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Compartment Syndrome

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Author:    Patricia Hartley (RNC, MSN)


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.


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 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.

Compartment Syndrome Pathophysiology

Compartment Syndrome Pathophysiology


History of Compartment Syndrome

Damage to limbs, particularly the legs, related to nerve damage and unchecked intra-compartmental pressures were documented as long ago as 1872 by Richard von Volkmann. The combination of nerve-related damage and compartment syndrome causing contracture related to a supracondylar fracture is still referred to as Volkmann contracture. Damage caused by hypertension or ischemia related to the limbs, and the association with rhabdomyolysis, was described by surgeons during World War II in patients who had sustained severe muscle injury. Today compartment syndrome following prolonged pelvic surgery is an uncommon, but a well documented complication.

Abdominal compartment syndrome has been recognized for years, but the term abdominal compartment syndrome (ACS) was only introduced in the 1980s. The risk of life-threatening elevation in intra-abdominal pressure is not limited to postoperative patients. Other causes that may cause an increased pressure include hemorrhage, edema, distended bowel, mesenteric venous obstruction, tense ascites, peritonitis, and tumors.

Patient Factors

A delay in diagnosis is the most important determinant of a poor patient outcome. Patients with a history of trauma, surgery, extravasation, diabetes, poor neurovascular status, or infection are at risk. Although more commonly associated with trauma or surgery on the limbs, compartment syndrome has been reported as a complication of some positions adopted for surgery, particularly the lithotomy and knee-chest positions. Various studies identify serious complications following surgery, particularly when the lithotomy position was used during urological surgery. The consequences for the patient are devastating, often resulting in multiple fasciotomies, chronic pain, and weakness.

The possibility of developing compartment syndrome and rhabdomyolosis is especially high in the presence of other risk factors including obesity, peripheral vascular disease, and prolonged duration of surgery. Compartment syndrome has been described in instances of drug overdose where persons have remained in one position for several hours, with the force supplied by the weight of their body on the extremity being the causative mechanism for the syndrome developing.

Surgical Factors

Within the operating suites, the success of many surgical procedures depends upon satisfactory exposure of the operative site, which often is achieved by placing patients in physiologically abnormal positions. With perceptive powers of the patient no longer intact, postural insults may occur that normally would not be tolerated in the awake state.

Variations on the lithotomy position are used for many procedures. A modified lithotomy trendelenburg (with additional head-down tilt) provides optimal combination approaches (abdominal and perineal) for complex urological, colorectal, and gynecological surgical procedures. This position allows the legs to be supported on multi-jointed operating table leg supports rather than lithotomy pole stirrups that reduce the degree of hip flexion and support the calves in semi-cylindrical padded cushions. The lower leg may be secured by soft straps or bandaging. While the practitioner ensures that the patient is positioned safely and correctly to minimize joint strain and pressure points, there is very little done to prevent the possibility of compartment pressure increases.

It is difficult to prevent any increase in compartmental pressure by the very nature of the position. The patient may be wearing compression stockings (if these are too small the problem will be compounded) and will likely have intermittent compression devices attached to each lower leg. The leg will still receive a degree of direct compression against calf support and it is essential to ensure that surgical assistants do not lean on the leg and provide additional compression.

Reduced perfusion is inevitable. The elevation of the legs above the heart reduces limb perfusion that may be compounded by the head-down tilt. Other factors related to limb perfusion may be hypotension (induced by anesthesia or sympathetic block) and surgically-induced pressure on major vessels during episodes of the procedure which may also affect venous return for short periods.

Pre-existing arterial disease may also be a contributory factor. When surgery is prolonged, the risk of compartment syndrome is increased. Most literature refers to long surgical procedures (six hours or longer) but it is now thought that much shorter episodes can also be responsible.

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
  • 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
-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”


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.


Patient and staff education should include general education about compartment syndrome itself, treatment, healing, and prognosis. Staff should clearly understand what procedures should and should not be done to prevent compartment syndrome. Discharge education should include wound care, infection prevention, extremity mobility/range of motion as allowed, and continued neurovascular assessments.


Current knowledge related to the risk of compartment syndrome when caring for patients of trauma or when operating in positions that put the legs higher than the heart when not absolutely necessary can be deemed negligent. If it means repositioning and re-draping, thus adding extra minutes to the surgical time and costing a small amount in additional drapes, surely this is a small price to pay for excellent perioperative care. The main goal in care of the patient with compartment syndrome is to maintain tissue function and viability.


Anglen, J., Banoventz, J., 1994 Clinical Orthodedics & Related Research. (301): 239-42, Apr.

Bocca, G., van Moorselaar, J., Wout, F., van der Staak, F., Monnens, L., 2002 Compartment Syndrome, Rhabdomyolysis and Risk of Acute Renal Failure as Complication of the Lithotomy Position, Journal of Nephrology 15 (2) 183-185.

Pearse, M., Harry, L., Nanchahal, J., 2002 Acute Compartment Syndrome of the Leg, British Medical Journal 325: 558-559.

Raza, A., Byrne, D., Townell, N., 2004 Acute Compartment Syndrome After Urological Pelvic Surgery, Journal of Urology 171: (1) 5-11.

Tal A., Lask, J., Keslin, J., Livine, P.M., 2004 Abdominal Compartment Syndrome: urological aspects; British Journal of Urology International 93: 474-477.

Warrell, D., Cox, T., Firth, J., Benz, E., 2003 Oxford Textbook of Medicine 4th ed, Vol. 3, Sections 18-33, p 257, Oxford, Oxford University Press.