53. Principles of restricted mobility management
pressure area care
CHAPTER CONTENTS
Pressure-area care369
Common sites for pressure ulcer formation371
Classification of pressure ulcers371
Factors influencing development371
Assessment of skin integrity373
Principles of pressure area care373
Role and responsibilities of the midwife374
Summary374
Self-assessment exercises374
References374
LEARNING OUTCOMES
Having read this chapter the reader should be able to:
• discuss why pressure ulcers occur
• identify factors that increase the risk of pressure ulcer formation
• describe the four stages of pressure ulcer formation
• undertake assessment of the skin, recognising normal and abnormal changes resulting from pressure
• discuss the principles of pressure area care.
Women may have restricted mobility for many reasons – bed rest due to antepartum haemorrhage, pre-eclampsia, during and following epidural anaesthesia, general anaesthetic, following a postpartum haemorrhage or postoperatively, etc. – making them vulnerable to or at an accelerated risk of pressure ulcer formation. Babies who are unwell, particularly the very preterm babies, are also vulnerable to or have an elevated risk of developing pressure ulcers. Damage to skin and underlying fatty tissues from pressure ulcers causes pain. If the ulcer becomes infected, septicaemia and/or bone infection can ensue; muscle or bone may be destroyed in severe cases. These complications of restricted mobility, although they are not commonly seen within the midwifery setting, do occur (Butcher, 2004 and Hughes, 2001), increase morbidity and mortality and are often avoidable; it is important that the midwife develops the knowledge and skills to reduce their incidence. The Royal College of Nursing and the National Institute for Health and Clinical Excellence (RCN & NICE 2004) recommend that all healthcare professionals undergo relevant training and education in the assessment and prevention of pressure ulcers.
This chapter focuses on the principles of pressure area care including a discussion of the aetiology and classification of pressure ulcers. The factors that influence the development of pressure ulcers are given, followed by a discussion of the assessment of skin integrity.
Pressure-area care
This is undertaken to reduce the incidence of pressure ulcer formation. A pressure ulcer is a skin ulceration that forms due to localised tissue necrosis, commonly found on the parts of the body that have received unrelieved pressure or friction, or both. It has previously been referred to as a ‘decubitus ulcer’, ‘pressure sore’ or (less commonly) a ‘bedsore’.
A variety of risk assessment tools are available for use in the clinical setting (e.g. the remodified Norton Scale, Braden Scale, RAPS scale) with varying degrees of success. Their use does not appear to prevent pressure ulcers worsening or from further ones developing [EUAP (European Pressure Ulcer Advisory Panel), 2009a and RCN (Royal College of Nursing), NICE (National Institute of Clinical Excellence), 2005] but the presence of a grade 1 pressure ulcer should be considered a significant risk factor for the development of a more severe form of pressure ulcer. The RCN & NICE (2004) recommend these should not replace clinical judgement, but should be used only as an aide-mémoire. Moore & Cowman (2008) reviewed the studies of risk assessment tools compared to the use of clinical judgement for assessing the risk of pressure ulcer development, but found no randomised trials had been undertaken and were unable to form a conclusion as to their value. However, of the tools available, Pancorbo-Hidalgo et al (2006) found the Braden Scale offered the best balance between specificity and sensitivity and the best risk estimate for pressure ulcer formation and concluded that both this scale and the Norton Scale were more accurate than nurses’ judgement in predicting the risk of pressure ulcer formation.
It is important to identify individuals at risk of developing pressure ulcers (EPUAP 2009a) by considering the woman or baby’s general medical condition, undertaking an assessment of their skin, mobility, moistness (including level of continence), nutrition and pain levels. For those identified as being at increased risk, appropriate intervention should be utilised.
Aetiology of pressure ulcers
Pressure ulcers develop as a result of two processes, occurring either separately or together:
1. unrelieved pressure
2. shearing and friction.
Unrelieved pressure
Pressure within the capillaries varies from 35 mmHg (arterial) to 16 mmHg (venous) (South et al 2008). External pressures above this will result in occlusion of the capillaries. If the pressure is prolonged, even with low-intensity pressure, the resulting anoxia causes tissue ischaemia and necrosis. Necrosis may begin in the muscle that lies over the bone. The length of time the pressure needs to be applied for damage to occur will vary from person to person.
Healthy lightly pigmented skin with a good circulation blanches when blood flow is restricted (e.g. fingertip pressure). The skin whitens, replacing the usual red/darker skin tones. The effects of pressure can be seen when the pressure is removed and a sudden, large increase in blood flow occurs, up to 30 times the normal resting value. This results in a normal ‘reactive hyperaemia’, when blanching is replaced by a bright red flush, lasting usually less than 1 hour. Providing the lymphatic vessels are not damaged and excess interstitial fluid is removed, there is no permanent damage. However, if there is lymphatic vessel damage, tissue changes occur and large amounts of interstitial fluid are squeezed out. The cells rub together and the cell membranes rupture, releasing toxic intracellular material and normal skin colour is not restored. A deep pressure ulcer can arise when the lymphatic vessels and muscle fibres tear. In the healthy adult with full sensation, this will result in pain causing the individual to move (Benbow 2008). Where sensation is impaired (e.g. epidural anaesthesia) the change of position does not occur spontaneously.
Abnormal reactive hyperaemia and induration can occur with excessive pressure, causing the affected area to appear darker than the surrounding skin. Absence of blanching with a fingertip may also be seen. These effects can last for more than 1 hour after the pressure has been removed, possibly up to 2 weeks (Ayello 1999).
Darkly pigmented skin does not blanch or change colour when pressure is applied, making it more difficult to recognise impending tissue damage.
Shearing and friction
A shearing force is the pressure exerted against the skin in a direction parallel to the body’s surface, occurring when the body moves up or down the bed while in an upright position. As the layers of muscle and bone slide in the direction of the body movement, the skin and subcutaneous layers stick to the bed surface, causing the bone to slide down into the skin, with a force exerted onto the skin. A shearing force results at the junction of the deep and superficial tissues. The microcirculation is compressed and damaged, causing microscopic haemorrhage and necrosis deep within the tissues. This is compounded by the decreased capillary blood flow resulting from the external pressure pressing against the skin. Eventually, a channel opens through the skin and the necrotic area drains through this. The areas commonly affected by shearing forces are the sacrum and coccygeus. Benbow (2008) suggests the effects of shearing are exacerbated by moisture, highlighting the importance of ensuring the sheets underneath the woman are dry. Shearing forces can be reduced if the head is kept below 30° (Ayello 1999), i.e. place the chin on the chest when moving.
Friction is the mechanical force that is exerted when the skin is dragged across a coarse surface (e.g. bedding). The epidermis is rubbed away, giving the appearance of a shallow abrasion injury, often on the elbows and heels. The effects of friction are exacerbated by moisture (as for shearing) (Benbow 2008).
Common sites for pressure ulcer formation
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