Osteofascialcompartmentsyndrome is a series of early signs and symptoms of acute ischemia and hypoxia of muscles and nerves within the osteofascial compartment formed by bone, interosseous membrane, septum and deep fascia. It is most commonly seen on the palmar aspect of the forearm and lower leg. It is often caused by an increase in the volume of the intraosseous contents due to the hematoma and tissue edema of traumatic fractures or an increase in the intraosseous pressure due to the decrease in the volume of the osteoinfascial compartment due to local compression. When the pressure reaches a certain level [8.7kpa (65mmHg) in forearm and 7.3kpa (55mmHg) in calf], the small arteries supplying the muscle can be closed, forming a vicious cycle of ischemia-edema-ischemia, leading to the following stages according to the different degrees of ischemia: 1, near ischemic muscle contracture: early ischemia, after timely treatment to restore blood supply, it may not occur or only occur After timely treatment to restore blood supply, muscle necrosis may not occur or may only occur in a very small amount, which may not affect the function of the limb. 2, Ischemic muscle contracture: shorter time or more severe incomplete ischemia, after restoration of blood supply most of the muscle necrosis, forming contracture deformity, seriously affecting the function of the affected limb. 3, extensive gangrene: long time complete ischemia, a large number of muscle gangrene, often requiring amputation. If a large number of toxins enter the circulation, it can also lead to shock cardiac arrhythmia and acute renal failure. The early clinical manifestations of osteofascial compartment syndrome are predominantly localized. Only when muscle ischemia is longer and extensive necrosis has occurred, systemic symptoms will appear, such as increased body temperature, increased pulse rate, decreased blood pressure, increased white blood cell count, accelerated blood sedimentation, and myoglobulin in urine. 1.Pain: Persistent and severe pain in the limb after trauma, and progressively increasing, is the earliest symptom of this sign. It is an important manifestation of nerve compression and ischemia within the osteofascial chamber. The nerve tissue is the most sensitive to ischemia, and the sensory fibers show symptoms at the earliest, so it must be paid enough attention to this, and timely diagnosis and treatment. In the late stage, when the ischemia is severe and the nerve function is lost, the sensation disappears, that is, there is no pain. 2.Fingers or toes are flexed: muscle strength is weakened. When the finger or toe is passively stretched, it can cause severe pain, which is the early manifestation of muscle ischemia. 3.The skin of the affected ventricular surface is slightly red: slightly higher temperature, swelling, severe pressure pain, and increased intra-ventricular tension can be felt on palpation. 4.Distal pulses and capillary filling time are normal: However, special attention should be paid to the fact that the tissue pressure inside the osteofascial chamber rises to a certain degree:8.66kPa (65mmHg) in the forearm and 7.33kPa (55mmHg) in the lower leg, it can close the small arteries supplying blood to the muscle, but this pressure is far below the patient’s systolic blood pressure, so it is not enough to affect the blood flow in the main arteries of the limb. At this point, although the distal arterial pulsation exists and the capillary filling time of the fingers and toes is still normal, the muscle has already become ischemic. Therefore, the presence of distal arterial pulsation in the limb is not a safe indicator, but should be analyzed in conjunction with other clinical manifestations to assist in the diagnosis. The above symptoms and signs are not fixed. If left untreated, ischemia will continue to worsen and develop into ischemic myoclonus and gangrene, and the signs and symptoms will change as well. The five main clinical manifestations of ischemic myoclonus can be recorded as five “P “s: (1) pain (pain) to painlessness; (2) pallor or cyanosis, marbling, etc.; (3) paresthesia; (4) paralysis; (5) pulselessness; osteochondrosis Once the diagnosis of ventricular syndrome is confirmed, fascial decompression should be performed immediately by incision. Early and complete fascial decompression is the only effective way to prevent ischemic necrosis of muscles and nerves. It is important not to wait until the 5 “P” signs appear before performing an incision and decompression, which can lead to irreversible ischemic muscle contracture. The incised skin is usually not sutured due to excessive tension. The wound can be loosely filled with petroleum jelly gauze, wrapped with sterile dressing, and postponed after the swelling has subsided, or the wound can be closed with a free skin graft. Do not forcefully suture the skin and lose the role of incision and decompression. After local incision and decompression, blood circulation is improved, and a large amount of toxins from necrotic tissues enter the blood circulation, so water loss, acidosis, hyperkalemia, renal failure, cardiac arrhythmia, shock and other serious complications should be actively prevented and treated, and if necessary, amputation should be performed to save lives.