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Pain management in patients

following limb amputation
Chapman S (2010) Pain management in patients following limb amputation. Nursing Standard. 25, 19,
35-40. Date of acceptance: February 5 2010.

Summary
Phantom limb pain is common in patients who have amputations.
This article outlines the different theories that explain the
pathophysiology of phantom limb pain, including peripheral, spinal
and central mechanisms. Treatment options are targeted at
addressing these mechanisms, combining analgesic techniques
with physical and psychological rehabilitation.

Author
Suzanne Chapman, clinical nurse specialist, pain management,
The Royal Marsden NHS Foundation Trust, London.

Keywords
Amputation, neuropathic pain, phantom limb pain,
urogenital pain
These keywords are based on subject headings from the British
Nursing Index. All articles are subject to external double-blind peer
review and checked for plagiarism using automated software. For
author and research article guidelines visit the Nursing Standard
home page at www.nursing-standard.co.uk. For related articles
visit our online archive and search using the keywords.

PAIN CAN OCCUR following the amputation

of many body parts. Phantom limb sensation
and pain after the amputation of upper or lower
limbs is the most studied of these phenomena.
Amputation of upper or lower limbs can be
undertaken as a result of malignancy, trauma,
diabetes, congenital deficiency or peripheral
vascular disease.
The reported incidence of phantom limb pain
varies in the literature from 2-97% (Schug 2008),
but is thought to occur in 60-80% of amputees.
This variability may arise because of different
definitions of pain and data collection techniques.
Bloomquist (2001) reported that even seven years
after amputation, 50% of patients continue
to experience burning, cramping, throbbing
NURSING STANDARD

or crushing phantom pain, described as

continuous or intermittent.
Phantom pain is a type of neuropathic pain
caused by the mechanical severing of nerves by
amputation of a body part. Unlike nociceptive
pain, which is generated by the activation of
normal pain pathways and has a protective
function, neuropathic pain is generated by the
abnormal activation of pain pathways in response
to damage or dysfunction in the nervous system
and does not have a protective function (Callin
and Bennett 2008a). This damage or dysfunction
can occur in the peripheral and/or central nervous
system. The International Association for the
Study of Pain (1994) defined neuropathic pain
as pain initiated or caused by a primary lesion or
dysfunction of the nervous system. This definition
allows for the fact that a primary lesion does not
necessarily have to be evident and includes a wide
range of pain syndromes that can disrupt activity
in the nervous system and cause dysfunction or
abnormal activity. Neuropathic pain can exist
without an identifiable cause (Johnson 2004).

Definitions and characteristics of pain

following amputation
Definitions of pain and/or sensations experienced
following amputation can vary, but can be
subdivided into phantom limb pain, phantom
limb sensation and stump pain (Box 1). The
experience of any of these types of pain or
sensations has been described as a phantom
complex (Nikolajsen and Jensen 2005).
Phantom limb pain This is a painful sensation
perceived in the missing limb. Pain may be
described as shooting, severe burning, ischaemic or
crushing in nature, or severe and agonising caused
by the phantom limb being in a hyper-extended or
unnatural posture (Bloomquist 2001, Schug 2008).
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BOX 2
Phantom limb pain theories

Flor et al 2006 described phantom limb pain as

having many features that may be reported
anywhere along a spectrum from simple,
short-lasting and rarely occurring, painful shocks
in a missing body part to a constant, excruciating
painful experience during which the individual has
a vivid, intense perception of the missing body part
(Flor et al 2006).
Phantom limb sensation This is any sensation of
the missing limb except pain. Sensations include
pins and needles, tingling and prickling. Awareness
of movement and positional orientation of the
limb are widely reported (Casale et al 2009). The
phantom limb may move spontaneously or remain
fixed, while some patients are able to move the
phantom limb at will. Telescoping is a commonly
reported form of positional limb orientation
where, over time, the phantom limb changes in
size and length and in extreme cases, only the digits
can be felt on the end of or in the residual stump
(Richardson 2008).
Stump pain This is pain experienced in the
residual portion of the limb or stump (Prantl
et al 2006). Causes of stump pain may include
neuromas scarred nerve endings or nodules that
may cause abnormal ectopic firing of nerves
(Bloomquist 2001) bony spurs in the residual
stump, localised skin disease and infection (Prantl
et al 2006). Residual limb and stump temperature
can be affected by increased or decreased blood
flow to the stump (Siddle 2004). Often the
temperature in the stump and the remaining
limb is lower. This low stump temperature is
correlated to the burning sensation that may be
experienced as part of phantom pain (Schug
2008). Muscle tension in the residual limb can
increase the cramping and squeezing sensations
associated with phantom pain.
Risk factors proposed for the development
of phantom limb pain include the severity of
pre-amputation pain and post-operative pain
(Nikolajsen and Jensen 2001), older age
BOX 1
Pain and/or sensations that may be
experienced following amputation
4Phantom limb pain: painful sensation perceived in
the missing limb.

4Phantom limb sensation: any sensation of the

missing limb except pain, for example, pins and
needles, tingling or prickling.

4Stump pain: pain in the residual portion of the limb

or stump.
(Richardson 2008, Schug 2008)

36 january 12 :: vol 25 no 19 :: 2011

4Peripheral theories: assume that phantom limb pain

originates at the nerves around the injury.

4Spinal theories: attribute the cause to changes

inside the spinal cord.

4Central theories: assume that phantom limb pain

is caused by some mechanism in the brain.
(Siddle 2004)

(Schug 2008), and catastrophising and passive

coping styles (Richardson et al 2007).
Catastrophising refers to a coping style
characterised by excessively negative thoughts
and emotions in relation to pain (Vase et al 2010).

Theories of phantom limb pain

The exact mechanism of phantom limb pain is
not understood fully. There are several theories
proposed to explain the mechanism or
pathophysiology of phantom limb pain (Box 2).
It is unlikely that phantom limb pain is generated
and maintained by one mechanism alone and
it is more likely that elements from all theories
are involved. A summary of key points for these
mechanisms is outlined in Box 3.
Peripheral theories Wherever cell or tissue
damage occurs, chemicals and enzymes are
released. These chemicals and enzymes contribute
to the inflammatory process, sensitise the
peripheral pain receptors (nociceptors) and
stimulate nerves that carry pain signals (A delta
and C fibres) (Middleton 2003). As the
nociceptors are continuously exposed to these
chemicals they start to respond to lower
concentrations of these chemical mediators
(Mann 2008) and start to produce a rapid number
of action potentials, which the central nervous
system interprets as pain (Middleton 2003).
Structural changes in the nociceptive neurones
cause the release of neurotransmitters from the
nerve endings near the site of the damage, thereby
activating neighbouring nerve endings (Callin
and Bennet 2008b). Therefore nerves not
involved in the original damage are now involved,
expanding the area of the body the brain perceives
is involved in pain (Mann 2008). Alteration and
an increase in the sodium and calcium channels
play a role in the generation of spontaneous nerve
discharges from the peripheral damaged neurons
(Callin and Bennett 2008b). This sensitisation
process does not resolve spontaneously (as it does
in normal tissue healing) in neuropathic pain
states such as phantom limb pain.
Patients often report pain and sensitivity to
vibration and touch in the residual limb or stump
following amputation. As a consequence of injury
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and subsequent tissue healing, swelling and

regenerative sprouting of the injured nerve (axon)
end occurs and can form nodules called neuromas
(Siddle 2004). These neuromas display
spontaneous and abnormal activity to stimuli.
Tapping of the stump neuroma can cause stump
pain and phantom limb pain (Nikolajsen and
Jensen 2001). Local anaesthetic blockade of
neuromas can eliminate the spontaneous and
stimulation-induced pain in the stump, but not
ongoing phantom limb pain, suggesting that there
are other mechanisms involved in the process
(Flor et al 2006). Phantom pain is often present
soon after amputation and long before neuromas
have had time to develop so this theory does not
explain the early development of phantom pain
(Nikolajsen and Jensen 2001).
Vascular mechanisms have also been
considered as a potential explanation for the
peripheral mechanisms that relate to phantom
limb pain. As discussed previously, an increase or
decrease in blood flow to the stump can still cause
stimulation of the nerve endings (Siddle 2004).
Lower temperatures can cause increased firing of
nerve impulses, which are perceived by the patient
as phantom limb pain (Siddle 2004).
Spinal theories Continuous stimulation of the
peripheral pain receptors (nociceptors) will in
turn lead to continuous transmission of pain
signals to the spinal cord. In the presence of this
continuous transmission of signals from the
peripheral nervous system, the central nervous
system becomes more sensitive and responsive
a process known as central sensitisation
(Flor 2008, Mann 2008). Nerve injury, such as
that caused by amputation, can trigger a state of
hyperexcitability in the central nervous system,
characterised by increased neuronal firing,
changes within the structure of the peripheral
sensory neurones as they arrive at the spinal cord
and a reduction in the normal spinal cord
inhibitory processes (Flor 2008).
Another theory proposes that the severing of
nerves in limb amputation modifies the reception
of impulses to the central nervous system from the
areas distal to the site of the amputation there is
a loss of sensory nerve input from the amputated
portion of the body (Stannard and Booth 1998).
This results in a reduction in neurochemicals with
a resulting change in how receptive the dorsal
horn neurons are and the pain pathway (Siddle
2004). This causes neural reorganisation to occur
at spinal cord and brain level. It is unclear at
present how much these spinal mechanisms
contribute to phantom limb pain.
Central theories These include the reorganisation
of the somatosensory cortex, known as cortical
remapping or cortical reorganisation, and
theories regarding neurosignatures or
memories. Cortical remapping or cortical
NURSING STANDARD

reorganisation suggests that phantom limb pain

is a process of abnormal reorganisation in the
neuromatrix secondary to pre-existing pain or
the amputation process (Richardson 2008). The
concept of the neuromatrix was proposed by
Melzack (1990) to explain phantom limb pain.
It suggests that the human body is represented in
the brain by a matrix of neurones. Factors that
contribute to this neuromatrix include sensory
life experiences including pain, which creates a
neurosignature or memory of each body part in
the brain (Siddle 2004). Melzack (1990)
proposed that following amputation phantom
sensations or pain represent the persistence of this
neurosignature, despite the loss of the body part.
Amputation involves the severing of nerves
and, as discussed previously, this results in a
reduction of impulses from the severed limb to
the central nervous system. This causes neural
reorganisations to occur at both spinal cord and
brain level (Richardson 2008). As a result of this
reorganisation in the somatosensory cortex, the
brain undergoes changes where the area which
received or generated impulses for the missing
BOX 3
Peripheral, spinal and central mechanisms involved in the
generation of phantom limb pain
Peripheral changes
4Structural changes in the nerves (neurones and axons).

4Ectopic impulses (abnormal firing of nerves).

4Changes in the function of neurotransmitters: increased function
(up-regulation) or reduced function (down-regulation).

4Alterations in channels and transduction molecules (sodium and

calcium channels).

4Formation of neuromas.
Spinal changes
4Continued input from peripheral nociceptors causes an increase in the
responsiveness of neurones in the spinal cord (central sensitisation).
Central sensitisation process may include: increased firing of neurones
in the spinal cord, a reduction in normal spinal inhibitory mechanisms,
and structural changes in the nerve endings of the primary sensory
neurones as they arrive at the spinal cord.

4Severing of nerves for amputation modifies the reception of impulses

to the central nervous system causing neural reorganisation at spinal
cord and brain level.
Central changes
4Cortical remapping or reorganisation: the somatosensory cortex of the
brain undergoes changes where the area of the brain that received
or generated impulses for the missing body part is taken over by an
adjacent area of the brain.

4Neuromatrix theory: a matrix of neurones that represent the body in the

brain can be influenced by experiences in life, which creates a memory
or neurosignature. It is proposed that phantom limb pain or sensations
represent the persistence of this memory despite the loss of the body part.
(Melzack 1990, Stannard and Booth 1998, Siddle 2004, Flor et al 2006, Callin and
Bennett 2008b, Mann 2008, Richardson 2008)

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body part is taken over by an adjacent area of
the brain. An example of this is that non-painful
stimulation of another body part, such as
brushing a cheek, can produce phantom
sensations or pain in the missing upper phantom
limb (Flor et al 2006, Richardson 2008).
A physical basis for this theory has been
demonstrated. Using neuroimaging techniques
Flor et al (2006) were able to demonstrate
a pain memory and altered structure in the
somatosensory cortex in the brain that may
underlie phantom pain while peripheral factors
sustain the memory.
Flor et al (2006) listed the following as other
central mechanisms, that may contribute to
phantom limb pain:
4Alterations in sensory and motor feedback
perception of abnormal somatosensory
phenomena such as telescoping, which refers
to changes in the size and length of the
phantom limb.
4A pain memory hypothesis pain in the
phantom limb is similar to the pain that existed
in the limb before amputation, which is part
of the neurosignature or memory for the
amputated limb.
4Affective and motivational aspects of pain
depression and coping-related variables.
In summary, it is likely that the initiating events
for phantom limb pain, phantom limb sensation
and stump pain start in the periphery, which
generates a chain of events at the spinal and
central nervous system level.

Treatment options
In light of the theoretical mechanisms proposed
for phantom limb pain, a combination of
therapies should be considered. Treatment
usually consists of a combined approach
including medication and rehabilitation with
physical and psychological components.
Pre-amputation Analgesic medication such as
opioids, non-steroidal anti-inflammatory drugs
(NSAIDs) and paracetamol should be used to
manage pre-amputation pain as there remains
a link between this pain experience and chronic
pain such as phantom limb pain (Middleton
2003, Flor et al 2006). Evidence for the use of
local anaesthetics to reduce pre-amputation pain
in an effort to reduce phantom limb pain after
surgery is equivocal, with some studies reporting
a reduction in phantom limb pain (Bach et al 1988,
Schug et al 1995) and others reporting no
38 january 12 :: vol 25 no 19 :: 2011

reduction in phantom limb pain (Pinzur et al

1996, Nikolajsen et al 1997). It may be beneficial
to target patients identified as having passive or
catastrophising coping styles early and involve
psychological support teams to enable the
patient to develop more active coping strategies
(Vase et al 2010).
Post-amputation Strong, effective analgesia
needs to continue in the peri-operative and
post-operative period as there remains a weak
causal link between pain experienced in this
period and phantom limb pain (Richardson
2008). Analgesic therapy with opioids such as
patient-controlled analgesia, local anaesthetics
(such as epidural infusions) and NSAIDs should
continue, providing a balanced combined
analgesic approach. Patients should be assessed
carefully and if they are reporting phantom limb
pain, specific medicines that target neuropathic
pain should be commenced.
Antidepressants such as amitriptyline, used
in lower doses than for treatment of depression,
are now widely used for treating phantom limb
pain. They work by inhibiting the re-uptake of
neurotransmitters serotonin and noradrenaline
(norepinephrine) in the central nervous system.
This allows more neurotransmitters to be
available in the synaptic area to help inhibit
further relay of the pain signal (Middleton 2003).
Antidepressants also block sodium channels
peripherally and this reduces the ability of nerve
cells to transmit pain impulses.
Anticonvulsants such as gabapentin or
pregabalin stabilise cell membranes and work by
preventing the spread of neuronal excitation or by
enhancing the activity of neurotransmitters. They
are thought to inhibit the spread of neural activity
in the pain pathway by blocking synaptic
transmission (Siddle 2004).
Other analgesics that may be considered
include N-methyl-D-aspartate receptor
antagonists such as ketamine and membrane
stabilisers such as lidocaine and mexiletine.
Topical agents, such as lidocaine plasters,
capsaicin and eutectic mixture of local
anaesthetics (EMLA) cream, can be applied to
the stump once the wound is healed. There may
be a role for nerve blocks in the management of
stump pain. The infiltration of local anaesthetic
into a painful area can block the peripheral
sodium channels. This can then reduce
spontaneous ectopic nerve firing (Middleton
2003). Surgical treatment may be effective for
specific stump pathology, such as bone spurs and
neuromas, but does not generally have a role in
the management of phantom limb pain
(Nikolajsen and Jensen 2001).
Early involvement of acute and chronic pain
management teams will optimise treatment of
patients with this specific type of neuropathic
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pain. Pain management teams will also provide

support for the patient and for nurses and other
healthcare professionals involved in the patients
day-to-day care. Unresolved pain issues can
affect a patients ability to engage in the
rehabilitation process so early intervention
and management are essential.
Other therapies target the cortical
reorganisation that occurs after amputation.
One example is the visual feedback technique of
mirror therapy which, it is speculated, normalises
the cortical reorganisations in the brain. Chan
et al (2007) demonstrated that mirror therapy
reduced phantom limb pain in patients who had
undergone lower limb amputation. Patients
attempt to perform movements of the phantom
limb while viewing the reflected image of the
movement of the intact limb.
A study by MacIver et al (2008) used a mental
imagery technique with a group of 13 upper limb
amputees with phantom limb pain. The amputees
had six weeks of intensive training in mental
imagery. This involved a combination of a
body-scan exercise and imagined movement
and sensation in the phantom limb. MacIver et al
(2008) demonstrated changes in cortical
reorganisation using functional magnetic
resonance imaging (MRI) with a corresponding
reduction in some aspects of phantom limb pain.

Flor et al (2001) reported that using an

electrical prosthetic limb moved by signals from
the patients muscle in the residual portion of the
amputated limb could reduce pain if used for
several hours every day. The authors undertook
MRI scans that demonstrated a reversion of the
sensory cortex to its original state. In addition,
patients were asked to touch the skin over the
stump repeatedly to improve the sensory
discrimination in that area. This reduced
phantom pain, possibly by replacing some of the
sensory input that was lost following amputation.
Transcutaneous electrical nerve stimulation may
also be considered to relieve pain. The electrical
current between the skin electrodes stimulates the
nerve fibres that transmit pain in the dorsal horn of
the spinal cord and blocks pain impulses (Stannard
and Booth 1998, Siddle 2004). Evidence is
conflicting, but studies report a reduction in the
severity of phantom limb pain (Katz and Melzack
1991). However, a recent Cochrane review found
no studies that met the eligibility criteria for
inclusion in the review and recommended that a
large multicentre randomised controlled trial was
needed (Mulvey et al 2010).
Rehabilitation is important in physical and
psychological adjustment, which will in turn
influence the patients pain experience. Physical
therapy maximises function by training and

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art & science pain series: 17

strengthening muscle groups to compensate
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Role of the nurse

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Conclusion
Phantom limb pain is common following
amputation. In addition, patients may experience
phantom limb sensations and stump pain. The
cause of phantom limb pain is unknown, but it is
thought to result from a combination of different
mechanisms. A structured pain assessment and
management regimen is vital to allow the
patient to embrace rehabilitation and return
to a good quality of life following amputation.
A combination of pharmacological and
non-pharmacological techniques should be used
by the nurse and the multidisciplinary team
to improve the patients peri-operative and
post-operative pain experience and reduce the
risk of any long-term negative effects NS

Acknowledgement
Each of the articles in this series has been written
by a member of the Royal College of Nursing
London Pain Interest Group. Nursing Standard
would like to thank Felicia Cox, senior nurse,
pain management, Royal Brompton and Harefield
NHS Foundation Trust, and chair, Royal College
of Nursing London Pain Interest Group, for
co-ordinating and developing this series.

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