Next-generation tourniquet: Recommendations for future capabilities and design requirements.

BACKGROUND: Advances in tourniquet development must meet new military needs for future large-scale combat operations or civilian mass casualty scenarios. This includes the potential use of engineering and automation technologies to provide advanced tourniquet features. A comprehensive set of design capabilities and requirements for an intelligent or smart tourniquet needed to meet the challenges currently does not exist. The goal of this project was to identify key features and capabilities that should be considered for the development of next-generation tourniquets. METHODS: We used a modified Delphi consensus technique to survey a panel of 34 tourniquet subject matter experts to rate various statements and potential design characteristics relevant to tourniquets systems and their use scenarios. Three iterative rounds of surveys were held, followed by virtual working group meetings, to determine importance or agreement with any given statement. We used a tiered consensus system to determine final agreement over key features that were viewed as important or unimportant features or capabilities. This information was used to refine and clarify the necessary tourniquet design features and adjust questions for the following surveys. RESULTS: Key features and capabilities of various were agreed upon by the panelists when consensus was reached. Some tourniquet features that were agreed upon included but are not limited to: Capable of being used longer than 2 hours, applied and monitored by anyone, data displays, semiautomated capabilities with inherent overrides, automated monitoring with notifications and alerts, and provide recommended actions. CONCLUSION: We were able to identify key tourniquet features that will be important for future device development. These consensus results can guide future inventors, researchers, and manufacturers to develop a portfolio of next-generation tourniquets for enhancing the capabilities of a prehospital medical provider. LEVEL OF EVIDENCE: Prognostic and Epidemiological; Level V.

CAN POLYETHYLENE GLYCOL-20K REPLACE ALBUMIN FOR PREHOSPITAL TREATMENT OF HEMORRHAGIC SHOCK WHEN FULL RESUSCITATION IS UNAVAILABLE?

ABSTRACT: A solution of high concentration albumin has been used for temporal volume expansion when timely resuscitation was unavailable after hemorrhagic shock. However, during prolonged hemorrhagic shock, cell edema and interstitial dehydration can occur and impede the volume expansion effect of albumin. Polyethylene glycol-20K (PEG) can establish an osmotic gradient from swollen cells to capillary lumens and thus facilitate capillary fluid shift and volume expansion. We hypothesized that with similar osmolality, 7.5% PEG elicits more rapid and profound compensatory responses after hemorrhagic shock than 25% albumin. Rats were randomized into three groups (n = 8/group) based on treatment: saline (vehicle), PEG (7.5%), and albumin (25%). Trauma was induced in anesthetized rats with muscle injury and fibula fracture, followed by pressure-controlled hemorrhagic shock (MAP = 55 mm Hg) for 45 min. Animals then received an intravenous injection (0.3 mL/kg) of saline, PEG, or albumin. MAP, heart rate, blood gases, hematocrit, skeletal muscle capillary flow, renal blood flow, glomerular filtration rate, urinary flow, urinary sodium concentration, and mortality were monitored for another 2 hours. Polyethylene glycol-20K and albumin both improved MAP, renal and capillary blood flow, and renal oxygen delivery, and decreased hyperkalemia, hyperlactatemia, hematocrit, and mortality (saline: 100% PEG: 12.5%; albumin: 38%) over saline treatment. Compared with albumin, PEG had a more rapid decrease in hematocrit and more profound increases in MAP, diastolic pressure, renal blood flow, glomerular filtration rate, and urinary flow. These results suggest that PEG may be a better option than albumin for prolonged prehospital care of hemorrhagic shock.

Effects of extremity trauma on physiological responses to hemorrhage in conscious rats.

Although physiological responses to hemorrhage are well-studied, hemorrhage is often accompanied by trauma, and it remains unclear how injury affects these responses. This study examined effects of extremity trauma on cardiorespiratory responses and survival to moderate (37%; H-37) or severe (50%; H-50) hemorrhage in rats. Transmitter and carotid catheter implantation and extremity trauma (fibular fracture and muscle injury) were conducted 2 wk, 24 h, and 90 min, respectively, before conscious hemorrhage. Mean arterial pressure (MAP) and heart rate (HR; via telemetry), and respiration rate (RR), minute volume (MV), and tidal volume (TV; via plethysmography) were measured throughout the 25 min hemorrhage and remainder of the 4 h observation period. There were four groups: 1) H-37, no trauma (NT; n = 17); 2) H-37, extremity trauma (T, n = 18); 3) H-50, NT (n = 20); and 4) H-50, T (n = 20). For H-37, during and after hemorrhage, T increased HR (P ≤ 0.031) and MV (P ≤ 0.048) compared with NT rats. During H-50, T increased HR (0.041) and MV (P = 0.043). After hemorrhage, T increased MV (P = 0.008) but decreased HR (P = 0.007) and MAP (P = 0.039). All cardiorespiratory differences between T and NT groups were intermittent. Importantly, both survival time (159.8 ± 78.2 min vs. 211.9 ± 60.3 min; P = 0.022; mean ± SD) and percent survival (45% vs. 80%; P = 0.048) were less in T versus NT rats after H-50. Trauma interacts with physiological systems in a complex manner and no single cardiorespiratory measure was sufficiently altered to indicate that it alone could account for increased mortality after H-50.NEW & NOTEWORTHY In both civilian and military settings, severe hemorrhage rarely occurs in the absence of tissue trauma, yet many animal models for the study of hemorrhage do not include significant tissue trauma. This study using conscious unrestrained rats clearly demonstrates that extremity trauma worsens the probability of survival after a severe hemorrhage. Although no single cardiorespiratory factor accounted for the increased mortality, multiple modest time-related cardiorespiratory responses to the trauma were observed suggesting that their combined dysfunction may have contributed to the reduced survival.

Patterns of Palliation: A Review of Casualties That Received Pain Management Before Reaching Role 2 in Afghanistan.

INTRODUCTION: Battlefield pain management changed markedly during the first 20 years of the Global War on Terror. Morphine, long the mainstay of combat analgesia, diminished in favor of fentanyl and ketamine for military pain control, but the options are not hemodynamically or psychologically equivalent. Understanding patterns of prehospital analgesia may reveal further opportunities for combat casualty care improvement. MATERIALS AND METHODS: Using Department of Defense Trauma Registry data for the Afghanistan conflict from 2005 to 2018, we examined 2,402 records of prehospital analgesia administration to assess temporal trends in medication choice and proportions receiving analgesia, including subanalysis of a cohort screened for an indication with minimal contraindication for analgesia. We further employed frequency matching to explore the presence of disparities in analgesia by casualty affiliation. RESULTS: Proportions of documented analgesia increased throughout the study period, from 0% in 2005 to 70.6% in 2018. Afghan casualties had the highest proportion of documented analgesia (53.0%), versus U.S. military (31.9%), civilian/other (23.3%), and non-U.S. military (19.3%). Fentanyl surpassed morphine in the frequency of administration in 2012. The median age of those receiving ketamine was higher (30 years) than those receiving fentanyl (26 years) or nonsteroidal anti-inflammatory drugs (23 years). Among the frequency-matched subanalysis, the odds ratio for ketamine administration with Afghan casualties was 1.84 (95% CI, 1.30-2.61). CONCLUSIONS: We observed heterogeneity of prehospital patient care across patient affiliation groups, suggesting possible opportunities for improvement toward an overall best practice system. General increase in documented prehospital pain management likely reflects efforts toward complete documentation, as well as improved options for analgesia. Current combat casualty care documentation does not include any standardized pain scale.

A novel animal model to study delayed resuscitation following traumatic hemorrhage.

A focus of combat casualty care research is to develop treatments for when full resuscitation after hemorrhage is delayed. However, few animal models exist to investigate such treatments. Given the kidney's susceptibility to ischemia, we determined how delayed resuscitation affects renal function in a model of traumatic shock. Rats were randomized into three groups: resuscitation after 1 h (ETH-1) or 2 h (ETH-2) of extremity trauma and hemorrhagic shock, and sham control. ETH was induced in anesthetized rats with muscle injury and fibula fracture, followed by pressure-controlled hemorrhage [mean arterial pressure (MAP) = 55 mmHg] for 1 or 2 h. Rats were then resuscitated with whole blood until MAP stabilized between 90 and 100 mmHg for 30 min. MAP, glomerular filtration rate (GFR), creatinine, blood gases, and fractional excretion of sodium (nFENa+) were measured for 3 days. Compared with control, ETH-1 and ETH-2 exhibited decreases in GFR and nFENa+, and increases in circulating lactate, creatinine, and blood urea nitrogen (BUN) before and within 30 min after resuscitation. The increases in creatinine, BUN, and potassium were greater in ETH-2 than in ETH-1, whereas lactate levels were similar between ETH-1 and ETH-2 before and after resuscitation. All measurements were normalized in ETH-1 within 2 days after resuscitation, with 22% mortality. However, ETH-2 exhibited a prolonged impairment of GFR, increased nFENa+, and a 66% mortality. Resuscitation 1 h after injury therefore preserves renal function, whereas further delay of resuscitation irreversibly impairs renal function and increases mortality. This animal model can be used to explore treatments for prolonged prehospital care following traumatic hemorrhage.NEW & NOTEWORTHY A focus of combat casualty care research is to develop treatment where full resuscitation after hemorrhage is delayed. However, animal models of combat-related hemorrhagic shock in which to determine physiological outcomes of such delays and explore potential treatment for golden hour extension are lacking. In this study, we filled this knowledge gap by establishing a traumatic shock model with reproducible development of AKI and shock-related complications determined by the time of resuscitation.

Spectral Reflectance as a Unique Tissue Identifier in Healthy Humans and Inhalation Injury Subjects.

Tracheal intubation is the preferred method of airway management, a common emergency trauma medicine problem. Currently, methods for confirming tracheal tube placement are lacking, and we propose a novel technology, spectral reflectance, which may be incorporated into the tracheal tube for verification of placement. Previous work demonstrated a unique spectral profile in the trachea, which allowed differentiation from esophageal tissue in ex vivo swine, in vivo swine, and human cadavers. The goal of this study is to determine if spectral reflectance can differentiate between trachea and other airway tissues in living humans and whether the unique tracheal spectral profile persists in the presence of an inhalation injury. Reflectance spectra were captured using a custom fiber-optic probe from the buccal mucosa, posterior oropharynx, and trachea of healthy humans intubated for third molar extraction and from the trachea of patients admitted to a burn intensive care unit with and without inhalation injury. Using ratio comparisons, we found that the tracheal spectral profile was significantly different from buccal mucosa or posterior oropharynx, but the area under the curve values are not high enough to be used clinically. In addition, inhalation injury did not significantly alter the spectral reflectance of the trachea. Further studies are needed to determine the utility of this technology in a clinical setting and to develop an algorithm for tissue differentiation.

Valproic acid during hypotensive resuscitation in pigs with trauma and hemorrhagic shock does not improve survival.

BACKGROUND: Valproic acid (VPA) has been extensively used for treatment of anxiety and seizure. Recent studies have shown that VPA has cellular protective effects in preclinical models following severe hemorrhage. This study investigated the effects of VPA on coagulation and survival in pigs after traumatic hemorrhage and hypotensive resuscitation. METHODS: Following baseline measurements, femur fracture was performed in 20 anesthetized and instrumented pigs (41 ± 2 kg), followed by hemorrhage of 55% of the estimated blood volume and a 10-minute shock period. Pigs were then resuscitated for 30 minutes with normal saline (NS) alone (NS group, n = 10, 4 mL/kg) or VPA solution (VPA group, n = 10, 90 mg/kg, 2 mL/kg of 45 mg VPA/mL, plus 2 mL NS/kg). All pigs were then monitored for 2 hours or until death. Hemodynamics were recorded, and blood samples were taken for blood and coagulation analysis (Rotem) at baseline, after hemorrhage, resuscitation, and 2 hours or death. RESULTS: Femur fracture and hemorrhage caused similar reductions in mean arterial pressure and cardiac output, and increase in heart rate in both groups. Resuscitation with NS or VPA did not return these measurements to baseline. No differences were observed in hematocrit, pH, lactate, base excess, or total protein between the groups. Compared with NS, resuscitation with VPA decreased platelet counts and prolonged activated partial thromboplastin time, with no differences in fibrinogen levels, prothrombin time, or any of the Rotem measurements between the two groups. Neither survival rates (NS, 7 of 10 pigs; VPA, 7 of 10 pigs) nor survival times after resuscitation (NS, 97 ± 40 minutes; VPA, 98 ± 43 minutes) differed between the groups. CONCLUSION: Following traumatic hemorrhage and hypotensive resuscitation in pigs, VPA provides no benefit toward improving coagulation function or survival times.

Pathophysiology of Hemorrhage as It Relates to the Warfighter.

Saving lives of wounded military warfighters often depends on the ability to resolve or mitigate the pathophysiology of hemorrhage, specifically diminished oxygen delivery to vital organs that leads to multiorgan failure and death. However, caring for hemorrhaging patients on the battlefield presents unique challenges that extend beyond applying a tourniquet and giving a blood transfusion, especially when battlefield care must be provided for a prolonged period. This review describes these challenges and potential strategies for treating hemorrhage on the battlefield in a prolonged casualty care situation.

Extremity trauma exacerbates acute kidney injury following prolonged hemorrhagic hypotension.

BACKGROUND: The incidence of and mortality due to acute kidney injury is high in patients with traumatic shock. However, it is unclear how hemorrhage and trauma synergistically affect renal function, especially when timely volume resuscitation is not available. METHOD: We hypothesized that trauma impairs renal tolerance to prolonged hemorrhagic hypotension. Sprague-Dawley rats were randomized into six groups: control, extremity trauma (ET), hemorrhage at 70 mm Hg (70-H), hemorrhage at 55 mm Hg (55-H), ET + 70 mm Hg (70-ETH), and ET + 55 mm Hg (55-ETH). Animals were anesthetized, and ET was induced via soft tissue injury and closed fibula fracture. Hemorrhage was performed via catheters 5 minutes after ET with target mean arterial pressure (MAP) clamped at 70 mm Hg or 55 mm Hg for up to 3 hours. Blood and urine samples were collected to analyze plasma creatinine (Cr), Cr clearance (CCr), renal oxygen delivery (DO2), urinary albumin, and kidney injury molecule-1 (KIM-1). RESULTS: Extremity trauma alone did not alter renal hemodynamics, DO2, or function. In 70-H, CCr was increased following hemorrhage, while Cr, renal vascular resistance (RVR), KIM-1, and albumin levels remained unchanged. Compared with 70-H, ET + 70 mm Hg exhibited increases in Cr and RVR with decreases in CCr and DO2. In addition, ET decreased the blood volume loss required to maintain MAP = 70 mm Hg by approximately 50%. Hemorrhage at 55 mm Hg and ET + 55 mm Hg exhibited a marked and similar decrease in CCr and increases in RVR, Cr, KIM-1, and albumin. However, ET greatly decreased the blood volume loss required to maintain MAP at 55 mm Hg and led to 50% mortality. CONCLUSION: These results suggest that ET impairs renal and systemic tolerance to prolonged hemorrhagic hypotension. Thus, traumatic injury should be considered as a critical component of experimental studies investigating outcomes and treatment following hemorrhagic shock. LEVEL OF EVIDENCE: This is an original article on basic science and does not require a level of evidence.

Effects of ketamine analgesia on cardiorespiratory responses and survival to trauma and hemorrhage in rats.

Ketamine is the recommended analgesic on the battlefield for soldiers with hemorrhage, despite a lack of supportive evidence from laboratory or clinical studies. Hence, this study determined the effects of ketamine analgesia on cardiorespiratory responses and survival to moderate (37% blood volume; n = 8/group) or severe hemorrhage (50% blood volume; n = 10/group) after trauma in rats. We used a conscious hemorrhage model with extremity trauma (fibular fracture + soft tissue injury) while measuring mean arterial pressure (MAP), heart rate (HR), and body temperature (Tb) by telemetry, and respiration rate (RR), minute volume (MV), and tidal volume (TV) via whole body plethysmography. Male rats received saline (S) or 5.0 mg/kg ketamine (K) (100 µL/100 g body wt) intra-arterially after trauma and hemorrhage. All rats survived 37% hemorrhage. For 50% hemorrhage, neither survival times [180 min (SD 78) vs. 209 min (SD 66)] nor percent survival (60% vs. 80%) differed between S- and K-treated rats. After 37% hemorrhage, K (compared with S) increased MAP and decreased Tb and MV. After 50% hemorrhage, K (compared with S) increased MAP but decreased HR and MV. K effects on cardiorespiratory function were time dependent, significant but modest, and transient at the analgesic dose given. K effects on Tb were also significant but modest and more prolonged. With the use of this rat model, our data support the use of K as an analgesic in injured, hypovolemic patients.NEW & NOTEWORTHY Ketamine administration at a dose shown to alleviate pain in nonhemorrhaged rats with extremity trauma had only modest and transient effects on multiple aspects of cardiorespiratory function after both moderate (37%) and severe (50%) traumatic hemorrhages. Such effects did not alter survival.

Acute overventilation does not cause lung damage in moderately hemorrhaged swine.

Airway management is important in trauma and critically ill patients. Prolonged mechanical ventilation results in overventilation-induced lung barotrauma, but few studies have examined the consequence of acute (1 h or less) overventilation. We hypothesized that acute hyperventilation, as might inadvertently be performed in prehospital settings, would elevate systemic inflammation and cause lung damage. Female Yorkshire pigs (40-50 kg, n = 10/group) were anesthetized, instrumented for hemodynamic measurements and blood sampling, and underwent a 25% controlled hemorrhage followed by 1 h of 1) spontaneous breathing, 2) "normal" bag ventilation (4.8 L·min volume, ∼400 mL tidal volume, 12 breaths/minute), 3) bag hyperventilation (9 L·min volume, ∼750 mL tidal volume, 12 breaths/minute), 4) maximum hyperventilation (15 L·min volume, ∼750 mL tidal volume, 20 breaths/minute), or 5) mechanical ventilation. Pigs then regained consciousness and recovered for 24 h, followed by euthanasia and collection of blood and tissue samples. No level of manual ventilation had any significant impact on hemodynamic variables. Blood markers of tissue damage and plasma cytokines were not statistically different between groups with the exception of a transient increase in IL-1ß; all values returned to baseline by 24 h. On pathological review, severity and distribution of lung edema or other gross pathologies were not significantly different between groups. These data indicate hyperventilation causes no adverse effects, to include inflammation and tissue damage, and that acute overventilation, as could be seen in the prehospital phase of trauma care, does not produce evidence of adverse effects on the lungs following moderate hemorrhage.NEW & NOTEWORTHY Appropriate airway management is essential in trauma and critically ill patients. Prolonged mechanical ventilation can result in overventilation-induced lung barotrauma, but few studies have examined the consequence of acute overventilation. We investigated the outcome of hemorrhage followed by 1 h of overventilation in swine. We found that acute overventilation, as could be seen in the prehospital phase of trauma care, does not produce evidence of adverse effects on otherwise healthy lungs following moderate hemorrhage.

Early Fasciotomy and Limb Salvage and Complications in Military Lower Extremity Vascular Injury.

BACKGROUND: Military guidelines endorse early fasciotomy after revascularization of lower extremity injuries to prevent compartment syndrome, but the real-world impact is unknown. We assessed the association between fasciotomy and amputation and limb complications among lower extremitys with vascular injury. METHODS: A retrospectively collected lower extremity injury database was queried for limbs undergoing attempted salvage with vascular procedure (2004-2012). Limbs were categorized as having undergone fasciotomy or not. Injury and treatment characteristics were collected, as were intervention timing data when available. The primary outcome measure was amputation. Multivariate models examined the impact of fasciotomy on limb outcomes. RESULTS: Inclusion criteria were met by 515 limbs, 335 (65%) with fasciotomy (median 7.7 h postinjury). Of 212 limbs, 174 (84%) with timing data had fasciotomy within 30 min of initial surgery. Compartment syndrome and suspicion of elevated pressure was documented in 127 limbs (25%; 122 had fasciotomy). Tourniquet and shunt use, fracture, multiple arterial and combined arteriovenous injuries, popliteal involvement, and graft reconstruction were more common in fasciotomy limbs. Isolated venous injury and vascular ligation were more common in nonfasciotomy limbs. Fasciotomy timing was not associated with amputation. Controlling for limb injury severity, fasciotomy was not associated with amputation but was associated with limb infection, motor dysfunction, and contracture. Sixty-three percent of fasciotomies were open for >7 d, and 43% had multiple closure procedures. Fasciotomy revision (17%) was not associated with increased amputation or complications. CONCLUSIONS: Fasciotomy after military lower extremity vascular injury is predominantly performed early, frequently without documented compartment pressure elevation. Early fasciotomy is generally performed in severely injured limbs with a subsequent high rate of limb complications.

Spectral Reflectance Can Differentiate Tracheal and Esophageal Tissue in the Presence of Bodily Fluids and Soot.

Endotracheal intubation is a common life-saving procedure implemented in emergency care to ensure patient oxygenation, but it is difficult and often performed in suboptimal conditions leading to high rates of patient complications. Undetected misplacement in the esophagus is a preventable complication that can lead to fatalities in 5-10% of patients who undergo emergency intubation. End-tidal carbon dioxide monitoring and other proper placement detection methods are useful, yet the problem of misplacement persists. Our previous work demonstrated the utility of spectral reflectance sensors for differentiating esophageal and tracheal tissues, which can be used to confirm proper endotracheal tube placement. In this study, we examine the effectiveness of spectral characterization in the presence of saline, blood, "vomit", and soot in the trachea. Our results show that spectral properties of the trachea that differentiate it from the esophagus persist in the presence of these substances. This work further confirms the potential usefulness of this novel detection technology in field applications.

Fentanyl impairs but ketamine preserves the microcirculatory response to hemorrhage.

BACKGROUND: Peripheral vasoconstriction is the most critical compensating mechanism following hemorrhage to maintain blood pressure. On the battlefield, ketamine rather than opioids is recommended for pain management in case of hemorrhage, but effects of analgesics on compensatory vasoconstriction are not defined. We hypothesized that fentanyl impairs but ketamine preserves the peripheral vasoconstriction and blood pressure compensation following hemorrhage. METHOD: Sprague-Dawley rats (11-13 weeks) were randomly assigned to control (saline vehicle), fentanyl, or ketamine-treated groups with or without hemorrhage (n = 8 or 9 for each group). Rats were anesthetized with Inactin (i.p. 10 mg/100 g), and the spinotrapezius muscles were prepared for microcirculatory observation. Arteriolar arcades were observed with a Nikon microscope, and vessel images and arteriolar diameters were recorded by using Nikon NIS Elements Imaging Software (Nikon Instruments Inc. NY). After baseline perimeters were recorded, the arterioles were topically challenged with saline, fentanyl, or ketamine at concentrations relevant to intravenous analgesic doses to determine direct vasoactive effects. After arteriolar diameters returned to baseline, 30% of total blood volume was removed in 25 minutes. Ten minutes after hemorrhage, rats were intravenously injected with an analgesic dose of fentanyl (0.6 µg/100 g), ketamine (0.3 mg/100 g), or a comparable volume of saline. For each drug or vehicle administration, the total volume injected was 0.1 mL/100 g. Blood pressure, heart rate, and arteriolar responses were monitored for 40 minutes. RESULTS: Topical fentanyl-induced vasodilation (17 ± 2%), but ketamine caused vasoconstriction (-15 ± 4%, p < 0.01). Following hemorrhage, intravenous ketamine did not affect blood pressure or respiratory rate, while fentanyl induced a slight and transient (<5 minutes, p = 0.03 vs. saline group) decrease in blood pressure, with a profound and prolonged suppression in respiratory rate (>10 minutes, with a peak inhibition of 57 ± 8% of baseline, p < 0.01). The compensatory vasoconstriction observed after hemorrhage was not affected by ketamine treatment. However, after fentanyl injection, although changes in blood pressure were transiently present, arteriolar constriction to hemorrhage was absent and replaced with a sustained vasodilation (78 ± 25% to 36 ± 22% of baseline during the 40 minutes after injection, p < 0.01). CONCLUSION: Ketamine affects neither systemic nor microcirculatory compensatory responses to hemorrhage, providing preclinical evidence that ketamine may help attenuate adverse physiological consequences associated with opioids following traumatic hemorrhage. Microcirculatory responses are more sensitive than systemic response for evaluation of hemodynamic stability during procedures associated with pain management.

Analysis of Casualties That Underwent Airway Management Before Reaching Role 2 Facilities in the Afghanistan Conflict 2008-2014.

INTRODUCTION: Airway compromise is the second leading cause of potentially survivable death on the battlefield. The purpose of this study was to better understand wartime prehospital airway patients. MATERIALS AND METHODS: The Role 2 Database (R2D) was retrospectively reviewed for adult patients injured in Afghanistan between February 2008 and September 2014. Of primary interest were prehospital airway interventions and mortality. Prehospital combat mortality index (CMI-PH), hemodynamic interventions, injury mechanism, and demographic data were also included in various statistical analyses. RESULTS: A total of 12,780 trauma patients were recorded in the R2D of whom 890 (7.0%) received prehospital airway intervention. Airway intervention was more common in patients who ultimately died (25.3% vs. 5.6%); however, no statistical association was found in a multivariable logistic regression model (OR 1.28, 95% CI 0.98-1.68). Compared with U.S. military personnel, other military patients were more likely to receive airway intervention after adjusting for CMI-PH (OR 1.33, 95% CI 1.07-1.64). CONCLUSIONS: In the R2D, airway intervention was associated with increased odds of mortality, although this was not statistically significant. Other patients had higher odds of undergoing an airway intervention than U.S. military. Awareness of these findings will facilitate training and equipment for future management of prehospital/prolonged field care airway interventions.

Testing of novel spectral device sensor in swine model of airway obstruction.

Loss of a patent airway is a significant cause of prehospital death. Endotracheal intubation is the gold standard of care but has a high rate of failure and complications, making development of new devices vital. We previously showed that tracheal tissue has a unique spectral profile which could be utilized to confirm correct airway device placement. Therefore, the goals of this study were twofold: 1- to develop an airway obstruction model and 2- use that model to assess how airway compromise affects tissue reflectance. Female swine were anesthetized, intubated, and instrumented. Pigs were allowed to breathe spontaneously and underwent either slow- or rapid-onset obstruction until a real-time pulse oximeter reading of ≤50%. At baseline, 25%, 50%, 75%, and 100% obstruction, a fiber-optic reflection probe was inserted into the trachea and esophagus to capture reflectance spectra. Both slow- and rapid-onset obstruction significantly decreased arterial oxygen concentration (sO2 ) and increased partial pressure of CO2 (pCO2 ). The presence of the tracheal-defining spectral profile was confirmed and remained consistent despite changes in sO2 and pCO2 . This study validated a model of slow- and rapid-airway obstruction that results in significant hypoxia and hypercapnia. This is valuable for future testing of airway device components that may improve airway management. Additionally, our data support the ability of spectral reflectance to differentiate between tracheal and esophageal tissues in the presence of a clinical condition that decreases oxygen saturation.

Noninvasive diagnostics for extremity compartment syndrome following traumatic injury: A state-of-the-art review.

Acute compartment syndrome (ACS) is a serious medical condition that can occur following traumatic injury to an extremity. If left undiagnosed, ACS can eventuate in amputation of the limb or even death. Because of this, fasciotomy to release the pressure within the muscle and restore tissue perfusion is often performed upon suspicion of ACS, as the sequelae to fasciotomy are less severe than those associated with not performing the fasciotomy. Currently, the "gold standard" of diagnosis is based on clinical assessment of such symptoms as pain out of proportion to the injury, obvious high pressure and swelling, pain on passive stretch of the muscles in the affected compartment, and deficits in sensory and/ormotor functions. Diagnosis is often confirmed using invasive measurements of intramuscular pressure (IMP); however, controversy exists as to how direct IMP measurement should be accomplished and threshold pressures for accurate diagnosis. Because of this and the attendant issues with invasive measurements, investigators have been searching over the last 25 years for a noninvasive means to quantitatively measure IMP or perfusion to the limb. The purpose of this review is to summarize the current state of the art of noninvasive devices that could potentially be used to diagnose ACS accurately and objectively. To do this, we divide the discussion into those medical devices that primarily measure mechanical surrogates of IMP (e.g., tissue hardness or myofascial displacement) and those that primarily measure indices of tissue perfusion (e.g., tissue oxygen saturation via near-infraredspectroscopy). While near-infrared spectroscopy-basedtechnologies have shown the most promise, whether such technologies will be of diagnostic benefit await the completion of ongoing clinical trials. LEVEL OF EVIDENCE: Systematic Review, level II.

Indices of muscle and liver dysfunction after surviving hemorrhage and prolonged hypotension.

BACKGROUND: This study determined the long-term effects of prolonged hypotension (PH) on liver, muscle, and kidney dysfunction. The hypothesis was that longer duration of PH after hemorrhage will result in greater organ dysfunction. METHODS: Baboons were sedated and hemorrhaged (30% blood volume). Systolic blood pressure greater than 80 mm Hg was maintained for 1 hour (1 hr-PH; n = 5), 2 hours (2 hr-PH; n = 5), or 3 hours (3 hr-PH; n = 5). After PH, hemorrhage volume was replaced. Animals were recovered and monitored for 21 days. Control animals were hemorrhaged and immediately resuscitated (0 hr-PH, n = 3). Data are Mean ± Standard Deviation, and analyzed by 2-way repeated measures ANOVA and Holm-Sidak test. RESULTS: Hemorrhage resulted in mild hypotension. Minimal resuscitation was required during the hypotensive phase, and survival rate was 100%. Significant increases (p < 0.001) in alanine aminotransferase, aspartate aminotransferase, creatine phosphokinase, and lactate dehydrogenase occurred on Day 1 after PH, and were significantly greater (p < 0.001) in the 2 hr- and 3 hr-PH groups than the 0 hr-PH group. Maximum alanine aminotransferase levels (U/L) were 140 ± 56 (0 hr-PH), 170 ± 130 (1 hr-PH), 322 ± 241 (2 hr-PH), and 387 ± 167 (3 hr-PH). Maximum aspartate aminotransferase levels (U/L) were 218 ± 44 (0 hr-PH), 354 ± 219 (1 hr-PH), 515 ± 424 (2 hr-PH), and 711 ± 278 (3 hr-PH). Maximum creatine phosphokinase values (U/L) were 7834 ± 3681 (0 hr-PH), 24336 ± 22268 (1 hr-PH), 50494 ± 67653 (2 hr-PH), and 59857 ± 32408 (3 hr-PH). Maximum lactic acid dehydrogenase values (U/L) were 890 ± 396 (0 hr-PH), 2055 ± 1520 (1 hr-PH), 3992 ± 4895 (2 hr-PH), and 4771 ± 1884 (3 hr-PH). Plasma creatinine and blood urea nitrogen were unaffected by PH (p > 0.10). CONCLUSION: These results indicate that PH up to 3 hours in duration results in transient liver and muscle dysfunction that was most severe after 2 hr-PH and 3 hr-PH. Prolonged hypotension produced minimal effects on the kidney. LEVEL OF EVIDENCE: Basic science research, Level of evidence not required for basic science research.

Time course of compensatory physiological responses to central hypovolemia in high- and low-tolerant human subjects.

Lower body negative pressure (LBNP) simulates hemorrhage in human subjects. Most subjects (67%) exhibited high tolerance (HT) to hypovolemia, while the remainder (33%) had low tolerance (LT). To investigate the mechanisms for decompensation to central hypovolemia in HT and LT subjects, we characterized the time course of total peripheral resistance (TPR), heart rate (HR), and muscle sympathetic nerve activity (MSNA) during LBNP to tolerance determined by the onset of decompensation (presyncope, PS). We hypothesized that 1) maximum (Max) TPR, HR, and MSNA would coincide, and 2) PS would result from simultaneous decreases in TPR, HR, and MSNA in LT and HT subjects but occur earlier in LT than in HT subjects. Max TPR was lower and occurred earlier in LT ( n = 59) than in HT ( n = 113) subjects (LT: 24 ± 1 mmHg·min·1-1 at 756 ± 31 s; HT: 28 ± 1 mmHg·min·1-1 at 1,265 ± 37 s, P < 0.01). Max TPR occurred several minutes before PS. During subsequent decrease in TPR, HR and MSNA continued to increase. Max HR (LT: 111 ± 2 beat/min at 923 ± 27 s; HT: 130 ± 2 beats/min at 1489 ± 23 s, P < 0.01) occurred several seconds before PS. Higher MSNA ( P < 0.01) was attained in HT ( n = 10; 51 ± 5 bursts/min at max TPR; 54 ± 5 bursts/min at max HR) than LT subjects ( n = 4; 41 ± 8 bursts/min at max TPR; 39 ± 8 bursts/min at max HR). The onset of cardiovascular decompensation is a biphasic process in which vasodilation occurs before bradycardia and sympathetic withdrawal. This pattern was similar in LT and HT but occurred earlier in LT subjects. We conclude that sudden bradycardia plays a critical role in the determination of tolerance to central hypovolemia.

Walter B. Cannon's World War I experience: treatment of traumatic shock then and now.

Walter B. Cannon (1871-1945), perhaps America's preeminent physiologist, volunteered for service with the Army Expeditionary Force (AEF) during World War I. He initially served with Base Hospital No. 5, a unit made up of Harvard clinicians, before moving forward to the front lines to serve at a casualty clearing station run by the British. During his time there, he performed research on wounded soldiers to understand the nature and causes of traumatic shock. Subsequently, Cannon performed animal experimentation on the causes of traumatic shock in the London laboratory of Dr. William Bayliss before being assigned to the AEF Central Medical Laboratory in Dijon, France, where he continued his experimental studies. During this time, he also developed and taught a curriculum on resuscitation of wounded soldiers to medical providers. Although primarily a researcher and teacher, Cannon also performed clinical duties throughout the war, serving with distinction under fire. After the war, Cannon wrote a monograph entitled Traumatic Shock (New York: Appleton, 1923), which encapsulated the knowledge that had been gained during the war, both from direct observation of wounded soldiers, as well as laboratory experimentation on the causes and treatment of traumatic shock. In his monograph, Cannon elucidates a number of principles concerning hemorrhagic shock that were later forgotten, only to be "rediscovered" during the current conflicts in Iraq and Afghanistan. This paper summarizes Cannon's wartime experiences and the knowledge gained concerning traumatic shock during World War I, with a comparison of current combat casualty care practices and knowledge to that which Cannon and his colleagues understood a century ago.