Acute Soft Tissue Injury Management

Background

For three decades, Protection, Ice, Rest, Compression and Elevation (PRICE) has been widely accepted in the management of acute soft tissue injuries (1-5). Whilst it remains the most common approach, little high quality scientific evidence exists to support its efficacy (6). This article will first look at the concept of injury, then the latest research and Clinical Guidelines for the practical application of PRICE.

 

ACPSM guidelines

In 1998, using research evidence published up to 1996, the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM, 1998) endorsed and published their original Clinical Guidelines for the practical application of each component of PRICE. These Clinical Guidelines have recently been superseded by new guidelines endorsed by the Chartered Society of Physiotherapy’s Supporting Knowledge in Physiotherapy Practice Programme, after peer review from their Good Practice Panel in October 2010 (ACPSM, 2010).

Concept of injury and rehabilitation

All connective soft tissue injuries, regardless of their severity, must undergo the same healing process (8,9,10). A consensus exists, consisting of 4 overlapping, interlinked phases (Figure 1); bleeding, acute inflammation, proliferation, and remodeling (11,12). Following injury, damaged blood vessels bleed causing hypoxia, so the injured tissue contains dead cells and extravasated blood (8). This triggers a natural but essential inflammatory response, involving a very complexed vascular and cellular response, the result being fluid exudate, oedema and phagocytic activity (6,12).

Figure 1

Inflammatory phase

The inflammatory phase prepares the wound for healing; the proliferation phase rebuilds the damaged structures; and the remodeling phase modifies the scar tissue into its mature form. The duration of each phase varies to some degree, dependent upon severity of injury and tissue type amongst others. The immediate protective response attempts to destroy, dilute, or isolate the cell or agents that may be at fault (15). Typically, the acute inflammatory phase lasts between 46 days, and prepares the wound for the proliferation phase (16). Acute inflammation results from vasodilatation and vasopermeability of the blood vessels, initiated and controlled by a wide array of chemical mediators released by the damaged tissues (17). Clinically, acute inflammation manifests as swelling, erythema, increased temperature, pain, leading to loss of function (9). The physical characteristics of acute inflammation were first formulated by Celsus in (30 BC – 38 AD) using Latin words; rubor, calor, tumor and dolor (18).

 

Changes in fluid exchange at the vascular bed

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Figure 2, shows normal tissue conditions. Healthy tissue maintains a dynamic balance of fluid movement between the vascular system and interstitial tissue space. Thus blood flow and fluid exchange remains in balance at the vascular bed and many of the capillaries remained closed.

Figure 3 shows the effects of the acute inflammatory response. Most of the capillaries open contributing to the localised increased blood flow. Vasodilatation and vasopermeability increase of local blood vessels and infiltration of the fluid into the interstitial spaces of the injured area. As a result, the normal fluid balance becomes disturbed at the vascular bed. The net effect is increased fluid movement from the blood vessel, into the surrounding interstitial space resulting in swelling / oedema formation at the injury site.

Figure 4 shows how the capillaries become more permeable (leaky), resulting in chemicals and blood cells migrating to the injury site. This response accounts for the swelling, heat, redness and pain.

Figure 4 (Adapted from 15: Cameron, 2003)

Whilst PRICE remains the most common approach in the management of acute soft tissue injuries, little high quality scientific evidence exists to support its efficacy. PRICE is used to control inflammation, thus, limit haemorrhaging, oedema, swelling, pain, and promote optimal healing (7,19,20). Limiting inflammatory exudate reduces the amount of fibrin, and ultimately excessive scar tissue (7), while limiting adhesions and excessive crosslink formation (21). Below,  the individual components that make up PRICE are discussed.

Early controlled mobilisation after injury

Although a short period of immobilisation (Protect / Rest) following injury is necessary (9,11), early controlled mobilisation is essential for decreased healing time, increased vascular ingrowth, quicker regeneration of scar tissue (23-25), resulting in stronger mobile ligaments (10,26).

   

Conversley, prolonged immobilization can lead to deleterious tissue effects such as; random deposition of collagen, excessive crosslink formation (Figure 5) and atrophy. Consequently this leads to functional implications such as losses in range of movement (Figure 5) and tensile strength (21). New tissue is fragile and easily interrupted, consequently, mobilisation too early or too intensively may rerupture the injured tissue (19).

Ice (cryotherapy)

Although largely based on anecdotal evidence, cryotherapy is widely recommended to reduce tissue temperature and metabolism, thereby minimising secondary hypoxic injury, cell debris, oedema, and pain (6,28,29). Many studies have failed to report details of the ice protocols used and lack internal validity (6). Crushed ice provides effective cooling and is probably the safest method. Ideally a damp barrier should be placed between the skin and ice. This approach will not mitigate the cooling effect on the skin - a thick dry barrier will mitigate the clinical effect (22).         

 

 

Crushed ice and polythene film compression wrap are applied to the lateral knee ligaments using an intermittent icing protocol of 10 minute every 2 hours (Figure 6), as recommended by Bleakley et al (30). Care is needed to avoid cold induced injury to any superficial tissues (e.g. peroneal nerve); therefore application times should reflect the amount of superficial body fat (22).

  

Compression & Elevation

Healthy tissue maintains a dynamic balance of fluid movement between the vascular system and interstitial tissue space (Figure 2). Acute soft tissue injury and the ensuing inflammatory response disturb this balance. The net effect is increased fluid movement from the blood vessel, into the surrounding interstitial space resulting in swelling / oedema formation at the injury site (Figures 3 & 4). One of the primary reasons for using elevation or compression after injury is to try to restore the pressure gradients within the affected tissue. This is achieved through external pressure (compression) or by gravity (elevation). The latest ACPSM (2010) recommendations are to continue using compression and elevation. However, probably don’t use high levels of compression with simultaneous elevation.

 

General Recommendations for use of PRICE

The following generally recommendations are a composite from the latest research and the ACPSM (2010) recommendations.

 

Protection & Rest - during the acute stage (Protection/Rest) is necessary. Movements in the plane of injury should be avoided. However, the duration, degree and mode of (Protection/Rest) are dependent on the severity of the injury. Research clearly demonstrates that low level mechanical loading (exercise) is crucial for effective healing of damaged tissues and helps minimise the risk of abnormal crosslink (adhesion) formation (Figure 5). As healing progresses, so should the level of loading – but under close supervision. The level of loading and speed of progression should be guided by the severity of the injury and tissue type performed within the limits of pain. New tissue is fragile and easily interrupted; consequently, loading too early or too intensively may rerupture the injured tissue.

 

Ice – should definitely be applied after an acute injury. Crushed ice appears the preferred choice, complete with a damp thin barrier between ice and skin (Figure 6). Typically, a duration of between 10 and 15 minutes for superficial tissue, and between 20 and 25 minutes for larger areas of deep tissue. The maximum duration should not exceed 30 minutes for safety. Intermittent ice applications of approximately every 2 hours appear optimum and safest.

 

Compression & Elevation -  healthy tissue maintains a dynamic balance of fluid movement between the vascular system and interstitial tissue spaces (Figure 2). Following injury, the inflammatory response disturbs this balance (Figure 3 & 4). This increased fluid movement from the blood vessel, into the surrounding interstitial space resulting in bleeding and swelling / oedema formation at the injury site. It is believed, compression forces the fluid (oedema / swelling) from the injury site towards the capillary, lymph vessels, or tissue spaces away from the damaged area. The clear physiological aims of Compression & Elevation are to prevent further bleeding, to increase intestinal pressure and to increase venous return. Thus, control inflammation, by limiting the accumulation of blood, oedema / swelling and pain to promote optimal healing. The compressive bandages should provide firm graduated compression that configures / moulds to the limb.

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References

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  2. Clanton, T., & Coupe, K.J. (1998). Hamstring strains in athletes: Diagnosis and treatment. Journal of American Academy of Orthopaedic Surgeons, 6, 237-248.

  3. Drezner J., (2003) Practical management: Hamstring muscle injuries. Clinical Journal of SportsMedicine, 13, 48-52.

  4. O’Sullivan, K., & Keane, N. (2009). Female Gaelic football players’ acute soft tissue injury management. Physiotherapy Ireland, 30, 13-18.

  5. Jarvinen, T.A.H., Kaariainen, M., Jarvinen, M., Kalimo, H. (2000). Muscle injuries. Current Opinion in Rheumatology, 12(2), 155-161.

  6. Bleakley, C.M. (2009). Current concepts in the use of PRICE for soft tissue injury management. Physiotherapy Ireland, 30(2), 19-20.

  7. ACPSM, (1998). Guidelines for the management of soft tissue injury with protection, rest, ice, compression and elevation (PRICE) during the first 72 hours: The Chartered Society of Physiotherapy.

  8. Evans, P. (1980). The healing process at cellular level: a review. Physiotherapy, 66(8), 256-259.

  9. Kannus, P., Parkkari, T.L., Jarvinen, T., et al. (2003). Basic science and clinical studies coincide: active treatment approach is needed after a sports injury. Scandinavian Journal of Medicine and Science in Sports. 13, 150-154.

  10. Vailas, A., Tipton, C., Matthes, R., Gart, M. (1981). Physical activity and its influence on the repair process of medial collateral ligaments. Connective Tissue Research, 9, 25-31.

  11. Jarvinen, M.J., Lehto, M.U. (1993). The effects of early mobilisation and immobilisation on the healing process following muscle injuries. Sports Medicine Journal, 15 (2), 78-89.

  12. Watson, T. (2006). Tissue repair: the current state of art. Journal of Sportex Health. 19, 812.

  13. Bandy, W. D. (1992). Functional rehabilitation of the athlete. Orthopaedic Physical Therapy Clinics of North America.1, 269-281

  14. Smith, G.N. (1998). Return to fitness. In M. Tidswell (Ed.), Orthopaedic Physiotherapy (pp.255270). London: Mosby.

  15. Cameron, M.H. (2003). Physical agents in rehabilitation: From research to practice. USA: Saunders

  16. Hunter, G. (1998). Specific soft tissue mobilisation in the management of soft tissue dysfunction. Manual Therapy. 3(1), 211.

  17. Watson, T. (2003). Soft tissue healing. In Touch. 104, 29.

  18. Underwood, J.C.E. (2000). General and systematic pathology. Third edition. Edinburgh: Churchill Livingstone.

  19. Kannus, P. (2000). Immobilization or early mobilisation after an acute soft tissue injury. The Physician and Sports Medicine. 28(3), 55-63.

  20. Jarvinen, T.A.H., Jarvinen, T.L.N., Kaariainen, M., Kalimo, H., Jarvinen, M. (2005). Muscle injuries: Biology and treatment. The American Journal of Sports Medicine, 33(5), 745-764

  21. Lederman, E. (2005). The science and practice of manual therapy. Second edition. Edinburgh: Churchill Livingstone.

  22. ACPSM, (2010). Management of acute soft tissue injury using PRICE guidelines. Executive Summary Recommendations.

  23. Arem, A.J., Madden, J.W. (1976). Effects of stress on healing wounds: Intermittent noncyclical tension. Journal of Surgical Research, 20 (2), 93-102.

  24. Buckwalter, J.A., Grodzinsky, A.J. (1999). Loading of healing bone, fibrous tissue, and muscle. Implications for orthopaedic practice. Journal of American Academic Orthopaedic Surgery. 7, 291-299.

  25. Culav, E.M., Clark, C.H., Merrilees, M.J. (1999). Connective tissues: matrix composition and its relevance to physical therapy. Physical Therapy, 79(3), 308-319.

  26. Glasgow, P. (2007). Sports rehabilitation: principles and practice. Sportex Medicine. 32, 10-16.

  27. Bleakley, C., McDonough, S., MacAuley, D. (2004). The use of ice in the treatment of acute softtissue injury: A systematic review of randomised controlled trials. The American Journal of Sports Medicine. 32(1), 251-261.

  28. Knight, K.L., Brucker, J.B., Stoneman, P.D., Rubley, M.D. (2000). Muscle injury management with cryotherapy. Athletic Therapy Today. 5(4), 2630.

  29. Raynor, M.C., Pietrobon, R., Guller, U., Higgins, L.D. (2005). Cryotherapy after ACL reconstruction: A metaanalysis. Journal of Knee Surgery. 28 (2), 123-129.

  30. Bleakley, C., McDonough, S., MacAuley, D. (2006). Cryotherapy for acute ankle sprains: a randomised controlled study of two different icing protocols. British Journal of Sports Medicine. 40, 700-705.

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