REHABILITATION

that constitutes the healing process, provides the key for effective therapy.

The division of tissue repair into phases is a way of helping to understand and deal with a complex series of events. Phasing is useful in this context, but the body effectively treats this as a series of reactions with a change in emphasis rather than a series of discrete stages or phases.

Time scales for repair cause much controversy. Any cited here will be those that relate to the average injury in the average tissue in the average patient. Some will move more swiftly and others less so, and the response of the individual should always take prece- dence over the supposedly ‘normal’ reaction

Figure 1 illustrates the overall relationship between the ‘phases’ of healing. They overlap, interact and are interdependent to a greater extent. The diagram time scale is not linear in that the scale shifts from hours through to months. The essential components of each phase are identified below.

Bleeding phase This is a relatively short lived phase, and will occur following injury, trauma or other similar insult. Clearly if there has been no overt injury, this will be of little or no importance, but following soft tis- sue injury, there will have been some bleeding. The normal time for bleeding to stop will vary with the nature of the injury and the nature of the tissue in question. The more vascular tissues (eg. muscle) will bleed for longer and there will be a greater escape of blood into the tissues. Less vascular tissues (eg. ligament) will bleed less (both in terms of duration and volume). It is normally cited that the interval between injury and end of bleeding is a mat- ter of a few hours (6-8 hours is often quoted) though this of course is the average. Some tissues will continue to bleed for a signifi- cantly longer period, albeit at a significantly reduced rate. A crush type injury to a more vascular tissue – like muscle - could still be bleeding (minimally) 24 hours or more post trauma. Any interven- tion that has the capacity to increase local tissue blood flow dur- ing this period would be overtly inappropriate. Short duration cold treatments can be effective so long as the cold source is not left in place for sufficiently long to result in a vasodilatory response.

KEY POINT

Recently, an increased emphasis has been placed on the capacity of cold therapies to reduce the amount of sec- ondary cell death due to local hypoxia, and it may transpire that this is a more important aspect of the use of cold than the vascular effects that have been emphasised hitherto (10).

terms of tissue repair, it is normal and essential.

The complex chemically mediated amplification cascade that is responsible for both the initiation and control of the inflammatory response can be initiated by numerous events, one of which is trau- ma. Mechanical irritation, thermal or chemical insult, and a wide variety of immune responses are some of the alternative initiators, and for a wide range of patients experiencing an inflammatory response in the musculoskeletal tissues, these are more readily identified causes. Although the ‘inflammation following injury’ sequence will be addressed in this paper, other routes can be sub- stituted as appropriate.

There are two essential elements to the inflammatory events, name- ly the vascular and cellular cascades. Importantly, these occur in parallel and are significantly interlinked. Figure 2 summarises the essential elements of the inflammatory cascade. The chemical medi- ators that make an active contribution to this process are myriad. In recent years, the identification of numerous 'growth factors' had led to several important discoveries and potential new treatment lines (11). Some of these mediators directly contribute to the pain experienced at the injury site eg. interleukin-1 (IL-1) and tumour necrosis factor-α (TNF-α) released by macrophages (12). An inter-

INFLAMMATION

TISSUE DAMAGE & BLEEDING

mast cells platelets basophils

chemical mediators

VASCULAR RESPONSE

CELLULAR RESPONSE

chemical mediators increased

vasolidation & vasopermeability

attraction of phagocytes

increased phagocytosis

increased flow volume & increased exudate

TISSUE OEDEMA

Inflammatory phase The inflammatory phase is an essential component of the tissue repair process and is best regarded in this way rather than as an 'inappropriate reaction' to injury. The inflammatory phase has a rapid onset (few hours) and swiftly increases in magnitude to its maximal reaction (2-3 days) before gradually resolving (over the next couple of weeks). It can result in several outcomes but in

www.sportex.net MACROPHAGES = ‘tissue response’

phagocytosis of debris

site clearance

Release of mediators which stimulate PROLIFERATIVE phase

Fig.3 = ‘inflammatory cascade’ Figure 2: The major components of the inflammatory events 9