New Pain Pathophysiology DA DV 2020

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PAIN PATHOPHYSIOLOGY

AND TREATMENT

Dr Didem Akçalı
2020
Pain

 An unpleasant sensory and emotional


experience associated with actual or
potential tissue damage.
 Pain is whatever the experiencing person
says it is.
 May not be directly proportional to amount
of tissue injury.
 Highly subjective, leading to
undertreatment
PERCEPTION

Korteks

Talamocortikal
junction
MODULATION C
Thalamus
SYSTEMIC TRANSMISSION

C
OPİOİDs

TRANSDUCTION

SPİNOTALAMİK
Primer
efferent Ağrılı
nosiceptor uyaran
NOCICEPTION
 Nociceptors for pain
 A delta& C fibers
 SEROTONIN

 BRADYKININ

 PROSTAGLANDIN

 OTHER N. MEDIATORS ACTİVATE A delta& C fibers

NOCICEPTION
 A delta thin myelinated
 Fast pain

 Sharp pain

 C unmyelinated
 Slow pain

 Chronic pain
 FAST PAIN- A delta fibers
 First WARNING

 Slow pain-C fibers
 To protect
 To help recovery
Lamina II substantia gelatinosa
PERCEPTION

Korteks

Talamocortikal
junction
MODULATION C
Thalamus
SYSTEMIC TRANSMISSION

C
OPİOİDs

TRANSDUCTION

SPİNOTALAMİK
Primer
efferent Ağrılı
nosiceptor uyaran
Cell injury

Membrane
phospholipids

Steroids
Arachidonic acid

5-Lipooxigenase Cyclooxygenase

NSAID
5-LO inhibitors Prostaglandines
Leucotriens
Prostacyclines
LTC4, D4, E4
Natural Opioids-Endorphins

 released from their storage areas in the brain


when a pain impulse reaches the brain,

 bind to receptors in the pain pathway to


block transmission and perception of pain.
Gate Control Theory
Melzack and Wall 1965.

 Physiological and psychological interactions


 Suggested spinal gates in the dorsal horn at
each segment of the spinal cord
 Competition at each gate for heat, touch or
pain to be transmitted at each point
Ascending pathways

 Spinothalamic pathways
 Spinomezencephalic pathways
 Spinoreticular pathways
 Spinolimbic pathways
 Postsynaptic dorsal colon pathways
Neuromatrix
 Genetic effects
 somatosensorial inputs, experience
form NEUROMATRIX

 NEURAL SIGNATURE
 Genetic and sensorial effects
 Cognitive effects

 Sympathetic nervous system


 Immune system
 Chronic physical and physiologic stresses

 There are inadequacies of current


pain treatment!
Pain
Assessment
PAIN HISTORY
 Description: severity, quality, location,
temporal features, frequency, aggravating
& alleviating factors
 Previous history
 Context: social, cultural, emotional,
spiritual factors
 Meaning
 Interventions: what has been tried?
VAS (Visuel analog skala)
Types of Pain

 1. Acute
 2. Cancer
 3. Chronic non-malignant
The most common chronic pain

1. Persistent low back pain


– result of poor muscle tone,inactivity,
muscle strain, sudden vigorous exercise

2. Chronic pain associated with cancer


TYPES OF PAIN

NOCICEPTIVE NEUROPATHIC

Somatic Visceral
• bones, joints • Organs –
• connective tissues heart, liver,
• muscles pancreas, gut,
etc.

Deafferentation Sympathetic Peripheral


Maintained
Somatic Pain
• Aching, often constant
• May be dull or sharp
• Often worse with movement
• Well localized

Eg/
– Bone & soft tissue
– chest wall
Visceral Pain
• Constant or crampy
• Aching
• Poorly localized
• Referred

Eg/
– CA pancreas
– Liver capsule distension
– Bowel obstruction
Clinical Terms For The Sensory Disturbances
Associated With Pain

 Dysesthesia – An unpleasant abnormal sensation,


whether spontaneous or evoked.
 Allodynia – Pain due to a stimulus which does not
normally provoke pain, such as pain caused by light touch
to the skin
 Hyperalgesia – An increased response to a stimulus
which is normally painful
 Hyperesthesia - Increased sensitivity to stimulation,
excluding the special senses. Hyperesthesia includes both
allodynia and hyperalgesia, but the more specific terms
should be used wherever they are applicable.
FEATURES OF NEUROPATHIC PAIN
COMPONENT DESCRIPTORS EXAMPLES
Steady, • Burning, Tingling • Diabetic neuropathy
Dysesthetic • Constant, Aching
• Post-herpetic
• Squeezing, Itching neuropathy
• Allodynia
• Hypersthesia

Paroxysmal, • Stabbing • trigeminal neuralgia


Neuralgic
• Shock-like, electric • may be a component
• Shooting of any neuropathic
pain
• Lancinating
Pain
Treatment
Non-Pharmacological Pain Management

 Acupuncture
 Cognitive/behavioral therapy
 Meditation/relaxation
 Guided imagery
 TENS
 Therapeutic massage
 Others…
WHO Analgesic Ladder
= due to pain 7-10, Severe pa
severity
Morphine
4-6, Medium Fentanyl
Oxycodone

Codeine
1-3, Weak pain Tramadol

Aspirin Meperidine (pethidine)


Paracetamol
NSAID

WHO. Geneva, 1996.


Medication(s) Taken

• Dose
• Route
• Frequency
• Duration
• Efficacy
• Adverse effects
Opioid Side Effects
 Constipation – need proactive laxative use
 Nausea/vomiting – consider treating with dopamine
antagonists and/or prokinetics (metoclopramide, domperidone,
prochlorperazine [Stemetil], haloperidol)
 Urinary retention
 Itch/rash – worse in children; may need low-dose naloxone
infusion. May try antihistamines, however not great success
 Dry mouth
 Respiratory depression – uncommon when titrated in
response to symptom
 Drug interactions
 Neurotoxicity (OIN): delirium, myoclonus  seizures
Adjuvants Used In Pain Treatment

 General / Non-specific
 corticosteroids
 cannabinoids (not yet commonly used for
pain)
 Neuropathic Pain
 gabapentin
 antidepressants
 ketamine
 topiramate
 clonidine

 Bone Pain
 bisphosphonates
 (calcitonin)
Treatment of Neuropathic Pain
Pharmacologic treatment
• Opioids
• Steroids
• Anticonvulsants – gabapentin, topiramate
• TCAs (for dysesthetic pain, esp. if depression)
• NMDA receptor antagonists: ketamine, methadone
• Anesthetics

Radiation therapy
Interventional treatment
• Spinal analgesia

• Nerve blocks
WHAT DOES ALGOLOGIST DO?
Pain Assessment
Pain treatment
Interventional treatment
Chronic Pain Treatment

1.Pharmacological treatment
2.Physical treatment
3.Interventional techniques
4.Surgery
5.Comprehensive and Alternative Treatment
Transdermal fentanyl

 Strong Mu agonist
 Severe pain
 Changed every 72 hours
 Indications
 When patient cannot use oral drugs
 In morphine toxicity
 Severe nausea, vomiting
 GIS obstruction
Opioid antagonist
NALOXONE

<5Y. <20 kg: IV / IM 0.1 mg/kg.


>5Y >20 kg 2 mg
Adult: 0.4 mg - 2 mg, repeat in 2 - 3 min (maks 10 mg)

Partial reversal
<5Y 0.01 to 0.03 mg/kg
0.1 - 0.2 mg adolescent and adult
MEPERIDINE

• AVOID IN CHILDREN AND ELDERLY


• Half life 3 hr
• 100-150 mg / higher dose, Half life 4-5 hr
• In cirrhosis 10 hr
• In renal disease>34 hr!
• No definite analgesic effect
• METABOLITE NORMEPERIDINE IS
NEUROTOXİC, half life 24 hr
MEPERIDINE

• CANNOT BE REVERSED WITH NALOXONE !


OPIOID ROUTES
 Oral
 IV
 SC
 Transdermal
 Transmucozal
 Epidural /spinal catheter
 Peripheral nerve block/catheter
 Elastomeric pump
 PCA - Patient controlled
analgesia
INTERVENTIONAL TREATMENTS

 Facet block, radiofrequency


 Transforaminal injection, DRG PRF
 Stellate block
 Cervical epidural steroid injection
 Lumbal sympathetic block
 Caudal epidural steroid injection
 Epiduroscopy
 Spinal cord stimulator
CANCER PAIN
 75-85 % IS TREATED BY
PHARMACOLOGIC TREATMENT
 SC/ IV TREATMENT
 INTERVENIONAL TREATMENT

 Neurolysis, neuromodulation
 Spinal / Epidural port/pump
 NEUROSURGICAL TREATMENT
Sympathetic blocks

Stellat ganglion

Thoracal ganglion

CeliacPlexus

Hypogastric plexus

İmpar ganglion
Celiac Plexus Block-
Transaortic Approach

31.12.2020
ST: Sempatik Zincir grc: Gri
Komminikan
Port-pump systems
[email protected]

NO
COMMUNICATION
NO SUCCESS!

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