Compartment syndrome (CS) is the result of increased pressure within a closed anatomical space. Any area of the body that contains a compartment can be affected, namely the hand, forearm, upper arm, entire lower extremity, abdomen, and buttocks. As intracompartment pressures increase and exceed the perfusion pressure, tissues become ischemic and can become necrotic without timely intervention. Thus, CS is limb threatening and can be life threatening. Prognosis depends on the timeliness of diagnosis and intervention. Therefore, time is critical; 6 hours is accepted as the upper limit of tissue viability.2
Traditionally, the "6 P's" (pain, paresthesia, paresis, pallor, poikilothermia, pulselessness) were used to clinically diagnose CS; however, pulselessness and pallor are usually not present in CS.3 Additionally, poikilothermia is not a commonly used term, and it usually occurs at a point where the extremity is nonviable. Thus, only "3 P's" remain; learn them – pain, paresthesia, and paresis – and do not rely on the other three.
In the pathophysiology of CS, venous outflow resistance is increased, ultimately leading to a cessation in blood flow. CS is really a venous obstruction rather than an arterial infarction. Venous outflow is impeded when the compartment pressure exceeds about 30 mm Hg. As the compartment pressure rises, all the veins are compressed and venous outflow is blocked. Since venous outflow is blocked, perfusion of the tissues within the compartment ceases. There might still be arterial pulsation of the larger arteries within the compartment and distal to the compartment because the systolic pressure still exceeds the compartment pressure. In addition, arterial blood might continue to flow outside the compartment and/or through arteriolo-arteriolar shunts,2,4,5 thus, distal pulses might still be present. Pulsation within larger arteries, however, will not result in any capillary circulation (ie, no cellular perfusion is present) because venous outflow is blocked. Avoid this pitfall: pulselessness is not present in early cases of compartment syndrome. Do not use the presence of pulses to rule out a compartment syndrome: this will delay the diagnosis beyond the point of salvage.
Consider a more extreme example. If the two iliac arteries are ligated, there is obviously no flow through the iliac arteries. Yet, a finger placed on the iliac arteries (proximal to the ligation) would still yield pulsation. Again, the presence of pulsation does not necessarily equate to blood flow.
Similarly, pallor might not be evident in CS. The skin outside the compartment can be normally perfused since only intracompartment perfusion might be affected. Even if the venous outflow of the skin is impeded, the appearance of the skin would be that of venous congestion, not pallor.
Pain, however, is a reliable indicator of CS. Suspect CS if the patient complains of severe pain following any injury to an extremity. Often, the pain is more severe than one would expect from the injury. Severe pain after splinting or casting should raise the possibility of CS. The pain can occur at rest or with certain movements, such as passive stretching of the muscles or active flexion/extension. The pain can be described as a burning sensation, and it is not usually relieved by pain medication or splinting.
Paresthesia will ultimately develop as nerve conduction slows in hypoxic/ischemic conditions. A later finding in CS, paresis or paralysis might set in as motor neurons start to dysfunction. The extremity might also feel tense or hard.2,5
The anterior distal lower extremity is cited as the most common site of CS. The reason for this location is probably due to its high frequency of injury. The usual cause of CS is a fracture. However, the incidence of CS following a fracture is actually very small. In the setting of a fracture, CS is therefore a diagnosis of low probability but high morbidity. It is also estimated that 30% of limbs will develop CS following vascular injury.2
There are two main pathways to increasing intracompartment pressure:
Increasing the fluid content within the compartment, either by hemorrhage or from edema
Decreasing the compartment size, either by tissue constricture or by external compression2,6
Osseofascial compartments are relatively nondistensible and have a fixed volume. Thus, the introduction of fluid into or external compression of the compartment will undoubtedly raise the intracompartment pressure. There are several theories that attempt to explain the exact mechanism of the resulting decrease in tissue perfusion. One popular theory states that the increase in intracompartment pressure leads to a compression of the venous system. As the pressure in the venous system rises, the arteriovenous pressure gradient decreases. Hence, blood has a decreased tendency to flow into the capillaries. The body's compensatory mechanisms to increase perfusion pressure are eventually overwhelmed by increasing intracompartment pressures. The increased venous outflow resistance ultimately causes a retrograde blood stasis. Blood ceases to perfuse the cells, and the tissues become ischemic.4
A further complication is that hypoxic cells will release vasoactive substances such as histamine and serotonin, which serve to increase capillary permeability. As protein leaks into the interstitial space, water is pulled along with it. Thus, the intracompartment pressures continue to rise.
Prolonged ischemia (over 6 hours) will result in rhabdomyolysis and potential loss of limb. Rhabdomyolysis can lead to acute renal failure and eventual death. CPK and serum myoglobin levels might be elevated, indicating rhabdomyolysis. Dipstick urinalysis might be positive for blood but on microscopic review be negative for RBCs, indicating the presence of myoglobin in the urine.2
Radiographs of the extremity might show the presence of an underlying fracture, but the absence of a fracture does not rule out CS because there are other etiologies for CS. A CT scan might reveal areas of muscle necrosis. Obtaining a CT scan, however, should not delay treatment. Once CS is suspected, it should be acted on immediately to increase the patient's chance of recovery.
A measurement of the compartment pressure should be obtained as soon as CS is suspected. Commercial pressure measurement devices are available; there are also three generic procedures for measuring intracompartment pressure (see "Intracompartment Pressure Measurement Methods").
The level of intracompartment pressure that serves as the cutoff point for diagnosing CS is under debate. Some cite 30 mm Hg as indicative of CS, whereas others claim that 45 mm Hg is an appropriate cutoff.2
The threshold for developing CS is directly affected by the amount of blood flow to that area. As such, hypotensive patients can develop CS at lower intracompartment pressures. Thus, some advocate the use of perfusion pressure, rather than just intracompartment pressure, in determining CS. (Perfusion pressure = diastolic BP minus the intracompartment pressure.) McQueen used perfusion pressure measurements of less than 30 mm Hg as diagnostic of CS and an indication for fasciotomy.2
Intracompartment Pressure Measurement Methods
The Stryker Stic device (registered trademark, Stryker, Kalamazoo, MI) is a commercially available product made specifically for measuring intracompartment pressures. It is fast and accurate, but it is modestly expensive. Prep the skin with povidone-iodine solution. Administer local anesthesia if necessary, being careful not to inject within the compartment.
There are three generic alternatives to the Stryker Stic, two of which will probably work with equipment that is available in most hospitals.
The IV infusion pump method (probably the best alternative)
Electronic pressure transducer method
Mercury column manometer method (difficult and sometimes not reliable7).
IV Infusion Pump Method
This method is very simple, but it requires an IV infusion pump with a built-in pressure readout. Most modern IV infusion pumps have this feature, which is most commonly used to permit nurses to set limits on IV infusion pressure so that the pump will alarm if a high pressure condition is encountered, usually due to an infiltrated IV or a malpositioned IV catheter. These sophisticated pumps reduce the likelihood of an undetected infiltrated or obstructed IV catheter.
Uppal et al described the use of the IVAC infusion pump to measure the intracompartment pressure.8 The accuracy of this method has been confirmed by others7:
Prime the IV infusion pump with saline and remove all air bubbles.
Attach an 18-gauge needle to the end of the IV tubing. Infuse saline so that saline is primed through the entire needle.
Set the IV infusion pump to 25 cc/hr.
Set the pump to read pressure in mm Hg (rather than cm H2O).
Adjust the height of the IV infusion pump to be roughly level to the patient's extremity that is about to be measured.
Turn the pump on to begin infusion, then insert the 18-gauge needle with saline flowing through it at 25 cc/hr into the desired compartment.
Immediately read the infusion pressure on the pump when the needle is inserted. Some pumps have a feature to display the pressure continuously. The pressure should have gone from a value near zero to a higher value reflecting the pressure within the compartment. The pressure must be read immediately to prevent fluid from infusing into the compartment and elevating the pressure further.
Remove the needle from the compartment.
Electronic Transducer Method
Prime a standard arterial line electronic pressure transducer module with normal saline. There should be at least two IV connections. One connects to an IV pump, which should be set at a very low rate such as 10 mL/hr. The distal port should be connected to an 18-gauge needle. The pressure transducer module cable should be connected to a blood pressure module/amplifier on the patient’s monitor system.
Infuse IV fluid until the 18-gauge needle is filled with saline, then stop the IV infusion.
Place the tip of the needle at the level of the patient’s extremity to be tested, then "zero" the monitor at this level.
Insert the needle into the designated muscle compartment.
Start the IV infusion. The monitor should show the pressure rising. When it reaches a plateau, this reflects the intracompartment pressure. Stop the IV infusion.
Core Knowledge Points—Management
Since the pathophysiology of CS involves an ischemic event, it might be helpful to give the patient oxygen to increase Po2. The patient should be hydrated intravenously to prevent acute renal failure secondary to rhabdomyolysis.2,6 The involved extremity should be kept at body level so that arterial blood flow is not compromised and venous drainage is unhindered.5
The definitive therapy for CS is fasciotomy to relieve the intracompartment pressure. The emergency physician should seek immediate surgical consultation, usually with orthopedics.
Core Knowledge Points—Complications
Prognosis ultimately depends on the speed of diagnosis and treatment. However, even with timely intervention, the patient might still suffer some permanent neuromuscular dysfunction.
Volkmann ischemic contracture is the functionless, claw-hand deformity that results from untreated forearm ischemia.
Rhabdomyolysis will occur after approximately 6 hours of warm ischemia and can escalate into a bacterial gangrene infection, loss of limb, and sepsis. Acute renal failure can result from rhabdomyolysis, and if left untreated, will lead to death.9 Following a fasciotomy, there is a risk of infection. The procedure will also leave some cosmetic deformity.2
Core Knowledge Points—Clinical Pearls
CS can occur without trauma. Prolonged external compression of an extremity can occur in the setting of drug or alcohol overdose and lead to CS.
Prognosis depends on the speed of diagnosis and treatment.
Severe pain (especially with passive stretching of the muscles) and increasing neuromuscular deficits are the key clinical manifestations of CS.
The traditional sign of pulselessness is not a definitive criterion of CS. Pulses can still be palpable in CS due to arteriolo-arteriolar shunts. Do not be misled by palpable pulses.
CS is mainly a clinical diagnosis but can be confirmed by measuring intracompartment pressures.
Critically ill patients can present with a myriad of complicating factors.
Shock: Hence, a lower intracompartment pressure is needed to overcome a lower perfusion pressure. Additionally, patients who require large volume resuscitation are at risk for developing interstitial edema and subsequent CS.9
Altered mental/neurologic status: Thus, the patient might not complain of pain and/or paresthesia. Examples include patients with CNS injury or patients on narcotics.
Hypoxia and/or anemia: In which case ischemia will occur more quickly following smaller compromises in capillary perfusion pressure.
Treatment of rhabdomyolysis involves aggressive intravenous hydration to prevent acute renal failure.
Fasciotomy is the definitive treatment for CS.
An orthopedic surgeon performed a fasciotomy of the patient’s forearm.
Large areas of muscle necrosis were noted.
He developed renal insufficiency secondary to severe rhabdomyolysis.
After multiple debridement procedures, he was able to regain some forearm, wrist, and hand function, but he suffered permanent neuromuscular deficits.
One of the patient's friends revealed that he had taken 20 or 30 shots of liquor the previous night. After he fell off the bar stool, his friends carried him into the back of a pickup truck, where he slept until he awoke the next day. His compartment syndrome was caused by his sleeping on his arm and compressing it for an extended period of time. The alcohol intoxication was significant because it blunted his body's normal protective reflexes that stimulate moving and rolling while sleeping.
The bruised lesion on his back was probably caused by pressure necrosis that resulted from something pressing on his flank while he was unconscious in the pickup truck