Inflammation (Fig. 4.1)

Inflammation may have an acute and a chronic stage. Acute inflammation is the response of the tissues to injury. It is a common process which occurs following mechanical or chemical trauma, infection, extremes of temperature, ischaemia, bacterial invasion and faulty immune reactions (Box 4.1). It is a necessary and positive event, being an important defensive mechanism essential for adequate healing to occur. It can, however, be induced or maintained inappropriately, in which case it may cause severe tissue damage, pain, deformity and loss of function in the affected parts.

Figure 4.1 • Inflammation: a comparison of normal capillary exchange and inflammatory response.

Reprinted from Pathophysiology for the Health-related Professions, Gould (1997) with permission from Elsevier.

Immediately after injury to the tissues, damaged blood vessels constrict under the influence of noradrenaline (norepinephrine) to slow blood loss should that be occurring. During acute inflammation the tissues then undergo sequential change, which begins with arteriolar dilatation, induced by local chemical mediators, including histamine, released from Mast cells and bradykinins, causing relaxation of the smooth muscle in the vessel walls. There is a consequent increase in blood flow. This means that the capillaries become dilated with the increased volume of blood entering them from the arterioles, which is seen and felt as a reddening of the skin in the affected area.

There follows an increase in capillary permeability, which allows leakage of plasma into the tissue spaces. The intercellular gaps in the endothelium increase in size due to contraction of the endothelial cells, which contain contractile filaments. Fluid is forced out of the capillary into the extravascular tissue spaces by an increase in hydrostatic pressure within the vessel, created by the extra blood which has flowed into the area. Proteins are also lost from the vessel, as they can escape through the enlarged intercellular gaps; this causes decreased intravessel osmotic pressure and increased osmotic pressure in the tissues. The fluid is seen and felt as a swelling, or oedema, in the affected and surrounding tissues. It is thought that oedema dilutes any toxins that may be present in the tissues and carries important substances which assist in phagocytosis. The fluid is known as inflammatory exudate and the process by which it moves into the tissues is termed transudation.

White cells line and adhere to the venule walls (margination) immediately the inflammatory process begins. Once fluid and proteins have leaked into the tissues, blood flow diminishes and blood viscosity increases, with red cells undertaking rouleaux formation in which they are stacked together.

Outside the vessels, white phagocytic cells, mainly neutrophils, migrate to the area. They are attracted by chemotaxis and leave the blood vessels by pushing between the endothelial cells, forcing through their pseudopodia between the cells. They are followed by large numbers of macrophages. The exudate is now a cellular aggregate and is viscous in consistency and appearance. Phagocytosis then removes unwanted material from the damaged area. The target cells are coated with protein—antibodies or complement—in the process of opsonisation, which allows them to be engulfed by the phagocyte. The material is then ingested, requiring much lysosomal activity.

Once the causative factor has been dealt with and inflammation has slowed, the tissues must return to normal by resolution. The inflammatory debris (including fibrinogen) is removed by macrophages, plasmin and lysosomal enzymes. The exudate and its proteins are removed by the lymphatics. If, however, any exudate persists it must undergo the process of organisation. Macrophages, fibroblasts and new capillaries invade the area. The macrophages remove the remains of the exudate while the fibroblasts secrete fibrin, which eventually results in collagen formation (a process expanded upon later in this chapter). The new capillaries withdraw and the collagenous tissue shortens, forming a scar. If tissue has been lost and the damaged cells are able to reproduce, regeneration next occurs.

The subacute phase lasts from 2 to 4 weeks after injury and is the period when resolution becomes complete and symptoms gradually subside (Kloth et al 1990).

Chronic inflammation

Inflammation that persists for months or more is termed chronic. It results from a breakdown in the normal process of acute inflammation, caused, for example, by a persistent irritant, inadequate circulation or a failure of exudate, pus or bacterial removal. It may also be caused by an autoimmune response. The presence of increased numbers of macrophages in the tissues will attract collagen-producing fibroblasts, which aim to encapsulate the affected site to prevent the spread of pathogens. Thus, prolonged inflammation will produce excess scar tissue, which can have significant functional consequences.

Inflammation occurs in all damaged tissues; recognition and assessment of the presence and severity of the symptoms will inform accurate clinical decision-making concerning massage.

The symptoms of inflammation (see Box 4.2) are known as the four cardinal signs. Redness is caused by the capillary vasodilatation and increased blood flow; swelling is caused by the inflammatory exudate in the tissues, enhanced by a reduction in lymphatic drainage in the area due to fibrinogen clots; heat is due to increased blood flow; and pain results from the former events, particularly the distension of tissues, pressure exerted by the oedema in limited tissue space and chemical irritation from inflammatory mediators.

Healing (Fig. 4.2)

The next process to consider is that of wound healing. The process is essentially the same in soft tissues whether the wound is caused by a scalpel, a crush or blow, a tear, or non-mechanical trauma. Inflammation is an inherent part of healing as the initial inflammatory process serves to contain the damage, preventing bacterial spread, for example. The other phases of healing must also be considered as they should dictate the type and timing of different massage manipulations. During this process, the tissues show a diversity of the various stages of healing. Ongoing inflammation occurs alongside other healing processes and possibly pathologies, for example inflammatory exudate, scar tissue and tissue necrosis.

Figure 4.2 • The healing process.

Reprinted from Pathophysiology for the Health-related Professions, Gould (1997) with permission from Elsevier.

There are two types of healing, the distinction being whether there is tissue loss. If the wound is a neat incision (a cut with a knife, for example) there is no tissue loss, whereas in the case of a skin graze, or a blow leaving crushed muscle fibres which die, tissue loss leaves a gap. Wounds without tissue loss heal by ‘first intention’ and those with tissue loss heal with ‘second intention’ (Fig. 4.2).

In either case, granulation tissue is formed, this process beginning 38–72 hours after injury. The area contains large numbers of macrophages for debris removal; fibroblasts and surrounding capillaries ‘bud’ into the area, forming new growth to provide nutrition. Collagen, hyaluronic acid and fibronectin (a glycoprotein which enhances cellular adhesion and migration) surround these new leaky capillaries and newly formed lymphatics. This tissue is termed granulation tissue, as its new capillaries give it a red granular appearance.

Meanwhile, a few hours after injury, epidermal cells begin to migrate. The surrounding epidermal cells break their desmosomal attachment with neighbouring cells and produce actin filaments at the edges of their cytoplasm which give them the capacity to move more easily by reaching out with pseudopodia. The cells either roll over the top of each other in a continuous line until the gap is filled, or slide along in a chain until the lead cell reaches the other side of the wound. The surrounding epithelial cells also reproduce, until a thin covering of cells seals the wound surface, and the wound is then closed from the edges inwards, growing progressively smaller in diameter. It is thought that these events can occur because the natural inhibitors of tissue growth—chalones—are absent from the area of tissue loss and are therefore unable to prevent cell division, and because epidermal growth factor is present.

At this stage the connections between the cells are fragile and delicate, and manipulation may damage them, causing breakdown of the new tissue which delays healing. However, good nutrition via the bloodstream is essential for successful tissue repair and careful massage of the surrounding area may be beneficial, particularly where the circulation is poor.

The next visible occurrence is wound contraction. This begins before substantial collagen synthesis in the first 2 weeks after injury; it is thought to be due to the contractile abilities in the actin-containing fibroblast, the myofibroblast. These cells extend pseudopodia, attach to the collagen fibrous network and retract, reducing the surface area of the wound if the conditions are favourable, and if the number of cells is appropriate for the size of collagenous matrix.

Once cell migration is complete, a collagenous basement membrane is laid down and the cells form connections. In scar formation, cytokines stimulate fibroblasts which form collagen, and polypeptide chains aggregate into a triple helix to become procollagen, at which stage it is released from the fibroblast. Parts of the molecule are lost, leaving tropocollagen, and intramolecular and intermolecular cross-bridges are formed to give tensile strength to what is not yet a structural fibril. At this point, the collagen resembles type III collagen, which is eventually replaced by type I collagen in response to mechanical stress. This stage is a major part of skin healing, as dermis contains predominantly connective tissue.

Mechanical stress is important at this stage for the remodelling of collagen (replacement of type III with type I collagen) and also for alignment along the lines of stress. This alignment is due to the piezo-electrical effect whereby electrical streaming potentials result from mechanical stress and dictate the remodelling process. This stress is usually produced internally by normal functional activity, for example when muscle contraction exerts a pull on a tendon or when joint movement applies forces to ligaments. The effect may be enhanced with artificial stress, applied externally by manipulation of the tissues. Massage, therefore, will promote remodelling and thereby increase the tensile strength of the tissues. This effect is particularly important where immobility, either local or general, has been enforced. The lack of movement will have resulted in reduced stress being exerted on the tissues which has a weakening effect, even in normal tissues, as demonstrated by research (Akeson et al 1973).

The remodelling occurs during the maturation phase of scar formation. The bonding within the intercollagenous molecules strengthens, converting from the weaker hydrogen type to the stronger covalent type of bond. Hydrogen bonding permits stretching in response to gentle stress, whereas mature collagen is more resistant. This is important, as at this stage stress that is correctly applied and not excessive will ensure that the wound or scar heals at optimum length; any shortening is difficult to correct once healing is complete, owing to the stronger covalent bonding in mature collagen.

Occasionally, this remodelling mechanism fails and the balance between collagen removal (or lysis) and deposition (or synthesis) is lost. If excess collagen deposition occurs within the boundaries of a skin wound, a hypertrophic scar results. If it extends beyond the wound, and encroaches on normal tissue, then a keloid scar results. Keloid scarring is prone to occur in burned skin and the use of pressure garments is common in treatment of the burned patient. These exert a continuous pressure (they must be worn for 24 hours a day), creating a piezo-electrical streaming potential to maximise connective tissue remodelling. They have been found to be extremely successful in reducing hypertrophic and keloid scarring.

Friction massage has been found not to influence the vascularity, pliability or height of hypertrophic scarring (as assessed by the Vancouver Burn Scar Assessment Scale) when it was given to 30 children for 10 minutes daily over a 3-month period (Patino et al 1999). The choice of frictions as a massage technique in this study can be questioned. It placed a high level of dynamic mechanical stimulation in tissues in which, in the case of hypertrophic scarring, the balance between the lysis and synthesis of collagen has been lost. It is perhaps unsurprising that this study yielded negative results when there is evidence that continuous pressure is effective in reducing the effects of hypertrophic scarring.

This account of the physiological events that occur during the inflammatory and healing processes may serve to inform our intervention during or following these events. Massage should be employed to:

First, it may be appropriate to increase circulation to the area. Blood flow may be compromised as a result of the patient’s circumstances—confined to bed, for example, or immobilised for some other reason. The reduced mobility may be general if the patient is unable to function normally, or may be local if only the affected limb, or even joints above and/or below the injured area, is immobilised. Immobility may be of a more subtle nature, for example if pain, or a dressing, prevents normal gait or muscle action. This situation reduces muscle pump activity and consequently venous return, resulting in a reduction of general circulation and a gravitational pooling in the lower limb. Slight puffiness around distal joints, especially the ankles, in the absence of other possible factors (such as heart or kidney failure), indicates reduced muscle pump.

The circulation locally around the wound may need to be increased. If inflammation has reached a chronic stage and healing has been delayed for any reason, then the wound margins may be adherent and congested. Wound contraction may be compromised due to excess adherence of the margins to underlying tissue. Gentle circular kneadings around the edges, taking care not to touch any healing surfaces, or to disturb areas of healing, may bring nutrition to the area, mobilise the margins from adjacent layers of tissue and speed up wound contraction, and therefore healing.

As the wound heals beyond the cell adherence stage, gentle stress will facilitate remodelling of collagen and therefore maturation of the scar. At this stage, adherence and excessive contracture must be avoided. Massage can help to loosen the scar from underlying tissue, preventing or reducing adherence in a more chronic stage of healing. It can reduce contracture of the scar by repetitive stretching, facilitating a final optimum length of the collagen fibres.

At all times, the stage of healing must be considered—this guides the effectiveness and safety of the techniques. The timetable of healing is now well established and the summary in Table 4.1 provides a good basis for clinical decision-making and treatment planning.

Table 4.1 Phases of wound healing

We will return to the implications of the stages of the healing process in the clinical sections of this book, but from the preceding descriptions it is clear that in the early stages of healing, when the cell connections and collagen fibrils are delicate, manipulation should be avoided. The surrounding area can be massaged gently to increase circulation, an effect that may be enhanced by proximal massage. During the early stages of remodelling, gentle mechanical stress will facilitate healing at the optimum collagenous length and strength. As this period moves into consolidated healing, a stronger stress will correct any shortening and further strengthen the tissue.

Wound contracture is an essential part of the healing process, particularly where there is extensive tissue loss, and over time the scars tend to become smaller and paler in colour. However, occasionally this shrinkage occurs beyond a desirable level. This sometimes happens as healing occurs, but remodelling, stimulated by normal movement of the body part and stretching of the affected tissues, gradually restores the tissue to a more functional length. If local or general immobility reduces this normal process, or if pathological factors such as infection increase fibrous tissue formation, it may be appropriate to assist in the establishment of tissue length; depending on which tissues are involved, reduction in tissue extensibility, even temporarily, compromises joint movement and function causing possible joint complications such as stiffness and loss of accessory movements, which may alter the biomechanics of the joint and reduce its range of movement. Complications such as this produce the difficulties experienced by a patient as functional loss. This may be considerable, for example if the damage has occurred in the hand, with potentially serious psychological, social and financial effects. Eventually, if left, the tissue may remodel in its newly shortened length and contracture may be permanent. Manipulations that stretch the tissue in all directions are important here.

The effects of excess tissue contracture will vary with the tissues involved. Ligament contracture, for example, will compromise the function of its joint. The effects will be exacerbated if adherence of the scar to underlying tissue has occurred. This will result in loss of excursion, not only of the superficial layers but of the deeper layers also, resulting in increased functional loss. Each time a normal movement places the tissue on a stretch, rather than yielding normally, a pull will be exerted at the point of adherence (and the tissue interface), causing pain. The patient will tend to stop the movement short of that point, to avoid further pain. Remodelling of the tissue will therefore occur in response to non-functional stimuli, resulting in shortened, and initially weaker, collagen because of the reduction in stress. If muscle tissue is involved, shortening and muscle imbalance could result. Where movement is less well controlled, there will be pull exerted at the end-point of mobility, creating an inflammatory reaction at the adherent interfaces. This will result in the formation of further fibrin and collagen, causing thickening and excess scarring. The result will be a permanent adherence and loss of function.

At this chronic stage, massage should be vigorous, focusing on prolonged stretching manipulations.

It is likely that the circulation will be compromised, as chronic inflammation may result in its attendant problems, and there may be involvement of nerve endings, resulting in neural tension in the skin.

Oedema

Oedema is present in many of the patients who consult or are referred for physical therapy. It must be controlled immediately it occurs, as chronic oedema can cause fibrosis, adhesions, resultant loss of joint movement and pain. The excess fluid itself causes pain as pressure is exerted on nociceptors; it further prevents cells from being bathed in fresh, newly nourished tissue fluid, and thus reduces normal cellular metabolism. Metabolic circulation may be reduced together with metabolites, and protein remains in the tissues. Prevention, containment and removal of swelling is the essential hierarchy of care for the tissues, regardless of cause, and massage can be a cornerstone of effective treatment, with skilful application of manual lymphatic drainage (MLD) being essential in the treatment of lymphoedema.

Control of oedema is a significant feature of the massage therapist’s professional life. It is present in many of our patients’ tissues for a variety of reasons and hence occurs in many forms. It is essential that we are able to recognise it and identify its type so that we can establish its causative factors. This will enable us to decide whether massage can assist its removal, which type of massage will be most effective, whether an alternative intervention is required or whether massage should be avoided altogether. Excess tissue fluid is present in many people, from the ‘puffy ankles’ of the shop assistant on a hot day or the holiday-maker at the end of a long flight, to more long-standing intractable oedema, as in lymphoedema. Normal fluid balance in the tissues is dependent on many factors, any of which, if operating suboptimally, can result in excess tissue fluid.

Fluid balance in the body

To maintain a perfect balance of fluid between the circulatory system and the tissues, the circulation must be operating normally, in both the structure of the carrying vessels and the constituents of the blood itself. The heart pumps arterial blood into the periphery of the body, through the arterial system, so the veins must operate an efficient system of return. They must be sufficiently pliable to be squeezed by contracting muscles, to pump the blood from the superficial veins into the deep veins and then upwards along the venous system, against gravity. Valves stop the back-flow of blood when the muscles relax, thus contributing to the pumping effect. A strong dynamic muscle pump will make this system extremely efficient, and weakened muscles or immobility will decrease its effectiveness. The volume being returned to the heart must match the volume being pumped by the heart, and a system of fluid balance maintenance must operate successfully at the arteriovenous capillary loop, through pressure equalisation between the tissues and vessels (see Chapter 2). Adequate tissue pressure around the muscles created by the fascial layers will give the muscles a firm covering to contract against, ensuring that good squeezing of the veins occurs.

Causes of oedema

There are several components to the circulatory system, and oedema can occur when any component operates at less than optimum efficiency:

• Inflammation, as in an acute injury or an allergic response in the skin, causes increased permeability of the capillaries, and excess fluid will leave the circulation for the tissues.

• If pressure is placed on any part of the circulatory system, as in pregnancy, varicosity or thrombosis in the veins, the increased hydrostatic pressure within the vessels will be in excess of that in the tissues, resulting in oedema.

• Pressure can be increased in the circulatory system by heart malfunction. Cor pulmonale results from pulmonary conditions in which the pressure in the pulmonary artery is increased, exerting a back pressure on the right ventricle, resulting in hypertrophy and reduced output by the insufficient heart musculature. The back pressure causes congestion in the veins of the periphery, raising the hydrostatic pressure in the venous blood with inevitable oedema.

• Insufficiency of the lymphatic system, for example congenital absence or damage to the lymph glands by radiotherapy or surgery, means that proteinous fluid accumulates in the tissues.

• Other medical conditions can create oedema in the tissues. Heart failure, which lowers cardiac output, leads to a lowered capillary pressure, which affects perfusion in the kidneys. Sodium and water are retained by the body, some of the fluid being pushed into the tissues. Primary renal disease invariably leads to a reduced filtration rate with excess retention of salts and fluid (Woolf 1988).

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