Historically, acute compartment syndromes (ACSs) were more commonly reported in the forearm associated with supracondylar humerus (SCH) fractures and in the lower extremity associated with femur fractures. Likely, this was related to historical treatment methods, including casting of the elbow in hyperflexion (>90 degrees) for SCH fractures and the use of Bryant traction for the treatment of femur fractures. With advancing treatment methods, such as operative stabilization and immediate spica casting, the incidence of these causes of compartment syndromes has decreased.

Currently, ACS in the pediatric population most commonly involves the lower leg associated with fractures of the tibia and/or fibula.^12,15 Adolescents in particular are at risk and have an 8.3% rate of compartment syndrome after tibial fractures.⁹ In the upper extremity, ACS most commonly involves the forearm typically associated with both bone fractures of the forearm and SCH fractures.^4,12,15,20 Based on a national database review, the incidence of forearm compartment syndrome following upper extremity injuries has been estimated at 1%.¹⁵ High-risk fracture patterns include displaced SCH fractures with concomitant ipsilateral forearm fractures with a rate of compartment syndrome as high as 33%⁴ or supracondylar fractures with a median nerve injury, which can mask the pain of compartment syndrome.²⁵ One study found displaced fractures of the forearm that undergo multiple passes of intramedullary nails may be at a higher risk for compartment syndrome.⁵³

DIAGNOSIS

The diagnosis of ACS is challenging and can be more difficult in children, especially infants, who are too young to cooperate, nonverbal, or apprehensive and crying. A high index of suspicion is recommended, especially in the setting of at-risk injuries and conditions.

Pain, pressure, pallor, paresthesia, paralysis, and pulselessness (the six Ps) have been described as clinical markers of compartment syndrome. The reliability of these clinical findings is questionable; however, as they may be difficult to obtain in the pediatric or obtunded patient or may present too late (only after irreversible tissue damage has already occurred). Instead, the three As may be more useful in making a diagnosis of compartment syndrome in the pediatric population: Anxiety (or restlessness), agitation (or crying), and an increasing analgesia requirement.^2,21

Pain out of proportion to the injury, especially aggravated by passive motion of the involved, ischemic compartment, remains as one of the most sensitive and early physical findings of compartment syndrome.²⁷ In particular, an increasing analgesia requirement (both in dose and frequency) can be a helpful early marker.² Pain perception may be diminished or absent; however, and cases of “silent” compartment syndrome (i.e., absence of pain in a compartment syndrome) have been reported.^1,27 Restlessness, agitation, and anxiety may be present instead, as children may not be able to report or express pain. Pressure, swelling, and tenseness may be the only objective findings of early compartment syndrome; however, these findings also tend to be unreliable physical markers of compartment syndrome.^27,40 Paralysis is a late and poorly sensitive finding of compartment syndrome, and once a motor deficit develops, full recovery is rare. Pulse oximetry usually is not helpful.

Diagnosis or exclusion of compartment syndrome on clinical grounds alone may be impossible. In these questionable clinical situations, compartment pressure measurements are recommended. In the pediatric setting, compartment pressures usually are best measured under conscious sedation or anesthesia. Accurate placement of the needle is essential. Multiple measurements at different sites and depths within each compartment are recommended. Compartment pressure measurements close to the level of fracture may be most accurate. Although controversial, the thresholds/indications for fasciotomy are an absolute pressure greater than 30 to 40 mm Hg or pressures within 30 mm Hg of either the diastolic blood pressure or the mean arterial pressure.⁴³ Recently, normal baseline compartment pressures have been shown to be higher in (the legs of) children (13 to 16 mm Hg) compared to adults (5 to 10 mm Hg). The clinical application of this data remains unclear.

Delayed diagnosis of compartment syndrome in children is not uncommon. This may be related to the challenges in making the diagnosis clinically in children. Other risk factors that may delay diagnosis are altered conscious level, associated nerve injury, polytrauma, and altered pain perception (possibly related to certain types of analgesia [regional]). Certain anesthetic techniques, including local anesthetics, regional anesthesia (epidural, nerve blocks), and systemic analgesics, may obscure early signs of a developing compartment syndrome and have been shown to increase the likelihood of missed compartment syndromes.^2,27,52 Delay in diagnosis may also be related to longer elapsed time between the initial injury and peak compartment pressures in the pediatric setting.¹² Extended close monitoring (after injury) is recommended in light of the sometimes later diagnosis of compartment syndrome in children.

In the future, near-infrared spectroscopy (NIRS) may prove to be useful in the earlier diagnosis of compartment syndrome, as NIRS is noninvasive and capable of measuring the oxygenation state of at-risk tissues.⁴¹

Overall, the entire clinical picture must be considered, and a high index of suspicion, especially in children who are difficult to examine, obtunded patients with blunt head injuries, or patients who are sedated, must always be maintained.

CLASSIFICATION

Acute Compartment Syndrome: ACS occurs when tissue pressures rise high enough within an osseofascial compartment to cause tissue ischemia. The exact time of onset of ACS is difficult to determine. It can therefore be difficult to know the duration of tissue ischemia in a given patient.

Exercise-induced or Exertional Compartment Syndrome: Exercise-induced compartment syndrome is a reversible tissue ischemia caused by a noncompliant fascial compartment that does not accommodate muscle expansion occurring during exercise. It has been described in both the upper and lower extremities.⁵¹

Neonatal: Both neonatal compartment syndrome and neonatal Volkmann contracture have been reported. To our knowledge, this has only been reported in the upper extremity. It is possible that this diagnosis exists for the lower extremity but has been attributed to other causes. Awareness of this diagnosis is important, as early recognition and treatment can improve the functional outcome and growth in these patients. Although established neonatal Volkmann contracture cannot be improved by emergent intervention, awareness of this diagnosis can aid in counseling of the family and treatment of the patient (Fig. 6-1A, B).

Volkmann Ischemic Contracture: Volkmann ischemic contracture is the end result of prolonged ischemia and associated with irreversible tissue necrosis.

Several classification systems have been described for upper extremity Volkmann contracture. Most are based on the clinical severity of the presentation and are used to help direct the appropriate treatment for the identified disability. Most authors recognize the tremendous variability of the clinical presentations and the subsequent limitations of the classification system.^38,48,49,54

Seddon was the first to introduce the concept of the ellipsoid infarct involving the muscles of the proximal forearm. He further described a spectrum of contracture from mild to severe. The mild type responds to splinting with little to no residual sequelae, with the possible recurrence of contracture as a young child grows to maturity. The most severe type was described as a limb, which “apart from its envelope is gangrenous and whose treatment is futile.”³⁸ Between these two extremes, he described three separate patterns of presentation: (1) Diffuse but moderate ischemia; (2) intense but localized muscle damage, and (3) widespread necrosis or fibrosis.

Zancolli noted the significant variability in the involvement of the hand. His classification system was entirely based on the involvement of the intrinsic muscles.⁵⁴ Types I to IV describe the severity of the intrinsic muscle involvement. The variability in presentation depends on the ischemic insult and recovery potential to the median and ulnar nerves.

The most commonly used and our preferred classification system is that of Tsuge.⁴⁸ He classified established Volkmann contracture into mild, moderate, and severe types, according to the extent of the muscle involvement.

The mild type, also described as the localized type involves the muscles of the deep flexor compartment of the forearm, usually involving only the flexor digitorum profundus of the ring or middle fingers. It can involve all the flexor digitorum profundus and the flexor pollicis longus as well. Nerve involvement is absent or mild, typically involving sensory changes which resolve spontaneously. With wrist flexion, the fingers can be fully extended. The majority of the mild type resulted from direct trauma either from crush injury or forearm fractures, and was typically seen in young adults.

In the moderate type, the muscle degeneration includes all or nearly all of the flexor digitorum profundus and flexor pollicis longus with partial degeneration of the flexor superficialis muscles. Neurologic impairment is always present. Sensory impairment is generally more severe in the median than in the ulnar nerve, and the hand demonstrates an intrinsic minus posture. Moderate-type injury was most commonly the result of SCH fractures in children between ages 5 and 10.

The severe type involves degeneration of all the flexor muscles of the fingers and of the wrist. There is central muscle necrosis, and varying involvement of the extensor compartment (Fig. 6-2). Neurologic deficits are severe, including complete palsy of all the intrinsic muscles of the hand. Tsuge categorized as severe those cases with moderate involvement that are complicated by fixed joint contractures, scarred soft tissue, or previously failed surgeries. As with the moderate cases, the severe cases were most commonly the result of SCH fractures in children.

Within each classification type, there is a broad range of clinical presentation. This heterogeneity of presentation makes it difficult to apply a specific treatment based solely on classification systems, and makes it nearly impossible to provide meaningful outcome and comparison studies.

TREATMENT

Potentially devastating complications may be avoidable with early recognition and prompt intervention. The goal of treatment is to prevent tissue necrosis, neurovascular compromise, and permanent functional deficits.

The first step is to remove all possible extrinsic causes of pressure, including circumferential dressings, cast padding, and casts. Remember that excessive limb elevation may be counterproductive; the affected limb should not be elevated higher than the patient’s heart to maximize perfusion while minimizing swelling; however, a little elevation is probably better than risking a dependent limb. Optimizing overall medical management is also recommended, as shock and hypoxia may lower tissue pressure tolerance.¹⁵

Ultimately, emergent surgical decompression (fasciotomy, i.e., release of the fascia overlying the affected compartments) is recommended for established cases. At times, release of the epimysium is also necessary. Clearly necrotic tissue should be excised as it may become a nidus for infection, but in young children questionable tissue should be left in place for a second look at a later date as discussed below. Late fibrosis of necrotic muscle can lead to compression of the adjacent nerves and result in disability of the extremity. Other procedures may be indicated based on the etiology of the compartment syndrome, including vascular thrombectomy, repair, or grafting; nerve exploration, if indicated; and fracture reduction and stabilization. Nerve repair or reconstruction when necessary should be performed at the time of definitive wound closure.

Late diagnosis increases the risk for severe complications, including infection, neurologic injury, need for amputation, and death. Concerns about increased risk of infection have led to some recommendations not to perform fasciotomy after 24 hours of onset of symptoms. Good results however may be possible in children even when fasciotomy is performed as late as 72 hours after the injury (within acute swelling phase).¹² Dramatic, essentially full, recovery has been reported following compartment syndrome of the lower leg in children even after delayed presentation.⁶ The potential for recovery of muscle function may be greater in a child than in an adult. This is consistent with the increased potential for recovery observed from other types of injuries in children, such as fractures, traumatic brain injuries, and articular cartilage injuries.⁶ As has been suggested in open fractures in children, if in doubt as to the viability of soft tissue, we recommend not to debride questionable tissue at the initial fasciotomy because the potential for tissue recovery in a child is much greater than that of an adult.¹¹

In the case of a delayed (or late) compartment syndrome, where fasciotomy is not indicated, for example, no demonstrable muscle function in any segment of the involved limb, the limb can be splinted in a functional position. For the upper extremity, if the resources are available for immediate reconstruction with functional free muscle transfer, then early debridement and reconstruction can reduce the incidence of late contracture and improve neurologic recovery.^36,44,45 Supportive care, usually in the form of vigorous intravenous hydration, should be given for the potential risk of myoglobinuria. Myoglobinuria, as well as metabolic acidosis and hyperkalemia, can also occur during reperfusion and requires medical management especially to prevent sequelae such as renal failure, shock, hypothermia, and cardiac arrhythmias and/or failure.

LOWER EXTREMITY

Thigh

Compartment syndromes involving the thigh are particularly rare but have been reported in the pediatric population after blunt trauma, external compression with antishock trousers, and vascular injury with or without fracture of the femur. Historically, children with femoral shaft fractures treated by skin or skeletal traction were also at risk for compartment syndrome.

Three compartments—anterior, medial, and posterior—are described in the thigh (Table 6-2). In the thigh, a long single lateral incision can adequately decompress the anterior and posterior compartments (Fig. 6-3). Occasionally, a medial adductor incision is required as well.

Lower Leg

The most common presentation of ACS in children involves the lower leg following a tibia and/or fibula fracture. Compartment syndrome is also a well-known complication following tibial osteotomies for angular and/or rotational correction.

In the lower leg, a one- or two-incision technique can be employed for decompressive fasciotomy of all four compartments—anterior, lateral, superficial posterior, and deep posterior (Table 6-3). In the two-incision technique (Fig. 6-4A), the anterolateral incision allows access to the anterior and lateral compartments. The posteromedial incision must be lengthy enough to allow for decompression of the superficial posterior compartment (more proximal) and deep posterior compartment (more distal). The soleus origin should be detached from the medial aspect of the tibia. All four compartments of the lower leg can also be adequately decompressed with a single-incision technique (Fig. 6-4B). The long lateral incision typically extends 3 to 5 cm within either end of the fibula. First, identification of the septum between anterior and lateral compartments allows access to these compartments. Next, by elevating the lateral compartment musculature, the posterior intermuscular septum is visualized and access to the superficial and deep posterior compartments is possible.

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