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Blunt traumatic aortic injury (BTAI) patients are severely ill, with high mortality and morbidity. As 60% of BTAIs occur in the distal arch, left subclavian artery (LSCA) management is determined without knowing posterior cerebral or left arm circulation in emergent cases. Because we perform thoracic endovascular aortic repair (TEVAR) + debranching technique for thoracic BTAI, we assessed efficacy and safety of debranching TEVAR in BTAI patients. We retrospectively reviewed vital signs on arrival, injury mechanism, characteristics, clinical time-series, concomitant injuries, injury description, operative procedures, and results from patient records. We excluded patients in cardiopulmonary arrest on arrival. From April 2014 to December 2018, nine of 25 patients admitted with BTAI underwent TEVAR. Median Injury Severity Score was 34 (29–34) and probability of survival was 0.82 (0.16–0.94). Society for Vascular Surgery BTAI injury grade was III or IV in all patients. Three patients underwent simple TEVAR and six underwent debranching TEVAR (LSCA occlusion + left common carotid artery to LSCA bypass). Median operation time was 108 (75–157) min for simple TEVAR and 177 (112–218) min for debranching TEVAR. Concomitant injuries included intracranial hemorrhage (N = 1), intra-abdominal injuries (N = 3), pneumo- or hemothoraxes (N = 4) and pelvic/extremities fractures (N = 7). Only one complication of left-hand claudication occurred postoperatively in a patient with simple TEVAR with LSCA occlusion. Despite debranching TEVAR taking approximately 60 min longer than simple TEVAR, short-term results indicated it to be acceptable for BTAI in multiple trauma patients to avoid LSCA complications unless we fail to stop bleeding first.

Background When resuscitating patients with hemorrhagic shock following trauma, fluid volume restriction and permissive hypotension prior to bleeding control are emphasized along with the good outcome especially for penetrating trauma patients. However, evidence that these concepts apply well to the management of blunt trauma is lacking, and their use in blunt trauma remains controversial. This study aimed to assess the impact of vasopressor use in patients with blunt trauma in severe hemorrhagic shock. Methods In this single-center retrospective study, we reviewed records of blunt trauma patients with hemorrhagic shock and included patients with a probability of survival Results Forty patients admitted from April 2014 to September 2019 were included. Median Injury Severity Score in survivors vs non-survivors was 41 (36–48) vs 45 (34–51) (p = 0.48), with no significant difference in probability of survival between the two groups (0.22 [0.12–0.48] vs 0.21 [0.08–0.46]; p = 0.93). Despite no significant difference in patient characteristics and injury severity, non-survivors were administered vasopressors significantly earlier after admission and at significantly higher doses. Total blood transfusion amount administered within 24 h after admission was significantly higher in survivors (8430 [5680–9320] vs 6540 [4550–7880] mL; p = 0.03). Max catecholamine index was significantly higher in non-survivors (2 [0–4] vs 14 [10–18]; p = 0.008), and administered vasopressors were terminated significantly earlier (12 [4–26] vs 34 [10–74] hours; p = 0.026) in survivors. Although the variables of severity of the patients had no significant differences, vasopressor use (Odds ratio [OR] = 21.32, 95% confident interval [CI]: 3.71–121.6; p = 0.0001) and its early administration (OR = 10.56, 95%CI: 1.90–58.5; p = 0.005) indicated significant higher risk of death in this study. Conclusion Vasopressor administration and high-dose use for resuscitation of hemorrhagic shock following severe blunt trauma are potentially associated with increased mortality. Although the transfused volume of blood products tends to be increased when resuscitating these patients, early termination of vasopressor had better to be considered.

Background Mobile intra-aortic thrombus without atherosclerosis, aneurysm, or congenital coagulopathy is very rare, and there are few reports especially in young or middle-aged patients. Furthermore, there are presently no established guidelines or common strategies for the treatment of mobile intra-aortic thrombus. In this case report, we describe the first case of intra-aortic thrombus caused by secondary erythrocytosis and describe the recommended treatment strategy for intra-aortic thrombus. Case presentation We report a case of an independent 40-year-old Asian man with a current history of heavy cigarette smoking who had sudden onset of abdominal and lumbar pain. Contrast-enhanced computed tomography revealed partial renal and splenic infarction, and he was transferred to our hospital. He also had a large mural thrombus in his thoracoabdominal aorta. Blood analysis on admission showed a hemoglobin level of 19.4 g/dL and hematocrit of 54.3 %; his international normalized ratio of prothrombin time, fibrin degradation products, and activated partial thromboplastin time levels were 1.02, 2.8 μg/ml, and 26.9 seconds respectively. We could find no abnormalities in protein C and protein S activity levels. Lupus anticoagulant and anti-cardiolipin antibody were both negative. He had no past medical history of arrhythmia and we found no signs of an arrhythmic event during admission. We promptly started anticoagulant therapy, but as the thrombus seemed at high risk of causing further critical infarction, we performed emergency aortic thrombectomy using partial extracorporeal circulation. To prevent dissemination of the thrombus during extracorporeal circulation, we first clamped his proximal and distal aorta on either side of the thrombus just before initiating extracorporeal circulation. After the aortotomy we removed a 14-cm length of intra-aortic thrombus without residual lesion. He was discharged from our hospital 20 days after surgery. From the results of his blood analysis, we considered the only cause of this thrombus was secondary erythrocytosis, which was probably induced by his current heavy cigarette smoking. Conclusion We are the first to report such a thrombosis caused by secondary erythrocytosis and conclude that once the diagnosis of intra-aortic thrombus with systemic embolism is clear, emergency surgical removal of such a thrombus must be considered to prevent further embolic complications.

Purpose: Effective hepatic blood flow (EHBF) is thought to reflect splanchnic perfusion and the metabolic state of the liver. This study was conducted to examine the relationship between cardiac output (CO) and EHBF using pulse dye-densitometry (PDD) in nonseptic and septic patients, and to assess the prognostic value of this relationship. Methods: The subjects were 33 critically ill patients, 16 of whom met the criteria for sepsis. Indocyanine green (ICG) was given via a central venous catheter to each patient. CO (l/min) and EHBF (l/min) were assessed with PDD. Results: CO and EHBF were significantly correlated in the nonseptic patients (r = 0.92, P < 0.001), but not in the septic patients (r = 0.38, P = 0.15). The ratio of EHBF to CO (EHBF/CO) in the septic patients was significantly lower than that in the nonseptic patients (0.08 ± 0.04 vs 0.22 ± 0.05; P < 0.001). Moreover, in the septic patients, the EHBF/CO ratios of nonsurvivors were significantly lower than those of survivors (0.06 ± 0.04 vs 010 ± 0.02; P < 0.01). Conclusions: In nonseptic patients, the EHBF decreased in relation to the CO. However, the EHBF/CO ratio of septic patients was lower than that of nonseptic patients, suggesting that inadequate splanchnic perfusion or metabolic change occurs in septic patients. Furthermore, the lower EHBF/CO ratio was related with a fatal outcome in septic patients. PDD could be a clinically useful method of assessing splanchnic conditions in critically ill patients.

Although the suppressive effect of 3-hydroxybutyrate (3-OHB) on post-traumatic protein catabolism in traumatized patients is well documented, the oxidation of exogenously administered 3-OHB during catabolic stress has not been investigated. The present study was designed to evaluate, using radioactive isotopes, total body oxidation in rats with and without burn stress to which 3-OHB had been exogenously administered, in comparison with total body oxidation in such rats that had received glucose. The rats were divided into four groups, based on whether or not a 30% full-thickness burn was inflicted, and the type of infusate they received after the burn, namely, 3-OHB or glucose. The total exhaled CO2 was collected for 6h after the infusion was commenced, and 14CO2 was assayed in a liquid scintillation spectrometer. Oxidation of the infusate was calculated from the percentage of exhaled 14CO2 derived from the infused substrates. The plasma concentration of 3-OHB was significantly increased after the infusion in both the burned and non-burned rats. The total exhaled 14CO2 from the rats infused with glucose decreased from 48.2 +/- 2.4% to 40.8 +/- 3.7% (means +/- SD, P0.001) after thermal injury. However, the total exhaled 14CO2 from the rats infused with 3-OHB appeared sooner, and there was no difference in the total expired 14CO2 derived from 3-OHB between the burned and non-burned rats, at 68.1 +/- 2.7% vs 66.4 +/- 3.4%, respectively. These findings suggest that even under conditions of burn stress, 3-OHB can be oxidized normally if the plasma concentration of 3-OHB is elevated by exogenous administration.