The “C” in R.I.C.E.
- Indications for its use
The “R.I.C.E.” regime has become common knowledge, not only among health professionals, but also within the sporting community and to a large degree the general public, when it comes to the treatment of soft tissue injuries.
“Acute trauma such as sprains, dislocations or contusions evoke numerous physiological responses in the injured tissue, such as hemorrhage, elevated tissue metabolism, a local inflammation reaction, odema and elevated tissue temperature.” (Smith et al, 1993)
The acronym R.I.C.E. stands for Rest, Ice, Compression and Elevation. It was initially known as ICE back in the ‘60’s and ‘70’s, and then seemed to progress to RICE in the ‘80’s. Now in the new millennium you can see documentation of either P.R.I.C.E. or R.I.C.E.D. The “P” stands for prevention and the “D” for diagnosis. These two latter terms are seen in sporting and ACC literature.
The intention of this review is to briefly go over the process that occurs when there is an injury to soft tissue and what stages occur in the healing of these injuries. Then to broadly go over the application and intention of the R.I.C.E. regime as it is explained to many sporting and general populations, with literature to support this regime.
We will discuss the importance of each factor and go further into the component that Doctor Dave Gerrard is quoted saying he considers as the most important, that is compression. By reviewing some recent literature as well as some very sound older papers we will have a greater understanding of what compression actually does.
Our reading and increased understanding will lead on to recommendations and support in the treatment of soft tissue injuries as well as some idea’s that would require further investigation, but could be worth having a look at?
Soft Tissue Injury and Healing
Injury to vascularised tissue initiates a series of responses known as inflammation and repair. Nearly 2000 years ago Celsius described the signs associated with inflammation as swelling, heat, redness and pain.
The initial stages of inflammation are characterised by vascular changes. In the first few minutes vasoconstriction of the arterioles occurs and the walls of the capillaries become lined with white blood cells. This is soon followed by vasodilatation, which increases blood flow and vessel hydrostatic pressure, as well as increasing the permeability of the capillaries and venules. Odema occurs because the escaping cells and fluid create an osmotic gradient, which causes fluid to move into the interstitial spaces. The lymphatic vessels usually clear this fluid, but in the inflammatory state they are overwhelmed.
The vascular response is initiated by the release of chemicals such as histamines, bradykinin and prostaglandin’s. All of these substances cause vasodilatation, and histamines in particular are implicated in the increase in microvessel permeability
The symptoms observed following injury can be explained by the sequence of vascular events. The heat and redness is due to vasodilatation, over expanded interstitial spaces are responsible for the swelling and associated discomfort and the bradykinin and prostaglandin’s stimulate pain.
As well as the vascular response described platelets aggregate and deposit fibrin, creating a blood clot. This fibrin also occludes lymphatic vessels, further preventing the draining of fluid. Leukocytes are attracted to the site of injury, and via phagocytosis rid the site of contaminating bacteria and debris, clearing the injury site and setting the stage for tissue repair.
b) Tissue Repair and Remodeling
The process of tissue repair is a very complex one and for the purpose of this assignment the details are not necessary. Suffice to say that early tissue repair is characterised by proliferation of new blood vessels and the formation of new connective tissue. This phase lasts from approximately 48 hours through to 3-6 weeks. The remodeling stage begins around 2 weeks and can last up to 12 months or more. In this later phase remodeling of the connective tissue takes place and further increases tissue strength.
Lehto et al, looked at the healing of muscle injury and highlighted that there are two processes competing, that is, the regeneration of injured muscle and the production of connective scar tissue. Extensive scar tissue can lead to a dense mechanical barrier, preventing the regeneration of muscle tissue.
The phases of inflammation, repair and remodeling are not of set duration and often overlap, however it is important for the physiotherapist to have an understanding of the process and the approximate time frames.
R.I.C.E. – Rest, Ice, Compression and Elevation
The intentions of the R.I.C.E. regime are not to speed healing, but to ensure the body has the best environment to have effective healing, in the shortest duration possible, and avoiding any complications. With the understanding of inflammation and repair it can be seen that the R.I.C.E. regime is targeting the inflammation, attempting to minimise this stage and therefore promote the repair and remodeling phases
Before focussing on the compression aspect let us look at the full picture of RICE as it is intended to be a complete package approach to the first aid of soft tissue injury.
Rest – this means specific rest of the injured part. ACC literature suggests this resting is to avoid any further damage to the injury. It assists in the formation of a blood clot and reducing ongoing bleeding. Lehto et al demonstrated, specifically in muscle injury, that immobilisation after injury accelerates granulation tissue production, but if continued for too long, leads to contractions of the scar, and poor structural reorganisation of the muscle and connective tissue. From their study they conclude that in the inflammation stage it is ideal to adequately rest the injured site, but then progress activity in the remodeling phase.
Ice – the ACC recommendations are to apply ice wrapped in a towel over the injured site for 20 mins, every 2 hours awake for the first 48 hours. The goal being to decrease pain, swelling and bleeding.
Ice has been advocated as the initial management of soft tissue injuries because of cold induced vasoconstriction reducing the inflammatory reaction, including odema. A very enlightening study by Smith et al in 1993 studied the microcirculation in the muscle of a rat following a contusion, and subsequent cryotherapy (ice application). In this study the investigators inserted a chamber into the muscle allowing microvascular observations in the conscious rat. This appears to be a very helpful investigative tool, and it is a shame this method isn’t utilised in more studies. The results of this study showed that following a contusion the arteriolar diameters are increased, with or without the application of ice. Ice alone, (nil contusion) has no effect on arterial diameter, however, has an effect of increasing venular diameter. Contusion alone does not effect venuals.
This study concludes that ice application favours filtration and reabsorption of fluid, and thus reduces odema.
The above study was the only one cited that truly investigated the microcirculation. Other studies quoted “vasoconstriction” as a result of cooling, which decreased blood flow and therefore modified the inflammatory reaction. Herme et al, 1993 identified some important reactions to early cryotherapy. As well as mentioning vasoconstriction, they pointed out that if cold therapy is applied for lengthy periods and the tissue temperature falls below 25 degrees Celsius, blood vessels dilate and therefore has an adverse effect due to increased bleeding and inflammatory response. These authors found that cryotherapy did not alter the outcome of muscle regeneration, but did seem to reduce pain and muscle spasm.
A study by Thorsson et al in 1985 looked at the effect of local cold application on intramuscular blood flow. Blood flow was measured using Xe clearance technique, technique described in many blood flow papers, which appears to be the gold standard (Lindbjerg, 1965). This study showed that during the first 5 mins of cold pack application there was no reduction in blood flow. However after 10 mins there was 35% (after running) and 50% (at rest) reduction in blood flow as compared to the opposite – control leg. Once the cold packs were removed blood flow continued to reduce by a further 65-70% over the next 10 mins. The authors concluded that because of the 10 min delay in blood flow reduction, compression was the best instant option to reduce haematoma size.
Interesting to note these authors did discuss that direct cooling did cause vasoconstriction of the blood vessels as well as a possible increased blood viscosity, thus reducing blood flow.
Briefly another study showed that the temperature of the water going through the cryocuff didn’t have an effect on the reduction in swelling, rather the pressure was the key indicator.
This literature suggests that the main role of ice in the acute injury is to reduce pain, and decelerate the local cellular metabolic rate minimising damage by tissue hypoxemia, rather than reduce swelling. Cold application also impairs conduction of afferent sensory input and decreases muscle spindle sensitivity to stretch thus reducing muscle spasm.
Elevation – ACC literature suggest that elevation will assist in the reduction of bleeding and swelling. A paper looking at the arterial blood flow during elevation showed that the arterial pressure was reduced with elevation and this in turn reduced blood flow. The elevated foot showed signs of vascular ischaemia. (Nielsen, 1983).
Compression – the key role of compression is to reduce swelling and bleeding. The objective of this assignment is to look into this in further detail.
The Use of Compression
One of the key objectives of the R.I.C.E. regime is to reduce the presence of odema, and thus prevent delayed healing due to poor oxygenation. Odema is also documented to reduce tendon gliding and causes joint lining and ligamentous adhesions, as well as general immobility (Airaksinen, 1989). It appears that the use of external pressure devices help the body’s own mechanisms to reduce interstitial fluid, by encouraging lymphatic and venous return (Michlovtz).
Curry first employed the principle of using external pressure in 1966, with the use of air splints in fractured limbs. The manufactures suggested the pressure of 40mm Hg, however in 1966 Ashton reported this pressure resulted in marked decrease in blood flow and she recommended 30mm Hg. This recommendation was supported by a study done by Campion et al two years later, 1968.
Pressure and Blood Flow – the theory
Before reviewing, both recent and older papers in the effectiveness of the use of compression in the reduction of blood flow and odema, let us first gain an understanding of the theoretical considerations of pressure on blood flow. This has been very well explained by Ashton in 1975, in a paper titled “The Effect of Increased Tissue Pressure on Blood Flow”.
The greatest factor determining the rate of blood flow through a vascular bed is the diameter of the arterioles. The forces acting upon the arteriole walls determine this diameter. Very simply that is the intravascular pressure pushing the diameter out and this is opposed by the surrounding tissue pressure pushing the diameter in.
If the surrounding tissue pressure is negative the intravascular pressure will have a vascular expanding force resulting in vasodilatation, and if the surrounding tissue pressure is positive this will result in vasoconstriction. It is important to note this is a very simplistic model, and this relationship is not necessarily linear due to the distensibility of the vascular walls.
The capillaries are vulnerable to changes in tissue pressure due to their intimate relationship to extracellular spaces. “Some investigators believe that tissue pressure has an important autoregulatory role and have suggested that in situations of elevated tissue pressure, capillary collapse rather than arteriolar closure may be an important factor in limiting blood flow” (Ashton, 1975).
In 1983, Nielsen found that if the compression on a blood vessel were equal to that of local diastolic blood pressure, blood flow would cease.
Odema as the Increased Pressure
Zelis et al, in 1969, measured the influence of odema on blood flow, in the dog’s forelimb. It was concluded “that the increased transudation of fluid into the surrounding tissue during partial venous occlusion results in an elevated tissue pressure which leads to compression of the distal end of the capillaries”. So, increased tissue pressure does limit blood flow.
Evidence for the Use of Compression
On the field and in the clinics, sports practitioners use elastic bandage to create compression. Immediately following an injury maximal compression should be applied in order to stop bleeding to the site of trauma. In the rehabilitation stage compression is useful in minimising the risk of new bleeding and assisting in the prevention and reabsorption of odema.
Thorsson et al, 1987, investigated the effects of different compression techniques on blood flow in large muscles. Blood flow in the thigh was measured in two degrees of compression. The maximum compression exerted a cutaneous pressure of 85 mm Hg and caused an immediate ceasation of blood flow. Moderate compression exerted a pressure of 40 mm Hg and reduced blood flow by approximately 50%. This external pressure was transmitted to tissue at least 3 cm below the skin.
As mentioned earlier, Neilsson found that intramuscular blood flow ceased when the pressure reached the level of diastolic blood pressure. Thorsson’s study supported this concept noting that every individual in his study had a diastolic pressure of less than 85 mm Hg. They suggested that individuals with hypertension would require greater compression forces.
A study which showed the compression bandage to not be useful was by Airaksinen et al., 1990. These investigators compared elastic bandaging Vs elastic bandaging and Intermittent Pneumatic Compression in the treatment of acute ankle sprains. They concluded that elastic bandages alone were not as effective as the use of IPC daily for 30 mins with elastic bandaging in between. The results showed decreased swelling, improved ankle ROM and less pain, over a 5-day treatment period and 4 weeks follow up. My criticism of this paper was that the bandaging technique and pressure exerted by the bandaged was not measured. The only measurement they gave was that the IPC was at 60mm Hg. It is conceivable that the bandage was of poor quality and not providing the necessary pressure, thus the group that did receive some 60mm Hg pressure at times was getting better results.
These same authors did a study a year earlier looking at IPC vs. no treatment in a chronic condition such as post cast immobilisation in fractured lower limbs. The IPC certainly showed significant benefits vs. nil treatment. This study would have been interesting to see had they used continuous high quality compression bandages. We would therefore have some interesting data on bandaging in the chronic situation.
The papers briefly outlined above give very strong indications that compression is key in the reduction of swelling in the acute injury. The frustration is the lack of evidence of what is the best type of compression modalities. The IPC looks very good, but as mentioned above, how good was the bandaging it was compared with.
The most recent paper found on this compression topic was titled “Influence of Compression Therapy on Symptoms Following Soft Tissue Injury from Maximal Eccentric Exercise”. This was by Kraemer and colleagues – 10 of them to be exact! And was published in 2001.
In the literature the use of eccentric exercise is often used to induce an injury. It is obviously not the same as a sprain or contusion but does result in similar symptoms that are pain, swelling, decreased ability to generate force and loss of motion. A paper in 1995 by Chleboun showed that IPC temporarily decreased swelling and muscle stiffness, but had no effect on the loss of strength following eccentric exercise.
Kraemer et al, looked at the use of constant compression via a compressive arm sleeve following eccentric exercise. The compressive force was determined at 10mm Hg. The experiment group wore this sleeve for 5 days immediately following the eccentric exercise. This study showed convincing significant results, in favour of the use of compression. By day 3 the compressed group had less strength and power deficits than the control group, they had no increase in arm circumference, as compared to the control group having 2 – 3cm increases in relation to pre exercise measurements. The experimental group also had no change in resting elbow angles, whereas control group had increased flexion and the experiment group also had less perceived soreness than the control group.
The authors discussed that the inability to generate tension in the biceps following the exercise may be due to both pain and structural damage. The absence of swelling and the reduced soreness in the experimental group may have resulted from the compression. They also commented that the sleeve might have acted as an external mechanical support to the muscles, thus assisting in a more rapid recovery of force production. They concluded that the compression reduced the swelling, and therefore compression looks to be a useful intervention in the management of soft tissue injuries.
This last reported investigation shows some very strong support for the use of compression. It is a very recent paper, had reasonable numbers (20 total), and showed statistically significant differences in 4 factors attributing to improved recovery following injury. The obvious concern is that this was injury due to eccentric exercise, not to an actual sprain or contusion. The insult was to muscle tissue, so we would be assuming that the positive results would hold true in a sprained ligament, and joint dysfunction situation.
It was interesting to see the marked positive results in this study given that the level of surface pressure was so low. Previous discussed pressure levels were in the domain of 40 – 80mm Hg, and this study was only 10mm Hg. Does this suggest that greater pressures are not necessary, or the positive outcomes could have been even greater had the compression sleeve exerted more force. It would have been interesting had they had a second and even third experimental group receiving pressure of say 40 and 80mm Hg each respectively.
It is important to understand why we want to reduce this inflammation time. As explained, we want to provide the ideal environment for the repair and remodeling phase of healing. The presence of odema for lengthy periods of time interferes with proper oxygenation, resulting in poor healing.
There is very good evidence to suggest that compression in particular, reduces the presence of swelling. This can then be supported by rest to reduce any further damage, by elevation to reduce blood flow and by ice to decrease pain and slow down metabolism.
The use of compression is best if immediate, and of a strong nature. Instead of the immediate application of ice onto soft tissue injuries, the immediate application of compression will lead to an improved healing environment. In practice this would mean that following an ankle sprain, a quadriceps contusion or a muscle tear a firm elastic bandage like the ACE brand would be utilised. In the event of an ankle sprain, specific compression such as the horseshoe, would be further advantageous.
Ice should be applied over the compression, as well as the limb being elevated. After 20 mins of ice it should be removed, but the compression should remain constant.
This is not new information, but does give us a better understanding of each of the roles of the rice regime, and in particular the importance of compression and the need for it to be immediate.
Where I think compression perhaps could be used, and is currently not, is in the recovery of muscles post exercise. Kraemer’s study with the compression sleeve after biceps curls gives good indications for this purpose. Obviously trials and investigations would be needed, but maybe we will see our national team athletes in compression suits between games and races at major events! – WATCH THIS SPACE!
- Andersson, S. Ibuprofen and compression bandaging in the treatment of ankle sprains. Acta Orthop. Scand. 54, 1983.
- Ashton, H. The effects of increased tissue pressure on blood flow. Clin. Orthop. 1966.
- Airaksinen O. Elastic bandages and intermittent pneumatic compression for treatment of acute ankle sprains.. Arch. Phys. Med. Rehab Vol 71, 1990.
- Airaksinen O. Changes in posttraumatic ankle joint mobility, pain, and edema following intermittent pneumatic compression therapy. Arch. Phys. Med. Rehab Vol 70, 1989.
- Campion, E.C., D.C. Hoffmann, and R.P. Jepson. The effects of external pneumatic splint pressure on muscle blood flow. Aust. N.Z. Journ. Surg. 1968.
- Chlebourn, G. S. Intermittent pneumatic compression effect on eccentric exercise-induced swelling, stiffness and strength loss. Arch. Phys. Med. Rehab. Vol 76, 1995.
- Dahn, I., N.A. Lassen, and H. Westling. Blood flow in human muscles during external pressure or venous statis. Clin. Sci. 1967.
- Kraemer, W. J. Influence of compression therapy on symptoms following soft tissue injuries from maximal eccentric exercise. JOSPT. 31(6), 2001..
- Lehto, M. et al. Collagen and fibronectin in a healing skeletal muscle injury. Jrn Bone and Joint Surg. 1985
10. Michlovitz, S. (1996) Thermal Agents in Rehabilitation. Third Edition. Philadelphia : F.A. Davis.
11. Nielsen, H.V. External pressure – blood flow relations during limb compression in man. Acta Physio. Scand. 1983
12. Nielsen, H.V. Arterial pressure – blood flow relations during limb elevation in man. Acta Physio. Scand. 1983
13. Smith, T.L. New skeletal muscle model for the longitudinal study of alterations in microcirculation following contusion and cryotherapy. Microsurgery Vol.14, 1993
14. Thorsson, O., L et al. The effect of local cold application on intramuscular blood flow at rest and after running. Med. Sci. Sports. 1985.
15. Thorsson, O., L et al. The effect of external pressure on intramuscular blood flow at rest and after running. Med. Sci. Sports. 1987.
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Katrina is a NZ trained physio holding a Masters degree. She is one of the few qualified Manipulative Physiotherapists on the beautiful Sunshine Coast in Australia.
Still a strong All Blacks New Zealand Rugby supporter, (we will forgive her for that!!) Katrina enjoys what the coast offers, paddling and swimming regularly with the Maroochydore SLSC. As a former international athlete (1992 World Surf Ski Champion), a national kayak coach and a recent finisher of the Coolangatta Gold, Katrina has a very good understanding of the athletic body and the need to keep training. Kat’s passion is her two dogs, Mana and Kia. Her canine and physio interests combined in completing a Level 1 Canine Physio course last year, and she is very happy to exchange ideas about your four legged family members.
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