Chronic Pain (Rob Bevan) Flashcards
(33 cards)
International Association for the Study of Pain (IASP) definition of pain:
“An unpleasant sensory and emotional
experience associated with, or resembling that
associated with, actual or potential tissue damage,
Classification of pain:
What is the difference between Acute and Chronic Pain?
Duration –
Acute – usually due to tissue damage - pain is a symptom –self-limiting
Chronic – pain that lasts longer than 3 months - pain is the disease
Cause – Cancer or Non-cancer, Iatrogenic, Cardiac, MSK, Dermatology, GI, Surgery
Mechanism - Nociceptive or Neuropathic or Nociplastic
Six key notes + Etymology
- Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.
- Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
- Through their life experiences, individuals learn the concept of pain.
- A person’s report of an experience as pain should be respected.
- Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.
- Verbal description is only one of several behaviours to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.
Features of Acute Pain?
Obvious tissue injury (e.g., trauma, injury, burn, etc.)
May be mild/ severe
Intensity related to extent of injury
Predictable time course – gets better with time
Treatments usually successful
Is helpful – warning sign - protective effect
All pain is affected by how we are feeling at the time
What are the 3 Classifications of Pain? (mechanism)
Nociceptive Neuropathic Nociplastic
Nociceptive Pain
Definition?
Causes?
Treatment?
Def= Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.
Causes:
Somatic:
* Bones (fracture, metastases)
* Muscles (dystonia, muscle spasm)
* Joints (Osteoarthritis)
* Skin (burns, post op)
Visceral: (internal rel to organs)
* Mucosal injury (peptic ulcer)
* Obstruction (gall stones)
* Ischaemia (angina)
Treatments:
* Opioids
* NSAIDs
* Paracetamol
* Anti-spasmodic
* Treat cause e.g., angina
The WHO analgesic ladder:
3 steps?
Step 1: Non-opioid analgesics
Step 2: Weak opioid for mild to moderate pain
Step 3: Strong opioid for moderate to severe pain
All are +/- adjuvant
Neuropathic Pain
Definition?
Causes?
Treatments?
Pain caused by a lesion or disease of
the somatosensory nervous system
Causes
Central
* Traumatic (spinal cord injury)
* Neurodegenerative (Parkinson’s D)
* Autoimmune (MS)
Peripheral
* Infections (Herpes Zoster)
* Nerve Compression (carpal tunnel)
* Trauma (CRPS)
* Metabolic (nutritional deficiencies)
* Auto-immune (Guillian Barre Syndrome
Treatment:
* Tricyclic anti-depressants (TCA)
* Gabapentinoids
* Pregabalin
* Gabapentin
* SNRIs - Duloxetine
* Carbamazepine (Trigeminal neuralgia)
What is Nociplastic Pain?
Definition?
Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain
Nociplastic Pain
Causes?
Features?
Causes
* Diffuse Sensitisation
(Fibromyalgia)
* Functional visceral pain
(Irritable bowel syndrome)
* Regional Somatic Sensitisation
(CRPS type 1, temporomandibular joint (TMJ) disorder)
Features:
* Peripheral Sensitisation (due to
Proliferation of sodium channels)
* Central sensitisation (due to NMDA
activation, cortical reorganization)
* Diminished descending inhibition
(i.e. due to NA, GABA, etc)
* Immune system activation (glial
cells, chemokines, cytokines, etc.)
Nociplastic Pain- Treatment:
Non-pharmacological treatments?
Pharmacological treatments
- (1st line) – exercise, sleep management, stress reduction, diet.
- Pregabalin.
- Duloxetine?
- Discussed in next lecture
Aim for decreased pain and improved QoL
but effect sizes for each could be small. Important to use multi-modal approach
What is Acute Pain?
- Obvious tissue injury (e.g.,
trauma, injury, burn, etc.) - May be mild/severe
- Intensity related to extent of injury
- Predictable time course
- Treatments usually successful
Is helpful –protective effect
Persistent/ Chronic pain:
Features?
Mild or severe?
Time course?
- e.g. Lower back pain, fibromyalgia
- Often severe
- ? no obvious pathologic process
- Intensity unrelated to tissue injury
- Unpredictable time course
- Difficult to treat
- Maladaptive pain response - unhelpful
Acute to Chronic pain
Pathophysiology:
What are the two types of sensitisation?
- Peripheral sensitisation due to repeated stimulation leading to increased sensitivity to pain (hyperalgesia)
- Central sensitisation –persistent transmission of pain signals from peripheral nervous system + reduction in GABA and inhibitory signals.
Acute to Chronic pain
Risk factors?
- Surgery
- Chronic opioid use
- Patient factors
- Pain syndromes
- Genetic predispositions
- Mood disorder, anxiety
- Personality disorder
- Female
- Obesity
- Young age
Important Practice Points for the Use of Opioids in chronic pain
- No good evidence of dose-response with opioids beyond 120mg/day morphine equivalent
- Patients who do not achieve useful pain relief from opioids within 2-4 weeks are unlikely to gain benefit in the long term
- Short-term efficacy does not guarantee long-term efficacy
- Data regarding improvement in quality of life with long-term opioid use are inconclusive
- No evidence for efficacy of high dose opioids in chronic non-malignant pain
High dose opioids:
120mg Morphine Oral
60mg Oxycodone oral
50micrograms/hr Fentanyl Transdermal Patches
52micrograms/hr Buprenorphine patches
300mg Tapentadol tablets
Side-effects & problems with opioid medication:
Morphine Equivalent Dose ≥ 120MG
Hyperalgesia
Addiction
Dependency
Sexual Dysfunction
Respiratory Depression
Immunosuppression
Changes in hormone levels
Opioid Induced Hyperalgesia
- Defined as “… state of nociceptive sensitization caused by
exposure to opioids” - Widespread pain
- More sensitive to certain painful stimuli.
- Pain may be the same as the underlying pain, or may be
different. - Worsening pain even with increasing opioid dose.
- Diffuse allodynia
- Could explain loss of opioid efficacy in some patients
- Unclear mechanism for OIH but thought to be due to
neuroplastic changes in peripheral & central nervous system. - Treatment:
- Lower/ stop opioid dose
- Evidence demonstrates stopping opioids for 1 month, other studies suggest 3 months
Wider impact of pain
- Individual and family
- Mood
- Sleep
- Mobility
- Role within the family
- Ability to work or engage in pleasurable
activities/ hobbies.
Painkillers do not cure..
chronic pain
Formula for Pain?
Somatosensory
Cognition
Affective
NICE - Pharmacological management of
chronic primary pain
What to reccomend?
What to not inititiate?
- Duloxetine
- Citalopram
- Fluoxetine
- Paroxetine
- Sertraline
- For 18 years and over – unlicensed for
this indication - Discuss benefits & risks
with patient - Anti-epileptics
- Anti-psychotics
- Benzodiazepines
- Corticosteroid trigger point injections
- Ketamine
- Local anaesthetics
- Opioids
- Paracetamol
Tricyclic anti- depressants
- Tricyclic anti-depressants (affect NA &
serotonin) - Amitriptyline (up to 50mg od) Half-life= 25 hours
- Nortriptyline (? Less drowsiness) Half-life= 26 hours
- Side effects:
- Drowsiness, anti-cholinergic (dry mouth,
difficulty with micturition, constipation,
glaucoma, CV disease (arrythmias). - ?dementia
- CI – heart problems, especially conduction
abnormalities.
