Patrick F. Walker

Background: Porcine liver injury models are used to study non-compressible torso hemorrhage and hemorrhagic shock; however, many existing models demonstrate variability in injury pattern and hemorrhage dynamics that may limit reproducibility. We developed an ultrasound-guided hepatic vein injury model in swine designed to produce controlled hemorrhage while enabling integrated hemodynamic and biochemical characterization throughout shock progression. Methods: Five Yorkshire swine underwent ultrasound-guided hepatic vein injury following standardized preparation and monitoring. Continuous hemodynamic monitoring and transesophageal echocardiography were performed throughout hemorrhage. Arterial, venous, and intra-abdominal shed blood samples were collected serially for point-of-care laboratory analysis and biomarker assessment. Hemorrhage progression, blood loss, metabolic parameters, and cardiovascular responses were evaluated. Results: All animals progressed to class IV hemorrhagic shock with reproducible physiologic deterioration. Mean time from injury to cardiac standstill was 25±7 minutes with mean total blood loss of 61±7% estimated blood volume. Mean hemorrhage rate was 2.60±0.87% blood volume loss/minute. Lactate increased from 2.4 to 4.6 mmol/L (P=0.01), while base deficit worsened from 2 to −10 mmol/L (P=0.01). Mixed venous oxygen saturation decreased from 88.5% to 37% (P=0.03), and fibrinogen decreased from 3.28 to 0.88 mg/dL (P=0.001). Shed blood demonstrated progressive metabolic derangement with rising potassium and lactate levels during hemorrhage. Conclusions: This ultrasound-guided hepatic vein injury model produces reproducible hemorrhagic shock in swine with clinically relevant hemodynamic and metabolic responses. The model provides a translational platform for investigating hemorrhage physiology, shed blood characteristics, and emerging resuscitative strategies and therapeutics.

Background: Choledocholithiasis complicates 10–15% of patients undergoing cholecystectomy. While endoscopic retrograde cholangiopancreatography (ERCP) followed by cholecystectomy is common, access to ERCP is inconsistent in rural and military hospitals, highlighting the role for single-stage laparoscopic common bile duct exploration (LCBDE). Methods: We describe a technical approach for fluoroscopy-guided, wire-based transcystic LCBDE using standardized endovascular tools, the “Biliary Endovascular Toolkit”. We performed a retrospective review of five patients undergoing cholecystectomy and transcystic LCBDE at our military hospital between May 2024 and October 2025. The operative technique employed percutaneous micropuncture sheath access, fluoroscopy-guided transcystic wire cannulation of the ampulla, and balloon dilation with sphincteroplasty for stone clearance. Results: Five patients (mean age 35.4 years) underwent single-stage cholecystectomy with transcystic LCBDE. Transcystic cannulation, duodenal wire access, and ductal clearance were successful in all cases (100%), without conversion or postoperative ERCP (0%). Mean operative time was 208 min (range 161–275). No patient experienced postoperative pancreatitis, pleural complications, or other 30-day adverse events. Conclusions: The Biliary Endovascular Toolkit offers a standardized, wire-guided workflow for transcystic LCBDE using off-the-shelf equipment. This technical note provides a practical framework for general surgeons managing choledocholithiasis, particularly in resource-limited settings.

Background: Thoracic damage control (TDC) is an operative strategy for physiologically depleted patients with severe thoracic injuries. The relationship of TDC complications and mortality has not been comprehensively examined. This study analyzed the association of complications and mortality following TDC. Methods: A retrospective registry review at a Level 1 trauma center identified patients ≥16 years undergoing TDC. Demographics, physiological data, injuries, operations, complications, and mortality were abstracted. Univariate and multivariate analyses for mortality risk factors were performed. Results: A total of 98 patients met the inclusion criteria. The median age was 31 (23-44) years, 52% male, and 69% had penetrating trauma. The median Injury Severity Score (ISS) was 32 (26-41), chest Abbreviated Injury Scale 4 (4–5), admission systolic blood pressure 112 (77-138), pH 7.16 (6.99–7.25), base deficit −11 (−17 to −7), and lactate 8.1 (5.7–11.3). The operative procedures performed included pulmonary 63.5%, cardiac 29.6%, great vessels 16.2%, and 66.3% had a concomitant damage control laparotomy. Of the entire cohort, 72 (73.5%) patients developed at least one complication, including bacteremia 35%, renal failure requiring continuous renal replacement therapy (CRRT) 23%, pneumonia 18%, and empyema 12%. Mortality was 25.5% (25/98), with 72% (18/25) occurring prior to chest closure. Univariate analysis demonstrated that blunt trauma (p<0.001), male sex (p=0.006), lower pH (p=0.007), higher ISS (p<0.001), and CRRT (p=0.031) were statistically significant risk factors for mortality. On multivariate analysis, only blunt trauma (OR 3.82, 95% CI 1.1 to 13.3, p=0.035) and admission pH <7.1 (OR 3.13, 95% CI 1.03 to 9.5, p=0.044) were independently associated with mortality. Conclusion: TDC is an essential operative strategy in patients with severe thoracic injuries presenting in advanced shock. Both blunt trauma and degree of shock are independent risk factors for mortality, which are present on admission. Although complications are frequent and severe, they do not predict mortality. Level of evidence: IV, diagnostic test/criteria.

Large-scale combat operations will generate casualty volumes and injury patterns that fundamentally differ from routine civilian trauma, yet contingency planning increasingly relies on civilian surgeons and hospitals to deploy, absorb, and definitively treat combat-injured patients through frameworks such as the National Disaster Medical System and Health Care Personnel Delivery System. Decades of experience, from World War II and the Global War on Terrorism to the current war in Ukraine, demonstrate that civilian surgical volume alone does not reliably translate into readiness for combat casualty care. Contemporary warfare produces blast and high-velocity fragment trauma, severe polytrauma, extensive contamination, complex extremity and vascular injuries, burns, and prolonged evacuation delays, requiring serial operative management and decision making under resource constraints. In contrast, civilian trauma systems are predominantly blunt injury-based with rapid access to definitive resources and subspecialty support. The Military Health System mitigates this readiness gap through the Clinical Readiness Program (CRP), a Knowledge, Skills, and Abilities (KSA) based framework that standardizes combat-relevant education, procedural training, and experience validation. No comparable readiness requirement exists for civilian surgeons despite their anticipated wartime role, creating a mismatch between assumed capacity and validated capability. This opinion argues that civilian clinicians expected to support combat casualty care should be incorporated into a civilian combat casualty care readiness framework modeled on the CRP. Key elements include specialty-specific curricula, knowledge assessments, periodic skills-based training aligned to deployment requirements, and KSA scoring using case log review to enable role assignment across echelons of care. Before activation, clinicians would undergo standardized education, skills verification, and team-based training. A scalable civilian readiness framework would enable rapid, effective, and safe integration of civilian surgeons into large-scale combat operations and responses, ensuring that providers are objectively prepared and ready before the call. ( J Trauma Acute Care Surg . 2026;000: 000–000. Copyright © 2026 Wolters Kluwer Health, Inc. All rights reserved.)

BACKGROUND: Exsanguination cardiac arrest (ECA) remains a formidable challenge in trauma surgery with a persistently dismal prognosis. Extracorporeal cardiopulmonary resuscitation (ECPR) has shown promise in medical cardiac arrest and may translate to trauma. We hypothesized that aortic cardiopulmonary resuscitation in trauma (ACT)—a controlled ECPR approach aimed at mitigating reperfusion injury—would improve sustained return of spontaneous circulation (ROSC) compared with resuscitative thoracotomy (RT) in a porcine ECA model. METHODS: Twelve swine were bled to mean arterial pressure 2 50 mm Hg with a sinus rhythm—at the end of the critical care period. Secondary outcomes included coronary and carotid flow to assess critical organ perfusion during resuscitation. RESULTS: The primary endpoint was achieved in 100% of ACT animals versus 0% of controls ( p p =0.060). During the critical care phase, ACT led to increased mean left-anterior-descending coronary artery flow (41.6±0.2 mL/min vs. 31.7±0.6 mL/min in RT) and right carotid artery flow (214.8±0.5 mL/min vs. 90.7±1.0 mL/min, both p <0.0001). CONCLUSIONS: Following ECA, ACT produced a markedly higher rate of sustained ROSC compared with conventional RT and significantly augmented coronary and carotid perfusion—highlighting its potential as a trauma-focused ECPR modality. LEVEL OF EVIDENCE: Preclinical—large animal model.

Background: Methadone blocks several ionic currents with different half‐maximal inhibitory concentrations, including the rapid component of the delayed and inward (I _K1 ) rectifier potassium current, the L‐type calcium current, and the late sodium current. Despite the well‐known proarrhythmic effect of methadone, the underlying mechanisms remain less well understood. Methods: Computer simulations were used to explore the proarrhythmic effects of methadone by investigating how its blocking effects on ionic currents act alone or together in arrhythmogenesis. Results: The major findings are (1) blocking I _K1 potentiates QT prolongation‐related arrhythmogenesis by enhancing a tissue‐scale dynamical instability for the spontaneous genesis of ectopic excitations; blocking I _K1 and the rapid component of the delayed rectifier potassium current together results in a synergistic effect, greatly increasing the arrhythmia propensity, much larger than that of blocking either one alone; (2) blocking I _K1 in combination with lowering L‐type calcium current potentiates phase 2 reentry caused by spike‐and‐dome action potential morphology, an arrhythmia mechanism of early repolarization or Brugada syndrome, whereas blocking the rapid component of the delayed rectifier potassium current exhibits little effect for this mechanism of arrhythmias; and (3) hypoxia, often comorbid in methadone populations, can potentiate QT prolongation‐related arrhythmias at high sympathetic activity and phase 2 reentry at low sympathetic activity, mainly via its effect on the L‐type calcium current. Conclusions: Methadone promotes both early and delayed repolarization arrhythmias. Early repolarization may be responsible for methadone‐related deaths occurring mainly during sleep and occurring more often in men. Blocking I _K1 can work synergistically with other channel blockers to disproportionately increase arrhythmia propensity, greatly increasing methadone's risk when it is combined with other proarrhythmic drugs or under disease conditions.

Background/Objectives: Hemorrhage is associated with most preventable combat-related deaths. Management of non-compressible truncal and junctional hemorrhage remains challenging, especially with prolonged evacuations. This study evaluated the efficacy of commercial topical hemostatic agents in uncontrolled hemorrhage models under coagulopathic conditions, examining differences based on applicator experience. Methods: Sixty Yorkshire swine were randomized to 5 groups: Combat Gauze (CG), Celox Rapid (CR), ChitoSAM 100 (CS), EVARREST® Fibrin Sealant Patch (EP), and X-Stat 30 (XS). After 50% hemodilution, a 5 mm femoral arteriotomy or 6 cm liver laceration was created, and the agents were applied as per device instructions. Hemostatic agents were placed by experienced (≥5 previous applications) or non-experienced (<5 previous applications) users. Animals were then monitored for rebleeding for 60 minutes. Results: In the junctional hemorrhage model, only ChitoSAM required more applications by novice applicators (2.3 vs. 1, p = 0.0104). No significant differences in rebleed rates among devices (CG 0%, CS 33%, CR 17%, EP 17%, XS 33%, p = 0.73) or by user experience were observed. No differences in perfusion were noted on angiography. In the hepatic laceration model, no significant differences in applications or rebleed rates for any agent (CG 0%, CS 50%, CR 17%, EP 17%, XS 0%, p = 0.21) or by user experience were found. Overall survival did not significantly vary by device. Conclusion: All 5 hemostatic agents showed similar efficacy in controlling junctional and intra-abdominal hemorrhage, with no significant differences in hemostasis, rebleed rate, or survival by experience level. However, more ChitoSAM applications were needed for junctional hemorrhage control in the absence of experience. All tested dressings show promise for rapid hemorrhage control.

Purpose In patients with hemorrhagic shock and an intracranial space occupying lesion (SOL), brain perfusion is severely compromised due to raised intracranial pressure (rICP), significantly worsening outcomes. This study aims to develop a swine model of a SOL with rICP and shock and characterize the effect on brain perfusion. Methods Ten male swine were divided into two groups– normal ICP (nICP) and rICP. rICP animals had an intracranial Fogarty balloon catheter inserted, which was infused with saline to simulate a SOL. Animals underwent hemorrhage to systolic blood pressures (SBP) of 60, 40, and 20mmHg. Cerebral blood flow (CBF) and cerebral blood volume (CBV) were measured using CT perfusion. Results The CBF/Mean arterial pressure (MAP) and CBV/MAP curves were modeled using non-linear regression, with both groups demonstrating a sigmoid relation. In both the CBF/MAP and CBV/MAP curves, animals with rICP had loss of autoregulation at a higher MAP compared to nICP. The curves were an excellent fit for CBF (nICP R² = 0.95; rICP R² = 0.77) and CBV (nICP R² = 0.96; rICP R² = 0.78). Conclusions This study aids in quantifying the compounding insult of raised ICP and hemorrhage with regard to brain perfusion. Raised ICP results in autoregulatory failure at a higher MAP compared to animals with nICP. These results can help inform future studies that should be aimed at evaluating novel interventions for this complex clinical scenario.