week 13 Acute Pain Management.pdf

Transduction: The harmful stimulus is turned into an electrical signal. Transmission: singnal travel along peripheral n...

Transduction: The harmful stimulus is turned into an electrical signal. Transmission: singnal travel along peripheral nerve fibers (peripheral transmission) to the dorsal horn of the spinal cord, and are further transmitted via neurons which cross the spinal cord and ascend to the thalamus and branches to the brainstem nuclei (central transmission) and somatosensory cortex. The Pain Pathway Perception: The brain recognizes the signal as pain. Descending Modulation: release of neurotransmitters such as serotonin, noradrenaline, and endogenous opioids to tone down the pain. Recent onset and limited duration Identifiable cause Acute Indicates injury or illness Predictable course Persistent for more than 3 months Cause is sometimes obscure or non- specific Chronic Sensitization of nociceptors or nerves Poorly responsive to drug therapy, including opioids Unpredictable course Most common in acute clinical settings Types of Pain Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors (pain sensing Nociceptive nerve fibers) Characteristics: Somatic (sharp, hot/stinging, usually localized) or Visceral (dull, crampy, poorly localized) Pain caused by a lesion or disease of the somatosensory nervous system Characteristics: Burning, electric shocks, Neuropathic tingling, pins and needles Often not responsive to opioids Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain. Nociplastic Patient advocate: Humanitarian, patient comfort and satisfaction, psychological outcomes Prolonged Injury Response: Hyperglycemia, increased risk of infection and length of stay, Fatty Acids: Increases heart’s oxygen needs. More Clotting: Higher risk of blood clots (DVT/PE). Bio-Psycho Social Model of Pain Muscle Breakdown: Slows healing and Pain Experience weakens immunity. Why Treat Acute Pain? Prolonged Sympathetic Response: Increased heart rate, blood pressure, myocardial oxygen demand, decreased myocardial oxygen supply (cardiac ischemia), decreased gastrointestinal motility (ileus) Other Complications: Increased pulmonary complications, increased thromboembolism, prolonged hospital admission, persistent/chronic pain Verbal Numerical Rating Scale Verbal Descriptor Scale FACES pain scale Measuring Pain If pain scores are high, but FAS A or B, more opioid Functional Activity Score (FAS) may not be necessary or appropriate Titrate dose of analgesia to –Level of sedation and not respiratory rate –Level of function and not pain scores alone Physical: Rest, positioning, compression, Non-Pharmacological elevation Management Acute Pain Psychological: Explanation, reassurance, distraction, manage expectation Management Combination for Severe Pain: Paracetamol Reduces need for opioids in stronger pain situations. Processed by liver, removed by kidneys Affects both COX-1 and COX-2 (e.g., Non-selective Ibuprofen). watch out for kidney, asthma, stomach Avoid If: NSAIDs bleeding risk. Heart issues Selective Mainly affects COX-2 (e.g., Celecoxib) Severe kidney problems: Ketamine’s Role: Effective in controlling Age over 75 severe and persistent pain. Mechanism: Blocks NMDA receptors to reduce pain and improve opioid effectiveness. Ketamine Side Effects: Primarily hallucinations and vivid dreams at higher doses. TCAs (e.g., Amitriptyline) nerve pain, but may cause sleepiness and dry mouth Help with nerve pain and seizures, but may cause drowsiness and dizziness; be Adjuvants Anticonvulsants (e.g., Pregabalin) careful if you have kidney problems. Useful for pain and calming, but can lower Alpha-2 Agonists (e.g., Clonidine) blood pressure and heart rate. Hydrophylic- slower onset & longer action Analgesic Management Active metabolites M3G & M6G Morphine Renal Excretion- caution in elderly & renal impairment Nausea & Vomiting itchness Lipophilic- rapid onset, shorter action Adverse Fentanyl No active metabolites- safer in renal Effects Of Urinary retention impairment Opioids Opioids Constipation OIVI First line oral opioid Semi-synthetic opioid derivative of thebaine- not related to codeine Oxycodone No harmful metabolites – safer in renal impairment with dose adjustment roviding pain relief while also affecting the reuptake of noradrenaline and serotonin. Care should be taken with active metabolites in renal impairment, and caution is warranted with certain drug interactions and the potential for lowering the seizure threshold. Tramadol inhibits noradrenaline reuptake, Atypical Opioids minimal serotonin effect No active metabolites – ok in mild-mod renal impairment Tapentadol Safer with MAOIs, SSRIs, SNRIs, high dose TCAs Lower risk of seizures Opioid-Induced Ventilatory Impairment (OIVI) Increasing sedation is a better clinical indicator of respiratory depression Risk of OIVI increases with concurrent administration of sedating medications LA Mechanism of action Na+ channel blockade Erector Spinae Plane Block (ESPB) A regional anesthesia technique where a local anesthetic is injected between two Regional Analgesia for Chest Fascial Plane Blocks layers of fascia Serratus Anterior Plane (SAP) Block Wall Trauma Sub-Pectoral Plane Block Administering oxygen, stopping bolus, initiating medical emergency response, seizure management, and using ACLS protocols,20% lipid emulsion local anesthetic systemic toxicity (LAST) Epidural infusions Up to 14 ml/hr Ropivacaine 0.2% Peripheral nerve block (continuous or intermittent) Up to 10 ml/hr