Identify which modalities are effective and clinically useful for particular pathologies.
Identify incorrect modality application techniques that can compromise clinical effectiveness.
Choose the appropriate clinical use or uses for a specific modality.
Explain the effect that cryotherapy has on certain biologic functions in the acute care of an injury.
Explain the effect that compression and elevation have on certain biologic functions with an acute injury.
Choose appropriate modalities based on their clinical efficacy for use during the rehabilitation process.
Explain when to initiate, modify, and discontinue modality protocols based on patient needs and rehabilitative goals.
Optimal care of athletic injuries is different from the typical care that most musculoskeletal/orthopedic patients receive. Typical care of nonathletic patients with musculoskeletal injury produces good outcomes over time, but the time line is frustratingly slow for an athlete trying to return to full levels of play this season. Typical care takes too long to initiate, is reevaluated too infrequently, is too conservative in approach, and leads to considerable noncompliance by the patient. To meet the more aggressive time line and functional demands of an athletic patient, we must recognize the interrelated nature of evaluation, acute management, and rehabilitation and see them as a continuum. This continuum begins the moment the injury occurs, and immediate initiation of care for an athlete offers a critical time savings that is lost when care is delayed until the next day or next week. It is often the difference between returning to play in 2 weeks instead of 6.
Appropriate therapeutic techniques, when applied at appropriate times, can radically reduce complicating factors, such as edema and neuromuscular inhibition, which delay the patient’s eventual return to normal function. Therapeutic modalities are one set of tools that can play a central role throughout the rehabilitative continuum but are most important early in the process. Like all tools, however, modalities have specific uses in specific situations. They are of little benefit when used for the wrong reason, with the wrong technique, or at the wrong time. At their best, therapeutic modalities are an exceptionally useful complement to the rehabilitative process but are not a replacement for it. At their worst, therapeutic modalities can be blindly applied and ineffective tools that waste the time of both the patient and clinician. This chapter explores the general use, rehabilitative timing, and specific application of therapeutic modalities for the care of the injured athlete. More importantly, the literature on the clinical efficacy of common therapeutic modalities is examined to identify which appear to be effective and which do not.
General principles of theapeutic modalities
What Are Modalities and Why Use Them?
Simply stated, modalities are therapeutic techniques. They include such dissimilar things as surgery, medications, and psychologic counseling, none of which are appropriate for independent use by allied health practitioners, such as athletic trainers and physical therapists. The modalities with which we are more familiar and that are more appropriate for our use are generally referred to as therapeutic modalities and include primarily physical agents, such as heat, cold, sound, electromagnetic energy, and mechanical energy (such as massage and compression).
Modalities As Part of a Comprehensive Rehabilitative Program
The single most important point to remember about therapeutic modalities is that they are tools and should never be used as replacements for a comprehensive rehabilitative program. Modalities are an adjunct to rehabilitation. That is, they can help a clinician and patient to accomplish a goal, but therapeutic modalities are not usually capable of accomplishing goals in isolation. Instead, they should generally be combined with other rehabilitative techniques (especially therapeutic exercise) and should not be viewed as a substitute for these techniques. For example, using only ice massage before practice for someone with patellar tendinitis is not the same as using a comprehensive rehabilitative program that involves counteracting chronic inflammation; minimizing sclerosis; correcting biomechanics; improving strength, endurance, and power; and limiting overuse. Conversely, some practitioners will make statements such as, “I don’t use modalities, I prefer exercise instead,” as though their choices were between exercise and modalities. It is seldom correct to choose between these approaches because they are not used for the same purposes. Instead, it would be better to understand how each approach can be useful to achieve a goal and then choose a plan of care that combines the best available elements, often both exercise and modalities, to achieve the goal.
When to Use Modalities
Like any tool, a therapeutic modality should be used for a specific purpose and at a specific time. You would use a screwdriver to tighten a screw but not to drive in a nail. Likewise, you would use cryotherapy to counteract acute inflammation but not to counteract the loss of range of motion associated with prolonged immobilization. Although it seems obvious, the key to using modalities appropriately is to match the specific physiologic effects of the modality with the specific rehabilitative goal for the patient. The apparent corollary to this statement is that if the physiologic effects of the modality do not match the rehabilitative goals, the modality should not be used, or if the goals have been met, the modality should be discontinued. Even though these principles are almost self-evident, it is not uncommon for novice clinicians to make the mistake of using a modality without having a specific goal in mind or failing to discontinue a modality after the goal for which it was chosen has been achieved.
Most practitioners do a fine job of identifying patient problems, creating specific goals related to these problems, and choosing modalities to help achieve these goals. However, advanced practitioners are also skilled at determining when a modality should be initiated within the rehabilitative continuum. With modality use, the timing is often critical. If cryotherapy and compression are applied within the first few minutes following trauma, the secondary injury response can be substantially suppressed, thereby saving time and tissue. Waiting until the next day—or even perhaps just a few hours to begin such care—will almost certainly be pointless.
Likewise, it is critical to understand when use of a modality should be discontinued. In the current era in which health insurance providers are attempting to limit billed charges, it is important to be cost-effective in using rehabilitative programs, and efficient and effective use of therapeutic modalities is an important element of a cost-effective program. However, some practitioners continue to use a modality even after the modality’s goal has been achieved because they lack a goal-oriented focus in the use of modalities. To avoid this error, practitioners should ask themselves four questions before each modality treatment ( Box 8-1 ).
What specific goal am I trying to achieve today by using this modality?
Am I using the best available modality (and correct application technique) to achieve this goal?
What specific criteria am I looking for to indicate that I should stop today’s treatment with this modality?
What specific criteria am I looking for to indicate that I have finished using this modality as part of this patient’s treatment plan? (This final question is often overlooked.)
How to Use Modalities
This chapter is not intended to be a substitute for a formal course in the application of therapeutic modalities. That topic is somewhat more comprehensive, and quite a few very good modalities texts provide a greater level of instruction in the application of modalities. This chapter instead reviews the general elements common to all modality applications and discusses some specific aspects of the application and the efficacy of each modality presented.
Legal and Appropriate Use of Modalities
Physical agents are appropriate for application by clinicians in any of several different professions, such as physicians, athletic trainers, and physical therapists, although their actual use is generally governed by the practice acts of individual states. Consult your state’s regulations before applying therapeutic modalities. A general provision in most practice acts is that practitioners are required to have specific training in both therapeutic modality theory and the application techniques for these modalities. A good principle to follow is that you should never use a therapeutic modality that you have not been specifically trained to use. Although this seems obvious, it is particularly relevant where students are concerned. Students should not apply therapeutic modalities until they have completed the relevant course work to support their modality use.
In addition to state regulation, many therapeutic modalities, including ultrasound, diathermy, lymphedema pumps, lasers, and others, are classified as medical devices and are therefore regulated in the United States by the Center for Devices and Radiological Health, part of the Food and Drug Administration ( www.fda.gov/cdrh/consumer/mda/index.html ). Different devices within the same category, such as lasers, may carry different classifications and be subject to different levels of regulation.
Another important aspect of the legal and appropriate use of modalities involves prescriptions for treatment. In most states, prescriptions for outpatient rehabilitation are required. Although specific prescriptions for each modality are sometimes required, frequently they are not, and use of therapeutic modalities is left to the professional judgment of the clinician. However, some modalities, particularly those involving pharmaceutical delivery (iontophoresis or phonophoresis), always require a specific prescription.
As is true with any rehabilitative procedure, practitioners assume some degree of liability with the use of therapeutic modalities. To maximize patient safety and minimize the liability associated with the use of therapeutic modalities, a number of policies and procedures should be adopted ( Box 8-2 ).
Good professional judgment must be used. Exercise of good professional judgment and application of a modality that you have not been trained to use are mutually exclusive. Therefore, modalities should be used only by those formally trained (and legally permitted) to use them.
Every modality must be in good working order and have recently been calibrated to ensure safe use of it.
Every planned modality treatment for every patient should be evaluated to ensure that it is appropriate with regard to the indications and contraindications for use of the modality.
Every modality treatment should be monitored for both safety and efficacy throughout the treatment. Treatments causing adverse effects should be discontinued immediately, as should treatments that are not effective.
Unattended modality treatments are obviously to be avoided, as are patient self-applications of most modalities.
General Application Procedures
Even though the specific application procedures for each therapeutic modality differ, all modality treatments have some commonalities. One of the most important, actively involving patients in their own care, is frequently overlooked. Before any modality is applied, it should be explained thoroughly to patients. Such explanations allow patients to make informed decisions about consent to treatment. Similarly, it also helps patients understand the specific goals and effects of the treatment. In addition, it helps patients understand any potentially harmful complications, such as excessive heating, and lets them know that the practitioner should be told if a treatment causes discomfort so that it can be modified before becoming a problem. Patients should also be asked whether they have any questions about the use of the modality in their treatment. An additional bonus of involving patients in their own care is that those who feel like a partner in their own care are frequently more compliant with their rehabilitative programs. Box 8-3 lists some common items that should be explained to patients before application of a modality.
State which modality is to be used: for example, “We’re going to use some ice on your knee for about 20 minutes after your exercise today.”
Inform the patient of the specific goal for the modality and what the modality does: for example, “The ice helps reduce any inflammation we may have caused today and it helps reduce your soreness.”
Rule out contraindications: for example, “Do you have any circulatory or neurologic problems, such as Raynaud disease?”
Explain what the patient should expect: for example, “It will feel very cold and it’ll probably be a little bit uncomfortable until you get used to it.”
Explain the precautions and reasons to discontinue the treatment: for example, “You shouldn’t feel any pain, numbness, or tingling down in your leg or foot, but if you do, let me know right away and I’ll take the ice off.”
Explain the criteria for discontinuing the use of this modality overall: for example, “We’ll quit using the ice if it’s not giving the result we want or when you quit having inflammation or soreness after your exercises.”
In addition to making patients partners in their own care, another commonality with all modality treatments is in the actual setup for the treatment. The physical preparations for use of a modality involve two items. The first is preparation of the patient. Before any other aspect of patient preparation, you should determine whether a prescription for the modality treatment is required and present and whether the prescription has expired or the number of permissible treatments has been exceeded. When this step is completed, the remainder of patient preparation generally involves reviewing the specific goal of the treatment along with the indications for the modality to ensure that no contraindications are present, review the patient’s previous response to the treatment (ask the patient), and ensure that the patient consents to the treatment. The outcome of any previous treatments should also be reviewed. Physical preparation of the patient generally involves removing or adjusting clothing as necessary for the specific modality and positioning the patient as comfortably as possible. This last aspect is critically important when modality treatments are given for more than just a few minutes.
The second aspect of physical preparation is the physical setup of the modality equipment and treatment area. First and foremost, the patient’s safety must be ensured through a quick but complete safety inspection of the equipment and area before use of any modality ( Box 8-4 ). After the equipment safety inspection is completed, you should make sure that all the necessary accessories for the treatment are present before actually beginning the treatment.
Check the condition of any patient cables or electrodes and ensure that they meet the required standards.
Confirm that the equipment is operational.
Confirm that patient safety switches are operational.
For electrical modalities, ensure that the equipment is properly grounded and that the equipment is used only with outlets equipped with ground-fault circuit interrupters.
Evaluate the treatment area to make sure no hazards are present, such as standing water or unstable treatment tables.
Just as there are commonalities in the setup for all modality treatments, there are also commonalities in the posttreatment procedures. Most of these are obvious and include removing the patient from any equipment, returning the equipment to its appropriate storage area, and assisting the patient in wiping off any treatment-related water, gel, or other material as necessary. The most important aspects of the postapplication period are less obvious and often overlooked, particularly in competitive athletic settings. The first is record keeping. It is absolutely critical that practitioners record the treatment parameters used during application of the modality. Recording the parameters allows a different practitioner to continue the course of treatment if you are unavailable. Without such a record, other practitioners are either forced to guess your protocol or ask the patient what has been done. At no time should a practitioner ever have to ask the patient which treatment parameters have been used because even the most involved of patients cannot be expected to understand the parameters or explain them correctly. It is also important to make specific note of any complications that occurred during the treatment, as well as the patient’s response to the treatment.
Another postapplication procedure often overlooked is reviewing the response to the modality treatment to determine whether the goal of the modality has been met, whether the treatment has been effective, or whether the treatment should be continued. A plan for discontinuing the modality treatment should be in place to help with this last issue.
Separating facts from fiction
Determining whether specific modalities are effective and clinically useful is often more difficult than it would outwardly appear. We will see that a number of clinically common modalities may not be as effective as once thought and that the clinical efficacy of modalities that are known to be useful can easily be compromised by incorrect application techniques. Unnecessary, incorrect, or inappropriate use of modalities has been a topic of discussion for clinicians and researchers, as well as for health insurance providers, who are carefully scrutinizing outcomes research to determine whether they should reimburse for certain modalities treatments. Unfortunately, poorly designed modality clinical trials or trials in which modalities are used incorrectly have led to poor outcomes that have negatively influenced the use of modalities in clinical practice. In addition, several very effective therapeutic modalities, such as short wave diathermy and low-power lasers, are not in common use because we are either not sufficiently aware of them, not trained to use them, or not able to afford to purchase them. To adequately examine the efficacy of therapeutic modalities, a few basics about modality research must first be reviewed.
In examining the history of modality use, one obvious trend is that clinical practice has almost always preceded scientific research. That is, clinicians pass along anecdotes about how they have used modalities and the results that they have observed. This has led to a great deal of modality folklore that in reality has very little basis in fact. We really did not see a meaningful body of scientific research on therapeutic modalities until the last few decades. This modality research has been conducted by scientists and clinicians from a number of different professional fields, including early work by physicians such as Lewis, who examined cold, and Lehmann et al, who examined heat. Most of the more recent research has been conducted by researchers from allied health fields, such as athletic training and physical therapy. In fact, the overwhelming majority of recent research on the clinical use of therapeutic modalities has been completed by athletic trainers, yet ironically, some states still prohibit athletic trainers from using these modalities.
The frequently observed trend of clinical practice preceding scientific inquiry with therapeutic modalities has greatly influenced research on modalities. Many, if not most modality researchers began their careers as clinicians. This clinician background has resulted in the use of many clinically relevant and relatively unsophisticated dependent variables in modalities research. Such clinical variables typically include range of motion, strength (usually isometric or isokinetic), swelling, pain/soreness, and various functional measures. There is also a body of research that has gone beyond clinical variables and examined slightly more basic variables, such as temperature, electromyographic activity, blood flow, and tissue stiffness. In recent years, a small number of laboratories have also examined very basic variables such as cell metabolism, protein expression, gene expression, enzyme activity, and cell proliferation.
The simpler and more clinical variables have obvious value to clinicians and are very useful in establishing outcomes, a type of research that is very helpful in supporting reimbursement activities. Unfortunately, these variables are generally less useful in helping establish modality theory. Most clinical variables are, at best, secondary manifestations of the effects of modalities. That is, modalities generally do not directly cause the effects seen in clinical variables, but instead they cause these clinical effects indirectly. For example, continuous ultrasound treatments do not improve range of motion directly or meaningfully. Instead, continuous ultrasound causes vibration between molecules in the tissue. The vibrations increase the temperature of the tissue, and the increased tissue temperature may allow tissues to become more elastic. In turn, increased elasticity may allow stretching techniques to be more effective. Finally, more effective stretching or joint mobilization may improve range of motion and do so more easily because of the improved elasticity. Without combining the stretching or mobilization with the ultrasound, the ultrasound is probably useless in this scenario.
The indirect relationship between most modalities and clinical variables presents problems in establishing theories because the clinical variables are easily confounded. That is, many factors might influence the clinical variables and can potentially mask or intensify the effects of the modality. The more steps between the modality’s believed direct effect and the clinical variable, the greater the chance that something can become confounded along the way. If this happens, we may not be able to observe a strong effect that we can use to support or refute the underlying theory regarding the modality. Likewise, the more steps that the clinical variable is removed from the direct effect, the greater the number of opportunities for a methodologic mistake to prevent the desired outcome. When we are examining only a relatively limited number of modality protocols and do not see an effect, it is difficult and probably inappropriate to make broad generalizations about the modality. A classic example of this problem is an ultrasound review paper by Robertson and Baker ( Table 8-1 ). The conclusion drawn in this review was that therapeutic ultrasound is not an effective adjunct for improving range of motion or pain. The effect of this review was a reluctance by many to use therapeutic ultrasound because they feared that insurance providers, in the wake of this paper, might not reimburse for such treatments. Unfortunately, the research studies reviewed in this paper generally used clinical variables and rather ineffective ultrasound application protocols, and most did not observe a positive effect. The use of substandard ultrasound protocols meant that the expected direct effect of ultrasound would have been smaller. A smaller than expected effect would have been further diluted because there were a number of physiologic steps between the presumed effect of ultrasound and the clinical variables studied. In fact, in examining the methods in the studies from this review, it is clear that most were wholly inappropriate and were very unlikely to cause a useful effect, and not surprisingly, no useful effects were seen.
|Problem Area||Problematic Protocol Used||Problem With the Protocol|
|Effective radiating area (ERA)||Thermal ultrasound applied to an area 5 times the size of the faceplate||The ERA is always smaller than the ultrasound faceplate, and the treatment area should be no larger than twice the ERA to induce an effective increase in temperature.|
|Thermal ultrasound applied to an area 10-25 times the size of the faceplate|
|Thermal ultrasound applied to an area 10 times the size of the faceplate|
|Nonthermal ultrasound applied to an area 10 times the size of the faceplate||No published evidence has shown that nonthermal ultrasound applied to such a large area produces an increase in healing.|
|Ultrasound frequency||1-MHz ultrasound used to treat superficial tissues (epicondylalgia)||1-MHz ultrasound is effective at depths of 2.5 to 5 cm. The epicondyles are considerably more superficial and should have been treated with 3-MHz ultrasound.|
|Treatment time||1-MHz ultrasound applied for a 3-minute treatment to test joint mobility with a treatment size at least 12 times as large as the ERA||This would not have produced any meaningful change in temperature because of the huge treatment area. Even with an appropriate treatment area, it would be estimated to produce only a 1.2°C increase in temperature. An increase in temperature of at least 3°C to 4°C would be required to produce changes in elasticity.|
|7 of the 10 studies used a 25% pulsed duty cycle, with treatment times varying from 2 to 15 minutes||The two studies that did show an effect of ultrasound both used 15-minute treatment times. The shorter treatment times very likely explain the lack of effect.|
Although much of the research on the use of modalities has focused on clinical variables, a surprisingly large number of effects of modalities are commonly accepted by clinicians but have little, if any, scientific support. In some cases there is even scientific evidence to the contrary, yet these widely held clinical beliefs still persist. One common example of this is cold-induced vasodilation with cryotherapy. Similarly, incorrect beliefs still circulate regarding contrast baths for reduction of edema and transcutaneously applied microcurrent for muscle injuries.
Cold-induced vasodilation, the notion that cryotherapy treatments can cause blood flow to increase above baseline levels, is still touted as an effect of cryotherapy by some clinicians. In fact, you may still occasionally hear someone incorrectly suggest that cold should not be used for more than about 30 minutes to avoid this phenomenon. This is completely false. In reality, cryotherapy does not increase blood flow above baseline levels at all. This has been repeatedly demonstrated for more than 60 years!
Where to Go From Here
In the future, modality research needs to accomplish two important tasks. First, we need to establish a body of suitable outcomes research documenting the efficacy of our modality treatments. Although we are continuing to learn about the physiologic effects of modalities, there is a wholly inadequate body of outcomes research related to the use of these modalities. Research is sorely needed to confirm whether our physiologically based treatments actually improve the outcomes of the patients whom we treat. This outcomes research must examine multiple protocols for each modality to refine our clinical techniques and maximize the benefits that our patients receive. Second, we need research that focuses more on the direct effects that we think are caused by the modalities. Generally, this means more research on the basic science variables that we think are the root of the clinical effects. When we establish and understand the very basic effects caused by our modalities, we will be better able to refine our treatments to maximize the clinical benefits of modality treatments. For example, we are very confident that cryotherapy is useful in minimizing the unwanted consequences of acute injury. However, we are not completely certain of the precise mechanisms by which this modality is effective. Even though a number of papers have proposed theories, these theories have yet to be confirmed. In fact, we do not yet know the answers to such basic cryotherapy questions as how cold the injured tissues need to be or how long the cold should be applied to be most effective. Answering the basic questions of how a modality works physiologically will allow us to better examine the clinically relevant questions of how to maximize the benefit of the modality.
Modalities for acute care
The use of therapeutic modalities for acute injuries is governed by a specific set of clinical goals ( Table 8-2 ). The most important of these goals is thought to be limiting the total quantity of tissue damage associated with the injury. Because we know that the time required for tissue healing is partially dependent on the quantity of tissue damaged, a smaller amount of damaged tissue should translate into a quicker repair and faster return to sport.
|Acute Care Goal||Choice of Modality|
|Reduce pain||Cryotherapy, TENS|
|Minimize edema formation||Cryotherapy, compression, elevation, microcurrent(?)|
|Minimize bleeding||Cryotherapy, compression, elevation|
|Minimize secondary injury||Cryotherapy|
|Minimize acute inflammation||Cryotherapy, microcurrent(?)|
|Prevent further injury||Immobilization/protection|
When an injury occurs, the immediate tissue damage associated with that injury is referred to as the primary injury. This damage includes disruption of a variety of structures, including ligamentous, tendinous, muscular, vascular, nervous, and bony tissues. Because primary injury occurs immediately with the trauma, it has already occurred before the injury is even evaluated. We can do nothing to limit the magnitude of this primary tissue damage apart from immobilizing the injured area to prevent further tearing of partially torn tissues. However, primary damage is not the end of the story. The pathophysiologic response to primary injury can lead to additional tissue damage, known as secondary injury, in tissues that were otherwise not initially injured. For example, disruption of blood flow resulting from an injury to vascular tissue can lead to ischemic injury of the otherwise uninjured tissues that they supply. Although ischemia is probably one of the leading villains of secondary injury, there are actually a number of other suggested causes as well. Unlike primary injury, secondary injury may be inhibited by our acute interventions. For example, some evidence shows that immediate application of cryotherapy inhibits secondary injury following acute trauma. By limiting secondary injury, the total quantity of injured tissue is limited, which should reduce the time necessary to repair the damage and return to sport.
A second but equally important goal of the acute use of modalities is to limit the sequelae of the acute inflammatory response. Because acute inflammation occurs with every injury to perfused tissues, all five signs of inflammation can be expected to occur to some extent. These signs—redness, heat, pain, edema, and loss of function—can lead to an unnecessarily prolonged time needed for healing. By limiting these signs, particularly the pain and edema, function can be restored sooner and patients thereby returned to activity sooner. Likewise, the biochemical consequences of acute inflammation include the release of a number of damaging enzymes and radicals that are capable of producing additional tissue damage (see Chapter 2 ). Obviously, limiting the quantity or activity of these damaging molecules could help reduce the total quantity of damaged tissue and therefore lead to quicker repair.
The traditional management of acute injuries is described by the acronym RICE, which stands for rest, ice, compression, and elevation. , Cryotherapy, or the therapeutic use of cold, is by far the most commonly used and probably the most effective modality for managing acute musculoskeletal injuries. , There is almost certainly no more familiar modality to practitioners than the ice bag; however, in clinical practice, cryotherapy takes many forms and can be used to help accomplish a variety of goals, both acute and postacute. From a scientific standpoint, there is perhaps no modality that we know more about; even so, our understanding of cryotherapy is somewhat more limited than probably imagined. This section discusses only the acute use of cryotherapy. Its postacute use in facilitating early exercise is discussed in conjunction with the other postacute modalities later in the chapter.
Cryotherapy is one of the most broadly defined of the therapeutic modalities. Quite simply, it involves the therapeutic application of cold. Many different forms of cold therapy are commonly used in clinical practice, and new forms are being developed and marketed continually. Although one of the most common forms of cryotherapy is the ice bag, cold modalities also include ice massage, ice slush immersions, cold-water immersion, frozen gel packs, vapocoolant sprays, cold-compression devices, and even “instant” cold packs. Please note that virtually all of these involve the local use of cold rather than the global (whole body) application of cold. The physiology of local cooling is somewhat different from that of global cooling, and it is this local cooling that is of most interest in rehabilitation.
The wide array of cryotherapy options is reflective of both the obvious efficacy of this modality and our inadequate understanding of what constitutes an ideal treatment. All these various forms of cryotherapy are capable of cooling tissues to different extents; however, only limited data are available to suggest which of these forms of cryotherapy is the most effective.
How We Think It Works
Like all modalities, cold treatments produce a variety of physiologic effects ( Table 8-3 ). These physiologic effects can easily be translated into goals for cryotherapy treatments. Although each of these effects is generally discussed separately, it should be remembered that they all occur simultaneously. Therefore, we need to consider all the effects of a modality when we use it, and we need to balance the desired effects with the unwanted effects to determine whether use of the modality is judicious or inadvisable.
|Physiologic Effect||Clinical Use|
|Reduced temperature||↓ secondary injury, ↓ edema formation, ↓ bleeding, ↓ pain|
|Reduced metabolic rate||↓ secondary injury|
|Reduced perfusion||↓ bleeding, ↓ edema formation|
|Reduced inflammation||↓ secondary injury, ↓ edema formation, ↓ pain|
Reduction in temperature
The most easily recognizable effect of cryotherapy is a reduction in tissue temperature. In fact, virtually all the effects observed with cryotherapy are a direct result of this change in tissue temperature. In the past 10 years alone, a great deal of cryotherapy research has used temperature reduction as the variable of interest. Most of these studies have examined skin temperature ( Fig. 8-1 ), but a growing body of literature is also reporting on deep temperatures during cryotherapy ( Fig. 8-2 ). From this literature we know that during many forms of cryotherapy the skin can easily reach single-digit temperatures (°C) and that the change in intramuscular temperature is quite variable depending on the depth at which temperature is measured and the duration of the treatment. Typical intramuscular temperatures during most forms of cryotherapy are in the range of 25°C to 31°C.
The most important factor that determines the change in tissue temperature during cryotherapy is heat transfer. An important concept to remember when we speak of tissue cooling is that cold cannot be transferred because cold is merely the absence of heat. Heat is transferred from one body to another, with the net transfer always being in the direction of high heat moving toward lower heat. Therefore, body tissues (high heat) are cooled because they lose heat that is absorbed by the cold modality (low heat); the greater the ability of a cold modality to absorb heat, the greater the potential for reducing tissue temperatures.
The heat-absorbing capacity of cold modalities is determined by a number of factors ( Box 8-5 ). Cold modalities with more mass can absorb more heat than those with a small mass. Similarly, the greater the contact area, the greater the heat transfer. Greater differences in temperature also lead to more rapid heat transfer. Conversely, the greater the tissue thickness, particularly adipose thickness, the slower the heat transfer.
Size of the contact area
Difference in temperature between the modality and the tissue
Distance across which heat must be transferred (tissue thickness)
One of the most important factors controlling heat transfer is the specific heat of the tissue and modality. Specific heat is the amount of heat necessary to raise the temperature of 1 kg of the material by 1°K (or 1°C because the units are the same size). The greater the specific heat, the more energy required to raise the temperature of the material. Therefore, material with a greater specific heat can absorb more heat energy per degree of change in temperature than can material with a lower specific heat. Perhaps even more important is whether the cold modality goes through a change of state (solid to liquid) when it absorbs heat. Changes in physical state occur at specific temperatures. For example, ice at 0°C becomes water at 0°C as it melts. The amount of heat required to cause this change in state during melting is known as the heat of fusion and is much higher than the material’s specific heat. For example, at 0°C the specific heat of ice is 2090 J/kg/°C, the specific heat of water at the same temperature is 4190 J/kg/°C, and the heat of fusion for ice melting to water is 333,000 J/kg. In other words, a cold modality changing from ice at 0°C to water at 0°C absorbs roughly 80 times as much heat as raising the temperature of cold water from 0°C to 1°C!
From a thermodynamics standpoint, it is clear that modalities that undergo a phase change (e.g., ice) are capable of absorbing more heat than those that do not (e.g., frozen gel). This notion received some clinical support when it was demonstrated that lower skin and intramuscular temperatures are observed when using ice-based modalities than when using flexible gel cold packs. Another important factor in reduction of tissue temperature is the use of compression. Cryotherapy used in combination with compression has been shown to produce greater reductions in temperature than cryotherapy used alone can.
In addition to the thermodynamic properties of the modality itself, the tissue temperatures observed during cryotherapy are also largely dependent on factors related to the tissues being treated. Of these factors, the thickness of the adipose layer at the treatment site appears to be the most important. In a noteworthy study, Otte et al compared the duration of treatment required to produce a uniform change in temperature in patients with different adipose thickness ( Fig. 8-3 ). Remarkably, to produce an identical 7°C drop in temperature of the quadriceps with the application of an ice bag, subjects with anterior thigh skinfolds of 11 to 20 mm required 23 minutes, whereas subjects with skinfolds of 31 to 40 mm required an almost unthinkable 59 minutes! Clearly, the days of “one duration fits all” for cryotherapy treatments are long gone.
Reduction in metabolic rate
Perhaps the most important goal of acute cryotherapy is a reduction in the metabolic rate of the cooled tissue. Such a reduction in metabolic rate would be quite beneficial in improving a tissue’s ability to survive the proposed secondary injury events that follow primary trauma. Although the exact mechanics of secondary injury is still being defined, it is clear that several of the mechanisms suggested would be altered by a change in temperature. For example, one of the two most common theories is that secondary injury results from the activity of damaging enzymes or free-radicals that are released during the inflammatory process. We know that the rate of chemical reactions is reduced at lower temperatures, so lowering a tissue’s temperature with cryotherapy would reduce the rate of activity of the detrimental enzymes or radicals and thereby reduce the quantity of damage that they cause. Likewise, the other suggested principal mechanism of secondary injury is that it is the result of postinjury ischemia. We know that without oxygen, tissues fail metabolically in a relatively short time. A reduction in temperature and its related drop in metabolic rate have clearly been shown to reduce a tissue’s demand for oxygen and thereby improve tissue survival under such conditions.
The temperature-dependent alteration in metabolic rate is generally described by using a physical chemistry concept referred to as Q 10 . Q 10 is simply the change in the rate of chemical reactions observed with a 10°C change in temperature as calculated with the Arrhenius equation. In physiology, Q 10 is generally used to describe the metabolic rate and is most commonly determined by examining either O 2 consumption or NH 3 excretion. A common misconception among biologists is that Q 10 = 2; that is, the rate of reaction doubles with each 10°C increase in temperature. In reality, Q 10 is somewhat variable and depends on the organism, the specific temperature range, and the metabolic pathway of interest. It generally falls between 1.2 and 2.5. That is, increasing the temperature by 10°C will lead to a 1.2- to 2.5-fold increase in the reaction rate (i.e., a 20% to 150% increase). Though normally defined for an increase in temperature, we can also use Q 10 to understand the physiologic effect of cryotherapy, which decreases temperature and therefore the metabolic rate. For example, let us arbitrarily say that the Q 10 is 1.5 for temperature increasing from 27°C to 37°C. This would mean that the metabolic rate increases 1.5-fold for this increase in temperature (i.e., a 50% increase). If we were to apply cryotherapy to a tissue whose temperature is 37°C to decrease it to 27°C, the metabolic rate would then be reduced by 1.5-fold, or 50%.
Although a decline in metabolic rate is clearly an important aspect of the acute use of cryotherapy, we still do not know much in this area. For example, even though the arguments for the role of damaging enzymes and free radicals are getting stronger, most of this research has been performed on organs and neurologic tissues, and we still know very little about the progression of secondary injury in musculoskeletal tissues. Likewise, the postinjury ischemia theories have not yet been well examined.
The gaps in the area of research regarding ischemia lead to several significant shortcomings in our current understanding of cryotherapy. We do not yet have a definitive answer about the most effective tissue temperature, duration of cryotherapy, or on-off ratio for using cryotherapy for the treatment of acute injury. These questions are addressed later in the chapter.
As is true with the metabolic rate, perfusion is also reduced with a decline in tissue temperature. , The decrease in blood flow is an effect of constriction of the vessel walls in response to cold. Some practitioners and even educators still suggest that cold can also cause dilation of blood vessels. This concept, known as cold-induced vasodilation, does not occur and is discussed in Box 8-6 .
As is the case with virtually every modality, a number of anecdotal beliefs about cryotherapy do not stand up to scrutiny in the laboratory. Unfortunately, modality myths have great tenacity and refuse to die quietly, and cold-induced vasodilation (CIVD) is no exception, even though the idea was discredited by Knight et al more than 20 years ago. Some clinicians and even a few modality instructors still cite CIVD, sometimes called rebound vasodilation, as an important physiologic effect of cryotherapy. CIVD is generally described as an increase in blood flow, above baseline levels, that accompanies cryotherapy treatments. This phenomenon is often used as a rationale for limiting cryotherapy treatments to less than 20 to 30 minutes in duration. Originally, the notion of CIVD grew from a study by Lewis in 1930 when he described cyclic fluctuations in finger temperature during immersion in ice water. He did not examine blood flow or vessel diameter, and his subjects were very likely hypothermic as a result of being underdressed in a very cold room. He observed that finger temperature fluctuated; it became warmer after a period immersed in cold water. This has been incorrectly translated to mean increased blood flow and was a popular rationale for the use of cryotherapy in rehabilitation for a number of years.
In reality, CIVD does not occur. Limb blood flow during cryotherapy is clearly depressed and never increases above baseline as long as the temperature is below normal. However, as is often the case with misunderstood ideas, there is a hint of truth buried in the legend of CIVD. That hint is known as the hunting response. During local hypothermic conditions, we see clear and profound vasoconstriction in vessels with muscular walls, such as arterioles. However, during prolonged local hypothermia, the degree of vasoconstriction in these vessels fluctuates and the resulting blood flow undergoes a cyclic increase and decrease. The important thing to note is that this cycling of blood flow occurs at flow levels that are considerably below their normal baseline. Said another way, the cyclic increase in blood flow during prolonged hypothermia does not approach the precryotherapy baseline blood flow and certainly does not go above baseline levels. Therefore, practitioners can use cryotherapy for longer than 15 to 30 minutes without fear of hyperperfusing an acutely inflamed tissue.
As vessels become colder, their muscular walls begin to contract, which causes the vessel to constrict in diameter. The constriction is generally thought to be more pronounced in arteries and veins with smaller diameters and in arterioles and venules. It is important to note that constriction does not occur in capillaries because their walls are single-cell-thick endothelium and do not contain muscular tissue that can contract. Vasoconstriction causes a decrease in blood flow that has been well documented over the past few decades. , A decrease in blood flow is a mixed blessing and causes a bit of a dilemma for injury management theory. On the beneficial side, less blood flow would translate to less hemorrhaging from damaged vessels, less edema formation, and decreased accumulation of inflammatory cells that might cause secondary injury. These effects would all translate to improved outcomes of the injury. On the detrimental side, less blood flow would also mean less delivery of O 2 and nutrients and less removal of metabolic waste products. These effects could all worsen the secondary damage following injury. In reality, topical application of cold only reduces blood flow and does not completely prevent it. Therefore, we are probably not imposing too great of an ischemic stress, so the pros are thought to outweigh the cons.
It is well accepted that cryotherapy inhibits inflammation, , , but the specific effects of cold on inflammation are somewhat complex because inflammation itself is extremely complex. Most introductory texts , describe inflammation in terms of its vascular, chemical, and cellular events, and all three of these events are altered by acute cryotherapy. The vascular effects of inflammation, most notably vasodilation, are counteracted by the vasoconstriction that results from cold treatments, as already described. The chemical effects—release of more than 100 chemicals that mediate the inflammatory process—are also affected by cold. Even though the effects of cold have not been explored for the majority of these inflammatory chemicals, we do know that the release or activity of several of the key inflammatory chemicals is inhibited during cryotherapy. The cellular events of inflammation are marked by the early activity of neutrophils, which gradually give way over a period of hours to the activity of macrophages. Through a cold-induced reduction in metabolism, the activity of all these cells is reduced. This is thought to be quite beneficial in the early stages of inflammation in which neutrophils dominate but less useful later when macrophages are active in removing inflammatory debris in preparation for tissue repair. Neutrophils account for roughly 60% to 70% of all circulating white blood cells. Their primary function is to fight an expanding bacterial infection by phagocytizing the bacteria and releasing a variety of damaging chemicals and free radicals—the immune system equivalent of hand grenades—to destroy additional bacteria. They are also very active in amplifying the overall immune response by releasing an assortment of chemical messengers. Because most musculoskeletal athletic injuries do not involve open wounds and infection, the activity of neutrophils with such injuries is generally greater than necessary and can lead to unwanted secondary damage to otherwise uninjured tissue (see Chapter 2 ). The use of cryotherapy to retard neutrophil activity and thereby limit this damage is a promising area of future cryotherapy research.
One of the most important physiologic effects of acute cryotherapy is its ability to retard the formation of edema/effusion. , The primary mechanism by which cryotherapy retards edema formation is thought to be its effect on Starling forces. These forces cause movement of fluid across the capillary wall, with two forces causing fluid to escape from the vessel and two forces attempting to retain fluid in the vessel. Under normal circumstances, the balance of these forces is such that a small amount of fluid is constantly escaping and being collected by the lymphatic system. When an injury occurs, tissue osmotic pressure, one of the escape forces, is thought to dramatically increase because of the release of free protein and other molecules from the damaged tissue. This would shift the balance of forces even further in the direction of fluid loss and edema formation. Cryotherapy is thought to minimize the total tissue damage and thereby hinder the release of free protein and thus the increase in tissue osmotic pressure. Coupled with the lowered blood flow resulting from vasoconstriction, cryotherapy results in a decrease in the other escape force, capillary hydrostatic pressure. With both escape forces reduced but not completely eliminated, the formation of edema or effusion is lessened, but not entirely prevented. Obviously, compression is a critical adjunct
The ever-popular phrase “ice reduces swelling” is not used here, and with good reason. “Swelling” is a troublesome word because it is sometimes used as a noun in place of edema or effusion, or it can be used as an action verb meaning that fluid is accumulating.
The problem with the phrase “ice reduces swelling” is that it is misleading and frequently misunderstood. It is well accepted that cryotherapy retards the accumulation of fluid both intraarticularly and extraarticularly. , However, cryotherapy by itself is not effective in removing that fluid once it has accumulated. Cryotherapy and compression in combination are somewhat effective in removing accumulated fluid, but this is most likely a function of the compression and not the cold.
Aside from selected pharmaceuticals, no modality is more effective than cryotherapy in managing both the acute and chronic pain associated with athletic injuries. Three primary theories attempt to explain cold’s pain-relieving efficacy, and in reality, all three probably occur simultaneously ( Box 8-7 ). ,
Gate Control Theory. The first and best known of these theories is gate control theory, in which the cold causes stimulation of Aβ afferent nerve fibers, which in turn inhibit transmission of pain to second-order neurons through gating at the substantia gelatinosa in the dorsal root ganglion of the spinal cord.
Reduction in Nerve Conduction Velocity. Nerve conduction velocity has been shown to be reduced by as much as 30% following typical cryotherapy treatments. Slower conduction would translate into a diminished sensation of pain.
Reduction in Sensitivity to Pain Receptors. A lesser known theory is that local application of cold reduces the sensitivity of pain receptors much in the same way that it reduces the sensitivity of touch and pressure receptors.
Ironically, although cold is an outstanding pain control modality, its application can actually be quite painful. This is particularly true of cryotherapy treatments that involve immersion in ice water and patients who are not accustomed to the treatment. The pain with cold application can initially be intense but often subsides after several minutes. Repeated application over a period of days or weeks generally leads to better tolerance by patients as they grow accustomed to the treatment.
The neuromuscular effects of cryotherapy are not generally used as a goal for cryotherapy treatment of acute injuries, but these effects can be quite useful in managing muscle spasms and in rehabilitation and are discussed with the rehabilitative use of cryotherapy.
Techniques and Dosage
At the present time, we use cryotherapy under the assumption that colder tissue temperatures are better, provided that tissue freezing and frostbite does not occur. Therefore, cryotherapy treatment of acute injuries is aimed at reducing tissue temperature as greatly and quickly as possible.
Topical application and insulating barriers
The most common application technique for cryotherapy involves the direct application of a cold modality, generally an ice bag or frozen gel pack, to the injured area with some sort of a compressive wrap, usually an elastic bandage or plastic wrap ( Table 8-4 ). As a general rule, cold packs made from ice are superior to frozen gel packs for the thermodynamic reasons discussed previously. Ice-based cold packs are also generally safer than frozen gel packs. It is very possible to cause further injury with cryotherapy, and there are three primary ways that patients are injured ( Box 8-8 ).
|Cold Modality||Application Technique||Comments|
|Ice bag||Apply directly to skin and use a compression wrap and elevation (ICE); the duration depends on adipose tissue and should be 20-40 minutes for most athletes.||Crushed ice conforms better than cubed. Ice from an unrefrigerated bin on an ice machine will not cause frostbite, but ice directly from a freezer may. Use appropriate caution.|
|Ice immersion||With submersion in water with ice, consider using a thin layer of elastic tape for compression (less insulating than elastic bandages).||Durations are not scientifically described, but most mimic ice bag durations.|
|Frozen gel pack||Do NOT apply directly to skin. Use a compression wrap and elevation. The duration should be 20-40 minutes for most athletes.||Because they are stored in a freezer at temperatures below 0°C, they can cause frostbite. They also rewarm much more quickly than ice bags.|
|Vapocoolant sprays||The spray and stretch technique is used for muscle spasms and trigger points.||Sprays are not used for most injuries (e.g., sprains, strains, fractures, contusions). They can quickly cause frostbite, so care must be exercised.|
It is possible to cause injury by using too much compression over too small an area and create a tourniquet-like effect. For this reason, compression wraps should not be applied with more than moderate force, generally defined as 45 to 50 mm Hg.
Extended use of cryotherapy over superficial portions of peripheral nerves can cause further injury. In several cases, nerve palsy has resulted from cryotherapy treatments, typically over the common peroneal nerve on the lateral aspect of the knee or the ulnar nerve at the medial aspect of the elbow. When using cryotherapy over these areas, we must diligently monitor the treatment, control the compression, and limit the duration of treatment.
Cold-induced injury is frostbite. Frostbite occurs when tissue has been destroyed by freezing. For frostbite to occur, the tissues must be cooled to the point at which ice crystals begin to form. This occurs when the tissue temperature drops below 0°C and is accelerated by greater than required compression. Therefore, care must be used with cold modalities that are colder than 0°C, and compression should be applied carefully.
Typically, ice bags are filled with either cubed or crushed ice made by an ice machine and stored in an unrefrigerated hopper below the ice machine. Because this ice is not stored in a refrigerated container, it is continually melting. Because melting ice, by its very definition, has a temperature of 0°C and heat is being added to the ice from the tissues being treated, it is physically impossible for such ice to freeze the skin and cause frostbite. For this reason, ice bags filled with ice stored in unrefrigerated hoppers should be applied directly to the skin without the addition of an insulating layer. The same cannot be said for ice stored in a freezer or frozen gel packs, however. Because their temperatures will most likely be below 0°C, they pose a risk of causing frostbite and therefore require some type of barrier, such as a wet elastic wrap, between the pack and the skin. Unfortunately, such barriers have been shown to severely limit the ability of the modality to cool the tissues and are therefore assumed to meaningfully impair the efficacy of the modality.
As a general rule, a barrier should be used only when applying a cold modality that has been stored at a temperature below 0°C; because cubed or crushed ice stored in an unrefrigerated hopper does not meet this criterion and is continually melting and heat is being added to the ice from the tissues being treated, no barrier should be used.
Cold combined with compression
One of the most overlooked aspects of applying ice packs for an acute injury is the use of compression. Practitioners are taught to treat injury with ice, compression, and elevation (ICE), with the compression and elevation being used to retard the formation of edema. However, we often overlook the fact that compression also plays a valuable role in cooling. When compression is used in combination with cryotherapy, we observe that deep tissues cool more rapidly and that lower temperatures can be achieved ( Fig. 8-4 ). Merrick et al were the first to describe this combined effect on cooling, and they speculated that the improved cooling resulted from the combination of better contact between the tissue and the modality and compression-induced reduction in blood flow.
Gaining in popularity are devices that automatically combine cryotherapy and compression. These devices, considered lymphedema pumps for regulatory purposes by the Food and Drug Administration, typically use a fluid-filled (hydraulic) sleeve that is filled with cold water to provide both cooling and compression. Many of these devices have partitioned sleeves that either fill sequentially in an effort to move edematous fluids proximally or use different pressure in each partition (gradient pressure) for the same purpose. Most devices allow the clinician to control the compression pressure, and some also allow control of the temperature of the water used for the compression. Although these devices make sense intuitively, like nearly all therapeutic modalities, few data describing their clinical outcomes are available.
Cold immersion treatments can be performed either with cold water, typically in the form of a cold whirlpool, or with an ice and water bath. Ice immersion has two important advantages over ice packs. First, immersion treatments are able to treat larger areas and do so more uniformly. Second, immersion allows heat transfer through water, which has much greater thermal conductivity than ice packs do. This greater thermal conductivity may permit more rapid cooling. Cold immersion has disadvantages as well. The first is that it is nearly impossible to use elevation with immersion treatment. The second disadvantage of immersion treatment is that the water develops thermal gradients. Thermal gradients are regions where the water has been heated by the somewhat warmer tissues that are being immersed. The water around these tissues becomes warmer than the rest of the water in the immersion container. As these regions of water are warmed, they are less able to absorb heat and a reduction in cooling occurs. To avoid this gradient effect, the water should periodically be mixed throughout the treatment. Patients typically do not enjoy the mixing, however, because it brings colder water back into contact with their limb and is somewhat uncomfortable.
Ice and water baths, often referred to as ice slushes, are considerably more uncomfortable than cold water baths, but their lower temperatures make them a more effective choice. Patient tolerance of ice slush treatments of the foot and ankle can be improved with the use of toe covers, which prevent the cold water from coming in direct contact with the toes.
When making an ice slush, a good analogy is to put the ice in first and then add water to the ice, just as you would add milk to breakfast cereal. The ice should just begin to float so that when the limb is added, the ice surrounds the area to be treated.
Ice massage, or rubbing a block of ice against the tissue, is an effective and common, but somewhat messy practice. Towels must be used beneath the treated tissue because the ice is constantly melting but the water is not collected in the ice bag. Ice massage treatments are generally of briefer duration than ice pack or cold immersion treatments and are capable of producing similar intramuscular temperatures. Care must be taken to avoid using excessive pressure over peripheral nerves.
Spray and stretch
A somewhat different type of cryotherapy treatment known as spray and stretch is used to induce brief, intense cooling to relieve myofascial pain and spasm. The technique has also been used to treat muscle cramps, but this technique has not been examined in the literature. The spray and stretch technique involves the application of a vapocoolant spray, typically ethyl chloride or Pain Ease (Gebauer Company, Cleveland, OH), which rapidly cools the skin during evaporation. Ethyl chloride is very flammable and therefore nonflammable Pain Ease is becoming more popular and is just as effective.
The technique involves spraying the vapocoolant liquid in parallel strokes over the skin overlying a muscle with myofascial trigger points and then immediately stretching the muscle. The brief, intense cooling is thought to act as a distracting neurologic stimulus that may cause reflexive motor inhibition and thus allow more effective stretching. Amazingly, some recent work has demonstrated that skin temperatures can reach − 10°C or colder with these products, yet they do not cause cold injury to the skin unless applied for a prolonged period (usually in excess of 8 seconds). A general guideline for their use is to stop applying the product when the skin surface “blanches” to a white color or when skin frosting begins to appear. Stopping at these points produces clinically meaningfully cooling without causing cold injury. In addition to spray and stretch, these products are commonly used to minimize the discomfort of needlesticks and venipuncture. They do cool deeply enough to be of much use in treating acute musculoskeletal injury.
For all that we have learned about cryotherapy, answers to the most important questions still elude us. The vast majority of cryotherapy research has used clinically convenient or easy-to-measure variables such as temperature. We now know a great deal about the response of skin and intramuscular tissue to cryotherapy. For example, we know that skin temperature drops almost immediately and that muscle temperature does not begin to fall until 3 to 5 minutes into the treatment. We also know that when the cold modality is removed, skin temperature begins to climb immediately but deep temperature actually continues to fall for nearly 5 minutes. We know that following cryotherapy treatments, temperature does not return to normal for more than an hour in resting subjects. However, we do not yet know the temperature that we need a tissue to reach to have a positive outcome with cryotherapy, and we certainly do not yet know the optimum intramuscular temperature for retarding secondary injury or inflammation. To answer these critically important questions, we will need to examine variables related to secondary injury or inflammation itself.
Because we do not yet know the optimum temperature that we need to reach during cryotherapy, we do not know how long our cryotherapy treatments should be applied to produce this temperature. We do know that there is a point of diminishing return with cryotherapy duration. In examining the time required for rewarming of the skin following cryotherapy, researchers have shown that longer, colder applications lead to longer rewarming periods only up to a point. Applications that exceeded 30 minutes had nearly identical rewarming times as 30-minute applications. We also know that adipose thickness is an important factor that we need to consider when choosing the duration of applications. In fact, to produce a typical cryotherapy effect in many of our athletes, we need to double or even triple the treatment durations that are commonly in use now (see Fig. 8-3 ). A third important question about cryotherapy is related to these first two. We do not yet know how often we need to reapply cold modalities. A typical recommendation is 20 minutes per hour for the first 5 or 6 hours following injury. Though typical, few data support any specific on-off cycling for cryotherapy.
Compression, or the application of external pressure, is a commonly used adjunct to acute cryotherapy, but it also has usefulness in isolation. Compression, the “C” in RICE, is one of the cornerstones of traditional management of acute injury, although it has not been well studied. The effectiveness of compression is thought to largely be related to its effect on Starling forces, the forces governing transcapillary fluid movement, although compression has other useful effects not related to these forces. This section discusses only the acute use of compression. Its postacute use in resolving existing edema is discussed in conjunction with the other postacute modalities later in the chapter.
Compression involves the application of external pressure to a tissue or tissues in either a circumferential or focal manner. Although the most common forms of compression involve circumferential application with either an elasticized bandage or elastic tape, quite a few other compression modalities are actually available. Among the best of these are pneumatic or hydraulic lymphedema pumps, which provide circumferential compression in either a constant or intermittent manner. Pneumatic lymphedema pumps use air to fill a compression garment and provide nearly uniform circumferential compression. Hydraulic lymphedema pumps, in contrast, use water or some other liquid to fill the compression garment. Although many of the early lymphedema pumps used single-chamber compression garments, most contemporary units use multichambered garments, which allow sequential filling (distal to proximal), gradient compression (more pressure in the distal chambers than in the proximal chambers), or both. For the management of acute injury, a large and important advantage is found with hydraulic pumps because they allow the use of precooled water, thereby providing concurrent cryotherapy. Both pneumatic and hydraulic lymphedema pumps are considered to be medical devices and are therefore regulated by the Food and Drug Administration through the Center for Devices and Radiological Health.
How We Think It Works
Compression produces several physiologic effects that can be used to explain its effectiveness. As is the case with cryotherapy, these effects probably do not work in isolation but instead work in concert to produce the desired outcome. Compression is thought to be effective in managing acute injuries by three primary means. One is that compression increases the cooling efficacy of cryotherapy, as discussed previously in the cryotherapy section. The other two mechanisms involve resisting the formation of edema. The first of these antiedema mechanisms entails a manipulation of Starling forces. The second involves lessening bleeding from the vessels damaged during the injury.
The most common explanation for the obvious effects of compression on retarding the formation of edema is through its effect on Starling forces ( Table 8-5 ). These forces, sometimes called capillary filtration forces, govern movement of plasma from the vascular system into the extravascular space through the intact walls of capillaries. Under normal homeostatic conditions, three forces, capillary hydrostatic, tissue hydrostatic, and tissue osmotic, cause fluid to migrate from the capillary into the extravascular space, and one force, capillary osmotic, resists the extravascular migration of fluid. Normally, a net loss of fluid from the vascular system occurs because of a slight imbalance in the Starling forces, with the “out” forces causing loss of fluid from the capillary being slightly larger than the “in” forces. As discussed in the cryotherapy section, acute injury causes a dramatic increase in the “out” forces through both a decrease in plasma osmotic pressure and an increase in interstitial osmotic pressure. These changes in pressure result from loss of plasma proteins into the surrounding tissues and from the release of free proteins from cells damaged by the injury.
|Force||Description||Direction||Mean Value (mm Hg)||Effect of Injury (mm Hg)|
|Capillary hydrostatic||Fluid pressure from inside the capillary||Vascular fluid loss||− 17.3||− 17.3 (no change)|
|Interstitial osmotic||Osmotic pressure exerted by extravascular solutes||Vascular fluid loss||− 8||− 28|
|Interstitial hydrostatic||Extravascular fluid pressure in the tissue||Vascular fluid loss †||− 3||+ 4|
|Capillary osmotic||Osmotic pressure exerted by interstitial fluid||Vascular fluid retention||+ 28||+ 14|
|Net force under normal conditions||Vascular fluid loss||− 0.3||− 27.3|
† Normally, a negative (outward) interstitial hydrostatic force (a partial vacuum) is present that helps hold tissue layers together, but as edema accumulates, this vacuum disappears, which allows tissues to separate and retain even more fluid. The fluid eventually develops positive pressure and can even occlude vessels if the pressure is great enough.
External compression is thought to work primarily by increasing tissue hydrostatic pressure and thereby reducing the magnitude of the pressure gradient favoring the formation of edema. Reduction of this gradient would lessen fluid loss from the vascular system and consequently retard the formation of edema. Note, however, that it is unlikely that external pressure will completely compensate for the increase in tissue osmotic pressure, and therefore some edema can be expected to form even with the use of external compression.
The edema or effusion associated with injury does not form solely from plasma fluid and protein that leak through intact capillary walls. A significant portion of the fluid accumulation associated with injury is from blood that spills out of blood vessels damaged in the injury. It is this blood that causes most of the ecchymosis seen in the injured area over the days following the injury. Compression is effective in the management of this blood loss is several ways. First, it reduces the quantity of blood flow to the damaged vessels and therefore limits the volume of blood available to be spilled from these vessels. Second, compression slows the rate of flow and allows more rapid development of the fibrin scaffolding that eventually forms a clot and stops the blood loss.
Technique and Dosage
Very little is found in the literature on the appropriate compression technique or dosage for managing acute injuries. Most often, compression is used in combination with cryotherapy, and the duration is based on the cryotherapy and not the compression. A small body of research examining typical compression pressures with elastic wraps and surface pressures of 40 to 50 mm Hg has been reported. These pressures correspond to applying an elastic bandage at medium stretch in which roughly half the stretch capacity of the wrap is used during application. Some evidence has shown that compression in this pressure range improves the cooling observed with cryotherapy by producing both lower tissue temperatures and slightly faster cooling. Other evidence, however, has shown that varying application pressures has little effect on tissue temperatures.
The use of focal compression, such as that achieved with a felt or foam “horseshoe” pad around the malleolus in treating an acute ankle sprain, can provide increased compression. This type of focal compression can be very useful in limiting the accumulation of fluid at specific sites, such as around the malleoli with ankle injuries or in the peripatellar region with knee injuries.
In addition to compression wraps, the other common form of compression used with acute injuries involves the use of lymphedema pumps, typically combined with cryotherapy. The application parameters for these devices when used for acute injury management have also not been well described. Although ideal parameters have not yet been identified, typical guidelines include 20 to 40 minutes of intermittent compression consisting of a 30- to 40-second inflation time and a 20- to 30-second deflation or rest time. Appropriate application pressure for these devices is not yet clear, but manufacturers have recommended pressures between 50 and 90 mm Hg; however, these recommendations are generally intended for the postacute removal of edema rather than retarding the formation of edema. On the other hand, there is a good argument for using pressures that are just below the patient’s diastolic blood pressure in an effort to apply as much pressure as possible without occluding the vasculature.
Obviously, the acute use of compression is a very common clinical practice. As common as it is, very few studies have attempted to describe the physiologic effects of compression and even fewer that have examined its use for the management of acute injuries. This leaves many questions still unexamined. Among the most important would be the appropriate pressure, appropriate duration, use of intermittent versus continuous compression, intermittent cycling parameters, and whether compression or elevation is a more important factor in retarding the formation of edema.
Elevation, the “E” in RICE, is the least studied of the trio of ice, compression, and elevation, but its use is widespread in the management of acute injuries. Elevation of an injured body part can be accomplished in a variety of ways ranging from specially designed treatment tables to simple, on-the-field techniques, such as resting an injured ankle on a football helmet or equipment bag.
How We Think It Works
The underlying premise with elevation is that gravity will limit the amount of blood delivered to the acutely injured area. Limiting blood flow to the injured area immediately following the injury is perceived to have three benefits. First, it would help control bleeding from damaged vessels, and this would be a benefit in terms of limiting edema and hematoma formation, as described previously in this chapter. Second, it would alter the transcapillary Starling forces in the injured area by reducing capillary hydrostatic pressure, one of the major forces causing fluid to move from the vessel out into the extravascular space. This has obvious implications for retarding edema formation. The third and most often overlooked benefit is that the reduced blood flow and capillary hydrostatic pressure would also limit the transport of neutrophils to the injury site. The neutrophil is the most numerous leukocyte population and plays a vital role in early magnification of the inflammatory process. It is also thought to be among the most likely villains in secondary injury. Limiting the delivery of neutrophils and other proinflammatory agents to the injury site would be of potential benefit in limiting the total amount of tissue damage and inflammation that would have to be resolved before repair could take place.
Unfortunately, the magnitude of the actual benefits from elevation has not been described. Although the arguments for elevation are intuitive and make good physiologic sense, it is unclear whether elevation plays an important role, a minor role, or no role in improving outcomes after injury. Therefore, several important questions need to be examined, including the effects of elevation on edema formation, the magnitude and duration of elevation necessary, and a relative comparison of the importance of elevation and compression. For example, a number of clinicians treat acute ankle sprains by applying elastic tape compression wraps and then immersing the ankle in an ice bath. The more rapid cooling with an ice bath than with an ice bag may be of some benefit; however, the gravity-dependent position goes against the commonly accepted importance of elevation. The actual importance of elevation needs to be established to resolve this clinical dilemma.
Other modalities are claimed to be efficacious in the management of acute injuries, and some appear to hold some degree of promise. High-voltage electrical current has been proposed as an acute treatment and has been suggested to limit retraction of endothelial cells, thereby minimizing the increases in vascular permeability that accompany acute inflammation. However, the efficacy of this approach in the actual management of acute musculoskeletal injuries in humans has not been well examined, and therefore claims about outcome must be made sparingly. Another valuable adjunct to acute injury management is transcutaneous electrical nerve stimulation.
Modalities for rehabilitation
Whereas the goals for acute injury management were centered on minimizing the immediate sequelae of the injury, including limiting additional tissue damage, retarding the acute inflammatory process, slowing the formation of edema, and minimizing pain, goals for the rehabilitative use of modalities are somewhat different ( Table 8-6 ). In postacute rehabilitation, the goals are focused mostly on removing the unwanted remnants of inflammation, repairing the tissue, and restoring more normal physiologic function of the repaired tissue. This is an important distinction that is sometimes lost on inexperienced practitioners. To make appropriate choices of modalities, you must first understand the patient’s stage in the progression of injury and what the next logical stage would be. It is vital to understand that all injuries progress through a predefined set of stages and that these stages are sequential and progressive. That is, you cannot truly begin to restore normal function to an acutely inflamed tissue until you first control the inflammation, second remove the inflammatory debris and fluid, and third repair the damage.
|Rehabilitative Phase||Goals for Use of Modalities||Choices of Modalities|
|Postacute||Remove edema and inflammatory debris||Intermittent compression, thermotherapy, ultrasound, massage, electrotherapy, exercise|
|Retard atrophy||Exercise, electrotherapy|
|Repair/regeneration||Increase perfusion/oxygen delivery||Thermotherapy, ultrasound, short wave diathermy, exercise, hyperbaric oxygen|
|Increase healing stimulus||Exercise, ultrasound, low-power laser, microcurrent(?)|
|Retard atrophy||Exercise, electrotherapy|
|Restore function (early)||Limit pain||Preactivity cryotherapy, cryokinetics, TENS, electrotherapy, microcurrent(?)|
|Counteract neuromuscular inhibition||Preactivity cryotherapy, cryokinetics, electrotherapy|
|Restore ROM||Thermotherapy, ultrasound, short wave diathermy, joint mobilization, ROM exercise|
|Restore adequate muscular strength, power, and endurance for activities of daily living||Exercise, electrotherapy|
|Minimize recurrence of inflammation following activity||Postactivity cryotherapy and compression|
|Restore function (middle)||Reduce preactivity stiffness as needed||Preactivity thermotherapy|
|Increase muscular strength, power, and endurance to functional/competitive levels||Exercise only|
|Restore muscular speed||Exercise only|
|Restore cardiopulmonary endurance||Exercise only|
|Minimize recurrence of inflammation following activity as needed||Postactivity cryotherapy and compression|
|Restore function (late)||Reduce preactivity stiffness as needed||Preactivity thermotherapy|
|Restore agility||Exercise only|
|Restore sport-specific skills||Exercise only|
|Controlled sport activity||Exercise only|
|Uncontrolled sport activity||Exercise only|
|Minimize recurrence of inflammation following activity as needed||Postactivity cryotherapy and compression|
Generally, the goal should be to move to the next stage of the injury. When signs of acute inflammation are present, the choice of modalities should focus on minimizing the inflammation. When examination reveals that the acute phase of inflammation has been controlled, the choice of modalities should focus on removing the unwanted leftovers from inflammation and promoting tissue repair. When the debris has been removed successfully and tissue repair promoted, focus should be directed to remodeling the new tissue and restoring adequate function for mobility and activities of daily living. When these goals have been achieved, return to sport can be addressed. Fortunately, most athletic injuries are able to progress through the early phases quickly, and athletes are often able to begin addressing competitive function early in the postinjury time line. It should be kept in mind that the choice of modalities and goals of rehabilitation for each of these phases are not mutually exclusive. There is almost never a clear dividing point between these phases on examination of the patient, and likewise there is no clear dividing point between the rehabilitative goals and the modalities that can help in achieving these goals. There should often be a degree of overlap between goals and therefore an overlap in modalities. This is particularly true in the repair and remodeling phases. For example, we know that appropriate rehabilitation can influence both the quantity and orientation of scar tissue made by the body. It is of great benefit to use modalities and controlled exercise to minimize the quantity of scar tissue produced while at the same time improving the strength of that scar tissue.
It is also very important to note that the role of traditional therapeutic modalities is almost exclusively limited to the earlier phases of rehabilitation and that the later phases concerned with restoring athletic performance are almost exclusively dependent on exercise as the modality of choice (see Table 8-6 ). Modality use in the later phases of rehabilitation seldom consists of more than preactivity thermotherapy with the aim of increasing perfusion and decreasing stiffness or postactivity cryotherapy with the goal of minimizing any activity-related inflammation. This notion is very closely tied to concepts presented in the beginning of this chapter, where the importance of having criteria for discontinuation of a modality was discussed. When a modality is used to accomplish a specific goal, the modality can and should be discontinued when that goal has been accomplished or when the modality is proving to no longer be effective for the patient. For example, if electrotherapy is being used for muscle reeducation and to overcome postinjury inhibition, its use can be discontinued when neuromuscular function appears normal and the athlete is ready to begin resistance training.
The hallmark of an experienced practitioner is using modalities for a specific purpose and replacing them with more appropriate measures when the goal has been met and they are no longer needed.
Cryotherapy for the management of acute injuries was addressed in great detail earlier in the chapter. The rehabilitative use of cryotherapy is somewhat different, however. Rehabilitatively, cryotherapy is used for two main purposes and at two different times in a rehabilitation session. First and most commonly, it is used to minimize any inflammation that develops as a result of the rehabilitation session and is applied following the session. For this purpose, use of cryotherapy is virtually identical to that already described for the management of acute injuries. The second use of cryotherapy rehabilitatively is to control pain and neuromuscular inhibition. When used for this purpose, cryotherapy is typically used before activity or is alternated with activity, a highly effective technique known as cryokinetics.
How We Think It Works
Cryokinetics is perhaps the single most effective rehabilitative technique for the early restoration of function following joint injuries, particularly ankle sprains. In this technique, several bouts of cryotherapy and exercise are alternated within a single rehabilitative session, usually very early following injury as discussed later. The preliminary rationale for the dramatic effectiveness of cryokinetics was that the cold reduced pain. Pain is thought to cause neuromuscular inhibition, and such inhibition is thought to be the primary limiting factor in the patient’s ability to perform rehabilitative exercise in the early postinjury period. We know that early exercise is the most important modality in our arsenal, and the sooner that controlled rehabilitative exercise can be initiated, the faster the progression of the injury toward normal function and presumably the better the outcome. We know that cold is effective in reducing pain and most other sensations as well. Therefore, if cold reduces pain and pain causes inhibition, cold should help overcome inhibition and therefore allow the patient to begin controlled rehabilitative exercise at an earlier point in the rehabilitative process.
Cold actually plays a contradictory role with respect to pain. Anyone who has placed their bare feet into an ice slush can tell you in great detail that cold can absolutely cause pain. On the other hand, if you have ever burned your finger and then held it under running cold water, you can also testify to the fact that cold reduces pain. So how do we explain the contradiction? First, cold-induced pain seems to be much more common with ice slush immersions than with any other form of cryotherapy, although no explanation for this frequent observation has been offered. The magnitude of the pain also appears to be inversely related to the temperature of the ice bath. In addition, those with injury-related pain are often observed to tolerate cold applications better than do normal, uninjured subjects. It appears that when pain is already present, cold acts to inhibit that pain, whereas when cold is applied to patients without pain, the cold itself becomes uncomfortable.
The primary suggestions of how cryotherapy may inhibit pain lie in cold’s effects on neurologic function. Cryotherapy has been shown to decrease nerve transmission in pain fibers and to decrease the excitability of free nerve endings, one of the most important pain receptors. Cold also has been shown to cause asynchronous transmission in pain fibers, to induce the release of endorphins, and to inhibit spinal nerve conduction. All of these effects are capable of altering the perception of pain.
Because cold reduces nerve conduction velocity on both afferent and efferent nerves, its effect is not limited to altering sensory function. Motor function is altered as well. The changes in motor function have often been overlooked but have some important implications for clinicians.
Among the more controversial neuromuscular effects of local cryotherapy is whether cold decreases maximal force production. The literature is mixed on the subject. Decreased force production has been shown in a number of studies examining isometric force, as well as in some evaluating concentric and eccentric force. In a few studies examining isometric force, an increase in force production was noted roughly 60 to 80 minutes following treatment with cold, but this effect has not yet been examined adequately with regard to concentric or eccentric force. The authors speculated that the increase was the result of either increased temperature or increased blood flow to the limbs following removal of the cold. These explanations seem unlikely because intramuscular temperatures remain depressed for quite some time following cryotherapy.
The initial decrease in strength following cryotherapy has created concern in some clinicians regarding the appropriateness of preactivity cryotherapy. They have questioned whether athletes are being placed at risk for injury by having them practice or compete under circumstances in which nerve conduction velocity and maximal strength are diminished. In an effort to address this issue, a growing body of research is examining the effects of cryotherapy on proprioception. As is often the case, the literature is divided, with studies some showing no alterations in proprioception or functional performance and others showing a decline in functional performance. Unfortunately, the body of research in this area is still small, so a definitive answer has yet to be made. However, because maximal strength is seldom used and because a clear detriment in performance has not been shown, many believe that it is safe to use cryotherapy before activity.
Some of the most exciting new cryotherapy research relates to motor neuron pool availability. Following injury, a period of neuromuscular inhibition occurs and results in motor weakness, impaired coordination of motor activities, and impaired proprioception. Clearly, these impairments present a significant hurdle in the early rehabilitation of injuries. One of the more common research strategies for examining inhibition is to look at the availability of the motor neuron pool. Under normal circumstances, we can voluntarily recruit only a portion of our total motor neuron pool. The body does not allow total recruitment of the pool because the forces that would be generated would cause us to pull muscles off their bony attachments and result in fractures and other injuries. During an injury and the subsequent postinjury rehabilitative period, the percentage of the motor neuron pool that can be recruited is less than normal and can be quantified by measurement of the Hoffmann reflex (H-reflex).
In several studies, neuromuscular inhibition, as indicated by a diminished H-reflex, has been created artificially by inducing joint effusion via the injection of sterile saline into the synovial space. This research strongly suggests that the neuromuscular inhibition following cryotherapy is not only related to pain (as suggested in cryokinetics theory) but also related to joint effusion. Interestingly, not only has the use of cryotherapy been shown to counteract this effusion-induced reduction in motor neuron pool availability, but cryotherapy has actually also led to motor neuron pool facilitation. That is, the application of cold actually increased the amount of the motor neuron pool that was available for recruitment. This suggests that cryotherapy can be used not only to counter the pain that limits early rehabilitation following injury but also to overcome the neuromuscular inhibition following injury. Perhaps even more interesting, Krause et al demonstrated that cryotherapy-induced facilitation also occurs when the cold modality is placed on a different body part, away from the injury (different dermatome). They showed that the knee effusion-induced reduction in motor neuron pool availability was counteracted by applying cryotherapy to the armpit! This suggests that facilitation is mediated by the central nervous system rather than by action on local nerves. On the other hand, members of this same research group have also shown than artificial effusion-induced inhibition is not present in the contralateral limb, so there is still much to learn in this area.
Techniques and Dosage
Many cryotherapy techniques were discussed in the acute management section. Those presented here are more appropriate for rehabilitative use than for acute use.
An old favorite among therapeutic modalities is the whirlpool, and virtually no athletic health care facility is without one. Cold whirlpools use water that is typically as cold as is available from the tap, usually around 50°F to 60°F. , Some clinicians add ice to the whirlpool to reduce its temperature, but to date no ideal temperature has been described in the literature. Whirlpools function by using a turbine to circulate the water around the body part, but they would probably be just as effective without the turbine. The key feature of the whirlpool is the water temperature itself and not the fact that the water is moving. Cold whirlpools were not discussed in the acute management section of this chapter because most are probably too warm to work well for acute injuries and other cold modalities are more likely to be effective. Cold whirlpools are very well suited to the rehabilitative use of cryotherapy, however, because emphasis is not placed on cooling a tissue as quickly as possible or to the greatest degree possible. Typical cold whirlpool treatments last from 15 to 30 minutes, thus mimicking the durations of other cold treatments, such as ice bags, but again, little evidence suggests that this duration is most appropriate.
An important safety consideration with whirlpools is that they should be appropriately grounded and connected to circuits only with a ground-fault circuit interrupter (GFCI). Whenever possible, it is recommended that an electrician be employed to disconnect the turbine on/off switch on the whirlpool and instead connect the whirlpool to a circuit with a GFCI and a timer switch that is out of reach of the patient in the whirlpool. This prevents the patient from operating the switch while standing in the water and provides an effective means of controlling the duration of the treatment. This second benefit is probably more important with warm whirlpool treatments, where athletes tend to not want to get out of the whirlpool.
Cryokinetics is a rehabilitative technique consisting of alternating bouts of cryotherapy and exercise ( Table 8-7 ). The technique is used primarily in the early phases of a rehabilitative program in an attempt to allow exercise to be initiated sooner than might otherwise be possible because of pain and neuromuscular inhibition. It is frequently started as soon as the day following the injury or even the day of the injury for relatively minor injuries. Cryokinetics is particularly useful for joint sprains, especially ankle sprains, but is not as effective for muscle injuries. The cold helps lessen the pain and reverse the inhibition so that exercise can take place. It has been suggested that early cryokinetics can cut days or even weeks from the rehabilitation of an ankle sprain. The real benefits from cryokinetics are found in the exercise because exercise is the single most important modality available to us in terms of its ability to cause positive changes following injury.