The Iceman Cometh….again! Back in February researcher and sports therapist Peter Thain wrote us a fantastic piece on ice application in sport. Now he's back by popular demand, albeit a little melted by the recent heat wave!
After arriving home from work (where I had been administering cryokinetic protocols), I was greeted with an erupting debate on Twitter. The main questions were regarding the use of ice, compression and elevation in acute injury management. Additionally, there was some suggestion that these modalities may interfere with the natural healing process of the tissue; however, I tend to disagree. Rather than responding to each tweet and trying to get my views across in 140 characters, I thought with such a widespread debate a little blog may be of some use! Thanks to Tom for allowing me to write this and hopefully it may answer some questions, or if not, hopefully provide more debate to excite further research.
So, after thinking about the questions for some considerable time, I went back to the original premise of the inflammatory response I had read in “Cryotherapy in Sports Injury Management” by Kenneth Knight. This is a text on cryotherapy, but also underpins the inflammatory response. The following points made below are taken from the classic text by Knight (1995) and are in no way credit to me. I think the work by Kenneth Knight is excellent, and although nearly 20 years old, the rationale for the use of modalities to control swelling may still be relevant today. So just a brief recap before I give my own views….
Inflammation has a threefold purpose:
- To defend the body against alien substances
- To dispose of dead and dying tissue
- To promote regeneration of tissue
There are five main signs of inflammation, one of which is swelling. In my experience of teaching students at university, speaking to athletes, and even some therapists, there is a common misconception that ‘swelling’ and ‘inflammation’ are the same; they are not. Swelling or edema is an indicator that the inflammatory process is taking place, not the inflammatory response itself. Inflammation IS VERY IMPORTANT in the healing process and diminishing the inflammatory response only delays healing and should therefore be discouraged. However, limiting the swelling, a possible waste product of inflammation may be advantageous.
The part of the inflammatory response I shall focus on is the second point: ‘to dispose of dead and dying tissue’. As a direct result of trauma, the inflammatory response is initiated with pathological and ultrastructural changes occurring in the affected tissues (Merrick, 2002). The disruption of cell membranes leads to a loss of homeostasis and therefore necrosis of the tissues. Whilst the cellular debris releases chemical mediators to initiate the further stages of the inflammatory response, this tissue debris has to be removed from the area before new cells can replace the damaged ones (Knight, 1995). As the inflammatory response continues, not all is positive. As a result of the primary injury, there will be a slower blood flow on the periphery of the injury and decreased blood flow from the damaged vasculature, resulting in less oxygen being delivered to the cells in the vicinity of the primary injury. If prolonged ischemia occurs, healthy cells will die on the periphery to the primary trauma and this is termed secondary ischemic injury (Merrick, 2002).
The swelling at the site of injury results from direct haemorrhaging and edema. The swelling that occurs immediately after injury is the result of haemorrhaging; as therapists we have little control over this. Clotting may take place within 5 minutes and therefore by the time the extent of the injury has been determined, the haemorrhaging has probably stopped. Therefore, it is the delayed swelling which is termed edema that therapists should be concerned with (Knight, 1995). If secondary hypoxic ischemia occurs, there is an increase in cellular debris and destruction of healthy tissue which may take longer to remove and therefore may delay the inflammatory process. With an increase in edema, the distance between the blood vessels and tissue cells increases further, making the diffusion of oxygen more challenging and further cell death will occur. This is a vicious circle, so how can we control and reduce this inflammatory bi-product in order to stop further damage to healthy cells from occurring?
The original premise of ice application by Knight was not to stop the initial haemorrhaging, but to reduce the effects of secondary injury which causes disruption to healthy cells. The idea was that ice application would reduce metabolism, which in turn would limit the demands for oxygen in the tissue on the periphery of the injury, reduce secondary injury, and consequently edema (Knight, 1995). However, following the work of Bleakley and Hopkins (2010), it is now accepted that there is no evidence for the ability of ice to reduce metabolism in the human tissue. This is why in my previous blog “Ice application and its use in sport”, I recommend compression an ice application in the acute setting, rather than ice alone. I still apply ice as it acts as counterirritant and analgesic, but it is the compression that is of value.
So why compression?
Well, according to Knight (1995), compression helps control edema formation and reduces the swelling by promoting reabsorption of this fluid. Personally, I have witnessed greater reductions in swelling when I have compressed the ankle following a lateral ankle sprain in comparison to when I have not. Not only does the compression aid reabsorption, it shuts down the area and therefore will not allow for additional edema to formulate. If there is less tissue debris, there is less free protein which will lower the tissue oncotic pressure. Tissue oncotic pressure pulls fluid from the capillaries and will increase edema (Knight, 1995).
So why elevation?
Elevation lowers capillary hydrostatic pressure and therefore reduces the rate of fluid moving out of the capillary and into the tissues causing a build-up of edema. Just as the pressure increases when you swim to the bottom of the swimming pool due to the volume of water above you, the same is true in the body with the fluid portion of the blood. In elevation, there is less pressure from fluid above and therefore the rate of fluid leaving the capillaries is reduced, therefore reducing edema.
What does this all mean?
Make no mistake, the inflammatory response is an essential part of healing, and no attempt to stop it should be made. Recently, we have all come to understand that taking Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) for acute injuries may be contraindicated for the very reason they halt the required inflammatory response. However, it is prudent to suggest that the application of compression and elevation does not interfere with the inflammatory response, but rather aids it. If it is possible to limit the secondary injury which causes death of healthy cells, there will be a reduction in edema which may enable the latter stages of the inflammatory response to start sooner. I don’t see these modalities as interfering with the inflammatory response but rather aided the removal of its waste products.
Where is the evidence, should we bother?
It must be noted that there is a large void in good quality clinical based evidence for the use of compression and elevation, and therefore it is important to question the use of such modalities. There is a clear need for further research to be conducted in this area to aid our understanding. Despite the lack of research, this does not mean the modalities should be considered contraindicated. It could be argued that we should not use them, although I believe in the rationale provide by Knight (1995) where there is a need to limit secondary injury and therefore the formation of edema. Although perhaps I should not rely on this to make clinical decisions, until evidence suggests the implementation of compression and elevation is contraindicated, I will continue to apply them.
Cryokinetics on the other hand has been shown to be effective in early studies (Grant, 1964; Hayden, 1964), and more recently Pincivero, Gieck and Saliba (1993) presented a case study and conclude that cryokinetic protocols hastened the return to activity. Unfortunately we are limited to these three studies solely examining cryokinetics. Although no randomized controlled trials exist to date, these three studies all report improved outcome with cryokinetics. In my own practice I tend to have a good outcome when using cryokinetics too, so again, I will continue to implement such protocols until research identifies them as contraindicated or that they have no effect. This may not be ideal, but ultimately all reported studies investigating cryokinetics highlight positive outcomes.
In the incidence of an acute injury I still recommend applying crushed ice in a plastic bag and applied to the injury with a compression wrap. The ice will act as an analgesic, whilst the compression and elevation will hopefully control or limit the cellular debris and thus edema formation. I would send the athlete home with the compression, and after 48 hours I would begin cryokinetics. As previously mentioned in “Ice application and its use in sport”, cryokinetics is powerful, and enables exercises to be performed sooner than normally would be possible, thus aiding the removal of swelling. The initial main goal in rehabilitation may be to restore range of movement, with an increased range of motion occurring simultaneously to a reduction in swelling. So, essentially I would suggest the main goal in the acute treatment of an injury and during rehabilitation is to limit and then aid the removal of swelling.
To conclude, it is important to remember that swelling is a sign of inflammation. We do not want to prevent or discourage the inflammatory response but we do want to aid the removal of swelling which may be considered as a waste product. I would suggest that compression and elevation in the immediate management of an acute injury, and cryokinetics in the rehabilitation stage are inflammatory optimisers. Cryokinetics is commonly referred to its ability to facilitate exercise, but ultimately, compression, elevation and cryokinetics may actually facilitate the inflammatory process by removing swelling at an optimal rate to encourage the latter stages of tissue formation and remodelling to take place.
The latter paragraphs in this blog are very much my own views and due to the limited literature these are merely postulated rationales.
Follow Peter on Twitter via @MrThain
Bleakley, C. M. & Hopkins, J. T. (2010). Is it possible to achieve optimal levels of tissue cooling in cryotherapy?Physical Therapy Reviews, 15(4), 344-350.
Grant, A. E. (1964). Massage with ice (cryokinetics) in the treatment of painful conditions of the musculoskeletal system. Archives of Physical Medicine and Rehabilitation, 45, 233-238.
Hayden, C. (1964). Cryokinetics in an early treatment program. Journal of American Physical Therapy Association, 44(11), 990-993.
Knight, K. (1995). Cryotherapy in Sport Injury Management. Champaign, IL: Human Kinetics.
Merrick, M. A. (2002). Secondary injury after musculoskeletal trauma: A review and update. Journal of Athletic Training, 37(2), 209-217.
Pincivero, D., Gieck, J. & Saliba, E. (1993).Rehabilitation of the lateral ankle sprain with cryokinetics and functional progressive exercise. Journal of Sports Rehabilitation, 2, 200-207.