Compartment Syndrome

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.

Tibial fractures are the most common cause of compartment syndrome, other causes being compromise of the blood vessels, tight dressings or plasters, crush injuries and other fractures. Established compartment syndrome shows itself by a loss of sensation, loss of movement of the part and loss of pulses. Decompression of the tight compartment is the typical and most effective treatment for this syndrome. Complications include breakdown of muscle tissue which can progress to renal failure and Volkmann contracture, a non-reversible damage to the muscles of the forearm.

Acute onset of compartment syndrome is the most common presentation after a traumatic event, chronic compartment syndrome has been described secondary to excessive exercise by measuring the pressure occurring within the leg compartments. Inside the compartment composed of the muscle and fascia the pressure rises, steadily reducing the blood flow into the area until muscle and nerve damage occurs. Acute compartment syndrome comes on quickly with the irreversible damage following closely after unless it is treated promptly.

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.

If compartment syndrome is going to be present there have to be either internal or external reasons for the heightened pressure in the limb segments. Outside contributing factors can be clothes which are too tight or similar dressings or plasters. Internal factors may be many and cover tissue oedema secondary to crush injury, internal bleeding, fractures and even doing too muscle building. The pressure levels exceed the blood pressure and this starves the nerves and muscles, allowing muscle tissue death with chemical changes attracting large amounts of water into the areas, further increasing the pressure. Arterial blood flow can be fully compromised eventually.

Elevated pressure in a compartment requires prompt decompression surgically, a delay of 6 to 10 hours would lead to nerve damage, death of muscle tissue and of more widespread tissue areas. Muscle damage can result in the release of the chemical myoglobin into the vascular system which can induce fatal renal damage. In chronic compartment syndrome the muscles increase in volume as they exercise and this raises the compartment pressure, keeping the pressure elevated between the contractions of the muscles and so impairing blood flow. Cramp in the muscles then develops as the necessary amounts of blood are not supplied.

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, editor of the Physiotherapy Site, writes articles about Physiotherapists, physiotherapy, Physiotherapists in Coventry, back pain, orthopaedic conditions, neck pain and injury management. Jonathan is a superintendant physiotherapist at an NHS hospital in the South-West of the UK.

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