A historical perspective on crush syndrome: the clinical application of its pathogenesis, established by the study of wartime crush injuries

Peiris, Dilini

doi:10.1136/jclinpath-2016-203984

Cited by 28 publications

(29 citation statements)

References 10 publications

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“…When comparing the main findings of our review with this literature, we identified some similar patterns. Both compartment syndrome, crush syndrome, and vascular injury were characterized by ischemia–reperfusion injury . Compartment syndrome and crush syndrome are to a major degree associated with elevated interstitial pressure, and more specifically intracompartmental pressure, as a consequence of edema.…”

Section: Discussionmentioning

confidence: 99%

“…Both compartment syndrome, crush syndrome, and vascular injury were characterized by ischemia-reperfusion injury. [86][87][88] Compartment syndrome and crush syndrome are to a major degree associated with elevated interstitial pressure, and more specifically intracompartmental pressure, as a consequence of edema. Moreover, in all four conditions, neutrophils are the first invading inflammatory cells, followed by macrophages, and promote further muscle damage.…”

Section: Discussionmentioning

confidence: 99%

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Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review

Damme

Hecke

Remue

et al. 2019

Wound Repair Regeneration

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Deep tissue injuries are pressure ulcers which initiate in the subcutaneous tissues and extend through a bottom‐up pathway. Once deep tissue injuries are visual at skin level, serious irreversible tissue damage has already occurred. In pressure ulcer development, inflammation and edema are coupled physiological processes associated with tissue damage arising due to sustained mechanical loading. This study aimed to provide an in‐depth overview of the physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues, in the context of pressure ulceration. A scoping review was performed according to the framework by Arksey and O'Malley. The databases MEDLINE, EMBASE, Web of Science, and Scopus, and the reference lists of included studies were searched for in vivo (animal, human), and in vitro studies matching the study objectives (from inception to 28 May 2018). No restrictions for inclusion were applied for study design, setting, participants, and year of publication. A total of 12 studies were included, varying in study design, sample characteristics, amount and duration of mechanical loads that were applied, follow‐up time, and assessment methods. Neutrophil infiltration and edema occur in the subcutaneous tissues nearly immediately after the application of load on soft tissues. The amount of neutrophils and edema increase in the first days after the mechanical insult and decrease once healing has been initiated and no supplementary mechanical load was applied. One study indicated that edema may extend up to the level of the dermo‐epidermal junction. Further research should focus on how deep tissue inflammation and edema are reflected into unique tissue changes at skin level, and how abnormal inflammatory responses manifest (e.g. when the nervous system is not functioning normally).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review

Damme

Hecke

Remue

et al. 2019

Wound Repair Regeneration

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“…Acute kidney injury (AKI) is the most common complication of rhabdomyolysis in crush syndrome, and it is an important factor that causes death and poor prognosis in patients. 3 Abbreviations: AKI: acute kidney injury BUN: blood urea nitrogen ELISA: enzyme-linked immunosorbent assay HE: Haematoxylin and Eosin stain IL-6: interleukin-6 JNK: c-Jun N-terminal kinase Mb: myoglobin mRNA: messenger ribonucleic acid NF-κB: nuclear factor-kappa B PCR: polymerase chain reaction TBS: tris-buffered saline TLR: toll-like receptor TNF-α: tumor necrosis factor-α Toll-like receptors (TLRs) are the members of the membrane protein family which can identify pathogen-associated molecules and mediate innate immune response; 4 TLR4 is an important member of the TLRs receptor family and belongs to I transmembrane receptor. Binding of stimulating factors to the TLR4 receptor is the first step in activating the innate immune system.…”

Section: Introductionmentioning

confidence: 99%

TAK-242 Attenuates Crush Injury Induced Acute Kidney Injury through Inhibiting TLR4/NF-κB Signaling Pathways in Rats

Wang

Chen

Hou

et al. 2020

Prehosp. Disaster med.

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Background: To investigate if toll-like receptor (TLR) 4/nuclear factor-kappa B (NF-κB) signaling pathways mediated crush injury induced acute kidney injury (AKI) in rats, and if TAK-242 (a specific inhibitor of TLR4) attenuates the injury through inhibiting the signaling pathways. Methods: This study was divided into two parts: (1) Establish the crush injury model: 50 rats were randomly divided into control group and four crush injury groups (n = 10/group). Crush injury groups were given 3kg pressure for eight hours and were sacrificed at the time points of 0h, 6h, 12h, and 24h after relieving pressure. And (2) Select the most obvious injury group (12h group) for drug intervention group. Thirty rats were randomly divided into control group, 12h group, and 12h+TAK-242 group (n = 10/group). Two parts detection were as follows: pathological changes of kidney tissues were observed in Haematoxylin and Eosin (HE) staining. Serum creatinine, blood urea nitrogen (BUN), myoglobin (Mb), and blood potassium were examined by automatic biochemical analysis instrument. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). The TLR4 messenger ribonucleic acid (mRNA), TLR4, and P65 were detected by real-time polymerase chain reaction (PCR), western blot, immunohistochemistry staining. Results: Compared with the control group, kidney tissues were damaged in crush injury groups, and most obvious in the 12h group. The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, and TLR4mRNA were increased in the crush injury groups and significantly increased in the 12h group (P <.05). The TLR4 and P65 were significantly increased in the 12h group (P <.05). Compared with the 12h group, kidney tissue damage was significantly reduced in the TAK-242 group (P <.05). The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, TLR4mRNA, TLR4, and P65 in the TAK-242 group were significantly reduced (P <.05). Conclusion: The present findings conclude that TLR4/NF-κB signaling pathways mediated crush injury induced AKI in rats, and TAK-242 attenuates the injury through inhibiting the signaling pathways.

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“…6 –8 As a result of I/R injury (especially in the lower extremities, which contain a large amount of skeletal muscle), serious systemic conditions including the acute renal failure can be caused by secreted chemical mediators derived from ischemic skeletal muscles, as represented by crush syndrome. 3,7…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of edaravone on systemic inflammation and local damage in skeletal muscles following long-term ischemia to murine hind limb

Yokoyama

Tsujii

Iino

et al. 2019

J Orthop Surg (Hong Kong)

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Purpose: The purpose of this study was to evaluate local and systemic pathology in a murine model of ischemia–reperfusion (I/R) injury induced by long-term application of a tourniquet on the hind limbs and to assess the protective effects of edaravone, a potent systemic scavenger of free radicals, using this model. Methods: Sixty C57BL6 mice were divided in two groups, with one group receiving a 3 mg/kg intraperitoneal injection of edaravone and the other group receiving an identical amount of saline 30 min before ischemia under deep anesthesia. The left thigh of each animal was constricted for 4 h with a 4.5-oz. orthodontic rubber band to induce ischemia; 4 h was the critical duration for skeletal muscles. After ischemia, specimens of skeletal muscles, both kidneys, and plasma were collected at 0, 2, 12, 24, 48, and 72 h. Injury to the skeletal muscles and vacuolar degeneration of the kidneys were histologically assessed. Additionally, apoptosis of skeletal muscle cells was assessed by analysis of caspase 3/7 activity and TUNEL staining. Plasma tumor necrosis factor (TNF)-α levels were measured using an enzyme-linked immunosorbent assay kit. Results: Skeletal muscles exhibited prominent injury of myofibers at 12 h after I/R injury, with clear upregulation of plasma TNF-α expression and histologic evidence of tubular dysfunction of the kidneys. Plasma TNF-α levels declined and histologic renal damage was ameliorated in edaravone-treated mice, but treatment did not protect skeletal muscle following ischemia for 4 h. Nonetheless, compared with group S, expression of the apoptosis marker caspase 3/7 was significantly inhibited in the skeletal hind limb muscles of Ed-group mice affected by reperfusion injury following ischemia for 4 h. Conclusion: The present study demonstrated that edaravone is a potentially useful drug for systemic or local treatment of reperfusion injury resulting from long-term ischemia.

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A historical perspective on crush syndrome: the clinical application of its pathogenesis, established by the study of wartime crush injuries

Cited by 28 publications

References 10 publications

Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review

Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review

TAK-242 Attenuates Crush Injury Induced Acute Kidney Injury through Inhibiting TLR4/NF-κB Signaling Pathways in Rats

Inhibitory effect of edaravone on systemic inflammation and local damage in skeletal muscles following long-term ischemia to murine hind limb

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