PERI-OPERATIVE PAIN MANAGEMENT Dr P Chalmers CP

IASP definition “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

Mechanism of Pain Cell Injury→Cytokines,prostanoids→Plasma Leakage→macrophages, monocytes, mast cells, platelets→Cytokines,prostanoids→ nociceptive nerve endings (C and Aδfibres)

IASP definition “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

Process of Nociception 1. Transduction conversion of pain stimulus into a nerve impulse by sensory receptors 2. Transmission of nerve impulses from the periphery to the brain and spinal cord 3.Perception the recognition of these impulses or signals as pain 4.Modulation whereby descending neuronal tracts from the brain modify the nociceptive transmission in the spinal cord Opioid system, noradrenergic, GABA, serotonin

Effects of Pain Neurohumoral Psychological Anxiety Resp:hypoventilation →hypercarbia and hypoxia hyperventilation CVS: tachycardia, hypertension, subendocardial ischaemia Nausea and vomiting Sweating Increased stress response → catabolism Outcome: Prolonged immobilisation and recovery Prolonged hospital stay

Effects of Analgesia Reduces anxiety and stress response Reduces respiratory complications Reduces cardiovascular complications Reduces autonomic effects Outcome: Earlier mobilisation Shorter hospital stay

Factors influencing pain Age Site of surgery Quality of care Patient autonomy Patient motivation

Assessment of pain Intraop: Monitoring CVS, RS Postop: Visual cues facial expression body language Psychological anxiety, restlessness, withdrawal Verbal response VAS Imagery Universal

Categorical Scale Mild Moderate Severe Verbal 1-10

Visual Analogue Scale

Facial Scale

Management of Acute Pain Multimodal Pharmacological Neural Blockade

Why multimodal Synergism Opioid sparing Reduced risk of tolerance and morphine sensitisation Reduced side effects and complications Pre-emptive

Pharmacological Opiods Paracetemol NSAIDS

Mode of Administration Oral IM IV Boluses continuous infusion PCA PR

0 4 8 Hours Plasma conc → PCA IM

Advantages and disadvantages of im v PCA administration IM PCA Delayed onset Rapid onset Fixed dose Dose matches pain Painful Painless Fluctuating plasma levels Continuous plasma levels Gradual onset of Technical error or failure side effects may be fatal Enhances patient autonomy

Neural Blockade

Neuroaxial: Spinal Epidural Regional Blockade Skin Infiltration Local anaesthetics Adjuvants

Requirements for Neural Blockade Consent Sterile condition Vascular access Monitoring Resuscitation equipment No clinical contraindications (coag,infections,allergies)

Epidural procedure

Spinal Epidural

Epidural Infusion Pump

Effects of Neural Blockade Sensory Loss Muscle Paralysis Autonomic Effects (spinal, epidural) ALWAYS aspirate before injection beware of accidental intravascular administration

Complications Neuro-axial Block (spinal/epidural) Hypotension Backache Spinal cord/nerve root compression (haematoma/abscess) Dural headache (epidural) Overextensive block Total Spinal Block Accidental Intravascular injection Side Effects of drugs LA’s Opiods

Advantages of epidural analgesia Excellent analgesia for 72hrs or longer Avoids side effects of opiods Improves postop respiratory function Reduces thromboembolic phenomena Reduces incidence of persistent post surgical pain

Local anaesthetics Lignocaine Bupivicaine Levobupivicaine

LignocaineBupivicaine Onset of Action FastMedium Pka % unionised2515 Weak bases mostly ionised at pH 7.4

LignocaineBupivicaine Potency14 Lipid solubility

LignocaineBupivicaine Duration of actionmediumLong % protein bound7095 Vasoactivity Dilatation at lo doses ++ Constriction at hi doses+ Dilatation at lo doses + Constriction at hi doses++

LignocaineBupivicaineLaevo- bupivicaine Onset of action 2-4 min rapid 10 min Duration30-90min medium 3-7hrs (16hrs) Long 3-7hrs (16hrs) Dosage 3mg/kg/4hrs (adr 6mg/kg) 2mg /kg/4hrs (adr 2 mg/kg ) Max dose 150mg; 400mg/24hrs

Local anaesthetics Adrenaline 1:200,000=5micrograms/ml Never used in spinals and epidurals Max dose 8ug/kg/hr = 20mls of 1in 200,000/hr

LignocaineBupivicaineLaevo- bupivicaine Toxic plasma conc ug/ml >5>1.5 ToxicityCNS +++Cardiac +++ Cardiac +

Management of toxicity R/Lipid emulsion 20% a bolus of 100mls followed by an infusion of 400mls over 20min (approx 0.25mls /kg/min) Repeat if necessary PLUS supportive measures anticonvulsants, inotropes etc

Adjuvants in neural blocks Opiods→pruritus,delayed onset resp depression, nausea, vomiting Clonidine

Pain Syndromes Sensitisation occurs in response to repeated or prolonged noxious stimuli: lower activation threshold,increased rate of firing a. peripheral: Increased sensitivity and excitability of nociceptive receptors and damaged nerves b.central: hyperexcitability of spinal neurones and descending modulating pathways Activation of NMDA receptors

Pain Syndromes Opioid Induced Hyperalgesia : the use of opioid paradoxically increases the patient’s perception of pain excitatory descending modulating pathways Persistent Post Surgical Pain Syndrome The response outlives the initiating stimulus and lasts for 3 months or more

Risk Factors History of poorly controlled pain (preoperatively and perioperatively) Intraoperative nerve damage (surgical, anaesthetic) History of preoperative neuropathic pain Co-morbidities associated with neuropathy: Diabetes, alcohol abuse, uraemia Drug induced neuropathy Nutritional deficiency,vitB12, B6, Malignancy Chem/radiotherapy Impaired immune system Fibromyalgia Major trauma Depression/anxiety (the unemployed)

Prevention of Pain Syndromes Efficient and effective pain management in the perioperative period Multimodal analgesia with neuroblockade regular acetaminophan and Nsaids and opioids On going research regarding perioperative use of antihyperalgesic agents: Pregabalin gabapentin NMDA receptor antagonists eg Ketamine Alpha agonists eg clonidine

Any questions ? ? ?