The most common causes of anterior compartment syndrome are trauma (fractures, crush injuries, contusions, gunshot wounds), tight casts or dressings, extravasation of IV infusion, burns, post-ischemic swelling, bleeding disorders, and arterial injury. When the pressure inside the anterior compartment increases, tissue perfusion can be compromised, which may lead to irreversible muscle and nerve damage – muscle necrosis. The anterior compartment of the lower leg is the most common site for acute compartment syndrome. Errors in Hox gene expression can lead to malformations in the limbs. These genes control patterning and consequently morphology of the developing limb in the human embryo. SHH activates specific HOX genes – Hoxd-9, Hoxd-10, Hoxd-11, Hoxd-12, Hoxd-13 – which are essential in limb polarization and regional specification. The zone of polarizing activity (ZPA) produces SHH, promoting the organization of the limb bud along the anterior-posterior axis. The specific fibroblast growth factor involved in hindlimb development is Fgf10, which is stimulated by Tbx4. The apical ectodermal ridge (AER) produces a fibroblast growth factor (Fgf), which promotes the outgrowth of the limb buds by stimulating mitosis. Retinoic acid is a global organizing gradient that initiates the production of transcription factors that specify regional differentiation and limb polarization. Several factors influence the formation of the limb bud vasculature and musculature including retinoic acid, sonic hedgehog (SHH), HOX genes, apical ectodermal ridge (AER) and the zone of polarizing activity (ZPA). The limb buds of the embryo begin to form about 5 weeks after fertilization as the lateral plate mesoderm migrates into the limb bud region and condenses along the central axis to eventually form the vasculature and skeletal components of the lower limb.
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