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Compartment Syndromes in the Pediatric Patient

Noonan, Kenneth J. MD; McCarthy, James J. MD

Journal of Pediatric Orthopaedics: March 2010 - Volume 30 - Issue - p S96-S101
doi: 10.1097/BPO.0b013e3181d07118
Trauma
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In this manuscript the authors review essential and new information on compartment syndrome in children. The article stresses the three A's of pediatric compartment syndrome: agitation, anxiety and increasing analgesic requirement which precede the classic presentation by several hours. Non-invasive methods of assessing compartment syndrome are highlighted and the medical-legal implications of missed compartment syndrome are further reviewed.

Department of Orthopaedics, University of Wisconsin School of Medicine and Public Health, Madison, WI

Reprint: Kenneth J. Noonan, MD, Department of Orthopaedics and Rehabilitation, K4/732 Clinical Science Center, 600 Highland Ave, UWHC, Madison, WI 53792. E-mail: noonan@orthorehab.wisc.edu.

Compartment syndrome is one of the most feared clinical scenarios, and can occur as a result of systemic disorders or local limb trauma in a pediatric patient. In the former case, elevated compartment pressures can result from bleeding or clotting disorders (Fig. 1), septicemia, animal bites, or after prolonged vascular reconstruction.1 Other possible causes include inadvertent fluid infiltration into the soft tissues from intravenous fluids or arthroscopy. However, the most common inciting event results from trauma inflicted to the limb. In this instance, venous outflow is compromised by elevated compartment pressures, which results in a positive feedback cycle of ischemia leading to increased vascular permeability resulting in increased interstitial fluid and greater compartment pressure. If left uncorrected, muscle and nerve ischemia can lead to profound disability. In addition to limb morbidity, potential systemic effects of muscle necrosis from compartment syndrome also exist. In cases of profound and extensive compartment syndrome (such as seen in the thigh), muscle damage can lead to significant hyperkalemia, acidosis, and myoglobulinuria; acute renal failure requiring dialysis has been seen in these unfortunate cases.

FIGURE 1.

FIGURE 1.

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NEONATAL COMPARTMENT SYNDROME

Compartment syndrome in the neonate is a rare, but commonly missed diagnosis, which presumably results from a combination of birth trauma and low neonatal blood pressure.2 Some children can be misdiagnosed as having hemiplegia; however, muscular contracture and growth arrest herald an ischemic limb etiology (Fig. 2). Recently, Ragland et al3 reported on 24 cases of neonatal compartment syndrome; only 1 case was diagnosed within the first 24 hours. The authors note that a unique sign is the presence of a “sentinel skin” lesion over the forearm of the affected limb. Ragland et al3 described a soft tissue sore on the forearm of children who were later diagnosed with neonatal compartment syndrome. The lesion was thought to represent the damaged soft tissue necrosis seen in retrospect and should be considered a sign of neonatal compartment syndrome. The authors termed this as the “sentinel” lesion. In the 1 patient who underwent fasciotomy within 24 hours, a functional result ensued. The remaining cases resulted in significant limb dysfunction because of contracture and growth arrest. The authors conclude that high clinical suspicion, especially in the instance of a sentinel skin lesion, may lead to prompt treatment and improved outcome.

FIGURE 2.

FIGURE 2.

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CLINICAL SIGNS OF COMPARTMENT SYNDROME

Accurate and timely diagnosis of compartment syndrome depends on the detection of clinical signs of increasing compartment pressure. For decades, orthopaedic residents have been trained to observe the 5 Ps. The most important of these is increasing pain, which has been described as out of proportion to the level of trauma, pain at rest, or pain with passive stretch of the muscles in the suspect compartment. Parasthesias may be the earliest subjective complaint and results from increased pressure on the nerve that passes through the tight compartment. Paralysis is another sign of muscle and nerve dysfunction but in the author's experience, this finding is difficult to discern in the acute setting from muscle guarding as a result of pain. Pallor and pulselessness imply arterial insufficiency and are included to complete this discussion; yet, it has been said that “when pulses are diminished, the damage has been done.”

In the ideal clinical setting, the diagnosis is easy to make when a patient with a hard swollen compartment has increasing pain that is worsened with passive stretch. Tingling in the distribution of a nerve that passes through the compartment simply cements the diagnosis and emergent treatment is indicated. The problem is that scared and anxious children are rarely the ideal patients to evaluate. Furthermore, these patients often reside on a pediatric floor that only occasionally cares for orthopaedic patients and whose staff is not experienced in detecting a patient with compartment syndrome.

Another finding that is related to pain is increasing agitation and anxiety seen in children with rising compartment pressures. In a series from Boston published in 2001, the increasing analgesic requirements preceded the noted change in the vascular status by an average of 7 hours in pediatric patients.4 Although greater than 90% of patients in the Boston study reported pain, only 70% had been in association with another “P”, the presence of the 5 Ps indicates prolonged ischemia and more advanced disease. The authors suggest that increasing analgesic requirement may precede the classic symptoms by greater than 7 hours. It is therefore important to completely and fully evaluate any pediatric patient who may require increasing amounts of medication for pain and especially if increased agitation and anxiety are present. A patient whose pain was controlled on oral medicine and now requires increasing doses or intravenous narcotics should be immediately examined and compressive and constricting dressings, splints, and casts removed to allow for swelling and examination of the limb.

In summary, the frightened pediatric patient is rarely the ideal patient to evaluate for increased compartment pressure and the development of compartment syndrome. The astute clinical team is trained to identify which patients are at risk and to monitor for increased pain and parasthesias and the 3 “As”: increasing anxiety, agitation, and analgesic requirement.

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PATIENTS AND TREATMENTS AT HIGH RISK FOR COMPARTMENT SYNDROME

Excluding the rare causes of compartment syndrome discussed above, the most common inciting event is limb trauma resulting in elevated compartment pressures. Some common traumatic events include fractures of the femur, forearm,5 supracondylar humerus, tibial tubercle, and tibial shaft. Tibial tubercle avulsion fractures, although benign appearing and not a result of crushing forces, can lead to anterior compartment syndrome as a result of injury to vessels that bleed into this compartment. In addition, open injuries and fractures associated with nerve injury are at higher rates of developing a compartment syndrome; in the later instance, the associated nerve injury presumably masks the clinical signs and symptoms of compartment syndrome.6 Common at-risk fractures include supracondylar humerus fracture with ipsilateral median nerve palsy, and the tibia fracture associated with concomitant peroneal nerve palsy. Finally, when displaced multiple fractures in the same limb are present, the clinician should have a high index of suspicion for the development of compartment syndrome. For instance, Blakemore et al7 reported a 33% rate of compartment syndrome in patients with displaced distal humerus and forearm fractures. Finally, it is important to remember that in the case of vascular disruption, prolonged ischemia (greater than 6 h) can lead to increased compartment pressures once revascularization is completed.

It is important for clinicians to realize that certain treatment algorithms can increase the incidence of compartment syndrome; these need to be appreciated in executing appropriate care of these injuries. For example, femur fractures treated with overhead skin traction should be avoided in all but the smallest patients (less than 2 y of age) because of increased risk of compartment syndrome. In addition, Mubarak et al8 have recently reported a series of compartment syndrome from the use of immediate spica casting in femur fractures; compartment syndrome may result from increased traction to the limb while the cast is being applied. The authors suggest an alternative method of spica cast application, which may prevent this complication.

Treatment of upper extremity fractures can also result in compartment syndrome because of vascular compromise. For instance, after fixation of supracondylar humerus fractures, flexion of the elbow to 120 degrees is associated with much higher pressures than those elbows immobilized in 90 degrees of flexion.9 Operative fixation is recommended for both ipsilateral supracondylar humerus and radius fracture seen in patients with floating elbow injuries. On account of the high rate of compartment syndrome, it is ideal to obtain stable fixation of both fractures to carefully monitor the limb for signs and symptoms of compartment syndrome. Finally, Yuan et al10 noted an increased risk of compartment syndrome in those patients that underwent intramedullary fixation for displaced forearm fractures. They found that multiple reduction attempts and longer operating room time presumably resulted in higher rates of compartment syndrome. Alternatively, these limbs may have been subject to more significant trauma resulting in more difficult fracture fixation. Regardless of the cause, significantly displaced forearm fractures treated with open or closed methods need to be carefully monitored for the development of compartment syndrome.

In addition to problems with spica casts, circumferential casts can decrease the ability of a limb to accommodate increased pressures and therefore surgeons need to be cognizant that fractures and surgery can result in soft tissue swelling that might not have been present during the cast application and may lead to compartment syndrome. In this frequent scenario, the first intervention should be relieving the circumferential pressure by splitting the cast. Briefly, plaster cast cutting and spreading (univalve) can be expected to decrease 40% to 60% of the external cast pressure and release of padding may increase this from 40% to 80%. Fiberglass casts applied without stretch relaxation are known to be 2 times tighter than those applied with plaster and in these cases, bivalving the fiberglass cast would be needed to see similar decreases in pressure. Casts that are applied with the stretch relaxation method are among the least constrictive of fiberglass casts and therefore univalving may be sufficient as long as the cast can be spread and held open. However, many of these synthetic casts spring back to their original position after simply cutting 1 side of the cast. In summary, bivalving casts is advised if there are concerns regarding excessive swelling.

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REGIONAL ANESTHESIA AND COMPARTMENT SYNDROME

It is appropriate that today's physician and society are focused on preventing as much pain as possible in all patients, and especially children.11–13 In addition, anesthesiologists and pain specialists have greater tools at their disposal to treat pain.14 Unfortunately, injudicious use of these modalities may mask the primary symptom of increased pain seen in compartment syndromes.15–18 It is further possible that use of sympathetic blocking agents could increase flow and possibly potentiate the development of compartment syndrome. Although our institution strongly endorses regional pain management, the use of these modalities is contraindicated after fracture fixation or in high-risk patients such as those undergoing tibial osteotomy, even though prophylactic fasciotomy is a matter of routine.

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COMPARTMENT PRESSURE MONITORING

The diagnosis of compartment syndrome is predominantly a clinical one and high compartment pressure measurements must be viewed in light of the clinical scenario. This concept was observed by Prayson et al,19 who studied isolated lower extremity fractures without compartment syndromes. The average compartment measure was 36 mm Hg in the injured leg versus 16 mm Hg in the uninjured leg. The authors concluded that the use of the Stryker Monitor (Stryker Corporation, Allendale, NJ) may not be specific for the diagnosis of compartment syndrome. In addition, pressures greater than 30 mm Hg can occur in the deep volar compartment of asymptomatic children treated for supracondylar humerus fracture.9 Yet, despite the potential for false-positive readings, compartment measures are a useful adjunct in some cases of potential compartment syndrome in which the clinical symptoms are contradictory and in patients that are obtunded or under general anesthesia.

The normal pressure in a muscle compartment is less than 10 to 12 mm Hg. Animal studies have shown that pressures maintained above 30 mm Hg for 8 hours are able to cause irreversible damage to muscle and significant nerve conduction impairment. After a leg injury, it is known that the anterior compartment is usually the highest pressure elevation and the superficial posterior compartment usually has the lowest pressure elevation. Heckman et al20 reported the relationship between compartment tissue pressure and the distance from fracture; they concluded that measures should be taken within all compartments, particularly within 5 cm of the level of injury.

There are both continuous and noncontinuous methods of monitoring compartment pressure, and there are several types of invasive instruments with which to measure pressure. The slit catheter and side-ported needles are the most accurate as standard needles produce values that are up to 20 mm Hg different in comparison with the slit catheter or side-ported needles. The Stryker instrument and the arterial line monitoring devices seem to be the most reliable methods to measure pressure.

There is no consensus about the ideal measuring device or the pressure threshold for fasciotomy in each of the anatomic regions. Some investigators have recommended fasciotomy if the compartment pressure is greater than 30 or 45 mm Hg. Others have recognized that a limb may be adequately perfused if the diastolic blood pressure (DBP) is 30 mm Hg greater than the measured compartment pressure. Therefore, fasciotomy may be indicated if the ΔP (ΔP=DBP–compartment pressure) is less than 20 to 30 mm Hg. Importantly, one needs to recognize the effect of general anesthesia when calculating these values. For instance, Kakar et al21 found that intraoperative DBP of patients treated with tibial intramedullary nailing decreased approximately 18 mm Hg while under anesthesia. The investigators suggest that the intraoperative pressure differential between the DBP and the compartment pressure may be lower because of general anesthesia and the surgeon should consider this when deciding whether to perform a fasciotomy or not.

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NEW DEVELOPMENTS IN NONINVASIVE MONITORING

Unfortunately, standard needle monitoring is painful and anxiety producing for children; as such, some endeavored to develop a noninvasive methodology as an alternative to needle-based compartment monitoring. Three recently published methods are described below.

Near-infrared spectroscopy measures tissue levels of hemoglobin and myoglobin and is somewhat similar to the method that a pulse oximeter uses to assess blood oxygenation.22 Decreased values of tissue oxygenation have been used to diagnose chronic compartment syndrome, and although preliminarily tried in the acute setting, the use of this method in acute compartment syndrome remains unclear.23 For instance, although the method is applied transcutaneously, the depth of measurement is limited to 2 to 4 cm, which would be problematic for the deep posterior compartment of the leg. Pulse phase-locked loop ultrasound is a technique in which ultrasound measures fascial displacement, which can be correlated with intramuscular pressure.24 Early testing in humans and in patients with acute compartment syndrome is promising but limitations may exist in deep tissue compartments or in cases in which fascia is significantly disrupted from trauma. Finally, and similar to direct pressure measurements of the cornea for the detection of glaucoma, several investigators have looked at soft tissue hardness as a means of diagnosing compartment syndrome.25 Recently, Joseph et al26 studied normal tissue hardness in unaffected individuals; in addition, they studied the relationship between tissue hardness and compartment pressure in an external model and in 3 freshly amputated limbs. Experimental data from this study suggest there is a nonlinear relationship between compartment pressure and tissue hardness. Factors that affect specificity include age, site of measurement (muscle bellies were less hard than tendons), hand dominance, and active muscle contraction.

Despite these important efforts to develop a noninvasive method to document compartment pressure, many technical and practical obstacles remain to be dealt with. Yet, even if a reliable noninvasive method is actualized, it is doubtful that it will supplant the concept that compartment syndrome is a diagnosis that is usually made clinically and whose signs and symptoms guide treatment.

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TREATMENT OF ACUTE COMPARTMENT SYNDROME

Once the diagnosis of compartment syndrome has been made, emergent fasciotomy of the compartment at risk is indicated. While simultaneously planning and performing the fasciotomy, the surgeon needs to consider and treat the inciting etiology or any other associated pathology. For instance, in cases of vascular compromise, bypass surgery or temporary shunting is performed by our vascular colleagues. Internal and external fixation options for limb stability are weighed and individualized for each patient. External fixation provides an excellent way to temporize and align limb fractures and dislocations while allowing exposure to soft tissue wounds and fasciotomy defects. In addition, some consideration for limb splinting and fracture reduction is needed to avoid exacerbation of elevated pressures. For instance, temporarily leaving a foot in plantarflexion will likely decrease pressures in the deep posterior compartment of the injured leg. Some investigators suggest that keeping a fractured limb in a malreduced and stable alignment in the short term may decrease pressure in that limb as opposed to reducing the fracture out to length.14,19

In cases in which forearm compartment syndrome is suspected, a curvilinear volar incision is used to allow release of the superficial and deep fascial compartments as well as the carpal tunnel. We have not routinely performed dorsal incisions but these may be indicated with increased pressure in the extensor mobile wad of muscles. Forearm fractures are usually stabilized with intramedullary devices, yet external fixation may be needed in more severe trauma. At our institution, leg compartment syndrome is treated with medial and anterolateral skin incisions whereby the deep posterior and superficial posterior compartments are released medially while the anterior and lateral compartments are released from the lateral incision. Although it may be tempting to perform limited skin incisions with wider subcutaneous fascial release, this should be discouraged in favor of ensuring complete release of the offending compartments; this is more easily guaranteed with longer skin incisions. In cases of open fractures, skin and soft tissue debridement precedes copious irrigation with saline and antibiotic solution.

Despite the relative paucity of literature regarding the role of vacuum-assisted closure sponges in compartment syndrome,27 we routinely use this technology to keep the wounds sealed before eventual closure. It could be hypothesized that negative pressure may decrease interstitial fluid, thus improving the ability for later closure. Delayed primary skin closure may be performed in some of the open wounds but split thickness skin grafting is a mainstay of closure, which can be performed as early as 3 days after fasciotomy. Other factors may dictate later closure but we usually try to accomplish this within 7 days.

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TREATMENT FOR VOLKMANN CONTRACTURE

If there is marked muscle necrosis and contractures, complex reconstruction, including potential free muscle transfer, may be indicated to restore useful hand function. A variety of factors must be taken into consideration when contemplating a reconstruction after the Volkmann ischemic contracture of the upper extremity.28 The child and the family should be given realistic expectations regarding reconstruction, and a detailed outline as to what will be required postoperatively. It is important to have a well-motivated patient. The situation may be complicated by medico-legal considerations. There will be a rather complex and time-consuming rehabilitation program that will be needed to affect the most gain from any reconstruction. Thus, the patient must be compliant and the family must be prepared to work with the child in the postoperative rehabilitative phase. Surgery will improve but not normalize the situation. There may be long-term issues with growth.

Staged surgical procedures may be needed to effect improvements in limb function. In rare situations, vascular inflow may need to be optimized to provide improved blood supply to the hand. At least protective sensation in the hand is important before reconstruction. Neural decompression or reconstruction of the median and ulnar nerves may be required. A full passive range of motion is a prerequisite of reconstruction. Thus, extensive physiotherapy and surgical capsulotomies and muscle lengthening may be necessary before undertaking motor reconstruction. Finally, the overlying soft tissues must be in optimal condition to provide adequate coverage and a base for muscle contraction and tendon gliding. This may require vascularized soft tissue coverage. Once all of this has been optimized, the patient may become a candidate for free muscle transfer.

Free functioning muscle transplantation to the forearm has changed the care of childhood Volkmann ischemic contracture. The initial work for free muscle transplantation was performed in China and Japan during the early 1970s to the 1990s. Transfer of the gracilis muscles had been found to improve the function of the hand in patients with the Volkmann ischemic contracture. This procedure requires 2 teams of surgeons; one group will harvest the gracilis muscle identifying and mobilizing its nerve input and vasculature. A second group of surgeons must prepare the bed in the forearm for muscle transplantation. Typically, the anterior interosseous nerve is selected for reinnervation of finger and thumb flexion. Identifying an origin for the muscle placement at the medial epicondyle, and the location of the tendons to the finger flexors and thumb flexors are needed. In addition, preparation for an end-to-end or end-to-side repair of the arteries and veins is made. A skin pedicle can be harvested with the free gracilis for coverage. Split thickness skin grafts can be applied over the muscle to diminish tension on the soft tissues and vascular pedicles. Postoperatively, the limb is rested for 3 weeks, after which passive range of motion of the fingers and wrists begins.

The results of muscle transplantation after ischemic contracture have been successful. Muscle contraction can begin at 2 months postoperatively and continue to improve for up to a year and a half. Barring significant complications, viability and improved function of the muscle can be expected. Late problems may arise after treatment of the Volkmann ischemic contracture and may include altered limb growth from growth plate damage, diminished forearm rotation, and progressive deformities of the wrist and fingers may occur because of muscle imbalance.

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MEDICAL AND LEGAL ASPECTS OF COMPARTMENT SYNDROME

The diagnosis and treatment of compartment syndrome exposes the treating physician to significant risk for legal action. In a 23-year review of the single malpractice carrier, a risk of a malpractice claim was 0.2% per year of practice.29 In general, because the symptoms of compartment syndrome are so classically defined, it is possible for an attorney to prove deviation from the standard of care. As such, decisions in favor of the patient are at a much higher rate (56%) than those for litigation because of other orthopaedic diagnoses, which are classically settled in favor of the plaintiff in less than 30% of cases. Common contributing factors include failure to act on symptoms, poor physician-patient communication, and fasciotomy occurring greater than 8 hours after the time of diagnosis. In addition, Cascio et al30 found that greater than 70% of the patients with compartment syndrome have inadequate documentation, which confuses the picture.

It appears that the plaintiff success rate for lawsuits for compartment syndrome is greater than for other orthopaedic lawsuits. Malpractice claims for compartment syndrome are uncommon on a per surgeon basis, yet treating surgeons must remain vigilant with regard to compartment syndrome. Careful physician documentation of an abnormal finding on physical examination without intervention, poor physician-patient communication, and an increased time for fasciotomy are associated with a decision in favor of the plaintiff.

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SUMMARY

Compartment syndrome is a dreadful result of significant trauma and pathology, which requires thoughtful assessment and prompt treatment to minimize limb damage and optimize eventual function. It remains a clinical diagnosis that can be confirmed with invasive monitoring in selected cases. Eventual development of noninvasive techniques would be a welcome addition in those patients that are at risk for this complication and who are difficult to assess clinically. Reconstruction for established contractures is challenging and requires compliant patients who are willing to consider staged surgery to improve functional outcome.

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REFERENCES

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18. Whitesides TE. Pain: friend or foe. J Bone Joint Surg. 2001;83:1424–1425.
19. Prayson MJ, Chen JL, Hampers D, et al. Baseline compartment pressure measurements in isolated lower extremity fractures without clinical compartment syndrome. J Trauma. 2006;60:1037–1040.
20. Heckman MM, Whitesides ET, Grewe SR, et al. Compartment pressure in association with closed tibia fractures. J Bone Surg. 1994;76:1285–1292.
21. Kakar S, Firoozabadi R, McKean J, et al. Diastolic blood pressure in patients with tibia fractures under anaesthesia: implications for the diagnosis of compartment syndrome. J Orthop Trauma. 2007;21:99–103.
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24. Wiemann JM, Ueno T, Leek BT, et al. Noninvasive measurements of intramuscular pressure using pulsed phase-locked loop ultrasound for detecting compartment syndromes: a preliminary report. J Orthop Trauma. 2006;20:458–463.
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26. Joseph B, Varghese RA, Mulpuri K, et al. Measurement of tissue hardness: can this be a method of diagnosing compartment syndrome noninvasively in children? J Pediatr Orthop. 2006;15-B:443–448.
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Keywords:

pediatric; compartment syndrome; trauma

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