The Basics 😖
Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
The physiology of pain is classically described in four parts…
- Transduction of a noxious stimulus into neurological information. Free nerve endings (primarily in the epidermis and viscera) convert chemical, thermal and mechanical insults into action potentials.
- Transmission of action potentials to the dorsal horn of the spinal cord, mediated by Aδ fibres (fast, sharp pain) or C fibres (slow, dull pain).
- Modulation within the spinal cord by descending inhibition, which decides the magnitude of noxious stimulus transmitted to the somatosensory cortex.
- Cognition by the brain into a subjectively unpleasant experience.
The first three points describe nocioception: the relaying of noxious stimuli from potentially-injured tissue to the brain. A noxious stimulus is only considered painful when it is interpreted as being unpleasant.
The experience of pain can originate from any level in the pathway.
Acute and Chronic 🧠
Acute pain typically starts with nocioception due to tissue damage (e.g. stepping on a Lego brick). This pain is generally straightforward to manage and makes up the bulk of an anaesthetist’s work.
Chronic pain persists after the initial insult has resolved for a period of more than three months. Common features include…
- Hyperalgesia: pain out of proportion to a stimulus
- Allodynia: painful interpretation of non-painful stimuli
- Neuropathic pain: pain originating from conducting nerve damage
- Phantom limb pain: pain after amputation of a limb
Chronic pain is more difficult to treat because it typically originates from all the harder-to-target levels above transduction, including within the brain itself.
WHO Ladder 🪜
Multi-modal analgesia is the standard of care for pain management. The aim is to maximise pain relief at every level and minimise side-effects.
We take a stepwise approach based on the WHO pain ladder. A starting dose is informed by the anticipated degree of pain and adjusted according to the patient’s reported pain level.
Medications 💊
Non-opioids
Paracetamol is an effective and relatively-harmless analgesic that should feature in (almost) every pain management plan.
NSAIDs block the formation of inflammatory prostaglandins by inhibiting cyclo-oxygenase enzymes (COX). Be wary of renal impairment, GIT ulceration, ischaemic heart disease, and bronchospasm.
Opioids
Opioids do the heavy lifting in acute pain but have a limited role in chronic pain management. The original opiate was morphine, but it’s very common to use semi- or fully-synthetic opioids in contemporary practice (e.g. fentanyl).
- Tramadol
- Hybrid opioid and SSRI (increases descending inhibition)
- Good analgesia for most patients
- Avoid in older patients (delirium)
- Tapentadol
- A metabolite of tramadol
- Less delirium, more expensive
- Buprenorphine
- A “partial agonist” at μ opioid receptors
- Less respiratory depression, equal analgesia
- Safe to co-prescribe with other opioids at normal doses
- Slow onset, limited potential for abuse
- Oxycodone
- Pretty fast onset
- Excellent for severe acute pain
- Immense potential for abuse
- Morphine
- The original opiate, not so common today
- Very nauseating (co-prescribe an antiemetic)
- Accumulates toxic metabolites in renal failure
- Fentanyl
- Very fast and short-lived
- Perfectly safe in renal failure
There is no role for codeine in modern pain management.
The primary adverse effects of opioids are nausea, sedation and dose-dependent respiratory depression. In the name of multi-modal analgesia, try to use more “weak” opioids to minimise these effects.1
Most opioids come in slow-release and immediate-release formulations. Availability is subject to local policy and cost, among other things. Try to use the same drug for both.
Adjuvants
There is limited need for junior doctors to prescribe these, but it’s good to know what they are. Adjuvants mitigate the risks of using high-dose opioids but usually come with their own side-effects.
- Ketamine
- Pregabalin (and gabapentin)
- Clonidine
- Tricyclic antidepressants
- SNRIs
Local Anaesthesia 💉
The propagation of action potentials requires the inward flux of sodium ions through voltage-gated channels. Local anaesthetics prevent action potential propagation (in all neurons, not just pain fibres) by blocking sodium influx.
There are three common local anaesthetics in Australia. You’ll mostly use lignocaine in day-to-day practice. The others are longer-lasting, more dangerous, and largely confined to regional or neuraxial anaesthesia.
- Lignocaine (1% or 2%)
- Bread and butter for local anaesthesia
- Often pre-mixed with adrenaline
- Bupivacaine (0.25% or 0.5%)
- Popular for spinal blocks
- Sometimes pre-mixed with adrenaline
- Ropivacaine (0.2%, 0.75% and and 1%)
- Popular for regional blocks
- Sometimes pre-mixed with adrenaline
Local anaesthetic systemic toxicity (LAST) is characterised by arrhythmia, seizure, and in coma in severe cases. Toxicity is almost always caused by accidental intravenous injection, so always draw back before your inject.
These are the “safe” doses for the common agents:
Agent | Adrenaline ⛔️ | Adrenaline ✅ |
---|---|---|
Lignocaine | 4 mg/kg | 7 mg/kg |
Bupivacaine | 2 mg/kg | 2 mg/kg |
Ropivacaine | 3 mg/kg | 3 mg/kg |
These doses are subject to wide inter-source variability. Don’t panic.
You can practice your local anaesthetic dosing using LocalBot.
Regional Anaesthesia 📍
The aim is to bathe a single nerve (or plexus) in local anaesthetic to prevent nocioceptive transmission. Most anaesthetists use ultrasound guidance.
Regional anaesthesia is an excellent opioid-sparing technique. Be mindful that local anaesthetic almost always causes a degree of motor blockade too.
Intravenous regional anaesthesia is an old-school technique where a limb was isolated from the circulation by tourniquet and flooded with intravenous local anaesthetic. Bier’s block is a famous example. This carries an insanely high risk of toxicity and is made redundant by the wide availability of ultrasonography.
Neuraxial Anaesthesia 🧠
Neuraxial anaesthesia is like local anaesthesia applied to the spine. It allows you to numb the entire lower half of the body with only a small dose of anaesthetic but it’s risky, invasive, time-consuming and difficult.
Neuraxial techniques are only relevant to surgery below the umbilicus. They are particularly useful for avoiding general anaesthesia in high-risk patients where large doses of opioids and hypnotics would be required.
Anatomy
The spinal cord terminates by L2 in most adults, leaving a long tail of nerve roots and CSF beneath it (the lumbar cistern). When doing a block, we avoid the spinal cord by aiming for the L3/4 interspace or lower.
The intercristal line is an imaginary line drawn between the highest points of the iliac crests that corresponds with the L4/5 interspace (in patients who have read the textbook). It is the go-to landmark for neuraxial needling.
Spinal Blocks
Spinal blocks are a single shot of local anaesthetic (sometimes mixed with other agents) injected into the lumbar cistern. They’re relatively simple and reliable but cannot be “topped up” once they wear off.
On its way to the subarachnoid space, the needle will pass through…
- Skin
- Subcutaneous fat
- Supraspinous ligament
- Interspinous ligment
- Ligamentum flavum
- Epidural space
- Dura mater
- Arachnoid mater
- Lumbar cistern
Local anaesthetic is slightly less dense than cerebrospinal fluid (it’s hypobaric), so it’s sometimes made “heavy” (hyperbaric) by mixing it with dextrose. The heavy mixture sinks to produce a unilateral block (if the patient lies on their side).
Epidural Blocks
Epidurals blocks are a related technique where a flexible catheter is threaded into the epidural space. Local anaesthetic is periodically injected to anaesthetise the nerve roots as they exit the vertebral column.
Epidurals are best suited to long-lasting pain like labour and delivery.
Risky Business
Despite patients’ reservations, neuraxial blocks are generally safe and well-tolerated. The main risks to warn them about are…
- Failure (especially epidurals)
- Headache
- Bleeding
- Infection
- Neurological injury
- High block2
Contraindications
- Patient refusal (ick factor)
- Impaired coagulation (including by medicines)
- Raised ICP
- Uncooperative patient
- Underlying neurological or spinal disease
- Fixed cardiac output
- Shock
Further Reading
- Nerve Block is a website (and app) that provides a great atlas of ultrasound anatomy for the common regional techniques.
- SafeLocal is an app that helps you calculate the safe maximum volume of local anaesthetic to use.
- Better Pain Management is a popular pain management course run by ANZCA.
- Deranged Physiology has a great chapter on pain (physiology).
Tramadol and tapentadol are sometimes referred to as “weak” opioids because they have significant activity at non-opioid receptors. It has nothing to do with opioid receptor affinity or agonism. ↩
A phenomenon where local anaesthetic migrates above the level of T4 and causes profound bradycardia, hypotension and eventual diaphragmatic paralysis. If the local anaesthetic reaches the cranium, it’s a life-threatening “total spinal” anaesthetic. ↩