Write a paper in which you do the following:
Write a 1-pararaph introduction of how you conducted your literature search and the databases consulted in your search in relation to your practice area or area of interest. Be specific and provide examples.
Write a 1-paragraph summary of each of the articles you have selected (a total of 3 paragraphs).
burns 35 (2009) 921–936
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
Review
The management of pain in the burns unit
P. Richardson *, L. Mustard
St. Andrews Centre for Plastic Surgery and Burns, Broomfield Hospital, Chelmsford, Essex, CM1 7ET, UK
article info
abstract
Article history:
The adverse sequalae of inadequate pain control in the burn population have been long
Accepted 16 March 2009
recognised, yet control of pain remains inadequate globally. The dynamic evolution of burn
pain both centrally and peripherally, and the many factors which influence pain perception
Keywords:
illustrate the need for a therapeutic plan which is similarly dynamic and flexible enough to
Burn pain
cope with the facets of background, breakthrough, procedural and post-operative pain.
Analgesia
Regular, ongoing and documented pain assessment is key in directing this process.
Burn pathophysiology
The family of opioid analgesics provide the backbone of analgesia to burn patients.
Together, they provide an excellent range of potencies, duration of actions and routes of
administration. However, they must be used judiciously as side-effects may be clinically
relevant and furthermore, recent data has implicated them as being capable of inducing
pain. NMDA receptor antagonist such as ketamine and gabapentin are increasingly recognised as useful adjuncts, capable of marked opiate sparing effects in this population. The
simple analgesic paracetamol (acetaminophen) has both anti-pyretic and opioid-sparing
properties and justly deserves its place in the pharmacological treatment of every burn
patient.
Non-pharmacological methods of pain control can play an important role in suitable
patients but resources vary widely between units.
With this review article, we have set out to give practical guidance to all healthcare
professionals with examples from our practice. We have found the addition of pain
specialists as an integral part of the burns multi-disciplinary team, and an environment
where pain is given a high clinical priority to be invaluable in our approach to pain control.
# 2009 Elsevier Ltd and ISBI. All rights reserved.
Contents
1.
2.
3.
Pain mechanisms after burn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pain assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pharmacological methods of burn pain control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1. Opioid analgesics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2. Morphine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3. Oxycodone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4. Fentanyl . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.5. Remifentanil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.6. Alfentanil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
* Corresponding author. Tel.: +44 1245514080.
E-mail address: patricia.richardson@meht.nhs.uk (P. Richardson).
0305-4179/$36.00 # 2009 Elsevier Ltd and ISBI. All rights reserved.
doi:10.1016/j.burns.2009.03.003
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4.
5.
6.
7.
8.
9.
burns 35 (2009) 921–936
3.7. Methadone. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Simple analgesics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1. Paracetamol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2. Non-steroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Other drugs useful in burn pain management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1. Gabapentin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.2. Ketamine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3. Clonidine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.4. Benzodiazepines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5. Amitriptyline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6. Lignocaine by intravenous infusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.7. Entonox . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Non-pharmacological methods of pain control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Practical considerations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.1. Background pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.2. Breakthrough pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.3. Procedural pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.4. Post-operative pain control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Standardisation and guidance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Burn pain is severe and good pain control is necessary for more
than simply humane reasons. The negative consequences of
poor pain control are wide ranging. Fear and anxiety induced
by a bad acute pain experience risk poor compliance with
rehabilitation therapies, increased pain perception and loss of
faith in the burn team [1]. Uncontrolled acute burn pain
increases the incidence of chronic pain and associated
depression [2], and correlates with suicidal ideation at time
of discharge from hospital [3]. Post-traumatic stress disorder is
a notable sequaelae of major burn and is linked both as a cause
and effect with poorly controlled burn pain [4,5]. Failure to
implement effective acute pain control increases the stress
response [6,7].
Despite major advances in burn wound management and
survival, burn pain is inadequately treated globally [8]. This is
attributed to its complexity and to lack of specific education in
health care professionals [9–11]. Burn pain evolves and
changes over time; drug handling is altered and the patients’
psychological needs evolve. Staff caring for burn patients face
unique challenges including the repeated infliction of pain on
already traumatised patients, with therapeutic procedures,
physiotherapy and provision of hygiene needs all having the
potential to cause pain and distress. Personal coping strategies
used by burns staff to distance themselves from a patient’s
pain have been identified as a barrier to effective pain
management [12]. A multi-disciplinary approach and a culture
where pain is given a high clinical priority increase the chance
of getting it right.
This review seeks to identify currently available methods of
achieving effective pain management and to provide practical
guidance in the adult burn population. Specialist groups, such
as children and the cognitively impaired are mentioned but
not addressed in full.
An understanding of the mechanisms of burn pain is a
necessary starting point.
1.
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Pain mechanisms after burn
Burns are classified by thickness and area affected, yet pain
does not always correlate accordingly. Afferent nerve destruction associated with deeper burns theoretically reduces the
amount of pain experienced, but in clinical practice this is not
a reliable predictor [9,13]. Different individuals do not feel the
same pain from the same wound or injury. In addition, the
pain experienced will change with tissue regeneration and
evolving physiological, psychological and environmental
influences.
Pain is perceived at the time and site of burn, due to
stimulation of local nociceptors and transmission of the nerve
impulse in Ad and C fibres thereby relaying the pain message
to the dorsal horn of the spinal cord. The magnitude of
impulse is modulated here by both concurrent peripheral
sensory inputs and descending influences from higher cortical
areas. Each of these has the potential to exert powerful effects
and may have the capability to override the unpleasant
sensation of pain entirely in extreme situations. Conscious
perception of pain occurs as the resultant impulse is
transmitted onwards to the brain and into areas collectively
known as the pain matrix. These remain to be fully defined
anatomically, but activity appears centred on cortical areas
and the thalamus [14]. Many factors influence the conscious
perception of pain (Fig. 1). Those that are subject to external
influence are targets for therapeutic manipulation. These
varied contributory factors are what make the pain experience
unique to each sufferer. Successful pain management plans
are consequently highly individual.
The inflammatory response is initiated within minutes of
injury and persists for days. The ‘inflammatory soup’ of
irritant chemicals continues to sensitise and stimulate pain
fibres throughout this time. The site of burn injury remains
painful, and markedly sensitive to mechanical (touch and
burns 35 (2009) 921–936
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Fig. 1 – Factors influencing the patient’s perception of pain from a burn wound.
movement) and thermal stimuli. This is known as primary
hyperalgesia. Secondary hyperalgesia, increased sensitivity
and pain perception to mechanical stimuli (yet not thermal) is
observed within minutes in the adjacent undamaged skin as C
fibres facilitate Ad input from neighbouring neurons [15].
Continued or repeated pain stimuli, which occur when
inadequate background or procedural analgesia is provided,
will give rise to adaptations throughout the central nervous
system whereby pain signals, and hence perception, become
facilitated and amplified to a given stimulus: hyperalgesia.
With time, these changes may become irreversible and
chronic pain is risked as a result. This ‘wind-up’ mechanism
involves sensitisation of peripheral receptors, increased
excitability at the dorsal horn centred on NMDA receptor
systems and activation of facilitating pathways descending
from higher centres [16]. The NMDA receptor modulating
drugs ketamine [17,18] and gabapentin [19,20] are of benefit in
the multi-modal pharmacological management of pain.
Opioids, while mainstay analgesics, are recognised as
having the potential to induce hyperalgesia through central
sensitisation [16] and this is discussed more fully later.
As the acute inflammatory response abates, the pain may
change in quality. Reported pain intensity may vary but is
typically maximal at sites of upper/mid-dermal skin loss, such
as areas of skin donation, and decreases with wound closure.
Infection of a burn at any stage of the healing process will be
accompanied by a resurgence of the inflammatory response
and augmentation of pain. Rebirth of new tissue is associated
with parasthesia and local discomfort [21] and healed burn
areas remain primed to show enhanced mechanical hyperalgesia following subsequent injury [22]. Anxiety and poor
pain experience will increase the perception of pain [13].
The pain experienced will alter with treatment of the burn.
Surgery to debride or excise the burn will adjust the depth of
the tissue injury. Covering the burn area with autograft or
allograft skin, or a synthetic dressing typically reduces the
pain. Skin harvest donor sites are usually associated with
more pain than the injured area itself.
Severely damaged nerves in deep dermal or full thickness
burns may lead to a relatively insensate area initially, but
regeneration will occur within 5–6 weeks of wound closure
[23]. Neuropathic pain can result from disordered regrowth
with sprouting to neighbouring nerves, spontaneous firing or
neuroma formation. The nature of this pain is described as
tingling, lancing, shooting and like electric shocks. Neuropathic pain often responds poorly to traditional analgesics
such as opioids, and therapeutic strategies for managing this
particular type of pain need to be employed.
Long-term or chronic pain remains a problem for a
significant number of burn survivors and this has been
estimated at 52% [24]. Phantom limb pain has a higher
incidence in amputations following electric shock injury [25].
2.
Pain assessment
Regular, ongoing pain assessment is essential to guide the
dynamic analgesic regime necessary to cope with the evolving
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burns 35 (2009) 921–936
Table 1 – Burn pain assessment.
How to assess burn pain
Ensure the patient understands the pain score.
Question the patient about background, breakthrough
and procedural pain.
Ask ‘Do you have any pain?’ and listen.
Pitfalls in pain assessment
Do NOT alter a pain score from a self-reporting scale, to what you think
it should be!
Some well intentioned questions are misleading e.g. ‘Would you like any
pain killers?’. They may be making the patient feel sick and the answer
will be ‘No’ despite pain.
If you are reviewing pain control – ask the patient yourself about their
pain, not your colleague.
Stick to the present tense.
Ask where and when the pain is felt, and what
makes it better or worse.
Record the answer the patient gives.
Any patient in pain should have pain scores
recorded hourly. All patients should be assessed a
minimum of twice a day.
nature of burn pain and its response to medication. Background pain (at rest and during movement), breakthrough
(unpredictable pain surges through the day), and procedural
pain all warrant individual assessment and recording
throughout the phases of burn recovery [4]. Site of pain,
aggravating and alleviating factors are important to define, in
particular the response to analgesics. A thorough pain
assessment may require examination of the patient in order
to guide the clinician towards the cause of the pain and
therefore effective management of it. For example pain may
result from a tight dressing needing release, tissue oedema in
a dependant limb requiring elevation, wound infection or
muscle necrosis in compartment syndrome. The words used
to describe the pain may guide the clinician to suspect a
particular pain mechanism, for example the ‘electric shock’
quality of neuropathic pain.
Accurate recording of a subjective experience, by another
individual, can be skewed by a number of things, including
bias and assumption. Several papers reported discrepancies
between patient and nurse pain scoring [26–29] and education
is undoubtedly the key to improving practice. Table 1
illustrates points that we have found to be useful when
teaching staff. Some patients are concerned to be on as few
drugs as possible and may deny pain to themselves and to
staff. Stressing the importance of good analgesia to allow
maximum gain from therapies, and potentially faster rehabilitation, is important.
Scoring pain conveys a sense of staff empathy and makes
the patients’ ‘complaint’ valid. Simple, patient-friendly scales
yield useful practical data and show trends and ‘hot-spots’ in
the patient’s day. Assessment scales are of many types.
Adjective scales require a word to be selected to equate with
the pain intensity (e.g. none, mild moderate severe) and
numeric require selection of a number (e.g. 0–3, 0–5, 0–10). The
visual analogue thermometer has been validated as a sensitive
and useful tool in the burned population [30]. Use of this device
requires the assessor to slowly move a strip from a position of
‘No Pain’ to ‘Unbearable Pain’ with the patient indicating when
to stop. Other more complex tools, such as the McGill Pain
Questionnaire [31] are useful for research or audit purposes.
The abbreviated burn specific pain anxiety scale will identify
and quantify anxiety [32].
Pictorial representation of the scale may be more suitable
to guide self-report in young children [33]. Tools based on
behavioural observations have been validated for use in those
who may not be able to reliably self-report pain; amongst
these are the Abbey pain scale [34] for use in the elderly and
cognitively impaired, and the FLACC score [35] in young
children and infants.
Staff scoring pain will need to be aware of target pain scores
and this will depend on the system used. Fig. 2 is an example of
a pain score record chart used in our institution and this
guides and documents a cycle of evaluation and appropriate
drug adjustments. We advocate assessment occurring 2–4
hourly in the early phase and at a minimum of 12 hourly in the
pain controlled patient to ensure that optimal management
efficacy is maintained. It is our experience that the simplicity
of a 0–3 scale is adequately sensitive for the purposes of
identifying trends in pain severity, and effectiveness of
analgesic regimes.
3.
Pharmacological methods of burn
pain control
Before prescribing any drug to a burn patient, the clinician
must have an understanding of the altered pharmacokinetic
state resulting from well-described pathophysiological
changes that follow burn injury. During the first 48 h,
decreased organ blood supply will reduce clearance of drugs,
but the subsequent hypermetabolic phase (48 h after injury) is
associated with increased clearance. Variations in levels of
acute phase plasma proteins lead to changes in drug binding
and free fractions available for end action. The volume of
distribution of a drug may be further affected by alterations in
total body water. Using regular and repeated pain assessment
to quantify the effect of analgesic agents reduces the impact of
these changes. Doses vary widely between individuals and
over time with the same individual. This review therefore will
not comment on doses other than in specific cases.
3.1.
Opioid analgesics
Opioids are the cornerstone of burn pain control. They are
effective and the variety of drugs available provides a range of
potencies, methods of administration and duration of actions.
The positive effects extend beyond the subjective feeling of
pain-free comfort. Morphine has been shown to correlate with
burns 35 (2009) 921–936
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Fig. 2 – St. Andrew’s Burns Centre Pain Score and Itch Chart.
reduced post-traumatic stress syndrome symptoms [36]. The
effects of opioids are wide ranging and include clinically
relevant side effects such as respiratory depression, itch,
nausea and vomiting.
Doses can vary widely and escalate rapidly during burn
treatment. This relates not only to wound healing and pain
modulation, but may also occur with the development of
opioid tolerance or the more recently defined state of opiateinduced hyperalgesia (OIH). Tolerance is defined as increasing
doses of a particular opioid being required to achieve the same
analgesic effect and applies equally to side effects. It is more
common following the use of short acting opioids, particularly
when administered as an infusion [37] but is otherwise
unpredictable. It is no more common in the burn patient
than any other [38]. The precise mechanism of tolerance is
unclear but its link to OIH is increasingly recognised [39]. OIH is
demonstrated clinically by increased pain sensitivity, diffu-
sely and throughout the body following opiate exposure.
Although opiates provide excellent analgesia they are poor at
preventing central sensitisation to pain [40]: pain scores and
opiate requirements have been shown to higher in postoperative surgical patients following the use of intra-operative
remifentanil infusions [41]. Mu-agonist opioids induce this
hyperalgesic state through effecting neuroplastic pro-nociceptive changes in afferent neurons and the spinal cord,
which may persist long-term [16]. NMDA/glutamate receptor
systems play a critical role supported by the fact that both
gabapentin [42] and ketamine [43] have been demonstrated as
reducing these changes. Ketamine is effective in reversing
opiate tolerance [44,45]. Although the relationship between
opiate tolerance and hyperalgesia is complex and poorly
understood, it has been suggested that mechanisms of
hyperalgesia may be responsible for inducing the state of
tolerance [46].
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burns 35 (2009) 921–936
It would be imprudent to extrapolate these findings and
suggest that opioids should be avoided for the control of acute
or burn pain. Their role remains valuable, but there is a
rationale for using them in reduced doses and in combination
with other non-opioid analgesics [47]. Non-steroidal antiinflammatory drugs and paracetamol reduce central hyperalgesia [48] and are opiate sparing [49,50] – effects also
demonstrated by ketamine [44,17,18] and gabapentin [19].
Changing to a different opioid, ‘an opioid switch’, can help
to restore analgesia in a tolerant patient [51] and switching to
methadone has been reported as successful in burn patients
[52,53]. Methadone has weak NMDA receptor properties [54]
which may provide an explanation for this.
Physical dependence commonly occurs in patients on longterm opioids and they should not be stopped abruptly, to avoid
precipitating withdrawal symptoms. Physical dependence is
not to be confused with addiction or psychological dependency, which is characterised by an alteration in behaviour
with cravings and compulsive opiate use despite evidence of
harm. The development of this latter state is extremely rare in
patients taking medically indicated opioid drugs, yet unfortunately patients continue to have these drugs withheld for fear
of addiction [55].
Burns patients potentially require long-term opioids, and
the aim is to establish an effective background regime based
upon oral slow-release preparations, with short acting elixirs
for breakthrough pain. Procedural pain is managed separately,
using well-timed and effective doses of opioids adjusted
according to patient response.
Any opioid drug may be used for burn pain management, but
the following offer particular benefits in the burns unit setting.
3.2.
Morphine
Morphine is the gold standard opioid drug against which all
others are measured. The oral preparation undergoes extensive
first pass metabolism meaning that to achieve an equianalgesic
dose, the intravenous dose to be increased two- to threefold for
oral administration. Accumulation of the active metabolite
morphine-6-glucuronide can occur in renal impairment when a
dose reduction or change of opioid may be needed.
Intravenous morphine will provide more rapid control of
pain than an oral preparation with peak effect occurring at
10 min compared to 30–90 min and may be useful for initial pain
control upon presentation. Oral (elixir and sustained release)
use is preferred in the burns patient, although intravenous
medication is more appropriate during the resuscitation phase
when delayed gastric emptying may occur. The peak effect of
intravenous dosing is at 10 min, compared to 30–90 min
following an oral dose. Absorption from subcutaneous and
intramuscular injections may be unreliable and these are best
avoided. The efficacy of morphine as a topical agent in burns
has been studied with no convincing evidence of benefit [56,57].
3.3.
hallucinations and histamine-induced itching are less with
oxycodone [58].
Oxycodone has superior bioavailability than morphine,
and only half the oral morphine dose is administered as oral
oxycodone. They are equipotent when administered intravenously.
3.4.
Fentanyl
Fentanyl is a rapid onset, potent, short acting synthetic opiate. It
is consequently well placed to provide good procedural
analgesia. It can be administered by a variety of routes, and
recent developments have led to novel techniques, most notably
transmucosal administration. Intravenously it is a potent
respiratory depressant and continuous infusions induce both
rapid tolerance and drug accumulation. Short-term fentanyl
infusions as sole agent for burns dressing change [59] or as
patient controlled analgesia (PCA) can be safe and effective [60].
Fentanyl administered intranasally (IN) reaches therapeutic levels within 2 min [61] and this may offer a practical
advantage over bitter tasting oral morphine preparations. In
adults using patient-controlled IN a mean total dose of
1.48 mcg/kg PCIN equates to 0.35 mg/kg of oral morphine
[62]. There is evidence of safe use in paediatric patients [63].
Fentanyl lozenges (for absorption via the buccal mucosa)
were originally developed for the management of breakthrough
cancer pain, usually at a starting dose of 200 mcg. There are now
reports of its use for control of procedural burn pain, for which
higher doses are required; 10 mcg/kg as a starting dose and
subsequently titrated according to response [64]. The lozenge is
rubbed over the oral mucosa rather than swallowed and onset
of analgesia is at 3–5 min, with peak effect at 20–40 min. In
paediatric patients 10 mcg/kg is equianalgesic to oxycodone
0.2 mg/kg [65]. The fast clearance time of the drug makes this
particularly attractive in patients with renal impairment.
3.5.
Remifentanil
Remifentanil is an ultra-short acting opiate, useful only as an
infusion. Peak effect is reached within 1–3 min and it has a
very short half-life (3.5 min) as a result of its organindependent yet predictable metabolism. The high incidence
of respiratory depression, especially in the opiate naı̈ve
patient requires that it is given only by trained anaesthetic
personnel and in a suitable environment. It has gained an
established place in the Intensive Care Unit for the management of short bursts of pain, and to assist with weaning from
mechanical ventilation.
Experience of its use as a sole agent for undertaking dressing
changes in spontaneously breathing, non-intubated burn
patients shows it to provide good analgesia and high levels of
patient satisfaction [66]. The clinician must be prepared for the
abrupt offset of analgesia and appropriate background pain
relief should be administered in a timely fashion.
Oxycodone
3.6.
Oxycodone is an effective alternative to morphine, some
patients tolerating one more than the other. There is no
evidence that oxycodone is more effective than morphine.
Both can cause opiate side effects, but there are reports that
Alfentanil
Alfentanil is a short acting opiate with peak effect reached
within 1 min of injection. Its half-life is 90 min and, unlike
remifentanil, can provide some post-procedural analgesia.
burns 35 (2009) 921–936
It is shorter acting than fentanyl and for this reason it is
favoured by some as the opiate of choice for control of
procedural burn pain both as a sole agent [67] and in
combination with propofol [68].
Alfentanil undergoes hepatic metabolism to inactive, nontoxic metabolites which are renally cleared [69]. Of all the
strong opioids, it has the most evidence to support its safety in
severe renal impairment.
3.7.
Methadone
Methadone is a synthetic opioid drug with excellent bioavailability and long duration of action. Once daily dosing gives
predictable action and avoids the ‘highs and lows’ of shorter
acting opiates. This is why it is widely used for the control of
opiate cravings in addicts. The steady state blood levels of
methadone vary between individuals due to genetic influences in hepatic metabolism and this raises safety concerns
particularly with regard to respiratory depression [54].
Methadone exerts its analgesic effect not only through
opiate receptor binding, but also through a weaker action
influencing pain modulation at spinal NMDA receptors. For
this reason, it is a useful drug to consider when undertaking an
opiate switch described in burns patients in both in the acute
and chronic settings [52,53].
4.
Simple analgesics
4.1.
Paracetamol
Paracetamol (acetaminophen) acts both centrally and peripherally to inhibit pain. A weak analgesic as a single-agent, when
used in combination with opioids it has a synergistic effect
producing an analgesic effect comparable to a higher opioid
dose. It has an excellent risk profile and few contraindications. Paracetamol should be used, regularly, in all
(non-contra-indicated) burn patients at its maximal dose of
90 mg/(kg day) with 4 or 6 hourly dosing. A review of paediatric
burn patients showed that 7.3% of children require paracetamol alone for pain relief, although interestingly this was
judged higher at 50.6% a decade earlier [70].
Paracetamol is established as an effective anti-pyretic,
probably through reduction in thermoregulatory set point, an
effect seen in both adults and children [71].
4.2.
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs offer effective analgesia, anti-inflammatory properties and anti-pyretic effects. Like paracetamol, they are also
synergistic with opioids and can reduce doses and hence side
effects [49].
Although highly effective against inflammatory pain,
NSAIDs unfortunately cannot be recommended for routinely
use in patients with significant burn injuries due to the already
increased risk of renal failure [72] (particularly in the elderly),
and peptic ulceration. In our institution they are restricted to
cautious use in fit, younger patients with smaller burns
(10, 20
>20, 30
Mean (SD)
2
3
2 3
More than adequate
Adequate
Inadequate
Self-inflicted
Event
Criminal
p
CG
MG
TG
MTG
38.22 (12.58)
26 (57.79)
19 (42.21)
5 (11.11)
39 (86.67)
1 (2.22)
19 (42.21)
26 (57.79)
21 (46.67)
17 (37.78)
7 (15.55)
17 (37.78)
28 (62.22)
30 (66.67)
30 (66.67)
0 (0.00)
8 (17.78)
38 (84.45)
7 (15.55)
20 (44.44)
19 (42.28)
0 (0.00)
14 (31.11)
15 (33.33)
16 (35.56)
13.37 (2.56)
10 (22.22)
25 (55.56)
10 (22.22)
7 (15.55)
26 (57.79)
12 (26.66)
37 (82.22)
5 (11.11)
3 (6.67)
36.24 (13.67)
26 (57.79)
19 (42.21)
5 (11.11)
38 (84.45)
2 (4.44)
21 (46.67)
24 (53.33)
17 (37.78)
22 (48.89)
6 (13.33)
21 (46.67)
24 (53.33)
28 (62.23)
26 (57.79)
0 (0.00)
7 (15.55)
34 (75.56)
6 (13.33)
18 (40.01)
18 (40.01)
0 (0.00)
24 (53.33)
13 (28.89)
8 (17.78)
13.27 (3.21)
10 (22.22)
32 (71.12)
3 (6.67)
8 (17.78)
31 (68.89)
6 (13.33)
40 (88.89)
5 (11.11)
0 (0.00)
38.67 (10.86)
25 (55.56)
20 (44.44)
3 (6.67)
40 (88.89)
2 (4.44)
16 (35.56)
29 (64.44)
22 (48.89)
16 (35.56)
7 (15.55)
16 (35.56)
29 (64.44)
31 (68.89)
21 (46.67)
3 (6.67)
8 (17.78)
32 (71.11)
7 (15.55)
21 (46.67)
20 (44.44)
5 (11.11)
19 (42.21)
17 (37.78)
9 (20.01)
13.93 (4.13)
11 (24.44)
28 (62.23)
6 (13.33)
9 (20.01)
27 (58.98)
9 (20.01)
40 (88.89)
4 (8.89)
1 (2.22)
36.38 (11.04)
33 (73.34)
12 (26.66)
7 (15.55)
37 (82.22)
1 (2.22)
17 (37.78)
28 (62.22)
24 (53.33)
16 (35.56)
5 (11.11)
13 (28.89)
32 (71.11)
30 (66.67)
26 (57.79)
1 (2.22)
7 (15.55)
32 (71.11)
9 (20.01)
28 (62.23)
18 (40.00)
11 (24.44)
23 (51.12)
12 (26.66)
10 (22.22)
15.12 (1.79)
12 (26.66)
26 (57.79)
7 (15.55)
10 (22.22)
23 (51.12)
12 (26.66)
41 (91.11)
4 (8.89)
0 (0.00)
CG: control group; MG: music group; TG: tramadol group; MTG: music-plus-tramadol group; TBSA: total body surface area.
Chi-squared (x2) test.
b
Fisher exact-test.
c
Kruskal Wallis test.
a
0.54c
0.28a
0.89b
0.83a
0.80a
0.26a
0.99a
0.78a
0.12b
0.99a
0.94a
0.90a
0.64a
0.99a
0.0004b
0.56a
0.11c
0.16a
0.07a
0.37b
854
Table 2 – Tests of the intervention effects on pain.
Dependent variable
Source
T0
T1
T2
T5
T6
T1
T2
T5
T6
T1
T2
T5
T6
Intervention
Error
SS
df
MS
F
p
h2p
1035.14
654.23
192.34
335.68
71.34
30964.28
46019.45
52004.50
1778.11
2523.86
3354.37
2265.89
1
1
1
1
3
3
3
3
175
175
175
175
1035.14
654.23
192.34
335.68
23.78
10321.43
15339.82
17334.83
10.16
14.42
19.17
12.95
101.88
45.36
10.03
25.93
2.34
715.67
800.29
1338.81
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