Compartment syndrome occurs when excessive pressure develops in one of the body’s compartments, exceeding the arterial pressure entering the compartment and so preventing blood from flowing in to supply the tissues. This can cause severe problems including great pain and tissue death if it is not treated quickly. This problem occurs mostly in the lower leg and in the forearm, where the muscles are all enclosed in a soft tissue section called a compartment, with the walls made up of bone and strong connective tissue called fascia. This makes the compartment inextensible and liable to pressure build up in certain circumstances.
The largest cause of compartment syndrome is a tibial fracture, with other causes including other fractures, blood vessel compromise, crush injuries and tight plasters or dressings. Symptoms once compartment syndrome is established are a loss of the pulses, inability to move the part and loss of sensibility. If the doctor suspects that compartment syndrome is present then surgical decompression is the primary treatment. Complications can include muscle breakdown leading to renal failure and Volkmann contracture, an irreversible contracture of the forearm muscles.
Whilst most compartment syndrome is acute following some kind of event, careful measurements of the pressures within the compartments of the leg have shown chronic compartment syndrome to be a clinical entity in situations such as excessive exercise performance. As the tissue pressure increases in the muscular and fascial compartment it starts to compromise the blood flow into the compartment, damaging the muscles and nerves. In the acute type the onset is fast and leads quickly to muscle and nerve damage which is irreversible unless treated urgently.
Shin splints in athletes have been regularly confused with chronic compartment syndrome, with the pain often on both sides and occurring after a particular period of exertion. The criteria for this condition vary in various pursuits and the abnormality can now be sought by pressure measurements. Open tibial fractures give the highest levels of compartment syndrome, with closed tibial fractures being much less risky for this condition. Vascular injuries may also precipitate compartment syndrome but vascular surgeons typically perform decompression at the time of repair if required.
Two kinds of factors are important for triggering compartment syndrome, either internal or external factors acting on the area. Wearing clothes too tight and the application of plasters or dressings too tightly can produce the required compression. Many potential internal factors exist such as swelling from a crushing injury, bleeding internally, doing excessive muscle building and fractures. As the pressure rises and overwhelms the blood pressure then blood flow stops, damaging the muscles and nerves and causing muscle death, leading to chemical changes which pull water into the compartment, increasing the pressure again.
High compartment pressure need speedy surgical decompression as if it is left for six to ten hours the compartment will develop muscle death, nerve damage and more generalised tissue death. The damage to the muscles can allow the release of myoglobin into the circulation which can cause kidney damage which can be fatal. Chronic compartment syndrome is accompanied by an increase in the volume of muscles which increases the pressure, allowing this to remain raised between muscular contractions and interrupt blood flow. This develops into muscle cramps as the muscles are denied the required amounts of blood.
Diagnosis of acute lack of blood to a limb can be indicated by limb pallor, pulse loss, pins and needles, pain and coldness of the leg, however these signs are not reliable in terms of diagnosis in clinical practice. Presentation may be of unexpectedly elevated levels of pain not seemingly related to the injury level, with an aching, deep pain which is worse on muscle stretching. On examination of the limb it should be clear whether there is any likelihood of internal tissue damage. Sensory testing can be helpful as pressure shows more obviously in sensory nerve function.
The signs and symptoms of the acute lack of blood in a limb can be indicated by the leg looking pale, a reduction in pulses, a cold leg and pins and needles and pain. Diagnostically however these signs may be unreliable to establish the syndrome. Presentation may include high pain levels out of proportion to the injury level, giving a deep, aching pain which increases on stretching of the muscles. Significant trauma to the limb should be clear on examination and could indicate damage to the tissues. Testing for loss of sensation may be useful as sensory nerves are more susceptible to pressure.
Jonathan Blood Smyth is the Superintendent of Physiotherapy at an NHS hospital in the South-West of the UK. He writes articles about back pain, neck pain, and injury management. If you are looking for physiotherapists in bradford visit his website.
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