Preventing paediatric pressure ulcers

Prevention of pressure ulcers (PUs) in children involves accepting that the skin is the largest organ of the body and requires a complete understanding of the wound healing process as a complex and carefully regulated physiological response to traumatic skin injury. To maintain the integrity of the skin, it is necessary to solve the important wound care puzzle called ‘prevention,’ the key components of which comprise a full clinical examination, analysis of risk, educational strategies and a natural comprehension of the different stages of skin breakdown (SB) and PUs.

In children, PUs can be defined as localised areas of tissue destruction and death resulting from compression of soft tissues between bone or bone-like prominences and an external surface. For example, retroauricular tissues can become compressed between the ear cartilage and the processus mastoideus of the temporal bone resulting in a PU as the skin is too fragile for the heavy cartilage (see Figure 1). But undue pressure, decreased mobility, decreased activity (depending on age) and decreased sensorial perception are not the only risk factors involved in PU development. Others include body areas that are moist because of incontinence, salivary secretions or acid fluids, as in first degree diaper dermatitis (Stage I PU, mild), which is characterised by tenderness and blotchy erythema and superficial or deep folliculitis. 

Pressure ulcer prevention programs must minimise dangerous effects due to extrinsic factors such as external moisture, friction and shear from movement over a coarse surface. Paediatrics is a heterogeneous age group (Table 1) especially affected by PUs because of the natural fragility of the skin, the extreme thickness of the epidermis-dermis (<2.1mm) and the inclusion of ‘fragile’ patients at high risk for SB such as premature, small-for-age newborns. In particular, the neonatal age is a true challenge, as immature skin must pass from the aquatic to the aerobic condition, and the underdevelopment of subcutaneous tissue, poor cohesion between the epidermis and dermis, the dermal instability and the alkaline skin surface are all equally responsible for an increased risk of SB. Other peculiar aspects of the neonatal skin and the resulting skin injuries are listed in Table 2.

Children admitted to the neonatal intensive care unit (NICU), paediatric intensive care unit (PICU), and cardiothoracic, orthopaedic, neurosurgical, surgical and neurorehabilitation units have to be managed with aggressive prevention strategies. These children are more prone to develop PUs because they are submitted to a large number of long-lasting surgical procedures, including extracorporeal life support. This may result in a temporary reduction of blood flow to less vital tissues of the body such as the skin in comparison to the brain, heart, kidneys and liver. As a result, a non-blanchable erythema or a persistent, sometimes scarring alopecia may appear (see Figure 2). The subsequent evolution of these two conditions, if not recognised and prevented, is a PU. The current time-rotational protocol for children aged 18mmHg; the closure-pressure for the capillary network in newborns is 20mmHg, in children >3 years <24mmHg and in adults 26mmHg. At the same time, all kinds of undue friction or compression at the level of the occiput, ears, heels and back, which are the sites mainly affected by SB (60%) in children, must be avoided (Table 3). 

The first step of our PU prevention protocol involves a skin assessment and re-assessment, developing an awareness of the true mobility of the child, the child’s moistness–incontinence aptitude (sometimes physiological for the age), a nutritional assessment, identifying limited deficiencies and pain and an immediate counselling of the parents. 

In our opinion, education and gradual training of the caregiver is of great importance for preventing PUs and should have a tremendous impact in reducing SB. The pain associated with PUs is often undiscovered, and the patient may be misunderstood leaving the ability to feel and respond to pressure related pain completely in charge of the mother, the best caregiver we have. However, the presence and the activity of a psychologist in the prevention-team are mandatory. In addition, extended family members are as important as parents; these are devoted figures that provide more than the usual social support in human relationships, and they are the main carers in more than 40% of observed cases.

We recommend a learning strategy that includes knowledge at four different levels: 

1.   identifying areas of ‘contact’ with bony prominences and SB 

2.   developing ‘synergism’ between caregiver, nurse and surgeon

3.   recognising that a ‘multiplicity’ of body sites should be included in an observational protocol, and it is possible to have more than one PU in a short period

4.   ‘acceptance’ of the disease (PU) as a transient one, if diagnosed early (secondary prevention). 

If caregivers are familiar with these four main points, prevention becomes easier.

If we consider the intrinsic factors able to induce a PU other than young age and faint tissue perfusion, nutrition plays a very important role. In our experience, 46% of children with a Stage I or Stage II PU are malnourished. Moderate mucosal bleeding, temporary alopecia, multilamellar and exfoliating peeling and peristomal hyperaemia are early signs of an impaired nutritional status that we have to assess, considering serum albumin, haemoglobin, iron and transferrin. If there is prompt and appropriate intake of calories, vitamins and minerals, all skin signs of deficiencies disappear within two to four weeks after the diet has been instituted. When a poor nutritional status is clearly evident and is associated with SB or a Stage I–II PU, a hyperproteic diet (proteins, 2.5–3g/kg; arginine 10–15g/24hours; proline/hydroxyproline 250–500mg/24hours) reverses all signs of skin disease. Other support for the skin includes selected vitamins; we consider 500% of the recommended daily amount (RDA) for vitamin A, vitamin C, beta-carotenes, vitamin E and selenium and 150% of the RDA for folic acid, niacin and vitamins B1 and B2 to be beneficial.

The second step involves the appropriate classification of admitted patients because, in our experience, there are six classes of high-risk children. These include children who are disabled, still-motionless, mentally-impaired, incontinent, spinal and syndromic patients. 

When we consider a child at high risk for SB and PU, we have to pay attention to their ‘primary system dysfunction’ and the ‘Paediatric Cerebral Performance Category.’ In a series of more than 850 paediatric patients with more than 1200 PUs, 36 and 21% were neurologically and pulmonary impaired, respectively, and 55% had a mild to severe (25%) brain disability. 

In children admitted to the NICU or PICU, the five most important risk factors responsible for developing a PU are:

1.  weight loss

2.  albumin <2.5mg/dl

3.  haemoglobin <10g/dl

4.  iron levels <20mcg/dl

5.  transferrin <10%

Another very important factor is biometry. Biometry is the ability to maintain natural conscious positions during both mobility and immobility. In high-risk patients, biometry is drastically impaired. When the anatomy is altered and distorted, unusual anatomical body sites are more prone to be affected by PUs. If more than three points of altered biometry are present, the possibilities for a SB and rapid development of a PU are nearly 95%. In these cases, instant prevention and articular as well as neuromuscular rehabilitation are needed (see Figure 3).

The third step is to pay attention to oedema development. Whatever the cause, in this pathological condition the pre-arteriolar space is increased, the distance between the capillary bundles and cells is increased, and as a result the diffusion of oxygen to the tissues is reduced. When oedema occurs, the depth of the anatomical folds and cavities of the body increase, and undue movements of friction and shear forces induce breaks and tears in the swollen skin.

The fourth step involves accurate surveillance of devices. These medical or surgical tools are ‘cheek to cheek’ with the skin of the child all day long, so we have to put a close watch on various skin sites and at the same time a rotational protocol, when possible, is advocated (see Figure 4). Children with more complex medical problems have a larger number of devices, a higher risk of SB and a more rapid appearance of multiple PUs. We must approach these situations with strategies for aggressive prevention.

In children, the accurate study of external pressures (repositioning and its frequency; appropriate bed, pillow, chair; avoiding direct skin contacts) and rehabilitation are important in reducing risk and SB. Indeed, postural, articular, psychological and neurological rehabilitation may reduce the risk for a subsequent PU to a minimum. 

In summary, the author suggests the use of an individualised prevention care plan that includes the four major actions that are able to prevent PUs. These include maintaining an ideal weight and providing proper nutritional support, mobilisation without a metabolic imbalance, mobility of the devices which ‘care for the life’ of the child and choice of caregiver(s).

All the above steps are part of a prevention program that educates caregivers about the anatomy, physiology and physiopathology of children aged 0–18 years and methodology such as anamnesis and clinical observation. If these goals are strictly pursued and optimal prevention provided, a drastic reduction of the incidence of PUs from 18 to 4.2% should be obtained.

1. Anthony D, Willock J, Baharestani M. A comparison of Braden Q, Garvin and Glamorgan risk assessment scales in paediatrics. J Tissue Viability 2010;19(3):98–105.
2. Baharestani MM, Ratliff CR. Pressure ulcers in neonates and children: an NPUAP white paper. Adv Skin Wound Care 2007;20(4):208–20.
3. Brook I. Microbiological studies of decubitus ulcers in children. J Pediatr Surg 1991;26(2):207–209.
4. Butler CT. Paediatric skin care: guidelines for assessment, prevention and treatment. Dermatol Nurs 2007;19(5):477–82.
5. Ciprandi G. Nutritional treatment in patients with pressure ulcers. Children. Acta Vulnologica 2011;9(3):11–19.
6. Curley MAQ, Quigley SM, Ming Lin MS. Pressure ulcers in paediatric intensive care: incidence and associated factors. Pediatr Crit Care Med 2003;4(3):284–90.
7. Ekmark EM. Risky business: preventing skin breakdown in children with spina bifida. J Pediatr Rehabil Med 2009;2(1):37–50.
8. Gershan LA. Scarring alopecia in neonates as a consequence of hypoxaemia-hypoperfusion. Arch Dis Child 1993;68(5 Spec No):591–93.
9. Grous CA, Reilly NJ, Gift AG. Skin integrity in patients undergoing prolonged operations. J Wound Ostomy Continence Nurs 1997;24(2):86–91.
10. Jaryszak EM et al. Paediatric tracheotomy wound complications: incidence and significance. Arch Otolaryngol Head Neck Surg 2011;137(4):363–66.
11. Mukherjee S, Coha T, Torres Z. Common skin problems in children with special healthcare needs. Pediatr Ann 2010;39(4):206–15.
12. Ouellet JA et al. Pressure mapping as an outcome measure for spinal surgery in patients with myelomeningocele. Spine 2009;34(24):2679–85.
13. Pasek TA et al. Skin care team in the paediatric intensive care unit: a model for excellence. Crit Care Nurs 2008;28(2):125–35.
14. Rana AR et al. Childhood obesity: a risk factor for injuries observed at a level-1 trauma centre. J Pediatr Surg 2009;44(8):160–65.
15. Rodriguez-Key M, Alonzi A. Nutrition, skin integrity and pressure ulcer healing in chronically ill children: an overview. Ostomy Wound Manage 2007;53(6):56–58.
16. Schindler CA et al. Skin integrity in critically ill and injured children. Am J Crit Care 2007;16(6):568–74.
17. Suddaby EC, Barnett S, Facteau L. Skin breakdown in acute care paediatrics. Pediatr Nurs 2005;31(2):132–38.