Perioperative Nursing: Pain Management

• The module focuses on the periop nurse, pain, and pain management.

Subject Coordinators

• Philippa Mann is the Subject Coordinator.
• Soumya Joseph is the Deputy Coordinator.
• The contact email is [email protected].

Expectations from Staff

• Staff will be prepared and on-time.
• Staff will provide professional, clear, and respectful communication.
• Staff will answer questions and help find the right resources if they don't know the answer.
• Consults are available in person or via Zoom.
• Staff is approachable and wants to assist the entire class to achieve their best.

Expectations of Students

• Students should arrive on time.
• Students should be prepared to engage in class and to study.
• Students should do the pre-readings and use the StintBook.
• Students should contact their tutors with any issues and seek help early.
• Students should be respectful of their tutor and peers.
• Tutorials are only 1/5 of expected study engagement; a 10cp subject requires 10 hours per week.

Subject Outline

• Access the Subject Outline on vUWS.
• The Subject Outline includes contact details, policies, semester structure, assessments, and attendance information.

Interactive Workbook on vUWS

• Open vUWS.
• Open NURS2037.
• Go to Learning Modules.
• Click on the StintBook link.
• Go to this week's Module.

Resources for the Week

• Craft & Gordon Textbook.
• HV1 interactive workbook.
• Readings and resources on vUWS.
• NSW Health website.
• Australian perioperative website.

Perioperative Nurse

• The module includes discussions on the term "perioperative" and the roles of a perioperative nurse.

Pain Definition

• Pain is defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage" (The International Association for the Study of Pain).
• Pain is influenced by overlapping physical (nociceptive and neuropathic), psychological, and environmental factors.
• Pain is a subjective individual experience.
• A person's attitudes, beliefs, and personality can strongly affect their pain experience.

Pathophysiological Processes of Pain

• Tissue injury leads to inflammation and the release of mediators such as substance P, prostaglandins, serotonin, and acetylcholine.
• These mediators stimulate nociceptors, resulting in signal transduction and conduction via peripheral nerves.
• The signal reaches the dorsal root ganglion, then the spinal cord, and ascends to the brain stem and thalamus.
• Inhibitory mediators (opioid peptides, norepinephrine, glycine, and GABA) modulate the pain signal.
• The signal reaches the cortex for central perception of pain.

Pain Perception Steps

• Contact with stimulus: Stimuli are mechanical or chemical.
• Reception: A nerve ending senses the stimulus.
• Transmission: A nerve sends the signal to the central nervous system.
• Pain center reception: The brain receives the information for further processing and action.

Anatomy of the Pain Pathway

• Transduction: Noxious stimuli are converted into electrical energy.
• Transmission: Electrical stimulus is sent to the dorsal horn of the spinal cord and synapse at the 2nd order neuron.
• Modulation: Inhibition vs amplification of the signal, by EAA.
• Perception: Conscious awareness of pain based on individual experiences.

Ascending and Descending Pathways

• Ascending pathway: Stimulus goes "up" to the brain.
• Descending Pathway: Brain processes and then sends a response "down" to modulate the pain.

Nociceptors

• Nociceptive pain arises from an identifiable lesion causing tissue damage, accompanied by stimulation of nociceptors in somatic or visceral structures.
• Nociceptors are receptors in tissues activated by painful stimuli, transducing 'noxious' information into an electrical signal transmitted to the central nervous system.
• High-threshold mechanoreceptors (HTM) respond to mechanical deformation.
• Polymodal nociceptors (PMN) respond to a variety of tissue-damaging inputs.
• Nociceptors are free nerve endings of nerve fibers, with two main types: Ad and C fibers.
• Ad fibers: Myelinated fibers with a low threshold for firing and fast conduction speed, responsible for transmitting the first pain felt.
• C fibers: Unmyelinated with slow conduction speed, responsible for secondary pain (dull, deep, throbbing), and lead to poor localization of pain.

Pain Signal Reception: 3 classes of Nociceptors

• Aδ mechanosensitive receptors respond to mechanical stimuli (pressure, touch).
• Aδ mechanothermal receptors respond to mechanical stimuli and heat.
• Polymodal nociceptors (C fibers) respond to a variety of stimuli.

Main Stages of Pain Perception

• Pain Sensitivity
• Signals are transmitted from the periphery to the dorsal horn (DH) (in the spinal cord) via the PNS
• Transmission of the signals to the higher brain via the CNS

Conscious Awareness of Pain: Cortical and Subcortical

• Cortical involves somatosensory cortex, insula, and anterior cingulate cortex
• Subcortical Involves hypothalamus, thalamus, amygdala, hippocampus

Pain Perception Revision

• Noxious stimuli cause cell damage, releasing sensitizing chemicals (prostaglandins, bradykinin, serotonin, substance P, histamine).
• These substances activate nociceptors, generating an action potential.
• Action potential goes from site of injury to the spinal cord, from the spinal cord to brainstem and thalamus, and then to the thalamus to the cortex for processing
• Neurons originating in the brainstem descend to the spinal cord and release substances (e.g., endogenous opioids) that inhibit nociceptive impulses.

Acute Pain

• Acute pain lasts for a short time and occurs following surgery or trauma.

Sub-Acute Pain

• Sub-acute pain progresses toward chronic pain and is known as the transition phase

Recurrent Pain

• Recurrent pain occurs on a cyclical basis (e.g., migraine or pelvic pain).

Chronic Pain

• Chronic pain lasts beyond the healing time for surgery or trauma.
• It can be associated with an increased pain experience and may exist without a clear reason.

Visceral Pain

• Visceral pain arises from internal organs and is "colicky" in nature.
• It is often accompanied by nausea and autonomic disturbance.

Somatic Pain

• Somatic pain is caused by stimuli such as cutting or crushing.

Neuropathic Pain

• Neuropathic pain is caused by a primary lesion or dysfunction of the nervous system, with possible motor, sensory, or autonomic dysfunction.
• Symptoms include spontaneous pain in the absence of a peripheral stimulus.
• The sensation is described as burning, tingling, shooting, stabbing, or numb.
• Shingles is an example.

Characteristics of Evoked Pains

• Allodynia: Painful response to a normally innocuous stimulus.
• Hyperalgesia: Pain of abnormal severity following a noxious stimulus.
• Hyperpathia: Exaggerated/prolonged response; may be delayed with explosive onset.
• Hyperaesthesia: Increased sensitivity to stimulation.
• Dysaesthesia: Altered sensation; discomfort rather than pain.

Role of the Sympathetic Nervous System in Neuropathic Pain

• Abnormal sympathetic outflow to an injured extremity occurs in response to neuropathic pain.
• Potential observations include abnormal regulation of vasculature, oedema, discolouration, changes in sweating, temperature changes, trophic changes in skin, and reduced motor activity.

Pain Information from the Face

• Pain information from the face comes from trigeminal nerve
• The three branches of the trigeminal nerve include the ophthalmic nerve (V1), maxillary nerve (V2), and mandibular nerve (V3).

Pain Relief Methods

• Non-opioid analgesics (aspirin, acetaminophen, ibuprofen) act at the site of pain.
• Opioid analgesics act on synaptic transmission in the central nervous system by binding to natural opioid receptors.
• Adjuvant analgesics (co-analgesics) are used for treating other conditions and also relieve pain.
• Anti-epileptic drugs reduce membrane excitability and action potential conduction in neurons of the central nervous system.

Where Pain Relief Works

• Opioids and alpha 2 agonists can affect through descending modulation or at the dorsal horn
• Local anesthetics, opioids, and alpha 2 agonists act at the dorsal root ganglion/dorsal horn.
• Local anesthetics act in the peripheral nerves and peripheral nociceptors.
• Anti-inflammatory drugs can affect the peripheral nociceptors.

Nursing Considerations for Opioid Use

• Monitor for constipation, pain relief, other side effects, and appropriate usage.
• Monitor blood pressure, heart rate, and respiratory rate, especially for the first 24 to 72 hours after initiating therapy or increasing dosage.

Non-Pharmacologic Interventions

• Physical (Sensory) Interventions: Comfort positioning, cutaneous stimulation, nonnutritive sucking, pacifier +/- sucrose solution, pressure, massage. hot or cold treatments
• Cognitive-Behavioral Interventions: Psychological preparation, education, or coaching, distraction tools (movies, games, videos, apps, toys with light/sound, bubbles), relaxation techniques (breathing, meditation, etc.), music and singing, guided imagery, conversation and therapeutic language.