Threshold Model for Extremity Compartment Syndrome in Swine

Kalns, John; Cox, Jennifer; Baskin, Jonathan Z.; Santos, Adrienne; Odland, Rick M.; Fecura, Stephen

doi:10.1016/j.jss.2010.12.041

Cited by 19 publications

(23 citation statements)

References 10 publications

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“…Nucleated cells (4) were also seen in the interstitial spaces between the necrotic fibers but in far less abundance than in the inflammatory regions bordering the periphery of the TA. Necrotic fibers were also observed in the damaged skeletal muscle (5).…”

Section: Use Of External Compression Creates Cs-like Injury Inmentioning

confidence: 90%

“…As a result, CS leads to severe soft tissue damage of the muscles, nerves, and vasculature . Pressure elevation also leads to vascular collapse and compromised perfusion of the enclosed tissues, including muscles and nerves . This results in muscle necrosis and nerve damage, which can lead to contractures, amputation, or even death .…”

mentioning

confidence: 99%

“…[1][2][3] Pressure elevation also leads to vascular collapse and compromised perfusion of the enclosed tissues, including muscles and nerves. 4,5 This results in muscle necrosis and nerve damage, which can lead to contractures, amputation, or even death. [6][7][8] It has been suggested that the progression of CS results from increased vascular permeability triggered by oxidative and inflammatory responses to the initial trauma.…”

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confidence: 99%

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Characterization of a compartment syndrome–like injury model

et al. 2015

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INTRODUCTION Acute compartment syndrome (CS) is caused by an elevation of pressure within a muscular compartment which can be caused by numerous factors, including blunt trauma. In this study, we characterized a rodent model of CS-like injury. METHODS Forty male athymic rats received a standardized injury of ischemia and compression to their hindlimbs, while the intracompartmental pressure (ICP) was measured using an implantable transmitter. Tetanic muscle function was evaluated, and histology was performed on the tibialis anterior (TA) muscle. RESULTS ICPs were held at 260.70±2.70mmHg during injury. Injured muscles recovered 59% of their total function 4 weeks after injury, and histology showed high levels of edema, inflammation (CD68+), angiogenesis (CD31+), and fibrosis within 72 hours following injury. DISCUSSION We describe a novel CS-like injury model and a novel method to measure ICP which could potentially be used to develop innovative therapies to manage CS injury in humans.

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Section: Use Of External Compression Creates Cs-like Injury Inmentioning

confidence: 90%

mentioning

confidence: 99%

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confidence: 99%

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Characterization of a compartment syndrome–like injury model

et al. 2015

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“…To minimize the fluctuation of pressures experienced in our high pressure model, plasma or a balloon, rather than saline solution, could have been used to maintain elevated compartment pressures 15 . Although not tested in this study, a technical tip that could have been used to ensure that the needle was inserted into the correct compartment would have been to manually squeeze or depress the compartment of interest while measuring the pressure; this should have caused the readings to elevate if needle placement was correct.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Focused Instruction on Orthopaedic Surgery Residents’ Ability to Objectively Measure Intracompartmental Pressures in a Compartment Syndrome Model

Morris

Harper

Hetzel

et al. 2014

The Journal of Bone and Joint Surgery

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“…in the face of patent vessels. As such, the pathologic contribution of inflammation to the pathophysiology of CS is being increasingly recognized; studies from our group 10 and others 11,12 have broadly implicated leukocytes as playing a primary role in both microvascular and parenchymal injury during CS. Few therapeutic options have been shown to be effective.…”

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confidence: 99%

Carbon monoxide‐releasing molecule‐3 (CORM‐3) offers protection in an in vitro model of compartment syndrome

et al. 2019

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Objective Limb compartment syndrome (CS), a complication of trauma, results in muscle necrosis and cell death; ischemia and inflammation contribute to microvascular dysfunction and parenchymal injury. Carbon monoxide‐releasing molecule‐3 (CORM‐3) has been shown to protect microvascular perfusion and reduce inflammation in animal models of CS. The purpose of the study was to test the effect of CORM‐3 in human in vitro CS model, allowing exploration of the mechanism(s) of CO protection and potential development of pharmacologic treatment. Methods Confluent human vascular endothelial cells (HUVECs) were stimulated for 6 h with serum isolated from patients with CS. Intracellular oxidative stress (production of reactive oxygen species (ROS)) apoptosis, transendothelial resistance (TEER), polymorphonuclear leukocyte (PMN) activation and transmigration across the monolayer in response to the CS stimulus were assessed. All experiments were performed in the presence of CORM‐3 (100 μM) or its inactive form, iCORM‐3. Results CS serum induced a significant increase in ROS, apoptosis and endothelial monolayer breakdown; it also increased PMN superoxide production, leukocyte rolling and adhesion/transmigration. CORM‐3 completely prevented CS‐induced ROS production, apoptosis, PMN adhesion, rolling and transmigration, while improving monolayer integrity. Conclusion CORM‐3 offers potent anti‐oxidant and anti‐inflammatory effects, and may have a potential application to patients at risk of developing CS.

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Threshold Model for Extremity Compartment Syndrome in Swine

Cited by 19 publications

References 10 publications

Characterization of a compartment syndrome–like injury model

Characterization of a compartment syndrome–like injury model

The Effect of Focused Instruction on Orthopaedic Surgery Residents’ Ability to Objectively Measure Intracompartmental Pressures in a Compartment Syndrome Model

Carbon monoxide‐releasing molecule‐3 (CORM‐3) offers protection in an in vitro model of compartment syndrome

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