acute inflammation
Acute inflammation is a complex series of events controlled by chemical mediators, the function of which is to remove harmful microorganisms and necrotic tissue, to defend against any further injury and to replace injured cells and restore architecture and function.
Arteriolar and capillary bed dilatation cause blood flow to be massively increased in the injured area, and vascular permeability is increased resulting in the formation of an extracellular, protein-rich inflammatory exudates (Kumar et al 2005 pp.49-62; Alpar and Gosling 1999 p.42).
Vascular permeability is modulated by kinins, complement and coagulation cascades.
White blood cells, predominantly neutrophils, adhere to the vascular endothelium due to the expression of adhesion molecules and migrate to the site of injury under chemotactic influence. Neutrophils are phagocytic, and attempt to clear the wound of invading microorganisms and cell debris.
Monocytes infiltrate the injured area and differentiate into tissue macrophages – scavengers of necrotic tissue and bacterial remnants etc. They also stimulate the growth of endothelial, epithelial and fibroblastic cells via growth factors.
the host response to injurious stimuli
Use the presentations below to revise the components of the host response to injurious stimuli (i.e. acute inflammation). The first presentation provides a summary of the major components, whilst the second provides a more detailed view.
images
- Derm Atlas image - healing and bruised sutured wound 5 days post skin biopsy
- Derm Atlas image - 1 month old scar following surgery
- Wikipedia image - wound suturing
- Resident.net - wound suturing guide
healing by primary intention
Wounds that have minimal tissue loss, particularly surgical incised wounds, heal by primary intention. In these circumstances, wound edges are apposed by sutures, and the size of the defect, and amount of clot present are both small. Very little epithelialization and contraction is required, and these wounds generally heal well with minimal scar formation.
Approximate timetable for healing of wounds by primary intention (Cottran et al 1999 pp. 107-109)
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Time |
Activity |
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0 hours |
Incision filled with clot. Inflammatory cells attracted |
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3-24 hours |
Neutrophils infiltrate clot. Epithelial ‘closure’ of the wound takes place by 24-48 hours |
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Day 3 |
Macrophages predominate and granulation tissue appears. |
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Day 5 |
Wound filled with granulation tissue. Collagen appears. |
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Week 2 |
Fibroblasts proliferate and collagen accumulation produces a scar. |
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2 months |
Connective tissue within scar largely devoid of inflammation. |
inflammation via the Khan Academy
healing by secondary intention
Where wounds are large, more extensive tissue replacement is required, and the processes of re-epithliazation, scar formation and wound contraction are prolonged.
factors affecting wound healing
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Local factors |
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Systemic factors |
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references
- Alpar E.K., Gosling P. (Ed) (1999), ‘Trauma – A scientific basis for care’, Arnold Publishing
- Ashcroft GS, Horan MA, Ferguson MW (1995), 'The effects of ageing on cutaneous wound healing in mammals', J Anatomy 187(1):1-26
- Kumar V, Abbas AK, Fausto N (2005), ‘Robbins and Cotran Pathological basis of disease’, 7th Ed Elsevier Saunders, Philadelphia, USA
- McCance K.L, Huether S.E. (2002), ‘Pathophysiology – The biologic basis for disease in adults and children,’ 4th Ed 2002 Mosby Inc
- Russell R.C.G., Williams N.S., Bulstrade C.J.K. (2000) (Ed), ‘Bailey and Love’s Short Practice of Surgery’, 23rd Edition, Arnold Publishing
inflammation and wound healing
Physical trauma results in cell injury, which in turn initiates an inflammatory response – essential for defence, survival and wound repair.
Acute inflammation is characterised by a series of changes that allow the entry of phagocytic cells and plasma proteins to the damaged area. Tissue repair starts during the early phases of inflammation, but continues long after the injurious stimulus has been neutralised.
wound healing
The aim of wound healing is to provide a complete return to normal structure and function (‘resolution’). However, if the damage is extensive, or the tissues incapable of regeneration etc, repair takes place instead of resolution. This is the replacement of destroyed tissue with scar tissue composed of collagen (McCance and Huether 2002 p.219).
Resolution and repair of wounds involve 2 overlapping phases – reconstruction and maturation.
A skin wound is initially sealed by blood clot containing fibrin and trapped red blood cells and white blood cells. The fibrin mesh is created following the activation of the coagulation cascade. Platelets trapped in the mesh assist in sealing the wound. A jelly-like matrix provides a framework for cell migration into the wound.
Granulation tissue arises following activation of endothelial cells and fibroblasts, the latter secreting collagen which gives strength to the healing wound.
As the clot is dissolved and granulation tissue formed, epithelial cells are attracted by macrophage-derived chemokines, and migrate under the clot or scab to re-epithelise the skin.
Collagen fibres are initially deposited randomly in the wound, but during maturation re-orient along lines of mechanical stress and undergo chemical changes resulting in increased strength.
Myofibroblasts present in the granulation tissue give rise to wound edge contraction – noticeable 6-12 days post-injury and resulting in an inward movement of the edges by approximately 0.5 mm/day (McCance and Huether 2002 p.221).
Scar tissue is remodelled in the maturation phase and capillaries disappear from the granulation tissue leaving a white scar.
source: wikimedia