Most evidence suggests that ice can provide adequate pain relief after injury. There is moderate clinical evidence that cold therapy is effective at decreasing short term pain after acute ankle injury and general soft tissue contusions, and low quality clinical evidence that shorter intermittent applications are sufficient to induce short term analgesia(1) Based on a post-surgical model, there is high quality evidence that cold therapy provides effective short term analgesia(1) These clinical findings are supported by basic scientific evidence; and we found numerous laboratory based studies confirming that skin temperature is reduced to less than 13°C after 5-15mins of cooling(2). This is the currently accepted threshold for inducing effective local analgesia. Importantly not all modes of cryotherapy cool equally or at the same rate(2).
There is moderate clinical evidence that ice has little effect on other clinical outcomes, including recovery time, function and swelling. There may be many reasons for this lack of effect. Primarily, the major studies in the area have used post surgical models; few have used closed soft tissue injury. We must also acknowledge that it can be difficult to induce clinically significant temperature reductions on deep muscle and joints after injury; and currently accepted threshold temperatures for reducing cellular metabolism (5°C – 15°C) seem unattainable(2). There is very low quality evidence from human studies that ice may reduce metabolism or aspects of the inflammatory response(3), the effect that ice has on biomarkers of inflammation and muscle damage after Exercise Induced Muscle Damage (EIMD)on humans is inconsistent(3).
Another important mechanism associated with cooling in the immediate stages after injury is the vasoconstrictive effect it may have on the vasculature. The original PRICE guidelines found consistent evidence that various modes of cooling decreased blood flow in human models. We found further evidence that cooling reduced blood flow in healthy human tissue, with no evidence of cold induced vasodilation(3). Other cold induced effects included reduced Oxygen saturation and facilitated venous capillary outflow in healthy tendon models(3). There is a depth of related studies on injured humans; and the effect of ice on microcirculation in injured animal models is inconsistent(3).
Based on basic scientific evidence and clinical research, we would suggest that in some clinical scenarios, cold induced benefits may be limited to analgesia; particularly in situations associated with higher levels of body fat, deep soft tissue injury, or when insulating barriers are necessitated (eg. Post surgical models) at the cooling interface. We do however acknowledge that the current threshold temperatures for achieving analgesia (skin temperature <13°C) or metabolic reduction (reduction to 5-15°C at injury site) are not definitive and may be subject to change based on emerging understanding of the biomechanical and physiological events surrounding acute injury and inflammation(4).
Despite a relatively large number of studies into the effectiveness of external supports and bandages, much of the evidence of compression is conflicting(1). The exact physiological rationale has yet to be fully explicated, and there is little evidence for an optimal compressive force. The rationale for using high levels of compression pressure is to minimise initial tissue haemorrhage after injury. We found very low quality evidence that this approach is ineffective after muscle injury. This was based on one controlled study comparing immediate compression (bandaging) at 80mmHg, with rest/ice(1). A related rationale for compressing is to prevent oedematous fluid from accumulating within the interstitial space. The external mechanical pressure is thought to increase the hydrostatic pressure of the interstitial fluid thereby forcing fluid from the injury site towards the capillary, lymph vessels, or tissue spaces away from the traumatised area. Smaller external forces may achieve this effect; many standard protocols recommend pressures between 15 and 35mm/Hg(5,6).
- Bleakley CM, Glasgow PD, Philips N, Hanna L, Callaghan MJ, Davison GW et al. for the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM). Management of acute soft tissue injury using Protection, Rest, Ice, Compression & Elevation, 2011. Chapter 7; Which components of PRICE are effective in the clinical management of acute soft tissue injury?
- Bleakley CM, Glasgow PD, Philips N, Hanna L, Callaghan MJ, Davison GW et al. for the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM). Management of acute soft tissue injury using Protection, Rest, Ice, Compression & Elevation, 2011. Chapter 3; What is the magnitude & depth of cooling associated with Ice?
- Bleakley CM, Glasgow PD, Philips N, Hanna L, Callaghan MJ, Davison GW et al. for the Association of Chartered Physiotherapists in Sports and Exercise Medicine (ACPSM). Management of acute soft tissue injury using Protection, Rest, Ice, Compression & Elevation, 2011. Chapter 4; Can PRICE decrease inflammatory response after acute soft tissue injury?
- Scott A, Khan KM, Roberts CR, Cook JL, Duronio V. What do we mean by the term “inflammation”? A contemporary basic science update for sports medicine. British Journal of Sports Medicine 2004;38(3):372-80.
- Thomas S. Bandages & Bandaging: the science behind the art. Care Science & Practice 1990; 8(2):56-60.
- Mayrovitz H, Delgado M, Smith J. Compression bandaging effects on lower extremity peripheral and sub-bandage skin perfusion. Ostomy Wound Management 1998; 44(3):56-67.