GasGasGas – The FRCA Primary Anaesthetics Exam Podcast

The Local Anaesthetics Chapter:

The Best Podcast for FRCA Primary Exam Preparation

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Key Clinical Question: How does ropivacaine’s unique S-enantiomer structure translate to clinical advantages in regional anaesthesia, and why might it be your go-to alternative when levobupivacaine isn’t available?

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Quick Reference Tables

Drug Formulations & Presentations

Parameter	Details
Brand Name	Naropin
Available Concentrations	0.2%, 0.5%, 0.75%, 1.0%
Special Preparations	Hyperbaric preparation (for spinal use)
Adrenaline Combinations	None available (doesn’t alter kinetics)
Licensing Note	No UK license for intrathecal use

Dosing Guidelines & Clinical Applications

Route/Application	Onset Time	Duration	Maximum Dose	Clinical Notes
Epidural	Similar to bupivacaine (sensory)	Sensory: Similar to bupivacaine	3 mg/kg	Motor block slower onset, faster recovery
Regional Blocks	Site-dependent	Variable by block type	3 mg/kg	Less motor block than bupivacaine
Spinal (off-license)	Standard spinal onset	Motor recovery faster	15 mg typical dose	Unlicensed in UK

Absorption Hierarchy (Fastest to Slowest)

Rank	Injection Site	Clinical Implication
1	Intercostal	Highest systemic absorption
2	Caudal	High absorption rate
3	Epidural	Moderate absorption
4	Brachial Plexus	Lower absorption
5	Subcutaneous	Lowest systemic absorption

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Detailed Content Sections

Classification & Basic Properties

Property	Details
Full Name	Ropivacaine Hydrochloride Monohydrate
Brand Name	Naropin
Chemical Class	Amide Local Anaesthetic
Stem/Group	Pipecoloxylide group
Appearance	Clear, colourless solution
Molecular Weight	274 g/mol
pH	Contains sodium hydroxide (3.7mg sodium/ml)
Enantiomeric Status	Pure S-enantiomer preparation

Pharmacodynamics

Mechanism of Action

Ropivacaine works through the classic local anaesthetic pathway:

1. Penetration: Unionised fraction crosses neurolemma (nerve membrane)
2. Internal ionisation: Becomes ionised within the neuron cytoplasm
3. Channel binding: Ionised form binds to internal aspect of voltage-gated sodium channels
4. Blockade: Preferentially binds to open/activated channels (use-dependent blockade)

Clinical Applications

• Primary Use: Regional anaesthesia and epidural analgesia
• Unlicensed Use: Spinal anaesthesia (no UK license for intrathecal route)
• Topical Applications: Limited clinical utility

Unique Clinical Characteristics

• Differential Blockade: Less motor block relative to sensory block compared to bupivacaine
• Onset Profile: Sensory block onset similar to bupivacaine, motor block slower
• Recovery Pattern: Sensory blockade duration similar to bupivacaine, motor recovery faster
• Practical Implication: Patients may have numb but mobile limbs initially

Side Effect Profile by System

Cardiovascular Effects:

• Biphasic Response: Initial hypertension → hypotension as plasma levels rise
• Toxicity Mechanism: Blood pressure drop + contractility reduction
• Cardiac Conduction: Can cause VF, asystole, VT at toxic doses
• Key Advantage: Less cardiotoxic than bupivacaine

Central Nervous System:

• Biphasic CNS Response: Initial excitation → depression
• Early Signs: Altered sensorium, agitation, perioral tingling
• Progression: Seizures → coma → respiratory depression
• Important Note: CNS blockade is reversible (like spinal blockade)

Pharmacokinetics

Parameter	Value	Clinical Significance
pKa	8.1 (same as bupivacaine)	15% unionised at pH 7.4
Protein Binding	94%	Binds to α1-acid glycoproteins
Volume of Distribution	52-66 litres	Large Vd indicates extensive tissue distribution
Clearance	0.44-0.82 L/min	Hepatic metabolism dependent
Elimination Half-life	59-173 minutes	Variable based on patient factors

Metabolism & Drug Interactions

Primary Pathway: Hepatic metabolism via aromatic hydroxylation

• CYP1A2: Primary enzyme (dominant role) (doesn’t fully mature til around 6-8 years of age)
• CYP3A4: Secondary involvement

Clinically Significant Interactions:

• CYP1A2 Inhibitors: inhibited – 77% increase in plasma levels
  • Enoxacin (fluoroquinolone) –
  • Fluvoxamine (SSRI for OCD) –
• CYP3A4 Inhibitors:
  • Fluconazole – only 15% plasma concentration increase (less clinically significant)

Clinical Pearl: CYP1A2 inhibitors are rare in UK practice, making significant drug interactions unlikely.

Special Clinical Applications

Sodium Bicarbonate Enhancement

Adding sodium bicarbonate significantly prolongs epidural blockade duration – useful for extended procedures.

Spinal Use (Off-License)

• Typical Dose: 15 mg for spinal anaesthesia
• Hyperbaric Preparation: Available but unlicensed in UK
• Clinical Pattern: Similar sensory duration to bupivacaine with faster motor recovery

Supply Chain Considerations

Ropivacaine gained prominence during levobupivacaine shortages, highlighting the importance of understanding alternative agents.

Safety Considerations

Maximum Safe Dosing

• Toxic Dose: 3 mg/kg (higher than bupivacaine)
• Clinical Monitoring: Same LAST protocol as other local anaesthetics
• Risk Factors: Inadvertent intravascular injection, patient factors affecting metabolism

Contraindications & Precautions

• Standard local anaesthetic contraindications apply
• Caution with CYP1A2 inhibitor co-administration
• Enhanced vigilance with hepatic impairment

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Educational Elements

Three Viva-Style Questions with Model Answers

Question 1: “An examiner shows you a vial of 0.5% ropivacaine. Compare and contrast this with bupivacaine.”

Model Answer Framework:

• Similarities: Both amide local anaesthetics, same pKa (8.1), similar sensory block characteristics
• Key Differences:
  • Ropivacaine is pure S-enantiomer vs racemic bupivacaine
  • Less cardiotoxic (higher toxic dose: 3 mg/kg)
  • Differential blockade – less motor block relative to sensory
  • Different recovery profile – faster motor recovery
• Clinical Implications: Could be useful when motor sparing desired (knee blocks perhaps?) + safer cardiac profile.

Question 2: “A patient develops signs of local anaesthetic toxicity after a regional block with ropivacaine. Describe the expected progression and management.”

Model Answer Framework:

• Progression: Biphasic response in both CNS and CVS
  • CNS: Perioral tingling → excitation/agitation → seizures → coma → respiratory arrest
  • CVS: Brief initial hypertension → hypotension → conduction blocks → cardiac arrest
• Management: LAST guidelines
  • Stop injection, call for help, maintain airway
  • 20% lipid emulsion therapy
  • Standard ALS resuscitation with modified approach for local anaesthetic toxicity
• Ropivacaine-specific: Less cardiotoxic than bupivacaine but same management principles

Question 3: “Explain the concept of differential blockade and its clinical relevance with ropivacaine.”

Model Answer Framework:

• Definition: Different degrees of sensory vs motor blockade
• Mechanism: Related to nerve fiber characteristics and drug properties
• Ropivacaine-specific:
  • Sensory block onset similar to bupivacaine
  • Motor block slower onset, faster recovery
  • Pure S-enantiomer contributes to this profile
• Clinical Applications:
  • Obstetric epidurals (mobility during labour)
  • Post-operative analgesia with preserved motor function
  • Day-case procedures requiring early mobilisation

Key Clinical Pearls & Mnemonics

Memory Aids

• “ROPES are Safer”: Ropivacaine Offers Pure Enantiomer Safety (My climbing club nickname was safety James after all!)
• “S for Safer”: S-enantiomer = Safer cardiac profile
• “Motor Slower, Recovery Quicker”: Ropivacaine’s differential blockade pattern

Essential Facts to Remember

1. Pure S-enantiomer – key differentiator from racemic local anaesthetics
2. 3 mg/kg toxic dose – higher safety margin than bupivacaine
3. CYP1A2 > CYP3A4 – metabolism hierarchy (rare drug interactions)
4. 15 mg spinal dose – equivalent to standard bupivacaine spinal dose
5. No adrenaline preparations – doesn’t alter kinetics significantly

Clinical Tips and Tricks

Practical Advice

• Supply Issues: Keep ropivacaine knowledge current – it’s your backup when levobupivacaine isn’t available
• Patient Education: Warn patients about potential temporary leg numbness with preserved movement
• Block Selection: Consider for procedures where early mobilisation is desired

Exam Strategies

• Opening Gambit: “Ropivacaine is structurally similar to bupivacaine but is enantiomerically pure…”
• Differentiation Points: Always mention S-enantiomer, differential blockade, and cardiac safety
• Backup Knowledge: Understanding ropivacaine demonstrates breadth of local anaesthetic knowledge

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Historical Context: The Woolley and Roe Case (1947)

Background

A pivotal moment in spinal anaesthesia history occurred at Chesterfield Royal Hospital when Albert Woolley and Cecil Roe developed devastating paraplegia following spinal anaesthetics on the same day by the same anaesthetist.

Timeline of Events

• Same Day: Two patients, same list, same anaesthetist
• Outcome: Both developed permanent paraplegia
• Legal Action: High Court case seeking compensation
• Verdict: Ruled against compensation based on medical evidence from other physicians

Root Cause Analysis

• Initial Theory: Phenol contamination through micro-cracks in ampoules
• Likely Cause: Acidic descaling agent residue in sterilisation equipment
• Contributing Factor: Theatre sister absent due to illness (later found to have pituitary tumour[survived neurosurgery])
• System Failure: Multiple holes in the cheese – equipment reuse, inadequate sterilisation oversight

Historical Impact

• Immediate Effect: Significant reduction in UK spinal anaesthesia use
• Concurrent Developments: Rise of safer general anaesthesia (halothane, neuromuscular blocking drugs)
• Long-term Legacy: Emphasis on single-use equipment and sterile technique

Modern Safety Lessons

• Equipment: Single-use spinal needles eliminate recontamination risk
• Antisepsis: 0.5% chlorhexidine vs 2% (arachnoiditis risk)
• Technique: Unsheathed needle discipline, appropriate sterile barriers
• Vigilance: Recognition that system failures can have devastating consequences

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Supporting Materials

References and Further Reading

Primary Sources

• Miller’s Anaesthesia (latest edition) – Comprehensive local anaesthetic pharmacology
• Oxford Handbook of Drugs in Anaesthesia and Critical Care – Quick reference guide
• Spinal anaesthesia for elective surgery: a comparison of hyperbaric solutions of racemic bupivacaine, levobupivacaine, and ropivacaine
• Comparison of plain and hyperbaric solutions of ropivacaine for spinal anaesthesia
• British Journal of Anaesthesia – Ropivacaine pharmacokinetics and clinical applications

Key Historic Articles

• “The history of spinal needles: getting to the point” – N. Calthorpe, AAGBI website
• Spinal anaesthesia during the 19th and 20th Centuries – cocaine and controversy
• The Woolley and Roe case

Guidelines and Resources

• Association of Anaesthetists Guidelines on Local Anaesthetic Toxicity
• AAGBI recommendations for neuraxial anaesthesia safety

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Transcript

Gas, Gas, Gas Podcast: Ropivacaine

Introduction and Welcome

00:00-00:32

Please listen carefully. Hello, and welcome to Gas, Gas, Gas. This is the best podcast for the FRCA primary exam. Our goal is to fill your brain with all this highly useful information. You might be in the gym right now, commuting, or ironing your scrubs. Regardless, revision is eventually going to end, but for now expect facts, concepts, model answers and the odd tangent. Make sure to check out gasgasgas.uk. There’s show notes there, there’s loads more detail. Make sure to like and subscribe. Anyway, buckle up, get ready for your mind to be bent into a new shape, and let’s get on with the show.

Ropivacaine Introduction and Key Points

00:36-01:29

Hello, everyone, and welcome to Gas, Gas, Gas. Today we are chatting ropivacaine. Now, if you get asked this in an exam and your brain’s jangling along and you need some stuff to say whilst you’re actually thinking about the rest of the answer, then you could open with: ropivacaine is structurally very similar to bupivacaine. They’re both amide anaesthetics. It is, however, described as causing less motor block in relative terms compared to other local anaesthetic agents. Of note, it is enantiomerically pure and is made up of the S-enantiomer. Much like levobupivacaine, this enantiomer favours cardiac sodium channels less – i.e., it’s less cardiotoxic.

We’re going to get into the rest of the bulk of it in a moment, but I just wanted to say, folks, if you haven’t subscribed to the show yet, what are you waiting for? This is great, at least I think it is. Make sure you check out the show notes in the podcast description. Takes you to the website, all the information is there. And if this podcast is happening to preserve your sanity, feel free to fire off a donation. There’s a link there in the show notes to support the podcast. Anyway, now we’ve got that out of the way, let’s get on with the show.

Drug Presentation and Availability

01:29-02:54

Full name: ropivacaine hydrochloride monohydrate. Brand name: Naropin (or Naropin, depending on how you pronounce things). This is an amide local anaesthetic agent and it is of the pipecolic acid stem/group.

How is it presented? Well, it’s a clear and colourless solution, and it is a pure enantiomeric preparation of S-ropivacaine. It comes in 0.25%, 0.5%, 0.75%, and I think 1% concentrations. There are no adrenaline mixes pre-made with this as it doesn’t alter kinetics, and there is also a hyperbaric preparation which can be used for spinal anaesthesia. However, of note, there isn’t a UK licence for its intrathecal use. I’m sure people still do it.

Now you’re probably thinking, “Why, Doctor Gas, are you bothering to talk about ropivacaine? I’ve never seen that in the cupboard.” Arguably I hadn’t seen it in the cupboard until like a year or two ago where there was actually a shortage of levobupivacaine, courtesy of probably Brexit, or just someone forgetting to press a big button that’s like on the wall in some warehouse that says “order more bupivacaine.” And actually places were having to reach for ropivacaine because they could get hold of it.

So I think it is important to have at least an approximate understanding of this drug, so that when someone forgets to press that big red bupivacaine order button, maybe we can reach for ropivacaine and not be completely clueless.

Mechanism of Action – Local Anaesthetic Pharmacodynamics

02:54-04:20

So we’re going to talk pharmacodynamics of ropivacaine. But now comes part of the show where I describe how local anaesthetics work in a different way for the umpteenth time, because it’s going to fit into your brain and stay there.

So you squirt some local anaesthetic on a nerve, and it doesn’t just tell the nerve to shut up from the outside – it has to get inside the nerve, really get under its skin, in order to work. So it has to transit across the neurolemma (aka the membrane of the nerve). To do this, it has to be in its un-ionised form. However, as we well know, most local anaesthetic agents prefer to be ionised than un-ionised, so there’s a small fraction that can get under the skin of that nerve to exert its effect.

Now we’ve got the un-ionised fraction, it’s soaked into that nerve, we’re inside our neuron floating around in cytoplasm, we’ve got our eyes locked on to that internal aspect of a sodium channel, and we’re like, “Yeah, come on then.” However, unfortunately, we’re not in the right shape for that sodium channel in our un-ionised form, so we have to go and ionise again, and as such make friends with a hydrogen ion, change shape and then get stuck in quite literally to that sodium channel, causing blockade.

Now we know that a sodium channel that’s giving our local anaesthetic a bit of aggro and opening its mouth is actually more susceptible to that local getting stuck in its mouth (mouth being channel here, folks). And that’s how local anaesthetics work.

Clinical Uses and Dosing

04:21-05:36

Anyway, we’re going to look at clinical uses of ropivacaine now. So it’s generally going to be used for regional anaesthesia and epidural anaesthesia. It is not licensed, as I said, for spinal anaesthesia in the UK. Dosing wise, well, the toxic dose is 3 milligrams per kilogram, so you shouldn’t give that. Below that, it’s probably site-specific, isn’t it? Because you can squirt quite a lot in for a volume block, but less if you’re ultrasounding right next to a nerve.

Now, interestingly, sensory block onset times for ropivacaine are similar to bupivacaine, whereas motor blockade takes longer to develop. So you might have a patient with numb legs who can wave them all around and might find it all very strange and discoordinated if their proprioception is gone but their muscles still work. They might be quite almost ataxic, I suppose.

The converse is true for recovery, in that sensory blockade persists for a similar time to bupivacaine, whereas the motor blockade recedes more quickly. Of note, if anyone were to ask you and back you into a corner, an appropriate spinal dose is 15 milligrams of ropivacaine, which is similar to what we might stick in bupivacaine-wise.

Side Effect Profile

05:36-07:04

Moving on from the clinical uses of ropivacaine in our pharmacodynamics section, we need to think about the side effect profile of ropivacaine. And you can probably guess that it is quite similar to other local anaesthetic agents. So I’m not going to delve deep into this, but I want to be able to convey that you can say it is less cardiotoxic than bupivacaine. And you could raise that argument and support it by suggesting that the toxic dose is 3 milligrams per kilogram for ropivacaine versus lower amounts for the other agents.

Naturally it is still cardiotoxic, and if you were to squirt it all into someone’s vein, artery, et cetera, you will end up with side effects.

Now, from a cardiovascular perspective, there’s an interesting biphasic response with ropivacaine, much like there is with other agents, in that initially you get a little bit of a blip of high blood pressure, which gives way to hypotension as the plasma concentration climbs, ultimately leading to conduction issues and VF, asystole, VT – whatever floats your boat, it seems to have a tendency to do it all.

And then from a central nervous system perspective, again, you will see that biphasic response where they get altered sensorium with some excitability of sensation, agitation, seizures, coma, death. But remember, this is reversible CNS blockade – much like it’s reversible on your spinal cord, it’s reversible in your brain. Just takes a while.

Pharmacokinetics – Absorption

07:04-07:48

Pharmacokinetics of ropivacaine. So the absorption characteristics of local anaesthetics again stand here. So intercostal (i.e. your ribs) – very well perfused, soaks up local anaesthetic quite merrily relative to caudal injections (i.e. through that sacral hiatus) – quite good at soaking it up, not as much as your ribs. Epidural injections, you’ll find that in the middle ground. Brachial plexus – less blood flow in there, soaks up slower. And subcutaneous, which, as we all know, is going to have the slowest uptake profile of local anaesthetics out of everything we’re doing, unless I guess maybe you squirt it on their toenail. I’m sure that has less blood flow.

Pharmacokinetics – Distribution and Protein Binding

07:49-08:33

Distribution-wise, so conveniently its pKa is the same as bupivacaine. It is 8.1, which means it is 15% un-ionised at physiological pH. It is 94% protein bound, which, just to be moderately awkward, bupivacaine is 95% protein bound. But they both favour alpha-1 acid glycoproteins as their chief site of binding, although I think it probably also binds to albumin if anyone’s asking to quote you on that. Alpha-1 acid glycoproteins for local anaesthetic drugs.

This volume of distribution is 52 to 66 litres, which is massive, but you know it’s going to soak into people. It’s quite lipophilic. It wants to go where it needs to go.

Pharmacokinetics – Metabolism

08:33-10:09

How is it metabolised? Well, you should be able to tell me by now, but as it is an amide local anaesthetic agent, the liver is getting busy. It breaks it down by hydroxylation and it uses CYP1A2 and CYP3A4.

Now the important thing here is that technically you can find a patient who has been taking drugs that inhibit these agents. Now for CYP1A2, I think it’s some pretty niche drugs here. For those who are deeply curious, the drugs that would inhibit CYP1A2 are enoxacin (and that’s a fluoroquinolone antibiotic, like ciprofloxacin – enoxacin) and fluvoxamine, which is a selective serotonin reuptake inhibitor used to treat OCD.

Now these aren’t common agents in UK practice, so I don’t think we need to stress too much about that. And then CYP3A4 – so that is classically inhibited by fluconazole.

Now, in terms of which of these enzymes has the dominant role, it’s probably the CYP1A2, because if you inhibit that, you get a marked increase in plasma levels, whereas with the 3A4, it’s only a 15% increase. So conveniently for us, not that it’s probably too much of an issue anyway, we don’t need to worry about drugs really inhibiting the clearance of ropivacaine. It might come into play if you are abroad and the patient was on enoxacin for some sort of renal tract infection, and then you were using an infusion of ropivacaine into their epidural space for some reason – then maybe you might start seeing toxic plasma levels and you might have to think a bit harder. Unlikely in the UK.

Pharmacokinetics – Elimination

10:09-10:33

Its clearance is 0.4 to 0.8 litres per minute, and the elimination half-life is one hour to just under three hours. That is ropivacaine in a nutshell. It’s important just to have a grip of how it compares to other drugs, more than perhaps knowing how to reach for it in your day-to-day practice, unless, of course, you’re in a hospital which uses ropivacaine, which certainly exists in the UK. And if you do, drop us a comment and describe how you guys use it. It’ll be interesting. Are you sticking it in spinals? Are you doing it off-licence? Gosh.

Historical Context – The Woolley and Roe Case (1947)

10:50-12:28

Now, I’ve only been talking for the grand total of like ten minutes, so I’m going to indulge in a bit of spinal history. We’ve already touched on in our cocaine episode, sticking cocaine in people’s intrathecal spaces, causing awful headaches, but then being able to whack people in the shins with hammers. But now we’re going to talk a little bit more about the potted history in the twentieth century when it comes to spinals.

So everyone’s probably heard of Dr Bier sticking cocaine in people’s backs, and then the folks who developed these needles, you know, Sprotte and Whitacre and all that, and Tuohy. And I think we’re all pretty accepting that when you’re using massive needles you cause headaches and you might prang nerves, or you’re in an area of the back and body where you’re not quite sure what the side effect profile is.

And that’s really where history takes us, and it occurred in 1947, and it was at Chesterfield Royal Hospital, when Mr Albert Woolley and Mr Cecil Roe developed devastating paraplegia following a spinal anaesthetic. Same day, same list, same anaesthetist.

Now before all this there were other documented side effects in the literature – people getting sort of like a chronic arachnoiditis picture, infections, epidural abscesses, haematomas, et cetera, et cetera, et cetera. All a bit non-specific and a bit unclear. In 1936 there was a paper that described patients developing meningitis, radiculitis, cauda equina syndrome and transverse myelitis. And there was a lot of documentation, but no clear – you know, no one’s going to organise a national audit project in 1947.

The Legal Case and Implications

12:28-13:28

But what happened with Mr Woolley and Mr Roe? Well, they were terribly injured, and they sought compensation through the High Court. Ultimately, the High Court ruled against them seeking compensation based on evidence given by other physicians at the time. Ultimately they decided that the phenol they were using to clean the outside of the ampoules and sterilise them before they were used to do a spinal anaesthetic had been seeping through micro-cracks in the ampoules, contaminating them, and that’s what happened to cause these devastating complications.

At the time, this really knocked back the use of spinal anaesthesia in UK practice as, concurrently, neuromuscular blocking drugs and halothane (a non-flammable volatile anaesthetic agent) were becoming popularised, rendering general anaesthesia quite a bit safer and causing a lot of perceived concern about administering spinal anaesthetics if you could avoid them.

Historical Context – Pre vs Post-1947 Practice

13:28-13:56

This is counter to how general anaesthesia and spinal anaesthesia bore out prior to neuromuscular blocking agents and a safer volatile anaesthetic, because surgeons quite liked patients who’d had spinal anaesthesia because they didn’t wriggle, they didn’t move, they were delightfully flaccid and they could operate on a convenient surgical field. Whereas patients under ether anaesthesia, et cetera – bit wrigglier, weren’t paralysed, more challenging.

The Real Cause – Equipment Sterilisation Failure

13:56-15:55

But what perhaps really happened? Now you could say, well, that anaesthetist just pranged them with a needle and wasn’t paying attention. And you could focus down on the practitioner. But also, it’s unusual that this event happened twice, same day, same anaesthetist, same list. And you have to look towards the equipment used.

Nowadays we use one spinal needle, goes in a sharp spin, whereas they used to reuse equipment – syringes, needles – and they would sterilise them. And unfortunately, I think we are looking at an early multiple holes through cheese event in that the sterilising equipment had got quite scaled up. And when I say scaled up, folks, remember that depending on the nature of your water and if you’re on limestone or not, you can actually have quite a lot of calcium carbonate in your water, and that furs up things that get boiled in (i.e., you get furry kettles full of calcium carbonate) and you’ve got to knock it off, scrape it off, or just ignore it.

But naturally, if you’re using it in an environment where you’re trying to sterilise things and you’ve got more nooks and crannies courtesy of scaling, then you need to do something about it.

Now this is only a supposition, because there’s no true proof of this. But the theatre sister, who would normally have supervised the sterilisation process on this day, unfortunately left work early because she was very ill. She was profusely vomiting and had a headache. Now you could wonder what the differential diagnosis for that might be, but actually she ended up with a pituitary tumour being successfully removed later on – hole in the cheese. Therefore, this descaling process hadn’t really been completely completed. No one rinsed out the tank and then sterilised the necessary kit. This kit was then used. Unfortunately, it had a little bit of unplanned acid on it.

The Devastating Consequences

15:55-16:35

Now you can imagine putting acid into an intrathecal space causes quite a lot of mischief, and it’s something we wouldn’t do. And this is what they think is the cause for the unfortunate neurological sequelae occurring.

Now, in terms of the verdict, the judges said that anyone performing a task should be expected to do that to the average of all those around them who perform that task (i.e. you shouldn’t expect an individual to be in the top percentile performing spinal anaesthesias) and that someone who’s at 50th percentile may get just as many complications and side effects, and it’s not their fault. However, the way that legislation and sort of medical law in the UK bore out at the time meant that nobody was then to blame, and these people got no compensation. That wouldn’t happen these days. I’m not a medical-legal lawyer, so I’m not going to go into more detail on that.

Modern Safety Lessons

16:35-17:21

Suffice to say, I was just more interested in the mysterious cheese model that occurred to lead to this complication that has been designed out by virtue of single-use equipment. I think it does highlight that we have to be absolutely vigilant when doing spinal anaesthetics – that we don’t unsheathe our spinal needle and put it back down until we’re actually going to use it. We do appropriate sterile technique.

I think there’s some arguments that we don’t really need to gown and drape and the like at the moment. I’ll wait for that to become embedded in reality before I start doing something that’s out on the edges of that bell curve that might make me feel slightly more implicated if I were to have a patient with a complication.

Modern Antiseptic Practices

17:21-18:06

On last note, and something that we actually all do and probably don’t realise why: why do we use 0.5% chlorhexidine spray as opposed to the 2% stuff that we use to put cannulae in? Well, there is an implication for chlorhexidine to cause an arachnoiditis, so we wouldn’t want to inadvertently introduce that into an intrathecal space. Let your prep dry. I’m sure you’ve seen on the wards people using chlorhexidine for lumbar punctures. We should hopefully be able to advise our colleagues that they might cause a disaster. And whilst it’s perhaps out of abject caution that we use lower concentrations of chlorhexidine for intrathecal and epidural and regional access, we do that for a reason, and we are in a modern healthcare system.

Further Reading and Conclusion

18:06-18:35

Now if you’re super curious about the history of all these different spinal needles in their various permutations of shapes, sizes, lengths, bevels, cutting, not cutting, blunt, pencil point, et cetera, there’s an excellent AAGBI essay which is linked in the show notes – explores this in greater and greater detail.

I hope you forgive my indulgence on the history of spinal anaesthesia. I don’t think there’s anything else I can talk about on that matter, you’ll be happy to hear. Always keep an eye out for descaling agents on your spinal needles, folks. Thank you very much for listening. Cheerio!

Closing Remarks

18:41-19:06

Thanks for listening, guys. I hope you found it useful, but if you found it awful, do let me know. Please like and subscribe, register with whichever podcast platform you find yourself using, and leave a comment if you think I need to square something away.

I just want to make sure that you guys know that every day you are getting better at this. There is a bucket of content to try and consume, and it is like drinking from a fire hose. Take it day by day, don’t overcook yourself, don’t freak out, and keep studying.

This is the full Show Transcript – Courtesy of Whisper LLM