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The use of local anaesthetics in acute pain management

Created: 21/12/2017
Updated: 10/1/2018
 
A multimodal approach to postoperative pain management may include a combination of both regional techniques (such as wound infiltration, nerve blocks, epidural analgesia) and systemically administered analgesic agents (such as paracetamol, nonsteroidal anti-inflammatory drugs, opioids, other adjuncts). The benefit of this approach is more effective pain relief, with a reduction in opioid-induced side effects.
Local anaesthetics may be used as the sole anaesthetic agent, or as an adjunct in a multimodal regimen.

 

Classification


Local anaesthetics fall into two groups, amides and esters. This classification is based on the structure of the interlinking intermediate chain between the aromatic lipophilic group and the hydrophilic group in each molecule.

 

Examples


Esters

  • Cocaine 
  • Procaine
  • Amethocaine
  • Benzocaine
  • Tetracaine

Amides

  • Lignocaine
  • Bupivacaine
  • Levobupivicaine
  • Ropivicaine
  • Prilocaine

Local anaesthetics are weak bases and exist predominantly in the ionised form at physiological pH.

Amides undergo hepatic metabolism, while esters are metabolised by plasma cholinesterase. Compared with esters, amides are more stable in solution, and have a longer shelf life. Clinically, amides are the preferred agents due to their more predictable action, and low rate of hypersensitivity reactions. The metabolism of esters leads to the formation of the well-known allergen, para-aminobenzoic acid (PABA).

The amide local anaesthetics are extensively used in practice. The choice of agent depends on the duration of action required, nature of the procedure, site of action and anaesthetist preference. Of the ester group, cocaine is frequently used for the topicalisation of the airway.

Mechanism of action

Normal nerve conduction relies on an influx of sodium ions through ion-specific channels in the nerve membrane, resulting in depolarisation and impulse propagation. Local anaesthetics block these sodium channels, resulting in a reversible conduction block. This is achieved by the non-ionised fraction of local anaesthetic crossing the cell membrane of the nerve. Inside the nerve, at a lower pH (6.9 versus 7.4), the local anaesthetic becomes ionised. The ionised fraction then binds to an intracellular binding site of the sodium channel, preventing sodium ion influx, and thus, depolarisation.

The onset and duration of nerve block is influenced by various factors:

- Local anaesthetic factors (physicochemical properties)

  • pKa – the closer the agent’s pKa to normal pH, the faster the onset of action 
  • Lipid solubility – the more lipid soluble the agent, the slower the onset of action 
  • Plasma protein binding – the more protein bound the agent, the longer the duration of action 
  • Isomers – L(S) enantiomers are usually less toxic 
  • Additives – the use of additives such as adrenaline or sodium bicarbonate may speed onset and prolong the block 
  • Volume and concentration of agent used

- Nerve anatomy 

  • Smaller diameter, myelinated nerves are more easily blocked

- Other factors

  • Site of injection (peripheral versus neuraxial)
  • Regional blood flow
  • Patient factors: hepatic and renal impairment, pregnancy

Clinical applications

Local anaesthetic agents may be administered via multiple routes:

1. Topicalisation of mucous membranes

Oral, pharyngeal, laryngeal, tracheal and urethral mucosa may be anaesthetised for various procedures.

2. Topical skin application

Ametop gel (4% w/w tetracaine) or EMLA cream (5% w/w eutectic mixture of lignocaine and prilocaine) may be used to relieve pain during phlebotomy, cannulation or lumbar puncture.

3. Patches

Lignocaine-containing topical patches have been found to be efficacious in a variety of pain conditions such as post-herpetic neuralgia and mononeuropathies; as well as rib fractures.

4. Subcutaneous and wound infiltration

Skin and wound infiltration offers good analgesic benefit in the immediate postoperative period; however, care must be taken to avoid exceeding maximum recommended doses. The effect may also, unfortunately, be short-lived.

In the case of lignocaine, adding adrenaline will increase the duration of action and maximum safe dose permitted (lignocaine without adrenaline: 3 mg/kg; lignocaine with adrenaline: 7 mg/kg). Adrenaline-containing solutions should never be injected into an area adjacent to an end-artery.

5. Neuraxial and perineural administration

Regional anaesthetic techniques are invaluable in the effective multimodal management of acute pain.

6. Intravenous administration

Intravenous lignocaine for the management of acute pain will be discussed below.

Intravenous (IV) lignocaine for acute pain

The clinical benefit of intravenously administered lignocaine is well established in the management of refractory chronic neuropathic pain. Increasing evidence now suggests that it is also effective as a systemic analgesic in acute postoperative pain.

Evidence

The strongest evidence for the use of intravenous (IV) lignocaine infusion is in patients undergoing open or laparoscopic abdominal procedures. Multiple studies or meta-analyses have found the following benefits:

  • Good postoperative visceral pain control, with reduced pain scores
  • Improved postoperative bowel function and prevention of ileus
  • Reduced opioid use and side effects
  • Earlier mobilisation
  • Reduced length of hospital stay

Some evidence also suggests that IV lignocaine may be of benefit in patients undergoing prostate, breast, thoracic and spinal surgery.

Mechanism of action

IV lignocaine has been found to be effective even at very low systemic concentrations. Additionally, in most trials, the clinical effect of IV lignocaine has long exceeded the duration of infusion. These findings cannot be fully explained by the sodium channel-blocking effects of lignocaine.

Although the exact mechanism of action is largely unknown, IV lignocaine appears to exert an inhibitory effect on injured nerve fibres and the dorsal root ganglia. It may also play a role in the prevention of central sensitisation. In addition, it has been found to have anti-inflammatory effects, by blocking the priming of polymorphonuclear granulocytes (PMNs).

Applications

  • Potential applications of IV lignocaine include:
  • Alternative to regional anaesthesia (e.g. if an epidural is contraindicated, refused or failed)
  • Enhanced recovery protocols
  • Laparoscopic surgery
  • Prevention of ileus
  • Patients with chronic neuropathic pain requiring surgery
  • Patients with opioid dependence or tolerance
  • Opioid-sparing techniques (in bariatric surgery, obstructive sleep apnoea, the elderly, opioid intolerance or allergy)
  • Trauma (e.g. burns, or rib or sternal fractures)

Contraindications

  • Allergy to lignocaine or other amide local anaesthetic
  • Local anaesthesia by another route (e.g. epidural or regional infusion)
  • Cardiac arrhythmias (e.g. atrial fibrillation, heart block, implantable pacemaker, other anti-arrhythmic agents [e.g. amiodarone, phenytoin])
  • Recent myocardial infarction or heart failure
  • Cardiovascular instability (shock)
  • Severe renal or hepatic impairment
  • Reduced conscious state
  • Seizure disorder

 Dose

Follow local protocols. Suggested dosing is 1–2 mg/kg as an initial bolus over 5 minutes, followed by continuous infusion of 0.5–3 mg/kg/hour, which may be continued for up to 72 hours postoperatively.  

Safety and side effects

Toxicity from perioperative lignocaine infusion is very rare; however, intravenous lignocaine has a narrow therapeutic index, and central nervous system toxicity can be rapidly fatal if not recognised. Staff must therefore be appropriately trained in the administration of intravenous lignocaine, use of infusion pumps, assessment of pain and identification of the adverse effects of local anaesthetic agents.

Postoperative vital signs must be monitored and documented according to local protocols, and lipid emulsion should be readily available.

Factors that may potentiate side effects include acidosis, hypoxia, hypercapnia, renal or hepatic impairment, and low plasma protein levels.

Staff caring for patients on lignocaine infusions must be aware of potential side effects. If a patient develops mild side effects, the infusion should be stopped immediately, and anaesthetic help summoned. Side effects are progressive as serum levels increase. If left unchecked, side effects can progress to seizures, cardiovascular collapse and death.

Classification   Serum lignocaine levels Signs and symptoms
 Mild  3–8 mg/mL
  • Numbness and tingling in peripheries and tongue
  • Perioral numbness and tingling
  • Metallic taste
  • Tinnitus
  • Dizziness 

 

 Moderate  8–12 mg/mL
  • Nausea and vomiting
  • Severe dizziness
  • Hearing and visual disturbances
  • Tremor
  • Cardiovascular instability
 Severe  Above 12 mg/mL
  • Drowsiness and confusion
  • Muscle twitching
  • Convulsions
  • Loss of consciousness
  • Cardiac arrhythmias
  • Cardiovascular collapse

References


Eipe N, Gupta S, Penning J. Intravenous lidocaine for acute pain: an evidence-based clinical update. BJA Education 2016; 9: 292–8.

Dunn LK, Duieux ME. Perioperative use of intravenous lidocaine. Anesthesiology 2017; 126: 729–37.

Elliot JA, Smith HS. Handbook of Acute Pain Management. CRC Press. 2011. Chapter 3: Local anesthetics in the management of acute postoperative pain (pp 19–28).

Milner A, Welch E. Applied Pharmacology in Anaesthesiology and Critical Care. 2012. Chapter 10: Local anaesthetic agents (pp 331–58).

ArticleDate:20171221
SiteSection: Article
 
   
    
                                            
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