Acute compartment syndrome remains one of the few true emergencies in orthopedic traumatology. It is a condition in which increased compartment pressure within a confined space compromises the circulation and viability of the tissues within that space. In the orthopedic trauma setting, compartment syndrome is observed in both acute open and closed fracture settings, most often in the long bones of the forearm and leg.1 It can also be present in the absence of fracture following a severe soft tissue injury. Acute compartment syndrome is important for orthopedic surgeons to recognize because its diagnosis is not always straightforward, and it has a high risk of associated limb morbidity if left undiagnosed or untreated.
Early fasciotomy is of the utmost importance because definitive treatment through early and correct diagnosis is key in preventing morbidity.2 Classic cardinal signs for acute compartment syndrome have demonstrated less than optimal sensitivity but excellent specificity; as Ulmer3 stated: “these findings suggest that the clinical features of compartment syndrome of the lower leg are more useful by their absence in excluding the diagnosis than they are when present in confirming the diagnosis.”
Despite the ability to invasively measure compartment pressures, the diagnosis of acute compartment syndrome, which is an evolving pathologic process, is often based on the assessment of all related clinical factors. In this article, the authors review the pathophysiology, anatomy, diagnosis, and treatment of this potentially devastating condition.
When inflammation develops following trauma, the limiting envelope surrounding individual muscle compartments leads to increased pressures that, if untreated, will eventually produce a final common pathway of cellular anoxia and tissue damage.4 The limiting envelope is most often the fascia but can be the epimysium5 or skin.1 Fascial compartments are inelastic and do not change in size after development is complete, but the muscle within is not limited in growth. Patients with increased muscle mass have less space for swelling after muscle injury.6
The basic principle of ischemia stems from inadequate perfusion relative to demand. The ischemia produced by compartment syndrome is a self-perpetuating cycle involving increasing edema, pressure, and ischemia.7 Muscles and nerves tolerate ischemia for up to 4 hours with limited sequelae; however, 8 hours of ischemia results in irreversible damage.8 Fasciotomy allows for normalization of capillary blood flow and clears the local accumulation of anaerobic metabolite build-up via restoration of physiologic pressures within the compartment. Following decompression, if early enough in the cycle, cells may become edematous and histologically will appear to exhibit injury. However, normal morphology is returned after 1 week.9,10
Several hypotheses exist regarding the pathophysiology of compartment syndrome, and it is likely that this syndrome is more complex than the current state of knowledge. The most widely accepted hypothesis is the arteriovenous pressure gradient theory, in which reduction of this gradient and decreased microvascular flow through the capillaries perpetuates edema and pressure, leading to increased ischemia.1,7 Initially, and most often in the acute setting, an increase in local pressure and edema stem from the insult. Subsequently, an increase in local intravenous pressure occurs, as well as a reduction in arteriovenous gradient, and leads to a local decrease in perfusion.
Endothelial cells sustain damage via anoxia and increased vessel wall permeability.11 In addition to the decrease in perfusion, the decreased venous return increases tissue edema. Lymphatic drainage can only compensate to a point and will fail under high pressure.12 It is the venous flow and this local stasis that perpetuate the edema and elevate compartment pressures. The pressures then increase to equal the diastolic blood pressure, and local tissue perfusion ceases.13,14 Once muscle necrosis begins and cytolysis occurs, the osmotically active contents of the cell spill into the interstitium and further increase the edema.15
Whitesides et al16 recommended that compartment pressures be compared with systemic diastolic pressures rather than absolute compartment pressures when determining the need for fasciotomy. This may account for why hypotension has been reported as a risk factor for developing compartment syndrome and for why hypertension has a protective effect and elevated the threshold pressure for viability of peripheral nerves.17 Conversely, in a study of tibial fractures and compartment syndrome by Park et al,18 no association was found between diastolic pressure and acute compartment syndrome.
Increased understanding of the exact pathophysiology processes may guide the development of medical nonsurgical interventions that could be applied in the early stages of acute compartment syndrome development to stop its progression and eliminate the need for surgical intervention.
Anatomy of Extremity Compartments
Knowledge of the anatomy and contents of each compartment are of paramount importance during the physical examination for compartment syndrome (Table; Figure). In cases of compartment syndrome of the leg, specifically in the context of a tibia fracture, the anterior compartment is almost always involved.19 Clinical judgement is an important tool for a surgeon to use to determine the need to release deep investing fascia or epimysium of a specific muscle compartment.10
Table: Lower-leg Compartment Contents
Figure: Axial section of the lower leg. Abbreviations: AIS, anterior intermuscular septum; ATA, anterior tibial artery; ATV, anterior tibial vein; DPN, deep peroneal nerve; F, fibula; GSaV, great saphenous vein; IM, interosseous membrane; LSuCN, lateral sural cutaneous nerve; MSuCN, medial sural cutaneous nerve; PA, peroneal artery; PIS, posterior intermuscular septum; PTA, posterior tibial artery; PTV, posterior tibial vein; PV, peroneal vein; SaN, saphenous nerve; SPN, superficial peroneal nerve; SSaV, small saphenous vein; T, tibia; TIS, transverse intermuscular septum; TN, tibial nerve.
Epidemiology and Etiology
The mechanism of injury for acute compartment syndrome ranges from high- and low-energy trauma to nontraumatic causes.20,21 The reported incidence of high- and low-energy trauma leading to acute compartment syndrome is approximately equal.4 McQueen et al6 reported that routine traffic accidents (involving both vehicle vs vehicle and vehicle vs pedestrian) were the most common causes of acute compartment syndrome, followed by sport-related injuries. Tissue-crushing injuries, falls, direct blows, burns, and penetrating injuries were among other reported traumatic mechanisms.6,22 Of note, traumatic injury leading to acute compartment syndrome was associated with fracture and nonfracture injuries. Circumferential wraps and casts also have the potential to restrict compartment expansion, decrease venous flow, and result in acute compartment syndrome.4,23
Age and sex distributions indicated that men in their thirties have the highest likelihood of developing acute compartment syndrome, which may be explained by the relatively larger muscle mass in men within a fixed compartment size after growth is complete. McQueen et al6 reported that the average annual incidence of compartment syndrome for men was 7.3 per 100,000, with a mean age of 32 years, whereas the average annual incidence for women was 0.7 per 100,000, with a mean age of 44 years.
Fracture is the reason for initial presentation and a major contributing factor in approximately 75% of cases of acute compartment syndrome.4,6,13,24 Specifically, in a review of 164 patients with acute compartment syndrome, 113 (70%) patients had an associated fracture, with the most common fracture being tibial diaphyseal fractures in 59 (36%) patients.
Lower-leg acute compartment syndrome has been reported in 2% to 9% of tibial fractures.6,18,25 Park et al18 found that, depending on the location of tibial fractures, the incidence of acute compartment syndrome varied from 1.8% in proximal tibial fractures to 8.1% in diaphyseal fractures and 1.4% in distal fractures, with the predominance at the diaphysis because the majority of muscle mass surrounds this area. McQueen et al6 reported 68 tibial fractures with acute compartment syndrome, of which 59 were diaphyseal fractures, 5 were tibial plateau fractures, and 4 were tibial pilon fractures.
Hope and McQueen26 reported the first series of patients to develop acute compartment syndrome in the absence of a fracture and excluded crush syndrome as a diagnosis. They showed that these patients are typically older, have more comorbidities, and have an increased chance of delay to fasciotomy, leading to increased muscle necrosis at the time of fasciotomy, citing a low awareness for risk of acute compartment syndrome in an isolated soft tissue injury. Posterior compartment involvement is more common in acute compartment syndrome without a fracture.26
Clinical Features and Diagnosis
The “6 Ps” (pain, pallor, paresthesia, paralysis, and pulselessness), which were initially developed to describe the findings seen in vascular injuries, have been used to describe clinical signs associated with compartment syndrome. However, these clinical symptoms are subject to large variability and inconsistencies.27 Pulselessness and pallor are rarely associated with compartment syndrome unless an associated vascular injury or systemic hypotension occurs. Practitioners who are unfamiliar with the pathophysiology of compartment syndrome often place emphasis on the presence of pulses to incorrectly rule out compartment syndrome. The presence of paresthesia and paralysis represent late findings after acute compartment syndrome has likely been present for 4 hours or more.
Diagnosing compartment syndrome is difficult in clinical practice, even with the availability of intracompartmental pressure measuring, and it has been argued that there is no way to determine the true rate of compartment syndrome.28 In addition, the gold standard for diagnosis via measurement of compartment pressures has recently been questioned. Within a single Level I trauma institution, a significant variation was found in different surgeons’ rates of compartment syndrome diagnosis. Interestingly, when looking at individual surgeons, the “more commonly a surgeon decided to check compartment pressures, the more likely the surgeon was to perform fasciotomy,”28 which introduces the hypothesis that a high false-positive rate may exist when using compartment checks. In addition, Prayson et al29 prospectively looked at compartment pressures in lower-extremity fractures and showed that 84% of fractured extremities qualified for the diagnosis of compartment syndrome based on having a compartment pressure within 30 mm Hg of diastolic pressure. Prayson et al29 argued that “direct compartment measurement with existing thresholds and formulations to determine the diagnosis of compartment syndrome may not accurately reflect a true existence of the syndrome.”
Current methods for direct measuring and monitoring of the compartment pressures include slit catheters, side-port needles, and ultrafiltration catheters. Pressure measurement is done either by an arterial line set or another pressure-monitoring device.30 Contrary to previous studies questioning the usefulness of compartment pressure measurements, McQueen et al31 estimated the sensitivity and specificity to be high. In a large retrospective review of patients who sustained a tibial diaphyseal fracture and underwent documented continuous anterior compartment pressure monitoring, the sensitivity and specificity were estimated as 94% and 98%, respectively, and the positive and negative predictive values were 93% and 99%, respectively. The study diagnosed acute compartment syndrome only after 2 hours of continuous anterior compartment measurement with the differential pressure (diastolic-intracompartmental pressure) remaining higher than 30 mm Hg, and the authors recommended continuous monitoring over 1 single measurement.31
Ulmer3 reviewed prospective studies on compartment syndrome and, despite variability in the clinical history and examination, was able to draw conclusions about the usefulness of the clinical findings. He looked specifically at pain, pain with passive stretch, paresthesias, and paresis in the literature and was unable to determine a consensus regarding which sign was of the greatest value due to a paucity of data. However, regarding use of these clinical findings in diagnosing compartment syndrome, the sensitivity was low (13% to 19%), the positive predictive value was low (11% to 19%), and both the specificity and negative predictive values were high (both 97% to 98%, respectively).3
Pain out of proportion to the injury is often cited as an early sensitive sign,4 yet pain is often already present at varying levels in trauma patients.13,19 Pain with a passive stretch of the muscle in the area of the injury has been reported to be of greatest clinical value but has also been stated to be too subjective.3 Swelling and palpable tenseness may be early signs of compartment syndrome, but at best they are crude indications of acute compartment syndrome.32 It is critical to maintain a high index of suspicion in at-risk patients, and repeated serial examinations are necessary.4,33
Magnetic resonance imaging (MRI) has been shown to identify chronic exertional compartment syndrome34; however, the use of MRI in trauma settings is limited due to the time commitment of MRI vs the emergent nature of acute compartment syndrome. Edematous changes on MRI are partially due to the initial injury and, although MRI can show changes in late compartment syndrome, it is not effective in diagnosing early acute compartment syndrome.35 Ultrasonography techniques are still in the early stages of development for monitoring compartment and perfusion pressures. Noninvasive ultrasound devices and pulse phase-locked loops detect slight movements in the fascia corresponding with arterial pulsation and distinguish between normal and abnormal intramuscular pressures.36,37 The benefit of this technology is that it is noninvasive and can be performed serially to produce a trend of intramuscular pressures. This may allow clinicians to detect impending acute compartment syndrome in its early stages. Near-infrared spectroscopy technology is noninvasive, measures local soft tissue oxygenation approximately 2 to 3 cm below the skin, and could provide continuous monitoring for intracompartmental hypoxia. Near-infrared spectroscopy has shown promise to become a sensitive and specific monitor of oxygenation of individual muscle compartments and is inversely correlated with increasing compartmental pressures. However, its limitations include use for patients with total body hypoperfusion and for obtaining measurements over a deoxygenated soft tissue hematoma.35,38,39 Interestingly, a lack of information exists in the literature on this subject, but measuring somatosensory-evoked potentials to detect nerve dysfunction may play a role in future noninvasive monitoring for compartment syndrome.40,41
In a prospective study comparing different compartmental measuring devices, Collinge and Kuper42 reported that no single measurement should be used for determination for or against performing fasciotomy, recommending the necessity of clinical correlation in the diagnosis of acute compartment syndrome.
Treatment, Fasciotomy, and Outcomes
Definitive treatment for acute compartment syndrome is emergent fasciotomy to decompress the compartments involved and prevent critical ischemia. Soft tissue viability is of immediate concern and has a narrow treatment window. As little as 8 hours of critical ischemia results in irreversible damage to compartmental muscles and nerves.8 Both single- and double-incision fasciotomy techniques have been described for releasing the 4 compartments of the lower extremity. In the first analysis of single- vs double-incision fasciotomy techniques for tibial fractures in acute compartment syndrome, Bible et al43 showed similar infection and nonunion rates between the techniques and left the choice to the surgeon.
Surgical decompression is not always indicated if the compartment syndrome has been evident for more than 48 hours and no evidence exists of retained function of the components within the compartment.30 Timing of prophylactic fasciotomy is controversial, and outcome data comparing prophylactic vs therapeutic fasciotomy are retrospective and of mediocre quality. In a study of 94 patients (including trauma and vascular patients), Velmahos et al44 found higher complication and nonclosure rates in prophylactic fasciotomy cases. The authors make a valid point that prophylactic fasciotomy is not without major complications, and the risk-benefit ratio should be weighed heavily.
Acute compartment syndrome remains a true orthopedic emergency. Despite a large amount of research and many articles discussing novel diagnostic tools, clinical examination is paramount, and the documentation of findings, discussion with patients and family, and treatment plan are essential. The authors believe that measurements of compartment pressures or other nonclinical diagnostic means should have no bearing on the urgent “get out of bed and take the patient to the [operating room].”
Alternative methods for diagnosing compartment syndrome have been attempted, but none have replaced high clinical suspicion and clinical examination.34 Review of the literature demonstrates the need for prospective, randomized trials comparing prophylactic and therapeutic fasciotomy, as well as additional investigation into reliable methods of diagnosing acute compartment syndrome.
- Matsen FA III, Krugmire RB Jr, . Compartmental syndromes. Surg Gynecol Obstet. 1978; 147:943–949.
- Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg Am. 2004; 86:864–868.
- Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder?J Orthop Trauma. 2002; 16:572–577. doi:10.1097/00005131-200209000-00006 [CrossRef]
- Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity musculoskeletal trauma. J Am Acad Orthop Surg. 2005; 13:436–444.
- Eaton RG, Green WT. Epimysiotomy and fasciotomy in the treatment of Volkmann’s ischemic contracture. Orthop Clin North Am. 1972; 3:175–186.
- McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk?J Bone Joint Surg Br. 2000; 82:200–203. doi:10.1302/0301-620X.82B2 .9799 [CrossRef]
- Holden CE. The pathology and prevention of Volkmann’s ischaemic contracture. J Bone Joint Surg Br. 1979; 61:296–300.
- Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg. 1996; 4:209–218.
- Heppenstall RB, Sapega AA, Scott R, et al. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988; (226):138–155.
- Leversedge FJ, Moore TJ, Peterson BC, Seiler JG III, . Compartment syndrome of the upper extremity. J Hand Surg. 2011; 36:544–559. doi:10.1016/j.jhsa.2010.12.008 [CrossRef]
- Durán WN, Takenaka H, Hobson RW II, . Microvascular pathophysiology of skeletal muscle ischemia-reperfusion. Semin Vasc Surg. 1998; 11:203–214.
- Mars M, Hadley GP. Raised intracompartmental pressure and compartment syndromes. Injury. 1998; 29:403–411. doi:10.1016/S0020-1383(98)00062-X [CrossRef]
- Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003; 85:625–632.
- Dahn I, Lassen NA, Westling H. Blood flow in human muscles during external pressure or venous stasis. Clin Sci. 1967; 32:467–473.
- Perron AD, Brady WJ, Keats TE. Orthopedic pitfalls in the ED: acute compartment syndrome. Am J Emerg Med. 2001; 19:413–416. doi:10.1053/ajem.2001.24464 [CrossRef]
- Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res. 1975; (113):43–51. doi:10.1097/00003086-197511000-00007 [CrossRef]
- Gelberman RH, Szabo RM, Williamson RV, Hargens AR, Yaru NC, Minteer-Convery MA. Tissue pressure threshold for peripheral nerve viability. Clin Orthop Relat Res. 1983; (178):285–291.
- Park S, Ahn J, Gee AO, Kuntz AF, Esterhai JL. Compartment syndrome in tibial fractures. J Orthop Trauma. 2009; 23:514–518. doi:10.1097/BOT.0b013e3181a2815a [CrossRef]
- McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg Br. 1996; 78:95–98.
- Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury. 2004; 35:1221–1227. doi:10.1016/j.injury.2004.04.009 [CrossRef]
- Ramos C, Whyte CM, Harris BH. Nontraumatic compartment syndrome of the extremities in children. J Pediatr Surg. 2006; 41:e5–e7. doi:10.1016/j.jpedsurg.2006.08.042 [CrossRef]
- Demling RH. The burn edema process: current concepts. J Burn Care Rehabil. 2005; 26:207–227.
- Younger AS, Curran P, McQueen MM. Backslabs and plaster casts: which will best accommodate increasing intracompartmental pressures?Injury. 1990; 21:179–181. doi:10.1016/0020-1383(90)90091-8 [CrossRef]
- Patel RV, Haddad FS. Compartment syndromes. Br J Hosp Med (Lond). 2005; 66:583–586.
- Blick SS, Brumback RJ, Poka A, Burgess AR, Ebraheim NA. Compartment syndrome in open tibial fractures. J Bone Joint Surg Am. 1986; 68:1348–1353.
- Hope MJ, McQueen MM. Acute compartment syndrome in the absence of fracture. J Orthop Trauma. 2004; 18:220–224. doi:10.1097/00005131-200404000-00005 [CrossRef]
- Newton EJ, Love J. Acute complications of extremity trauma. Emerg Med Clin North Am. 2007; 25:751–761. doi:10.1016/j.emc.2007.06.003 [CrossRef]
- O’Toole RV, Whitney A, Merchant N, et al. Variation in diagnosis of compartment syndrome by surgeons treating tibial shaft fractures. J Trauma. 2009; 67:735–741. doi:10.1097/TA.0b013e3181a74613 [CrossRef]
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- McQueen MM, Duckworth A, Aitken S, Court-Brown CM. The estimated sensitivity and specificity of compartment pressure monitoring for acute compartment syndrome. J Bone Joint Surg Am. 2013; 95:673–677. doi:10.2106/JBJS.K.01731 [CrossRef]
- Mubarak SJ, Owen CA, Hargens AR, Garetto LP, Akeson WH. Acute compartment syndromes: diagnosis and treatment with the aid of the wick catheter. J Bone Joint Surg Am. 1978; 60:1091–1095.
- Shuler FD, Dietz MJ. Physicians’ ability to manually detect isolated elevations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010; 92:361–367. doi:10.2106/JBJS.I.00411 [CrossRef]
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- Garabekyan T, Murphey GC, Macias BR, Lynch JE, Hargens AR. New noninvasive ultrasound technique for monitoring perfusion pressure in a porcine model of acute compartment syndrome. J Orthop Trauma. 2009; 23:186–193. doi:10.1097/BOT.0b013e31819901db [CrossRef]
- Wiemann JM, Ueno T, Leek BT, Yost WT, Schwartz AK, Hargens AR. 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. doi:10.1097/00005131-200608000-00002 [CrossRef]
- Cole AL, Herman RA Jr, Heimlich JB, Ahsan S, Freedman BA, Shuler MS. Ability of near infrared spectroscopy to measure oxygenation in isolated upper extremity muscle compartments. J Hand Surg. 2012; 37:297–302. doi:10.1016/j.jhsa.2011.10.037 [CrossRef]
- Shuler MS, Reisman WM, Kinsey TL, et al. Correlation between muscle oxygenation and compartment pressures in acute compartment syndrome of the leg. J Bone Joint Surg Am. 2010; 92:863–870. doi:10.2106/JBJS.I.00816 [CrossRef]
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- Bronson WH, Forsh D, Qureshi SA, Deiner SG, Weisz DJ, Hecht AC. Evolving compartment syndrome detected by loss of somatosensory- and motor-evoked potential signals during cervical spine surgery. Orthopedics. 2012; 35:e1453–e1456. doi:10.3928/01477447-20120822-40 [CrossRef]
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Lower-leg Compartment Contents
|Anterior||Extensor hallicus longus, extensor digitorum communis, tibialis anterior, peroneous tertius||Deep peroneal nerve||Anterior tibial artery|
|Lateral||Peroneous brevis and longus||Superficial peroneal nerve, proximal portion of deep peroneal nerve||Peroneal artery|
|Posterior superfical||Gastrocnemius, soleus, plantaris||Tibial nerve branches||Posterior tibial artery, popliteal artery, peroneal artery, sural arteries|
|Posterior deep||Popliteus; tibilis posterior, flexor hallicus longus, flexor digitorum longus, popliteus||Tibial nerve||Posterior tibial artery, peroneal artery|