CG30 | VERSION 1.0 1/12
trust clinical guideline
Guideline ID
CG30
Version
1.0
Title
Pain Management Guideline
Approved by
Clinical Effectiveness Group
Date Issued
01/10/2014
Review Date
31/09/2017
Directorate
Medical
Authorised Staff
Clinical
Publication
Category
Ambulance Care Assistant
Emergency Care Assistant
Student Paramedic
Advanced Technician
Paramedic (non-ECP)
Nurse (non-ECP)
ECP
Doctor
Guidance (Green) - Deviation permissible;
Apply clinical judgement
1.Introduction
1.1
Pain is one of the most frequently encountered symptoms, resulting from a wide
variety of injuries and illnesses in the pre-hospital environment.
1.2
Ambulance clinicians now have more tools in their analgesic armoury than
ever before however, research indicates that simply improving the range of
analgesics available does not necessarily translate into improvements in practice.
Improvements will only occur when pain becomes recognised as a pre-hospital
priority, and every patient receives the most effective pain relief that can
safely be delivered. No clinician would unnecessarily inflict pain, yet poor pain
management is akin to just that.
1.3
Numerous studies both in and out of hospital have confirmed that acute pain is
often inadequately managed. The reasons that are suggested for this include:1-4
▲▲ Lack of understanding of the nature and pathophysiology of pain;
▲▲ Lack of understanding of methods available to control the pain;
▲▲ Failure to assess the degree of pain for the individual patient.
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2.
What is Pain?
2.1
The International Association for the Study of Pain define pain as “an
unpleasant, subjective, sensory and emotional experience associated with actual
or potential tissue damage or described in terms of such damage”.5
2.2
Pain is a subjective and personal experience, only known by the person who is
suffering, which can make pain assessment challenging. Several studies suggest
that pain assessment and scoring by clinical staff consistently underscores pain,
when compared with the scores assigned by patients themselves.6
2.3
Pain is a sensation generated in the brain, after the receipt of sensory stimulus
received through a number of neural pathways, which is modulated by two
primary groups of naturally occurring and synthetic substances that work on the
brain, central nervous system (CNS) or peripheral tissue; namely analgesics and
anaesthetics.7
2.4
Pain is a physiological response that warns us of danger. The process of
nociception describes the normal processing of pain and the responses to
noxious stimuli that are damaging or potentially damaging to normal tissue.
There are four basic processes involved in nociception:
▲▲ Transduction;
▲▲ Transmission;
▲▲ Perception;
▲▲ Modulation.
2.5
Transduction of Pain
2.5.1 Transduction begins when the free nerve endings (nociceptors) of C fibres
and A-delta fibres of primary afferent neurones respond to noxious stimuli.
Nociceptors are exposed to noxious stimuli when tissue damage and
inflammation occurs as a result of, for example, trauma, surgery, inflammation,
infection, and ischemia.
2.6
Transmission of Pain
2.6.1 The transmission process occurs in three stages, with the pain impulse
transmitted:
▲▲ From the site of transduction along the nociceptor fibres to the dorsal horn in
the spinal cord;
▲▲ From the spinal cord to the brain stem;
▲▲ Through connections between the thalamus, cortex and higher levels of the
brain.
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2.7
Perception of Pain
2.7.1 Perception of pain is the end result of the neuronal activity of pain transmission
and where pain becomes a conscious experience. The multidimensional
experience of pain has affective-motivational, sensory-discriminative, emotional
and behavioural components.
2.7.2 When painful stimuli are transmitted to the brain stem and thalamus, multiple
cortical areas are activated and responses are elicited:
▲▲ The reticular system: This is responsible for the autonomic and motor
response to pain and for warning the individual to do something, for
example, automatically removing a hand when it touches a hot saucepan. It
also has a role in the affective-motivational response to pain, such as looking
at and assessing the injury to the hand once it has been removed from the
hot saucepan.
▲▲ Somatosensory cortex: This is involved with the perception and interpretation
of sensations. It identifies the intensity, type and location of the pain
sensation and relates the sensation to past experiences, memory and
cognitive activities. It identifies the nature of the stimulus before it triggers a
response, for example, where the pain is, how strong it is and what it feels
like.
▲▲ Limbic system: This is responsible for the emotional and behavioural
responses to pain for example, attention, mood, and motivation, and also
with processing pain and past experiences of pain.
2. 8 Modulation of Pain
2.8.1 Pain is modulated by two primary types of drugs that work on the brain;
analgesics and anaesthetics. The term analgesic refers to a drug that relieves
pain without loss of consciousness. The term central anaesthesia refers to a
drug that depresses the CNS. It is characterised by the absence of all perception
of sensory modalities, including loss of consciousness without loss of vital
functions.
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3.
Pain Mechanism
3.1
There are several pain mechanisms related to the different natures and causes of
pain.7
3.2
Somatic Pain
3.2.1 Somatic pain is the pain a patient feels when they experience sudden or
unexpected damage to the skin or soft tissues. Somatic pain generally is
classified into two primary distinct sensation types:
▲▲ Cutaneous, superficial, peripheral pain which originates within the skin,
muscle or within the peripheral nerves;
▲▲ Sensation referred as deep pain which originates within joints receptors,
tendons and deep tissues (fascia).
3.3
Visceral Pain
3.3.1 Visceral pain is related to damage and irritation of viscera (organs) by stimulation
such as pressure, chemical damage, ischaemia and physical trauma. The pain
tends to be diffuse in nature (difficult to localise) and more difficult to apply a
description to. Visceral pain is often associated with autonomic symptoms such
as bradycardia, hypotension, sweating and nausea.
3.4
Neuropathic Pain
3.4.1 Neuropathic pain is caused by a functional change (neuronal hyperexcitment)
in the CNS secondary to an injury affecting a peripheral nerve. The pain is
generally persistent in nature with little relief from conventional means of pain
management. Neuropathic pain should not be confused with neurogenic pain
which describes pain resulting from injury to a peripheral nerve but without
necessarily implying any neuropathy.
3.5
Referred Pain
3.5.1 Referred pain is localised pain experienced distant to the site of injury. The exact
mechanism for referred pain is not entirely clear. It is linked to the assumption
that the axons responsible for transmission of pain information from viscera
enter the spinal cord via the same route as transmission carrying cutaneous
pain sensation. e.g. referred pain in the left arm as the result of a myocardial
infarction.
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3.6
Phantom Pain
3.6.1 Phantom pain is a condition where the patient experiences a physical sensation
in the absence of activation of the nociceptors of the peripheral or central
afferent nerves.
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3.6.2 The causes of phantom pain are unclear. In some cases, it is believed that may
relate to growths known as neuromas at the remaining cut ends of nerves.
3.7
Chronic Pain
3.7.1 Chronic pain is prolonged pain episodes spanning from months or longer which
arise from existing tissue injury, inflammation changes, nerve tissue damage,
neoplasm growth, circulatory problems or viral infection.
4.
Pain Assessment
4.1
Pain is one of the most frequently encountered symptoms, resulting from a
wide variety of injuries and illnesses in the pre-hospital environment. The Trust
recognises the importance of managing patients’ pain and considers that pain
should be monitored and managed as the fifth vital sign.9
4.2
Assessment is the cornerstone of effective pain management. Ambulance
clinicians must be aware that when they fail to utilise pain scoring, they are
likely to underestimate moderate to severe pain and overestimate the effect of
analgesics.
4.3
All ambulance clinicians are required to complete at least one pain assessment
on patient who may be experiencing pain and repeat the assessment after each
intervention. Given the subjective nature of pain, it is difficult for clinicians to
estimate the pain intensity themselves. The patient should be the centre of
pain assessment. Self-assessment should be used wherever possible, including
patients with cognitive impairment. Observational pain rating must only be
applied when a patient cannot complete a self-assessment.
4.4
The mnemonic SOCRATES should be used for pain assessment in all patients:10
▲▲ Site;
▲▲ Onset;
▲▲ Character;
▲▲ Radiates;
▲▲ Associate symptoms;
▲▲ Time/ duration;
▲▲ Exacerbating or relieving factors;
▲▲ Severity.
4.5
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The verbal numerical (0-10) rating scale is generally suitable for adults / older
children with no cognitive impairment. It requires the patient to rate the pain
intensity from an 11-point scale where 0 is considered ‘no pain’ up to 10
considered the ‘worst possible pain’.
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4.6
The Abbey pain scale is advocated as the tool for measuring pain in adults with
dementia and/or cognitive impairment that leaves them unable to verbalise.11 It
contains six questions that allow the clinician to measure the patients response
to pain:
▲▲ Vocalisation;
▲▲ Facial expression;
▲▲ Changes in body language;
▲▲ Behavioural change;
▲▲ Physiological change;
▲▲ Physical change.
4.7
Each question is scored out of 3 in the Abbey pain scale, giving a total pain score
between 0 to 18. A copy of the Abbey pain scale is available on the cover of
Patient Clinical Record.
4.8
JRCALC recommends the Wong and Baker pain scale and the face, legs, activity,
cry & consolability (FLACC) scale for pain assessment in children.10 Please refer to
JRCALC guideline for further details.
5.
Non-Pharmacological Methods of Pain Relief
5.1
Pain is a complex sensation involving not only physical aspects, but
psychological, emotional, and behavioural factors. A range of nonpharmacological methods can be used to complement conventional analgesics.
Simple measures should be taken to try and reduce the patient’s level of anxiety,
as fear and anxiety have been shown to increase pain levels. The common types
of non-pharmacological methods of pain relief include:
▲▲ Psychological;
▲▲ Cooling;
▲▲ Dressing;
▲▲ Splintage.
5.2Psychological
5.2.1 Fear and anxiety often worsen pain. Psychological methods of pain relief work
by providing a coping strategy, focusing the child’s attention away from the pain
onto something else.
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5.2.2 Reassurance is an interventional technique thought by many to improve the
efficacy of pain relief through reduction in anxiety and fear being experienced
by a patient in pain. Before commencing an assessment or procedure, it is vital
that the processes involved are explained to the patient in a way that they can
understand; increasing their level of understanding reduces stress and anxiety.
Providing the opportunity for children to make age appropriate choices will also
increase their sense of control. Giving false information, such as telling the child
that cannulation won’t hurt, must be avoided.
5.2.3 Distraction is the most frequently used behavioural therapy and is most effective
with relatively short duration pain, such as that caused by a specific procedure.
Strategies work by focusing attention on a distracter rather than on the pain
itself. In order to be effective, the chosen strategy must be appropriate to
the patient’s age and stimulate the major senses (hearing, vision, touch, and
movement). Something as simple as distracting the child using a toy can act as a
potent analgesic.
5.2.4 Guided imagery involves encouraging the patient to use their imagination to
modify their response to pain. Children for example should be asked to imagine
their favourite place, cartoon character or to imagine that the pain is flowing
out of their body. Relaxation reduces autonomic activity and because a patient
cannot be relaxed and anxious at the same time, pain tolerance should increase.
5.3.Cooling
5.3.1 The active cooling of an injured area of soft tissue or a joint could reduce
swelling, inflammation and pain as it removes noxious agents and reduces pain,
and may reduce oedema by stabilising mast cells and histamine release.
5.4Dressing
5.4.1 The use of dressings to cover exposed burns could reduce the air contact with
the exposed nerve endings reducing pain.
5.5Splintage
5.5.1 Splinting can provide support to and prevent motion of fractures. Correct
splinting of an injured extremity can reduce pain, reducing the risk of further
damage to muscles, nerves, blood vessels and skin.10
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5.5.2 A parent or guardian should travel with the child wherever possible, as their
presence has at least in Emergency Departments been demonstrated to reduce
the unpleasantness of procedures more than any other factor.35
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6.
Pharmacological Interventions for Pain Relief
6.1
The WHO pain relief ladder is the basis for administering all types of pain relief;
careful choice of appropriate interventions will increase the chance of effective
pain management:12
▲▲ Step One - Mild pain, non-opioid.
▲▲ Step Two - Moderate pain, weak opioid +/- non-opioid.
▲▲ Step Three - Severe pain, strong opioid +/- non-opioid.
6.2
Non Opioids - Careful consideration must be given to the choice of analgesia.
Non-opioids such as Entonox, paracetamol and non-steroidal anti-inflammatory
drugs (NSAIDs) have particular advantages in that they have very few side
effects.
6.3
Weak Opioids - These are used when non-opioids are ineffective. They include
codeine phosphate (ECPs/Doctors only) and are often used in combination with
paracetamol.
6.4
Strong Opioids - Morphine remains the first-line strong opioid of choice and
oral morphine forms the backbone of first-line therapy. It is important to titrate
any strong opioids to the patient’s response. Elderly patients are likely to need a
lower or less frequent dose, especially if they have renal or hepatic impairment.
6.5
The document ‘Medicines: Who can give what’ details the analgesics which can
be administered and in some cases supplied by each grade of clinician.
6.6Entonox:
▲▲ Medical gas mixture consisting of 50% nitrous oxide and 50% oxygen.
▲▲ Believed that its analgesic effects are due to the nitrous oxide component
which causes the release of biochemical substances to act on the brain and
spinal cord.13
▲▲ Suitable as the first line analgesia in the pre-hospital setting with its rapid
onset time (2-3 minutes) and has the benefit of not requiring cannulation.
▲▲ Analgesia of choice for child birth as it does not accumulate under normal
conditions and causes minimal side effects.
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6.7Paracetamol:
▲▲ Available in oral suspension, oral tablets and intravenous preparation (IV
Paracetamol should be for severe pain only).
▲▲ Thought to produce analgesia through a central inhibition of prostaglandin
synthesis and inhibits the activation of nociceptors at the site of injury.14
▲▲ Onset time for paracetamol is 3-5mins (intravenously) and 20-30mins (orally).
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▲▲ Analgesic effect is comparable with morphine in muscular injury. Intravenous
paracetamol can be used if morphine is contraindicated (i.e. the patient is too
hypotensive to allow safe administration) and to reduce opioid requirement
when used in combination.
6.8NSAIDs:
▲▲ There are a range of NSAIDs available in the Trust including: oral ibuprofen
suspension, oral ibuprofen tablet, oral naproxen tablet, rectal diclofenac
suppository and intramuscular diclofenac injection (the latter three are ECP/
Doctor only).
▲▲ NSAIDs act as an inhibitor of the enzyme cyclooxygenase (COX), inhibiting
both COX-1 and COX-2 isoenzymes to inhibit prostaglandin productions and
reduced inflammation at the injury site.15
▲▲ The onset time for oral and rectal NSAIDs is 20-30mins and 10-15mins for
intramuscular diclofenac injection.
▲▲ NSAIDs are useful for muscular and bone pain that is often poorly controlled
by opioids. But it should be avoided in the acute stage of injury (<72hrs), as
the anti-inflammatory effect of NSAIDs may delay the healing process.
▲▲ Caution must be used in patients with asthma, reduced renal or hepatic
function and in the elderly. The common adverse effects include GI bleeding,
renal or cardiac failure.
6.9Opioids:
The opioids available to Trust ambulance clinicians are:
▲▲ Oral codeine phosphate 15mg tablet (ECPs/Doctors only);
▲▲ Oral morphine sulphate solution ;
▲▲ Morphine sulphate 10mg injection (intramuscular, intraosseous and
intravenous). Note that there is no longer a lower age limit for IM
administration. Further guidance on administering morphine can be found in
SOP M05.
▲▲ Opioids modulate sensory information in the CNS, preventing the receipt
of pain information to the brain by blocking neurotransmitter release at the
pre-synaptic terminal of CNS neurones and blocking “open” the potassium
channels in CNS neuronal cells to block transmission of the pain stimulus
through the spinal cord.
▲▲ The onset time for oral opioids is about 20-30 minutes, 10-15 minutes for
intramuscular opioid and 2-3 minutes for intravenous opioid. It is important
to note that the onset of intramuscular injection could be delayed in a poorly
perfused (such as hypothermic or shock) patients.
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▲▲ It is important to titrate any strong opioids to the patient’s response and
it is worth noting that the peak effect of intravenous opioid is around
10-20minutes. Elderly patients are likely to need a lower or less frequent
dose, especially if they have renal or hepatic impairment.
6.10
Ketamine (CCPs/Doctors only)7:
▲▲ Ketamine is a phencyclidine (PCP) derivative providing specific significant
anaesthetic, analgesic and amnesic properties with minimal effects on the
respiratory system. This is particular useful in undertaking painful procedures
(such as difficult extrication or fracture reduction). It may be administered by
Doctors and Paramedics authorised by the Executive Medical Director.
▲▲ It interacts at the NMDA receptor complex promoting neurotransmitter
inhibition and affects the opioid receptors, which account for its analgesic
effect with a rapid onset time (30 seconds).
▲▲ Ketamine causes less hypotension than morphine which means it is useful
when the patient is haemodynamically unstable and the administration
of morphine could further compromise their condition, or in entrapment
situations where morphine has already been given and further analgesia is
required, with the added sedative and amnesic properties of ketamine.
7.
Special Considerations
7.1
Treatment of the underlying conditions may often help relieve the pain in many
situations.
7.2Burns
7.2.1 Active cooling removes heat and prevents progression of the burn. This is
effective if performed within 20 minutes of the injury. Immersion or irrigation
with running tepid water (15.5°C) should be continued for up to 20 minutes.16
Cover exposed burn with cling film to protect exposed nerve endings to reduce
pain.
7.2.2 If there is limited or no access to running water, specially designed dressing
(such as watergel) could be used to cool and cover burns.10 Caution should be
exercised to avoid overcooling.
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7.3
Cardiac Chest Pain
7.3.1 Cardiac chest pain is related to myocardium ischaemia. The use of glyceryl
trinitrate (GTN) may improve myocardium perfusion by dilation of coronary
arteries or relief of coronary spasm to reduce pain10. Intravenous opioids (e.g.
morphine) are recommended as the first line analgesia for cardiac chest pain,
with Entonox being used to initiate analgesia whilst an IV cannula is inserted and
morphine is prepared.17
7.4
Palliative Care
7.4.1 Further guidance can be found in Clinical Guideline CG29 - Palliative Care.
7.5 Sickle Cell Anaemia
7.5.1 Sickle cell anaemia is a genetic (inherited) blood disorder in which red blood
cells, which carry oxygen around the body, develop abnormally.18 These
abnormal red blood cells can then clog sections of blood vessels leading to
episodes of ischaemic pain which can be severe. These episodes are called a
sickle cell crisis. Oxygen and fluid therapy may supplement strong opioids in the
management of pain related to the crisis.19
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8.References
1.
Hennes, H., Kim, M. K., & Pirrallo, R. G. (2005), PREHOSPITAL PAIN MANAGEMENT. Prehospital
Emergency Care, 9(1), 32-39.
2.
Hwang, U., Richardson, L. D., Sonuyi, T. O., & Morrison, R. S. (2006), The effect of emergency
department crowding on the management of pain in older adults with hip fracture. Journal of
the American Geriatrics Society, 54(2), 270-275.
3.
Swor, R., McEachin, C. M., Seguin, D., & Grall, K. H. (2005), Prehospital pain management in
children suffering traumatic injury. Prehospital Emergency Care, 9(1), 40-43.
4.
Todd, K. H., Sloan, E. P., Chen, C., Eder, S., & Wamstad, K. (2002), Survey of pain etiology,
management practices and patient satisfaction in two urban emergency departments. Can J
Emerg Med, 4(4), 252-256.
5.
International Association for the Pain Study (2013), IASP Taxonomy (online resource), http://
www.iasp-pain.org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/default.htm
(accessed on 13th May 2013)
6.
Prkachin, K., Solomon, P. & Ross, J. (2007), Underestimation of pain by health-care providers:
towards a model of the process of inferring pain in others. Canadian Journal of Nursing
Research, 39(2), 88-106.
7.
Nicholls T. & Hawkes-Frost L(2012), Pain: an ambulance prospective, Bridgwater, Class Health
8.
Schaible, H. & Richter, F.(2004), Pathophysiology of pain. Langenbeck’s Archives of Surgery,
389(4), 237-243.
9.
Lanser, P., & Gesell, S. (2001). Pain management: the fifth vital sign. Healthcare Benchmarks,
8(6), 68.
10.
Joint Royal Colleges Ambulance Liaison Committee (2013), UK Ambulance Service Clinical
Practice Guidelines 2013, Bridgwater, Class Professional Publishing
11.
Royal College of Physicians, British Geriatrics Society and British Pain Society (2007), The
assessment of pain in older people: national guidelines. Concise guidance to good practice
series, No 8. London, RCP
12.
World Health Organisation (2013), WHO’s pain ladder for adults (online resources), http://www.
who.int/cancer/palliative/painladder/en/ (accessed on 13th May 2013)
13.
BOC (2011), Entonox® Pocket Guide, Manchester, BOC Healthcare
14.
Graham, G. & Scott, K.(2005), Mechanism of action of paracetamol. American journal of
therapeutics, 12(1), 46.
15.
Cashman, J. N. (1996). The mechanisms of action of NSAIDs in analgesia. Drugs, 52(5), 13-23.
16.
Hudspith, J., & Rayatt, S. (2004). ABC of burns: first aid and treatment of minor burns. British
responsive
committed
effective
Medical Journal, 328(7454), 1487.
17.
National Institute for Health and Care Excellence (2010), CG95 Chest pain of recent onset: NICE
guideline, London, NICE
18.
NHS (2013), Sickle cell anaemia (online resource), http://www.nhs.uk/conditions/Sickle-cellanaemia/Pages/Introduction.aspx (accessed on 13th May 2013)
19.
Yale, S., Nagib, N. & Guthrie, T.(2000), Approach to the vaso-occlusive crisis in adults with sickle
cell disease. American Family Physician, 61(5), 1349.
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