PAIN MANAGEMENT

III. GENERAL PRINCIPLES OF ANESTHESIA

PAIN

Click the links below to access content on each subject area pertaining to Pain.

PAIN THEORY

PAIN MANAGEMENT

QUESTIONS

BACK TO DASHBOARD

BACK TO GENERAL PRINCIPLES OF ANESTHESIA

Return to Top ^

Pain Theory (Anatomy, Physiology, and Psychodynamics)

Acute

TERM	DESCRIPTION
Algesia	Increased sensitivity to pain
Algogenic	Pain producing
Allodynia	Nonharmful stimulus that is perceived as pain
Analgesia	Normal painful stimulus in which there is no perceived pain.
Dysesthesia	Unpleasant, abnormal sensation, whether spontaneous or evoked.
Hyperalgesia	Normal painful stimulus with a heightened response.
Neuralgia	Pain in a nerve distribution.
Neuropathy	Disturbance of function or pathological change in a nerve.
Paresthesia	Abnormal sensation, spontaneous or evoked.

Pain associated with A-delta nerve fibers is described as acute, fast, and/or sharp.
Pain associated with C nerve fibers is described as slow, chronic, and/or dull.
Substance P is the neurotransmitter that acts on the G protein-linked neurokinin-1 receptor.
Substantia gelatinosa comprises laminae II and III.
The spinothalamic tract is associated with anterolateral pathway and primary afferent neurons.
- Starting in the dorsal cord, fibers either ascend or descend in the tract of Lissauer.
- Then, the axons of primary afferents enter the gray matter of dorsal horn and synapse with second-order neurons and terminate in Rexed laminae I, II, and V. There are 2 types of 2^nd order neurons: nociceptive neurons and wide-dynamic-range neurons.
- 2^nd order neurons cross midline of the spinal cord through the anterior commissure and ascend in the anterolateral pathway of the spinothalamic tract to the thalamus.
- In the lateral thalamus and intralaminar nuclei, 2^nd order synapse with 3^rd order and then send projections to the cerebral cortex.
- Perception of pain along this tract
The descending dorsolateral efferent pathway is activated by a noxious stimuli.
- Cerebral cortex, hypothalamus, thalamus, periaqueductal gray area (PAG), nucleus raphe magnus, and locus coeruleus (LC) axons from the dorsolateral funiculus synapse with and suppress pain transmission to the brainstem and the spinal cord.

The descending efferent modulatory pathway is the analgesic pathway.

PAIN-MODULATING NEUROTRANSMITTERS

Neurotransmitters	Receptor
Substance P (excitatory)	Neurokinin 1 (NK-1), neurokinin 2 (NK-2)
Glutamate (excitatory)	NMDA, AMPA, kainite, mGluRs
Glycine (inhibitory)	Chloride linked (GlyR)
GABA (inhibitory)	GABA_A, GABA_B, GABA_C
Enkephalin (inhibitory)	Mu, delta
Serotonin (inhibitory)	5-HT (5-HT_1-3)
Norepinephrine (inhibitory)	Alpha-2 adrenergic

Chronic

Transduction – A noxious mechanical, chemical, or thermal stimulus is converted into an electrical impulse called an action potential

Transmission – Transmission of action potentials to the central nervous system through a-delta and c fibers

Perception – Process where potential or actual tissue trauma is recognized by a conscious person

Modulation – Inhibition of painful perception through the release of neurotransmitters

Nociceptive pain:
- Can be somatic or visceral:
  - Somatic- pain that follows a somatic nerve; well localized and sharp
  - Visceral- pain involved with organs, can be distended or obstructed; dull and diffuse
- Neuropathic pain:
  - Caused by abnormal processing of painful stimuli resulting from a primary lesion or dysfunction in the PNS/CNS
- Causalgia (AKA complex regional pain syndrome type II):
  - Syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes.

Return to Top ^

Acute

Pharmacology

- NSAIDs
  - Mild to moderate pain
  - Multimodal remedies
  - Synergistic effects with opioids
  - These drugs work by inhibiting COX which prevents arachidonic acid converted to prostaglandins. Prostaglandins (specifically PGE₁ and PGE₂) sensitize the nociceptors and increase effects of mediators, like substance P, bradykinin, and serotonin.
    - Ketorolac
      - 30 mg IM is equivalent to morphine 12 mg IM.
      - Should not be administered more than 5 days

- Opioids
  - Moderate to severe pain
  - Binds to and activates G protein-coupled receptors
    - Central G protein-coupled receptors- Rexed lamina II of the substantia gelatinosa, and supraspinally in the periaqueductal gray area, medial thalamus, amygdala, and limbic cortex.
    - Peripheral G protein-coupled receptors- afferent sensory nerve fibers (mu, delta, kappa).
  - Fentanyl
    - 80-100 x more potent than morphine
    - Highly lipid soluble; short onset and duration
  - Morphine
    - Hydrophilic
    - Longer acting
  - Hydromorphone
    - Derivative of morphine
    - 7-8 x more potent than morphine

- Analgesic adjuncts
  - N-Methyl-D-Aspartate antagonists
  - Ketamine
    - Multimodal approach for perioperative pain control
    - Administered low dose for acute pain
  - Alpha-2 agonists
    - Interact with alpha-2 receptors centrally (dorsal horn) ad peripherally.
      - Clonidine
        Alpha 2: alpha 1 receptors selectivity 400:1
        Most commonly intrathecal or epidural
      - Dexmedetomidine
        Alpha 2: alpha 1 receptors selectivity 1600:1
        Most commonly IV

Local anesthesia
- Block sodium channels in both afferent and efferent neuronal membranes
- Topical, infiltration, neuraxial, peripheral nerve blocks, systemic (IV), and diagnostic/interventional (e.g. trigger point injection, epidural steroid injection)

Patient-controlled analgesia (PCA)
- IV pain medication with varying options for patient on-demand controls

Acute pain in patients with chronic pain
- Anticonvulsants
  - Inhibit neuronal excitation and stabilize nerve membranes (neuropathic pain)
  - 1^st generation
    - Carbamazepine and phenytoin
  - 2^nd generation
    - Gabapentin and pregabalin
  - These provide anticonvulsant, anxiolytic, and antihyperalgesic effects
  - Pregabalin requires less dosing with fewer side effects.

- Antidepressants
  - Neuropathic pain
  - Tricyclic antidepressants (TCAs)
    - Tend to have more side effects than SSRIs and SNRIs
  - Selective serotonin reuptake inhibitors (SSRIs)
  - Selective norepinephrine and serotonin reuptake inhibitors (SNRIs)

- Corticosteroids
  - Treats rheumatoid arthritis, osteoarthritis, chronic back and neck pain
  - Anti-inflammatory and antiedema

- Methadone
  - Synthetic opioid used in the treatment of opioid addiction
  - Racemic mixture
    - S-methadone antagonizes NMDA and inhibits serotonin and norepinephrine uptake
    - R-methadone binds opioid receptors
  - Long half-life makes its use in acute pain management difficult for dosing

- Buprenorphine
  - Alternative to methadone in opioid addiction
  - Semi-synthetic, partial mu agonist and full kappa antagonist
  - Extremely high affinity to mu receptor which makes reversal much more difficult

REFERENCE: Nagelhout Nurse Anesthesia 7^th edition, pages 1293-1321

Chronic

Corticosteroids are a commonly-used medication class is used in the interventional treatment of chronic pain and support anti-inflammatory while repressing proinflammatory proteins.

Multimodal Pain Therapy

Interlaminar epidural steroid injections are placed within the epidural space.
Transforaminal epidural steroid injections provides the concentrated medication on the affected nerve root.
Motor cortex stimulation is an interventional pain management procedure that is performed for neuropathic pain.
Two interventional pain management techniques for complex regional pain syndrome (CRPS):
- Stellate ganglion block
- Intravenous regional block
A sphenopalatine ganglion block is indicated for a headache.
The goal of radiofrequency ablation and cryotherapy is to destroy the nerve myelin covering and allowing the axon to remain intact.
The sympathetic ganglion block is indicated for hyperhidrosis and postherpetic neuralgia is the stellate.
The mechanism of the TENS unit in relieving pain is activation of inhibitory neurons.