) in injured areas of the traumatized brain. The NO-precursor L-arginine has been shown to counteract CBF decreases early after trauma, but microcirculatory and more long-term effects on CBF of L-arginine have not been investigated. In an attempt to analyze effects of L-arginine on the microcirculation in the traumatized brain, the present study was designed to evaluate the effects of L-arginine compared to vehicle (0.9% saline) following a standardized controlled cortical-impact brain trauma in mice. Cerebral blood flow (autoradiography [(14)C]-iodoantipyrine), number of perfused capillaries (FITC-dextran fluorescence technique), brain water content (wet vs. dry weight) and the blood to brain transfer constant K(i) for [(51)Cr]-EDTA were analyzed in the injured and the contralateral cortex. Cortical blood flow in the injured cortex was 0.43+/-0.3 mL/g/min and 0.81+/-0.3 mL/g/min 3 h after trauma in the vehicle and L-arginine groups, respectively (p<0.05), and no treatment effect was seen 24 h after trauma. The number of perfused capillaries decreased following trauma and was unaffected by L-arginine. K(i) increased following trauma and was unaffected by L-arginine. Brain water content was lower in the L-arginine group than in the vehicle group 3 h after trauma and there was no difference between the groups 24 h after trauma. We conclude that L-arginine reduces brain edema formation and improves cortical blood flow in the early phase after a brain trauma, whereas no circulatory effects can be seen after prolonged treatment.     

Disseminated intravascular coagulation in trauma patients.

Disseminated intravascular coagulation (DIC) is characterized by the in vivo activation of the coagulation system, which results in the intravascular deposition of fibrin and consumption bleeding. DIC is a serious hemostatic complication of trauma. It can be clearly distinguished from physiological hemostatic response to trauma by using sensitive coagulofibrinolytic molecular markers. Physiological hemostasis to injuries is similar in all kinds of trauma without exception. There is an increase in circulating proinflammatory cytokines in DIC patients after trauma. Elevated cytokines induce tissue factor-mediated activation of coagulation, suppression of the anticoagulant pathway, and plasminogen activator inhibitor-1 (PAI-1)-mediated inhibition of fibrinolysis followed by disseminated fibrin deposition in the microvasculature. In addition to the occlusive microvascular thrombosis and hypoxia, sustained systemic inflammatory response characterized by neutrophil activation and endothelial damage plays a pivotal role in the development of multiple organ dysfunction syndrome (MODS) in posttrauma DIC patients. DIC associated with sustained systemic inflammatory response syndrome (SIRS) after trauma leads to the development of MODS, which is the main determinant of patients' outcome after trauma.     

The influence of trauma,Dextran 1000, and Dextran 40 on the lodgement of circulating tumor cells

Summary Earlier studies have shown that trauma and infusion of Dextran 1000 increased the formation of pulmonary metastases after i.v. tumor cell injection in rats. Infusion of Dextran 40 enhanced the pulmonary metastasis formation in traumatized but not in non-traumatized animals. In this study tumor cells labelled with a radioactive isotope were used to register the lodgement circulating tumor cells after trauma and infusion of Dextran 1000 and Dextran 40. It was found that the pulmonary lodgement of tumor cells was increased after trauma and infusion of Dextran 1000. Dextran 40 did not influence the lodgement in a significant way either in normal or in traumatized animals. Thus, the increased formation of metastases after trauma and infusion of Dextran 1000 seems to depend upon an increased tumor cell lodgement.This study was supported by grants from the Göteborg Medical Society     

False aneurysm of left ventricle after nonpenetrating chest trauma (about one case)

Ischemic heart disease is the most common etiology of aneurysms of the left ventricle. The latter can also result from trauma. We report a case of a patient operated for false aneurysm of the left ventricle revealed by dyspnea and occurring six years after a nonpenetrating chest trauma. Follow-up after surgery was good with no complication occurring. In conclusion, this lesion must be considered in case of chest trauma and can be easily detected by echocardiography or CT scan.     

Post-traumatic pseudoaneurysm of the common hepatic artery with duodenal fistula

BackgroundPost-traumatic pseudoaneurysm of the hepatic artery is rare, especially after blunt abdominal trauma; an even more rare occurrence is enteric fistulisation.Case outlineA 29-year-old man was admitted with an acute episode of upper gastrointestinal bleeding three months after blunt abdominal trauma and was found to have an hepatic artery pseudoaneurysm with duodenal fistula. Surgical treatment was by ligature of the artery and duodenal closure with omental patch.DiscussionThere is one previous case report of hepatic artery pseudoaneurysm as a delayed complication of blunt abdominal trauma. The presence of a haematoma in the hepatoduodenal ligament after blunt trauma should raise the suspicion of hepatic artery injury, and surgical exploration may prevent the subsequent development of pseudoaneurysm. CT scan has become an important instrument both in diagnosis and in surgical planning.     

Rupture of a hepatic adenoma in a young woman after an abdominal trauma: A case report

Unlike hepatic haemorrhage following blunt abdominal trauma, spontaneous abdomen bleeding is rare, even in the presence of a hepatocellular adenoma (HA) or carcinoma. However, the diagnosis of a tumour underlying a haematoma after liver trauma is unusual, especially when it occurs more after two years after the accident. Here, we report a case of a ruptured HA due to blunt abdominal trauma. A 36-year-old woman was admitted to our hospital with sudden onset of upper abdominal pain. Her medical history revealed a blunt abdominal trauma two years prior. Initial abdominal computed tomography scan revealed a large haematoma measuring more than 16 cm in diameter in the right lobe of the liver. Magnetic resonance imaging showed haemorrhagic areas and some regions with hepatocyte hyperplasia, suggesting HA. The patient underwent right hepatic lobectomy, and a histopathological examination confirmed a diagnosis of HA. In conclusion, it is important to consider that abdominal trauma may hide old, asymptomatic and not previously detected injuries, as in the case reported.     

Post-traumatic stress disorder: medicine and politics

Regrettably, exposure to trauma is common worldwide, and can have serious adverse psychological results. The introduction of the notion of post-traumatic stress disorder has led to increasing medicalisation of the problem. This awareness has helped popular acceptance of the reality of post-traumatic psychiatric sequelae, which has boosted research into the pathogenesis of the disorder, leading to improved pharmacological and psychological management. The subjective experience of trauma and subsequent expression of symptoms vary considerably over space and time, and we emphasise that not all psychological distress or psychiatric disorders after trauma should be termed post-traumatic stress disorder. There are limits to the medicalisation of distress and there is value in focusing on adaptive coping during and after traumas. Striking a balance between a focus on heroism and resilience versus victimhood and pathological change is a crucial and constant issue after trauma for both clinicians and society. In this Review we discuss the advantages and disadvantages of medicalising trauma response, using examples from South Africa, the Armed Services, and post-disaster, to draw attention to our argument.     

晚期糖基化终产物引起老年小鼠创伤后继发心脏损伤加重的机制研究

目的 探讨衰老个体创伤后心肌损伤加重的机制,尤其是晚期糖基化终产物（AGEs）在其中发挥的作用。方法 C57雄性小鼠使用Noble-Collip创伤仪制备小鼠创伤模型。将成年C57小鼠（2月龄18只）和老年C57小鼠（20月龄18只）随机分为:非创伤组、创伤组、创伤干预组。采用彩色多普勒超声诊断仪检测左室射血分数(EF)和左室短轴缩短率(FS)。取心肌组织予Western blot检测磷酸化的AMP蛋白激酶（pAMPK）、AMP蛋白激酶（AMPK）、p16和p53 蛋白表达水平,使用ELISA 试剂盒检测血清可溶性晚期糖基化终产物受体（sRAGE）和羧甲基赖氨酸（CML）的水平。结果 与成年创伤小鼠对比,老年小鼠创伤后心肌损伤明显加重,表现为左室EF和左室FS显著减低（均P<0.01）。血MG-AGEs显著升高（P<0.05）以及AMPK活性下降（P<0.05）。预先采用sRAGE对AGEs进行干预,可显著改善老年小鼠创伤后心功能,表现为心肌AMPK活性显著提高（P<0.01）,心脏功能EF和FS值显著提高（P<0.01）。结论 衰老个体创伤后心肌损伤加重的机制与MG-AGEs系统有关,该系统可能是提高老年个体临床救治的有效靶点之一。     

Female urethral injury secondary to blunt pelvic trauma

Urethral injury after blunt pelvic trauma is rare in women. We report a case of urethral injury and vaginal laceration secondary to blunt pelvic trauma. Pelvic examination should be performed in any female patient who has sustained blunt pelvic trauma to avoid the morbidity associated with delayed diagnosis of urethral injury.