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 most common cause of compartment syndrome is a fracture of the tibia but there are other potential causes which include tissue crush injuries, tight dressings and plasters, other fractures and damage to blood vessels. If the syndrome develops the signs and symptoms are a loss of feeling in the area, loss of pulses and loss of the ability to move the limb. Surgical decompression is the primary form of management for diagnosed compartment syndrome. Potential complications include kidney failure, breakdown of muscle tissue and permanent contracture of the forearm muscles.
A traumatic event is the most common precipitating factor for compartment syndrome in the acute mode, but enthusiastic performance of exercises can show measureable increases in the pressure in a compartment, leading to a diagnosis of chronic compartment syndrome. The nerves and muscles are damaged by the acute loss of blood coming into the compartment due to the pressure gradually rising inside an inextensible area. Irreversible tissue damage can occur after the rapid acute onset of compartment syndrome without prompt management.
The athletic condition shin splints may be related to chronic compartment syndrome, the pain typically occurring in both legs and after a particular exercise period has elapsed. The criteria for diagnosing the problem are specific to particular activities and the problem can now be diagnosed via pressure measuring. The highest risk of this syndrome occurs after open fractures of the shin bone, with closed fractures being much less likely to cause problems. Injuries to the blood vessels can also set off compartment syndrome but this is dealt with by the vascular surgeons who decompress the area at surgery.
For compartment syndrome to occur there must be either external or internal reasons for a raised pressure in the segments of the limb. External forces can include over tight clothes or boots and tight dressings or plasters. Internal factors can be numerous and include tissue swelling due to crush injury, fractures or internal tissue bleeding and even overdoing weightlifting. The muscles and the nerves are starved of blood due to the excessive pressure, causing chemical changes due to muscle necrosis which attract greater amounts of water into the compartment, increasing the pressure again. Eventually arterial blood flow is completely obstructed.
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.