Muscle Microcirculatory Impairment Following Acute Compartment Syndrome in the Dog

Har-Shai, Y.; Silbermann, Michael; Reis, N. D.; Zinman, C.; Rubinstein, I.; Abassi, Zaid; Os, Better

doi:10.1097/00006534-199202000-00014

Cited by 11 publications

(4 citation statements)

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“…Crescentic nucleus of the endothelial cells might appear attached to the blood cells. An average of four vessels was found to supply each fiber, in a square or hexagonal arrangement, which in some way constitutes the optimal number of vessels for diffusion of oxygen into a cylindrical muscle fiber (16,19).…”

Section: Resultsmentioning

confidence: 99%

Involvement of nitric oxide system in experimental muscle crush injury.

Rubinstein

Abassi²,

Coleman³

et al. 1998

J. Clin. Invest.

104

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Muscle crush injury is often complicated by hemodynamic shock, electrolyte disorders, and myoglobinuric renal failure. In this study, we examined the involvement of the nitric oxide (NO) system in the development of muscle damage in an experimental model of crush injury induced by exertion of standardized mechanical pressure on tibialis muscle of rat. The intact limb served as a control. Four days after injury, the crushed muscle was characterized by extreme capillary vasodilatation as demonstrated by histological morphometric analysis. These changes were accompanied by muscle hyperperfusion as evaluated by measurements of femoral blood flow (ultrasonic flowmetry) and capillary blood flow (laser-doppler flowmetry). Treatment with Nomega-nitro-L-arginine methyl ester, a NO synthase (NOS) inhibitor, largely decreased the hyperperfusion. Furthermore, the expression of the different NOS isoforms, assessed by reverse transcription-PCR and immunoreactive levels, determined by Western blot, revealed a remarkable induction of the inducible NOS in the crushed limb. Similarly, endothelial NOS mRNA increased gradually after the induction of muscle damage. In contrast, the major muscular NOS, i.e., neuronal isoform remained unchanged. In line with the alterations in the mRNA levels, Western blot analysis revealed parallel changes in the immunoreactive levels of the various NOS. These findings indicate that muscle crush is associated with activation of the NO system mainly due to enhancement of iNOS. This may contribute to NO-dependent extreme vasodilatation in the injured muscle and aggravate the hypovolemic shock after crush injury.

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Section: Resultsmentioning

confidence: 99%

Involvement of nitric oxide system in experimental muscle crush injury.

Rubinstein

Abassi²,

Coleman³

et al. 1998

J. Clin. Invest.

104

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show abstract

“…In a canine study, after six hours of ischemia, only 20 % of pre-ischemic ATP remained which led to complete muscle necrosis [7]. Histologic analysis revealed central muscle necrosis with a surrounding zone of partial ischemia and peripheral tissue edema, often within areas of incomplete injury [8].…”

Section: Epidemiologymentioning

confidence: 99%

Acute compartment syndrome: obtaining diagnosis, providing treatment, and minimizing medicolegal risk

Taylor

Sullivan

Mehta

2012

Curr Rev Musculoskelet Med

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Acute compartment syndrome (ACS) is a surgical emergency. Diagnosis depends on a high clinical suspicion and an understanding of risk factors, pathophysiology and subtle physical exam findings. The typical high risk scenario for ACS is a male patient younger than 35 years of age, involved in a high energy sport or roadway collision, resulting in a tibial shaft fracture. He will go on to develop acute compartment syndrome of the leg in less than 10 hours and require emergent fasciotomy. Diagnosis of ACS in this patient is primarily a clinical one but can be confirmed with invasive intracompartmental pressure monitoring or noninvasive near infrared spectroscopy (NIRS). Delaying the diagnosis will likely result in some degree of permanent disability and places the surgeon at high risk for litigation. This article reviews the salient features of acute compartment syndrome that should be understood by all orthopaedic residents and surgeons.

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“…As compartment pressure rises an identical rise in venous pressure results in decreased perfusion pressure. Resultant decreased blood flow causes further tissue injury as a result of hypoxia and accumulation of products of metabolism, and further increased compartment pressure 16,17 . Ultimately, necrosis of nerve and muscle results in a spectrum of pathological change from discrete patchy necrosis reflected in isolated or limited neurologic deficit, to ischaemic contracture, infarction of large areas of muscle, and functional uselessness.…”

Section: Discussionmentioning

confidence: 99%

Axillary vein thrombosis and compartment syndrome in upper limb trauma

Cullen

1994

Emergency Medicine

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Axillary thrombophlebitis and compartment syndrome are potential complications of upper limb trauma with significant morbidity and mortality. A 25 year old man presented 24 hours following an isolated limb injury with these synchronous complications. Early systemic anticoagulation and fasciotomy resulted in significant bleeding and anaemia. Renal function remained normal despite evidence of significant rhabdomyolysis (CK>16 000U/L). Several attempts at closure of fasciotomies were frustrated by major swelling and finally, devitalised biceps brachii was debrided in toto. He was discharged with residual sensory and motor deficits. Three months later, he had marked disability from weakness, sensory disturbance and post‐phlebitic swelling.

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Muscle Microcirculatory Impairment Following Acute Compartment Syndrome in the Dog

Cited by 11 publications

References 0 publications

Involvement of nitric oxide system in experimental muscle crush injury.

Involvement of nitric oxide system in experimental muscle crush injury.

Acute compartment syndrome: obtaining diagnosis, providing treatment, and minimizing medicolegal risk

Axillary vein thrombosis and compartment syndrome in upper limb trauma

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