A wound can be described in several ways i.e. by its aetiology, anatomical location or whether it is acute or chronic. However, these definitions, serve a critical role in the assessment and proper management of the wounds. An actual account, its definition can be broken down into the skin’s protective functions: continuous epithelium loss with or without connective tissues being loosed. This is as a result of an injury caused to the skin by either surgery, blow, cut or even chemicals. A wound can also be said to be any type of an injury that causes harm to the skin. The following article will, therefore, discuss the kinds of wounds e.g. arterial, venous stasis, pressures ulcer etc.). It will also consider the pressure ulcer staging, assessment, prevention and its treatment.
The first type of wound is the arterial ulceration. It emanates from a reduction in the arterial blood supply to the limbs in the lower parts of the body. It causes the atherosclerotic disease of both the medium and large arteries. Its other causes include diabetes, vasculitis, thalassemia and even the sickle cell disease. These may predispose the atheroma formation. Arterial system can be further damaged by the concurrent hypertension which damages the artery’s initial layer. The reduction in supply of blood to the artery causes hypoxia, ulcer formations, as well as, tissue damage.(Mallon, 2007, P. 122)
Arterial ulceration appears over toes, heels and the bony parts of the foot. The wound appears punched-out with pale demarcated edges that are often necrotic bases. The surrounding skin do exhibit a dusky erythema which cools to touch, hairlessness and a brittle texture. Toenails become thick with the risk of being uprooted. Gangrene extremities also do occur. There is also a decreased pulse of the arterial system i.e. in the pedis and tibia arteries. Bruises that indicate the presence of atherosclerosis also appears.(Mallon, 2007, P. 146)
The second type of wound is called venous stasis. It is caused by a sustained venous hypertension. It appears in the gaiter part of the leg. The wound may be discrete or circumferential. The ulcer bed is covered with a fibrous layer which is laced with a granulation tissue. It is also surrounded by an irregular and a gently sloping edge. Such type of wounds that appear above the midcalf have their origins.(Mallon, 2007, P. 67)
The third type of a wound is called a peptic ulcer. They develop in the stomach’s lining i.e. the oesophagus and the small intestines. This is as a result of the erosion caused by the acidity of the stomach. Three types of pep tics i.e. gastric, oesophageal and duodenum wounds exists. They develop inside the stomach, oesophagus and the small intestines’ upper section respectively. Such wounds in stomach causes chest pains, vomiting, dark stools, nausea and changes in appetite. The contributing factors to peptic wounds include excessive alcohol consumption, radiation therapy, stomach cancer, smoking and frequent use of anti-inflammatory drugs.(Barbara, 2007, P. 178).
Laceration is also a type of a wound. It is an injury to the skin resulting to it being torn or open. They can either be shallow causing damage to the skin surface or even deeply causing injury to ligaments, nerves and blood vessels. They are mostly caused by blunt trauma e.g. by being hit with a baseball bat. The skin in a laceration is jagged since the skin is torn and not cut.
Broader sense, wounds can be categorised as penetrating, non-penetrating and miscellaneous wounds. (Barbara, 2007, P. 115).Penetrating wounds result from skin breakages thus reaching down to underlying tissues. They can either be stab wounds, skin cuts, surgical wounds and gunshot wounds. Non-penetrating wounds are as a result of friction with other surfaces. The wound does not manage to break through the skin. They include abrasions, contusions and concussions. Miscellaneous wounds, on the other hand,encompass thermal wounds, chemical wounds, bites and stings and even electrical wounds.
Lastly, pressure ulcers can be said to be injuries that break the skin and the underlying tissues. They are caused when pressure is applied to a section of the skin. They are at times called bed sores or pressure sores. They range from the severity of discoloured patches of skin to open wounds that fully exposes underlying muscles. The pressure applied causes a disruption in the blood flow which results in the affected area becoming starved of oxygen and nutrients. The skin eventually breaks down leading to ulcer formation.(Bader, 2005, P. 4)
Pressure sores go through four stages. In stage 1, the wounds are not yet open. The skin is painful, but it has no breaks. It is reddened and doesn’t blanch. The skin temperature becomes warmer and softer than the surrounding areas. At stage 2, the skin tears away forming a painful ulcer. A blister forms with the skin dying and becoming irreparable. At stage 3, the blister becomes worse forming a crater like beneath the skin. It extends to tissues below the skin. Fat starts showing in the sore. At stage 4, the sore is extremely deep and reaches into muscles and bones thus causing extensive damage tissues and tendons.
Treatment of pressure sores incorporates the use of dressings, creamy solutions and gels. They speed up healing of the sores and in relieving pressure. At times when the case becomes severe, surgery is recommended. For some individuals, their treatment involves an inconvenience of regularly nursing the affected area. For others, it can be complicated and life threatening. Firstly, pressure that caused it is reduced. This is achieved by repositioning and use of support bases. The second step is cleaning and dressing of the wounds. The last stage is removing the damaged tissues. This is because, for the tissues to heal properly; it should be free of the infectious skin.(Bader, 2005, P. 45)
References
Bader, L. (2005). Pressure Ulcer Research: Current and Future Perspectives. New York. Springer Science & Business Media.
Barbara, M. (2007). Wound Care: A Collaborative practise manual.Berlin. Lippincott Williams & Wilkins.
Mallon, C, P. (2007). The Aetiology of Deep Venous Thrombosis.New York. Springer Science & Business Media.
