Compartment Syndrome

Compartment Syndrome

Compartment syndrome, if not identified and acted upon early, will result in irreversible
damage to neuromuscular soft tissue. Therefore, the healthcare professional must be aware
of the risks, signs and symptoms, unusual circumstances, and appropriate interventions with
this syndrome. Compartment syndrome is a life-threatening condition in which increased
tissue pressure in a confined anatomical space causes decreased blood flow leading to
ischemia and dysfunction of contained myoneural elements. It is marked by pain, muscle
weakness, sensory loss, and palpable tenseness in the involved compartment. Ischemia can
lead to necrosis resulting in permanent impairment of function. Increased pressure within
the compartment results from bleeding and swelling into the closed space which in turn
causes pressure on the vital structures. There is elevation of interstitial pressure in a closed
fascial compartment that results in microvascular compromise. As the duration and
magnitude of interstitial pressure increases, myoneural function is impaired and necrosis of
soft tissues eventually develops. Compartment syndrome can occur where there is
significant edema in a compartment within the hand, forearm, upper arm, buttock, legs,
feet, and occasionally the abdomen. Usually compartment syndrome occurs due to
fractures of the tibia or forearm, in vascular injuries, or burns. Almost any injury or surgery
can cause the condition.

Physiology

Arteries and their subdivisions bring freshly oxygenated blood to the tissues, and the
associated venous system returns deoxygenated blood to the venous circulation. The
human body has a number of areas that function as closed compartments to this delivery
system. There are three main compartments in the forearm and four main compartments in
the lower leg. The long bones of the limbs, for example, are joined and surrounded by
sheets of tough and relatively inelastic tissue called fascia which create comparatively
inflexible boundaries. The placement of the fascia is such as to divide the leg, for instances,
into a number of sections or compartment. These compartments contain muscles, arteries,
veins, and nerves. These compartments generally have a fairly constant volume that permits
only slight variation. If swelling occurs in these compartments the subsequent rise in
compartment pressure can cause serious damage.

The arterial blood system continues to bring blood into the compartment, but low pressure
veins and their subdivision have a low intra-luminal pressure that is restricted. When this
occurs it is further compounded by the release of fluid from the blood vessels resulting in a
further rise in compartment pressure that perpetuates the cycle. Edema within the closed
compartment will increase the pressure within that compartment eventually compromising
the vascular supply. Such compromise will lead to further ischemia and edema formation. A
vicious cycle will be established as cells become deprived of oxygen.

Subsequent necrosis of muscle and loss of capillary wall integrity will lead to transudation,
exudation, and the development of massive edema within the compartment.
Rhabdomyolysis then occurs. Rhabdomyolysis is the dissolution or breakdown, of striated
muscle that results in the production of myoglobin. Myoglobin is known to cause acute
renal failure. If untreated, rhabdomyolysis may lead to myoglobinuria, permanent

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neurovascular damage, renal failure, sepsis, and even death. This occurs as the myoglobin is
released into the circulation where it can occlude the distal convoluted tubule and
precipitate renal failure.

Significant fluid loss into damaged tissues leads to hypovolemia and metabolic acidosis. This
not only acts as a potent pre-renal cause for renal impairment but also enhances the
nephritic effect of myoglobin. Severe metabolic complications may present after
reperfusion when the damaged membranes continue to leak, aggravating edema formation
and increasing the pressure in the closed osteofascial compartment. Rhabdomyolysis is well
documented as a secondary cause in a range of conditions related to skeletal muscle injury.

The syndrome may develop as quickly as within the first 30 minutes to 1-2 hours post
trauma. Or it may develop postoperatively, post fracture reduction, or in as late as 5-6 days.
If it is allowed to last for more than 6 hours, neuromuscular damage becomes irreversible.
Splinting, traction, early closed reduction with casting, or early surgery for fractures reduce
the risk of Compartment Syndrome.

There are three categories of etiology:

1. Decreased compartment size can be caused by restrictive dressings, splints or casts,

excessive traction, or premature closure of fascia.

2. Increased compartment content can be caused by a fracture that causes bleeding or from
a vascular injury, burns, infiltrated IV infusion, swollen or inflamed bowel, or snakebites.
The first response is to elevate the extremity. However, when the extremity is elevated
too high above heart level, this compromises arterial perfusion, which further compounds
the ischemic problem.

3. Externally applied C can be caused from restrictive dressings, prolonged compression

from lying on a limb or crushing injuries of soft tissue.

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Compartment Syndrome Pathophysiology

Insult/Injury

Vascular C
(Microvascular and Venous Congestion)

Hypoxia

Cell Death and Protein Release

Edema

Increased Intra-compartmental Pressure

Further Cell Damage

C Necrosis

Permanent
Death Amputation
Disability

Signs and Symptoms

Compartment syndrome usually presents after reperfusion of a limb. Pain and swelling may not
occur immediately. The first signs usually occur after the patient has regained consciousness,
undergone their post-anesthetic care, and returned to the unit. Often several hours are reported as
uneventful before the first signs and symptoms are reported. The first suspicions are usually aroused
when a patient complains of severe pain in the lower legs when they have recovered consciousness
or a few hours after surgery. Some patients may even describe pain despite postoperative epidural
anesthesia. The patient’s leg may appear tense and swollen. The level of pathological pain is found
to be far greater than the ordinary postoperative pain to be expected from the surgical intervention.

The diagnosis of compartment syndrome requires a high index of clinical suspicion. Timing of
identification and intervention with compartment syndrome is crucial to a positive patient outcome.
It is possible that an initial diagnosis of deep vein thrombosis (DVT) may interfere with the correct
diagnosis. The measurement of compartment pressures will confirm the suspicions of compartment
syndrome while venous Doppler studies will confirm a DVT. Remember the “6 P’s” of compartment
syndrome:

1. Paresthesia

Subtle first symptom

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Compartment Syndrome

Best elicited by direct stimulation

Complaints of tingling or burning sensations

Loss of 2 point discrimination

Can lead to numbness

2. Pain

Out of proportion to the injury

Elicited by passive stretching of the involved compartment

Described as throbbing or deep – localized or diffuse

Increases with the elevation of the extremity

Unrelieved by narcotics

May not be present if central or peripheral sensory deficits are also present

3. Pressure

Involved compartment or limb will feel tense and warm on palpation

Skin is tight and shiny

Skin may appear cellulitic

Direct compartment pressure of 30-40 mmHg as measured by a wick, continuous infusion, or

injection method such as the Stryker monitor – normal intracompartmental tissue pressure is
0-10 mmHg.

Differential pressure of greater than 30 mmHg – diastolic blood pressure minus compartment
pressure – as long as diastolic pressure remains high enough or at least 30 mmHg, the
compartment will be perfused and there may not be a need for surgical decompression.

Whiteside’s theory suggested that the development of compartment syndrome depends not
only on intra-compartmental pressure but also depends on systemic blood pressure – diastolic
pressure minus compartment pressure should be > 30 mmHg.

Example 1:
80 = patient diastolic B/P
-20 = direct compartment pressure
60 = differential pressure (adequate compartment perfusion)

Example 2:
80 = patient diastolic B/P

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Compartment Syndrome

-60 = direct compartment pressure

20 = differential pressure (adequate compartment perfusion)

4. Pallor

Late sign

Pale, grayish or whitish tone to skin

Prolonged capillary refill (>3 seconds)

Cool feel to skin upon palpation due to lack of capillary perfusion

5. Paralysis

Late sign

May start as weakness in active movement of involved or distal joints

Leads to inability to move joint or digits actively

No response to direct neural stimulation due to damage

6. Pulselessness

Late sign

Very weak or lack of palpable or Doppler audible pulse

Due to lack of arterial perfusion

Other warning signs of Compartment Syndrome:

1. Fractured blisters: represent areas of necrosis of the epidermis and separation of the skin layers.
Occur as the body attempts to relieve the pressure in the compartment.

2. Laboratory findings: elevated WBC (white blood cell count) and ESR (erythrocyte sedimentation
rate) levels due to the severe inflammatory response

3. Elevated temperature due to ischemia/necrosis of tissue and possible infectious response.

4. Elevated Serum Potassium due to cell damage.

5. Lowered Serum pH levels due to acidosis

6. Stretch pain or pain on passive extension or hyperextension of digits (toes or fingers, depending
on the site)

Don’t lose valuable time waiting for laboratory findings. Be vigilant to assessment of the “6 P’s”

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Treatment

When compartment syndrome is diagnosed and treated early, full recovery usually follows. When
initial signs and symptoms appear, loosen any external constrictive dressings or cut the cast. Other
measures are to position the extremity at the level of the heart not above the heart and provide
adequate hydration of the patient to maintain arterial blood pressure. Accurately monitor
compartment pressures.

Medical decompression may be instigated if compartment syndrome is suspected and intra-

compartment pressures are only marginally increased. A mannitol infusion has been reported as
effecting a complete resolution.

Fasciotomy, or surgical decompression, is a surgical incision of the affected compartments. It may be

required if conservative interventions are not effective in interrupting the edema-ischemia cycle. As
soon as the fascia is sectioned, or surgically split open by an incision through all layers down to and
including the fascia, the compartmental contents can bulge, thus allowing pressures to decline along
with reinstitution of the normal circulatory pattern.

If performed Fasciotomy should be done in less than 6 hours and no later than 12 hours after onset
of symptoms. If the procedure is performed during this time frame it is likely to prevent myoneural
deficits. Fasciotomy must be undertaken by a skilled surgeon, ensuring that all compartments (for
instance all four in the lower leg) are accessed through a single lateral incision or double vertical
whenever possible.

During fasciotomy it is vital to identify and protect nerves. Wounds are usually left open protected
by suitable sterile dressings. Inspection of the wound after 48 hours may necessitate further necrotic
tissue excision. Delayed skin closure or skin grafting may become treatment options. Adequate
analgesia and antibiotic coverage are essential for improving outcomes.

In cases where treatment and prophylaxis of renal failure associated with rhabdomyolysis is
suspected or diagnosed, prompt fluid and metabolic correction is essential to re-establish a good
urine output. Mannitol has also been beneficial as a renal vasodilator and intravascular expander
and aids to induce osmotic diruesis. If these methods fail dialysis may be necessary.

Source: http://www.ceufast.com/courses/176/176.htm

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