High Versus Low Volume Fluid Resuscitation Strategies in a Porcine Model (Sus scrofa) of Combined Thermal and Traumatic Brain Injury.

BACKGROUND: Combined burn and traumatic brain injury (TBI) treatment priorities may not align due to opposing fluid resuscitation paradigms used in treating burns and TBI. We developed a porcine model of combined thermal injury/TBI and compared an "aggressive" fluid resuscitation strategy using the Parkland formula and a "restrictive" resuscitation strategy using the modified Brooke formula. METHODS: Twenty-eight swine were deeply anesthetized and received a 40% total body surface area full-thickness burn injury and TBI. Swine were then randomized to receive restrictive or aggressive resuscitation for 8 h after which time animals were euthanized and necropsy was performed. Volume of brain injury was assessed after analyzing segmental slices of brain tissue. RESULTS: There were no differences between the restrictive and aggressive resuscitation groups in blood pressure, heart rate, central venous pressure, intra-cranial pressure (ICP), or serum lactate levels after 8 h of resuscitation. Urine output was higher in the aggressive resuscitation group. The restrictive group had a significantly higher serum blood urea nitrogen (BUN) compared with baseline and compared with the aggressive group. There was no significant difference in size of brain injury between groups. CONCLUSIONS: Both restrictive and aggressive resuscitation demonstrated adequate resuscitation at 8 h postinjury. Increased serum BUN in the restrictive group may be an indicator of early acute kidney injury, despite adequate urine output. Resuscitation strategy did not appear to affect ICP or the size of brain injury.

Does the pediatric hemodynamic cliff exist in response to hemorrhagic shock?

BACKGROUND: The paradigm that children maintain normal blood pressure during hemorrhagic shock until 30%-45% hemorrhage is widely accepted. There are minimal data supporting when decompensation occurs and how a child's vasculature compensates up to that point. We aimed to observe the arterial response to hemorrhage and when mean arterial pressure (MAP) decreased from baseline in pediatric swine. METHODS: Piglets were hemorrhaged in 20% increments of their total blood volume to 60%. MAP and angiograms of the thoracic aorta (TA) and abdominal arteries were obtained. Percent change in area of the vessels from baseline was calculated. RESULTS: Piglets (n = 8) had a differential vasoconstriction starting at 20% hemorrhage (celiac artery 36.3% [31.4-44.6] vs TA 16.7% [10.7-19.1] p = 0.0012). At 40% hemorrhage, the differential vasoconstriction favored shunting blood away from the abdominal visceral branches to the TA (celiac artery 54.7% [36.9-60.6] vs TA 29.5% [23.9-36.2] p = 0.0056 superior mesenteric artery 46.7% [43.9-68.6] vs TA 29.5% [23.9-36.2] p = 0.0100). This was exacerbated at 60% hemorrhage. MAP decreased from baseline at 20% hemorrhage (66.4 ±â€¯6.0 mmHg vs 41.4 ±â€¯10.4 mmHg, p < 0.0001), and worsened at 40% and 60% hemorrhage. CONCLUSION: In piglets, a differential vasocontriction shunting blood proximally occurred in response to hemorrhage. This did not maintain normal MAP at 20%, 40% or 60% hemorrhage. LEVEL OF EVIDENCE: Level II.

Esmolol reduces myocardial injury induced by resuscitative endovascular balloon occlusion of the aorta (REBOA) in a porcine model of hemorrhagic shock.

PURPOSE: Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes myocardial injury from increased aortic afterload and supraphysiologic cardiac output. However, pharmacologic methods to attenuate high cardiac output and reduce myocardial injury have not been explored. We hypothesized that the use of esmolol during REBOA would reduce myocardial injury. METHODS: Ten pigs were anesthetized and instrumented. Following 25% total blood volume hemorrhage, animals underwent 45 min of supraceliac (zone 1) REBOA with or without titration of esmolol to maintain heart rate between 80 and 100 beats per minute. Following the REBOA interventions, animals underwent 275 min of standardized critical care. RESULTS: During REBOA, heart rate was significantly lower in the esmolol group compared to control animals (100 [88 - 112] vs 193 [172 - 203] beats/minute, respectively, p < 0.001) and the average mean arterial pressure (MAP) was lower in the esmolol group (88.0 [80.3-94.9] vs 135.1 [131.7-140.4] mmHg, respectively, p = 0.01). During the critical care phase, there were no differences in heart rate or MAP between groups. Animals in the intervention group received 237.9 [218.7-266.5] µg/kg of esmolol. There was a significant increase from baseline in serum troponins for the control group (p = 0.006) and significantly more subendocardial hemorrhage compared to animals treated with esmolol (3 [3 - 3] and 0 [0 - 0], p = 0.009, respectively). CONCLUSION: In our porcine model of hemorrhagic shock, zone 1 REBOA was associated with myocardial injury. Pharmacologic heart rate titration with esmolol during occlusion may mitigate the deleterious effects of REBOA on the heart.

Resuscitative endovascular balloon occlusion of the aorta in a pediatric swine model: Is 60 minutes too long?

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is recommended in adults with a noncompressible torso hemorrhage with occlusion times of less than 60 minutes. The tolerable duration in children is unknown. We used a pediatric swine controlled hemorrhage model to evaluate the physiologic effects of 30 minutes and 60 minutes of REBOA. METHODS: Pediatric swine weighing 20 kg to 30 kg underwent a splenectomy and a controlled 60% total blood volume hemorrhage over 30 minutes, followed by either zone 1 REBOA for 30 minutes (30R) or 60 minutes (60R). Swine were then resuscitated with shed blood and received critical care for 240 minutes. RESULTS: During critical care, the 30R group's (n = 3) pH, bicarbonate, base excess, and lactate were no different than baseline, while at the end of critical care, these variables continued to differ from baseline in the 60R group (n = 5) and were worsening (7.4 vs. 7.2, p < 0.001, 30.4 mmol/L vs. 18.4 mmol/L, p < 0.0001, 5.6 mmol/L vs. -8.5 mmol/L, p < 0.0001, 2.4 mmol/L vs. 5.7 mmol/L, p < 0.001, respectively). Compared with baseline, end creatinine and creatinine kinase were elevated in 60R swine (1.0 mg/dL vs. 1.7 mg/dL, p < 0.01 and 335.4 U/L vs. 961.0 U/L, p < 0.001, respectively), but not 30R swine (0.9 mg/dL vs. 1.2 mg/dL, p = 0.06 and 423.7 U/L vs. 769.5 U/L, p = 0.15, respectively). There was no difference in survival time between the 30R and 60R pediatric swine, p = 0.99. CONCLUSION: The physiologic effects of 30 minutes of zone 1 REBOA in pediatric swine mostly resolved during the subsequent 4 hours of critical care, whereas the effects of 60 minutes of REBOA persisted and worsened after 4 hours of critical care. Sixty minutes of zone 1 REBOA may create an irreversible physiologic insult in a pediatric population.

Pharmacokinetics of Tranexamic Acid Given as an Intramuscular Injection Compared to Intravenous Infusion in a Swine Model of Ongoing Hemorrhage.

INTRODUCTION: Tranexamic acid (TXA) improves survival in traumatic hemorrhage, but difficulty obtaining intravenous (IV) access may limit its use in austere environments, given its incompatibility with blood products. The bioavailability of intramuscular (IM) TXA in a shock state is unknown. We hypothesized that IM and IV administration have similar pharmacokinetics and ability to reverse in vitro hyperfibrinolysis in a swine-controlled hemorrhage model. METHODS: Twelve Yorkshire cross swine were anesthetized, instrumented, and subjected to a 35% controlled hemorrhage, followed by resuscitation. During hemorrhage, they were randomized to receive a 1 g IV TXA infusion over 10 min, 1 g IM TXA in two 5 mL injections, or 10 mL normal saline IM injection as a placebo group to assess model adequacy. Serum TXA concentrations were determined using liquid chromatography-mass spectrometry, and plasma samples supplemented with tissue plasminogen activator (tPA) were analyzed by rotational thromboelastometry. RESULTS: All animals achieved class III shock. There was no difference in the concentration-time areas under the curve between TXA given by either route. The absolute bioavailability of IM TXA was 97%. IV TXA resulted in a higher peak serum concentration during the infusion, with no subsequent differences. Both IV and IM TXA administration caused complete reversal of in vitro tPA-induced hyperfibrinolysis. CONCLUSION: The pharmacokinetics of IM TXA were similar to IV TXA during hemorrhagic shock in our swine model. IV administration resulted in a higher serum concentration only during the infusion, but all levels were able to successfully correct in vitro hyperfibrinolysis. There was no difference in total body exposure to equal doses of TXA between the two routes of administration. IM TXA may prove beneficial in scenarios where difficulty establishing dedicated IV access could otherwise limit or delay its use.

Late Amputation Following Refracture After Removal of Multiplanar Circular External Fixator for Treatment of Severe Combat-Related Tibial Fracture: A Case Report.

CASE: The multiplanar circular external fixator is commonly used in the treatment of severe combat-related tibial fractures. We present the case of a patient who sustained a refracture after removal of such a fixator. This complication contributed to failure of the limb salvage and ultimately resulted in the patient undergoing transtibial amputation. CONCLUSION: The choice to pursue limb salvage or amputation must be a shared decision between the patient and provider. This discussion must now include the possibility of refracture if limb salvage is pursued using multiplanar circular external fixation. Further study is also required to define fracture stability after the removal of a multiplanar circular external fixator.

Characteristics of combat-related spine injuries: a review of recent literature.

Injuries to the spinal column in combat casualties sustained during the conflicts in Iraq and Afghanistan are common, and the highest in reported wartime history. High-energy blast mechanisms from improved explosive devices have resulted in complex polytrauma and injury patterns, which are often markedly different from those injuries encountered in civilian trauma. Herein, we review the most current literature with regard to the distinct types of combat-related spine injuries/concomitant comorbidities sustained in Operations Enduring Freedom, Iraqi Freedom and New Dawn.

Electron attachment to sulfur oxyhalides: SOF2, SOCl2, SO2F2, SO2Cl2, and SO2FCl attachment rate coefficients, 300-900 K.

Electron attachment to SOF(2), SOCl(2), SO(2)F(2), SO(2)FCl, and SO(2)Cl(2) was studied with two flowing-afterglow Langmuir-probe apparatuses over the temperature range 300-900 K. Attachment rate coefficients at 300 K are k(a) = 2.6+/-0.8x10(-10)(SOF(2)), 1.8+/-0.5x10(-8)(SOCl(2)), 4.8+/-0.7x10(-10)(SO(2)F(2)), 2.4+/-0.7x10(-9)(SO(2)Cl(2)), and 2.0+/-0.6x10(-7) cm(3) s(-1)(SO(2)FCl). Arrhenius plots of the data imply activation energies of 56+/-22 meV(SOF(2)), 92+/-40(SO(2)F(2)), 44+/-22 meV(SOCl(2)), and 29+/-15 meV(SO(2)Cl(2)). The rate coefficients for SO(2)FCl decrease slightly with temperature, commensurate with the decrease in the capture rate coefficient. Electron attachment to SOF(2) and SO(2)F(2) is nondissociative, while reaction with SOCl(2), SO(2)FCl, and SO(2)Cl(2) is dissociative. Dissociative attachment is dominated by channels arising from S-Cl bond cleavage but also includes a minor channel forming a dihalide product ion. Branching fraction data are reported for the dissociative attachment channels.

Variable electron and neutral density attachment mass spectrometry: temperature-dependent kinetics of electron attachment to PSCL(3) and PSCL(2) and mutual neutralization of PSCl(2)(-) and PSCl(-) with Ar(+).

We describe the VENDAMS (variable electron and neutral density attachment mass spectrometry) technique to measure the rate constants of various processes occurring as primary, secondary, and higher order chemistry in a flowing afterglow at high charge densities over a temperature range of 300 to 550 K. In particular, we report measurements of rate constants of ion-ion mutual neutralization and electron attachment to radical species, processes which have proven difficult to study through other means. The product negative ion abundances from the addition of PSCl(3) to an Ar(+)/e(-) plasma have been measured as a function of initial electron densities between 1 × 10(8) and 4 × 10(10) cm(-3). Data at lower electron densities yield branching ratios of the primary electron attachment to PSCl(3); determination of the reactions and rate constants occurring at low electron densities then allows for determination of the greater number of reactions and rate constants contributing at higher electron densities. Reaction rate constants and branching ratios of electron attachment to PSCl(2) are reported; this is the first measurement of electron attachment to a radical as a function of temperature. The data show an unusual negative temperature dependence; however, a zero or even slightly positive dependence is within the uncertainty. Measured electron attachment rate constants are 1.4 × 10(-7), 1.1 × 10(-7), and 9.1 × 10(-8) ± 40% cm(3) s(-1) at 300, 400, and 550 K, respectively; the dominant product channel is PSCl + Cl(-) (95, 87, and 77% at 300, 400, and 550 K), and the minor channel is PSCl(-) + Cl. Ion-ion mutual neutralization rate constants of both PSCl(-) and PSCl(2)(-) with Ar(+) are reported over the investigated temperature range; rate constants at 300 K are 4.9 × 10(-8) ± 20% cm(3) s(-1) and 4.5 × 10(-8) ± 15% cm(3) s(-1) and show temperature dependences of T(-0.5±0.3) and T(-0.9±0.3), respectively.