Acute Pain

Management
Presenter:
Ricky G. Jaleco, Level 2

Preceptors:
Dr. Ruel Trivilegio
Dr. Ted Anthony Kilayko
Dr. Michael Toledo
 Acute Pain
Management
OBJECTIVES:
TO DISCUSS THE FOLLOWING:
• ANATOMY OF ACUTE PAIN
• CHEMICAL MODULATORS
• SURGICAL STRESS RESPONSE
 Acute Pain
• “the normal, predicted, physiologic response to an adverse chemical, thermal, or mechanical
stimulus.”

• Generally, resolves within 1 month.

• Acute pain-induced change in the central nervous system is known as neuronal plasticity.

• This can cause sensitization of the nervous system, resulting in allodynia and hyperalgesia.
 Anatomy of Acute Pain
• The Nociceptive Pathway is an
afferent three-neuron dual
ascending (anterolateral and dorsal
column medial lemniscal
pathways) system

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 Anatomy of Acute Pain
• Descending modulation from:
• cortex,
• thalamus,
• and brainstem.

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 Anatomy of Acute Pain
• Nociceptors are free nerve
endings located in skin, muscle,
bone, and connective tissue with
cell bodies located in the dorsal
root ganglia.

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 Anatomy of Acute Pain
• The First-order neurons that make up the dual
ascending system have their origins in the
periphery as A-δ and polymodal C fibers.

• A-δ fibers transmit “first pain,”

• Sharp, stinging, localized

• Polymodal C fibers transmit “second pain,”

• Diffuse, associated with affective & motivational
aspects of pain

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PRIMARY AFFERENT NERVES

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NERVE FIBERS

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 Anatomy of Acute Pain

• First-order neurons synapse on second-order

neurons in the Dorsal Horn primarily within
Laminas I, II, and V, where they release
excitatory amino acids and neuropeptides.

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 Anatomy of Acute Pain

• Some fibers can ascend or descend in Lissauer tract prior

to terminating on neurons that project to higher centers.

• Second-order neurons consist of nociceptive-specific and

wide dynamic-range (WDR) neurons.

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 Anatomy of Acute Pain

• Nociceptive-specific neurons are

• located primarily in Lamina I,

• respond only to noxious stimuli, involved in the

sensory-discriminative aspects of pain.

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 Anatomy of Acute Pain

• Wide Dynamic Range (WDR) neurons

Laminae IV, V, and VI,

• respond to BOTH nonnoxious and noxious input,

• involved with the affective– motivational

component of pain.

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 Anatomy of Acute Pain
• Axons of both nociceptive-specific and WDR
neurons ascend the spinal cord via the Dorsal
Column–Medial Lemniscus and the Anterior
Lateral Spinothalamic tract

• to synapse on Third-order neurons in the

contralateral thalamus,

• which then project to the somatosensory cortex,

where nociceptive input is perceived as Pain.

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 Pain Processing
• A key development in our understanding of pain processing is that the pain pathway is
not “hardwired” and nociceptive input is not passively transmitted from the periphery
to the brain.

• Tissue injury tends to fuel neuroplastic changes within the nervous system, which
results in both peripheral and central sensitization.

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 Pain Processing
• Hyperalgesia - which is defined as an exaggerated pain response to a normally painful
stimulus.

• Allodynia - which is defined as a painful response to a typically nonpainful stimulus.

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 Pain Processing
The four elements of pain
processing include:

• Transduction
• Transmission
• Modulation
• Perception
 Transduction
• is the event whereby noxious
thermal, chemical, or
mechanical stimuli are
converted into an ACTION
POTENTIAL.

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 Transmission
• occurs when the action potential is conducted
through the nervous system via the first-,
second-, and third-order neurons, which have
cell bodies located in the dorsal root ganglion,
dorsal horn, and thalamus, respectively.

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 Modulation
• pain transmission involves altering afferent
neural transmission along the pain pathway.

• The dorsal horn of the spinal cord is the most

common site for modulation of the pain
pathway, and modulation can involve either
inhibition or augmentation of the pain signals.

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 Pain Processing
• Inhibitory spinal modulation include:
• 1) release of inhibitory neurotransmitters such as γ-amino butyric acid (GABA) and
glycine by intrinsic spinal neurons

• 2) activation of descending efferent neuronal pathways from the motor cortex,

hypothalamus, periaqueductal gray matter, and the nucleus raphe magnus, which
results in the release of norepinephrine, serotonin, and endorphins in the dorsal horn.

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 Pain Processing
• Spinal modulation, which results in augmentation of pain pathways, is manifested as
central sensitization, which is a consequence of neuronal plasticity.

• The phenomenon of “wind-up” is a specific example of central plasticity that results

from repetitive C-fiber stimulation of WDR neurons in the dorsal horn.

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 Perception
• is the final common pathway, which results
from the INTEGRATION of painful input into
the somatosensory and limbic cortices.

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 Pain Processing
• Generally speaking, traditional analgesic
therapies have only targeted pain perception.

• A multimodal approach to pain therapy should

target all four elements of the pain processing
pathway.

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• Four elements of pain
processing include:

• Transduction
• Transmission
• Modulation
• Perception

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My Chemical Modulators
 CHEMICAL MODULATORS
• Tissue damage following surgical procedures leads to the activation of small
nociceptive nerve endings and local inflammatory cells (e.g., macrophages, mast cells,
lymphocytes, and platelets) in the periphery.
 CHEMICAL MODULATORS
• Antidromic release of substance P and glutamate from small nociceptive afferents
results in vasodilation, extravasation of plasma proteins, and stimulation of
inflammatory cells to release numerous algogenic substances

• Peripheral sensitization of polymodal C fibers and high-threshold mechanoreceptors by

these chemicals leads to primary hyperalgesia an exaggerated response to pain at the
site of injury.

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 CHEMICAL MODULATORS
• As is the case in the periphery, the dorsal horn of the spinal cord contains numerous
transmitters and receptors involved in pain processing.

• Three classes of transmitter compounds integral to pain transmission include:

• The excitatory amino acids Glutamate and Aspartate
• The excitatory neuropeptides Substance P and Neurokinin A
• The inhibitory amino acids Glycine and GABA

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 CHEMICAL MODULATORS
• The various pain receptors include:

– The N-methyl- D-aspartate (NMDA)

– The α-amino-3-hydroxy-5-methylisoxazole-4- proprionic acid (AMPA)

– The kainate receptor

– The metabotropic receptor

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 CHEMICAL MODULATORS

• AMPA and Kainate Receptors - which are sodium channel dependent, are
essential for fast synaptic afferent input.

• NMDA Receptor - which is calcium channel dependent, is only activated

following prolonged depolarization of the cell membrane.

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 CHEMICAL MODULATORS
• Repetitive C- fiber stimulation of WDR neurons in the dorsal horn at
intervals of 0.5 to 1 Hz can precipitate the occurrence of windup and central
sensitization

• This leads to Secondary Hyperalgesia - increased pain response evoked by

stimuli outside the area of injury.

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Surgical Stress Response
 SURGICAL STRESS RESPONSE
• Surgical Stress causes release of cytokines:
• (e.g., interleukin-1, interleukin-6, and tumor necrosis factor-α) and precipitates adverse
neuroendocrine and sympathoadrenal responses,

• resulting in detrimental physiologic responses, particularly in high-risk patients.

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 SURGICAL STRESS RESPONSE

• Increased secretion of the Catabolic

• Decreased secretion of the Anabolic
Hormones such as
• Cortisol Hormones such as
• Glucagon • Insulin
• Growth hormone
• Testosterone
• Catecholamines.

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 SURGICAL STRESS RESPONSE
• The end result of this is Hyperglycemia and a Negative Nitrogen Balance, the
consequences of which include:

• poor wound healing,

• muscle wasting,
• fatigue, and
• impaired immunocompetency.

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SURGICAL STRESS RESPONSE

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 Preventive Analgesia
• Preventive Analgesia includes any antinociceptive regimen delivered at any time
during the perioperative period that will attenuate pain-induced sensitization.

• The term “Preventive Analgesia” replaces the older terminology “Preemptive

Analgesia,” which is defined as an analgesic regimen that is administered prior to
surgical incision and is more effective at pain relief than the same regimen
administered after surgery.

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 Preventive analgesia

• The goal of preventive analgesia is to block the development of sustained pain.

• Theoretically, this occurs by preventing NMDA receptor activation in the dorsal horn
that is associated with windup, facilitation, central sensitization expansion of receptive
fields, and long term potentiation, all of which can lead to a chronic pain state.

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 Preventive analgesia
• In order for preventive analgesia to be successful, three critical principles must be
adhered to:

1. The depth of analgesia must be adequate enough to block all nociceptive input
during surgery

2. The analgesic technique must be extensive enough to include the entire surgical field

3. The duration of analgesia must include both the surgical and postsurgical periods.
Patients with pre-existing chronic pain may not respond as well to these techniques
because of preexisting sensitization of the nervous system.

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THANK YOU!
SOURCE: BARASH 8TH ED.