1. Compartment syndrome is a surgical emergency and must be diagnosed and treated promptly.
2. Accurate diagnosis of the condition relies of the collation of clinical features and intracompartmental pressure measurements. Serial assessments can help establish the diagnosis when there is uncertainty.
3. Unrelenting pain out of proportion to the injury, paraesthesia or paresis of nerves within the affected compartments, and passive stretch exacerbation of pain are important clinical features.
4. Threshold for diagnosis in adults when using compartment pressure measurements is a perfusion pressure (diastolic blood pressure—intracompartmental pressure) of less than 30 mmHg for 2 consecutive hours.
5. Decompression in the leg is performed using the two-incision technique. The posteromedial incision is 12–15 mm posterior to the posteromedial border and the anterior incision 2 cm lateral to the crest of the tibia. All four compartments are to be released adequately to enable extrusion of enlarged muscle.
6. All non-viable muscle is excised and fasciotomy wounds covered immediately with meshed split skin grafts or within 72 hours at the latest.
Acute compartment syndrome of the limb is characterised by ischaemia of the soft tissues in association with raised tissue pressures within unyielding osseofascial compartments. It is a surgical emergency as the sustained high levels of pressure compromise capillary perfusion lead to hypoxia-induced death of tissue. Compartment syndrome may occur following a fracture or revascularisation of an ischaemic limb; sometimes it is associated with a crush injury (1). Irreversible muscle and nerve damage occur when hypoxic levels are sustained and the period beyond which the damage becomes permanent depends on the type of tissue and pressure levels. Consequently, prompt diagnosis and decompression may save limbs. A missed diagnosis is associated with significant morbidity arising from the ischaemic necrosis and, sometimes, putrefaction of tissues within the compartment. Late decompression, after the stage when tissue can be rescued, should be avoided because of the risks of infection and reperfusion injury.
The principles described in the foregoing account apply to the upper and lower limb except for the hand and foot.
Making the diagnosis
An increased awareness of the condition, particularly with some fracture types, and repeated clinical assessments and intracompartmental pressure measurements will enable early diagnosis and treatment. Heightened vigilance is recommended for young adults with mid-diaphyseal tibial fractures, tibial plateau fractures, or proximal tibial fractures associated with knee dislocation (2, 3). These injury types have a higher association with acute compartment syndrome, possibly from the high-energy nature of the underlying mechanisms producing greater soft tissue disruption. The key to making an accurate diagnosis is the serial collation of signs and symptoms. The greater the number of positive features, the more likely is the diagnosis to be accurate, especially if this is repeated over a short period of observation. Whilst a single positive finding has a probability of an accurate diagnosis of 25%, three findings increase this probability to 93% (4).
An important feature of compartment syndrome in the conscious patient is severe pain that is out of proportion to the injury and that fails to improve in the expected time course after surgery or after a judicious dose of analgesics. The pain is exacerbated by passive stretching of the muscles of the affected compartment but this sign is not valuable in children, who are influenced by apprehension and fear of pain. The classic five Ps of compartment syndrome (pain, pallor, paraesthesia, pulselessness, and paralysis) are not relevant to an early diagnosis of the condition; if anything, waiting for all five Ps would inevitably lead to a late diagnosis. Of the five, pain, paraesthesia, and weakness (paralysis) are likely to be found early and a clinical examination should look for signs of nerve impairment, e.g. sensory loss within the areas supplied by nerves traversing the involved compartments. In the lower leg the anterior compartment is most commonly involved and numbness in the first web space (deep peroneal nerve) is an early sign.
The clinical signs of compartment syndrome are affected if nerve blocks or regional anaesthesia has been used or if the patient is unconscious. The impediment introduced by such effective analgesic methods is not about the ability to make the diagnosis but about making the diagnosis early. Eliciting clinical signs can be difficult in non-compliant patients and young children. In such scenarios, continuous measurement of intracompartmental pressure has its advocates (5). In the unconscious or non-compliant patient, it may be the only available clinical parameter. The pressure is measured using purpose-made devices, which are solid state transducer intracompartmental catheters (STIC, Stryker, USA) or transducer-tipped catheters (Omnibar E5F, Raumedic, Germany). Both produce similar readings but single measurements should be used cautiously; corroborative clinical signs or repeated measurements help add weight to the diagnosis of compartment syndrome (6). The commonly used threshold for decompression in adults is when the perfusion pressure (diastolic pressure minus intracompartmental pressure) is less than 30 mmHg, especially when sustained for more than 2 hours. In a consecutive series of over 900 adults with tibial fractures, the sensitivity and specificity for making the diagnosis with this threshold were 94% and 98%, respectively, and led to fasciotomies in 18% (5). The balance between a prompt diagnosis and unnecessary fasciotomy can be difficult; both untreated compartment syndrome and unneeded surgery carry morbidity (7, 8, 9). Additionally, this perfusion pressure threshold can be unsuitable for young children who have diastolic blood pressures between 40 and 55 mmHg (this would suggest intracompartmental pressures of 10–25 mmHg would then prompt a fasciotomy). The incidence of acute compartment syndrome is lower in young children (<12 years) and may occur as late as 65 hours after injury (10). The recommendation for young children is to use serial clinical examination repeated over brief intervals whilst the limb is nursed flat and to note if there has been a record of increasing analgesic needs (11, 12).
Surgery to decompress the four compartments in the leg is the only treatment available; whilst preparing for surgery it is prudent to confirm that all circumferential dressings have been divided. Long incisions through skin and fascia are needed to decompress adequately and allow extrusion of the increased muscle bulk. Subcutaneous incisions in the fascia through shorter skin incisions are not recommended (13). We recommend the two-incision technique (14, 15). The positions of the incisions are different from classic descriptions (16); this represents a deliberate attempt to facilitate soft tissue cover of open fractures by preserving perforators arising from axial vessels such that local fasciocutaneous flap options remain viable (Figure 11.1a–d). There are added advantages: the incisions provide good access to the posterior and anterior tibial vessels should these be needed as recipient vessels for free flaps.
The superficial and deep posterior compartments are decompressed by an incision placed 12–15 mm just posterior to the posteromedial border of the tibia. At times the posteromedial border is difficult to palpate in the swollen limb but starting from the medial malleolus (a bony landmark always felt even in such scenarios) it is possible to gauge the position with some accuracy. The placement of this posteromedial fasciotomy incision is 12 mm from the posteromedial border of the tibia in children but closer to 15 mm when the patient is an adult. As a guide, if the child’s leg is approximately the size of an adult forearm, the distance of 12 mm should be used; as the limb approaches adult size, then the 15 mm distance is safe. The posterior tibial neurovascular bundle lies between the muscles of the two posterior compartments, just next to the investing fascia of the deep compartment. Care must be taken when decompressing this compartment from the posteromedial side. Proximally, the soleus originates from the posteromedial border of the tibia and needs to be taken down sharply to allow full access to the fascia of the deep posterior compartment.
The anterior and lateral (peroneal) compartments are decompressed by an incision 2 cm lateral to the crest of the tibia. Entry into the anterior compartment is immediate but the peroneal compartment is decompressed by retracting the muscles of the anterior compartment medially and identifying the septum separating anterior and lateral muscle groups and incising it carefully. This septum can be seen and felt lateral to the fibula. The surface anatomy—tibial crest and posteromedial border—for the placement of the two skin incisions can be difficult to define in a swollen limb but careful palpation will reveal these contours.
There has been a resurgence of interest in single incision fasciotomies for decompression of all four compartments (17, 18). We do not advocate the technique: reaching all four compartments from a single lateral incision involves undermining the skin anteriorly and posteriorly. This degloves the skin and can pose potential problems for wound healing in a zone of injury. The two-incision technique decompresses by allowing the greater volume of contents (muscle) within the compartments to spill out and thereby occupy a larger space.
Muscle viability must be checked after compartment decompression and excised if necrotic. If all devitalised tissue is removed, we favour immediate coverage with meshed, split thickness grafts secured with a negative pressure foam dressing using pressures of 50–70 mmHg only. This provides cover to the wounds and fracture with immediate effect. If closure is to be delayed because of uncertainty over tissue viability, a temporary dressing is applied (19). Return to theatre for final inspection, wound excision, and definitive fracture cover should be accomplished within 72 hours.
A late diagnosis of compartment syndrome and subsequent fasciotomy can lead to severe infection, renal failure and death (20, 21, 22). The definition of late diagnosis is unclear and there is evidence that even by 3 hours after trauma there is muscle necrosis (23). This suggests there may be varying degrees of the condition and that our current tools for establishing the diagnosis—whether clinical features or pressure measurements—are surrogates for the cell death occurring from impaired tissue perfusion. Newer modalities are being investigated and include near-infrared spectrometry and tissue ultrafiltration samples (24); at present, clinical examination and compartment pressure measurement remain at the forefront of diagnosis (25).
There is controversy over how best to manage a late presentation of compartment syndrome in adults as decompression enables reperfusion of necrotic muscle and leads to a rhabdomyolysis syndrome. Leaving the compartments closed will allow the necrosis to complete without reperfusion; this may be a safer prospect (26). Conversely there are those who advocate decompression even if the diagnosis is late but with removal of necrotic muscle (to the extent of compartment removal, if necessary, leaving the traversing neurovascular bundles intact). There is insufficient evidence to provide clear guidance but a late decompression without removal of necrotic muscle will lead to greater morbidity, and potentially death, from reperfusion and rhabdomyolysis. This contrasts with the situation when dealing with children where the syndrome may evolve more slowly and result in a late diagnosis; serial assessments are advised and fasciotomy, even when late, can be associated with recovery (27).
Acute compartment syndrome can occur in open tibial fractures; there is no spontaneous decompression of the compartments from the wound. The diagnosis involves vigilance, repeated clinical assessments and intracompartmental pressure measurements. Treatment is by a dual-incision fasciotomy and decompression of all four compartments of the tibia. Wound excision must follow if non-viable tissue is identified.
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