Sports and Soft Tissue Injuries

A Guide for Students and Therapists

Christopher Norris

• Publisher: Routledge
• Year: 2018
• ISBN:
  9781351589314
• Edition: 5
• Topic: Medicina
• Subtopic: Fisioterapia, medicina fisica e riabilitazione

The fifth edition of the retitled Sports and Soft Tissue Injuries sharpens its focus on the treatment of sports injuries, providing the most complete evidence-based guide for physiotherapists, sports therapists and medical practitioners working with athletes.

Opening with chapters that examine the underlying science of tissue healing and principles of rehabilitation, the book employs a systematic approach, with chapters covering each area of the body, from facial through to ankle and foot injuries. Every chapter includes in-depth discussion and guidance on the treatment of common sports injuries through physiotherapeutic modalities, drawing on the author's wealth of personal experience and the latest peer-reviewed research.

A complete pedagogical resource, Sports and Soft Tissue Injuries is highly illustrated in full colour, and is an important text for students of sports therapy, physiotherapy, sport medicine and athletic training, interesting further reading for sport and exercise science or kinesiology students with an interest in sports injury, and a crucial reference for practicing physiotherapists and athletic trainers and the related disciplines.

CHAPTER 1
Healing

Following injury, tissue which has been damaged must be replaced by living material. Two processes are possible, regeneration and repair. With regeneration, tissue is replaced by the proliferation of surrounding undamaged tissue. Therapy to produce this effect is currently in its infancy with stem cell therapy. With repair, however, lost material is replaced by granulation tissue which matures into a scar (Watson 2016), a process which most commonly reflects healing seen within the field of sports and soft tissue injury.

Therapists need to have knowledge of the processes which occur at each successive stage of healing to be able to select the treatment technique which is most appropriate for the stage the subject is presenting. A technique aimed at reducing the formation of swelling, for example, would be inappropriate when swelling had stopped forming and adhesions were the problem. Similarly, a manual treatment designed to mobilize soft tissue may not be helpful when inflammation is still forming and the tissues are highly irritable.

The stages of healing are, to a large extent, purely a convenience of description, since each stage runs into another in a continuum, the previous stage acting to initiate the next. The term phasing rather than separate stages may be more suitable. Traditionally, the initial tissue response has been described as inflammation, but some authors see inflammation as a response separate to the processes occurring at the time of injury. Both injury and inflammation may be viewed as a reactive phase of injury, with the classical inflammatory period preceded by a short (ten-minute) period before the inflammatory mechanism is activated. The reactive phase may also be viewed as a lag phase (Hunter 1998), before the strength of the healing tissues begins to change. In any traumatic injury the initial stage is bleeding, which is the precursor for the inflammatory cascade seen as both a vascular and cellular response.

The second stage of healing has been variously called repair, proliferation and regeneration. The tertiary stage is normally termed remodelling. The terms injury, inflammation, repair and remodelling will be used in this text

When describing the stages of healing, the terms acute, subacute and chronic are helpful. The acute stage (up to 48 hours following injury) is generally the stage of inflammation. The subacute stage, occurring between 14 and 21 days after injury, is the stage of repair. The chronic stage (after 21 days) may be viewed as the stage of remodelling. The term chronic is also sometimes used to describe self-perpetuating inflammation, where the inflammatory process has restarted due to disruption or persistent irritation of the healing tissues. The total healing process occurs over a continuum, shown in Fig. 1.1.

Figure 1.1 Timescale for Healing. from Oakes, B.W. (1992) the Classification of Injuries and Mechanisms of Injury, Repair and Healing. In Textbook of Science and Medicine in Sport (Eds J. Bloomfield, P.A. Fricker and K.D. Fitch). Blackwell Scientific Publications, Melbourne. with Permission.

Keypoint

Treatment must be adapted to the stages of healing, which are injury, inflammation, repair and remodelling.

Injury

This stage represents the tissue effects at the time of injury, before the inflammatory process is activated. With tissue damage, chemical and mechanical changes are seen. Local blood vessels are disrupted causing a cessation in oxygen to the cells they perfused. These cells die and their lysosome membranes disintegrate, releasing the hydrolysing enzymes the lysosomes contained. The release of these enzymes has a twofold effect. First they begin to break down the dead cells themselves, and second, they release histamines and kinins which have an effect on both the live cells nearby and the local blood capillary network.

The disruption of the blood vessels which caused cell death also causes local bleeding (extravasated blood). More vascular tissue such as muscle will bleed more than less vascular tissue such as ligament. On average, bleeding following soft tissue injury stops within four to six hours (Watson 2016). The red blood cells break down, leaving cellular debris and free haemoglobin. The blood platelets release the enzyme thrombin, which changes fibrinogen into fibrin. The fibrin in turn is deposited as a meshwork around the area (a process known as walling off). The dead cells intertwine in the meshwork, forming a blood clot. This network contains the damaged area.

The changes occurring at injury are affected by age. Intramuscular bleeding, and therefore haemorrhage formation, is more profuse in individuals over 30 years of age. The amount of bleeding which occurs will be partially dependent on the vascularity of the injured tissues. A fitter individual is likely to have muscle tissue which is more highly vascularized, and therefore greater bleeding will occur with muscle injury. In addition, exercise itself will affect gross tissue responses. Muscle blood flow is greatly increased through dilatation of the capillary bed, and again bleeding subsequent to injury will be greater.

Keypoint

The tissues of an active individual are more highly vascularized than those of an inactive subject. The subject’s tissues will therefore bleed more during injury, and bruising will be more noticeable.

Inflammation

The next phase in the healing sequence is that of inflammation, summarized in Fig. 1.2. This may last from ten minutes to several days, depending on the amount of tissue damage which has occurred, but generally reaches its peak by one to three days. Vascular and chemical cascades occur in parallel to drive the inflammatory process.

Figure 1.2 Inflammatory Elements.

Definition

A chemical cascade (signalling cascade) is a series of chemical reactions. As one reaches its completion, it triggers the next in a type of ‘chain reaction’.

The inflammatory response to soft tissue injury is much the same regardless of the nature of the injuring agent or the location of the injury itself. Inflammation is not simply a feature of soft tissue injuries, but also occurs when the body is infected, in immune reactions and with infarction. Some of the characteristics of the inflammatory response seen with soft tissue injury may be viewed as excessive and better suited to dealing with infection than healing injury.

The cardinal signs of inflammation are heat (calor), redness (rubor), swelling (tumor) and pain (dolor). These in turn give rise to the so-called fifth sign of inflammation: disturbance of function of the affected tissues (functio laesa).

Keypoint

Inflammation is often seen as undesirable. However, inflammation is the first stage of healing and so is a vital step on the road to recovery. The aim should be to prevent excessive inflammation and move the subject on through the phases of healing towards eventual full function.

Heat and Redness

Heat and redness take a number of hours to develop, and are due to the opening of local blood capillaries and the resultant increased blood flow. Chemical and mechanical changes, initiated by injury, are responsible for the changes in blood flow. Chemically, a number of substances act as mediators in the inflammatory process. The amines, including histamine and 5-hydroxytryptamine (5-HT or serotonin) are released from mast cells, red blood cells and platelets in the damaged capillaries and cause vessel dilatation and increased permeability. Kinins (physiologically active polypeptides) cause an increase in vascular permeability and stimulate the contraction of smooth muscle. They are found normally in an inactive state as kininogens. These in turn are activated by the enzyme plasmin, and degraded by kininases.

The initial vasodilatation is maintained by prostaglandins. These are one of the arachidonic acid derivatives, formed from cell membrane phospholipids when cell damage occurs, and released when the kinin system is activated. The drugs aspirin and indometacin act to inhibit this change – hence their use as anti-inflammatory agents in sports and soft tissue injury treatment (see Treatment Note 1.1). The prostaglandins E1 and E2 will stimulate nociceptors and also promote vasodilatation, blood-vessel permeability and lymph flow.

The complement system, consisting of a number of serum proteins circulating in an inactive form, is activated and has a direct effect on the cell membrane as well as he...