Unilateral Chest Trauma Research Articles

Buffalo chest in a not so high fall: a case report

Bufallo chest refers to an anatomical variation characterized by an ongoing connection between the two pleural spaces, a unique feature found in these animals, since they possess a single pleural space due to an incomplete mediastinum. When this condition is found in humans, a unilateral chest trauma can cause bilateral pneumothorax. We reported a case of a 91 year old male who, after a fall resulting in right ribs fractures, presented at the emergency department with an extensive bilateral pneumothorax. We described clinical and imagiological features and our approach. This case demonstrates an unusual presentation of a rare anatomical anomaly.

Predictors of Mortality in Patients with Isolated Chest Trauma

Background: Chest trauma remained an important type of trauma that carries the risk of morbidity and mortality. The Modified Early Warning Score [MEWS] is a unique score as it is a physiological and simple score which permits improvement in the patient management. The aim of the work: To assess frequency, risk factors of mortality and examine MEWS as a predictor of mortality in patients with isolated chest trauma. Patients and Methods: Prospective analysis of 157 patients presented to emergency department, with isolated chest trauma. Demographic data, MEWS, trauma characteristics, and laboratory data were recorded on admission. The patients received standard management and were followed up until discharge or death. Results: Age of patients ranged from 4 to 79 years. Male constituted 79.6%. About 29% admitted with penetrating chest trauma. About 98% and 82% presented within 24 hours and had unilateral chest trauma. MEWS of them ranged from 0 to 12. There is a significant relationship between mortality and hemoglobin levels, length of hospital stay and MEWS. There is a non-significant relationship between mortality and gender, type of trauma or duration of admission. Unilateral trauma indefinitely protects against mortality. MEWS [≥7] and length of hospital stay [≥4 days] increase mortality risk by 127.3 and 4.7 folds respectively. The cutoff of MEWS for prediction of mortality was ≥ 6.5, with sensitivity of 100%, specificity of 84.9%, [p <0.001]. Conclusion: High on-admission MEWS ≥7, late presentation after 24 hour and bilateral injury were risk factors of mortality in isolated chest trauma.

Erector spinae plane vs. paravertebral blockade for rib fracture analgesia

We would like to commend Adhikary et al. for their continued efforts to show benefit from novel regional techniques for chest trauma 1 and agree that patients with rib fracture(s) have significantly improved pain scores after regional analgesia. We would like to invite the authors to reply to a number of comments that we have about their work. Firstly, the authors make several comments about the technically challenging nature of paravertebral blockade. In our institution, ultrasound-guided thoracic paravertebral blockade is the regional technique of choice in unilateral chest trauma. Data from our experiences reveal an extremely low complication rate, with no significant complications from 314 paravertebral catheters over a 4-year period 1, inserted by consultant and registrar anaesthetists. This is consistent with our experience of thousands of single-shot blocks performed for breast surgery, and with similar experiences in other centres worldwide 2. We recognise that there is, undoubtedly, a learning curve associated with the paravertebral technique, but we believe this is similar in appearance to learning curves for any other new regional anaesthetic technique. Secondly, we note that only 79 patients were administered an erector spinae plane (ESP) block over 19 months. Can we ask whether there were other patients in the authors’ institution that received epidural or paravertebral blockade during this time, and whether comparative analysis has been possible? We are not aware of any published evidence that the ESP block is technically easier, and the results of any such analysis would be useful to know when organising training. Are there novices or non-anaesthetists performing the ESP block at the authors’ institution? Thirdly, the authors question the feasibility of paravertebral blockade in coagulopathy and haemodynamic instability. In our opinion, neither coagulopathy nor anticoagulation is a contra-indication to paravertebral techniques, necessarily. We assess each case individually, in line with the collaborative guideline from on regional anaesthesia techniques in patients with abnormalities of coagulation 3. This guideline classifies paravertebral block as ‘higher risk’ compared with more peripheral or superficial techniques, but provides no quantification of this risk, and does not reference any evidence documenting complications in patients with disorders of coagulation. Furthermore, we can find no case reports of spinal or epidural haematomas following ultrasound-guided paravertebral block performance. The practice of using curled catheters rather than straight in the paravertebral space further reduces the risk of accidental epidural placement. Our experience also reveals no associated haemodynamic instability following paravertebral blockade. Their analysis revealed a statistically significant increase in spirometry values, but such improvement would be expected normally over time, with or without regional anaesthesia. Are the authors confident about ascribing causality between the block and the spirometry improvement, given the 24-h gap between insertion and measurement? In our experience, spirometry improves very soon (within 30 min) after block insertion, and often improves further by the following day. We suggest that paravertebral block overcomes the variability in analgesia observed in the authors’ study, because it places local anaesthetic in close proximity to the target nerves, can be performed by a range of anaesthetist grades, is associated with minimal complications and side-effects, and performance of which is contra-indicated in very few patients. Regardless of the block choice however, we agree with the authors that good analgesia (under the aegis of a comprehensive pain service) remains critical in the successful management of rib fractures.

Characterization of blunt chest trauma in a long-term porcine model of severe multiple trauma.

Chest trauma has a significant relevance on outcome after severe trauma. Clinically, impaired lung function typically occurs within 72 hours after trauma. However, the underlying pathophysiological mechanisms are still not fully elucidated. Therefore, we aimed to establish an experimental long-term model to investigate physiological, morphologic and inflammatory changes, after severe trauma. Male pigs (sus scrofa) sustained severe trauma (including unilateral chest trauma, femur fracture, liver laceration and hemorrhagic shock). Additionally, non-injured animals served as sham controls. Chest trauma resulted in severe lung damage on both CT and histological analyses. Furthermore, severe inflammation with a systemic increase of IL-6 (p = 0.0305) and a local increase of IL-8 in BAL (p = 0.0009) was observed. The pO2/FiO2 ratio in trauma animals decreased over the observation period (p < 0.0001) but not in the sham group (p = 0.2967). Electrical Impedance Tomography (EIT) revealed differences between the traumatized and healthy lung (p < 0.0001). In conclusion, a clinically relevant, long-term model of blunt chest trauma with concomitant injuries has been developed. This reproducible model allows to examine local and systemic consequences of trauma and is valid for investigation of potential diagnostic or therapeutic options. In this context, EIT might represent a radiation-free method for bedside diagnostics.

Intrapleural versus epidural analgesia with local anesthetics in patients with thoracic trauma

This prospective, randomized and controlled study aimed to compare the efficacy of two methods for analgesia in patients with chest trauma and rib fractures: continuous epidural catheter analgesia and regional intrapleural analgesia (RIPA). Seventy-three patients with unilateral chest trauma were randomized into two groups. In Group 1 patients we placed an epidural catheter (level – TH 8–10), and in Group 2 patients we placed an intrapleural catheter (level – fifth intercostal space). We used 1% lidocain for analgesia in both groups. The control group received intravenous analgesia with opioid. We applied 10 ml lidocain bolus to the intrapleural catheter four to six times per 24 hours and clamped the catheter for 10 min. For epidural analgesia we applied 50–100 mg lidocain and started continuous infusion at a rate of 2–3 mg/kg/hour, not exceeding a dose 400 mg lidocain per 24 hours. We monitored the level of thermohipanesthesia, the level of analgesia (Visual Aanalogue Scale – 10 points), parameters of respiratory and cardiovascular function (respiratory rate, arterial O2 oxygen saturation [SaO2], heart rate, arterial blood pressure, central venous pressure, ability to expectorate). Thermohipanesthesia was unilateral and significantly shorter in Group 2 patients, whereas in Group 1 patients it was bilateral and of longer duration. The level of analgesia was similar in both groups (0–4 points) but in Group 2 patients it was achieved by more frequent applications of lidocain, which potentially is dangerous for toxicity. The respiratory rate decreased, O2 and SaO2 increased, and the ability to expectorate was improved. In Group 2 patients the heart rate and arterial blood pressure remained stable, and in Group 1 patients there were episodes of tachycardia and hypotension, which is undesirable in trauma patients. The technique of placing an intrapleural catheter is easier.

Macrophage cyclooxygenase expression, immunosuppression, and cardiopulmonary dysfunction after blunt chest trauma.

Two series of experiments were performed in swine who received severe blunt chest trauma. The goals were to determine the time course of constitutive and inducible cyclooxygenase (COX) isozyme expression in pulmonary macrophages (Mphis), and to determine whether COX expression and cardiopulmonary dysfunction were altered when neutrophils (PMNs) were pharmacologically depleted with cyclophosphamide (CYC). In series 1 (n = 17), anesthetized, mechanically ventilated swine were subjected to right chest trauma via captive bolt gun, hemorrhage, and a 60-minute shock period. In series 2 (n = 41), CYC (50 mg/kg intravenously) was administered 4 days before trauma, and the shock period was shortened to 30 minutes. In both series, hemodynamic support and supplemental oxygen were provided for an additional 60 to 90 minutes after shock. Mphis were isolated from serial bilateral bronchoalveolar lavages (BALs) and COX protein expression was measured with Western blots. In series 1, death occurred in 11 of 17. In survivors, Mphi COX-1 peaked at > 100 times baseline in both right BAL and left BAL by 60 minutes (before resuscitation). Changes in Mphi COX-2 were minimal. In series 2, before trauma, CYC (n = 16) reduced circulating and BAL PMNs by > 90% relative to control (n = 25, both p < 0.05) with no complicating side effects. After trauma, death occurred in 11 of 25 controls versus 9 of 16 with CYC. In survivors, PaO2/FIO2 was < 250 and PaCO2 was 25% higher on constant minute ventilation, indicating mismatched ventilation/perfusion; both changes were reduced with CYC (p < 0.05). In controls, bilateral histologic damage included edema, alveolar hemorrhage, and interstitial infiltrates. These changes were reduced by one third with CYC (p = 0.08). Trauma-induced changes in BAL protein, BAL elastase, or Mphi COX expression were not lessened by CYC. After unilateral chest trauma, Mphi COX-1, not COX-2, is induced bilaterally and before fluid resuscitation; CYC prevented PMN infiltration and attenuated structural and functional changes after resuscitation, which suggests that PMNs have a role in the pathogenic mechanism of secondary lung injury; Mphi COX expression and other injury markers were not altered by CYC; and since Mphis continued to express proinflammatory COX protein even after pretreatment with a powerful nonspecific immunosuppressant, and since there is residual alveolar capillary damage even in the absence of PMNs, it is logical to conclude that no single cell type or mediator is a practical therapeutic target and that novel resuscitation strategies must address multiple elements in the inflammatory cascade.

Differential ventilation with low-flow CPAP and CPPV in the treatment of unilateral chest trauma

A case of severe unilateral chest trauma with bronchopleural fistula is presented. Ventilatory therapy consisted of asynchronous independent lung ventilation (AILV). The injured lung was ventilated with intermittent positive pressure ventilation (IPPV) [tidal volume (TV) = 200 ml, f = 25/min, I:E = 0.5, minute volume (MV) = 5.0 l/min, FiO2 = 0.4], and the unaffected lung was ventilated with continuous positive pressure ventilation (CPPV) (TV = 600 ml, f = 12/min, I:E = 0.5, MV = 7.2 l/min, PEEP = 0.5 kPa, FiO2 = 0.4). Adequate gas exchange was obtained (PaO2 = 14.5 +/- 2.3 kPa, PaCO2 = 5.5 +/- 0.7 kPa), but high air leakage volumes persisted. Thus, differential low-flow CPAP (V = 5.0-7.5 l/min, PEEP = 0.5 kPa, FiO2 = 0.4) of the injured lung and CPPV (TV = 600 ml, f = 12/min, MV = 7.2 l/min, I:E = 0.5, PEEP = 0.5 kPa, FiO2 = 0.4) of the unaffected lung was applied for 36 hours. Further deterioration of pulmonary function was prevented, and the bronchopleural fistula closed after several hours. After another period of AILV the patient was treated with conventional mechanical ventilation, and finally weaned with high-flow CPAP.