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BACKGROUND: In major trauma patients, hypocalcemia is associated with increased mortality. Despite the absence of strong evidence on causality, early calcium supplementation has been recommended. This study investigates whether calcium supplementation during trauma resuscitation provides a survival benefit. METHODS: We conducted a retrospective analysis using data from the TraumaRegister DGU® (2015-2019), applying propensity score matching to balance demographics, injury severity, and management between major trauma patients with and without calcium supplementation. 6 h mortality, 24 h mortality, and in-hospital mortality were considered as primary outcome parameters. RESULTS: Within a cohort of 28,323 directly admitted adult major trauma patients at a European trauma center, 1593 (5.6%) received calcium supplementation. Using multivariable logistic regression to generate propensity scores, two comparable groups of 1447 patients could be matched. No significant difference in early mortality (6 h and 24 h) was observed, while in-hospital mortality appeared higher in those with calcium supplementation (28.3% vs. 24.5%, P = 0.020), although this was not significant when adjusted for predicted mortality (P = 0.244). CONCLUSION: In this matched cohort, no evidence was found for or against a survival benefit from calcium supplementation during trauma resuscitation. Further research should focus on understanding the dynamics and kinetics of ionized calcium levels in major trauma patients and identify if specific conditions or subgroups could benefit from calcium supplementation.

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BACKGROUND: To which extent trauma- induced disturbances in ionized calcium (iCa2+) levels have a linear relationship with adverse outcomes remains controversial. The goal of this study was to determine the association between the distribution and accompanying characteristics of transfusion-independent iCa2+ levels versus outcome in a large cohort of major trauma patients upon arrival at the emergency department. METHODS: A retrospective observational analysis of the TraumaRegister DGU® (2015-2019) was performed. Adult major trauma patients with direct admission to a European trauma centre were selected as the study cohort. Mortality at 6 h and 24 h, in-hospital mortality, coagulopathy, and need for transfusion were considered as relevant outcome parameters. The distribution of iCa2+ levels upon arrival at the emergency department was calculated in relation to these outcome parameters. Multivariable logistic regression analysis was performed to determine independent associations. RESULTS: In the TraumaRegister DGU® 30 183 adult major trauma patients were found eligible for inclusion. iCa2+ disturbances affected 16.4% of patients, with hypocalcemia (< 1.10 mmol/l) being more frequent (13.2%) compared to hypercalcemia (≥ 1.30 mmol/l, 3.2%). Patients with hypo- and hypercalcemia were both more likely (P < .001) to have severe injury, shock, acidosis, coagulopathy, transfusion requirement, and haemorrhage as cause of death. Moreover, both groups had significant lower survival rates. All these findings were most distinct in hypercalcemic patients. When adjusting for potential confounders, mortality at 6 h was independently associated with iCa2+ < 0.90 mmol/L (OR 2.69, 95% CI 1.67-4.34; P < .001), iCa2+ 1.30-1.39 mmol/L (OR 1.56, 95% CI 1.04-2.32, P = 0.030), and iCa2+ ≥ 1.40 mmol/L (OR 2.87, 95% CI 1.57-5.26; P < .001). Moreover, an independent relationship was determined for iCa2+ 1.00-1.09 mmol/L with mortality at 24 h (OR 1.25, 95% CI 1.05-1.48; P = .0011), and with in-hospital mortality (OR 1.29, 95% CI 1.13-1.47; P < .001). Both hypocalcemia < 1.10 mmol/L and hypercalcemia ≥ 1.30 mmol/L had an independent association with coagulopathy and transfusion. CONCLUSIONS: Transfusion-independent iCa2+ levels in major trauma patients upon arrival at the emergency department have a parabolic relationship with coagulopathy, need for transfusion, and mortality. Further research is needed to confirm whether iCa2+ levels change dynamically and are more a reflection of severity of injury and accompanying physiological derangements, rather than an individual parameter that needs to be corrected as such.

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BACKGROUND: Up to 25% of trauma deaths are related to thoracic injuries. OBJECTIVE: The primary goal was to analyse the incidence and time distribution of death in adult patients with major thoracic injuries. The secondary goal was to determine if potentially preventable deaths occurred within this time distribution and, if so, identify an associated therapeutic window. DESIGN: Retrospective observational analysis. SETTING: TraumaRegister DGU. PATIENTS: Major thoracic injury was defined as an Abbreviated Injury Scale (AIS) 3 or greater. Patients with severe head injury (AIS ≥ 4) or injuries to other body regions with AIS being greater than the thoracic injury (AIS other >AIS thorax) were excluded to ensure that the most severe injury described was primarily thoracic related. MAIN OUTCOME MEASURES: Incidence and time distribution of mortality were considered the primary outcome measures. Patient and clinical characteristics and resuscitative interventions were analysed in relation to the time distribution of death. RESULTS: Among adult major trauma cases with direct admission from the accident scene, 45% had thoracic injuries and overall mortality was 9.3%. In those with major thoracic trauma ( n  = 24 332) mortality was 5.9% ( n  = 1437). About 25% of these deaths occurred within the first hour after admission and 48% within the first day. No peak in late mortality was seen. The highest incidences of hypoxia and shock were seen in non-survivors with immediate death within 1 h and early death (1 to 6 h). These groups received the largest number of resuscitative interventions. Haemorrhage was the leading cause of death in these groups, whereas organ failure was the leading cause of death amongst those who survived the first 6 h after admission. CONCLUSION: About half of adult major trauma cases had thoracic injuries. In non-survivors with primarily major thoracic trauma, most deaths occurred immediately (<1h) or within the first 6 h after injury. Further research should analyse if improvements in trauma resuscitation performed within this time frame will reduce preventable deaths. TRIAL REGISTRATION: The present study is reported within the publication guidelines of the TraumaRegister DGU® and registered as TR-DGU project ID 2020-022.

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OBJECTIVE: The present study aimed to determine the difference in force required to puncture simulated pleura comparing Kelly clamps to fine artery forceps. The treatment of symptomatic traumatic pneumothorax and haemothorax involves puncture of the parietal pleura to allow decompression. This is usually performed using Kelly clamps or fine artery forceps. Over-puncture pulmonary injury risk increases with the force used. METHODS: An experienced single operator performed puncturing of simulated parietal pleura on a thoracic mannequin while wearing a force sensor under gloves. The force imparted at the device tip onto the parietal pleura was estimated by subtracting the force required to hold the device from the total force. Outcome variables were the total maximum force and force imparted by the device. RESULTS: There were 11 simulated procedures completed, seven using Kelly clamps and four using fine artery forceps. After subtracting the force required to hold the chosen forceps, the median value of pleural puncture force using Kelly clamps was 52.91 N (IQR 36.68-63.56) and 10.70 N (IQR 7.64-26.56) using fine artery forceps (P = 0.006). CONCLUSION: A significantly increased force was required to puncture simulated parietal pleura using Kelly clamps compared to fine artery forceps. This higher puncture force will be associated with increased instrument acceleration at the time of pleural puncture, which may result in an increased risk of injury to the underlying lung. Based on these data, clinicians may reduce the risk of pulmonary injury by using fine artery forceps rather than Kelly clamps when performing pleural decompression.

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Ricin is a highly toxic agent derived from the castor bean plant (Ricinus communis). Poisoning occurs commonly by oral ingestion of the beans. Injection of ricin is believed to be more lethal. Ricin is a large glycosylated protein difficult to detect in clinical samples. Instead, ricinine, a small alkaloid found in the same beans, is used as surrogate marker for ricin exposure. We describe a simple LC-MS/MS method for the detection of ricinine in serum, blood and urine, validated according to EMA guidelines and successfully applied to patient samples of a suicidal death after injection of a castor bean extract. A 26-year-old man self-presented to the emergency department with severe abdominal cramps and nausea after injection of a castor bean extract. Due to rapid deterioration of his hemodynamic function despite early aggressive fluid resuscitation, he was transferred to ICU. Abdominal cramps worsened and a fulminant diarrhea developed, resulting in hypovolemic shock and cardiorespiratory collapse. Despite full supportive therapy, the patient died approximately 10 hours after injection due to multiple organ failure. Ricinine was quantified by LC-MS/MS after LLE with diethyl ether using ricinine-D3 as internal standard. Six hours after injection, ricinine concentrations in serum and blood were 16.5 and 12.9 ng/mL, respectively, which decreased to 12.4 and 10.6 ng/mL, 4 hours later. The urinary concentration was 81.1 ng/mL 7 hours after injection, which amply exceeded the levels previously reported in similar cases with lethal outcome. Concentrations of ricinine, compatible with a lethal exposure to castor beans, were detected in serum, blood and urine. Ricinine was also found in bile and liver tissue.

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BACKGROUND AND OBJECTIVES: The transversus abdominis plane (TAP) block can be used as part of a multimodal analgesia protocol after abdominal surgery. This study investigated whether a pneumoperitoneum during abdominal surgery influences the spread of local anesthetics. METHODS: Nine fresh frozen cadavers were used for the study. Using an ultrasound-guided midaxillary technique, a unilateral TAP block-like injection with 20 mL of methylene blue dye was performed. After the injection, a pneumoperitoneum was immediately installed for 1 hour. After desufflation, this ipsilateral side was dissected, and a TAP block-like injection was performed on the contralateral side. One hour after injection, the contralateral side was also dissected. The anatomical dissection was used to determine the extent of dye spread and the nerves stained by the dye. RESULTS: In none of the specimens did the dye reach the posterior origin of the transverse abdominal muscle. There was no statistically significant difference in the number of stained nerves and spread of the dye in the insufflated side compared with the noninsufflated side. In 4 of 9 cadavers, we found a variant course of a nerve preventing staining of that nerve. CONCLUSIONS: The stretch of the abdominal wall caused by the insufflation of the abdomen does not influence the spread of dye in the abdominal wall. Because of the absence of posterior spread, regardless of the timing of a midaxillary ultrasound-guided approach, we believe that a posterior approach should be chosen if posterior spread is desired.

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