Short-term outcomes of robotic-assisted transthoracic diaphragmatic plication.

Background: Patients who are symptomatic from diaphragmatic dysfunction may benefit from diaphragmatic plication. We recently modified our plication approach from open thoracotomy to robotic transthoracic. We report our short-term outcomes. Methods: We conducted a single-institution retrospective review of all patients who underwent transthoracic plications from 2018, when we began using the robotic approach, to 2022. The primary outcome was short-term recurrence of diaphragm elevation with symptoms noted before or during the first planned postoperative visit. We also compared proportions of short-term recurrences in patients that underwent plication with extracorporeal knot-tying device alone versus those that used intracorporeal instrument tying (alone or supplemental). Secondary outcomes included subjective postoperative improvement of dyspnea at follow-up visit and by postoperative patient questionnaire, chest tube duration, length of stay (LOS), 30-day readmission, operative time, estimated blood loss (EBL), intraoperative complications, and perioperative complications. Results: Forty-one patients underwent robotic-assisted transthoracic plication. Four patients experienced recurrent diaphragm elevation with symptoms before or during their first routine postoperative visit, occurring on POD 6, 10, 37, and 38. All four recurrences occurred in patients whose plications were performed with the extracorporeal knot-tying device without supplemental intracorporeal instrument tying. Proportion of recurrences in the group that used extracorporeal knot-tying device alone was significantly greater than the recurrences in the group that used intracorporeal instrument tying (alone or supplemental) (P=0.016). The majority (36/41) reported clinical improvement postoperatively and 85% of questionnaire respondents also agreed they would recommend the surgery to others with similar condition. The median LOS and of chest tube duration were 3 days and 2 days, respectively. There were two patients with 30-day readmissions. Three patients developed postoperative pleural effusion necessitating thoracenteses and 8 patients (20%) had postoperative complications. No mortalities were observed. Conclusions: While our study shows the overall acceptable safety and favorable outcomes in patients undergoing robotic-assisted transthoracic diaphragmatic plications, the incidence of short-term recurrences and its association with the use of extracorporeally knot-tying device alone in diaphragm plication warrant further investigation.

No intravenous access, no problem: Intraosseous administration of tranexamic acid is as effective as intravenous in a porcine hemorrhage model.

BACKGROUND: The acute coagulopathy of trauma is often accompanied by hyperfibrinolysis. Tranexamic acid (TXA) can reverse this phenomenon, and, when given early, decreases mortality from bleeding. Establishing intravenous (IV) access can be difficult in trauma and intraosseous (IO) access is often preferred for drug administration. Currently, there are no data on the efficacy of IO administered TXA. Our objectives were to compare serum concentrations of TXA when given IV and IO and to compare the efficacy of IO administered TXA to IV at reversing hyperfibrinolysis. METHODS: Using a porcine hemorrhage and ischemia-reperfusion model, 18 swine underwent hemorrhagic shock followed by a tissue plasminogen activator infusion to induce hyperfibrinolysis. Animals then received an IV or tibial IO infusion of TXA over 10 minutes. Blood was then analyzed using rotational thromboelastometry to monitor reversal of hyperfibrinolysis. Serum was analyzed for drug concentrations. RESULTS: After hemorrhage and ischemia-reperfusion, there were no significant differences in mean arterial pressure (48 vs. 49.5), lactate (11.1 vs. 10.8), and pH (7.20 vs. 7.22) between groups. Intraosseous TXA corrected the lysis index at 30 minutes in EX-TEM and IN-TEM, like IV infusion. Peak serum levels of TXA after IV and IO administration show concentrations of 160.9 µg/mL and 132.57 µg/mL respectively (p = 0.053). Peak levels occurred at the completion of infusion. Drug levels were tracked for four hours. At the end of monitoring, plasma concentrations of TXA were equivalent. CONCLUSION: Intraosseous administration of TXA is as effective as IV in reversing hyperfibrinolysis in a porcine model of hemorrhagic shock. Intraosseous administration was associated with a similar peak levels, pharmacokinetics, and clearance. Intraosseous administration of TXA can be considered in hemorrhagic shock when IV access cannot be established.

Impact of a novel phosphoinositol-3 kinase inhibitor in preventing mitochondrial DNA damage and damage-associated molecular pattern accumulation: Results from the Biochronicity Project.

BACKGROUND: Despite improvements in the management of severely injured patients, development of multiple organ dysfunction syndrome (MODS) remains a morbid complication of traumatic shock. One of the key attributes of MODS is a profound bioenergetics crisis, for which the mediators and mechanisms are poorly understood. We hypothesized that metabolic uncoupling using an experimental phosphoinositol-3 kinase (PI3-K) inhibitor, LY294002 (LY), may prevent mitochondrial abnormalities that lead to the generation of mitochondrial DNA (mtDNA) damage and the release of mtDNA damage-associated molecular patterns (DAMPs). METHODS: Sixteen swine were studied using LY, a nonselective PI3-K inhibitor. Animals were assigned to trauma only (TO, n = 3), LY drug only (LYO, n = 3), and experimental (n = 10), trauma + drug (LY + T) groups. Both trauma groups underwent laparotomy, 35% hemorrhage, severe ischemia-reperfusion injury, and protocolized resuscitation. A battery of hemodynamic, laboratory, histological, and bioenergetics parameters were monitored. Mitochondrial DNA damage was determined in lung, liver, and kidney using Southern blot analyses, whereas plasma mtDNA DAMP analysis used polymerase chain reaction amplification of a 200-bp sequence of the mtDNA D-loop region. RESULTS: Relative to control animals, H + I/R (hemorrhage and ischemia/reperfusion) produced severe, time-dependent decrements in hepatic, renal, cardiovascular, and pulmonary function accompanied by severe acidosis and lactate accumulation indicative of bioenergetics insufficiency. The H-I/R animals displayed prominent oxidative mtDNA damage in all organs studied, with the most prominent damage in the liver. Mitochondrial DNA damage was accompanied by accumulation of mtDNA DAMPs in plasma. Pretreatment of H + I/R animals with LY resulted in profound metabolic suppression, with approximately 50% decreases in O2 consumption and CO2 production. In addition, it prevented organ and bioenergetics dysfunction and was associated with a significant decrease in plasma mtDNA DAMPs to the levels of control animals. CONCLUSIONS: These findings show that H + I/R injury in anesthetized swine is accompanied by MODS and by significant mitochondrial bioenergetics dysfunction, including oxidative mtDNA damage and accumulation in plasma of mtDNA DAMPs. Suppression of these changes with the PI3-K inhibitor LY indicates that pharmacologically induced metabolic uncoupling may comprise a new pharmacologic strategy to prevent mtDNA damage and DAMP release and prevent or treat trauma-related MODS. LEVEL OF EVIDENCE: Therapeutic study, level III.

Resuscitative endovascular balloon occlusion of the aorta for major abdominal venous injury in a porcine hemorrhagic shock model.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a rescue maneuver for unstable patients with noncompressible hemorrhage below the diaphragm. The efficacy of REBOA in the setting a major abdominal venous injury is unknown. Our objective was to examine the use of REBOA in a large animal model of major abdominal venous injury and characterize any impact on the hemodynamics, rate and volume of hemorrhage, and survival. METHODS: Ten swine (35-55 kg) underwent a controlled and validated hemorrhage and ischemia/reperfusion injury protocol to produce shock physiology. Animals were randomly assigned to a control arm (N = 5) or a treatment (REBOA) arm (N = 5). An injury was then created in the common iliac vein. Bleeding was allowed for 60 seconds and the balloon was then inflated in the REBOA arm. Hemodynamics were recorded for 45 minutes or until death. Blood loss was verified post-mortem and bleeding rate calculated. RESULTS: All animals demonstrated shock physiology at the time of randomization. There were no differences between control versus REBOA animals in baseline mean arterial pressure (42 vs. 50), pH (7.29 vs. 7.26), lactate (6.19 vs. 6.26), or INR (1.2 vs. 1.3, all p = NS). REBOA animals demonstrated immediate improvements in mean arterial pressure (50.6 vs. 97.2, p = 0.04). The mean survival time was 4.1 minutes for controls (100% died) versus 40.1 minutes for REBOA (p < 0.01). There was no difference in total blood loss (mean 630 mL for both). The rate of bleeding was significantly lower in the REBOA animals (control 197 mL/min vs. REBOA 14 mL/min, p = 0.02). CONCLUSION: In the setting of an abdominal venous injury, REBOA improved hemodynamics and lengthened survival time. Blood loss was similar between groups but the rate of bleeding was markedly decreased with REBOA. REBOA appears effective for central venous injuries and provides a sustained period of stabilization and window for surgical intervention.