Background story: Ever since I sprained my ankle 3 years ago and was, to my surprise, told not to ice it, I have been curious to understand the theories and evidence behind recommendations to ice/not ice. Really, I want to know once and for all, should I ice an acute soft tissue injury immediately so that I can return to the activities I want to do faster? (Spoiler alert: I still don’t have an answer.)
Theoretically, ice can enhance recovery from an acute soft tissue injury by decreasing tissue temperature, which reduces pain, muscle spasm, metabolism, and minimizes inflammatory processes (1). So does the research support this theory? One systematic review found that using ice shortly following an acute soft tissue injury may be effective in increasing the speed of return to participation; however, their conclusions are based on four randomized controlled trials (RCTs) on humans with weak study methodologies (2,3). With the limited evidence in the form of RCTs, and from my tutorial tutor’s advice, I decided to look at this issue from a physiology perspective to find my answer. It seems that a major assumption behind using ice is that inflammation is bad and since ice decreases inflammation, it should be used. However, is inflammation actually bad? If so, why?
All that being said, I present my learning objective for this post…
Learning Objective: what are the pathophysiological mechanisms behind the inflammatory response to an acute soft tissue injury and the implications of this on the use of modalities (e.g. ice) to decrease inflammation?
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Main take home messages (very simplified physiology; sorry for any physiology majors out there)
- neutrophils are the first white blood cells to arrive at the site of injury, followed by macrophages
- neutrophils act to clean up cell debris but can cause more tissue injury at the same time
- macrophages help promote tissue repair
- macrophages need neutrophils to function optimally –> thus, there is a balance between reducing secondary injury from neutrophils and ensuring there is enough neutrophilic activity to promote macrophage activity (tissue repair)
- this balance is currently unknown
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I am, by no means, a physiology expert and the following simplified summary is based on my interpretation of a literature review I found, titled “The dual roles of neutrophils and macrophages in inflammation: a balance between tissue damage and repair” by Butterfield et al. (4). Also, many of the studies they cited were done in vitro or using animal models so it’s questionable how applicable the results are to humans.
As implied by the title, there appears to be a need to balance the body’s inflammatory response as it can cause more damage but also help with repair. After an acute soft tissue injury, neutrophils are the first white blood cells that arrive at the site (highest concentration at 3 – 24 hours post-injury), followed closely by macrophages. In general, neutrophils are responsible for removal of cell debris and release inflammatory cytokines that can cause further tissue damage. On the other hand, macrophages are involved with cell signalling and the release of factors and cytokines that promote tissue repair.
Does this mean we want to decrease the neutrophilic response (i.e. inflammation in the first 24 hours) and increase the macrophage response (inflammation after the first 24 hours)? From in vitro studies, it seems that there is some communication between neutrophils and macrophages that enhances tissue repair; having neutrophils on their own increases the amount of early tissue damage but a lack of neutrophils inhibits the reparative function of macrophages. It’s thought that the clearing of cell debris by the neutrophils is necessary to allow for cellular regeneration and repair by the macrophages. However, having a prolonged neutrophilic response slows down the rate of tissue repair, possibly due to excess tissue destruction.
Clinical Implications
Based on this review, it is unclear to me whether or not we should be trying to decrease inflammation following an acute soft tissue injury. There needs to be some neutrophilic activity but not too much…the current problem is that we don’t know how much that “some” is and how much our therapeutic interventions (e.g. ice, NSAIDs) reduce the amount of activity by. Is the slowed rate of tissue repair from lower concentrations of neutrophils enough to offset the secondary tissue damage caused by neutrophils? I feel like this is a math optimization problem haha.
I doubt the relationship actually looks like this but I hope you get the idea – there’s a tradeoff!
Other Questions/Thoughts
- since ice can be used to decrease pain (5), it may be useful for those who need to use the injured area (e.g. for athletes, walking with a sprained ankle) and it may be useful to help people do more rehab exercises
- on the other hand, would the analgesic effect be so large that it would cause people to accidentally damage the tissue further?
- swelling in the knee joint has been linked with arthrogenic muscle inhibition of the quadriceps (6). Could this lead to altered joint mechanics, then altered joint stresses, and finally other injuries over time? If so, should we be concerned about reducing the swelling immediately to limit the amount of inhibition? Or will the muscle function return back to normal after the tissue has healed so we don’t need to worry about the acute swelling?
For any clinicians or trainers reading this, what are your thoughts and reasoning behind the use of ice (or other anti-inflammatory modalities) in the face of this uncertainty in the literature? As always, other perspectives are encouraged and more than welcome :). Shoot me an email or leave a comment below!
References
1. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: a systematic review of randomized controlled trials. Am J Sports Med. 2004 Jan;32(1):251–61.
2. Hubbard TJ, Aronson SL, Denegar CR. Does Cryotherapy Hasten Return to Participation? A Systematic Review. J Athl Train. 2004 Mar;39(1):88–94.
3. Collins NC. Is ice right? Does cryotherapy improve outcome for acute soft tissue injury? Emerg Med J. 2008 Feb;25(2):65–8.
4. Butterfield TA, Best TM, Merrick MA. The dual roles of neutrophils and macrophages in inflammation: a critical balance between tissue damage and repair. J Athl Train. 2006 Oct;41(4):457–65.
5. Bleakley CM, McDonough SM, MacAuley DC, Bjordal J. Cryotherapy for acute ankle sprains: a randomised controlled study of two different icing protocols. Br J Sports Med. 2006 Aug;40(8):700–5–discussion705.
6. Rice D, McNair PJ, Dalbeth N. Effects of cryotherapy on arthrogenic muscle inhibition using an experimental model of knee swelling. Arthritis Rheum. 2009 Jan 15;61(1):78–83.
