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PRINCIPLES OF PAIN MANAGEMENT & ANALGESIA “THERE IS NO COMING TO CONSCIOUSNESS WITHOUT PAIN.” -CARL JUNG PRINCIPLES OF PAIN & ANALGESIA WHAT IS PAIN? An unpleasant sensory or emotional experience associated with actual or potential tissue damage Pain results when nerve cells in the skin or deep tissues, called nociceptors, detect a noxious stimulus 2 types of sensory neurons that detect and transmit pain A delta fibers (large, myelinated) Transmit sharp, discrete pain signals that allow the patient to localize the source of pain. transmits somatic pain C fibers (small, nonmyelinated) Transmit dull, aching, throbbing pain that cannot be easily localized transmits somatic & visceral pain (visceral pain is only transmitted by C fibers) PRINCIPLES OF PAIN & ANALGESIA THE PAIN PATHWAY TRANSDUCTION: transformation of noxious thermal, chemical, or mechanical stimuli into electrical signals called action potentials by A-delta & C fibers TRANSMISSION: these sensory impulses are then conducted to the spinal cord MODULATION: in the spinal cord where the A-delta & C fibers terminate, the impulses can be altered by other neurons, which either amplify or suppress them. PERCEPTION: the impulses are transmitted to the brain, where they are processed and recognized. THE PHYSIOLOGY OF PAIN PRINCIPLES OF PAIN & ANALGESIA WHAT IS PAIN? Somatic pain arises from the skin, soft tissues, muscles, bones, or joints Easily localized through stabbing, throbbing, or aching Visceral pain arises from internal organs not easily localized and is characterized by cramping or burning Referred pain term used to describe the pain that is felt in a body part other than where the actual pain stimulus is coming from PRINCIPLES OF PAIN & ANALGESIA WHAT IS PAIN? Hyperalgesia is increased sensitivity to a stimulus Neuropathic pain arises from direct damage to peripheral nerves or the spinal cord. May be shooting, sharp, or tingling Phantom limb or stump pain is sensation or pain arising from the missing body part Pain can also be classified according to onset and duration Acute pain has an abrupt onset and a relatively short duration of action. *Effectively treated with analgesic drugs Chronic pain has a slow onset, and duration of several months to years. *May be unresponsive to drug therapy PRINCIPLES OF PAIN & ANALGESIA MYTHS ABOUT PAIN IN ANIMALS Consider how some people without medical backgrounds may view the animal’s response to pain PRINCIPLES OF PAIN & ANALGESIA THE 5 FREEDOMS OF ACCEPTABLE ANIMAL WELFARE Freedom from hunger Freedom from physical and thermal discomfort Freedom from pain, injury, & disease Freedom to express normal behavior Freedom from fear and distress PRINCIPLES OF PAIN & ANALGESIA WHAT ABOUT OUR ANIMAL PATIENTS AND/OR OUR JOBS COULD MAKE MONITORING FOR PAIN OR USING ANALGESICS DIFFICULT? PRINCIPLES OF PAIN & ANALGESIA MONITORING SIGNS OF PAIN Consider how we as humans display pain vs. how our animal patients display pain. Write some ways you can monitor for pain in animals. 3 TYPES OF BEHAVIORS ASSOCIATED W/PAIN IN ANIMALS PRINCIPLES OF PAIN & ANALGESIA PAIN ASSESSMENT The measurement of pain is important to: Pain scales Based on observer’s assessment of patient’s spontaneous behaviors, and behaviors on handling, interaction, and manipulation, & maybe physiologic parameters. Pain scores should be reassessed regularly and preferably by the same person to minimize observer variation. PRINCIPLES OF PAIN & ANALGESIA PAIN ASSESSMENT TOOLS: Simple descriptive scale PRINCIPLES OF PAIN & ANALGESIA PAIN ASSESSMENT TOOLS: Numeric rating scales PRINCIPLES OF PAIN & ANALGESIA PAIN ASSESSMENT TOOLS: Visual analogue scale PAIN ASSESSMENT TOOLS: Comprehensive scales PRINCIPLES OF PAIN & ANALGESIA CONSEQUENCES OF UNTREATED PAIN Consider the long term effects of untreated pain PRINCIPLES OF PAIN & ANALGESIA PHYSIOLOGICAL SIGNS OF PAIN PRINCIPLES OF PAIN & ANALGESIA WHAT IS ANALGESIA? Analgesia is the absence of the awareness of pain, achieved through the use of drugs or other modes of therapy. It applies to the relief of pain without the loss of consciousness. WHAT ARE THE GOALS FOR PAIN CONTROL? Control pain at every stage of treatment to administer analgesics before the patient has an awareness of pain. This is known as preemptive analgesia. Decreases the analgesic requirements Decreases CNS sensitization To prevent windup, an event caused by a buildup of chemical mediators that intensify the pain response PRINCIPLES OF PAIN & ANALGESIA METHODS OF PAIN CONTROL WITHOUT MEDS Endorphins are endogenous compounds produced by the pituitary gland and the hypothalamus that bind to opioid receptors during situations of trauma or stress. They resemble opiates in their ability to provide pain relief and a feeling of wellbeing. “natural pain reliever” Nursing care: Other therapies to control pain: PRINCIPLES OF PAIN & ANALGESIA METHODS OF PAIN CONTROL USING MEDS OPIOIDS NSAIDS OTHERS: alpha-2 agonists, ketamine, steroids LOCAL ANESTHETICS METHODS OF PAIN CONTROL USING MEDS OPIOIDS OPIOIDS MODE OF ACTION: Acts on 4 different receptors in the brain and spinal cord Mu Kappa Delta Sigma(only cause hallucination, euphoria/dysphoria) An opioid agent may act as an agonist (stimulating agent) or antagonist (blocking agent) at each receptor Some opioid agents are considered mixed agonist/antagonists in that they block one type of receptor and stimulate another or partial agonists in that they only partially stimulate some opioid receptors Binding to these receptors can result in a number of effects: ANALGESIA Respiratory depression Sedation Dysphoria And others,… OPIOIDS REVERSIBILITY One major advantage of opioids is their reversibility with pure antagonists such as NALOXONE, which is the most effective Naloxone competitively binds to opioid receptors It is also possible to use a mixed agonist/antagonist such as BUTORPHANOL or a partial agonist such as BUPRENORPHINE to reverse the effects of the pure agonists CONTROLLED OPIOIDS MORPHINE: a FULL AGONIST (stimulates all 4 receptors) Great for moderate to severe pain Produces significant sedation cardiovascular & respiratory depression SIDE EFFECT/CAUTIONS: Can cause excitement in cats (use lower doses) Often results in VOMITING due to its effects on the CRTZ Give slowly IV otherwise severe histamine release can lead to hypotension and pruritis Other FULL AGONISTS include oxymorphone, hydromorphone, and fentanyl OPIOIDS FENTANYL: a FULL AGONIST (stimulates all 4 receptors) the injectable has a rapid onset of action and short duration of action. Onset of action: 2 min; duration of effect: 20-30 min commonly used as a transdermal skin patch Fentanyl is slowly absorbed through the skin and may take 4-12 hrs in cats, and 1224 hrs in dogs to reach therapeutic levels See pg 230 in your book, Procedure 7-1 for instructions on placing a fentanyl patch. OPIOIDS BUPRENORPHINE: partial agonist of the mu receptor(aka bupi, buprenex) Delayed onset of action, (40 min IM) but longer duration of action than other opioids – 6-8 hrs Best used for mild to moderate pain The injectable product is effectively given to cats transmucosally (applied to the gingiva, under the tongue, in cheek pouch) Can be used to reverse the effects of pure agonists, while maintaining some analgesic effect. Not as effective as naloxone THIS DRUG IS PART OF THE VTI PROTOCOL FOR DOGS & CATS* OPIOIDS BUTORPHANOL: mixed agonist(kappa,sigma)/antagonist (mu)(aka torb, torbugesic) Best used for mild to moderate pain; and is commonly used as a cough suppressant Can be used to reverse the effects of pure agonists. Not as effective as naloxone Commonly combined with a sedative such as dexmedetomidine or acepromazine MIXING AN OPIOID & SEDATIVE IS KNOWN AS NEUROLEPTANALGESIA OPIOIDS TRAMADOL: a non-opiate drug that has agonist activity at the mu receptor Oral tablets Useful post-operative pain med in dogs and cats Not currently controlled METHODS OF PAIN CONTROL USING MEDS NSAIDS NSAIDS MECHANISM OF ACTION: Inhibits the synthesis of prostaglandins by blocking the enzyme cyclooxygenase ( aka COX-1 & COX-2) COX-1 leads to the production of beneficial prostaglandins COX -2 leads to the production of harmful prostaglandins that are present during tissue damage and inflammation. NSAIDS BENEFITS OF NSAIDS: No strict record keeping Little abuse potential Effective when given orally No sedative, cardiovascular, or respiratory effects Antipyretic effects SIDE EFFECTS/CAUTIONS: GI upset/GI ulcers due to inhibition of prostacyclin DO NOT USE CONCURRENTLY w/ STEROIDS renal toxicity due to inhibition of PGE2 hepatic toxicity Inhibits platelet aggregation due to blockage of thromboxane NSAIDS RIMADYL (carprofen) Approved for use in DOGS ONLY! Oral(chewable tablets) and injectable forms available Less likely to cause side effects mentioned previously due to its COX-2 selectivity Common uses: Post-operative pain relief Pain relief from osteoarthritis and other musculoskeletal injuries PART OF THE CANINE POST-OP PAIN CONTROL PROTOCOL AT VTI NSAIDS METACAM (meloxicam) Approved for use in dogs and cats COX-2 selective Oral and injectable formulations available PART OF FELINE POST-OP PAIN CONTROL PROTOCOL AT VTI METHODS OF PAIN CONTROL USING MEDS OTHERS: ALPHA-2 AGONISTS KETAMINE ALPHA-2 AGONISTS & KETAMINE ALPHA-2 AGONISTS (ex: dexdomitor, xylazine) Short duration of action (~90 minutes) Also causes profound sedation, bradycardia Commonly combined with butorphanol Reversible (analgesic effects are reversed as well) KETAMINE Works by antagonizing NMDA receptors in the spinal cord Blocking NMDA receptors prevents central sensitization & windup Effective for somatic analgesia, but limited visceral analgesia Duration of action is short 30min METHODS OF PAIN CONTROL USING MEDS LOCAL ANESTHETICS LOCAL ANESTHETICS WHAT IS LOCAL ANESTHESIA/ANALGESIA? The use of a chemical agent on sensory neurons to produce a disruption of nerve impulse transmission, leading to temporary loss of sensation LOCAL ANESTHETICS CHARACTERISTICS OF LOCAL ANESTHETICS Exert their effects on neurons in the peripheral nervous system and spinal cord that control pain, heat, cold, & pressure Relatively few effects of the cardiovascular and respiratory systems Exert their effects in the area closest to the site of injection Not normally transferred across the placenta Safe for c-sections LOCAL ANESTHETICS ROUTES OF ADMINISTRATION TOPICAL: must penetrate the epidermis to reach the dermis where the peripheral nerves are located Sprayed on intact skin for superficial procedures such as skin biopsies (ex: ethyl chloride) Creams can also be applied to desensitize skin for superficial minor procedures (ex: lidocaine/prilocaine) Splash blocks refer to the use of sprays or anesthetic soaked gauze sponges on open wounds or surgical sites Applied through a chest tube in patients having thoracic surgery Should be done when patient is awake Absorbed through the mucous membranes (larynx, eye, urethra) Short duration of action and less pain relief when compared to other routes of administration of local anesthetics LOCAL ANESTHETICS ROUTES OF ADMINISTRATION: INFILTRATION(injection): Local anesthetic can be injected subcutaneously, intradermally, or between muscle planes Ideally the site of injection is clipped and cleaned Small needle (23-25 gauge) used to prevent tissue damage Test efficacy by pricking the site with a needle Do not inject into infected or inflamed tissues Some local anesthetic drugs are combined with epinephrine Epinephrine causes vasoconstriction which decreases rate of absorption and prolonging effect It also decreases the amount of drug entering the circulation, decreasing chances of toxicity. CAUTION AROUND AN INCISION OR ON EXTREMITIES AND WITH PATIENTS WITH CV ABNORMALITIES LOCAL ANESTHETICS ROUTES OF ADMINISTRATION NERVE BLOCKS: Injection of a local anesthetic in the proximity of a specific nerve to desensitize a specific anatomic location. Location of target nerve must be known and palpated if possible. Lameness exams in horses Cornual blocks for dehorning cattle Dental blocks in dogs and cats Infiltration of nerves during amputation of a limb Declawing cats May take 15-20 minutes for absorption Nerve blocks include line blocks and ring blocks Cornual blocks for dehorning cattle THIS NERVE BLOCK IS ALSO A RING BLOCK Dental blocks for tooth extractions Maxillary Nerve block via The infraorbital foramen NERVE BLOCKS Nerve blocks help pinpoint areas of pain Paravertebral block THESE ARE EXAMPLES OF LINE BLOCKS NERVE BLOCKS THIS NERVE BLOCK IS ALSO A RING BLOCK LOCAL ANESTHETICS ROUTES OF ADMINISTRATION NERVE BLOCKS LINE BLOCKS: continuous line of local anesthetics placed SQ in an area served by numerous small nerves The needle is inserted along the line of infiltration and the anesthetic is injected as the needle is withdrawn If placed encircling an anatomic part, it is called a RING BLOCK INTRAARTICULAR: injecting local anesthetics directly into a joint usually after surgery of the joint, immediately after closure of the joint capsule LOCAL ANESTHETICS ROUTES OF ADMINISTRATION EPIDURAL: blockage of sensory and motor nerves in the rear, abdomen, pelvis, tail, hind limbs, and perineum Anesthetist must be familiar with the anatomy of the terminal spinal cord and lumbosacral vertebrae Epidural space Dura mater arachnoid Subarachnoid space w/CSF Pia mater Spinal cord LOCAL ANESTHETICS EPIDURALS http://www.youtube.com/watch?v=zmwv MHZG_5g SIDE EFFECTS OF LOCAL ANESTHETICS Allergy Rash or hives in the area Systemic toxicity Sedation, nausea, restlessness, hyperexcitability, seizures, respiratory suppression, coma Infection (esp. w/epidurals) Cranial infiltration of an epidural may cause serious toxicity, respiratory suppression death METHODS OF PAIN CONTROL Combining drugs from different categories (multimodal therapy, balanced analgesia) is more beneficial than using high doses of one medication. Pain is alleviated via different pathways SPECIAL TECHNIQUES NEUROMUSCULAR BLOCKING AGENTS MECHANICAL VENTILATION NEUROMUSCULAR BLOCKING AGENTS Aka muscle-paralyzing agents These agents act by interrupting normal transmission of impulses from motor neurons to the muscle synapse Site of action: neuromuscular junction, where acetylcholine is released by the neurons to attach to muscle end plates. NEUROMUSCULAR BLOCKING AGENTS Two ways for these agents to disrupt the nervous transmission Depolarizing agents – cause a single surge of activity at the neuromuscular junction, followed by a refractory period. (Ex: succinylcholine) Animals may show spontaneous muscle twitching followed by paralysis Reversal agents are not effective Non-depolarizing agents- block the receptors and the end plate. (ex: pancuronium, atracurium) No initial surge of activity at the neuromuscular junction, no spontaneous muscle movements. These agents can be reversed with neostigmine or edrophonium Not commonly used in vet med, but can be useful in the following situations. Thoracic or diaphragmatic surgery Orthopedic surgery Ophthalmic surgery C-sections Facilitating difficult intubation “balanced anesthesia” techniques NEUROMUSCULAR BLOCKING AGENTS Neuromuscular blocking agents allow relaxation of voluntary muscles only. Skeletal muscles are affected in a predictable order 1st- Facial, neck paralysis 2nd- Tail, limb, abdominal muscles Last- intercostal muscles, diaphragm ADMINISTRATION Normally given slowly IV Onset of action: 2 minutes Duration: 10-30 minutes Animals on these drugs will require manual or mechanical ventilation ADVERSE EFFECTS Hypothermia Respiratory failure Cardiac arrhythmias MECHANICAL VENTILATION Patient’s breathing is controlled by a ventilator rather than compression of a reservoir bag The ventilator automatically compresses a bellows, which forces oxygen and anesthetic gas into the patient’s airways The bellows is compressed at a specified rate and a specified volume USES: not normally used in healthy anesthetized patients, but can be helpful in: Patient’s with compromised respiratory system Thoracotomy surgery Lengthy operations MECHANICAL VENTILATION MECHANICAL VENTILATION Depending on the type of ventilator, the anesthetist can deliver gases according to a pressure cycle, a volume cycle, or a time cycle. Pressure cycle – supplies air until the pressure reaches a preset level. This is generally 12 cm to 20 cm. Timed cycle – supplies air according to a set inspiratory time. This is generally 1 to 1.5 seconds. I:E ratio is 1:2 to 1:3 Volume cycle – delivers a preset tidal volume regardless of the pressure required. This is generally 10-15 mL/kg MECHANICAL VENTILATION RISKS OF CONTROLLED VENTILATION Excessive airway pressure may rupture alveoli Cardiac output may be decreased if positive pressure is maintained throughout inspiration and expiration If ventilation rate is too high, excessive carbon dioxide may be exhaled leading to respiratory alkalosis Controlled ventilation is generally more efficient at delivering anesthetic gas which may lead to exacerbation of side effects such as hypotension and CNS depression. Anesthetist may be tempted to relax on the monitoring
