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It is imperative, as a sports therapist, to understand the process of soft tissue repair to develop a safe and effective management plan for clients’ injury problems. Understanding this, allows us to decide what modalities or interventions to apply. If certain therapy techniques or inappropriate exercises are applied, it can lead to further problems in the healing stages. A therapist cannot change the time is takes to heal an injury but can certainly make the stages more effective. There are four stages of healing that will be discussed in more detail later on in the essay.
In the event of an injury, the process of healing that follows depends on the extent of the injury and the approximation of the wound site’s stump ends. There are two types of tissue healing; primary and secondary intention. Healing by primary intention commonly occurs in minor wounds wherein the tissue separation is small and a bridge of cells bind the ends of the wound together, resulting in a small line of scar tissue. Healing by secondary intention occurs in more severe wounds, where the stump ends cannot be bridged as they are too far apart. The wound heals by producing tissue from around the wound to fill the space created by the wound. This can occur in second degree sprains where ligament tissue is torn and not surgically repaired. Secondary intention healing takes longer than primary and also results in a larger scar.
Healing can be described as a continuum of changing events. There are four common stages to healing; bleeding, inflammation, proliferation and re-modelling. All the stages overlap considerably and are not separate.
Diagram to illustrate the four stages of healing (Watson, 2009)
Figure 1 shows a basic overview of the four stages. The phases are shown individually, but in reality, they are overlapped. Some events associated with one phase act as stimulant for the next phase.
The first stage of soft tissue repair is bleeding. As a result of soft tissue damage; blood vessels are damaged as well. The severity of the bleeding depends upon the vascularity of the tissue involved. Muscles have a more increased vascularity than ligaments. This stage lasts around 6 to 8 hours depending on the tissue involved.
The main focus of a sports therapist’s management would be to rest. It would be advisable to use crutches, stopping any weight bearing activity, as bleeding can start if the wound opens up again. A compression bandage could be considered to delay the onset of the inflammation phase. Restricting the intake of alcohol, aspirins and medications could be beneficial for the patient as these can thin the blood considerably. Once the body has moved into the haemostasis stage, bleeding will stop and the repair phase moves into the inflammation stage.
The second stage of healing is inflammation. The shift from bleeding to inflammation is not clear, as there may be some bleeding in the start of the inflammation phase. Houglum (2005) identifies that there are five cardinal signs to inflammation; heat, redness, swelling, pain and loss of function. This is a normal and necessary process to healing and can take up to 2 to 3 days. The stage can be initiated by numerous events such as trauma, mechanical irritation and thermal or chemical insult. Houglum (2005, p.37) states that “During inflammation, the injury is contained and stabilized and debris removed”. There are two elements to the inflammatory events that occur in parallel; vascular and cellular.
The vascular phase consists of close interaction between cells and chemicals, the process of chemotaxis taking place causing vascular permeability. Vascular permeability allows cells and chemicals that are in the blood stream to enter the injury site and perform their functions to heal the tissue. It is initially caused by histamine, a local hormone that is released by cells that enter the area due to which blood vessels get larger and leaker. As a result of this unwanted fluids and waste material are cleared. Histamine is a short lived hormone and its function is carried on by serotin and kinins. Kinins presence at the injury site is also short term and is followed by prostaglandin formation. There are two prostaglandins, one continuing the vascular permeability and one attracts leukocytes to the injury site. These prostaglandins stimulate repair or the damaged site and stimulate the stage into proliferation. As a result of vasodilation and vasopermeability there is an increase in flow volume, an increase in hydrostatic pressure and swelling.
The other phase of the inflammation stage is cellular events where there is a migration of various cells to the injured area. Platelets release phospholipids which effectively stop the bleeding by stimulating a clotting mechanism. According to Houglum (2005, p. 38) “Platelets also bind to the collagen fiber stumps that were exposed by the injury”. Platelets can also release substances such as fibronectin, growth factors and fibrogen.
Watson (2009) suggests that following the bleeding phase, fibrin and fibronectin form a solid layer that helps the adhesion of various cells, like a plug stopping the bleeding. As the healing stage progresses, the plug is replaced by type III collagen. Leakage from the blood vessels is stopped by the fibrin plug, which compromises their ability to remove the extra fluid from the area. However, later on fibrinolysin is released allowing drainage of excess fluid from the area. Within the first few hours of injury, white blood cells such as neutrophils, eosinophils and basophils start to remove debris from the site. As these are short lived, they are replaced by monocytes and macrophages. These exhibit a strong phagocytic activity that is responsible for the tissue debridement that takes place.
Houglum (2005) argues that inflammation can become harmful if it is prolonged, further than the normal healing time. Generally an injury should be passed through to acute inflammation and then to healing. Conversely, if acute inflammation is interrupted there can be a negative effect and as a result the injury can move into chronic inflammation. Chronic inflammation will result in a pus formation consisting of dead white blood cells. Failure of the body to deal with the initial insult is where healing fails to take place. As a result of this healing by fibrosis takes place where scar tissue is formed.
The goal of a sports therapist would be to facilitate inflammation but minimizing it (Houglum, 2005). This would be accomplished by applying initial first aid using the price principles. Protection via bandages and supports to the injury would be applied to reduce the likeliness of further bleeding or swelling. Brukner and Khan (2007) suggest that rest, with the use of crutches for lower limb injury and a sling for upper limb, will help reduce the metabolic requirement around the injury site. Ice can slow down nerve conduction, which slows down the rate pain gets to the spinal cord, effectively reducing the pain sensation. Ice would also increase vasospasm, reducing uncontrolled swelling around the injury. Brukner and Khan (2007) also advise that compression and elevation reduce swelling around the area and can decrease the effect of hydrostatic pressure which helps to reduce pain around the site. Hands off techniques such as active movements in a pain free range can beneficial.
Inflammation takes place in an anaerobic environment. After the macrophages clean up the injury site they recruit and activate other cells that start through anaerobic respiration where lactic acid is produced. Lactic acid stimulates the next stage of tissue repair named proliferation.
The third stage of soft tissue repair is proliferation, the true phase of healing, when bleeding has completely stopped. Watson (2009) suggests that it is the restoration of tissue continuity with the deposition of repair tissue. The stage of proliferation has a rapid onset of 24 to 48 hours but takes much longer to reach its peak reactivity, between 2 to 3 weeks. If the tissue is more vascular, it will take a shorter time in reaching peak proliferation production. There are two fundamental processes involved in the repair which are fibroplasia and angiogenesis.
The migration of fibroblasts is principally responsible for the development of new capillaries and extracellular matrix. A production of substances made by the fibroblasts will make up a matrix of collagen, proteoglycans and elastin which are required for vital scar tissue formation and proliferation. This migration to the injured site, allows fibroblasts to lay down collagen type III. Although, the fibre structure of type III collagen is weak, it helps provide the wounds primary tensile strength. It can be easily torn if too much stress is applied.
Alongside fibroplasia, a process called angiogenesis takes place. Watson (2009) states “â€¦capillaries in the region of the tissue damage bud and grow towards the repair zone”. Blood flow through the region is re-established, providing oxygen and nutrients while removing metabolic waste products. Oxygen is essential for many of the repair processes, but more importantly for collagen production. This process of tissue maturation continues into the remodelling phase.
To facilitate the proliferation stage, a sports therapist should apply heat to increase the blood flow to the area, effectively bringing more oxygen to the injury site and allowing more collagen production. Houglum (2005) believes ultrasound promotes collagen and myofibroblast production. Ultrasound would facilitate the proliferation phase as there is an increased need of collagen and myofibroblasts. Brukner and Khan (2007) claim that proprioceptive work such as joint awareness and positional sense can help enhance general coordination which will help facilitate strength and endurance exercises required in the next stage. Nutritional support such as whey proteins and vitamin c can speed up the healing process.
Various authors (Houglum, 2005 and Watson, 2009) identify that the remodelling stage normally starts at the peak of proliferation around 2-3 weeks and can last up to 18 months. Wound contraction starts and type III collagen are converted to type I, to stabilise and restore the injury site. As there is more type I collagen, it becomes more insoluble and less resistant to damage. Collagen fibres produce more cross links as fluid is reduced in the area, strengthening the structure of the scar. Eventually this cross linking becomes the major source of the scars tensile strength. The large numbers of capillaries produced in the proliferation phase are no longer needed and start to retreat. Fibroblasts migrated from the previous stage will also reduce. Visible changes can be seen, with the cellular changes taking place including the loss of scars red colour changing to white and then evening out with natural skin tone.
Therapeutic interventions to facilitate the remodelling phase can be a range of exercises and deep tissue work. These can help the arrangement of collagen fibres. Houglum (2005, p.43) claims that:
“When collagen fibers are aligned in an organized, parallel fashion, collagen can form the greatest number of cross links and thereby possess optimal strength”.
In this organised arrangement, function and mobility is at its greatest degree and properly applied forces can enhance it. Khan and Scott (2009, p. 249) in their report confirm that:
“The benefits of loading include improved alignment of regenerating myotubes, faster and more complete regeneration, and minimisation of atrophy of surrounding myotubes”.
Physical stress is an important component in the development of quality tissue repair. With this in mind, resistance training can be considered. Brukner and Khan (2007) suggest that resistance training may stimulate collagen synthesis. Strength and power training such as squats, dead lifts, compounds lifts that use more than one joint will increase the strength not only in the wounded area but the overall body. Sports specific exercises and complex training can also help in this stage. Brukner and Khan (2007) identify that stretching will promote a flexible strong scar. These interventions can speed up the conversion of type III collagen fibres into type I.
General factors that delay the healing process are age, protein deficiency, low vitamin c levels, steroids and NSAID’s and temperature when low. The local factors known to delay healing are a poor blood supply, adhesion to bone or other underlying tissue, continued inflammation, drying of the wound and excessive movement can restart inflammation.
Bleeding, inflammation, proliferation and remodelling are the four stages of soft tissue repair that are distinct but overlapping. From a sports therapist’s perspective it is important we apply therapeutic intervention at the right time and the appropriate management in order to facilitate the repair process avoiding delays by entering the chronic inflammation phase. Each athlete or client has different post injury sporting goals, level of skill and degrees of competitiveness, which all influence the rehabilitation programme. Therapeutic exercise must be administered carefully without causing harm to the healing tissues if rehabilitation programs are to be successful.
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