Acute anterior thigh compartment syndrome in Premiership rugby

  1. Christopher Swallow and
  2. Daniel Walton
  1. School of Sport and Exercise Science, University of Worcester, Worcester, UK
  1. Correspondence to Christopher Swallow; c.swallow@worc.ac.uk

Publication history

Accepted:08 Feb 2022
First published:15 Mar 2022
Online issue publication:15 Mar 2022

Case reports

Case reports are not necessarily evidence-based in the same way that the other content on BMJ Best Practice is. They should not be relied on to guide clinical practice. Please check the date of publication.

Abstract

A case study of acute compartment syndrome in the anterior lateral thigh of a professional Rugby Union Flanker with no history of trauma is presented. The report covers all details from initial occurrence; medical history; investigations and surgical treatment; manual stimulus and rehabilitation; return to play; challenges and considerations—resulting in a positive outcome. Resultant observations/recommendations are that investigations should be swift and carefully considered to facilitate surgical intervention via decompressive fasciotomy as required.

Background

Acute compartment syndrome (ACS) is a condition where the intracompartmental pressure within an osseofascial compartment increases and compromises the circulation and viability of the enclosed tissues.1 The resulting swelling and oedema cause cellular anoxia and tissue damage.2 3 If ACS is not readily diagnosed, capillary perfusion exceeds normal rates which may lead to ischaemia, tissue necrosis2 and disruption of regular neural function.

Commonly, ACS aetiology is associated with compartments of the lower leg and forearm (with or without fractures) following direct trauma.2 However, isolated occurrences to the thigh have been noted2 4–7; even though the thigh contains a larger compartment encapsulated with dilative fascia and the anatomy of the hip naturally facilitates tissue expansion.8 Alternatively, instances of ACS have also been induced by exercise, known as exercise-induced compartment syndrome.9 Athletes may be considered at higher risk of ACS as muscular hypertrophy and increased exercise tissue perfusion9 may reduce the available space within compartments.7 10 In combination with the physical demand and contact nature of sport, this may contribute to sports being the second most common cause for ACS developing.10

The Professional Rugby Injury Surveillance Project (PRISP) report published in 2018/2019 noted that match and training injury incidence continues to grow and was documented at 103 per 1000 hours in fixtures and 2.9 per 1000 hours in training within English Premiership rugby.11 The severity of sustained injuries also rose; with severity determined by a greater number of days lost categorisation (more days=more severe). The biggest rise was seen in severe injuries classified within the >84 days category, which have become more diverse.11 All known ACS occurrences within professional rugby have arisen in the previous 2 years, which have included this subject, All Black Prop Atu Moli and 2019 world player of the year Springbok Pieter-Steph du Toit. However, there have been semiprofessional instances prior to this.2 7 12

Current empirical literature investigates ACS from a mechanical13 and clinical perspective, focusing on semiprofessional occurrences. Therefore, with recent recognised occurrences, it is prudent to discuss educatory details in relation to ACS rehabilitation within a professional sports setting, as documented in this report.

Initial case presentation

We introduce a case of a fit and healthy 29-year-old male professional rugby player (Flanker) with a height and weight of 188 cm and 108 kg. After completing an 80 min fixture on the 28 April 2019, the player developed ACS of the right anterior lateral thigh.

The player was clinically examined following the fixture by two club physiotherapists and a club doctor but could not recall an originating occurrence. The player reported symptoms of intramuscular haematoma including confined swelling and palpatory tenderness on the anterior lateral thigh. He also presented minor discomfort with resisted knee extension and full weight bearing but no reduction in range of movement (ROM); no pain on passive ROM; no distal paraesthesia and no pallor. Following assessment, he completed the ‘Protection, Rest, Ice, Compression and Elevation’ injury protocol, was given analgesia and a compression bandage was applied lightly.

The bandage was removed approximately 1.5 hours later due to pain while driving and the player’s symptoms worsened throughout the evening regardless of therapeutic interventions; hence concerns about ACS were formed. Club doctors decided to admit to John Radcliffe Hospital, Oxford due to exquisite pain/pressure/throbbing which was constant while sitting.

Medical history

The athlete sustained a right Rectus Femoris strain during training 1 month before injury which was managed conservatively; no imaging required. He returned to play within 14 days, with a small reduction in bilateral knee flexion. The athlete also suffered a left Semimembranosus/tendinosis strain 6 months prior to ACS occurrence as well as a surgically repaired left Anterior Cruciate Ligament (ACL) injury 2 years prior. Additionally, the athlete suffered bilateral grade 1–2 Biceps Femoris strains and sustained a left Adductor Longus tendon strain, both approximately 36 months preceding injury.

Investigations

Following admission, a decline in status was observed from initial assessment with pain on passive Quadriceps stretching and reduced knee flexion (less than 30°, pain on straight-legged raise and large suprapatellar effusion noted). An X-ray was instructed to exclude fracture and was negative.

Haematology, coagulation and clinical biochemistry status was normal other than reduced Haemoglobin levels (114 and 94 L) and erythrocyte count (3.75 and 3.03). Neovascular status was present, and the athlete had a blood pressure of 174/70 mm Hg. A decision was made to measure the pressure of the anterior compartment with a central venous pressure transducer with unilateral readings of 90 mm Hg in the affected area compared with 18 mm Hg in the uninjured thigh, confirming ACS.

Treatment

An emergency fasciotomy was performed with a lateral incision from the Greater Trochanter to the lateral femoral condyle.14 Further incisions were made to the Intramuscular Septum and Fascia Lata, of which there was no evidence of underlying injury.

Significant muscle haematoma was noted to the Vastus Lateralis and Rectus Femoris including visible fibre damage. Nerve stimulation confirmed viable twitches.15 The Adductor compartment was soft with no clinical evidence of ACS, so no incision was made on the balance of morbidity.

The haematoma was released, circa 50 mL expressed, and 2 L of saline were used to wash the area. No necrosis was noted.

Succeeding the initial procedure, the anterior compartment was dressed and left partially open to evacuate further haematoma, mitigate infection and ensure tissue status; a common procedure with ACS.16 Intravenous antibiotics and analgesia (oral Morphine) were also prescribed alongside elevation. Swelling had reduced to a point where full closure using Vicryl 3.0 via the shoelace method16 could be completed 8 days post injury.

The player was discharged 9 days post injury on 7 May 2019 as seen in figure 1, partially weightbearing with an analgesia prescription of Codeine 60 mg, Ibuprofen 400 mg and Paracetamol 1000 mg; to be taken as required within respective guidelines following a wound and dressings check. In addition, a vague return to play (RTP) timeframe was documented around 12 weeks post surgery.

Figure 1

Right anterior thigh when discharged from hospital.

Manual stimulus and rehabilitation

A 16-week structured RTP protocol was devised by the player’s assigned physiotherapist which included timely progressions, allowing objective multidisciplinary management. This protocol was divided into five phases covering the acute recovery and tissue healing; low loading and tissue capacity; moderate to high load and restoration of strength and a return to sport. The goals of each phase are set out in table 1.

Table 1

Physiotherapist led return to play protocol

Phase Acute post injury—site protection phase Low load Moderate load return to gym High load to run and train Return to sport and perform
Stage Overview Aims Physio led Physio led Transition S&C led S&C led
Protect repair, promote healing, control pain, reduce analgesia Protect repair, increase ROM, control pain, limit atrophy, commence loading programme Protect repair, reintegrate into lowers gym, tolerate running volume <70% max speed Re-integrate into unrestricted quadriceps loading, tolerate progressed running speeds from 70%–100%, tolerate increased running volume up to previous max training week Re-integrate into full training week, tolerate 80 min match demands, tolerate back-to-back fixtures, avoid reinjury, continue daily maintenance and top-ups
0–2 weeks 2–6 weeks 6–10 weeks 10–16 weeks 16+ weeks

  • ROM, range of movement; S&C, strength and conditioning.

Table 6

Soft tissue therapist manual stimulus protocol for scar healing

Phase Inflammatory and immediate homoeostasis Proliferation Remodelling Return to sport and perform
Stage Overview Aims Reduce inflammation, initial homoeostasis, wound closure and support tissue healing
Stimulate the early release and aggregation of collagen		 Manual stimulus to ensure increased levels of tissue stability, fibroblast alignment and hypervesiculating tissue for granulation. Normatrophy function around 70%. Normal levels of melanin, vascularity and contracture. Treatment combined to assist with the physical demands of training and fixtures alongside manual stimulus to support local tissue functionality.
Appropriate Manual Stimulus Deep Oscillation (0.2 Hz) over dressings, local lower body myofascial stretching and neural flossing/mobilisations.
Dry stretch/compression/traction manual stimulus around the scar once dressings removed.		 Promote tissue mobility by applying 5/10 min dry/wet stimulus linearly/ towards scar using combinations of IASTM/ScarWork/EWST (100 impulses per cm2)/Deep Oscillation (1 min 0.2 Hz)/HILT/CO2 laser and 20/30% Stretching 2/3 times a week.
Sonography—if required to ascertain levels of tissue elasticity and fibrosis.		 Specific invasive multidirectional stimulus for 10/15 min using aforementioned modalities 2/3 times a week depending on tissue status and healing. Global and local treatment. Further scar-based focus as required to support athlete.
0–6 days Day 6–21 Day 21–2 years 16+ weeks

  • EWST, Extracorporeal Shockwave Therapy; HILT, High Intensity Light Therapy; IASTM, Instrument Assisted Soft Tissue Massage.

Progression between phases was based on meeting objective data. For example, the athlete was required to achieve full and pain free ROM and equal knee extensor strength, as assessed by handheld and isokinetic dynamometry (IKD). Comparisons were made to previous IKD testing following ACL repair from December 2017, seen in tables 2–4, of which a low left-sided Quadriceps and Hamstrings deficit was noted.

Table 2

Range of motion and peak torque values

Concentric Eccentric
  L R   L R
Extension 0 0 Flexion 0 0
Flexion 79 76 Extension 79 76
Total 79 76 Total 79 76
Mean peak torques with comparison to normative values
_(Nm) 60°/s Concentric Eccentric
  Extensors Flexors Extensors Flexors
Left 217 122 304 118
Right 229 146 283 184
General normative 230 130 250 160
Matched normative 246 140
Table 3

Angles at peak torque

° Concentric Eccentric
60°/s Extensors Flexors Extensors Flexors
Left 41 31 49 27
Right 40 33 46 25
° Concentric Eccentric
180°/s Extensors Flexors Extensors Flexors
Left 33 35 43 22
Right 34 34 50 22
Table 4

Hamstring and Quadriceps concentric and eccentric ratios

Ratios: Hamstring concentric/Quadriceps concentric (Hc/Qc)—normative values~0.6
Speed (°/s) L R
60 0.56 0.64
180 0.55 0.57
Hc/Qc—normative value ~0.6 to 1
(a more functional ratio representing the agonistic/antagonistic nature of the muscles)
Speed (°/s) L R
60 0.54 0.8
180 0.73 0.92

Examples of the athlete’s phase four strength and conditioning led reintegration as well as return to performance physical data can be seen in table 5.

Table 5

Strength and conditioning led physical performance data and session content

Session date Session type Field time Total distance Max velocity Metres per minute Velocity distance covered (Zone 5—60%–70%) Velocity distance covered (Zone 6—70%–80%) Velocity distance covered (Zone 7—80%–90%) Velocity distance covered (Zone 8—90%–110%) Velocity number of efforts (Zone 5—60%–70%) Velocity number of efforts (Zone 6—70%–80%) Velocity number of efforts (Zone 7—80%–90%) Velocity number of efforts (Zone 8—90%–110%) Total player load
08/07/2019 Rehab Running 0.016041667 2220.34009 7.3765 96.11723 212.7 9.95 0 0 11 2 0 0 206.88322
09/07/2019 Rehab Running 0.020706019 1869.93408 8.1845 62.71439 85.04 160.21001 250.19 1.53 10 10 8 1 160.291
12/07/2019 Rehab Running 0.027534722 2468.67407 6.2695 62.23705 0 0 0 0 0 0 0 0 222.13034
16/07/2019 Conditioning Session 0.019664352 2765.543 6.5695 70.55760333 139.3 20.19 0 0 15 2 0 0 291.21146
22/07/2019 Rehab Running 0.031400463 2270.47314 8.3005 50.20172 91.55 104.32 139.48 8.19 13 9 8 1 254.01476
23/07/2019 Conditioning Session 0.046215278 4380.44807 6.4425 65.76426167 710.79003 5.67 0 0 27 2 0 0 469.71783
25/07/2019 Conditioning Session 0.037268519 4851.0765 7.9805 115.8409669 120.8 81.74 58.17 0 13 7 3 0 516.04682
26/07/2019 Conditioning Session 0.059618056 5605.92528 6.2875 80.664475 321.66999 4 0 0 29 1 0 0 572.16231
30/07/2019 Rehab Running 0.027685185 2134.19507 8.4065 53.52213 162.32001 274.98001 467.14999 13.59 20 20 17 1 194.19466
12/08/2019 Units 0.039583333 1017.40002 3.3285 17.91875 0 0 0 0 0 0 0 0 110.34767
29/08/2019 Attack Session 0.056608796 4696.32096 6.6555 74.07377556 175.99 29.09 0 0 21 4 0 0 456.93374
12/10/2019 Matchday 0.043391204 4151.31249 6.54491 66.94654333 200.64 20.6 0 0 19 3 0 0 473.34623

The club soft tissue therapist was also responsible for consulting with the assigned physiotherapist and devised a specific protocol to complement each phase of rehabilitation, to restore the integrity and function of the connective tissues as quickly as possible.17–19 This protocol had four phases and can be seen in table 6.

Manual stimulus was applied between two and three times per week to compliment the athlete’s rehabilitation and tissue healing objectives.16–21 Progression of manual stimulus depended on athlete tolerance, subjective feedback and healthy status of tissue healing.20 Additional manual stimulus such as Extracorporeal Shockwave Therapy (EWST) and High Intensity Light Therapy (HILT) pulsed dye (PDL), CO2 laser, Tecar Therapy and Sonography have all been discussed in literature18 19 22 and could have been used to ascertain and influence levels of tissue elasticity and fibrosis. However, they were not required in this instance as tissue healing was evident and treatment progressions were achieved at each stage as seen in figures 2 and 3.

Figure 2

Right anterior thigh 3 weeks post injury.

Figure 3

Scar remodelling 6 weeks post injury.

Outcome and follow-up

Following a successful 16-week rehabilitation programme, as discussed above, and a subsequent extended 6-week preseason the athlete returned to competitive play on 28 September 2019. He featured in four consecutive fixtures before sustaining a blow to the lateral thigh during the second half of a fixture. On 12 November 2019, a consultation was organised with a specialist orthopaedic surgeon to consider risk factors and agree an RTP following fluid aspiration and the 6–8 weeks rehabilitation programme. Following his return, the player featured in a further eight fixtures to conclude the campaign; amassing a total of 747 min across the back row: one of the most consistent seasons of his career.

Discussion

Occurrences of ACS within sport are rare.2 10 There is a paucity of examples associated with the anterior thigh2 4–7 and none previously of a professional rugby player which have been published within empirical research. Commonly, previously published cases investigate ACS from a mechanical12 and clinical perspective. However, they do not prepare professional athletes nor educate relevant professionals regarding suitable guidelines related to RTP; rehabilitation; tissue healing; complications/challenges or outcomes.

Empirical research emphasises the importance of early and effective diagnosis associated with ACS. Nevertheless, there appears to be no published consensus regarding this process either with or without fracture.2 15 23 Traditionally, observing indicatory symptoms such as the ‘six P’s’ (pain, pressure, pulselessness, paralysis, paraesthesia and pallor) would confirm diagnosis. However, confirming/verifying ACS can be complicated when considering the rapid progression of symptoms, preceding factors and location and invasiveness of devices measuring intracompartmental pressure.2 As found in this case, some or all observable symptoms can be absent, but ACS be present.24 In addition, research suggests that instances of ACS without fracture are more likely to have delayed diagnosis.15 Therefore, repeated examination and pressure monitoring in suspected cases should be undertaken during hospital admittance.12 15

Intracompartmental pressure thresholds have been commonly accepted as accurate triggers for intervention. Either having an ΔP of between 20 and 30 mm Hg or a difference in compartment pressure and perfusion pressure of greater than 30 mm Hg would be diagnostic indicators for surgical intervention. However, discussion of thresholds in the anterior thigh is not encompassed in the existing research.2

Severe consequences can develop should ACS not be recognised and treated rapidly. Such consequences may include necrosis caused by ischaemia; thereby subjecting the patient to higher risk of infection and potentially fatal complications.15 25 There is also no clear timeframe within literature to determine retrospectively when ACS should have been diagnosed. This is crucial as fasciotomy outcomes can be affected by the intervention timeline,12 26 with research indicating that sequalae was more common in those cases which were missed or delayed. Noted symptoms include ongoing pain; motor weakness and altered tissue sensations including paraesthesia and dysesthesia.27 In this instance, acute tissue alterations were present throughout the stages of tissue healing but have since subsided.

In 13% of fasciotomies,26 two divisions of the Fascia Lata were required to adequately release intracompartmental pressure. In addition, once healed, tissue herniation through the defect Iliotibial band may further reduce the strength of natural protective mechanisms.26 As such, it is reasonable to hypothesise the athlete concerned in this case study may be more prone to repetitive haematomas of his lateral thigh muscle. This is a common match injury detailed within five of the last six PRISP reports and having an occurrence rate of 4.0 per 1000 hours.11 Furthermore, the physical nature of rugby and the performer’s musculoskeletal adaptations suggest that training and/or playing modifications may need to be discussed between performers, medical/performance personnel, and coaches to successfully prevent recurrences. Suitable considerations may include a supportive guard to wear during training and fixtures and limiting the amount of contact training.

Learning points

  • Early and effective diagnosis of acute compartment syndrome (ACS) is imperative, especially without fracture when occurrences relate to sport.

  • Comprehensive return to play rehabilitation programmes, including input from various support personnel mitigate reinjury and facilitate athletes to return suitably to professional sport following ACS.

  • Return to play in professional sport should consider athletes musculoskeletal adaptations, sporting and positional demands as well as sequalae. Long-term performance modifications should be highlighted and discussed.

Ethics statements

Patient consent for publication

Acknowledgments

Harry Sharman provided GPS analysis details relating to athlete physical loading and rehabilitation. Aman Shergill assisted with GPS data table interpretation. Chloë Morris and Ricky Shamji provided language editing support and proofreading.

Footnotes

  • Contributors CS and DW: study conception; CS: procured investigational details from the relevant parties; CS conducted the literature search; CS and DW wrote the manuscript; CS has primary responsibility for final content. Both authors reviewed and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

References

  1. ↵
    1. Mauser N ,
    2. Gissel H ,
    3. Henderson C , et al
    . Acute lower-leg compartment syndrome. Orthopedics 2013;36:619–24.doi:10.3928/01477447-20130724-07 pmid:http://www.ncbi.nlm.nih.gov/pubmed/23937740
  2. ↵
    1. Smith RD ,
    2. Rust-March H ,
    3. Kluzek S
    . Acute compartment syndrome of the thigh in a rugby player. Case Reports 2015;2015:bcr2015210856.
  3. ↵
    1. Olson SA ,
    2. Glasgow RR
    . Acute compartment syndrome in lower extremity musculoskeletal trauma. J Am Acad Orthop Surg 2005;13:436–44.doi:10.5435/00124635-200511000-00003 pmid:http://www.ncbi.nlm.nih.gov/pubmed/16272268
  4. ↵
    1. Burns BJ ,
    2. Sproule J ,
    3. Smyth H
    . Acute compartment syndrome of the anterior thigh following quadriceps strain in a footballer. Br J Sports Med 2004;38:218–20.doi:10.1136/bjsm.2003.004762 pmid:http://www.ncbi.nlm.nih.gov/pubmed/15039263
  5. ↵
    1. Machold W ,
    2. Muellner T ,
    3. Kwasny O
    . Is the return to high-level athletics possible after fasciotomy for a compartment syndrome of the thigh? A case report. Am J Sports Med 2000;28:407–10.doi:10.1177/03635465000280032201 pmid:http://www.ncbi.nlm.nih.gov/pubmed/10843137
  6. ↵
    1. Rohman L ,
    2. Chan S ,
    3. Hadi S , et al
    . Recurrent spontaneous compartment syndrome of the thigh. BMJ Case Rep 2014;2014:bcr2013201859.doi:10.1136/bcr-2013-201859 pmid:http://www.ncbi.nlm.nih.gov/pubmed/25150230
  7. ↵
    1. Wadhawan H ,
    2. Upadhyay V ,
    3. Sabboubeh A , et al
    . Acute anterior thigh compartment syndrome revisited: a case report and review of literature. Eur J Trauma Emerg Surg 2007;33:430–3.doi:10.1007/s00068-007-6952-5 pmid:http://www.ncbi.nlm.nih.gov/pubmed/26814739
  8. ↵
    1. Riede U ,
    2. Schmid MR ,
    3. Romero J
    . Conservative treatment of an acute compartment syndrome of the thigh. Arch Orthop Trauma Surg 2007;127:269–75.doi:10.1007/s00402-006-0199-1 pmid:http://www.ncbi.nlm.nih.gov/pubmed/16896742
  9. ↵
    1. Cetinus E ,
    2. Uzel M ,
    3. Bilgiç E , et al
    . Exercise induced compartment syndrome in a professional footballer. Br J Sports Med 2004;38:227–9.doi:10.1136/bjsm.2003.004630 pmid:http://www.ncbi.nlm.nih.gov/pubmed/15039267
  10. ↵
    1. McQueen MM ,
    2. Gaston P ,
    3. Court-Brown CM
    . Acute compartment syndrome. who is at risk? J Bone Joint Surg Br 2000;82:200–3.doi:10.1302/0301-620.82b2.9799 pmid:http://www.ncbi.nlm.nih.gov/pubmed/10755426
  11. ↵
    1. England Professional Rugby Injury Surveillance Project Steering Group
    . England Professional Rugby Injury Surveillance Project [Internet]. RFU: Rugby Football Union, 2021: 1–45. https://www.englandrugby.com/dxdam/89/8994c1ba-17df-47a3-a4c6-8878ed6728d0/England%20PRISP%2018.19.pdf
  12. ↵
    1. Rööser B ,
    2. Bengtson S ,
    3. Hägglund G
    . Acute compartment syndrome from anterior thigh muscle contusion: a report of eight cases. J Orthop Trauma 1991;5:57–9.doi:10.1097/00005131-199103000-00010 pmid:http://www.ncbi.nlm.nih.gov/pubmed/2023045
  13. ↵
    1. Verwiebe EG ,
    2. Kanlic EM ,
    3. Saller J , et al
    . Thigh compartment syndrome, presentation and complications. Bosn J Basic Med Sci 2009;9 Suppl 1:S28–33.doi:10.17305/bjbms.2009.2751 pmid:http://www.ncbi.nlm.nih.gov/pubmed/19912116
  14. ↵
    1. Tarlow SD ,
    2. Achterman CA ,
    3. Hayhurst J , et al
    . Acute compartment syndrome in the thigh complicating fracture of the femur. A report of three cases. J Bone Joint Surg Am 1986;68:1439–43.doi:10.2106/00004623-198668090-00019 pmid:http://www.ncbi.nlm.nih.gov/pubmed/3782215
  15. ↵
    1. Mauffrey C ,
    2. Hak DJ ,
    3. Martin III MP
    1. Tillinghast CM ,
    2. Gary JL
    . Chapter 8, compartment syndrome of the lower extremity. In: Mauffrey C , Hak DJ , Martin III MP , eds. Compartment syndrome: a guide to diagnosis and management. Springer, 2019: 67–81.
  16. ↵
    1. Kakagia D
    . How to close a limb fasciotomy wound: an overview of current techniques. Int J Low Extrem Wounds 2015;14:268–76.doi:10.1177/1534734614550310 pmid:http://www.ncbi.nlm.nih.gov/pubmed/25256284
  17. ↵
    1. Koller T
    . Mechanosensitive aspects of cell biology in manual scar therapy for deep dermal defects. Int J Mol Sci 2020;21:2055.doi:10.3390/ijms21062055 pmid:http://www.ncbi.nlm.nih.gov/pubmed/32192136
  18. ↵
    1. Swallow C
    . Scarwork: A timeline for treatment stimulus in sport | BJSM blog - social media’s leading SEM voice. [online] BJSM blog, 2021. Available: https://blogs.bmj.com/bjsm/2021/01/09/scarwork-a-timeline-for-treatment-stimulus-in-sport [Accessed 5 Apr 2021].
  19. ↵
    1. Deflorin C ,
    2. Hohenauer E ,
    3. Stoop R , et al
    . Physical management of scar tissue: a systematic review and meta-analysis. J Altern Complement Med 2020;26:854–65.doi:10.1089/acm.2020.0109 pmid:http://www.ncbi.nlm.nih.gov/pubmed/32589450
  20. ↵
    1. Landén NX ,
    2. Li D ,
    3. Ståhle M
    . Transition from inflammation to proliferation: a critical step during wound healing. Cell Mol Life Sci 2016;73:3861–85.doi:10.1007/s00018-016-2268-0 pmid:http://www.ncbi.nlm.nih.gov/pubmed/27180275
  21. ↵
    1. Holly E ,
    2. Poulton H
    . Understanding scars. Recommendations and interventions (2), 2021. Available: https://restoretherapy.co.uk/understanding-scars/;
  22. ↵
    1. Enwemeka CS ,
    2. Parker JC ,
    3. Dowdy DS , et al
    . The efficacy of low-power lasers in tissue repair and pain control: a meta-analysis study. Photomed Laser Surg 2004;22:323–9.doi:10.1089/pho.2004.22.323 pmid:http://www.ncbi.nlm.nih.gov/pubmed/15345176
  23. ↵
    1. Maher M ,
    2. Mauffrey C
    . Diagnostic dilemma for the orthopedic surgeon. Compartment Syndrome 2019:1–7.
  24. ↵
    1. Seddon H
    . Volkmann's ischaemia. Br Med J 1964;1:1587–92.doi:10.1136/bmj.1.5398.1587 pmid:http://www.ncbi.nlm.nih.gov/pubmed/14134485
  25. ↵
    1. Finkelstein JA ,
    2. Hunter GA ,
    3. Hu RW
    . Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma 1996;40:342–4.doi:10.1097/00005373-199603000-00002 pmid:http://www.ncbi.nlm.nih.gov/pubmed/8601846
  26. ↵
    1. Fitzgerald AM ,
    2. Gaston P ,
    3. Wilson Y , et al
    . Long-Term sequelae of fasciotomy wounds. Br J Plast Surg 2000;53:690–3.doi:10.1054/bjps.2000.3444 pmid:http://www.ncbi.nlm.nih.gov/pubmed/11090326
  27. ↵
    1. Dover M ,
    2. Marafi H ,
    3. Quinlan J
    . Long term sequelae following fasciotomy in trauma patients. In: Orthopaedic proceedings. 93. The British Editorial Society of Bone & Joint Surgery, 2011: 180.

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