Dr. Dean Burrill, Anesthesiologist
Royal Columbian & Eagle Ridge Hospitals
Director, Acute & Chronic Pain Service RCH
 Current
status of pain
management in the trauma
population
 Identify types of pain in trauma
 Pain assessment
 Pharmacological management
 Regional anesthestic management
 Introduction to other options
 Summary
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Consider alternatives to the 0 to 10 pain scale
The CNS is “plastic”. Ongoing pain can lead
to real structural changes in the nervous
system.
Recognise current drug management of pain.
Consider newer current and future options.
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25 year old left-handed motorcyclist
travelling on highway.
Lost control, impacted at least two other
vehicles.
Stabilized at the scene and transferred by
helicopter to hospital.
Major injury to left arm, forearm, and
subclavian artery.
Fracture of right tibia.
Stable fracture of cervical spine.
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Over 50 units of blood.
Required left upper limb disarticulation.
Ligation of left subclavian artery.
IM nail of right tibia.
C-spine managed conservatively with
Philadelphia collar.
Initially managed in ICU, followed by High
Acuity Unit (non-ventilatory).
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Significantly influenced by current military
campaigns.
Soldiers with similar injuries require less
analgesics than civilians.
Beecher observed that soldiers expected
evacuation and safe recuperation but civilians
expected loss of wages and social hardship.
Pre-clinical studies suggest neuronal
sensitisation, remodelling, gene expression,
histological changes and behavioural changes
can occur within minutes to days after injury.
Keene et al. 2011
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450 trauma patients - pain was measured on
admission
Prevalence admission- 91%
Discharge (86%) – 2/3 moderate or severe pain
at discharge
Pain decreased in 37% of the patients, did not
change at all in 46%, or had increased in 17% of
the patients at discharge from the ED
Pain prevalence and pain relief in trauma patients in the Accident &
Emergency department (2008) Berben et. al. Injury; May;39(5):578-85
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Pain is the single most common presenting
symptom to ER – 78%
60% of patients in pain had analgesics given
with a median wait time of 90 minutes
Patients not given analgesics - 42% would have
like to have been given analgesic
74% of patients discharge home with modsevere pain
Pain in the emergency department: results of the pain and emergency medicine initiative
(PEMI) multicenter study. (2007) Todd, K., et al.. The Journal of Pain, Vol 8, No 6. 460466.
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Fear of masking injuries
Fear of impacting hemodynamic status
Fear of respiratory compromise
Lower priority
Underuse of effective analgesic techniques
Lack of pain protocols/order sets
Lack of pain management knowledge by
providers
Values and beliefs
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3047 adults patients admitted with acute trauma
(69 hospitals in 14 US states)
12 months post - 62.7% of patients reported
injury-related pain
Mean severity was 5.5/10
Pain at 3 months was predictive of both the
presence and higher severity of pain at 12 months
More common in women and those who had
untreated depression before injury
Lower pain severity was reported by patients with a
college education and those with no previous
functional limitations
Prevalence of Pain in Patients 1 Year After Major Trauma (2008) Rivara et. al Arch
Surg;143(3):282-287
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Studies in England and France have revealed
40 to 60 per cent of trauma patients have
other substances present on admission.
◦ Alcohol.
◦ Street drugs.
◦ Prescription medications: i.e. Strong opioids.
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Often a pre-existing pain condition also part
of the picture.
Presence of these substances may modify
administration of analgesics.
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Younger age
Multiple surgeries
◦ Length of sx
◦ Type of sx
Poorly managed pain
Nerve injury
Duration of disability (time to return to work)
Psychological -  anxiety, depression, stress,
pain catastrophizing
Macrae (2008), Keene et al (2011) , Sommer et al (2010)
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Vlaeyen and Linton, 2000
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screening
education, clear communication,
reassurance and advice to maintain usual
activities
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Remember, acute pain usually indicates
ongoing tissue damage and/or injury.
Acute pain can be protective, discouraging
activity that could cause further injury.
Trauma and pain almost synonymous
Chronic pain is pain that continues three to
six months after injury and usually continues
despite the fact that tissues have healed and
ongoing injury is unlikely.
Somatic
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Pain that is caused by
tissue damage, mild to
severe, that subsides as
healing occurs
Protective
Easily diagnosed
Potential to be treated
effectively
Usually limited short
duration
Visceral
Cardiovascular
Respiratory
GI
Heart Rage
Blood Pressure
Increased
myocardial demand
Hypercoagulation
Unstable angina
Myocardial
infarction
DVT
PE
Lung Volumes
Atelectasis
Decreased cough Pneumonia
Splinting
Hypoxemia
Gastric Emptying Constipation
 Bowel Motility
Anorexia
Ileus
National Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et al (2004)
Neuroendocrine
Altered release of
multiple hormones
Hyperglycemia
Wt loss/ muscle
wasting
Impaired wound
healing
Impaired immune
function
MSK
Muscle spasm
Impaired muscle
mobility & function
Immobility
Weakness
Fatigue
Psychological
Anxiety
Fear
Sleep deprivation
Impact on coping
Post traumatic
stress disorder
National Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et al (2004)
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Neuropathic pain is caused
by an injury or dysfunction
of the peripheral or central
nervous system
(Jovey, 2002)
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NP can be caused by infection,
trauma, ischemia, metabolic
disorders, tumors, toxins and
primary neurological diseases
Crush injuries
Burn injuries
Vertebral fractures
Discogenic pain
TBI – headache, neck pain, back
pain & limb spasticity
Occipital neuralgia
Phantom Limb pain
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1 to 8 weeks for most cases
Can be immediate or prolonged
Any injury can cause central imprinting of pain
sensation (central sensitization)
Trauma
Arthritis
Neuropathies
Surgery
Headache
When peripheral pain becomes central pain: diagnosis and treatment. (2011). Power
point presentation – Dr. Forest Tennant
Injury/related Surgery
Incidence of persistent
pain
Amputation
30-85%
Thoracotomy/Chest Wall
5 - 67%
Spinal Cord Injury
› 50%
Traumatic Brain Injury
32 – 51%
Vertebral fractures
› 25%
Burn Injuries
35- 52%
Complex Regional Pain
1-5%
Macintrye and Schug (2007), Kehlet et al.(2006), Sinha & Cohen (2011), Nampiaparampil
(2008), Dauber et al. (2002), Singh & Cailliet (2011)
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Numeric Pain Scale
No Pain
Mild
Moderate
Severe
Baker-Wong Faces Scale
Available in 22 languages – FHA Stores #253945
Online – FHA Intranet – RCH Pain Management
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Current “Gold Standard” used in most of our
hospitals.
But it has significant problems:
Subjective.
Wide variation between individuals.
Not thought to be linear.
Should consider changes more than actual
numbers.
◦ Often administered incorrectly:
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 Zero is no pain and ten is the worst pain.
DO:301
If the patient’s score is equal to or greater than 4, the
test is positive (sensitivity: 82.9%; specificity: 89.9%)
Pain Score
Level of Pain
Analgesic Action
3
Continuous pain at
rest, severe pain on
movement.
Morphine (or other
strong agent), and
consider those below.
2
Mild pain at rest,
moderate on
movement.
Weak opiate, NSAID
and consider those
below.
1
No pain at rest, mild
on movement.
Acetaminophen.
0
No pain at rest or on
movement.
None.
Looker and Aidington, 2009
McGrath, 1996
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Acetaminophen
NSAIDs
Cox-2 inhibitors
Ketamine
Gabapentinoids
Tricyclic antidepressants
Steroids
Opioids
Local anaesthetics
Biofeedbac
k
Guided
Imagery
Distraction
Tricyclic
Antidepressants
Opioids
SSRI
Anticonvulsants
http://www.pharmacology2000.com/Central/Opioids/postop_pain1.gif
MODIFIED
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Effective alone and in combination.
Mechanism of action not entirely understood
but inhibition of cycloxygenase receptors
believed to be involved.
Anti-pyretic.
Reduces opioid requirements.
Bioavailability and speed of onset improved
with IV form.
Concerns re. liver function.
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Maximum daily dose: 4000 mg.
3200 mg in chronic users (healthy adults).
2400 mg in elderly patients or those with
liver, renal or cardiac impairment.
◦ Combination drugs ending in: “-cet”.
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Analgesic, anti-inflammatory, anti-pyretic.
Inhibit cycloxygenase (COX) in the spinal cord
and periphery, thereby decreasing prostanoid
synthesis and diminish post-injury
hyperalgesia.
COX-1 versus COX-2: 1 present in all cells, 2
present in cell at sites of inflammation
(inducible enzyme).
COX-2 selective agents thought to have fewer
side effects, for example GI issues, but
instead have other concerns, such as cardiac.
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Acetylsalicylic Acid (ASA) the original. Differs
from most NSAIDs as irreversibly bound.
More COX-1 than COX-2 effects.
◦ Combination drugs ending in: “-sal”.
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Ibuprofen, Naproxen, Indomethacin,
Ketorolac: both COX-1 and COX-2.
Celecoxib (Celebrex): COX-2.
◦ Rofecoxib (Vioxx) withdrawn due to cardiac
concerns.
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Risk factors associated with GI haemorrhage:
◦ History of Peptic Ulcer Disease or Upper GI Bleed –
risk ↑ 4 – 5 x
◦ Oral steroid – risk ↑ 4 – 5 x
◦ Age > 65 – risk ↑ 5 – 6 x
◦ High (>2x normal) dose of NSAID – risk ↑ 10 x
◦ Anticoagulants – risk ↑ 10 – 15 x
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Gabapentin (Neurontin) & Pregabalin (Lyrica)
Structurally related but NOT the same.
Gabapentin indicated for chronic neuropathic
pain but has been tried in acute surgical pain
with some success.
Pregabalin indicated for neuropathic pain,
fibromyalgia and, in Europe, generalised
anxiety disorder.
Pregabalin is more potent, absorbs faster and
has greater bioavailability.
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These medications act on the
neurotransmitters in the brain and spinal
cord, chiefly on systems associated with
GABA (gamma-aminobutyric acid), the main
inhibitory neurotransmitter in the CNS.
Pregabalin may potentiate other depressant
medications such as barbiturates and
benzodiazepines.
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2010 prospective randomized trial, which
included pregabalin as part of a multimodal
analgesia regimen, has shown a significant
decrease in chronic pain at 6 months after
Total Knee Arthroplasty. Chronic pain six
months after TKA may be as high as 12%.
0% in the pregabalin group and 5.2% in the
placebo group with persistent neuropathic
pain at six months
Perioperative oral pregabalin reduces chronic pain after total knee arthroplasty: a
prospective randomized, controlled trial. Anesth Analg 2010;110(1):199-207.
Buvanendran A, et al
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N-methyl D-aspartate (NMDA) receptor
blocker.
Also:
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Sympathomimetic
Nor-epinephrine uptake blocker
Muscarinic cholinergic antagonist
Opioid receptor activity (controversial)
Competes against Glutamate at NMDA
receptor, blocking “wind-up” and central
sensitisation.
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Wide safety profile.
Can be used pre-hospital, as an adjunct to
opioids and other analgesics, and may have a
role in chronic narcotic dependence and
hyperalgesia.
Anaesthetic in doses >2 mg/kg
Analgesic at 10 – 15 times less, concurrent
with a significant decrease in side effects.
On WHO essential medicines list for
anaesthetic agents.
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May help to diminish “wind-up”, particularly
at the spinal cord level, which increases the
nociceptive perception of pain.
Has been shown to reduce post-operative
pain and opioid requirements.
Has a role in opioid tolerance and opioid
hypersensitivity.
May be used as an infusion post-operatively
◦ Many hospitals now have protocols.
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“Weak” versus “Strong”
Morphine is the classic and gold-standard to
which all others are compared.
Weak: Codeine, Tramadol.
Strong: Morphine, Hydromorphone, Fentanyl,
Oxycodone & Methadone.
Act on µ, κ and δ receptors.
Presynaptic receptors both excitatory &
inhibitory; postsynaptic receptors only
inhibitory.
Class
Definition
Example
Agonist
A drug which causes
maximal stimulation
of receptor when
bound.
Morphine, Fentanyl,
Sufentanil,
Remifentanil.
Antagonist
A drug which fails to
cause any stimulation
of the receptor when
bound.
Naloxone.
Partial Agonists
A drug which, when
bound to the receptor,
stimulates the
receptor below
maximal intensity.
Buprenorphine.
Mixed
Agonists/Antagonists.
A drug which acts
simultaneously on
several receptor
subtypes.
Nalbuphine,
Butorphanol.
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Oral, intramuscular, subcutaneous,
intravenous & rectal.
Intrathecal & epidural.
Transdermal, intranasal, transbuccal,
periocular, pulmonary and intra-articular.
Drug
Parenteral
Oral
Morphine
10
30
Buprenorphine
0.3
0.4 (sl)
Codeine
100
200
Fentanyl
0.1
N/A
Hydrocodone
N/A
30
Hydromorphone
1.5
7.5
Meperidine
100
300
Oxycodone
10
20
Oxymorphone
1
10
Tramadol
100
120
sl = sublingual
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Methadone is not on the previous list as it
cannot be equated with other opioids.
This is because in addition to being a full µopioid agonist it is an NMDA receptor
antagonist (like Ketamine) and may be a
nicotinic acetylcholine receptor antagonist.
“Equivalency” doses can have unpredictable
results and so a protocol has been developed
for converting to Methadone.
Methadone is very effective for weaning
opioids in chronic pain patients.
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Nausea & Vomiting – chemoreceptor zone in
4th ventricle.
Dysphoria – activation of κ.
Euphoria – activation of µ.
Confusion, delirium & seizures.
Respiratory depression.
Neuroendocrine effects.
Gastrointestinal effects.
Bladder & ureter.
Skin.
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Nothing really new but newer combinations
of old agents.
◦ Butrans Patch: Buprenorphine transdermal patch
for chronic pain.
◦ Suboxone: Buprenorphine compounded with
Naloxone in a tablet form.
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Transdermal patch applied for 7 days!
◦ Partial agonist at mu & delta opioid receptors
◦ Antagonist at kappa opioid receptors
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Relevance to trauma & emergency surgery pts
◦ May need increased short acting opioids to be
effective due to the strong binding effect at the mu
receptor & the antagonist effects of buprenorphine
Oral Morphine
Equivalent
Less than 30 mg
30- 80 mg
Burprenorphine
5 mcg/hr
10 mcg/hr
Analgesic
NNT
Ibuprofen 600/800
1.7
Ketorolac 20
1.8
Diclofenac 100
1.8
Acetaminophen 1000 + Codeine 60
2.2
Ibuprofen 400
2.5
Ketorolac 10
2.6
Acetaminophen 650 + Tramadol 75
2.6
Diclofenac 50
2.7
Ibuprofen 200
2.7
Meperidine 100 (i.m.)
2.9
Tramadol 150
2.9
Morphine 10 (i.m.)
2.9
Acetaminophen 1000
3.8
Tramadol 100
4.8
Codeine 60
16.7
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Act as cell membrane stabilisers, thus
reducing the depolarisation and
repolarisation of excitable membranes, such
as nerve cells.
Act at cellular level by blocking sodium
channels.
Movement of ions, such as sodium, from the
outside to the inside of cells (and vice versa),
is essential to allowing action potentials to
propagate along nerve fibres.
Biofeedbac
k
Guided
Imagery
Distraction
Tricyclic
Antidepressants
Opioids
SSRI
Anticonvulsants
http://www.pharmacology2000.com/Central/Opioids/postop_pain1.gif
MODIFIED
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Immediate:
◦ CNS and Cardiorespiratory toxicity
 Intralipid
◦ Allergies
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Delayed
◦ Infusions
 Excessive dose
 Migration of catheter
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Masking clinical symptoms and signs
◦ Compartment syndrome
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Have unique benefit and low risk.
Cutaneous anaesthesia (lidocaine, prilocaine,
TAC)
Simple neural blockade:
◦ Field block
◦ Digital nerve block
◦ Trigger point injection
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Complex nerve blocks and Continuous
Peripheral Nerve Blocks (CPNB)
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Intercostal
Ankle
Brachial plexus
Lumbar plexus
Sciatic nerve
Neuroaxial
◦ Epidural
◦ Spinal
Risks associated with any nerve
block:
Additional risks for catheter
techniques:
Infection
Increased risk of infection
Haematoma/bleeding
Catheter failure
Nerve damage (permanent &
temporary)
Catheter disconnection
Inadvertent intravascular injection
Catheter migration
Failure
Catheter leak
Pneumothorax (upper limb &
paravertebral blocks)
Catheter removal with bleeding
diathesis
Local anaesthetic toxicity
Retained catheter
? Masking of compartment
syndrome
DJ Connor, 2009
Anterior
Lateral
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As soon as possible once life-threatening
injuries have been dealt with.
Ideally pre-operatively has been shown to
have better efficacy, especially in
amputations, but these are rarely planned in
trauma.
If more traditional analgesic techniques are
failing to control the pain.
If multiple surgeries are planned on the area.
Meta-Analysis, Richman et al. 2006
Meta-Analysis, Richman et al. 2006
Side
Effects
Catheter
Opioid
P value
Odds ratio NNT
Nausea/
Vomiting
38/182
(20.9%)
95/195
(48.7%)
<0.001
0.28
4
Sedation
12/45
(26.7%)
23/44
(52.3%)
<0.012
0.33
4
Puritis
11/113
(9.7%)
29/109
(26.6%)
<0.001
0.30
6
Sensory/
Motor
Block
22/70
(31.4%)
9/60
(15.0%)
<0.023
0.39
Meta-Analysis, Richman et al. 2006
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Mariano et al. (2008) has demonstrated the
efficacy of ultrasound-guided CPNB catheter
insertion during humanitarian missions in
paediatric patients with limited
communication.
Could provide superior management of our
patients with language/communication
issues.
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Usually epidural but may include spinal
catheters.
Often limited in trauma due to bleeding
diathesis, access to insertion site or
associated injuries, and issues surrounding
catheter maintenance or removal.
Particularly suited to the management of rib
fractures in both non-ventilated and
ventilated patients.
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Epidural has been the gold standard in our
institution.
For bilateral fractures and sternal fractures,
epidural is the superior choice.
For unilateral fractures thoracic paravertebral
catheters can provide equal comfort with less
risk.
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Orthopaedic management of fractures.
Surgical fixation of rib fractures.
Neurosurgical management of spinal
fractures.
Surgical management of abdominal & thoracic
issues.
Radiological management of vertebral
compression fractures using vertebroplasty
and kyphoplasty.
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Following management in ICU and HAU
patient was discharged to ward. Initial
discharge complicated by delirium. Had
temporary readmission to HAU and psychiatry
involved. Psychotropic medication started.
Opioids (oral), NSAIDs, Acetaminophen and
Gabanoids initiated.
Significant phantom limb issues.
Brachial plexus catheter inserted.
Patient discharged mid-September
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Patient seen in follow-up this past week as
outpatient.
Stable pain at 2 – 3/10.
Gabapentin and Hydromorphone main
analgesics.
Attempting to slowly wean medication.
Still wearing hard collar so cannot be fitted
with prosthesis yet.
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Early initiation of appropriate treatment.
◦ Analgesics such as morphine and ketamine started
in the field.
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Early initiation of appropriate treatment.
◦ Analgesics such as morphine and ketamine started
in the field.
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Aggressive use of multimodal therapy during
diagnosis, management and recuperation.
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Acetaminophen.
NSAIDs.
Gabanoids
Ketamine.
Opioids.
Local anaesthetics
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Assessment and management of psychosocial
factors that may confound treatment or
contribute to development of chronic pain.
◦ Screening for those at risk.
 Pre-existing substance abuse.
 Pre-existing chronic pain.
 Crappy Life Syndrome
◦ Education, communication & rehabilitation.
◦ Minimising fear and encouraging early return to
normal activity.
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Insertion of CPNB and neuroaxial catheters as
indicated.
Surgical fixation of fractures and
management of wounds as appropriate.