Dr. Dean Burrill, AnesthesiologistRoyal Columbian & Eagle Ridge HospitalsDirector, Acute & Chronic Pain Service RCH

Current status of pain management in the trauma population

Identify types of pain in traumaPain assessmentPharmacological management Regional anesthestic management

Introduction to other options Summary

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.

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.

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).

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

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

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 mod-severe 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. 460-466.

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

providersValues and beliefs

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

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.

Often a pre-existing pain condition also part of the picture.

Presence of these substances may modify administration of analgesics.

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)

Vlaeyen and Linton, 2000

screening education, clear communication, reassurance and advice to maintain usual

activities

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.

• Pain that is caused Pain that is caused by tissue damage, by tissue damage, mild to severe, that mild to severe, that subsides as healing subsides as healing occursoccurs

• Protective• Easily diagnosed• Potential to be

treated effectively• Usually limited short

duration

SharpThrobbing

Gnawing

Aching

Constant

Somatic

Cramping Squeezing

Deep AchingDull

Visceral

CardiovascularCardiovascular Heart RageBlood PressureIncreased myocardial demandHypercoagulation

Unstable anginaMyocardial infarctionDVTPE

RespiratoryRespiratory Lung VolumesDecreased coughSplinting

AtelectasisPneumoniaHypoxemia

GIGI Gastric Emptying Bowel Motility

ConstipationAnorexiaIleusNational Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et

al (2004)

NeuroendocriNeuroendocrinene

Altered release of multiple hormones

HyperglycemiaWt loss/ muscle wastingImpaired wound healingImpaired immune function

MSKMSK Muscle spasmImpaired muscle mobility & function

ImmobilityWeaknessFatigue

PsychologicalPsychological AnxietyFear

Sleep deprivationImpact on copingPost traumatic stress disorder

National Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et al (2004)

Neuropathic pain is caused by an injury or dysfunction of the peripheral or central nervous system (Jovey, 2002)

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

1 to 8 weeks for most cases Can be immediate or prolonged

Any injury can cause central imprinting of pain sensation (central sensitization)TraumaArthritisNeuropathiesSurgeryHeadache

When peripheral pain becomes central pain: diagnosis and treatment. (2011). Power

point presentation – Dr. Forest Tennant

Injury/related Injury/related SurgerySurgery

Incidence of Incidence of persistent painpersistent pain

Amputation 30-85%

Thoracotomy/Chest Wall

5 - 67%

Spinal Cord Injury › › 50%50%

Traumatic Brain Injury 32 – 51%32 – 51%

Vertebral fractures › › 25%

Burn InjuriesBurn Injuries 35- 52%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)

Numeric Pain Scale

No Pain Mild Moderate Severe

Available in 22 languages – FHA Stores #253945

Online – FHA Intranet – RCH Pain Management

Baker-Wong Faces Scale

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:

Zero is no pain and ten is the worst pain.

DO:301DO:301

If the patient’s score is equal to or greater than 4, thetest 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

Acetaminophen NSAIDs Cox-2 inhibitors Ketamine Gabapentinoids Tricyclic antidepressants Steroids Opioids Local anaesthetics

BiofeedbackGuided ImageryDistraction

Tricyclic AntidepressantsOpioidsSSRI

Anticonvulsants

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www.pharmacology2000.com/Central/Opioids/postop_pain1.gif MODIFIED

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.

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”.

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.

Acetylsalicylic Acid (ASA) the original. Differs from most NSAIDs as irreversibly bound. More COX-1 than COX-2 effects.◦ Combination drugs ending in: “-sal”.

Ibuprofen, Naproxen, Indomethacin, Ketorolac: both COX-1 and COX-2.

Celecoxib (Celebrex): COX-2.◦ Rofecoxib (Vioxx) withdrawn due to cardiac

concerns.

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

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.

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.

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

N-methyl D-aspartate (NMDA) receptor blocker.

Also:◦ Sympathomimetic◦ Nor-epinephrine uptake blocker◦ Muscarinic cholinergic antagonist◦ Opioid receptor activity (controversial)

Competes against Glutamate at NMDA receptor, blocking “wind-up” and central sensitisation.

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.

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.

“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.

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

Methadone is not on the previous list as it cannot be equated with other opioids.

This is because in addition to being a full µ-opioid 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.

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.

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.

Transdermal patch applied for 7 days!◦ Partial agonist at mu & delta opioid receptors◦ Antagonist at kappa opioid receptors

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

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.

BiofeedbackGuided ImageryDistraction

Tricyclic AntidepressantsOpioidsSSRI

Anticonvulsants

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www.pharmacology2000.com/Central/Opioids/postop_pain1.gif MODIFIED

Immediate:◦ CNS and Cardiorespiratory toxicity

Intralipid◦ Allergies

Delayed◦ Infusions

Excessive dose Migration of catheter

Masking clinical symptoms and signs◦ Compartment syndrome

Have unique benefit and low risk. Cutaneous anaesthesia (lidocaine,

prilocaine, TAC) Simple neural blockade:

◦ Field block◦ Digital nerve block◦ Trigger point injection

Complex nerve blocks and Continuous Peripheral Nerve Blocks (CPNB)◦ 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

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

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.

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.

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.

3

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.

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

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.

Early initiation of appropriate treatment.◦ Analgesics such as morphine and ketamine

started in the field.

Early initiation of appropriate treatment.◦ Analgesics such as morphine and ketamine started

in the field. Aggressive use of multimodal therapy during

diagnosis, management and recuperation.◦ Acetaminophen.◦ NSAIDs.◦ Gabanoids◦ Ketamine.◦ Opioids.◦ Local anaesthetics

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.

Insertion of CPNB and neuroaxial catheters as indicated.

Surgical fixation of fractures and management of wounds as appropriate.