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Compartment Syndrome

Compartment syndrome is an acute medical condition taking place after surgery, injury or
extensive and repetitive muscle use. The problem causes increased pressure, typically by
inflammation, within a confined area, impairing the body's blood supply. Untreated,
compartment syndrome may lead to irreversible nerve damage or even muscle death.
The common mean pressure in interstitial tissue is near zero mmHg in muscles, when not
contracting. Should the pressure be elevated to or above 30 mmHg, small vessels in the tissue
may be compressed, leading to ischemia (restriction of blood flow) and pain. Compartment
syndrome is seen most often in either the anterior compartment or posterior compartment of the
Note the difference between diastolic blood pressure and compartment pressure. If the diastolic
blood pressure does not exceed the compartment pressure by at least 30 mmHG, then it is
considered a medical emergency.
Symptoms of compartment syndrome are sometimes known as the six P's:
Pain: Pain is beyond the proportion of what is expected with the injury, surgery or activity.
Paresthesias: Altered sensations such as numbness or pins and needles.
Passive stretch pain: Pain with passive stretching is encountered.
Pulseless: Although a rare symptom, a lack of pulse may be detected if the relevant artery is in
the affected compartment, and the pressure is high enough.
Paralysis: Limb paralysis can be a late symptom of compartment syndrome.
Pressure on passive extension: Passive extension of the compartment leads to increased
Typical compartment syndrome causes include burns, car accidents, circulation blockage, crush
injury, fractures of the forearm or tibia, hemorrhage, ischemic-reperfusion (after an injury), IV
drug injection, limb compression for an extended period, overly tight bandages, rigid cast usage,
severely bruised muscles, surgery and vascular puncture.
Individual compartments are defined by fascia, which are thick layers of connective tissue. As
this tissue does not stretch, pressure may rise dramatically due to even a minor amount of
bleeding into the compartment, or muscle swelling within it. This can compress the blood
vessels, muscles and nerves in the compartment.

Not all compartment syndrome cases are brought on as quickly. Continued and heavy use of the
muscles, such as done by an athlete, may also cause compartment syndrome. In this instance it is
known as chronic compartment syndrome. CCS is not normally a medical emergency, but due to
the loss of circulation, it may cause damage to local nerves or muscles, which in some cases is
In the end, the main cause of compartment syndrome is the fact that the pressure is too great. The
reason for this may either be due to increased fluid content in the compartment, or decreased
compartment size. One of those reasons is brought on by the underlying cause. Visit the
diagnosis page to learn more about a potential diagnosis of compartment syndrome.
Diagnosis of compartment syndrome is made by a doctor or medical professional. If an
individual suspects such a condition, he should immediately go to the nearest hospital or
emergency room. Do not try to self-diagnose or figure out your own treatment method for this
serious medical condition.
Testing for a case of compartment syndrome involves checking the pressure of the muscle
compartment(s) involved. A fasciotomy, a surgery of cutting the fascia to relieve pressure, may
be necessary should the pressure be great enough.
Some sources state that 30 mmHg or greater compartment pressure prescribes a fasciotomy. On
the other hand, others recommend the comparison of the intracompartmental pressure to the
diastolic blood pressure, where a 30 mmHg or greater difference is that level at which a
fasciotomy should be performed.
Compartment syndrome is most often treated with a fasciotomy, a procedure of cutting the fascia
to relieve pressure which should then return to its standard level. Acute compartment syndrome
is the "highest" level and is considered an emergency. Subacute compartment syndrome is not
commonly such an emergency, but nevertheless normally requires similar treatment.
Chronic compartment syndrome (CCS), often suffered by athletes, can often be treated either by
surgery or with conservative methods, including elevating the limb (typically leg), manually
decompressing the compartment, resting and taking anti-inflammatories. If symptoms continue,
however, the case should likely be treated with surgery. Left untreated, CCS has the potential to
develop into a case of acute compartment syndrome.
Necrosis of the compartment's tissue may result from the failure to relieve pressure in the
compartment. At that point, capillary perfusion will drop, which leads to a greater oxygen
deficiency (hypoxia) in the tissues. Untreated cases of acute compartment syndrome may lead to
other severe conditions such as kidney failure and rhabdomyolysis (rapid breakdown of skeletal
muscle tissue), and potentially death.

If compartment syndrome is not treated, or the treatment does not work as hoped, then the patient
may go through certain complications. Once the condition has been diagnosed, it is imperative
that the person receive treatment to avoid serious and potentially life-threatening issues. Some
things that may occur are discussed here.
Volkmann's contracture
This situation is brought on when pressure is not relieved, ultimately leading to necrosis due to
hypoxia (lack of sufficient oxygen). Volkmann's contracture is a condition where there is a
permanent deformity, such as in the hand. A contraction leads it to be shaped similar to a claw.
In rhabdomyolysis, the muscle tissues of the affected area break down quickly, letting certain
products into the patient's blood. It is often found in those who are injured during disasters,
although crush injuries of any kind, as well as other causes, can lead to it. Whether caused by
compartment syndrome or another issue, it requires medical treatment. A suspected diagnosis
might be made in certain circumstances, with confirmation given later when kidney function
decreases. Please keep in mind that a professional makes this kind of diagnosis.

Compartment syndrome (CS) is a limb-threatening and life-threatening condition observed when
perfusion pressure falls below tissue pressure in a closed anatomic space. The current body of
knowledge unequivocally reflects that untreated compartment syndrome leads to tissue necrosis,
permanent functional impairment, and, if severe, renal failure and death.
The original description of the consequences of unchecked rising intracompartmental pressures
is widely attributed to Richard vonVolkmann. His 1872 publication documented nerve injury and
subsequent contracture from compartment syndrome following supracondylar fracture.1 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
vonVolkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused
by limb hypertension after experimentally induced venous obstruction. 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.2
Almost simultaneously, Matsen published his findings, which are the most commonly annotated
group of articles in present literature.
Compartment syndrome has been found wherever a compartment is present: hand, forearm,
upper arm, abdomen, buttock, and entire lower extremity. Almost any injury can cause this
syndrome, including injury resulting from vigorous exercise.
This article presents current thoughts and findings regarding compartment syndrome. Most
importantly, it urges physicians to maintain a high level of suspicion when dealing with
complaints of extremity pain.3

Compartment syndrome pathophysiology follows the path of ischemic injury.
Intracompartmental structures cannot withstand infinite pressure. When fluid is introduced into a
fixed volume, or when volume decreases with fixed volume, pressure rises. Various osseofascial
compartments have a relatively fixed volume; introduction of excess fluid or extraneous
constriction increases pressure and decreases tissue perfusion, until no oxygen is available for
cellular metabolism.
Elevated perfusion pressure is the physiologic response to rising intracompartmental pressure. As
intracompartmental pressure rises, autoregulatory mechanisms are overwhelmed and a cascade
of injury develops. Tissue perfusion is determined by measuring capillary perfusion pressure

(CPP) minus the interstitial fluid pressure. When this pressure falls below a critical threshold,
injury results.
Normal cellular metabolism requires 5-7 mm Hg oxygen tension; this is easily maintained with
the CPP averaging 25 mm Hg and interstitial pressure 4-6 mm Hg. However, rising interstitial
pressure overwhelms perfusion pressure.
Matsen demonstrated that as intracompartmental pressure rises, venous pressure rises. When
venous pressure is higher than CPP, capillaries collapse. The pressure at which this occurs is
under debate; however, intracompartmental pressures greater than 30 mm Hg are generally
agreed to require intervention.
At this point, blood flow through the capillaries stops. In the absence of flow, oxygen delivery
stops. Hypoxic injury causes cells to release vasoactive substances (eg, histamine, serotonin),
which increase endothelial permeability. Capillaries allow continued fluid loss, which increases
tissue pressure and advances injury. Nerve conduction slows, tissue pH falls due to anaerobic
metabolism, surrounding tissue suffers further damage, and muscle tissue suffers necrosis,
releasing myoglobin. The end result is loss of the extremity and, possibly, the loss of life.

United States
Anterior distal lower extremity is the most common studied cause of compartment syndrome.
Tibial fracture is quoted as the most common, likely secondary to its frequency of injury. Ranges
of 2-12% have been published. Another frequency rate cited is that 30% of limbs develop
compartment syndrome following vascular injury; however, this is not well documented and is
most likely an estimate. McQueen retrospectively looked at 164 patients with diagnosed
compartment syndrome; 69% were associated with a fracture, one half of those involved the

Compartment syndrome outcome depends on both the diagnosis and the time from injury to
intervention. Rorabeck and Macnab reported almost complete recovery of limb function if
fasciotomy was performed within 6 hours.5 Matsen found necrosis after 6 hours of ischemia,
which currently is the accepted upper limit of viability.6

In the retrospective study by McQueen, compartment syndrome was diagnosed more often in
men than in women; however, this likely represents selection bias because most patients with
traumatic injuries are male.4



Suspect compartment syndrome (CS) whenever significant pain occurs in an extremity.

Pressure rises and ischemic injury begins to impair nerve function.

Nerve impairment causes the patient to complain of severe pain, out of proportion to
examination, often described as a burning sensation or tightness.

The traditional 5 Ps (ie, pain, paraesthesia, pallor, poikilothermia, pulselessness) are not
diagnostic of compartment syndrome. Literature warns that, with the exception of pain
and paraesthesia, these traditional signs are not reliable, and the presence or absence of
them should not affect injury management.

Importantly, note that these symptoms assume a conscious patient who did not
suffer any additional injury that hinders sensory input (eg, spinal cord injury).

In young children, the ability to gather a history of complaints is limited.

Maintain a high level of suspicion in any injury that causes limb pain.

High-velocity injuries are particularly worrisome.

Determine the mechanism of injury.

Long bone fractures

High-energy trauma

Penetrating injuries (eg, gunshot wounds, stabbings) - Often cause arterial injury,
which can quickly lead to compartment syndrome

Venous injury - May cause compartment syndrome (do not be misled by palpable

Crush injuries

Anticoagulation therapy significantly increases the likelihood of compartment syndrome;

remember to ask if patients are anticoagulated for any reason.

Compartment syndrome requiring fasciotomy has been observed after simple

venipuncture in an anticoagulated patient.

Vigorous exertion may lead to compartment syndrome.

Compartment syndrome has been found in soldiers and athletes without any
trauma. This can be acute or chronic with acute compartment pressures as high as
those found in severe trauma.

If compartment syndrome is suspected, check intracompartmental pressure, even

with no presence of any trauma.7


Certain physical signs are associated with compartment syndrome. After initial symptoms
of pain or burning, decreased strength and eventually paralysis of the affected extremity
occur. Follow-up physical examinations are important to determine if any progression of
symptoms is noted.
Severe pain at rest or with any movement should raise suspicion.

Pain with certain movements, particularly passive stretching of the muscles, is the earliest
clinical indicator of compartment syndrome.

A patient may report pain with active flexion.

If a patient complains of pain, determine if any neural compromise is present.


Sensory nerves begin to lose conductive ability, followed by motor nerves.

Some nerves may reveal effects of increasing pressure before others.

For example, in the anterior compartment of the lower leg, the deep peroneal
nerve is quickly affected, and sensation in the web space between first 2 toes may
be lost.

The affected limb may begin to feel tense or hard, as if filling with fluid.

Compare the affected limb to the unaffected limb.

Any discharged patient should be given these specific signs and return immediately if
they develop.


A myriad of precipitating injuries leading to compartment syndrome share some

The cause of compartment syndrome is extremely simple: the pressure is too high.

The underlying reason for increasing pressure, as proposed by Mubarak and Hargens, is
increased fluid content or decreased compartment size.8

Increased fluid content can be caused by the following:


Intensive muscle use (eg, tetany, vigorous exercise, seizures)

Everyday exercise activities (eg, stationary bicycle use, horseback riding9 )


Intraarterial injection (frequently iatrogenic)


Decreased serum osmolarity (eg, nephrotic syndrome)

Infiltrated infusion

Hemorrhage (particularly from a large vessel injury)

Decreased compartment size can be caused by the following:


Military antishock trousers (MAST)



Lying on a limb can cause compartment syndrome. In 1979, Owen et al published a

landmark study in which researchers measured intracompartmental pressures in various
positions common in drug overdoses.2 Average pressures of 48 mm Hg with the
head resting on forearm, 178 mm Hg when the forearm was under ribcage,
and 72 mm Hg when one leg was folded under the other were reported.

Differential Diagnoses
Peripheral Vascular Injuries
Coelenterate and Jellyfish Envenomations
Deep Venous Thrombosis and Thrombophlebitis
Gas Gangrene
Necrotizing Fasciitis

Other Problems to Be Considered

Differentials listed above often occur concurrently with compartment syndrome (CS).

Laboratory Studies
Laboratory results are often normal and are not necessary to diagnose compartment syndrome
(CS) and are not helpful to rule out compartment syndrome.

Complete metabolic profile (CMP)

CBC count with differential

Creatine phosphokinase (CPK) and urine myoglobin levels

Serum myoglobin level

Urine toxicology screen: This subsequently may help define the etiology, but it is rarely
helpful in patient treatment.

Initial urinalysis: This may be positive for blood but negative for RBC on microscopic
analysis, which may indicate myoglobin in the urine (rhabdomyolysis).

Prothrombin time (PT) and activated partial thromboplastin time (aPTT)

Imaging Studies

Radiography of the affected extremity


Ultrasonography aids in evaluating arterial flow as well as in visualizing any deep

venous thrombosis (DVT).

Ultrasonography is not helpful in diagnosis of compartment syndrome; however,

it aids in the elimination of differential diagnoses.

Other Tests

Compartment pressure measurement

o This measure should be at the top of the list when searching for compartment
syndrome; perform it as soon as the diagnosis of compartment syndrome is

Numerous commercial model tonometers are available (eg, Stryker, ACE). The
Stryker STIC device is shown in the image below.

Stryker STIC Monitor. Image courtesy of Stryker Corporation, used

with permission.

Stryker STIC Monitor. Image courtesy of Stryker Corporation, used with


Numerous "build-it-yourself" techniques, without evidence of reliability, are also

available; their use is not recommended.
A diagram of a measuring device for use when commercial devices are
unavailable is pictured below.

Picture of compartment pressure measuring device for use when

commercial devices are unavailable.

Picture of compartment pressure measuring device for use when commercial

devices are unavailable.

Pulse oximetry
o Pulse oximetry is helpful in identifying limb hypoperfusion.

Pulse oximetry is not sensitive enough to exclude compartment


Prehospital Care
Compartment syndrome (CS) can develop rapidly after an arterial injury. Therefore, speed of
transport is essential. Perform only the necessary lifesaving procedures in the field if
compartment syndrome is suspected.

Emergency Department Care

Time is of the essence in diagnosing and treating compartment syndrome. Irreversible nerve
damage begins after 6 hours of intracompartmental hypertension. If compartment syndrome is
suspected, pressure measurements and appropriate consultation must be performed quickly.

Many cases of compartment syndrome are due to trauma. Follow advanced trauma life
support (ATLS) guidelines to stabilize the patient before attempting to address
compartment syndrome.
Ischemic injury is the basis for compartment syndrome. Additional oxygen should be
administered because it slightly increases partial pressure of oxygen (PO2).

Keeping extremities level with the body decreases limb mean arterial pressure without
changing intracompartmental pressure.

Do not elevate the affected extremity. Styf and Wiger measured, after an elevation of 35
cm, a decrease in the mean arterial perfusion pressure of 23 mm Hg and no change in
intracompartmental pressure.10

Intravenous (IV) hydration is essential, hypovolemia worsens ischemia.

Fasciotomy remains the definitive therapy for CS because of its well-documented, limbsaving results.

Recently, timing and use of fasciotomy have been questioned. Fasciotomy extends
hospital stay and changes a closed injury to an open injury, greatly increasing the
chance of infection.

As mentioned above, debate surrounds the threshold for fasciotomy. Numerous

authors recommend 30 mm Hg, while others cite 45 mm Hg. Still others urge
prophylactic fasciotomy at normal pressures to prevent compartment syndrome.

Convincing evidence reflects that debate should center on delta-p. Delta-p is a

measure of perfusion pressure (diastolic blood pressure minus intracompartmental
pressure). Originally used in dogs, delta-p measurements of less than 30 mm Hg
were used by McQueen for fasciotomy.11 As a result, several patients with
intracompartmental pressures of 40 mm Hg or greater were observed because the

delta-p was greater than 30 mm Hg. Criteria were used in 116 patients without
sequelae. The converse is also true because patients with intracompartmental
pressures less than 30 mm Hg but with high delta-p values have developed
compartment syndrome.

Recent studies have confirmed previously postulated theories that myonecrosis associated
with compartment syndrome after envenomation is multifactorial and that fasciotomy
may not prevent myonecrosis. Myonecrosis is thought to be due to a direct toxic effect of
the venom and the inflammatory response. Therefore, these patients should be
aggressively treated with antivenom if available because this has been shown to decrease
limb hypoperfusion.


General surgeon
Orthopedic surgeon

Vascular surgeon


Some authors have advocated the use of mannitol for compartment syndrome (CS). Although its
use in rhabdomyolysis is well documented, its use in acute compartment syndrome is new. More
recently, Daniels and Reichman treated an Israeli soldier who developed compartment syndrome
with mannitol.12 After resolution, he was discharged without a fasciotomy. Unfortunately,
intracompartmental pressures were not measured, since the diagnosis was based on limb
circumference and nerve conduction studies. Further investigation is warranted in this area.
Hyperbaric oxygen (HBO) therapy is a logical choice for compartment syndrome because it
addresses the primary concern of ischemic injury. HBO has many beneficial effects. It reduces
edema through oxygen-induced vasoconstriction while maintaining oxygen perfusion and
supports tissue healing in a similar mechanism by allowing oxygen delivery when perfusion
pressure is low. Reperfusion injury following CS often is voiced as an argument against HBO.
However, HBO actually protects against reperfusion injury.
Bouachour performed a well-controlled randomized study with 31 patients following crush
injury and demonstrated significant increase in complete healing (p <0.0005) with HBO. Wattel
et al have given an appraisal of the current literature regarding HBO therapy for compartment
syndrome and justifiably concluded that studies demonstrate HBO effectiveness in improving
wound healing, reducing amputation rate, and lowering surgical procedure rate.13
Although HBO is currently only adjunctive therapy because of its limited availability,
it should not be ignored. It may extend treatment duration and it may not reverse
the compartment syndrome etiology but has been shown to be beneficial.