Analgesic Options & Pain Management in the Trauma Population

2. Analgesic Options & Pain Management in the Trauma Population Dr. Dean Burrill, Anesthesiologist Royal Columbian & Eagle Ridge Hospitals Director, Acute & Chronic Pain Service RCH

3. Overview • 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

4. Objectives • 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.

5. Case Presentation: • 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.

7. 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).

8. Current status • 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.

9. Keene et al. 2011

10. Prevalence of Pain in Trauma Patients • 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

11. Pain in ER • 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.

12. Barriers to Pain Management in Trauma Population • 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

13. Prevalence of Pain after Major Trauma • 3047 adults patients admitted with acute trauma (69 hospitals in 14 US states) • 12 months post - 62.7% of patients reportedinjury-related pain • Mean severity was 5.5/10 • Pain at 3 monthswas predictive of both the presence and higher severity of painat 12 months • More common in women and thosewho had untreated depression before injury • Lower pain severity was reported by patients witha 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

14. Trauma and Associated Substances • 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.

15. Factors associated with the development of persistent pain after Trauma • 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)

16. The Fear-Avoidance Model. • Vlaeyen and Linton, 2000

17. Preventing Fear-Avoidance • screening • education, clear communication, • reassurance and advice to maintain usual activities

18. Acute Pain vs Chronic Pain • 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.

19. Acute Pain Somatic • 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 Throbbing Sharp Aching Gnawing Constant Visceral Cramping Squeezing Deep Aching Dull

20. Adverse effects of unrelieved Pain National Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et al (2004)

21. Adverse effects of unrelieved Pain National Pharmaceutical Council (2001). Macintyre & Schug (2007).Cohen et al (2004)

22. 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 Neuropathic Pain

23. Time to central pain imprinting • 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

24. Incidence of Chronic/Persistent Pain after Trauma Macintrye and Schug (2007), Kehlet et al.(2006), Sinha & Cohen (2011), Nampiaparampil (2008), Dauber et al. (2002), Singh & Cailliet (2011)

25. Pain Severity Tools Numeric Pain Scale 0 1 2 3 4 5 6 7 8 9 10 No Pain MildModerate Severe Baker-Wong Faces Scale Available in 22 languages – FHA Stores #253945 Online – FHA Intranet – RCH Pain Management

26. One to Ten Pain 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.

27. Pain in the ICU DO:301

28. Pain Assessment in Advanced Dementia (PAINAD) Scale

29. If the patient’s score is equal to or greater than 4, thetest is positive (sensitivity: 82.9%; specificity: 89.9%)

30. Pain score, definition and analgesic action Looker and Aidington, 2009

31. WHO analgesic ladder for management of increasing pain McGrath, 1996

32. Initial Management Using Drugs • Acetaminophen • NSAIDs • Cox-2 inhibitors • Ketamine • Gabapentinoids • Tricyclic antidepressants • Steroids • Opioids • Local anaesthetics

33. Analgesics and Sites of Action

34. Pain Pathway – Pain Management Biofeedback Guided Imagery Distraction Tricyclic Antidepressants Opioids SSRI Anticonvulsants http://www.pharmacology2000.com/Central/Opioids/postop_pain1.gifMODIFIED

35. Acetaminophen • 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.

36. Acetaminophen cont’d • 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”.

37. NSAIDs • 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.

38. NSAIDs cont’d • 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.

39. NSAIDs cont’d • 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

40. Gabapentinoids • 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.

41. Gabapentinoids cont’d • 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.

42. Gabapentinoids cont’d • 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 pregabalingroup and 5.2% in the placebo group with persistent neuropathic pain at six months • Perioperative oral pregabalinreduces chronic pain after total knee arthroplasty: a prospective randomized, controlled trial. AnesthAnalg 2010;110(1):199-207. Buvanendran A, et al

43. Ketamine • 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.

44. Ketamine cont’d • 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.

45. Ketamine cont’d • 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.

46. Opioids • “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.

47. Classification of opioids according to receptor activity.

48. Routes of adminstration • Oral, intramuscular, subcutaneous, intravenous & rectal. • Intrathecal & epidural. • Transdermal, intranasal, transbuccal, periocular, pulmonary and intra-articular.

49. EquianalgesicOpioid Doses (mg) sl = sublingual

50. Methadone • 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.