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Wound management in a young woman with special needs

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Elizabeth McArthur, RSCN, BSc (Advanced Nursing); Frances Dooley, RSCN, RN, DipHE.

Elizabeth-Clinical Nurse Specialist, Paediatric Pain, Royal Liverpool Children’s Hospital, Liverpool; Frances-Ward Sister, Royal Liverpool Children’s Hospital, Liverpool

This case study highlights the difficulties experienced by health-care professionals caring for children with profound special needs, in particular, the problems encountered when the child’s pain and distress is not adequately assessed and managed.




Pain is a major problem in people with cerebral palsy. Schwartz et al’s study (1999) found that most of those questioned experienced pain daily. Chronic pain promotes an extended and destructive response and can result in fatigue and physical stress. A prolonged stress response can lead to a compromised immune system, affecting the length of hospital stay and long-term outcomes (Chapman and Gavrin, 1999).



Alice Farrell, one of twins, was delivered by emergency section. As a result of birth asphyxia she had severe cerebral palsy, causing multiple limb contractions and kyphoscoliosis, leading to respiratory and gastrointestinal problems. She was fed via a gastrostomy tube, had an active seizure disorder and developmental delay. Although Alice had a severe physical disability and was unable to speak, she could understand what was happening around her and could communicate with those who knew her well. Her mother was her main carer.



At the age of 17 Alice was admitted to hospital for a right-sided Castle’s procedure, excising of the femoral head and repositioning the local muscles to straighten the femur. She had various complications and was finally transferred to a medical ward, and then referred to the pain service. Initial assessment revealed a number of problems, the nature of treatment for which are outlined below.



The problems
An acute surgical wound colonised with methicillin-resistant Staphylococcus aureus
A variety of treatments was used, including hydrocolloid, alginate and wound-cavity dressings. Initially, the wound was dressed with Granuflex (ConvaTec) and Steristrips (3M). The wound broke down at the lower end, allowing the femur to break through the skin surface. This was treated with Kaltostat rope (ConvaTec) and packed with Allevyn cavity dressing (Smith and Nephew). The wound bed was treated with Intrasite Gel (Smith and Nephew) and vancomycin.



The treatment for MRSA-colonised wounds in our hospital comprises topical vancomycin combined with a hydrogel to treat the MRSA, rehydrate non-viable tissue and maintain a moist wound-healing environment (Vernon, 2000).



Other problems and their treatments were:



- Systemic infection: treated with oral and intravenous vancomycin and intravenous gentamicin



- Gastrostomy site: this was leaking profusely and was treated with topical Bactroban (Beecham) and covered with a stoma bag



- Reduced oxygen saturation levels: this was due to factors that included spinal curvature, which led to decreased lung volumes and distress, causing Alice to arch her back to a greater degree. This in turn led to a pooling of secretions in the back of her throat, increasing her distress even more.



Alice required oxygen therapy (2-6L/min) via a face mask. An ongoing chest infection further complicated the problem. This was treated with netilmicin, nebulisers and physiotherapy.



Inability to tolerate fluids or diet orally Alice became dehydrated and had severe weight loss. Gastro-oesophageal reflux is common in this population of children and can lead to respiratory problems (Schwartz et al, 1999). However, this was not a problem on this current admission.



Increased muscle spasm This was due to surgery, wound breakdown and the application of traction. Alice was treated with baclofen (5mg three times daily), which reduces the frequency and severity of spasms and clonus in patients with spinal lesions (Drug and Therapeutics Bulletin, 2000). Brain damage in cerebral palsy affects descending inhibitory neurones, resulting in inadequate release of gamma amino butyric acid (GABA) and relative excess of glutamate (Nolan et al, 2000). Baclofen acts as an agonist at the GABA receptors in the dorsal horn of the spinal cord and reduces pain associated with muscle spasms.



Risk of pressure damage Alice was at high risk of pressure damage as she had reduced mobility, an acute illness and was malnourished and dehydrated (NICE, 2000). Young et al (1998) describe the difficulties associated with the orthopaedic patient who, because of the nature of their surgery, may have restricted movement and require great care when their position is changed. In Alice’s case, the risk of wound breakdown and pressure ulcer development was exacerbated by poor nutritional intake (Box 1) (Russell, 2000).



Alice was initially nursed on a foam mattress, but as her condition deteriorated an air-fluidised bed (Clinitron, Hill-Rom) was required to prevent further tissue damage.



Pain management
No formal pain assessment was undertaken. There was no history of how Alice coped with pain or what behavioural cues she might display. Nolan et al (2000) advocate taking a pain history/questionnaire detailing how pain is manifested and what alleviates it. However, there are no validated pain assessment tools for use with children or adults with profound special needs (Biersdorff, 1994; Guisano et al, 1995; McGrath, et al, 1998; Oberlander et al, 1999).



At the time of referral, Alice was receiving dihydrocodeine, oral morphine and chloral hydrate on an as-required basis. Diclofenac and paracetamol were also given.



Following referral, the nursing, medical, physiotherapy and pharmacy staff became involved in a multiprofessional pain-management plan co-ordinated by the acute pain service. The family was involved at all stages and in all decisions. Multi-modal analgesia was used to achieve an optimum effect and to lessen potential side-effects (Box 2).



Melzack and Wall (1965) postulated that pain was a far more complex phenomenon than had previously been thought. In the light of the presence of persistent noxious (painful) stimuli, research shows that the c-fos oncogene is implicated in the development of pain ‘memory’. It is therefore vital to address pain management problems in the earlier stages to minimise the effect on the patient because, if poorly treated, pain results in long-term neurological memory (WorldWide Anaesthetist, 2001).



Trying to unravel pain mechanisms in a patient with multiple problems such as Alice is difficult. It was clear that, in this case, we needed to try a variety of pharmacological interventions to identify which mechanism was active at that time.



LeMone and Burke (1996) describe the pain pathway simply as the ‘sensation of pain as perceived by nociceptors in the periphery of the body. Pain is then transmitted through the afferent A-delta (myelinated and rapid transmitters, not opioid responsive and usually associated with acute pain) and small C fibres (not myelinated slow transmitters) which usually respond to pain from deep structures such as muscle and viscera resulting in a diffuse burning and aching.’



Alice was experiencing pain as a result of stimulation of both A-delta and C fibres due to the many interventions she required, including wound dressing changes, intravenous cannulation and physiotherapy.



‘Wind-up’ pain is also a recognised phenomenon. Dickenson (1997) points to the significance of the mediating role of the N-methyl-D-aspartate receptor in enhancing spinal processing of painful messages and long-term events in the brain.



To create the ideal conditions for this receptor to work, certain conditions need to be met. These are the release and binding of the co-agonists for the receptor, glycine and glutamate, together with a non-NMDA-induced depolarisation to remove the resting magnesium block of the channel. Once these conditions have been reached, this system becomes activated, leading to hypersensitivity - that is, wind-up pain. The threshold of A-delta fibres that normally perceive touch and sensation is lowered and the sensations are perceived as painful stimuli.



Besson (1999) points out that the release of substance P into the spinal cord has a similar effect. Substance P is a neurotransmitter normally released for a short period due to noxious (painful) stimuli. In our experience, acute pain need only be present for a short time in a patient with long-term pain management problems before a ‘wind-up’ element becomes a problem. Preclinical studies point to neuronal expression of new genes occurring within 20 minutes of injury. Studies in the neonatal population using heel lances and babies undergoing circumcision show an exaggerated behavioural response to pain much later (Carr and Goudas, 1999).



As morphine attacks pain modulated through the c polymodal receptor, it has little influence on the NMDA receptor sites, except when it is given in very large doses. Ketamine, derived from the phencyclidine (PCP) family, appears to have both central nervous system and local anaesthetic properties (Granry et al, 2000). It is thought to react with mu, delta and kappa opioid receptors, but with a preference for mu receptors. These receptors are significant, as they can influence the way pain is experienced. However, anecdotal evidence suggests that children aged under eight years given analgesic doses of ketamine do not experience these effects.



Ketamine has a high bio-availability following intravenous, caudal and intramuscular administration but first-pass metabolism and lower absorption necessitate higher doses if given via the rectal or oral routes (Reich and Silvay, 1989). First-pass metabolism is ‘the proportion of an orally administered drug that is metabolised by the liver and gut wall after absorption from the gastrointestinal tract, determining the amount of unchanged drug that reaches the systemic circulation’ (Macintyre and Ready, 1992).



Ketamine preserves airway patency and respiratory function and does not have a significant sedative effect at low doses, important in patients who have respiratory problems and where sedation has a considerable impact on quality of life.



The effect of pain and distress on the healing capacity of a patient is thought to be considerable (Kremer, 1999; Kiecolt-Glaser et al, 1995; Rook, 1996) but little research has been carried out.



On reflection, a very basic lesson was learnt by our involvement in Alice’s care. ‘Pain is whatever the person says it is,’ wrote McCaffrey and Beebe (1989), but what do we do about the child or adult who cannot tell you about it?



As health professionals, we must listen to parents and/or carers. They have a wealth of information that can help us manage their child’s pain with greater success. In the very complex patient with many different pain experiences, it is evident at the outset that our understanding of pain, its causes and effects on the individual is limited. Indeed, we are still in the infancy stage of comprehending it. Practitioners must also consider a wider range of analgesics for the management of complex pain in patients with wounds.



Eventually, with family and multiprofessional support, and Alice indicating what worked and what did not, we succeeded in making her comfortable and, after two months, her wounds healed.



- The patient’s name has been changed.



- This article is based on a paper published in the October 2001 issue of the Journal of Wound Care.



The authors would like to thank the patient, her family and the staff of D3 at Alder Hey Hospital.



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