You are on page 1of 9

ARTICLE IN PRESS

Current Orthopaedics (2004) 18, 468476

www.elsevier.com/locate/cuor

EMERGENCY CARE

Acute compartment syndrome


S. Singha,, S.P. Trikhab, J. Lewisc
a

7 Ardmay Gardens, Surbiton, Surrey, KT6 4SW, UK Flat 3, 9 Grange Road, Kingston-upon-Thames, Surrey, KT1 2QU, UK c Worthing and Southlands NHS Trust, West Sussex, UK
b

KEYWORDS
Compartment syndrome; Volkmanns ischaemic contracture; Fasciotomy; Compartment pressure monitoring

Summary Compartment syndrome can occur in any myofascial muscle compartment. If left untreated it can lead to ischaemic contractures and severe disabilities. A high index of suspicion is required in at risk cases. Compartment pressure monitoring is a useful adjunct in the diagnosis of raised compartment pressure especially when clinical assessment is difcult. The key to a successful outcome is early diagnosis and decompression of affected compartments. & 2005 Elsevier Ltd. All rights reserved.

Introduction
Compartment syndrome has been dened as a condition in which the circulation and function of tissues within a closed space are compromised by an increased pressure within that space.1 The muscles and nerves of the extremity are enclosed in fascial spaces or compartments and are therefore susceptible to this condition. It is a surgical emergency which if not recognised and treated early can lead to ischaemic contractures, neurological decit, amputation, renal failure and even death. Richard von Volkmann was the rst to report this complication.2 He reported post-traumatic

muscle contracture of acute onset with increasing deformity despite splinting and passive exercises. Compartment syndrome is most commonly seen following trauma, but may occur after ischaemic reperfusion injuries,3 burns4 and positioning during surgery 5 Fractures of the tibial shaft and the forearm account for 58% of compartment syndromes.6 A high index of suspicion is required and early decompression of all at risk compartments is the treatment of choice.79

Pathophysiology
The common pathogenic factor in compartment syndrome is increased pressure within a fascial compartment. Three theories have been proposed to explain the development of tissue ischaemia: (1) The increased compartmental pressure may lead to arterial spasm.10

Corresponding author. Tel.:+44 07968 013803;

fax: +44 208 390 7029. E-mail addresses: sameer.singh@virgin.net (S. Singh), ptrikha@doctors.org.uk (S.P. Trikha), mrlewis@totalise.co.uk (J. Lewis).

0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2004.12.006

ARTICLE IN PRESS
Acute compartment syndrome (2) The critical closing pressure theory states that because of the small luminal radius and the high mural tension of arterioles there must be a signicant transmural pressure difference (arteriolar pressure minus tissue pressure) to maintain patency. If tissue pressure rises or arteriolar pressure drops so that this critical pressure difference does not exist then the arterioles will close.11 (3) If tissue pressure rises then the veins will collapse due to their thin walls. If blood continues to ow from the capillaries the venous pressure will rise until it exceeds tissue pressure and patency of the veins is reestablished. This leads to an increase in venous pressure and therefore reduces the arteriovenous gradient and as a result reduces tissue blood ow.12 The response of skeletal muscle to ischaemia or trauma is similar regardless of the mechanism of injury.13 When muscles become anoxic histaminelike substances are released and these dilate the capillary bed and increase endothelial permeability. Transudation of plasma occurs into the intramuscular compartment and this increases the pressure within the muscular compartment. To compensate the lymphatic drainage increases, however when this reaches a maximum the intracompartmental pressure (ICP) causes collapse of lymphatic vessels.14 Due to the high pressure in the arterial system there is continuing blood ow into the compartment and this increases the swelling and oedema. It is only in the late stages of compartment syndrome that arterial ow into the compartment is compromised. The amount of pressure required to produce a compartmental syndrome depends on many factors, including the duration of pressure elevation, metabolic rate of tissues, vascular tone and the mean arterial pressure. The data on effects of ischaemia to tissues are derived from research in which sudden, total ischaemia was imposed. Neural tissues demonstrate functional abnormalities (parasthesia and hyperesthesia) within 30 min of the onset of ischaemia, and irreversible functional loss after 12 h.12,1517 Muscle shows functional changes after 24 h and irreversible changes beginning at 412 h.1618 Ischaemia of 4 h gives rise to signicant myoglobinuria, reaching a maximum at about 3 h although it can persist up to 12 h.1922 Compartment syndromes lasting longer than 12 h produce chronic functional decits, such as contractures, motor weakness and sensory disturbance.23,24 Any cause of increased compartmental pressure can result in a compart469
Table 1 Aetiology of compartment syndrome as described by Matsen. Decreased compartment size Closure of fascial defects Tight dressings Localised external pressure Increased compartment content Bleeding Vascular injury Bleeding disorder Increased capillary permeability Post Ischaemic swelling Exercise Seizure and eclampsia Trauma Burns Orthopaedic surgery Increased capillary pressure Exercise Venous obstruction Muscle hypertrophy Inltrated infusion Nephrotic syndrome

ment syndrome. See Table 1 for a list of aetiologies as described by Matsen1.

Diagnosis
Clinical
The key to successful treatment of acute compartment syndrome is early diagnosis and decompression of the affected compartments.1,7,9,23,24 The classical signs of impending compartment syndrome are pain, pallor, parasthesia, paralysis and pulselessness (The 5 ps). However by the time all these symptoms have developed (especially pulselessness) the limb will be non-viable. A high index of suspicion is required to make the diagnosis. Clinical diagnosis is made on a combination of physical signs and symptoms. These include pain out of proportion to the stimulus, pain on passive stretch of the affected muscle compartment, altered sensation, muscle weakness and tenderness over the muscle compartment. The symptoms and signs which are the most reliable in making the diagnosis are increasing pain, and pain on passive stretching of the muscle within the affected compartment.2528 However these symptoms are subjective and impossible to elicit in the unconscious, non-cooperative patient and those

ARTICLE IN PRESS
470 who have had regional blocks. There has been concern raised with the use of patient controlled analgesia and regional anaesthesia in high risk cases.28,29 S. Singh et al. blood leading to inaccurate readings. Due to these potential draw backs a solid-state transducer (STIC) intracompartment catheter has been developed.32 This has a multiperforated polyethylene tip with a STIC which can remain patent for up 16 h. The STIC catheter has been shown to be functionally superior to conventional systems (needle, wick and slit) and easier to assemble, calibrate, maintain and interpret. The wick, slit and STIC methods require specialised equipment which may not be readily available, while the needle system as proposed by Whitesides30 can be constructed from equipment which is readily available in most hospitals. If on clinical examination an obvious compartment syndrome is present pressure measurement may not be necessary. However it can be useful adjunct in the diagnosis of compartment syndrome especially in children, unconscious patients and those with equivocal clinical ndings.

Intracompartmental pressures
Pain can be unreliable especially in the trauma patient. It can range from being mild to severe, and in the unconscious patient important clinical symptoms and signs can be difcult to elicit. Techniques have been developed to measure ICPs. Technique for monitoring intracompartmental pressures Whitesides 30 introduced a method for measuring ICP that required simple equipment available in most hospitals (Fig. 1). Using a needle, plastic tubing lled with saline and air attached to a mercury manometer they established tissue pressure measurement criteria as determinants of the need for fasciotomy. However this technique involved the injection of saline into the compartment and this may aggravate an impending compartment syndrome. The slit and wick techniques require a polyethylene tubing connected to a pressure transducer. The tubing is lled with water and it is important that there are no air bubbles present within the tubing. The wick and slit catheter allow continuous monitoring of compartments, and have been shown to be more accurate than the needle manometer technique.31 However the end of the tubing in the fascial compartment may become blocked with

At what pressure to decompress?


The normal tissue pressure within closed compartments is about 010 mmHg. This pressure markedly increases in compartment syndrome. There is inadequate perfusion and relative ischaemia when the tissue pressure within a closed compartment rises to within 1030 mmHg of a patients diastolic blood pressure. Whitesides believed that fasciotomy is indicated when the tissue pressure rises to 40 mmHg in a patient with a diastolic pressure of 70 mmHg. Using these criteria no functional decits developed in patients, and all showed conclusive

Figure 1 Apparatus for measuring compartment pressure.

ARTICLE IN PRESS
Acute compartment syndrome evidence of compartment syndrome at the time of operation.30 McQueen 33 recommended a differential pressure (diastolic pressure minus ICP) of 30 mmHg as a threshold for fasciotomy in tibial fractures. ICPs between 30 and 50 mmHg have been suggested that a fasciotomy should be performed.34 The lower level of 30 mmHg is most commonly used as when the tissue pressure rises above this the capillary pressure is insufcient to maintain capillary blood ow. It has also been shown that fascial compliance decreases sharply at an ICP of 33 mmHg as the fascia has reached its maximum stretch.35 It is important to state that tissue viability is dependant on adequate perfusion and blood ow within the microcirculation. Setting an absolute pressure ignores the role that blood pressure plays in maintaining adequate blood ow within a compartment. It has been shown that muscle damage occurring at a specic level relative to the blood pressure is more consistent that relying on a xed compartment pressure.36 The diastolic pressure minus the ICP is called the delta pressure. The critical level has been found to range from 10 to 35 mmHg. The most commonly used delta pressure is 30 mmHg or less.1,10,33 In tibial fractures it has been shown that by using a delta pressure of 30 mmHg unnecessary fasciotomies can be avoided. No clinically signicant complications were identied in patients with a delta pressure greater than 30 mmHg. The ICP or delta pressure at one point in time does not necessarily conrm that a compartment syndrome is present. During intramedullary nailing there are short increases in ICP, however these are not always associated with clinical signs of compartment syndrome.37 The higher the ICP and the longer it is maintained the greater the muscle damage, however an ICP of 30 mmHg maintained for 8 h caused signicant muscle necrosis in canines 35 and biochemical changes have been observed in the experimental situation with a delta pressure of 20 mmHg for 4 h. When the delta pressure approached zero these changes were present in 2 h.38 As stated earlier the sooner the decompression the better the outcome. If decompression is delayed for more than 12 h permanent disability may occur, however if decompression is performed under 6 h of making the diagnosis a full recovery can be expected.24,25,39,40,41 However conrming the exact time of the start of compartment syndrome can be difcult. 471 clinical studies relate to this region of the body. The site at which the compartment pressure is measured should be within a few centimetres of the maximal pressure as it cannot be assumed that the ICP equilibrates throughout the compartment.42 The pressure is always highest 5 cm from the fracture in tibial fractures, and therefore it is recommended that ICP should be measured as close to the site of injury as possible.43 In the lower leg there are four fascial compartments and one or all of these may be involved in compartment syndrome. The highest pressures are recorded in the anterior compartment then the deep posterior compartment.9,42 It would seem logical therefore in tibial fractures to measure the pressure within 5 cm of the fracture and to monitor the pressure in the anterior tibial compartment. However other compartments may need to be monitored depending on the clinical picture. Within the UK practices for monitoring ICP vary. In a postal questionnaire 46% of trauma centres had equipment available for monitoring compartment pressures, and 42% of respondents were unsure at what ICP they would perform fasciotomies. Only 9% used a delta pressure of 30 mmHg as a guide to perform fasciotomies as suggested by Whitesides 30 and McQueen.33 Failing to diagnose and treat a compartment syndrome urgently can be disastrous for patients. Pressure monitoring can be a useful adjunct to help conrm the diagnosis. McQueen et al. 37 suggest monitoring all patients at risk as an aid to clinical diagnosis. Others have suggested that this can lead to over treatment.44 Certainly pressure monitoring should be used in unconscious patients, those who are difcult to assess and when equivocal clinical ndings are present. All centres involved in trauma should have equipment available for monitoring compartment pressures and clinicians involved in trauma need to be aware of interpretation of these results.

Other methods for measuring compartment pressures


Near-Infrared Spectroscopy (NIRS) NIRS is an optical technique that allows tracking of variations in the oxygenation of muscle tissue.45 The technique involves monitoring the absorption of light transmitted through muscle tissue at two distinct wavelengths. A change in the oxygenation state of haemoglobin results in opposite changes in the absorption of light. By calculating the differences in the absorption signal the device provides a continuous index of tissue oxygenation. It can be of

Problems with interpreting pressures


The majority of compartment syndromes occur in the lower limb and hence the majority of the

ARTICLE IN PRESS
472 use in investigating chronic compartment syndrome in adults, as it can detect changes in relative oxygenation, but it is of little value in acute compartment syndrome as changes in the relative oxygenation may have already occurred.46 Laser Doppler owmetry This uses a exible bre optic wire which is introduced into the muscle compartment. The signals from this wire are recorded on a computer. It can be used as an adjunct in the diagnosis of chronic compartment syndrome,47 however it was suggested that further work needs to be carried out into the pathophysiology of chronic compartment syndrome and laser Doppler owmetry needs analysis in larger population groups. S. Singh et al. ICP adequate decompressive fasciotomies should be performed. Several surgical approaches have been tried in the leg. The surgical goal is the prevention of permanent disability, and the adequacy of decompression should not be compromised by cosmesis or the number and lengths of incisions. It is essential to decompress all compartments at risk. In the lower limb bulectomy via a single lateral incision has been suggested, however this only allows limited views and an adequate release may not be achieved. A two incision approach allows safe access to all four compartments of the lower leg and is the treatment of choice. The deep posterior compartment has been neglected in descriptions of fasciotomies however this is the 2nd most commonly involved compartment and access can be gained behind the posteromedial border of the tibia in the distal third of the leg where the belly of exor digitorum longus is exposed. The technique of double incision fasciotomy is described below. It is important to perform a complete decompression and incisions less than 15 cm may result in inadequate decompression.49 In the emergency treatment of compartment syndrome there is no place for short cosmetic incisions. Lower limb fasciotomy (Fig. 2) Anterolateral incision. This incision allows approach to the anterior and lateral compartments of the leg. A 1520 cm incision is placed halfway

Treatment
Raised ICP threatens the viability of the limb and this represents a true management emergency. As stated earlier early diagnosis is the key to a successful outcome. Removal of all dressing down to skin, followed by open extensive fasciotomies with decompression of all muscle compartments in the limb is the treatment of choice. Experimental evidence shows that the circular cast can substantiate the adverse effects of raised ICP.48 Splitting of the cast on one side led to an average fall in ICP 30%, and 65% if split on both sides. Splitting of the padding led to a further fall in ICP by 10%. Complete removal of the cast reduced the pressure by another 15%. In patients whom the diagnosis is being considered and in those in whom resuscitation is proceeding the following steps should be performed:14 (1) Ensure the patient is normotensive, as hypotension reduces perfusion pressure and facilitates tissue injury, (2) Remove any circumferential or constricting bandages as these may increase ICP, (3) Maintain the limb at heart level as elevation reduces the arterio-venous pressure gradient. (4) Give supplemental oxygen to ensure optimal saturation.

Fasciotomies
If the tissue pressure remains elevated despite the above, and the clinical scenario indicates increased

Figure 2 The safe incisions. These are designed to avoid the perforating arteries. The antero-lateral incision is 2 cm lateral to the medial border of the tibia. The postero-medial incision is 1 or 2 cm prosterior to the medial border of the tibia.

ARTICLE IN PRESS
Acute compartment syndrome 473

Figure 3 Anterior and peroneal compartment decompression (acanteriror compartment; Iclateral compartment). The fascia is shown in dark grey.

Figure 4 Decompression of the posterior compartments (ssoleus; ggastrocneumius; tptibialis posterior).

between the bula and the tibial crest. The skin edges are undermined. A short longitudinal incision is made over the muscle bellies allowing palpation of the intramuscular septum between the anterior and lateral compartments. By identifying the septum the supercial peroneal nerve can be identied adjacent to the septum where it crosses the junction of the middle and distal thirds of the leg. The anterior compartment fascia is opened throughout the leg by extending the rst incision in the fascia (Fig. 3). It is important not to damage the supercial peroneal nerve in the distal third of the wound. The peroneal compartment is decompressed by incising the fascia in line with the bular shaft posterior to the intermuscular septum. Proximally the incision is directed to the bular head and distally to the lateral malleolus remaining posterior to the supercial peroneal nerve. Posteromedial incision. This incision is used to decompress the supercial and deep posterior compartments of the leg. It is placed 2 cm posterior to the posterior tibial margin and is about 1520 cm long. Care should be taken to avoid damage to the saphenous nerve and vein and they should be retracted anteriorly. The supercial posterior compartment is decompressed rst, and the fascia is incised throughout its length (Fig. 4). The Achilles tendon helps to identify this compartment. The fasciotomy is extended distally as far as the medial malleolus. The deep posterior compartment is then released by incising the fascia distally and then proximally under the bridge of soleus. It may be necessary to detach the soleus from the back of the tibia.

A technique for forearm fasciotomy is now described. Forearm fasciotomy A single incision can be used to decompress the volar aspect of the forearm (Fig. 5). It is similar to the volar approach to the radius as described by Henry.50 It begins 1 cm proximal and 2 cm lateral to the medial epicondyle. It is carried obliquely across the antecubital fossa and over the volar aspect of the mobile wad of three muscles (brachioradialis, extensor carpi radialis longus and extensor carpi radialis brevis). It is curved medially reaching the midline at the junction of the middle and distal third of the forearm. It is continued straight distally to the proximal skin crease over palmaris longus. The incision is curved across the wrist crease to the mid palm area. The median nerve should be decompressed at the carpal tunnel. In cases of median nerve symptoms the median nerve should also be explored in the proximal forearm. The median nerve can be constricted at the proximal end of pronator teres and at the proximal edge of exor digitorum supercialis. The dorsal muscle compartment can be released by a single incision. This begins 2 cm distal to the lateral epicondyle and carried distally to the wrist. The skin edges are undermined and the dorsal fascia incised directly in line with the skin incision. Foot fasciotomies Excessive bleeding and oedema can produce compartment syndromes in the closed spaces of the foot. Foot compartment syndrome should be suspected in all crushing and high energy foot

ARTICLE IN PRESS
474 S. Singh et al. wound.53 Closure of the wound takes about 10 days. There are some commercially available devices to aid fasciotomy closure.54 The Suture Tension Adjustment Reel (STAR) is placed parallel to the wounds at the time of fasciotomy, and when the swelling has subsided the reels are tightened to gradually close the wound. This method requires 24 days of bedside tightening for wound closure. Split skin grafting can lead to a poor cosmetic result, with insensate skin and donor site morbidity. Delayed primary closure using the skins elasticity provides a more cosmetically acceptable outcome for the patient but requires greater nursing care. However a poor cosmetic result is preferable to the outcome of a missed compartment syndrome.
Figure 5 The incision for decompression of the volar aspect of the forearm. If posterior compartment pressure doesnt concomitantly fall then the posterior compartment requires to be opened by an additional linear posterior incision.

Intramedullary nailing
Over the last 2 decades intramedullary nailing of tibial fractures has increased. Initially there was concern that nailing may increase ICPs and precipitate compartment syndrome and it was thought that nailing should be delayed for up to 7 days to allow the swelling to subside.55 Further research in this area has shown that during reaming the pressure may rise to 180 mmHg,37 however this high ICP fell back to normal after removing the reamer. The application of traction also increases ICPs but these immediately dropped with release of the traction. Despite high pressures being reached during the reduction of tibial fractures and during reaming no patients in the study developed any sequelae of compartment syndrome. Transient increases in compartment pressures seam to be well tolerated and return back to normal after the stimulus is removed. Controversy still exists if monitoring should be performed during intramedullary nailing. McQueen9,33 advocates routine monitoring of all patients with tibial fractures if facilities are available. Others have suggested that this may lead to over treatment44 and unnecessary fasciotomies.

injuries. With crush injuries of the foot Myerson found acute compartment syndrome in 16 of 58 patients.51 Tense swelling of the foot should alert the clinician to this possibility, particularly because pain on passive stretch of the toes and the presence or absence of pedal pulses are less reliable indications of compartment syndrome in the foot. There are a number of different approaches to decompress foot compartments. A dorsal approach along the 2nd and 4th metatarsals is simple to perform and provides effective decompression of all four compartments.52 Associated Lisfranc injuries and metatarsal fractures can also be stabilised via this approach.

Closure of fasciotomy wounds


After decompression of fascial compartments the wounds are left open and sterile dressings are applied. Delayed primary closure can be performed when swelling has subsided, however this may be difcult due to skin retraction and oedema. If the wound edges cannot be approximated without tension, skin grafting may be required. Various methods have been described using the elastic properties of the skin to aid fasciotomy closure. An elastic vessel shoelace can be applied with the staples at the side of the wound. This can be gradually tightened without the need for anaesthesia, providing gradual closure of the fasciotomy

Conclusion
Compartment syndrome can have disastrous consequences if not recognised and treated appropriately. In conscious patients the diagnosis can be made by careful examination of the patient. Invasive monitoring is a useful adjunct especially in unconscious patients and those who are difcult to assess. As the tissue pressure rises the viability of the cells are threatened. The tissue pressure level at which perfusion threatens cell viability varies

ARTICLE IN PRESS
Acute compartment syndrome according to the age and circulatory status of the patient. A delta pressure (Diastolic pressure-Tissue pressure) of 30 mmHg or less is an accepted level that fasciotomy should be performed. 475
23. McQuillan WM, Nolan B. Ischaemia complicating injury. J Bone Joint Surg 1968;50B:482. 24. Matsen FA, Clawson DK. The deep posterior compartmental syndrome of the leg. J Bone Joint Surg 1975;57A:34. 25. Rorabeck CH, Macnab I. Anterior tibial compartment syndrome complicating fratures of the shaft of the tibia. J Bone Joint Surg 1976;58A:54950. 26. Halpern AA, Nagel DA. Anterior compartment pressures in patients with tibial fractures. J Trauma 1980;20:78690. 27. Ellis H. Disabilities after tibial shaft fractures: with special reference to Volkmanns ischaemic contracture. J Bone Joint Surg 1958;40B:1907. 28. Thonse R, Ashford RU, Williams IR, Harrington P. Differences in attitudes to analgesia in post-operative limb surgery put patients at risk of compartment syndrome. Injury 2004;35:2905. 29. Richards H, Langston, Kulkarni R, Downes EM. Does patient controlled analgesia delay the diagnosis of compartment syndrome following intramedullary nailing of the tibia. Injury 2004;35:2968. 30. Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:4351. 31. Rorabeck CH, Castle GSP, Hardie R, Logan J. Compartment pressure measurements: an experimental investigation using the Slit Cathter. J Trauma 1981;21:4469. 32. McDermott AGP, Marble AE, Yabsley RH. Monitoring Acute Compartment Pressures with the STIC Catheter. Clin Orthop 1984;190:1928. 33. McQueen MM, Court-Brown CM. Compartmet monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg 1996;78-B:99104. 34. Elliot KGB, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg 2003;85-B:62532. 35. Hargens AR, Akeson WH, Murbarak SJ, et al. Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg 1978;60-A:499505. 36. Heppenstall RB, Sapega A, Scott R, et al. The compartment syndrome: an experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop 1998;226:13855. 37. McQueen MM, Court-Brown CM. Compartment pressures after intramedullary nailing of the tibia. J Bone Joint Surg 1990;72-B:3957. 38. Heppenstall RB, Sapega A, Izant T, et al. Compartment syndrome: a quantative study of high energy phosphorus compounds using 31P-magnetic resonance spectroscopy. J Trauma 1989;29:11339. 39. Sheridean GW, Matsen III FA. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg 1976; 58-A:1125. 40. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg 1996;78-B:958. 41. Mullet H, Al-Abed K, Prasad CVR, OSullivan M. Outcome of compartment syndrome following intramedullary nailing of tibial diaphyseal fractures. Injury 2001;32:4113. 42. Heckman MM, Whitesides TE, 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 1994;76-A:128592. 43. Matava MJ, Whitesides TE, Seiler JG, Hewan-Lowe K, Hutton WC. Deterioration for the compartment pressure threshold of muscle ischaemia in a canine model. J Trauma 1994;37: 508.

References
1. Matsen FA. Compartment Syndrome. Clin Orthop 1975;113:814. 2. Volkmann R. Die ischaemischem Muskellamungen und Kontrakturen. Zentralbl. Chir 1881;8:801. 3. Perry MO, Thal E R, Shires G T. Management of arterial injuries. Ann Surg 1971;173:4028. 4. Brown RL, Greenhalgh DG, Kagan RJ, Warden GD. The adequacy of limb escharotomies-fasciotomies after referral to a major burns centre. J Trauma 1994;37:91620. 5. Goldsmith AL, MacCallum MID. Compartment syndrome as a complication of the prolonged use of the LloydDavies position. Anaesthesia 1996;51:104852. 6. McQueen MM, Gatson P, Court-Brown CM. Acute compartment syndrome: who is at risk? J Bone Joint Surg 2000; 82-B:2003. 7. Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg 1984;66-B:937. 8. Matsen FA, Winquist RA, Krugmire RB. Diagnosis and management of compartment syndromes. J Bone Joint Surg 1980;62-A:28691. 9. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg 1996;78-B:958. 10. Ashton H. The effect of Increased Tissue pressure on Blood ow. Clin Orthop 1975;113:1526. 11. Burton AC. On the physical equilibrium of small blood vessels. Am J Physiology 1951;164:31929. 12. Parkes AR. Traumatic Ischaemia of peripheral nerves with some observations on Volkmanns Ischaemic Contracture. Br J Surg 1944;32:40313. 13. Sanderson RA, Foley RK, McIvor G, Kirkaldy-Willis WH. Histological Response on Skeletal Muscle to Ischaemia. Clin Orthop 1975;113:2735. 14. Mars M, Hadley GP. Raised intracompartmental pressure and compartment syndromes. Injury 1998;29:40311. 15. Bowden REM, Gutmann E. The fate of voluntary muscle after vascular injury in man. J Bone Joint Surg 1949;31-B:356. 16. Holmes W, Highet WB, Seddon HJ. Ischaemic nerve lesions occurring in Volkmanns Contracture. Br J Surg 1944;32:259. 17. Malan E, Tattoni G. Physiological and anatomopathology of acute ischaemia of the extremities. J Cardiovasc Surg 1963;17:212. 18. Whitesides TE, Hirada H, Morimoto K. The response of skeletal muscle to temporary ischaemia: an experimental study. J Bone Joint Surg 1971;53A:1027. 19. Klock JC, Sexton MJ. Rhabdomyolysis and acute myoglobinuric renal failure following herion use. Calif Med 1973; 119:5. 20. Montagnani CA, Simeone FM. Observations on the liberation of myoglobin and haemoglobin after release of muscle ischaemia. Surgery 1953;34:169. 21. Schreiber SN, Liebowitz MR, Bernstein LH. Limb compression and renal impairment (crush syndrome) following narcotic overdose. J Bone Joint Surg 1972;54A:1683. 22. Spinner M, Mache A, Silver L, Barsky AJ. Impending ischaemic contracture of the hand. Plast Reconstruct Surg 1972;50:341.

ARTICLE IN PRESS
476
44. Janzig HMJ, Broos PLO. Routine monitoring of compartment pressure in patients with tibial fractures: beware of over treatment. Injury 2001;32:41521. 45. Chance B, Nioka S, Kent J, McCully K, Fountain M, Greeneld R, Holtom G. Time resolved spectroscopy of haemoglobin and myoglobin in resting and ischaemic muscle. Anal Biochem 1988;174:698707. 46. Breit GA, Gross JH, Watenpaugh DE, Chance B, Hargens A. Near-Infrared Spectroscopy for monitoring of tissue Oxygenation of Exercising Skeletal Muscle in chronic compartment syndrome model. J Bone Joint Surg 1997; 79-A:83843. 47. Abraham P, Leftheriotis G, Saumet JL. Laser Doppler Flowmetry in the diagnosis of chronic compartment syndrome. J Bone Joint Surg 1998;80-B:3659. 48. Garn S, Mubark S, Evans K, Hargens A, Akeson W. Quantication of Intracompartmental pressure and volume under plaster casts. J Bone Joint Surg 1981;63A:44953.

S. Singh et al.
49. DeLee JC, Stiehl JB. Open tibia fracture with compartment syndrome. Clin Orthop 1987;160:17584. 50. Henry AK. Extensile exposure. Edinburgh and London: Churchill Livingstone; 1973. 51. Myerson MS, McGarvey WC, Henderson MR, Hakim J. Morbidity after crush fractures to the foot. J. Orthop Trauma 1994;8:3439. 52. Murabak SJ. Hargens AR, Compartment syndromes and volkmanns contracture. Philadelphia WB: Saunders; 1981. 53. Harris I. Gradual closure of fasciotomy wounds using a vessel loop shoelace. Injury 1993;24:5656. 54. McKenney MG, Itzhak N, Fee T, Martin L, Lentz K. A simple device for closure of fasciotomy wounds. Am J Surg 1996; 172:2757. 55. Donald G, Seligson D. Treatment of tibial shaft fractures by percutaneous Kuntscher nailing: Technical difculties and a review of 50 consecutive cases. Clin Orthop 1983;178: 6473.