Acute compartment syndrome occurs
when the tissue pressure within a closed muscle compartment exceeds the
perfusion pressure and results in muscle and nerve ischemia. It
typically occurs subsequent to a traumatic event, most commonly a
fracture.
The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and decreased peripheral sensation secondary to nerve irritation.
Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, and extremity paresis, because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb contracture, called ults. Severe cases may lead to renal failure and death.
The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.
Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although CSS is more common in the anterior compartment of the lower leg, it has been described in the forearm of motocross racers and other athletes.[1, 2, 3] For more information, see the Medscape Reference article
The incidence of compartment syndrome depends on the patient population studied and the etiology of the syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior compartment syndrome[4] ; compartment syndrome was seen in 1-9% of leg fractures.
Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, buttock,[5] and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous exercise. Clinicians need to maintain a high level of suspicion when dealing with complaints of extremity pain.[6]
The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. (See Treatment.)
Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common antecedent to compartment syndrome. Approximately 50 years after von Volkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction.[8]
Wilson first described the initial case of exertional compartment syndrome in 1912. Mavor, in 1956, first reported a case of chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in the literature, and pathophysiology and treatment options have been discussed.
In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of compartment syndrome. In the 1970s, the importance of measuring intracompartmental pressures became apparent.
Owen et al published a series of articles describing the use of the wick catheter for pressure measurement and then documented high compartmental pressures in various circumstances.[9] Almost simultaneously, Matsen published his findings, which are the most commonly annotated group of articles in present literature.[10]
The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and decreased peripheral sensation secondary to nerve irritation.
Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, and extremity paresis, because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb contracture, called ults. Severe cases may lead to renal failure and death.
The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.
Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although CSS is more common in the anterior compartment of the lower leg, it has been described in the forearm of motocross racers and other athletes.[1, 2, 3] For more information, see the Medscape Reference article
The incidence of compartment syndrome depends on the patient population studied and the etiology of the syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior compartment syndrome[4] ; compartment syndrome was seen in 1-9% of leg fractures.
Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, buttock,[5] and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous exercise. Clinicians need to maintain a high level of suspicion when dealing with complaints of extremity pain.[6]
The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. (See Treatment.)
Historical aspects
The original description of the consequences of unchecked rising intracompartmental pressures is widely attributed to Richard von Volkmann. His 1872 publication documented nerve injury and subsequent contracture from compartment syndrome following supracondylar fracture.[7] That injury remains known as Volkmann contracture.Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common antecedent to compartment syndrome. Approximately 50 years after von Volkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction.[8]
Wilson first described the initial case of exertional compartment syndrome in 1912. Mavor, in 1956, first reported a case of chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in the literature, and pathophysiology and treatment options have been discussed.
In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of compartment syndrome. In the 1970s, the importance of measuring intracompartmental pressures became apparent.
Owen et al published a series of articles describing the use of the wick catheter for pressure measurement and then documented high compartmental pressures in various circumstances.[9] Almost simultaneously, Matsen published his findings, which are the most commonly annotated group of articles in present literature.[10]
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