Aims: Pharmacological modulation of skeletal muscle reperfusion injury after trauma associated ischaemia may improve limb salvage rates and prevent the associated systemic sequelae. Resuscitation with hypertonic saline restores the circulating volume and has favourable effects on tissue perfusion and blood pressure. The purpose of our study was to evaluate the effects of hypertonic saline on skeletal muscle ischaemia reperfusion (I/R) injury and the associated endorgan injury. Methods: Adult male Sprague Dawley rats (n=24) were randomised into three groups: control group, I/R group treated with normal saline and I/R group treated with hypertonic saline. Bilateral hind-limb ischaemia was induced by rubber band application proximal to the level of the greater trochanters for 2.5 hours. Treatment groups received either normal saline or hypertonic saline prior to tourniquet release. Following twelve hours reperfusion, the tibialis anterior muscle was dissected and muscle function assessed electrophysiologically by electrical field stimulation. The animals were then sacrificed and skeletal muscle harvested for evaluation. Lung tissue was also harvested for measurement of wet-to-dry ratio, myeloperoxidase content and histological analysis. Results: Hypertonic saline significantly attenuated skeletal muscle reperfusion injury as shown by reduced twitch and tetanic contractions of the skeletal muscle (Table). There was also a significant reduction in lung injury as demonstrated by differences in wet-to-dry ratio, myeloperoxidase content and histological analysis. Conclusion: Resuscitation with hypertonic saline may have a protective role in attenuating skeletal muscle ischaemia reperfusion injury and its associated systemic sequelae

This study was undertaken to assess the contribution of fat embolism (FE) to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock and FE (HR/FE), resuscitated hemorrhagic shock, FE, and control. FE was induced via intramedullary femoral canal pressurization using a 1–1.5 ml bone cement injection. Only HR/FE animals displayed significant proinflammatory cytokine release as compared to controls. These findings suggest that the combination of resuscitated shock with FE initiates an inflammatory response, which may lead to the development of fat embolism syndrome.

The objective of this study was to assess the contribution of fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock.

Only the animals that underwent resuscitated shock and fat embolism displayed amplified BALF proinflammatory cytokine expression.

These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

Only HR/FE BALF IL-8 and MCP-1 levels were significantly higher than controls (0.72 ng/ml vs. 0.26ng/ ml, p=0.03; 18.3 ng/ml vs. 2.0 ng/ml, p=0.01, respectively).

Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Shock was induced via carotid bleeding for one-hour prior to resuscitation. For FE induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. Four hours later, postmortem bronchoalveolar lavage was performed through the right mainstem bronchus. Analyses of bronchoalveolar lavage fluid (BALF) of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were carried out in triplicate and blinded fashion using the ELISA technique.

Our findings suggest that FE by itself does not initiate inflammatory lung injury, as there were no apparent differences between the control and FE cytokine levels. Only the HR/FE animals revealed elevated levels of pro-inflammatory cytokines in BALF. These findings are in agreement with our previous results, which displayed neutrophil activation only in the HR/FE group.

This study was undertaken to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock and fat embolism, resuscitated hemorrhagic shock, fat embolism, and control. Fat embolism was induced via intramedullary cavity with a 1–1.5 ml bone cement injection. Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

The objective of this study was to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock.

Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration.

These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

CD11b mean channel florescence was only significantly elevated in the HR/FE group at two and four hours post knee manipulation. Moreover, greater infiltration of alveoli by leukocytes was only significantly higher in the HR/FE group as compared to controls.

Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Hypovolemic shock was induced via carotid bleeding for one-hour prior to resuscitation. For fat embolism induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. For evaluation of neutrophil activation, blood was stained with antibodies against CD45 and CD11b and analyzed with a flow cytometer. Animals were mechanically ventilated for four hours post surgical closure. Postmortem thoracotomy was performed, and three stratified random blocks of each lung were processed for histological examination.

Our findings suggest that FE by itself does not cause lung injury, as there were no apparent differences between the control and FE animals. Only the HR/FE animals revealed a higher number of infiltrating neutrophils into alveolar spaces and greater neutrophil activation.

Purpose. In patients with multiple trauma delayed fracture healing is often diagnosed, but the pathomechanisms are not well known yet. The purpose of the study is to evaluate the effect of a severe hemorrhagic shock on fracture healing in a murine model. Methods. 10 male C57BL/6N mice per group (Fx, TH, THFx, Sham) and point in time were used. The Fx-group received an osteotomy after implantation of a fixateur extern. The TH-group got a pressure controlled hemorrhagic shock with a mean arterial blood pressure of 35 mmHg over 90 minutes. Resuscitation with 4 times the shed blood volume of Ringer solution was performed. The THFx group got both. Sham-animals received the implantation of a catheter and a fixateur extern but no blood loss or osteotomy. After 1, 2, 3, 4 or 6 weeks the animals were sacrificed. For the biomechanics the bones were analyzed via X-ray, µCT and underwent a 3-point bending test. The nondecalcified histology based on slices of Technovit 9100. The signaling pathway was analyzed via RT. 2. Profiler™ PCR Array Mouse Osteoporosis, Western Blot and Quantikine ELISA for RankL and OPG. Statistical significance was set at p < 0.05. Comparisons between groups were performed using the Mann–Whitney U (Fx vs. THFx) or Kruskal-Wallis Test (other groups). Results. The experiment showed that after 1 week the bones of the Fx- and THFx-mice were macroscopically instable. After 2 weeks the Fx-group showed macroscopically a stable bridging whereas the bones of the THFx-group were partly not stable bridged. 3 weeks after surgery the bones of both groups were stable bridged. Analysis via µCT showed that trauma hemorrhage leads to decreased density of the bone and callus and also to increased share of callus per bone volume after 2 weeks. The 3-point-bending test showed that the maximum bending moment is decreased in the group THFx compared to Fx after 2 weeks. The studies of the histology showed after 2 weeks a decrease in bone and cartilage after trauma-hemorrhage by optical analysis of photographs of the slices. The analyses of the signaling pathway pointed to an involvement of the RankL/Opg and IL6 pathway. Conclusion. A hemorrhagic shock has a negative effect on fracture healing in terms of reduced density of the bone and callus, increased share of callus per bone volume, decreased maximum bending moment, reduced mineralization of the callus and leads to changes in the RankL/Opg and IL6 pathways

The beneficial effects of therapeutic hypothermia have been capitalised upon in fields such as cardiac surgery for several decades. Hypothermia not only slows metabolism and consumption of metabolic substrates, but also confers cellular protection against ischaemia and reperfusion. Hypothermia has historically been considered as something to avoid in trauma casualties, with coagulopathy being the main concern. There is now increasing evidence for the role of controlled therapeutic hypothermia in trauma, particularly improved functional outcomes following brain injury and the utility of ‘suspended animation’ or ‘emergency preservation’ in the resuscitation of severe haemorrhagic shock. With the ongoing ‘Eurotherm’ trial of hypothermia in the treatment of traumatic brain injury, and the imminent launch of the ‘Emergency Preservation and Resuscitation (EPR) for Cardiac Arrest From Trauma’ clinical trial in the USA, this presentation will provide a timely overview of the developments of therapeutic hypothermia in trauma management

Resuscitation decisions are part of routine practice and raise difficult, sensitive issues. We present experience of Do-Not-Attempt-Resuscitation (DNAR) decision-making in our unit. Patients and staff (medical, nursing) completed a questionnaire to ascertain current practice, knowledge, and patient feeling regarding DNAR decisions. Consultants and Registrars make DNAR decisions, junior-doctors and nurses feel they have insufficient knowledge. Senior-doctors were most familiar with BMA and Trust guidelines. The majority of all staff felt every patient should be asked. Consultants thought DNAR decision-making was least necessary. Half of patients felt doctors had not explained the necessity of DNAR decisions and half felt conversations could have been handled better. Half said they had not been asked their opinion. Two-thirds would like more visual information. UK-wide figures show 15% survival to discharge of in-hospital arrest; a-third of medical staff knew this. Registrars were most optimistic and consultants and ward doctors most pessimistic. All patients believed survival rate was 50%. Important DNAR decisions are based on poor knowledge and communication. We developed an education programme for staff and information-video for patients and relatives to improve service. Video for DNAR discussions has not been previously used; it will provide a framework on which to approach this sensitive issue

Objectives

Local corticosteroid infiltration is a common practice of treatment for lateral epicondylitis. In recent studies no statistically significant or clinically relevant results in favour of corticosteroid injections were found. The injection of autologous blood has been reported to be effective for both intermediate and long-term outcomes. It is hypothesised that blood contains growth factors, which induce the healing cascade.