Javascript not enabled
TraumaFocus On...

Diagnosis of acute compartment syndrome

A. D. Duckworth, M. McQueen

Acute compartment syndrome (ACS) is defined by a critical pressure increase within a confined compartmental space, causing a decline in the perfusion pressure to the compartment tissue,1-6 which without timely diagnosis and treatment will lead to ischaemia, necrosis and ultimately permanent disability of the affected region.6-9 Management is with immediate fasciotomy and decompression of all tissues within the affected compartment.6,10-13



The diagnosis of ACS throughout the literature often uses a combination of clinical signs and/or compartment pressure monitoring, with a recent systematic review on compartment syndrome of the forearm documenting the use of monitoring in 50% of cases.6,14-16 O’Toole et al17 documented that compartment pressure monitoring was only used as the primary diagnostic tool in 11.7% of cases when they reviewed the notes of 386 tibial diaphyseal fractures at a large level I trauma centre. An older United Kingdom survey of compartment pressure monitoring revealed that over 50% of all consultant orthopaedic surgeons did not use monitoring within their institution.14

A delay in the diagnosis and management of ACS leads to a prolonged time of inadequate perfusion and has been found to result in a poor outcome for the patient,10,13,18-20 as well as being associated with increased medical costs.21 A prompt diagnosis is necessary to minimise the risk in a predominantly young and active population of potentially devastating long-term complications such as muscle necrosis, contractures, neurological deficits, fracture nonunion, infection, chronic pain, and in the worst cases amputation and even death.6,10,16,22-24 Along with providing an improved patient outcome, an early diagnosis is associated with decreased indemnity risk for legal claims.25 A delay in diagnosis has been attributed to a lack of awareness for the condition, inexperience of the surgeon, general or regional anaesthesia, patients with polytrauma, soft-tissue injuries and the reliance solely on the clinical signs used to diagnose ACS.6,24,26-32



Knowledge of the incidence, and an understanding of the demographic risk factors, is invaluable when assessing a patient for a suspected ACS. The annual incidence of ACS in the literature has been quoted as 3.1 per 100 000 population, with the incidence in males ten times that of females.15,16 The mean age ranges from 30 to 35 years with males affected at a significantly younger age than females.15,33,34 The most frequently affected sites are the leg13,20,35,36 and forearm,16,37-39 although the arm,40-43 hand,43-45 gluteal region,32,46 thigh,24,47-50 foot51-55 and abdomen56 can all be affected.

Over two-thirds of all ACS presentations are associated with a fracture, with a tibial diaphyseal fracture accounting for a third of all ACS cases (Table I).15 In the early days of intramedullary nailing of tibial diaphyseal fractures there was some concern that the technique might cause an increased rate of ACS,19,57-61 but subsequent studies have documented no increase in incidence.61,62 The incidence of ACS associated with a fracture of the tibia or distal radius has been found to be significantly increased in patients under the age of 35 years at the time of injury.15 In a large study of 1403 fractures of the tibial shaft from Edinburgh, risk factors for developing ACS were identified as male gender and youth.6 Furthermore, in a recent study of 414 tibial fractures, risk factors for the development of ACS were young patients with diaphyseal fractures.63 A proposed explanation for this is related to the increased muscle size in these patients, and hence a reduced capacity for swelling. In elderly patients, the protective effects of an increased perfusion pressure (hypertension) and small atrophied muscles has been postulated.

Although commonly associated with fractures, it is important to appreciate that almost a quarter of ACS presentations arise in the absence of a fracture.15,16,23 The mean age of patients who develop an ACS associated with a soft-tissue injury is significantly older than those associated with a fracture.23 A variety of causes has been identified and includes crush injuries, crush syndrome, drug overdose and anti-coagulation therapy.15,22,24,34,37,48,49,55,64-66 ACS in the absence of fracture has been found to be associated with a delay to diagnosis and fasciotomy.23

High-energy injuries including sports, road traffic accident and falls from height accounted for only half of all the modes of injury in one study of ACS.15 Although commonly perceived to be associated with high-energy injuries and open fractures, data has demonstrated an increased rate of ACS complicating closed low energy tibial diaphyseal fractures.15,67-69 This is perceived to be related to the ‘auto-decompression’ of the affected compartment at the time of a high energy injury. However, high energy fractures of the forearm and femur are associated with an increased rate of ACS, which is probably related to the high number of young males who sustain these injuries.15,16,43,48



Symptoms and signs associated with a diagnosis of ACS are pain out of proportion to the injury, pain on passive stretch, swelling, sensory disturbance and motor disturbance. Weakness or absence of peripheral pulses is not an associated sign as this indicates either a vascular injury or the late stages of ACS, in which scenario amputation is usually necessary.6 A clinical diagnosis can be made on a combination of these clinical signs. However, there is literature documenting the poor diagnostic performance characteristics of these signs,28 and they have been felt to be unreliable in the assessment of ACS in adults6,24,51,54,70 and in children.71

Ulmer28 performed a systematic review to determine the efficacy of four clinical signs in the diagnosis of ACS (Table II). He found that the sensitivity of clinical findings for diagnosing ACS to be low at 13% to 19%, with a specificity of 97% (Table II), and concluded that all the signs are better at excluding than confirming a diagnosis. In this analysis, it was found that with only one positive sign, the odds of ACS being present never reached above 26%. With three positive signs the odds were 93%, however, the third sign was paresis. This is a late sign of ACS and it is not acceptable to wait for this to develop before making the diagnosis and instituting treatment. If the diagnosis is delayed until paresis is established only 13% of patients will make a full recovery.35



Severe pain that is out of proportion to the associated injury and refractory to analgesia is judged to be the primary symptom of ACS. However, pain is subjective, already present post injury, of variable intensity, can be reduced when affecting the deep posterior compartment, can be absent when there is a concomitant nerve injury, and has been found to have very poor sensitivity (Table II).13,18,22,28,72 It has also been proven to be inadequate when assessing children or in the patient with poly-trauma and suspected ACS.71,73 Pain on passive stretch is equally unreliable with comparable diagnostic performance characteristics (Table II).28,72,74 Badhe et al74 reported four cases of ACS in which any form of pain was absent, with diagnosis confirmed on subsequent fasciotomy.



Although palpable swelling is a common presenting feature of ACS, it is a very subjective sign and is often hindered due to either the necessity of immobilisation masking the affected compartment or the fact that some compartments are deep and therefore difficult to assess.18,75



This sign can be related to either nerve ischaemia as it runs through the affected compartment or can be related to a concomitant nerve injury.72,76 There were initial suggestions that this sign might be more useful than pain in the diagnosis of ACS75 but it has since been suggested this is a late sign.20 On analysis, sensitivity is even lower at 13%, with a marginally increased specificity (98%).28



This is a late sign of ACS and is the poorest performing clinical finding on diagnostic performance analysis.28 Positive pre-fasciotomy motor symptoms have been found to negatively influence the outcome in patients with compartment syndrome,12,35,48 with one study reporting that only 13% of patients achieve a full recovery.35 Furthermore, there is noted difficulty in determining the presence of limb paralysis in a trauma patient who may have limited motor function due to pain.77



Given the necessity for a timely diagnosis, the variable aetiology and presentation of ACS, as well as the poor performing diagnostic performance characteristics of the clinical signs at presentation, continuous intracompartmental pressure (ICP) monitoring in all at risk patients is recommended.6,13,15,23,28,31,74,78-81 Pressure monitoring has been proven to detect ACS prior to the onset of clinical signs in addition to reducing the time to fasciotomy and the development of subsequent sequelae,13,82 whilst not increasing the rate of fasciotomy or associated complications.69,83-85

McQueen, Christie and Court-Brown13 reviewed 25 patients (13 monitored, 12 not monitored) with tibial diaphyseal fractures that had been complicated by an ACS. They found a significant increase in the time from injury to fasciotomy (16 hour difference, p < 0.05), no complications in the monitored group compared with 83% in the non-monitored (p < 0.01), and a significant delay in tibial union in the non-monitored group (p < 0.05).13

Al-Dadah et al85 compared 109 patients with a tibial diaphyseal fracture who underwent continuous ICP monitoring (fasciotomy rate 15.6%, time to fasciotomy 22 hours) with a historical control group of 109 patients who were assessed using clinical signs alone (fasciotomy rate 14.7%, time to fasciotomy 23 hours). Although they found no significant increase in the fasciotomy rate, they did not demonstrate a significant difference in terms of clinical outcome or time to fasciotomy.85

Harris, Kadir and Donald86 performed a randomised trial of 200 consecutive tibial fractures comparing monitored and non-monitored patients. The primary outcome measure was the presence of late sequelae by six months after injury. According to the protocol, monitored patients underwent continuous ICP monitoring for 36 hours (no cases of ACS) and the non-monitored group received standard clinical assessment (five cases of ACS). They documented no difference between groups regarding the complication rates recording 27 soft-tissue complications and 29 nonunions in the 177 patients available for review.86 A criticism of this study is that like was compared with like as the indication for fasciotomy in alert patients in both groups was clinical symptoms and signs.86 Furthermore, issues regarding timing were ignored. For the ICP monitoring to be compared accurately with clinical symptoms and signs it must be the primary indication for fasciotomy.


Methods of ICP monitoring (Table III)

Techniques for ICP monitoring include indirect measures using the needle manometer with or without the infusion of saline into the compartment,11,87,88 the wick catheter,75,89 the slit catheter90-92 or the solid state transducer intracompartmental catheter (STIC) with or without the transducer at the tip.78,93,94 The slit catheter is currently recommended and used by many authors, including within our unit.13,69,90

Boody and Wongworawat95 compared three ICP monitoring devices (Stryker ICP pressure monitor, Whitesides apparatus, arterial line manometer) using an in vitro model. They concluded that side-port needles and slit catheters were more accurate than straight needles, with the arterial line manometer and the Stryker monitor the most accurate devices.95 Collinge and Kuper96 performed a clinical study in 26 patients with suspected ACS (31 limbs, 97 compartments) to compare three ICP monitoring devices (STIC, electronic transducer-tipped catheter, modified Whitesides needle). They concluded all techniques were comparable but not completely reliable for ICP monitoring in trauma patients.96

Innovative techniques include near infrared spectroscopy, which is a direct non-invasive measure of tissue oxygenation and has demonstrated good correlation with ICP measurements in both experimental and human studies,97-100 though further work is required.



Technique and placement 

Whichever method of ICP monitoring is employed, appropriate placement is within or on the affected compartment using an aseptic technique.101 In the presence of an associated fracture, the device should be placed within 5 cm of the level of the fracture to give accurate readings.6,80,102,103

In the leg, the anterior compartment is routinely used as it is the most frequently affected and accessible.69,85 However, despite being potentially difficult to manage and uncomfortable for the patient, some authors do recommend monitoring the deep posterior compartment as well given the associated risk of missing an isolated deep ACS.18,102 We would routinely recommend this if there is a clinical reason to suspect its presence. For other suspected compartment syndromes of the lower limb, the anterior compartment of the thigh is recommended as it has been found to be most frequently affected.24,47-50 Isolated posterior thigh compartment syndromes have been reported and should always be excluded.104 In the case of a suspected foot ACS, the interosseous compartments are suggested, with consideration of the calcaneal compartment in hindfoot injuries.51,54,55

The forearm is the most commonly affected site in the upper limb and measurement of the flexor compartment is routine.16,22,37,39,43,105,106 Again, in the suspected case of a rare isolated dorsal ACS, that compartment should be measured.16 The anterior compartment of the arm and the interosseous compartment of the hand are the recommended placements for ICP monitoring for the remainder of the upper limb.6,41,43,44


Threshold and timing for decompression

Evidence has demonstrated that the normal ICP of healthy muscle is 10 mmHg.107 Much of the literature attempting to determine the threshold pressure for decompression has focused on whether to use ICP alone or whether to consider the ICP in relation to perfusion pressure. Despite initial studies suggesting an absolute ICP of 30-50 mmHg to be the threshold,12,44,68,75,83,87,108 it is now recognised that a patient’s tolerance to the ICP is dependent on perfusion, or the systemic blood pressure.69,103,109-111 Whitesides et al109 was the first to suggest this using an animal model, with ranges from 10 mmHg to 35 mmHg considered diagnostic.103,111,112 However, there is now experimental and clinical work suggesting a pressure difference or delta pressure (∆P = diastolic pressure – intra-compartmental pressure) of less than or equal to 30 mmHg should be considered diagnostic.13,69,82,101 McQueen and Court-Brown69 studied 116 patients with tibial diaphyseal fractures who underwent continuous pressure monitoring of the anterior compartment for 24 hours. The use of a ∆P of ≤ 30 mmHg as a threshold for fasciotomy led to no missed cases of ACS, no unnecessary fasciotomies and no complications in any patients.69 White et al101 validated the clinical use of a ∆P of ≤ 30 mmHg in a study of 101 patients followed for over a one year period. They found no significant difference in muscle power or return to function in 41 patients with an absolute pressure of over 30 mmHg and a ∆P over 30 mm Hg for more than six hours continuously, with the 60 patients who had absolute pressures of less than 30 mmHg.101

It should be noted that much of the above work does not include children and was carried out solely in association with ACS of the leg. Other regions of the body may have different pressure thresholds but in the absence of evidence to the contrary it seems reasonable to retain the threshold of a ∆P of 30 mmHg. Furthermore, in children, the mean arterial pressure rather than the diastolic pressure has been suggested a more appropriate measure to calculate the ∆P as the diastolic pressure is often lower in this group of patients.113

Confusion in the literature regarding time to fasciotomy relates to the definition of the start point. Time to fasciotomy has been found to correlate with outcome,10,13,18-20 with six to 12 hours quoted as critical in both clinical and experimental studies.83,108,114,115 The variation is likely to be due to varying pressure levels. It is probable that a lower pressure can be tolerated for a longer period of time and vice versa.108,115 We would suggest that time to fasciotomy would be most accurately determined as time from admission as this is closest to the time of injury.6,23,69 Time from diagnosis is not relevant as once the diagnosis has been made, urgent fasciotomy should be performed without delay.      

When using ICP monitoring, the trend and duration of pressure measurements are important to consider when determining the appropriate point to perform fasciotomy.6,62 By employing a protocol of fasciotomy to be carried out based on the trend of readings over a two hour period, authors have found a reduction in the time to fasciotomy and complications whilst not increasing the rate of fasciotomy.69 One study has suggested overtreatment can occur with continuous ICP monitoring,116 although this study does not consider the trend over time. A diagnosis of ACS should not be made on the basis of a single reading. Another consideration is the effect of anaesthesia on blood pressure. Kakar et al117 performed a prospective cohort study of 242 tibial fractures treated with intramedullary nail fixation under GA. When calculating the ∆P using ICP monitoring, they found the pre-operative diastolic pressure correlated well with the post-operative pressure, with a significant difference seen in the intra-operative pressure (mean difference 18 mmHg, p < 0.05).117 They concluded that fasciotomy should not be performed on an isolated ∆P measurement intra-operatively and that serial measurements are recommended.



The literature would benefit from further long-term outcome studies examining the usefulness and effect of ICP monitoring, as well as data on the diagnostic performance characteristics of ICP monitoring. Further work is needed to determine the critical ∆P for other regions of the body and in children, as well as more data on the innovative techniques of ICP monitoring.

Large prognostic prospective studies would help identify and clarify high-risk patients. Optimally, adequately powered prospective randomised controlled trials of continuous ICP monitoring versus clinical signs would provide level 1 evidence. However, several issues arise with this. Firstly, for ICP monitoring to be effective it needs to be the primary indicator for fasciotomy including consideration of time factors. Secondly, during the conduct of any such trial there is a high risk of changing behaviour by encouraging more stringent and frequent examination of the patient than is normal practice, thus biasing the results. Thirdly, there is no gold standard reference for diagnosing ACS and the incidence in the literature is quoted as well below 30%.15,17,63 In this situation, statistical methodology including latent class analysis and Bayes theorem should be used when determining the diagnostic performance characteristics of the clinical tests used.



In conclusion, acute compartment syndrome can occur following either a fracture or soft tissue injury, with males and youth being most at risk. Because of the poor diagnostic performance characteristics of the clinical diagnosis, we would recommend continuous compartment pressure monitoring as the prime diagnostic tool in the following situations:

·  All patients with tibial diaphyseal fractures

·  All patients with high-energy tibial pilon and plateau fractures

·  All young patients with high-energy forearm or femoral injuries, with or without an associated fracture

·  All patients with soft tissue swelling suggestive of compartment syndrome, irrespective of age, gender or causality

·  All patients at risk who are unable to co-operate with clinical assessment (e.g. patients with polytrauma, ventilated patients, children)


Until further evidence is available, we would recommend the slit catheter technique for continuous ICP monitoring, with a ∆P of ≤ 30 mmHg diagnostic of ACS using a trend of readings over a two hour period.



1. Ashton H. Critical closing pressure in human peripheral vascular beds. Clin Sci 1962;22:79-87.

2. Ashton H. The effect of increased tissue pressure on blood flow. Clin Orthop 1975:15-26.

3. Matsen FA 3rd, Krugmire RB Jr. Compartmental syndromes. Surg Gynecol Obstet 1978;147:943-9.

4. Matsen FA 3rd, King RV, Krugmire RB Jr, Mowery CA, Roche T. Physiological effects of increased tissue pressure. Int Orthop 1979;3:237-44.

5. Hartsock LA, O'Farrell D, Seaber AV, Urbaniak JR. Effect of increased compartment pressure on the microcirculation of skeletal muscle. Microsurgery 1998;18:67-71.

6. McQueen MM. Acute compartment syndrome. In: Bucholz RW, Court-Brown CM, Heckman JD, Tornetta P 3rd, eds. Rockwood and Green's Fractures in Adults. Seventh ed. Philadelphia: Lippincott Williams & Wilkins, 2010:689-708.

7. Gelberman RH, Zakaib GS, Mubarak SJ, Hargens AR, Akeson WH. Decompression of forearm compartment syndromes. Clin Orthop 1978;134:225-9.

8. Holden CE. The pathology and prevention of Volkmann's ischaemic contracture. J Bone Joint Surg [Br] 1979;61-B:296-300.

9. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma 1996;40:342-4.

10. Sheridan GW, Matsen FA 3rd. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg [Am] 1976;58-A:112-15.

11. Matsen FA 3rd, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartmental syndromes. J Bone Joint Surg [Am] 1980;62-A:286-91.

12. Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg [Br] 1984;66-B:93-7.

13. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg [Br] 1996;78-B:95-8.

14. Williams PR, Russell ID, Mintowt-Czyz WJ. Compartment pressure monitoring: current UK orthopaedic practice. Injury 1998;29:229-32.

15. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome: who is at risk? J Bone Joint Surg [Br] 2000;82-B:200-3.

16. Kalyani BS, Fisher BE, Roberts CS, Giannoudis PV. Compartment syndrome of the forearm: a systematic review. J Hand Surg Am 2011;36:535-43.

17. O'Toole RV, Whitney A, Merchant N, et al. Variation in diagnosis of compartment syndrome by surgeons treating tibial shaft fractures. J Trauma 2009;67:735-41.

18. Matsen FA 3rd, Clawson DK. The deep posterior compartmental syndrome of the leg. J Bone Joint Surg [Am] 1975;57-A:34-9.

19. Mullett H, Al-Abed K, Prasad CV, O'Sullivan M. Outcome of compartment syndrome following intramedullary nailing of tibial diaphyseal fractures. Injury 2001;32:411-13.

20. Rorabeck CH, Macnab L. Anterior tibial-compartment syndrome complicating fractures of the shaft of the tibia. J Bone Joint Surg [Am] 1976;58-A:549-50.

21. Schmidt AH. The impact of compartment syndrome on hospital length of stay and charges among adult patients admitted with a fracture of the tibia. J Orthop Trauma 2011;25:355-7.

22. Eaton RG, Green WT. Volkmann's ischemia: a volar compartment syndrome of the forearm. Clin Orthop 1975;113:58-64.

23. Hope MJ, McQueen MM. Acute compartment syndrome in the absence of fracture. J Orthop Trauma 2004;18:220-4.

24. Mithofer K, Lhowe DW, Vrahas MS, Altman DT, Altman GT. Clinical spectrum of acute compartment syndrome of the thigh and its relation to associated injuries. Clin Orthop 2004;425:223-9.

25. Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg [Am] 2004;86-A:864-8.

26. Mubarak SJ, Wilton NC. Compartment syndromes and epidural analgesia. J Pediatr Orthop 1997;17:282-4.

27. Harrington P, Bunola J, Jennings AJ, Bush DJ, Smith RM. Acute compartment syndrome masked by intravenous morphine from a patient-controlled analgesia pump. Injury 2000;31:387-9.

28. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder? J Orthop Trauma 2002;16:572-7.

29. Richards H, Langston A, Kulkarni R, Downes EM. Does patient controlled analgesia delay the diagnosis of compartment syndrome following intramedullary nailing of the tibia? Injury 2004;35:296-8.

30. Davis ET, Harris A, Keene D, Porter K, Manji M. The use of regional anaesthesia in patients at risk of acute compartment syndrome. Injury 2006;37:128-33.

31. Mar GJ, Barrington MJ, McGuirk BR. Acute compartment syndrome of the lower limb and the effect of postoperative analgesia on diagnosis. Br J Anaesth 2009;102:3-11.

32. Roberts CS, Gorczyca JT, Ring D, Pugh KJ. Diagnosis and treatment of less common compartment syndromes of the upper and lower extremities: current evidence and best practices. Instr Course Lect 2011;60:43-50.

33. Simpson NS, Jupiter JB. Delayed onset of forearm compartment syndrome: a complication of distal radius fracture in young adults. J Orthop Trauma 1995;9:411-18.

34. Morin RJ, Swan KG, Tan V. Acute forearm compartment syndrome secondary to local arterial injury after penetrating trauma. J Trauma 2009;66:989-93.

35. Bradley EL 3rd. The anterior tibial compartment syndrome. Surg Gynecol Obstet 1973;136:289-97.

36. Halpern AA, Nagel DA. Anterior compartment pressures in patients with tibial fractures. J Trauma 1980;20:786-90.

37. Gelberman RH, Garfin SR, Hergenroeder PT, Mubarak SJ, Menon J. Compartment syndromes of the forearm: diagnosis and treatment. Clin Orthop 1981:252-61.

38. Peters CL, Scott SM. Compartment syndrome in the forearm following fractures of the radial head or neck in children. J Bone Joint Surg [Am] 1995;77-A:1070-4.

39. Botte MJ, Gelberman RH. Acute compartment syndrome of the forearm. Hand Clin 1998;14:391-403.

40. Vitale GC, Richardson JD, George SM Jr, Miller FB. Fasciotomy for severe, blunt and penetrating trauma of the extremity. Surg Gynecol Obstet 1988;166:397-401.

41. Diminick M, Shapiro G, Cornell C. Acute compartment syndrome of the triceps and deltoid. J Orthop Trauma 1999;13:225-7.

42. Prasarn ML, Ouellette EA, Livingstone A, Giuffrida AY. Acute pediatric upper extremity compartment syndrome in the absence of fracture. J Pediatr Orthop 2009;29:263-8.

43. Prasarn ML, Ouellette EA. Acute compartment syndrome of the upper extremity. J Am Acad Orthop Surg 2011;19:49-58.

44. Halpern AA, Greene R, Nichols T, Burton DS. Compartment syndrome of the interosseous muscles: early recognition and treatment. Clin Orthop 1979;140:23-5.

45. Schnall SB, Holtom PD, Silva E. Compartment syndrome associated with infection of the upper extremity. Clin Orthop 1994;306:128-31.

46. Brumback RJ. Traumatic rupture of the superior gluteal artery, without fracture of the pelvis, causing compartment syndrome of the buttock: a case report. J Bone Joint Surg [Am] 1990;72-A:134-7.

47. Tarlow SD, Achterman CA, Hayhurst J, Ovadia DN. Acute compartment syndrome in the thigh complicating fracture of the femur: a report of three cases. J Bone Joint Surg [Am] 1986;68-A:1439-43.

48. Schwartz JT Jr, Brumback RJ, Lakatos R, et al. Acute compartment syndrome of the thigh: a spectrum of injury. J Bone Joint Surg [Am] 1989;71-A:392-400.

49. Mithöfer K, Lhowe DW, Altman GT. Delayed presentation of acute compartment syndrome after contusion of the thigh. J Orthop Trauma 2002;16:436-8.

50. Mithoefer K, Lhowe DW, Vrahas MS, et al. Functional outcome after acute compartment syndrome of the thigh. J Bone Joint Surg [Am] 2006;88-A:729-37.

51. Myerson M. Diagnosis and treatment of compartment syndrome of the foot. Orthopedics 1990;13:711-17.

52. Manoli A 2nd, Weber TG. Fasciotomy of the foot: an anatomical study with special reference to release of the calcaneal compartment. Foot Ankle 1990;10:267-75.

53. Kym MR, Worsing RA Jr. Compartment syndrome in the foot after an inversion injury to the ankle: a case report. J Bone Joint Surg [Am] 1990;72-A:138-9.

54. Myerson M, Manoli A. Compartment syndromes of the foot after calcaneal fractures. Clin Orthop 1993;290:142-50.

55. Frink M, Hildebrand F, Krettek C, Brand J, Hankemeier S. Compartment syndrome of the lower leg and foot. Clin Orthop 2010;468:940-50.

56. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdominal compartment syndrome. J Trauma 1998;45:597-609.

57. Tischenko GJ, Goodman SB. Compartment syndrome after intramedullary nailing of the tibia. J Bone Joint Surg [Am] 1990;72-A:41-4.

58. Moed BR, Strom DE. Compartment syndrome after closed intramedullary nailing of the tibia: a canine model and report of two cases. J Orthop Trauma 1991;5:71-7.

59. Koval KJ, Clapper MF, Brumback RJ, et al. Complications of reamed intramedullary nailing of the tibia. J Orthop Trauma 1991;5:184-9.

60. Williams J, Gibbons M, Trundle H, Murray D, Worlock P. Complications of nailing in closed tibial fractures. J Orthop Trauma 1995;9:476-81.

61. Tornetta P 3rd, French BG. Compartment pressures during nonreamed tibial nailing without traction. J Orthop Trauma 1997;11:24-7.

62. McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary nailing of the tibia. J Bone Joint Surg [Br] 1990;72-B:395-7.

63. Park S, Ahn J, Gee AO, Kuntz AF, Esterhai JL. Compartment syndrome in tibial fractures. J Orthop Trauma 2009;23:514-18.

64. Mubarak S, Owen CA. Compartmental syndrome and its relation to the crush syndrome: a spectrum of disease: a review of 11 cases of prolonged limb compression. Clin Orthop 1975;113:81-9.

65. Reis ND, Michaelson M. Crush injury to the lower limbs: treatment of the local injury. J Bone Joint Surg [Am] 1986;68-A:414-18.

66. Geary N. Late surgical decompression for compartment syndrome of the forearm. J Bone Joint Surg [Br] 1984;66-B:745-8.

67. DeLee JC, Stiehl JB. Open tibia fracture with compartment syndrome. Clin Orthop 1981;160:175-84.

68. Blick SS, Brumback RJ, Poka A, Burgess AR, Ebraheim NA. Compartment syndrome in open tibial fractures. J Bone Joint Surg [Am] 1986;68-A:1348-53.

69. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg [Br] 1996;78-B:99-104.

70. Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996;4:209-18.

71. Bae DS, Kadiyala RK, Waters PM. Acute compartment syndrome in children: contemporary diagnosis, treatment, and outcome. J Pediatr Orthop 2001;21:680-8.

72. Wright JG, Bogoch ER, Hastings DE. The 'occult' compartment syndrome. J Trauma 1989;29:133-4.

73. Kosir R, Moore FA, Selby JH, et al. Acute lower extremity compartment syndrome (ALECS) screening protocol in critically ill trauma patients. J Trauma 2007;63:268-75.

74. Badhe S, Baiju D, Elliot R, Rowles J, Calthorpe D. The 'silent' compartment syndrome. Injury 2009;40:220-2.

75. 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-A:1091-5.

76. Robinson CM, O'Donnell J, Will E, Keating JF. Dropped hallux after the intramedullary nailing of tibial fractures. J Bone Joint Surg [Br] 1999;81-B:481-4.

77. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg [Br] 2003;85-B:625-32.

78. McDermott AG, Marble AE, Yabsley RH, Phillips MB. Monitoring dynamic anterior compartment pressures during exercise: a new technique using the STIC catheter. Am J Sports Med 1982;10:83-9.

79. Heppenstall B, Tan V. Well-leg compartment syndrome. Lancet 1999;354:970.

80. Saikia KC, Bhattacharya TD, Agarwala V. Anterior compartment pressure measurement in closed fractures of leg. Indian J Orthop 2008;42:217-21.

81. McQueen MM, Court-Brown CM. Early diagnosis of compartment syndrome: continuous pressure measurement or not? Injury 2010;41:431-2.

82. Ozkayin N, Aktuglu K. Absolute compartment pressure versus differential pressure for the diagnosis of compartment syndrome in tibial fractures. Int Orthop 2005;29:396-401.

83. Allen MJ, Stirling AJ, Crawshaw CV, Barnes MR. Intracompartmental pressure monitoring of leg injuries: an aid to management. J Bone Joint Surg [Br] 1985;67-B:53-7.

84. Ovre S, Hvaal K, Holm I, Stromsoe K, Nordsletten L, Skjeldal S. Compartment pressure in nailed tibial fractures: a threshold of 30 mmHg for decompression gives 29% fasciotomies. Arch Orthop Trauma Surg 1998;118:29-31.

85. Al-Dadah OQ, Darrah C, Cooper A, Donell ST, Patel AD. Continuous compartment pressure monitoring vs. clinical monitoring in tibial diaphyseal fractures. Injury 2008;39:1204-9.

86. Harris IA, Kadir A, Donald G. Continuous compartment pressure monitoring for tibia fractures: does it influence outcome? J Trauma 2006;60:1330-5.

87. Matsen FA 3rd, Mayo KA, Sheridan GW, Krugmire RB Jr. Monitoring of intramuscular pressure. Surgery 1976;79:702-9.

88. Whitesides TE Jr, Haney TC, Harada H, Holmes HE, Morimoto K. A simple method for tissue pressure determination. Arch Surg 1975;110:1311-13.

89. Mubarak SJ, Hargens AR, Owen CA, Garetto LP, Akeson WH. The wick catheter technique for measurement of intramuscular pressure: a new research and clinical tool. J Bone Joint Surg [Am] 1976;58-A:1016-20.

90. Rorabeck CH, Castle GS, Hardie R, Logan J. Compartmental pressure measurements: an experimental investigation using the slit catheter. J Trauma 1981;21:446-9.

91. Moed BR, Thorderson PK. Measurement of intracompartmental pressure: a comparison of the slit catheter, side-ported needle, and simple needle. J Bone Joint Surg [Am] 1993;75-A:231-5.

92. Shakespeare DT, Henderson NJ, Clough G. The slit catheter: a comparison with the wick catheter in the measurement of compartment pressure. Injury 1982;13:404-8.

93. McDermott AG, Marble AE, Yabsley RH. Monitoring acute compartment pressures with the S.T.I.C. catheter. Clin Orthop 1984;190:192-8.

94. Willy C, Gerngross H, Sterk J. Measurement of intracompartmental pressure with use of a new electronic transducer-tipped catheter system. J Bone Joint Surg [Am] 1999;81-A:158-68.

95. Boody AR, Wongworawat MD. Accuracy in the measurement of compartment pressures: a comparison of three commonly used devices. J Bone Joint Surg [Am] 2005;87-A:2415-22.

96. Collinge C, Kuper M. Comparison of three methods for measuring intracompartmental pressure in injured limbs of trauma patients. J Orthop Trauma 2010;24:364-8.

97. Arbabi S, Brundage SI, Gentilello LM. Near-infrared spectroscopy: a potential method for continuous, transcutaneous monitoring for compartmental syndrome in critically injured patients. J Trauma 1999;47:829-33.

98. Gentilello LM, Sanzone A, Wang L, Liu PY, Robinson L. Near-infrared spectroscopy versus compartment pressure for the diagnosis of lower extremity compartmental syndrome using electromyography-determined measurements of neuromuscular function. J Trauma 2001;51:1-8.

99. 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-A:863-70.

100. Shuler MS, Reisman WM, Cole AL, Whitesides TE Jr, Moore TJ. Near-infrared spectroscopy in acute compartment syndrome: case report. Injury 2011;42:1506-8.

101. White TO, Howell GE, Will EM, Court-Brown CM, McQueen MM. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma 2003;55:1133-8.

102. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures: the relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg [Am] 1994;76-A:1285-92.

103. Matava MJ, Whitesides TE Jr, Seiler JG 3rd, Hewan-Lowe K, Hutton WC. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma 1994;37:50-8.

104. Mallo GC, Stanat SJ, Al-Humadi M, Divaris N. Posterior thigh compartment syndrome as a result of a basketball injury. Orthopedics 2009;32:923.

105. Stockley I, Harvey IA, Getty CJ. Acute volar compartment syndrome of the forearm secondary to fractures of the distal radius. Injury 1988;19:101-4.

106. Hwang RW, de Witte PB, Ring D. Compartment syndrome associated with distal radial fracture and ipsilateral elbow injury. J Bone Joint Surg [Am] 2009;91-A:642-5.

107. Giannoudis PV, Tzioupis C, Pape HC. Early diagnosis of tibial compartment syndrome: continuous pressure measurement or not? Injury 2009;40:341-2.

108. Hargens AR, Akeson WH, Mubarak SJ, et al. Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg [Am] 1978;60-A:499-505.

109. Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:43-51.

110. 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 1988;226:138-55.

111. Heckman MM, Whitesides TE Jr, Grewe SR, et al. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma 1993;7:199-210.

112. Brooker AF Jr, Pezeshki C. Tissue pressure to evaluate compartmental syndrome. J Trauma 1979;19:689-91.

113. Mars M, Hadley GP. Raised compartmental pressure in children: a basis for management. Injury 1998;29:183-5.

114. Hargens AR, Romine JS, Sipe JC, et al. Peripheral nerve-conduction block by high muscle-compartment pressure. J Bone Joint Surg [Am] 1979;61-A:192-200.

115. Heppenstall RB, Sapega AA, Izant T, et al. Compartment syndrome: a quantitative study of high-energy phosphorus compounds using 31P-magnetic resonance spectroscopy. J Trauma 1989;29:1113-19.

116. Janzing HM, Broos PL. Routine monitoring of compartment pressure in patients with tibial fractures: beware of overtreatment! Injury 2001;32:415-21.

117. Kakar S, Firoozabadi R, McKean J, Tornetta P 3rd. Diastolic blood pressure in patients with tibia fractures under anaesthesia: implications for the diagnosis of compartment syndrome. J Orthop Trauma 2007;21:99-103.

118. Styf JR, Crenshaw A, Hargens AR. Intramuscular pressures during exercise. comparison of measurements with and without infusion. Acta Orthop Scand 1989;60:593-6.

119. Breit GA, Gross JH, Watenpaugh DE, Chance B, Hargens AR. Near-infrared spectroscopy for monitoring of tissue oxygenation of exercising skeletal muscle in a chronic compartment syndrome model. J Bone Joint Surg [Am] 1997;79-A:838-43.

120. Mohler LR, Styf JR, Pedowitz RA, Hargens AR, Gershuni DH. Intramuscular deoxygenation during exercise in patients who have chronic anterior compartment syndrome of the leg. J Bone Joint Surg [Am] 1997;79-A:844-9.