Acute Compartment Syndrome
Compartment syndrome describes the state of increased pressure in a closed tissue space that impairs blood flow to that space. In turn, the lack of perfusion leads to hypoxia and damage to the muscles and nerves in the space or passing through it.
Compartment syndrome is often caused by trauma, such as a tibia fracture, but can be seen after vascular surgery (a so-called reperfusion injury). Compartment syndrome can also be caused by tight casts, or by infiltration of an intravenous line. Avoiding complications from compartment syndrome requires timely diagnosis and expeditious treatment. The diagnosis can be made on the basic clinical signs and symptoms (especially increasing pain as lactate – the product of anaerobic metabolism – builds up). Diagnosis can be confirmed with measurement of the pressure inside the compartment, but diagnosis can be made on clinical grounds alone in high-risk patients to expedite treatment. Definitive treatment is surgical with urgent fasciotomy: cutting the fascia that surrounds the compartment, thereby relieving the pressure.
Structure and Function
Muscles in the extremities are enveloped by a band of strong connective tissue known as fascia. The space surrounded by a given fascial covering is known as a compartment.
The lower leg, the region most commonly involved in compartment syndrome, has four anatomical compartments: the anterior, lateral, deep posterior, and superficial posterior compartments (Figures 1 and 2).
The anterior compartment contains the muscles that primarily dorsiflex (extend) the ankle and the toes: the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. Also in this compartment are the deep peroneal nerve and the anterior tibial artery and vein.
When the anterior compartment is under pressure, patients may complain of a “pins and needles” sensation in the first web space of their foot, which is innervated by the deep peroneal nerve.
Missed compartment syndrome in the anterior compartment can result in “foot drop,” a condition where patients cannot dorsiflex their foot when ambulating.
The lateral compartment contains the peroneus longus and peroneus brevis muscles and the superficial peroneal nerve. The vascular supply is through the peroneal artery. Notably, the peroneal artery lies in the posterior compartment and supplies the lateral compartment through anastomotic branches that course around the fibula. (That this compartment does not contain an artery is of particular interest to those who write student examination questions.)
The superficial posterior compartment contains the gastrocnemius, soleus and plantaris muscles, along with the sural nerve — a purely sensory nerve.
The deep posterior compartment contains the following muscles: tibialis posterior, flexor hallucis longus, and flexor digitorum longus. The neurovascular contents comprise the tibial nerve and posterior tibial vessels. The tibial nerve is exceptionally important as it provides sensation to the plantar surface of the foot. Without normal function of the tibial nerve, a person can begin to damage the skin on the sole of the foot without being aware of it; inevitably, the skin will break down. (Loss of protective sensation is commonly seen with diabetic peripheral neuropathy.)
Compartment syndrome may also affect more than one compartment at a time, causing a variety of symptoms during presentation.
When there is bleeding or edema within a compartment, the pressure within the compartment increases, because the surrounding fascia does not stretch. The increased pressure impairs blood flow to the tissues (see Figure 3).
In the setting of decreased perfusion and resulting ischemia, the tissues within a compartment will switch from aerobic to anaerobic metabolism. This causes increased production of lactate (lactic acid). The increased level of lactate creates the burning pain characteristic of compartment syndrome.
Ultimately, increased pressure and decreased perfusion leads to necrosis of the muscles and nerves within the compartment.
Critical to an understanding of compartment syndrome is that capillaries are occluded by an increasing compartment pressure before arteries are occluded. Arteries may still flow, and distal pulses may still be palpable, even if capillary perfusion is blocked. As such, ordering serial vascular observations (“check pulses every 2 hours”) to detect compartment syndrome is unhelpful and indeed potentially harmful: if distal pulses are charted as present, a physician may gain a false confidence that all is well and ignore other signs and symptoms of ischemia.
Compartment syndrome may result from a decrease in compartment size, or an increase in compartment pressure.
A decrease in compartment size can occur with: constrictive dressings, tight casts, burns (eschar tissue), or localized external pressure that occurs in crush injuries or prolonged immobilization in drug overdose.
An increase in intra-compartmental pressure leading to acute compartment syndrome may be seen in a variety of conditions. These associated conditions include fractures, internal bleeding, extensive damage of the muscles (“rhabdomyolysis”), infiltration of IV infusions, increased capillary permeability caused by trauma (including surgical procedures) or burns, and reperfusion after a prolonged period of ischemia (e.g., after performing surgery to re-vascularize a limb).
Acute compartment syndrome may be iatrogenic. For example, anticoagulants (leading to bleeding in the compartment) and constrictive dressings are possible physician-induced causes.
Traditionally, students have been taught to memorize the “six P’s” of compartment syndrome. Reliance on the presence of these features can be misleading and delay diagnosis. (For that reason, the “six P’s” are not listed here but in the miscellaneous section below.)
The most sensitive and important finding is “pain out of proportion to the injury,” in association with a tense compartment.
Paresthesia in the distribution of the sensory nerve of the affected compartment(s) may present after 2 hours of ischemia, due to hypoxic injury of the nerve. Sensory fibers are more sensitive to ischemia and hence sensory changes will generally precede motor changes. The additional presence of paresthesia therefore indicates that irreversible muscle damage will soon follow if it hasn’t already started (from about 4 hours).
On examination, muscle compartments are swollen; they are often described as “tense and non-compressible.”
Paralysis, pallor, and pulselessness suggest arterial compromise and are not usually seen in acute compartment syndrome until irreversible damage has already occurred.
It is reasonable to ask what exactly is “pain out of proportion to the injury?” After all, it is impossible to truly know what another person is feeling. It would seem that “pain out of proportion to the injury” requires not only knowing how the person feels, but how much a given injury should hurt. One could hazard a guess based on clinical experience, but that method is still imprecise and will be colored by the patient’s anxiety and baseline pain tolerance. Yet an outsider can know something: namely, the expected time course of symptoms and a particular patient’s deviation from that. Specifically, a reduced fracture in a splint should hurt a bit less than one that is not reduced; it certainly should not hurt more. Thus, if the patient reports an increase in pain an hour after having the fracture immobilized, that suggests a problem. If in doubt, seek a second opinion, or refer the patient to another consultant. It is better to incorrectly make a diagnosis of compartment syndrome than to miss the diagnosis and have the patient develop ischemic contractures or lose a leg.
Plain x-rays are useful in the case of trauma to evaluate the fracture pattern if one is present.
Laboratory values such as elevated serum creatine kinase can be used to quantify muscle injury; however, this alone is not diagnostic of acute compartment syndrome, and the time taken to get the results may be detrimental to the viability of the patient’s leg.
First and foremost, however, compartment syndrome remains a clinical diagnosis. Objective confirmation is reassuring but waiting for that evidence must not create an unacceptable delay.
In a patient who is awake and cooperative, diagnosis is based on the exam and patient history – e.g., is the pain “out of proportion” to the injury?
In cases in which the patient is unable to participate in the exam, compartment pressures can be measured using needle manometry (see Figure 4).
Although it has been suggested that a given value for compartment pressure can be used to make the diagnosis, the best criterion for the diagnosis is the pressure differential between the mean arterial blood pressure and the measured compartment pressure. (The mean arterial blood pressure can be calculated as [(diastolic blood pressure x 2) + systolic blood pressure] divided by 3.)
Considering the difference (or “delta”) between compartment pressure and mean arterial blood pressure accounts for not only increased resistance from high compartment pressures but also decreased driving pressure and in turn represents the extent to which tissue perfusion might be limited. Specifically, perfusion may be limited not only because of elevated compartment pressure, but also because mean arterial pressure is low or some combination of the two. For example, a compartment pressure of 25 mm Hg ordinarily would not lead to tissue ischemia if mean arterial pressure were normal; it very well might if the patient is hypotensive because of hemorrhage.
Although the precise “delta” value to diagnose compartment syndrome is perhaps debatable and should be governed by clinical judgment (with lower values having greater sensitivity at the price of lost specificity), a commonly used consensus criterion is that if the difference is less than 40 mm Hg, perfusion will be impaired.
Acute compartment syndrome is most commonly associated with fractures. Tibia fractures have the highest association, followed by distal radius fractures.
The differential diagnosis of acute compartment syndrome includes conditions that may lead to compartment syndrome, such as an arterial thrombus leading to ischemia, necrotizing infection, or rhabdomyolysis. A deep venous thrombosis may also present with seemingly disproportionate pain with passive stretch of the great toe; however this is unlikely in the acute trauma setting.
Here are some ways to miss the diagnosis of compartment syndrome. Avoid them all.
- “One and done.” That is, after demonstrating one normal examination, the patient is assumed to be forever fine. As noted, ‘pain out of proportion to the injury’ is best determined by consideration of the symptoms over a period of time, and thus multiple serial exams are required.
- The extremity is not properly immobilized, or the fracture is inadequately reduced.
- There are tight bandages or casts around the extremity, which can cause external compression and limit the ability of soft tissue to swell.
- A patient is given (or allowed to self-administer) ever-increasing doses of narcotic medications without repeat evaluation.
In addition, conditions beyond fracture have a higher association with compartment syndromes. Suspicion for acute compartment syndrome should be raised if a patient has increasing pain with a gunshot wound, a circumferential cast or dressing, an extravasated intravenous infusion, a burn, coagulopathy, or recent arterial injury or surgery.
In a patient that is intubated and sedated, it is not possible to gather a clinical history or perform an exam. Therefore, any injury classically associated with compartment syndrome should result in a low threshold to measure the compartment pressure in order to obtain a diagnosis.
Treatment Options and Outcomes
Acute compartment syndrome is a surgical emergency. Treatment requires surgical release of the fascia around the compartments to allow the contents to expand. This procedure is known as a fasciotomy (see Figure 5).
Typically, all compartments of the affected extremity will be released at the same time; for example, acute compartment syndrome of the anterior compartment of the leg will result in fasciotomies of all four compartments of the leg. This procedure allows direct visualization of the muscles, and diagnosis is often confirmed by seeing muscle bulge out of the compartments as the pressure is released.
During the procedure, sections of muscle that appear necrotic should be excised (“debrided”), as they can be a source of infection. The skin incisions can be covered with Vacuum-Assisted Closure [VAC] dressings. VAC dressings, as their name implies, can suction fluid from the wound, reduce swelling and help pull the edges of the wound together. Alternatively, incisions may be left open and covered with conventional dressings for a few days. The patient should return to the operating room every 2-3 days for irrigation and debridement. Skin coverage is typically delayed 7-10 days after the fasciotomy and may require the use of a skin graft (see Figure 6).
Note that even if the fracture is an open one (that is, the skin is broken), a compartment syndrome may still develop: the wound may simply be insufficient to relieve the pressure.
Failure to treat compartment syndrome can result in muscle ischemia or necrosis, resulting in muscle contractures, infection and/or loss of limb. Again, note that loss of nerve function will lead to loss of protective sensation and skin breakdown distally – and whereas muscle loss may be tolerated by use of an orthosis, for example, continual skin breakdown is not tolerated well at all.
Risk Factors and Prevention
Again, the conditions associated with compartment syndromes include fracture, gunshot wound, circumferential casts or dressing, extravasation of intravenous lines, burns, coagulopathy and arterial injury, or surgery. Compartment syndrome cannot be prevented, per se, but its complications can be prevented by vigilance and expeditious treatment.
The discussion above, as the chapter title suggests, centers on acute compartment syndrome, but there is a chronic form as well: the chronic exertional compartment syndrome. Chronic exertional compartment syndrome typically is seen in young endurance athletes, especially runners. Because muscle volume can increase during exercise, some people may experience increased pressure within a muscle compartment with activity. Why some people suffer chronic exertional compartment syndrome is not known with certainty but may relate to a person’s greater propensity to increase muscle volume or to an individual’s stiffer, less compliant fascia around the muscles. The symptoms of chronic exertional compartment syndrome usually abate with rest without causing tissue damage, but a full-blown compartment syndrome can occur in rare circumstances. (Technically speaking, this is not a “chronic” compartment syndrome, but rather a chronic condition of recurrent and reversible acute events.) The diagnosis of chronic exertional compartment syndrome is made by measuring compartment pressures before and after activity. Non-operative treatment, including activity modification, non-steroidal anti-inflammatory medication, and use of orthotics, is usually successful, but in rare cases fasciotomy is needed.
Acute compartment syndrome can be seen with seizures. The mechanism of injury is likely ischemia caused by prolonged and uncontrolled muscle contractions. Acute compartment syndrome can also be seen in obstetrics, especially in cases with eclampsia, constriction of blood vessels by prolonged use of the lithotomy position and hypotension induced by postpartum hemorrhage.
The “beetle in the box” paradox introduced by the philosopher Ludwig Wittgenstein in his book, Philosophical
Investigations, hints at the problem of comprehending a patient’s report of pain. Wittgenstein imagined a scene
where people are each holding a box that only they can examine. When a person reports that her own box contains a
“beetle,” we don’t know what is in the box because we can’t be sure what that person means by the word “beetle.”
On the other hand, if that the person had two boxes, and said that both held a beetle, we can know that the boxes
have similar contents. Likewise, if a person says that his or her pain is “7 out of 10,” we really don’t know how
much pain that signifies – for pain scales are certainly not universal – yet if an hour ago the pain was reported
as “6 out of 10,” we do know that pain has subjectively increased. All this to say, serial observations can
“objectify” subjective symptoms, and are thus required to avoid the complications of compartment syndrome.
The 6 P’s of compartment syndrome – in case somebody were to ask – are pain, pallor, paralysis, paresthesia, pulselessness, and poikilothermia (cold limb). These “classic” findings are more accurately associated with acute vascular occlusion rather than with compartment syndrome.
Fasciotomy, compartment syndrome, high-energy trauma, crush injuries