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PERIOPERATIVE MANAGEMENT

Management of acute
pain

noxious stimuli, whereas neuropathic pain is the result of


dysfunction of the nervous system. Although these may coexist
as mixed pain, the acute post-surgical pain pattern is regarded as
nociceptive.
Pain may also be classified into somatic and visceral pain, for
example pain from cholelithiasis, renal calculi, etc. It is important to understand the type of pain to direct appropriate treatment and to understand the need for traditional and nontraditional analgesia.
An alternative classification is based on duration. Acute pain
is defined as pain of recent onset and probable limited duration.
It usually has an identifiable temporal and causal relationship to
injury or disease. The point at which acute pain becomes
chronic has been suggested at about 12 weeks or when the pain
is no longer thought to be due to the initial insult. Chronic pain
commonly persists beyond the time of healing of an injury and
frequently there may not be any clearly identifiable cause.1 It is
increasingly recognized that acute and chronic pain may represent a continuum rather than distinct entities.2,3

Kiran K Koneti
Martin Jones

Abstract
Acute pain is an important fear for most patients and inuences their
recovery and overall experience. Poorly treated, it could lead to undesirable effects and patient dissatisfaction. Hence, it is important to understand, assess and treat acute pain effectively. Pain is regarded as
the fth vital sign and should be addressed as important as other vital
parameters. Management of pain involves team work, including acute
pain services, especially in dealing with complex problems. Management of pain ideally starts at the pre-assessment visit or from rst presentation to the clinician. It is important to anticipate and treat acute
pain effectively, which may prevent the development of chronic pain
syndromes. Patients should be given information about analgesic options, the risk:benet ratio of the treatment options at the earliest opportunity and ideally have an individualized management plan.

Physiology of pain
The ability of the somatosensory system to detect noxious and
potentially tissue-damaging stimuli is an important protective
mechanism that involves multiple interacting peripheral and
central mechanisms. The neural processes underlying the
encoding and processing of noxious stimuli are defined as
nociception. The detection of noxious stimuli requires activation of peripheral sensory organs (nociceptors) and transduction
into action potentials for conduction to the central nervous
system. Nociceptors are stimulated by chemical, thermal or
mechanical damage and trigger the nociceptive impulses.
Nociceptive primary afferents are widely distributed throughout
the body (skin, muscle, joints, viscera, meninges) and comprise
both lightly myelinated A-delta fibres (diameter 2e5 mm) and
slow-conducting unmyelinated C-fibres (diameter <2 mm).
These fibres enter the dorsal horn of the spinal cord and synapse
at different sites (Ad at Rexed laminae II and V; C at Rexed
laminae II). The substantia gelatinosa (lamina II) integrates
these inputs and second-order neurons form the ascending
spinothalamic and spinoreticular pathways on the contralateral
side (Figure 1). The larger Ab fibres conducting touch and
descending pathways stimulate inhibitory interneurons within
the substantia gelatinosa and inhibit C fibre nociceptive inputs.
This is the basis of the gate theory of pain. Pain may be modified
by altering the neural pathway from its origin at the nociceptor
to its interpretation within the central nervous system by
various agents.
Psychological factors that influence the experience of pain
include the processes of attention, other cognitive processes (e.g.
memory/learning, thought processing, beliefs, mood), behavioural responses, and interactions with the persons
environment.

Keywords Acute pain; acute pain management; acute pain service;


adjuvant analgesics; non-opioid analgesics; opioid analgesics;
postoperative pain

Introduction
By any reasonable code, freedom from pain should be a basic
human right, limited only by our knowledge to achieve it.
Ronald Melzack
It is the basic duty of all healthcare professionals to relieve
pain, and the most important indication for treating pain after
surgery is humanitarian. Pain is defined by the International
Association for the Study of Pain (IASP) as an unpleasant sensory and emotional experience associated with actual or potential
tissue damage, or described in terms of such damage.1 Since pain
is highly subjective, it may also be described as being what the
patient says it is. Pain is an individual, multifactorial experience
influenced, among other things, by culture, previous pain experience, belief, mood and ability to cope. Pain may be an indicator
of tissue damage but may also be experienced in the absence of
an identifiable cause. The degree of disability experienced in
relation to the experience of pain varies; similarly there is individual variation in response to methods to alleviate pain.1
Pain may be classified according to its presumed aetiology.
Nociceptive pain is due to the stimulation of nociceptors by

Kiran K Koneti MBBS DA FCARCSI FRCA EDRA is an Advanced Pain


Fellow, Northern Deanery, Newcastle upon Tyne, and a Consultant
Anaesthetist and Pain Specialist at Sunderland Royal Inrmary, UK.
Competing interests: none declared.

Adverse physiological and psychological aspects of pain


Acute pain is one of the activators of the complex neurohumoral
and immune response to injury. Both peripheral and central
injury responses have a major influence on acute pain mechanisms. Thus acute pain and injury of various types are inevitably

Martin Jones MBChB FRCA is a Consultant Anaesthetist at the


Freeman Hospital, Newcastle upon Tyne, UK. Competing interests:
none declared.

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Please cite this article in press as: Koneti KK, Jones M, Management of acute pain, Surgery (2016), http://dx.doi.org/10.1016/j.mpsur.2015.11.008

PERIOPERATIVE MANAGEMENT

Effect of postoperative analgesia on surgical outcome

Physiology of pain

By reducing the unwanted effects of surgery on the pulmonary


and cardiac systems and by reducing ileus, the stress response
and thromboembolic complications, effective multimodal analgesia may improve patient morbidity. However, these benefits
are only achieved when dynamic pain relief is targeted to allow
early mobilization and other interventions are facilitated such as
early feeding with analgesia forming only part of a multidisciplinary approach.5

Substantia gelatinosa

Dorsal root ganglion

Dorsal horn

Pain assessment

Ventral horn

Rexeds laminae II and V

The assessment and measurement of pain are fundamental to the


process of assisting in the diagnosis of the cause of a patients
pain, selecting an appropriate analgesic therapy and evaluating
then modifying that therapy according to response. Pain should
be assessed within a biopsychosocial model that recognizes that
physiological, psychological and environmental factors influence
the overall pain experience.
The assessment of acute pain should include a thorough
general medical history and physical examination, a specific
pain history and an evaluation of associated functional
impairment along with any side effects of treatment. In acute
pain management, assessment must be undertaken at appropriately frequent intervals. It is useful to draw the distinction between the different types of pain because the likely duration of
the pain and the response to analgesic strategies may vary.

Spinothalamic
and spinoreticular
tracts

Figure 1

interrelated and if severe and prolonged, the injury response


becomes counterproductive and can have adverse effects on
outcome.1
Clinically significant injury responses can lead to a range of
physiological effects that may lead to adverse clinical effects
(Table 1). Patients at greatest risk of adverse outcomes from
unrelieved acute pain include very young or elderly patients,
those with concurrent medical illnesses and those undergoing
major surgery.1
Sustained acute nociceptive input, as occurs after surgery,
trauma or burns, can also have a major influence on psychological function, which may in turn alter pain perception. Failure to relieve acute pain may result in increasing anxiety,
inability to sleep, demoralization, a feeling of helplessness, loss
of control, inability to think and interact with othersdin the most
extreme situations, where patients can no longer communicate,
effectively they have lost their autonomy.4

Pain history and contents


SOCRATES is a useful mnemonic acronym commonly used by
healthcare professionals to evaluate pain (Box 1).
The definition of pain underlies the complexity of its measurement. It is difficult to objectively measure the intensity of
pain an individual is suffering from. This is usually assessed by
individual patients own report. These self-reporting measures
may be influenced by mood, medication and sleep disturbance.
Sometimes associated factors such as hyperalgesia (e.g. mechanical withdrawal threshold), the stress response (e.g. plasma

Effects and consequences of pain


System

Effects

Consequences

Clinical issues

Cardiovascular

Increased sympathetic activity

Risk of cardiac ischaemia, particularly


with pre-existing cardiac disease

Gastrointestinal
Respiratory

Increased sympathetic activity


Ineffective cough and reduction in
functional residual capacity
Activation of sympathetic and hormonal
systems (catecholamines, cortisol,
endorphins, etc.)

Increased heart rate, inotropy, and blood


pressure resulting in increased
myocardial oxygen demand
Reduced gastrointestinal motility
Inability to cough effectively and a
reduction in functional residual capacity
Inflammation, hyperglycaemia, protein
catabolism, increased free fatty acid
levels (lipolysis)
Changes in water and electrolyte flux
Hypercoagulable state
Reductions in natural killer cell function,
proliferative responses

Metabolic

Other

Reduction in patient movement


Suppression of cellular and humoural
immune function

Ileus
Atelectasis, ventilation-perfusion
mismatch and hypoxaemia
Delayed wound healing, reduced
immune function
Diminished muscle strength
Poor wound healing
Thromboembolism
Possible effects on tumour growth/
metastasis

Table 1

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consciousness or cognitive impairment, young children, elderly


patients or where there are failures of communication due to
language barriers, unwillingness to cooperate or severe anxiety.
In these circumstances other methods of pain assessment need to
be adopted (e.g. FACES pictorial scale).

SOCRATES assessment of pain


Site and radiation
Onset
Character
Radiation
Associated symptoms or signs
Time course and treatment
Exacerbating/relieving factors
Severity e at rest/movement/cough

Treatment
Treatment of acute pain should be tailored to individual patients assessment and requirements prior to admission. It is
initiated usually by anaesthetists in the perioperative period
and carried on by the surgical team. It involves prior planning
with the acute pain service (APS), if necessary along with the
use of protocols for managing specific types of surgeries and to
identify at risk patients. The APS involves the multidisciplinary
team including medical, nursing, and pharmaceutical expertise. The APS plays a major role in day-to-day management of
acute pain after surgery along with provision of training for
medical nursing staff involved in the management of postoperative pain.6 It is important to use appropriate other services (e.g. physiotherapists) to facilitate early recovery and
mobilization.
Traditionally the analgesic ladder introduced for treatment of
cancer pain by the World Health Organization (WHO) ladder has
been adapted for the treatment of acute pain (Figure 3).
It is made up of three steps in the increasing intensity of pain.
The first step involves the use of non-opioid  adjuncts (e.g.
paracetamol, aspirin or non-steroidal anti-inflammatory drugs
(NSAIDs)). If pain is still unsettled or there is increasing intensity, in addition to step 1 medication weak opioids (e.g. codeine, tramadol) can be added. In moderate to severe pain or
pain persisting or increasing in spite of step 2 treatment, stronger
opioids are considered in addition. All these involve the concept
known as multimodal analgesia. It is important to include the
analgesic ladder in individual patient analgesic plan along with
the adjunctive therapies, although it is used in reverse order in
acute pain. The analgesics act at different sites. Some may act at
the site of injury and decrease pain associated with inflammatory
reaction (e.g. NSAIDs), some may alter nerve conduction (e.g.

Box 1

cortisol concentrations), behavioural responses (e.g. facial


expression), functional impairment (e.g. coughing, ambulation)
or physiological responses (e.g. changes in heart rate) may provide additional information. Recording pain intensity as the fifth
vital sign aims to increase awareness and utilization of pain
assessment. Regular and repeated measurements of pain should
be made to assess ongoing adequacy of analgesic therapy. Uncontrolled pain should always trigger a reassessment of the
diagnosis and consideration of alternatives such as developing
surgical or other complications, or the presence of neuropathic
pain. Review by an acute pain service or other specialist group
should be considered. Although there are multidimensional
scales available to assess the pain, for practical purposes, unidimensional scales are used for assessment of post-surgical
pain. Commonly described options (Figure 2) are used according to the departmental preference.
In some instances it may not be possible to obtain reliable selfreports of pain, for example, patients with impaired

Pain rating scales


0

10

Numerical Rating Scale (NRS)


No pain

Mild pain

Moderate pain

Severe pain

WHO pain management stepladder

Visual Rating Scale (VRS)

No pain

Visual Analogue Scale (VAS)

Step 3
Strong opioid
non-opioid
adjunct

Worst possible
pain

Step 2

0
No hurt

1
Hurts a
little bit

2
3
4
Hurts a
Hurts
Hurts a
little bit even more whole lot
more

Weak opioid
non-opioid
adjunct

5
Hurts
worst
Step 1

Non-opioid
adjunct

Wongs Faces Scale


Note: VAS is usually a research tool

Figure 2

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Presentation: paracetamol is presented as 500 mg tablets alone


and in combination with weak opioids. It is available in oral/
rectal and intravenous preparations. The adult dose is 15e20
mg/kg and could be administered 4 hourly with a maximum dose
of 90 mg/kg/day. The intravenous form has more rapid onset of
action and superior early analgesia. However, repeated use of the
intravenous preparation has not shown a sustained advantage
compared to the oral form. Hence, intravenous paracetamol has
limited role in regular use and limited to patients who are not
able to take oral medication or the ones with gut malabsorption.
Suppositories are commonly used in children and have limited
use in adults also due to cost implications.

local anaesthetics), some may modify transmission in the dorsal


horn (e.g. opioids and antidepressants) while some may affect
the central component and the emotional aspects of pain (e.g.
opioids and antidepressants).
Based on information from systemic reviews of randomized,
double-blind, single-dose studies in patients with moderate to
severe pain the Oxford analgesic league table was constructed as
shown in Figure 4. The numbers needed to treat (NNT) are
calculated for the proportion of patients with at least 50% pain
relief over 4e6 hours compared with placebo.
Paracetamol
Paracetamol is the most commonly used analgesic with analgesic
and antipyretic action. Even though it has been widely available
for long time, its exact mechanism of action is still unknown.
NNT (95% confidence interval (CI)) for 1 g of paracetamol is 3.8
(3.4e4.4). Opioid requirements may be reduced by 20e30%
when administered with regular paracetamol.

Side effects: it is well tolerated with very few side effects and
contraindications. Since it is metabolized in liver, any form of
liver impairment would necessitate cautious administration.
NSAIDs
NSAIDs are widely used to treat mild to moderate pain and also
to reduce opioid consumption in the perioperative period. The
NNTs of various NSAIDs are as in Figure 4.

Mode of action: its antipyretic actions are due to the inhibition


of prostaglandin synthesis within the central nervous system.
Although the mechanism of paracetamol remains elusive, it may
involve direct and indirect inhibition of central cyclooxygenases, but the activation of the endocannabinoid system
and spinal serotonergic pathways also appear to be essential.1
Paracetamol has also been shown to prevent prostaglandin
production at the cellular transcriptional level, independent of
cyclo-oxygenase activity.1 As one of the mechanisms of action of
paracetamol appears to be linked to the serotonergic system, it is
possible that other drugs with serotonergic effects could affect
pain relief.

Mode of action: NSAIDs act primarily by inhibiting the enzyme


cyclo-oxygenase (COX) thereby preventing the production of
both prostaglandins (anti-inflammatory action) and thromboxanes (platelet aggregation) from membrane phospholipids. The
enzyme cyclo-oxygenase (COX) exists as two isoenzymes, COX-1
and COX-2. COX-1 (constitutive form) is responsible for the
production of prostaglandins that control renal blood flow, haemostatic function and form the protective mucosal barrier. COX2 (inducible form) is produced in response to tissue damage and

Oxford analgesic league table


Etoricoxib 120
Valdecoxib 40
Celecoxib 400
Paracetamol/codeine 1000/60
Rofecoxib 50
Ibuprofen 400
Lumicoxib 400
Naproxen 500/550
Diclofenac 50
Morphine 10 IM
Paracetamol 1000
Aspirin 600/650
Tramadol 100
1

95% confidence interval of number needed to treat for at least 50% pain relief compared with placebo
http://www.medicine.ox.ac.uk/bandolier/booth/painpag/Acutrev/Analgesics/Leagtab.html

Figure 4

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facilitates the inflammatory response. They also act as antipyretics due to inhibition of centrally produced prostaglandins.

Presentation e available in doses of 50/75/100 mg, sometimes in combination with paracetamol. Tramadol 100 mg has
NNT (95% CI) of 4.8 (3.8e6.1). It is well absorbed orally with
bio-availability of 70e90%.
Side effects: it has potential to interact with drugs that inhibit
central 5-HT or noradrenaline re-uptake (e.g. tricyclic antidepressants, selective serotonin re-uptake inhibitors) resulting in
seizures and hence should be avoided in epileptic patients.

Presentation: NSAIDs are broadly classified based on their


preferential inhibition of COX enzyme. The commonly used
NSAIDs (e.g. ibuprofen, diclofenac) are non-specific COX inhibitors while specific COX-2 inhibitors avoid the side effects of
COX-1 inhibition. However only the incidence of gastrointestinal side effects appear to be reduced while there is no
reduction in the incidence of other NSAID-associated side effects. There has been an increase in cardiac side effects with
some (typically e COX inhibitors) and these have since been
withdrawn.

Strong opioids
Strong opioids form the third step in the WHO analgesic ladder
for severe pain. These are common drugs used in the perioperative period for most intermediate and major surgeries. The
prototype and standard against which other drugs are compared
is morphine. Other commonly used strong opioids in the perioperative setting include oxycodone, diamorphine, fentanyl, and
alfentanil. The use of pethidine has decreased over the years due
to adverse central side effects.

Side effects: reduced prostaglandin synthesis in gastric mucosal


cells may lead to mucosal ulceration and hence may cause peptic
ulceration. NSAIDs should be used cautiously in renal impairment and brittle asthmatics.
Weak opioids
The term opiate refers to all naturally occurring substances with
morphine-like properties while opioid is a general term that
describes substances with affinity for opioid receptors. The
opioid receptors are of various types and are widely distributed
within central nervous system, spinal cord and periphery.

Presentation: strong opioids are administered orally or parenterally as intermittent boluses or continuous infusions. It is vital
to provide supplemental oxygen and frequently monitor vital
signs, especially respiratory rate and oxygen saturations (SpO2)
for patients on strong opioid infusions or patient controlled
analgesia (PCA) systems. PCA is the preferred method of
administering strong opioids for most major surgeries for the
initial 48e72 hours with a step down to oral route when
tolerated.

Mode of action: the activation of opioid receptors is associated


with hyperpolarization at the cellular level. The opioid drugs
produce analgesia by reducing neuronal excitability and inhibition of neurotransmitter release from the primary afferent terminals in the spinal cord and activation of descending inhibitory
controls in the midbrain. The commonly used weak opioids are
codeine and tramadol, which are used along with the WHO step
1 medication in step 2.

Side effects: all opioids share a similar side effect profile such as
sedation, nausea and vomiting, constipation, itching commonly
and the more serious side effect of respiratory depression. It is
always important to prescribe regular medication for combating
the common side effects of opioids. Respiratory depression
should be diagnosed early and initial treatment will be according
to an ABC approach along with use of the opioid antagonist
naloxone. It is important to consider urinary catheterization for
patients with impaired mobility or major surgery.

Codeine is the commonly used drug in this group.


Presentation e its route of administration is usually oral or
intramuscular (IM) and occasionally rectally in children. It is 10
times less potent than morphine and codeine 60 mg has an NNT
(95% CI) of 16.7 (11e48). It is widely used orally in doses of 30
e60 mg in 4e6 hourly intervals up to a maximum dose of 240
mg/day. It is also available in combination with paracetamol (cocodamol) in various strengths. Its use is now contraindicated in
children below the age of 18 undergoing tonsillectomy due to
serious adverse events.
Side effects: these are typical of any opioid (e.g. constipation,
nausea). The use of codeine and dihydrocodeine is limited in
bowel surgery and disadvantageous due to constipation. Its high
NNT and side effect profile, particularly on gastrointestinal
motility, limit its usefulness in postoperative pain.

Adjuvant drugs
Complex pain is fraught with challenges in the use of traditional
analgesia. Pain-modifying adjuvant medication has a role in these
situations. Adjuvants used in acute pain include nitrous oxide
(N2O), gabapentinoids, ketamine, magnesium, lignocaine, and
clonidine. N2O has been used as Entonox (50% mixture of oxygen
50% N2O) mainly for labour analgesia and procedural analgesia
(intravenous cannulation, ulcer care, sigmoidoscopy) in a ward or
emergency setting. It has modest analgesic and sedative properties
and causes minimal respiratory and cardiac depression. N2O diffuses more rapidly than nitrogen and can expand enclosed aircontaining spaces within the body. Its use is therefore contraindicated in the presence of a pneumothorax, obstruction of
middle ear and sinus cavities, recent vitreoretinal surgery, pneumocephalus, bowel obstruction and gas embolism.1
N-Methyl-D-aspartate receptor antagonists (e.g. ketamine,
dextromethorphan, amantadine, magnesium) have been used in
acute pain to modify central sensitization at spinal cord level. The
principal effect of low-dose ketamine is as an anti-hyperalgesic,
antiallodynic and antitolerance agent and not as a primary

Tramadol:
Mode of action e tramadol has affinity for opioid receptors
and also inhibits synaptic noradrenaline and serotonin (5-HT) reuptake, while stimulating presynaptic 5-HT release. This provides an alternative pathway for analgesia involving descending
inhibitory pathways within the spinal cord. It causes less respiratory depression and constipation in equianalgesic doses relative to morphine.

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analgesic per se.1 Consequently, ketamines main role is as an


adjuvant in the treatment of pain associated with central sensitization such as in severe acute pain, neuropathic pain and opioidresistant pain. It may also reduce the incidence of chronic postsurgical pain (CPSP) and attenuate opioid-induced tolerance and
hyperalgesia. Ketamine may also be useful for the treatment of
opioid-resistant or breakthrough cancer pain and, in higher
doses or combined with agents such as midazolam, can provide
effective and safe analgesia for painful procedures. Perioperative
ketamine has preventive, but not pre-emptive analgesic effects
in the immediate postoperative period.
Gabapentinoids (gabapentin/pregabalin) have been shown to
improve analgesia and reduce postoperative opioid consumption, along with reduced vomiting and pruritus. The incidence of
sedation is, however, increased compared with placebo.1 The
effects of gabapentin do not appear to be dose-dependent in the
range of 300e1200 mg.1
Perioperative intravenous (IV) lignocaine (lidocaine) infusion
and magnesium can be opioid-sparing and significantly reduce
pain scores, nausea, vomiting and duration of ileus up to 72
hours after abdominal surgery, contributing to a reduced hospital
length of stay.1 The use of systemic a-2-agonists (e.g. clonidine)
consistently improves perioperative opioid analgesia but the
frequency and severity of side effects (bradycardia, hypotension)
may limit their clinical usefulness.

Single-dose peripheral nerve blockade: peripheral nerve blocks


(PNBs) are useful in ambulatory surgery as they provide sitespecific anaesthesia with prolonged analgesia and minimal haemodynamic changes. Provided patients are given verbal and
written information regarding the risks as well as appropriate
follow-up, it would seem reasonable to discharge these patients
with the benefit of prolonged analgesia. Common blocks pertaining to surgical site include transverse abdominal plane
blocks, paravertebral blocks, ilioinguinal/iliohypogastric blocks
and plexus blocks for limbs. Careful choice of technique is
required to prevent prolonged motor block and restrict early
mobilization.
Continuous peripheral nerve blockade (CPNBs): although
providing maximal pain relief in the first 12e24 hours, patients
may suffer intense pain following resolution of a peripheral nerve
block. CPNBs using perineural catheters and continuous infusions of local anaesthetic lead to sustained postoperative
analgesia, opioid-sparing and result in less sleep disturbance
and improved rehabilitation.
Neuraxial techniques (epidural/spinal): local anaesthetics can
be administered via the epidural or intrathecal route along with
opioids to provide extended analgesia. The technique is determined by the site of surgery. The analgesia provided is usually
excellent. The decision to proceed is guided by the risk:benefit
ratio and prior agreement with patients. The UK Royal College of
Anaesthetists national audit project (NAP 3) estimated the permanent harm from epidurals in the perioperative period between
8.2 and 17.4 per 100,000 procedures. The risk for spinals was 1.6
e2.6 per 100,000.8 The risk of paraplegia or death after perioperative epidurals was 1.0e6.1 per 100,000 compared with 1.1
e2.1 per 100,000 spinals.7 These absolute risks are very small
compared to many associated with anaesthesia and surgery.
Thoracic epidural analgesia has been shown to reduce the stress
response after abdominal surgery.

Local/regional anaesthesia
Commonly used local anaesthetics in the perioperative period are
lignocaine, bupivacaine and its L-isomer (levobupivacaine) and
ropivacaine. Local anaesthetics can provide good pain control
with minimal side effects, and are usually used as part of a
balanced multimodal approach. Recent studies have also shown
extended benefit with the use of local anaesthetics with regional
anaesthesia in decreasing the recurrent rate of breast and prostate cancers. Loco-regional techniques play a vital role in a
number of enhanced recovery programmes pertaining to
different surgeries.7
Local anaesthetics can be administered by different routes and
delivery methods. Care must be taken to avoid exceeding the
recommended maximum dose. Cardiovascular collapse is an
infrequent but a serious risk with inadvertent intravenous
administration. Resuscitation should proceed along life support
guidelines and treatment with lipid emulsion instituted following
local guidance.
The various techniques of local anaesthetic administration
include:

Specic patient groups


The assessment and treatment of pain in certain patient groups is
challenging. Among them, children and elderly people with
cognitive impairment, or sedated patients in critical care are
particular examples. For these groups, evaluation by behavioural
assessment and specialized pain scales (such as the Wong Faces
scale) may be helpful. The situation in elderly patients is sometimes complicated by multiple pathologies and types of pain.
Management of acute pain can be challenging in patients
with substance abuse disorder. They exhibit tolerance to opioid
analgesia sometimes along with a low pain threshold. Ward
staff may find themselves in a confrontational situation due to
demands for adequate analgesia. The effective use of pain services along with good communication from the general practitioner and local community drug teams can make a difference
in this group. It is also not unusual to be confronted with patients with chronic pain on large doses of strong opioids.
Although it is ideal to tailor their analgesic regime with the use
of pain service, it is also important to maintain their background dose of opioid to prevent withdrawal and to achieve
effective analgesia.

Local infiltration: infiltration of local anaesthetic reduced requirements for opioid analgesics after day surgery and leads to a
lower incidence of nausea and vomiting. After day-stay hernia
repair, wound infiltration with levobupivacaine provided analgesia for 24 hours. Local infiltration was superior to opioid and
tenoxicam after minor laparoscopic surgery. Infiltration of the
trocar site for day-case laparoscopic cholecystectomy was more
effective if done prior to incision than postoperatively.1
Continuous wound infusions with local anaesthetics: these
provide only limited analgesic benefit for the first postoperative
day after outpatient inguinal hernia repair.

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(30e85%), thoracotomies (5e67%), mastectomies (11e57%)


and inguinal hernia repairs (0e63%). Although the link between nerve damage during surgery and development of CPSP
is complex,9 a number of preoperative (persistent preoperative
pain, genetic susceptibility), intraoperative (longer surgeries,
repetitive surgeries) and postoperative (severity of
postoperative pain, adjuvant radiotherapy) risk factors have
been identified for CPSP. While the identification of risk factors for the development of CPSP is important, their validity in
predicting CPSP is not clear. Considering the complexity and
multifactorial pathogenesis of the problem, it is likely that
multimodal approach to preventive analgesia and attention to
psychosocial risk factors may influence the development of
CPSP.

Specic surgical conditions


One of the most common sources of pain is postoperative pain
and the management principles discussed could be applied to the
management of acute pain in general. In addition to this
approach, there is also a need for information on postoperative
pain management that relates to the site of surgery and specific
surgical procedures. An ambitious project to develop such
evidence-based guidelines for the management of postoperative
pain was initiated by the PROSPECT group.9 Guidelines for the
treatment of pain after a number of specific operations can be
found at the PROSPECT website.
Acute causes of neuropathic pain can be iatrogenic, traumatic,
inflammatory or infective. Nerve injury is a risk in many surgical
procedures and may present as acute neuropathic pain in the
postoperative period with an incidence of 1e3%. The majority of
these patients had persistent pain at 12 months, suggesting that
acute neuropathic pain is a risk factor for chronic pain.2,3 The
role of acute neuropathic pain as a component of postoperative
pain is possibly underestimated; after sternotomy 50% of patients had dysaesthesia in the early postoperative period, which
was closely associated with severity of post-operative pain.3

Summary/conclusion
Treatment of pain after surgery is central to the care of postoperative patients. Failure to relieve pain is morally and ethically unacceptable. Effective pain relief is an essential element of
good quality care. Early and regular pain assessment on par with
other vital parameters along with appropriate treatment by all
healthcare providers, if need be with the use of acute pain services, will lead to improved patient outcomes and satisfaction.
This can be achieved by education, use of departmental guidelines/protocols, regular audit of practice, and feedback to the
professionals involved.
A

Acute post-amputation pain syndrome


Following amputation of a limb, and also breast, tongue, teeth,
genitalia and even inner organs such as the rectum, or a deafferentation injury such as brachial plexus avulsion,1 a number of
phenomena can develop. These are:
 Stump pain e pain localized to the site of amputation.
 Phantom sensation e this is defined as any sensory
perception of the missing body part with the exclusion of
pain.
 Phantom limb pain e this is defined as any noxious sensory phenomenon in the missing limb or organ. The incidence of phantom limb pain is estimated to be 30e85%
after limb amputation and occurs usually in the distal
portion of the missing limb. This can be immediate or
delayed. Usually it is intermittent and diminishes with
time.
Continuous regional blockade via nerve sheath catheters
provides effective postoperative analgesia after amputation, but
has no preventive effect on phantom limb pain. Various agents
like calcitonin, morphine, ketamine, gabapentin, amitriptyline
and tramadol reduce phantom limb pain.

REFERENCES
1 Australia and New Zealand College of Anaesthetists and Faculty
of Pain Medicine. Acute pain management: scientic evidence.
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we now? Br J Anaesth 2011; 107: 25e9.
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outcome. Br J Anaesth 2001; 87: 62e72.
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Chronic post-surgical pain (CPSP)


Chronic post-surgical pain (CPSP) is one of the most common
and serious complications after surgery.10 CPSP is defined by
pain developing after surgical procedure, lasting at least 2
months, while other causes of pain (malignancy, infection)
and pain continuing from a pre-existing pain problem are
excluded. Nerve injury during surgery has been implicated in
the development of CPSP2 and some patients with CPSP have
neuropathic pain. Inflammatory and immune reactions after
damage to axons results in release of neurotransmitters that
act locally and in the spinal cord to produce hypersensitivity
and ectopic neural activity which contributes to central
sensitization. The incidence of CPSP is high with amputations

SURGERY --:-

2016 Published by Elsevier Ltd.

Please cite this article in press as: Koneti KK, Jones M, Management of acute pain, Surgery (2016), http://dx.doi.org/10.1016/j.mpsur.2015.11.008