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Compartment syndrome-induced microvascular dysfunction: an experimental rodent model.

Abdel-Rahman Lawendy¹, David W Sanders, Aurelia Bihari

¹Division of Orthopaedic Surgery, University of Western Ontario, London, Canada. arlawend@uwo.ca

Canadian Journal of Surgery. Journal Canadien De Chirurgie

|March 30, 2011

Summary

Acute compartment syndrome (CS) significantly impairs skeletal muscle microcirculation and increases cellular injury due to elevated intracompartmental pressure. This study reveals CS causes microvascular dysfunction and inflammation, highlighting its limb-threatening nature.

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Area of Science:

Vascular Surgery
Trauma Surgery
Skeletal Muscle Physiology

Background:

Acute compartment syndrome (CS) is a critical condition caused by elevated intracompartmental pressure, leading to limb-threatening ischemia.
The precise pathophysiologic mechanisms underlying CS remain incompletely understood.
This study investigates the impact of increased intracompartmental pressure on skeletal muscle microcirculation, inflammation, and cellular injury.

Purpose of the Study:

To elucidate the effects of elevated intracompartmental pressure on skeletal muscle microcirculation.
To quantify the inflammatory response in acute compartment syndrome.
To assess the degree of muscle cellular injury induced by CS.

Main Methods:

Acute compartment syndrome (CS) was induced in Wistar rats using a saline infusion technique, maintaining pressure between 30-40 mm Hg for 45 minutes.
Intravital videomicroscopy (IVVM) was employed to visualize and quantify microcirculation in the extensor digitorum longus muscle post-fasciotomy.
Leukocyte recruitment was measured to assess inflammation, and differential fluorescent staining was used to quantify muscle cellular injury.

Main Results:

Elevated intracompartmental pressure significantly increased nonperfused capillaries (from 12.7 to 30.0 per mm) and decreased continuously perfused capillaries (from 78.4 to 41.4 per mm).
The proportion of injured muscle cells increased from 5.0% to 16.3% in the CS group.
Activated leukocyte counts rose significantly (from 3.6 to 8.6 per 100 μm²), indicating a pronounced inflammatory response.

Conclusions:

Early CS-induced microvascular dysfunction is characterized by reduced nutritive capillary perfusion.
Acute compartment syndrome leads to significant skeletal muscle cellular injury.
A severe acute inflammatory component is associated with CS-induced microvascular dysfunction.