October 13, 2025 • 25 mins
An extensive overview of local anesthesia in dentistry, detailing the pharmacology of various anesthetic agents like lidocaine, mepivacaine, and articaine, including their dosages, duration, and effects when combined with vasoconstrictors such as epinephrine. It also covers the armamentarium used for injections, discussing syringes, cartridges, and needle gauges, and introduces modern delivery systems like Computer-Controlled Local Anesthetic Delivery (C-CLAD). Significant attention is given to patient evaluation through medical history and physical status classification, as well as the techniques for administering local anesthetics for both maxillary and mandibular procedures, including various nerve blocks. Finally, the text addresses potential complications like needle breakage, paresthesia, overdose, and allergic reactions, offering guidance on their prevention and management, while also touching on legal considerations and future trends in pain control.
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Episode Transcript
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Speaker 1 (00:00):
Welcome to the deep dive. Today. We're really digging into
the absolute bedrock of pain control in dentistry local anesthesia.
We've got the textbooks, the core knowledge, and we're going
to break it all down exactly.
Speaker 2 (00:13):
Our mission really is to synthesize this foundational science. We're
talking molecular level stuff right up to the latest clinical protocols.
Speaker 1 (00:21):
Right for everyone listening, especially if you're newer to the field.
This is about connecting the dots why things work, not
just how to do them, from the nerve impulse itself
to keeping patients safe.
Speaker 3 (00:32):
Absolutely, we need to be thorough.
Speaker 2 (00:33):
We're covering nerve structure, how the drugs actually work, the equipment,
the armamentarium, patient evaluation, those crucial ASA classifications, drug interactions.
Speaker 1 (00:42):
Injection techniques, maxillary mandibular, all the supplemental.
Speaker 2 (00:45):
Methods, and importantly, managing complications if things don't go quite
as planned. It's a big picture and every piece matters.
You can't just know the dose limits without understanding why
aspiration is non negotiable.
Speaker 1 (00:57):
Okay, perfect setup. Let's dive right into the very beginning.
How does local anesthetic actually stop that pain signal? I
always like the analogy of water on a lit fuse
heading for dynamite.
Speaker 2 (01:10):
That's a good starting point. The anesthetic is the water,
the nerve impulses the fuze, and the dynamite is the
brain registering pain. But that water needs to get inside
the fuse casing.
Speaker 1 (01:21):
Okay, So talk us through the nerve structure itself.
Speaker 2 (01:23):
Well, you've got the axon, which is the core filled
with axoplasm and it's wrapped in the nerve membrane, the axilemma.
Now for faster nerves, the myelinated ones, they have this
fatty mile in sheaf acting as insulation.
Speaker 1 (01:36):
And the signal jumps between gaps in that sheath.
Speaker 3 (01:38):
Right exactly.
Speaker 2 (01:39):
Those gaps are the nodes of ranvier. The membrane's exposed
there and the impulse leaps from node to node. That
saltatory conduction much faster. But the anesthetic has to work
at that nerve.
Speaker 1 (01:49):
Membrane and getting it there is the challenge. It has
to cross layers, and you mentioned the perinurium is the
main barrier.
Speaker 3 (01:55):
It's the biggest turtle.
Speaker 2 (01:56):
Yeah, And the drug needs to be in the right
chemical form to get through that fatty nerve sheath. The
anesthetic molecule needs to be uncharged lepophilic. That's the free
base form the.
Speaker 1 (02:07):
RN so RN gets it through the door.
Speaker 2 (02:09):
RN diffuses a cross. Once it's inside the axoplasm, where
the pH is pretty stable, around seven point four, those
RN molecules pick up a proton and become positively charged.
Speaker 1 (02:18):
Again.
Speaker 3 (02:19):
That's the cassionic form RNH.
Speaker 1 (02:21):
Plus INN and that's the actusor that's.
Speaker 2 (02:23):
The one that does the work. The RNH plus ion
physically binds to a receptor site inside the sodium channel.
It's like putting a key in the lock and breaking
it off. Sodium ions can't rush in.
Speaker 1 (02:33):
No sodium influx, no depolarization.
Speaker 2 (02:35):
No nerve impulse, pain signal blocked.
Speaker 1 (02:38):
Okay, this immediately brings up something clinically vital. You mentioned
the pH inside is stable, but outside that matters for
getting the RN form in hugely.
Speaker 2 (02:48):
The pH of the surrounding tissue dictates how much of
the drug is in that RN form ready to diffuse.
Speaker 1 (02:53):
And this is where visoconstrictors come in. Chemically speaking, adding
one makes the solution quite acidic, right like pH three point.
Speaker 2 (02:59):
Five compared to maybe six point five for a plain solution. Yes,
significantly more acidic. And that means initially fewer RN molecules
are available to penetrate the nerve sheath.
Speaker 1 (03:11):
So the clinical result is two things.
Speaker 2 (03:13):
First, that initial burning sensation patients sometimes feel. That's often
the acidity. Second, it means a slower onset of anesthesia.
You need to be patient and jack slowly let the
tissue buffer the solutions so more RN can form and
get inside.
Speaker 1 (03:27):
Got it, slow onset potential burn good points. Now let's
think bigger picture systemic effects. Ideally in LA is totally reversible,
low toxicity. Yeah, but it always gets.
Speaker 2 (03:38):
Absorbed eventually, always, every last bit gets into the bloodstream. Yeah,
and how fast depends entirely on where you put it.
Oral absorption pretty poor. Lightikin gets hit hard by the
liver first pass, like seventy two percent wiped out.
Speaker 1 (03:49):
But other roads are faster.
Speaker 2 (03:50):
Oh yeah, tracheal nucosa. It's almost like an IV injection.
Super fast absorption. And when those blood levels climb too high,
LAS start depressing excitable membranes. Thinks C think cardiovascular system,
So what are.
Speaker 1 (04:02):
The warning signs? What do we look for if toxicity
is developing.
Speaker 2 (04:05):
Initially you see CNS excitation. The patient might feel lightheaded, dizzy,
maybe some slurred speech, muscle twitches, tremors. Numbness of the
tongue or around the mouth is a classic early sign.
Speaker 1 (04:17):
And if levels keep rising.
Speaker 2 (04:19):
Then it flips to CNS depression. Seizures might actually stop,
the EG could flatten out, breathing slows down respiratory depression,
and then you start seeing serious cardiac effects.
Speaker 1 (04:30):
Which leads us directly to why we add vasoconstrictors vps.
It's not just about making the numbness last longer. It's
a key safety factor. Can you list those core benefits again?
Speaker 3 (04:40):
Sure?
Speaker 2 (04:41):
Five main reasons. One they constrict blood vessels locally. Two,
this slows down the absorption of the LA into the.
Speaker 1 (04:47):
Bloodstream, lowering the peak blood level.
Speaker 2 (04:49):
Exactly, which number three drastically cuts the risk of systemic toxicity.
Four slower absorption means the LA stays at the nerve longer,
so you get increased duration in depths of anesesia. And
five for surgery, that vasoconstriction means less bleeding hemostasis.
Speaker 1 (05:04):
Okay. These vps are sympathomometic, mimicking adrenaline and nor adrenaline.
They act on specific receptors elfin beta correct.
Speaker 2 (05:12):
Alpha receptors primarily cause that vasoconstriction we want. Beta receptors
are more complex. Beta one stimulates the heart, Beta two
causes vasodilation in some areas and importantly bronchodilation.
Speaker 1 (05:24):
And different vps hit these receptors differently.
Speaker 2 (05:26):
Right, like norpinefrin, it doesn't have much beta two actions,
so you get really intense peripheral vasoconstriction. Oh. In an
interesting side note, cocaine is the only LA that always
causes vasoconstriction itself because it blocks nora pineffrine reuptake.
Speaker 1 (05:39):
Fascinating. Let's talk dosage in dilutions. This math has to
be second nature. A one to one hundred thousand dollars dilution,
how much drug is.
Speaker 2 (05:47):
That permeli leader that's zero point zero one milligrams per
milileader or often easier to think in micrograms ten micrograms
per mL. Knowing this is crucial for calculating safe limits.
Speaker 1 (05:58):
So what are those limits? For epinephron the common VP
for a.
Speaker 2 (06:01):
Healthy adult patient, the maximum recommended dose is zero point
two milligrams, which is two hundred micrograms.
Speaker 1 (06:07):
Okay, two hundred micrograms for healthy but for someone with
cardiovascuar issues. Maybe an ASA class three or fall.
Speaker 2 (06:12):
That limit drops sharply. It's only zero point zero four
milligrams or forty micrograms.
Speaker 1 (06:17):
That's a big difference, and this is important. Some might
think any epinephrine is bad for these patients, but you're
saying using a small, controlled amount within that forty microgram
limit might actually be safer than using a plain.
Speaker 2 (06:28):
LA that fails often, yes, because if the plane LA
doesn't achieve profound anesthesia, the patient gets stressed, maybe feels pain,
and their body releases its own catecholamines, its own adrenaline.
That endogenous release can be way higher and much less
controlled than the tiny amount we inject.
Speaker 1 (06:49):
So successful, stress free anesesia is the goal, and sometimes
a limited VP dose is the best way to achieve that,
even in an ASA three patient. Just stick rigorously to
that forty microgram limits.
Speaker 3 (07:00):
Precisely, it's about risk management, right.
Speaker 1 (07:02):
We've covered the chemistry, the safety limits. Let's move to
the tools, the armamentarium. The classic aspirating syringe. That palm
thumb grip not always the easiest to control, is it No?
Speaker 2 (07:12):
Ergonomically it's not ideal, which is why the development of
computer control local anesthetic delivery systems. The CEA slids like
the wand or STA system back in ninety seven, was
such a step forward.
Speaker 1 (07:22):
How do they help?
Speaker 2 (07:23):
They allow a pen like grasp, much more like how
you'd hold an explorer or a scaler. It gives you
fingertip control and accuracy. Plus the machine controls the flow rate,
keeps it slow and consistent.
Speaker 1 (07:34):
So the operator can just focus on needle placement and
angulation exactly.
Speaker 2 (07:38):
It takes one variable out of the equation and generally
leads to a more comfortable injection for the patient because
the pressure is managed set.
Speaker 1 (07:45):
Peak of needles. I find it amazing that patients apparently
can't tell the difference between a twenty five, twenty seven
or thirty gauge needle in mucous membrane. So why the
preference for twenty five or twenty seven gage for deeper
blocks like the IAMB.
Speaker 2 (07:59):
It really comes down to aspiration. The larger lumen of
the twenty five or twenty seven gauge makes aspiration pulling
back to check for blood more reliable than with a
thirty gauge.
Speaker 3 (08:08):
You get a truer reading the needle.
Speaker 1 (08:09):
Safety Yeah, huge topic. What are the absolute must know rules.
Speaker 2 (08:13):
Number one, Never ever insert the needle all the way
to the hub. That's the weakest point. If it's going
to break, it'll likely break there. Leaving some needle visible
is crucial.
Speaker 1 (08:23):
Okay, never to the hub. What us?
Speaker 2 (08:24):
Never change the direction of the needle while it's deeply
embedded in tissue. If you need to redirect, withdraw it
almost completely first, then re angle and advance again. Trying
to bend it inside tissue puts huge stress.
Speaker 1 (08:37):
On it, and gauge relates to breakage risk too.
Speaker 2 (08:40):
Yes, physics tells us the smaller diameter needles the thirty
and twenty seven gage are statistically more likely to break
than a twenty five gauge needle.
Speaker 1 (08:48):
Got it. Let's look inside the cartridge itself. Standard is
about one point eight millimel, though some manufacturers list one
point seven milimel. We know it has the LA drug
maybe a VP. What else is in there?
Speaker 2 (08:59):
Distilled water as the vehicle and sodium chloride to make
the solution isotonic with the body tissues reduces.
Speaker 1 (09:05):
Irritation, and if there's a vasoconstrictor.
Speaker 2 (09:07):
Then you must have an antioxidant preservative, usually sodium bisulfite.
That's what gives the cartridge its shelf life maybe eighteen months,
but it's also what makes the solution acidic.
Speaker 1 (09:16):
Bringing us back to that pH point again, the bisulfite
lowers the pH causing potential burning and slower onset.
Speaker 3 (09:23):
Correct.
Speaker 2 (09:24):
Oh and one thing that used to be in cartridges
was methyl parabin another preservative, but it caused some allergy issues,
so it was removed from single use dental cartridges back
in nineteen eighty four.
Speaker 1 (09:34):
Good historical note. Okay, all this leads into the actual
process of giving a shot. The a traumatic injection protocol.
This isn't just about technique, it's a systematic approach.
Speaker 2 (09:44):
Absolutely starts with using a sharp sterile needle. Check it
for barbs, maybe on gauze, Identify your target site.
Speaker 1 (09:51):
Then prep the tissue, yes.
Speaker 2 (09:52):
Dry it thoroughly with gauze first. Then apply your topical anesthetic.
And here's a key point, leave it on for a minute,
not ten or fifteen seconds. A full minute is needed
for it to really work on the surface layers. Topical
antiseptic is optional.
Speaker 1 (10:07):
After that, okay, minute of topical, then.
Speaker 2 (10:09):
What stabilize your hand? Stabilize the syringe, don't rest it
on the patient's arm or shoulder that introduces movement, Advance
the needle slowly into the tissue.
Speaker 1 (10:18):
And for block injections like the IAMB or.
Speaker 2 (10:20):
Infurbital, deposit just a few drops of anesthetic before you
anticipate contacting the periostium. That's sensitive bone lining it numbs
the area ahead of the needle tip makes sense. Then
the critical safety steps asprit pull back gently on the plunger,
do it in at least two planes, meaning rotate the
bevel slightly, and aspirate again. This confirms you're not inside
(10:42):
a blood vessel. Essential, especially with those larger gauge needles
in vascular areas.
Speaker 1 (10:47):
Absolutely critical. And the final.
Speaker 2 (10:49):
Step deposit the solutions slowly. A milliter per minute is
a good benchmark. Too fast causes pain, can tear tissues,
leading to soreness later, and drastically increases the risk of
a toxic reaction if you did happen to be intravascular
despite aspiration. Slow injection is paramount.
Speaker 1 (11:07):
Okay, excellent breakdown of the technique. Now let's shift focus
from the needle to the person holding it, the patient evaluation,
medical history dialogue. This is an optional right.
Speaker 2 (11:17):
It's a moral and legal necessity. You have to know
who you're treating. Using comprehensive medical history forms like the
standard UOP or met life ones and actually talking to
the patient about their health is fundamental and a key.
Speaker 1 (11:29):
Part of that assessment is using the ASA Physical Status classification.
Can you quickly recap that?
Speaker 4 (11:34):
For us?
Speaker 2 (11:34):
Sure, it's a scale from one to six, but clinically
we mainly focus on one through four. ASAS one is
a normal, healthy patient, ASA two has mild systemic disease,
maybe well controlled diabetes or hypertension, or perhaps extreme anxiety
about dentistry.
Speaker 1 (11:49):
Okay, ASA two is mild disease or significant anxiety. What
about three?
Speaker 2 (11:54):
ASA three means severe systemic disease that limits their activity,
but isn't incapacitating stable angina, a heart attack more than
six months ago, maybe poorly controlled hypertension COPD.
Speaker 1 (12:05):
So definite limitations. Yeah, An ASA.
Speaker 2 (12:08):
Four that's severe systemic disease that's a constant threat to life,
maybe unstable angina, recent heart attack or stroke, severe heart failure,
and stage renal disease. These patients often need treatment in
a hospital setting. Knowing the ASA class directly impacts our
treatment plan, especially our vasoconstrictor use.
Speaker 1 (12:24):
Right. Tying back to those dose limits, let's revisit a
couple of specific conditions you mentioned ASA two or three.
Heart failure patients often need good pain control, and VPS
used carefully can help achieve that. What about lung conditions.
Speaker 2 (12:35):
Patients with significant emphysema maybe ASA three or four rely
on what's called a hypoxic drive to breathe. Giving them
too much supplemental oxygen, say more than three liters per minute,
can actually knock out that drive and potentially cause respiratory arrest.
So caution with oxygen is needed.
Speaker 1 (12:53):
Good point. And while we're on patient factors allergies, how
common is a true allergy to a mid local anesthetic
like latyicane or articane.
Speaker 2 (13:02):
Virtually nil? It's incredibly rare. Most reported novocane allergies remember
novocane was an ester different class or even allergies to
modern amides turn out to be something else like way.
Often it's a psychogenic reaction, feinting due to fear or
perhaps mild ob of symptoms that were misinterpreted as allergy.
True IgE mediated anaphylaxis to an amid la is almost
(13:24):
unheard of.
Speaker 1 (13:25):
Okay, that's crucial context. Let's hammer down the most important
drug interactions we need to worry about, specifically with vasoconstrictors.
Speaker 2 (13:31):
Top of the list has to be tricyclic antidepressants TCAs,
things like amatrypto line. They can seriously potentiate the effects
of vasoconstrictors with levinordifrin or neropaneffern it could be a
five to ten fold enhancement of press to effects with
epanephrine maybe about twofold. The clinical advice is clear avoid
levenordifran and norpinifrin completely. Impatients on TCAs limit up an
(13:55):
effort strictly, maybe to that point zero four or point
zero five milligram dose range.
Speaker 1 (14:00):
TCAs are a big one.
Speaker 2 (14:01):
What else non selective beta blockers like propranolol. If you
give a patient on propranolol a vasoconstrictor like epinephrine, the
beta blocker prevents the vasodilation effect beta too, leaving the
alpha receptor vasoconstriction unopposed, resulting in potentially a sharp rise
in blood pressure and then a reflex slowing of the
heart rate bradycardia. It can be dangerous. Careful dose limitation
(14:23):
of epinephrine is needed here too.
Speaker 1 (14:25):
What about MAO inhibitors used to be a big contraindication.
Speaker 2 (14:28):
Yeah, that's changed. More recent evidence suggests that the typical
vasoconstrictors used in dentistry Epinepherne, levener de friend nor panfrin
don't actually cause a hypertensive crisis in patients taking MAOIs.
So that's less of a concern now than previously thought.
Speaker 1 (14:41):
Good update. How about malignant hyperthermia MH. They used to
be an absolute no for a my DA.
Speaker 3 (14:47):
LA's also updated.
Speaker 2 (14:49):
It's now generally considered a relative contraindication. Importantly, MH has
never actually been triggered when an amid local anesthetic was
the only drug given. The consensus is that 'ides are
likely safe, but consultation with the patient's physician is still wise.
Speaker 1 (15:04):
Okay. One more specific toxicity methemoglobinemia. What causes that?
Speaker 2 (15:09):
This one is primarily associated with prelocaine and also sometimes
benzicane topical It's caused by a metabolite called orthotoluidine.
Speaker 1 (15:18):
It's dose related and the signs are quite distinctive.
Speaker 2 (15:20):
Yes, it usually shows up maybe three to four hours
after the drug was given, the patient becomes lethargic, might
have trouble breathing, looks cyanotic, kind of bluish, But crucially,
the cyanosis doesn't improve much with oxygen. If you drew
arterial blood, it would look chocolate brown.
Speaker 1 (15:35):
And the treatment is specific too.
Speaker 2 (15:36):
Very specific. Slow intravenous administration of methylene blue is the antidote.
You need to recognize it and know the treatment protocol.
Speaker 1 (15:44):
Moving from risks to actual practice, choosing the right drug
and technique duration is key. Liticane two percent with one
point one hundred zer an epi gives about sixty minutes
of pople anesthesia.
Speaker 2 (15:55):
Roughly yes, and maybe three to five hours of soft
tissue numbness. Compare that to boop of a cane zero
point five percent with one point two hundred thousand epi
that gives you ninety minutes, maybe even up to one
hundred and eighty minutes of polple and soft tissue anthesia
for four to nine hours, much longer acting.
Speaker 1 (16:14):
So using that long acting boop of a gane for
just say a single filling that takes twenty minutes probably overkill.
Speaker 2 (16:21):
Absolutely, you're leaving the patient profoundly numb for hours longer
than needed, increasing that risk. We talked about self inflicted
injury to the lipper tongue, especially in kids or patients
who might not understand. Choose the drug that fits the
procedures required.
Speaker 1 (16:34):
Duration makes sense. Let's talk specific injection techniques. Maxillary first
infiltration the superperio steel injection is common, but maybe not
for multiple teeth.
Speaker 2 (16:44):
Right, it's great for one or two teeth. For molars,
we often use the posterior superior alveolar block, the PSA,
but it's got that well known quirt miss.
Speaker 1 (16:51):
Is the mesiobucle route of the first molar in a.
Speaker 3 (16:53):
Fair number of people, about twenty eight percent of the time.
Speaker 2 (16:55):
Yeah, the nerve supply sometimes comes from a different branch.
That's where supplemental infiltration might be needed.
Speaker 1 (17:00):
Are there other maxillary options, maybe for anterior teeth without
numbing the face.
Speaker 2 (17:05):
Yes, the more advanced palatal approaches, the AMSA anterior and
middle superior alveolar and the pasa palatal approach anterior superior
alveolar blocks.
Speaker 3 (17:15):
They can numb in.
Speaker 2 (17:16):
Sizors, canines, premolars, and the associated palatal tissue all from
a palatal injection site. Great for esthetic work where you
don't want lipdroop.
Speaker 1 (17:24):
And the nesicipalatine block for the anterior palet, known for
being a bit spicy.
Speaker 2 (17:28):
Can be uncomfortable, yes, but slow injection is key and
you only need a tiny amount like zero point three
milli mile usually does the trick for broad bilateral anesthesia
of the anterior palette.
Speaker 1 (17:39):
Okay, let's tackle the mandible. The big one is the
inferior alveolar nerve block, the IAANB, but it's notoriously unreliable.
Speaker 2 (17:47):
Sometimes it has the highest failure rate of any common block. Unfortunately,
success rates vary in the literature, but missing isn't uncommon. Plus,
it has that high positive aspiration rate maybe ten fifteen percent,
meaning you hit a blood vessel farly often.
Speaker 1 (18:00):
Which is why alternatives are so important.
Speaker 2 (18:02):
The Gaugates technique the Gugate's mandibular nerve block. Yes, it's
a true V three block, aiming higher up, closer to
the mendibular foreman. It anesthetizes almost all the branches of
mendibular nerve, inferior alveolar, lingual buckle, mylohyoid, auricular, temporal, and
the benefits much higher success rate. Often cited above ninety
(18:22):
five percent and a significantly lower positive aspiration rate maybe
around two percent. Because your higher up away from the
main vessels accompanying the.
Speaker 1 (18:31):
Ann so higher success, lower risk seems like a strong contender.
What about numbing just one tooth without widespread numbness.
Speaker 2 (18:38):
That's where supplemental technique shine. The periodontal ligament injection or
PDL injection, also intriossious IO injection directly into the cancellus
bone and intraceptal injection into the interdental septum.
Speaker 1 (18:50):
These give very localized anesthesia exactly.
Speaker 2 (18:53):
Single tooth may be adjacent soft tissue, but minimal lip
or tongue numbness. Great for isolated procedures or when bilateral.
Speaker 1 (18:59):
Blocks are and technology helps here too.
Speaker 2 (19:01):
Definitely, the c clad systems like the STA are really
advantageous for PDL and IO injections. They control the pressure
and flow rate very precisely. The SDA system even has
dynamic pressure sensing technology that helps guide the operator to
the optimal injection site in the PDL space, improving success
and comfort.
Speaker 1 (19:21):
What about that last resort, the intrapulple injection when nothing else.
Speaker 2 (19:25):
Works, usually for the hot tooth often a mandibular molar.
You drill into the pulp chamber and deposit directly. It
works partly by the drug action, but also significantly by
the applied pressure. It causes brief intense pain, followed almost
immediately by profound anesthesia. It's effective, but definitely a last resort.
Speaker 1 (19:45):
Okay, let's round this out by discussing complications. What can
go wrong? Parasgia seems to be a big concern.
Speaker 2 (19:50):
Parasesia persistent numbness or altered sensation lasting beyond the expected
duration of the anesthetic. It's distressing for patients. The lingual
nerve is involved in the vast majority of reporting cases,
maybe ninety percent.
Speaker 1 (20:01):
Is there an association with certain drugs.
Speaker 2 (20:04):
There's a statistically higher incidence reported with the four percent
local anesthetics, specifically arcticane and prelocane, compared to lower concentrations
like two percent lytocine. The thinking is it might relate
to the higher concentration itself potentially being neurotoxic to the
nerve fibers, especially if injected directly into the nerve bundle.
Speaker 1 (20:24):
That's a really important point for drug selection, especially for iambs.
What other common complications trismus.
Speaker 2 (20:30):
That's muscle soreness or limited opening. Basically a spasm of
the jaw muscles, usually mild after an imb maybe from
muscle trauma by the needle, managed with heat, gentle stretching,
maybe some anti inflammatories.
Speaker 3 (20:43):
Usually resolves in a few days.
Speaker 2 (20:44):
Ebaituma bruising happens when a blood vessel is nicked, most
common after the PSA block because of the vascular plexus
back there. Best management is immediate pressure applied to the
area for several minutes. It can look dramatic, but usually
resolves on its.
Speaker 1 (20:57):
Own overtime and fatal paralysis for the patient.
Speaker 2 (21:01):
Transient facial nerve paralysis hitting CMBF. This happens if you
inject anesthetic into the parotid gland, usually by inserting the
needle too far posteriorly during an IAANB or maybe a
vasiraniaknosi block. Its temporary lasts as long as the anesthetic,
but very alarming, preventable by adhering strictly to anatomical landmarks
and depth limits.
Speaker 1 (21:21):
Okay, last critical area managing emergencies. Let's reemphasize the difference
between overdose.
Speaker 2 (21:26):
And allergy, absolutely crucial distinction overdose is dose related. It
happens because the blood level of the drug gets too
high too fast. Allergy is not dose related, it's an
immune response. Even a minuscule amount can trigger a reaction
in a sensitized individual.
Speaker 1 (21:41):
How do we manage a mild to moderate overdose that
develops slowly?
Speaker 2 (21:45):
Basic life support is key. Position the patient comfortably administer oxygen,
provide reassurance, monitor vital signs. Most reactions are self limiting
as the drug redistributes and is metabolized. If seizures occur
in are prolonged, say four or five minutes, then an
anticondulcant like mitazolum might be needed, but only if you're
trained in its administration and advanced airway management.
Speaker 1 (22:07):
And allergy management. Especially the worst case anaphylaxis.
Speaker 3 (22:11):
Speed is everything.
Speaker 2 (22:12):
If you see signs of a severe, rapidly progressing allergic reaction,
difficulty breathing, hive spreading, drop in blood pressure, the primary
treatment is immediate epinephrine.
Speaker 1 (22:22):
What dosin root usually zero.
Speaker 2 (22:24):
Point three milligrams of one point one zero zero zero epinephrine,
given intramuscularly or subcutaneously for an adult, repeat every five
to fifteen minutes as needed, then basic life support, oxygen
call for emergency medical services. You might administer histamine, walkers
and corticosteroids later, but epinephrine is the first line life
(22:44):
saving drug.
Speaker 1 (22:45):
And just to be absolutely clear, is there any absolute
contraindication to using epinefin in a true anaphylactic emergency.
Speaker 2 (22:52):
Now, in the context of anaphylaxis, the benefits of epinephrine
far outweigh any potential risks. It's the drug of choice, period,
powerful reminder.
Speaker 1 (23:00):
Okay, looking ahead briefly, what are some key trends or
advancements changing practice?
Speaker 2 (23:04):
Well, two things stand out recently. One is the increasing
acceptance and evidence supporting the use of articane, that four
percent drug for simple infiltration anesthesia for mandibular posterior teeth
and adults potentially avoiding the IAANB for some procedures.
Speaker 1 (23:19):
Interesting infiltration instead of a block in the mandible.
Speaker 3 (23:23):
Yeah.
Speaker 2 (23:24):
And the other the development of a local anesthetic reversal
agent phantolamine mesylate brand name or VERSE. It's an alpha
adrinergic blocker.
Speaker 1 (23:33):
So it counteracts the vasoconstrictor.
Speaker 2 (23:34):
Exactly, it counteracts the epi or levo, allowing blood flow
to return to the area more quickly, which washes the
anesthetic away faster. It significantly speeds up the return of
normal soft tissue sensation, lip tongue numbness goes away much quicker.
Speaker 1 (23:48):
That seems huge for patient comfort and reducing that risk
of accidental biting, especially in kids.
Speaker 2 (23:53):
It's a major benefit, particularly in pediatric dentistry or for
patients having procedures before needing to speak or eat soon after.
Speaker 1 (24:00):
Fantastic. So we've really got an end to end here
from the axon level drug chemistry pH all the way
through equipment techniques, patient safety, ASA complications, emergencies, and even
future trends.
Speaker 2 (24:12):
It's a complex field. Administering local anesthetic is probably the
most common invasive procedure and dentistry, but it's never truly benign.
There are always risks, but.
Speaker 1 (24:22):
Adherence to the principles we've discussed, thorough patient evaluation, understanding
the drugs, meticulous technique like slow injection and aspiration, maybe
utilizing technology like c key lad it all draftically minimizes
those risks.
Speaker 2 (24:36):
That's the goal, predictable, profound and safe pain control.
Speaker 4 (24:39):
Okay, here's a final thought for everyone listening, particularly related
to that parastgia discussion. We know four percent local anesthetics
are widely used, but they carried that statistically higher risk
of nerve issues, especially with blocks. So the practical question
is what step can you take in your practice, maybe
even tomorrow, to ensure you're balancing the need for effective
anesthesia with the standard of care for protecting peripheral nerves.
(25:01):
Is it always about choosing a different drug or could
it be about refining your technique? Something to consider and
to wrap up, here's a quick review exercise based on
today's deep dive. You're treating an ASA three patient with
a history of stable cardiovascular disease. They need about sixty
minutes of pople anesthesia for a crown prep on a
lower molar. Which of these anesthetic options would likely be
the most suitable keeping in mind both efficacy and the
(25:23):
VP limits one point two percent lightocane plane NOVP two
point three percent mepvicane plan NOVP three point two percent
lightokane with one point one hundred thousand epifrine using maybe
one two cartridges, staying under the forty annoining limit. Four
point five percent pupvcane with one point two hundred thousand epinephrine.
Speaker 1 (25:39):
Again respecting the forty r ing gooing limit four per
one point five percent PVV came with one one think
about the need for profound anesthesia to minimize stress, versus
the duration needed versus the strict VP limit for this patient.
We'll let you ponder that one. Thanks for joining us
on the deep dive.
Welcome to the deep dive. Today. We're really digging into
the absolute bedrock of pain control in dentistry local anesthesia.
We've got the textbooks, the core knowledge, and we're going
to break it all down exactly.
Speaker 2 (00:13):
Our mission really is to synthesize this foundational science. We're
talking molecular level stuff right up to the latest clinical protocols.
Speaker 1 (00:21):
Right for everyone listening, especially if you're newer to the field.
This is about connecting the dots why things work, not
just how to do them, from the nerve impulse itself
to keeping patients safe.
Speaker 3 (00:32):
Absolutely, we need to be thorough.
Speaker 2 (00:33):
We're covering nerve structure, how the drugs actually work, the equipment,
the armamentarium, patient evaluation, those crucial ASA classifications, drug interactions.
Speaker 1 (00:42):
Injection techniques, maxillary mandibular, all the supplemental.
Speaker 2 (00:45):
Methods, and importantly, managing complications if things don't go quite
as planned. It's a big picture and every piece matters.
You can't just know the dose limits without understanding why
aspiration is non negotiable.
Speaker 1 (00:57):
Okay, perfect setup. Let's dive right into the very beginning.
How does local anesthetic actually stop that pain signal? I
always like the analogy of water on a lit fuse
heading for dynamite.
Speaker 2 (01:10):
That's a good starting point. The anesthetic is the water,
the nerve impulses the fuze, and the dynamite is the
brain registering pain. But that water needs to get inside
the fuse casing.
Speaker 1 (01:21):
Okay, So talk us through the nerve structure itself.
Speaker 2 (01:23):
Well, you've got the axon, which is the core filled
with axoplasm and it's wrapped in the nerve membrane, the axilemma.
Now for faster nerves, the myelinated ones, they have this
fatty mile in sheaf acting as insulation.
Speaker 1 (01:36):
And the signal jumps between gaps in that sheath.
Speaker 3 (01:38):
Right exactly.
Speaker 2 (01:39):
Those gaps are the nodes of ranvier. The membrane's exposed
there and the impulse leaps from node to node. That
saltatory conduction much faster. But the anesthetic has to work
at that nerve.
Speaker 1 (01:49):
Membrane and getting it there is the challenge. It has
to cross layers, and you mentioned the perinurium is the
main barrier.
Speaker 3 (01:55):
It's the biggest turtle.
Speaker 2 (01:56):
Yeah, And the drug needs to be in the right
chemical form to get through that fatty nerve sheath. The
anesthetic molecule needs to be uncharged lepophilic. That's the free
base form the.
Speaker 1 (02:07):
RN so RN gets it through the door.
Speaker 2 (02:09):
RN diffuses a cross. Once it's inside the axoplasm, where
the pH is pretty stable, around seven point four, those
RN molecules pick up a proton and become positively charged.
Speaker 1 (02:18):
Again.
Speaker 3 (02:19):
That's the cassionic form RNH.
Speaker 1 (02:21):
Plus INN and that's the actusor that's.
Speaker 2 (02:23):
The one that does the work. The RNH plus ion
physically binds to a receptor site inside the sodium channel.
It's like putting a key in the lock and breaking
it off. Sodium ions can't rush in.
Speaker 1 (02:33):
No sodium influx, no depolarization.
Speaker 2 (02:35):
No nerve impulse, pain signal blocked.
Speaker 1 (02:38):
Okay, this immediately brings up something clinically vital. You mentioned
the pH inside is stable, but outside that matters for
getting the RN form in hugely.
Speaker 2 (02:48):
The pH of the surrounding tissue dictates how much of
the drug is in that RN form ready to diffuse.
Speaker 1 (02:53):
And this is where visoconstrictors come in. Chemically speaking, adding
one makes the solution quite acidic, right like pH three point.
Speaker 2 (02:59):
Five compared to maybe six point five for a plain solution. Yes,
significantly more acidic. And that means initially fewer RN molecules
are available to penetrate the nerve sheath.
Speaker 1 (03:11):
So the clinical result is two things.
Speaker 2 (03:13):
First, that initial burning sensation patients sometimes feel. That's often
the acidity. Second, it means a slower onset of anesthesia.
You need to be patient and jack slowly let the
tissue buffer the solutions so more RN can form and
get inside.
Speaker 1 (03:27):
Got it, slow onset potential burn good points. Now let's
think bigger picture systemic effects. Ideally in LA is totally reversible,
low toxicity. Yeah, but it always gets.
Speaker 2 (03:38):
Absorbed eventually, always, every last bit gets into the bloodstream. Yeah,
and how fast depends entirely on where you put it.
Oral absorption pretty poor. Lightikin gets hit hard by the
liver first pass, like seventy two percent wiped out.
Speaker 1 (03:49):
But other roads are faster.
Speaker 2 (03:50):
Oh yeah, tracheal nucosa. It's almost like an IV injection.
Super fast absorption. And when those blood levels climb too high,
LAS start depressing excitable membranes. Thinks C think cardiovascular system,
So what are.
Speaker 1 (04:02):
The warning signs? What do we look for if toxicity
is developing.
Speaker 2 (04:05):
Initially you see CNS excitation. The patient might feel lightheaded, dizzy,
maybe some slurred speech, muscle twitches, tremors. Numbness of the
tongue or around the mouth is a classic early sign.
Speaker 1 (04:17):
And if levels keep rising.
Speaker 2 (04:19):
Then it flips to CNS depression. Seizures might actually stop,
the EG could flatten out, breathing slows down respiratory depression,
and then you start seeing serious cardiac effects.
Speaker 1 (04:30):
Which leads us directly to why we add vasoconstrictors vps.
It's not just about making the numbness last longer. It's
a key safety factor. Can you list those core benefits again?
Speaker 3 (04:40):
Sure?
Speaker 2 (04:41):
Five main reasons. One they constrict blood vessels locally. Two,
this slows down the absorption of the LA into the.
Speaker 1 (04:47):
Bloodstream, lowering the peak blood level.
Speaker 2 (04:49):
Exactly, which number three drastically cuts the risk of systemic toxicity.
Four slower absorption means the LA stays at the nerve longer,
so you get increased duration in depths of anesesia. And
five for surgery, that vasoconstriction means less bleeding hemostasis.
Speaker 1 (05:04):
Okay. These vps are sympathomometic, mimicking adrenaline and nor adrenaline.
They act on specific receptors elfin beta correct.
Speaker 2 (05:12):
Alpha receptors primarily cause that vasoconstriction we want. Beta receptors
are more complex. Beta one stimulates the heart, Beta two
causes vasodilation in some areas and importantly bronchodilation.
Speaker 1 (05:24):
And different vps hit these receptors differently.
Speaker 2 (05:26):
Right, like norpinefrin, it doesn't have much beta two actions,
so you get really intense peripheral vasoconstriction. Oh. In an
interesting side note, cocaine is the only LA that always
causes vasoconstriction itself because it blocks nora pineffrine reuptake.
Speaker 1 (05:39):
Fascinating. Let's talk dosage in dilutions. This math has to
be second nature. A one to one hundred thousand dollars dilution,
how much drug is.
Speaker 2 (05:47):
That permeli leader that's zero point zero one milligrams per
milileader or often easier to think in micrograms ten micrograms
per mL. Knowing this is crucial for calculating safe limits.
Speaker 1 (05:58):
So what are those limits? For epinephron the common VP
for a.
Speaker 2 (06:01):
Healthy adult patient, the maximum recommended dose is zero point
two milligrams, which is two hundred micrograms.
Speaker 1 (06:07):
Okay, two hundred micrograms for healthy but for someone with
cardiovascuar issues. Maybe an ASA class three or fall.
Speaker 2 (06:12):
That limit drops sharply. It's only zero point zero four
milligrams or forty micrograms.
Speaker 1 (06:17):
That's a big difference, and this is important. Some might
think any epinephrine is bad for these patients, but you're
saying using a small, controlled amount within that forty microgram
limit might actually be safer than using a plain.
Speaker 2 (06:28):
LA that fails often, yes, because if the plane LA
doesn't achieve profound anesthesia, the patient gets stressed, maybe feels pain,
and their body releases its own catecholamines, its own adrenaline.
That endogenous release can be way higher and much less
controlled than the tiny amount we inject.
Speaker 1 (06:49):
So successful, stress free anesesia is the goal, and sometimes
a limited VP dose is the best way to achieve that,
even in an ASA three patient. Just stick rigorously to
that forty microgram limits.
Speaker 3 (07:00):
Precisely, it's about risk management, right.
Speaker 1 (07:02):
We've covered the chemistry, the safety limits. Let's move to
the tools, the armamentarium. The classic aspirating syringe. That palm
thumb grip not always the easiest to control, is it No?
Speaker 2 (07:12):
Ergonomically it's not ideal, which is why the development of
computer control local anesthetic delivery systems. The CEA slids like
the wand or STA system back in ninety seven, was
such a step forward.
Speaker 1 (07:22):
How do they help?
Speaker 2 (07:23):
They allow a pen like grasp, much more like how
you'd hold an explorer or a scaler. It gives you
fingertip control and accuracy. Plus the machine controls the flow rate,
keeps it slow and consistent.
Speaker 1 (07:34):
So the operator can just focus on needle placement and
angulation exactly.
Speaker 2 (07:38):
It takes one variable out of the equation and generally
leads to a more comfortable injection for the patient because
the pressure is managed set.
Speaker 1 (07:45):
Peak of needles. I find it amazing that patients apparently
can't tell the difference between a twenty five, twenty seven
or thirty gauge needle in mucous membrane. So why the
preference for twenty five or twenty seven gage for deeper
blocks like the IAMB.
Speaker 2 (07:59):
It really comes down to aspiration. The larger lumen of
the twenty five or twenty seven gauge makes aspiration pulling
back to check for blood more reliable than with a
thirty gauge.
Speaker 3 (08:08):
You get a truer reading the needle.
Speaker 1 (08:09):
Safety Yeah, huge topic. What are the absolute must know rules.
Speaker 2 (08:13):
Number one, Never ever insert the needle all the way
to the hub. That's the weakest point. If it's going
to break, it'll likely break there. Leaving some needle visible
is crucial.
Speaker 1 (08:23):
Okay, never to the hub. What us?
Speaker 2 (08:24):
Never change the direction of the needle while it's deeply
embedded in tissue. If you need to redirect, withdraw it
almost completely first, then re angle and advance again. Trying
to bend it inside tissue puts huge stress.
Speaker 1 (08:37):
On it, and gauge relates to breakage risk too.
Speaker 2 (08:40):
Yes, physics tells us the smaller diameter needles the thirty
and twenty seven gage are statistically more likely to break
than a twenty five gauge needle.
Speaker 1 (08:48):
Got it. Let's look inside the cartridge itself. Standard is
about one point eight millimel, though some manufacturers list one
point seven milimel. We know it has the LA drug
maybe a VP. What else is in there?
Speaker 2 (08:59):
Distilled water as the vehicle and sodium chloride to make
the solution isotonic with the body tissues reduces.
Speaker 1 (09:05):
Irritation, and if there's a vasoconstrictor.
Speaker 2 (09:07):
Then you must have an antioxidant preservative, usually sodium bisulfite.
That's what gives the cartridge its shelf life maybe eighteen months,
but it's also what makes the solution acidic.
Speaker 1 (09:16):
Bringing us back to that pH point again, the bisulfite
lowers the pH causing potential burning and slower onset.
Speaker 3 (09:23):
Correct.
Speaker 2 (09:24):
Oh and one thing that used to be in cartridges
was methyl parabin another preservative, but it caused some allergy issues,
so it was removed from single use dental cartridges back
in nineteen eighty four.
Speaker 1 (09:34):
Good historical note. Okay, all this leads into the actual
process of giving a shot. The a traumatic injection protocol.
This isn't just about technique, it's a systematic approach.
Speaker 2 (09:44):
Absolutely starts with using a sharp sterile needle. Check it
for barbs, maybe on gauze, Identify your target site.
Speaker 1 (09:51):
Then prep the tissue, yes.
Speaker 2 (09:52):
Dry it thoroughly with gauze first. Then apply your topical anesthetic.
And here's a key point, leave it on for a minute,
not ten or fifteen seconds. A full minute is needed
for it to really work on the surface layers. Topical
antiseptic is optional.
Speaker 1 (10:07):
After that, okay, minute of topical, then.
Speaker 2 (10:09):
What stabilize your hand? Stabilize the syringe, don't rest it
on the patient's arm or shoulder that introduces movement, Advance
the needle slowly into the tissue.
Speaker 1 (10:18):
And for block injections like the IAMB or.
Speaker 2 (10:20):
Infurbital, deposit just a few drops of anesthetic before you
anticipate contacting the periostium. That's sensitive bone lining it numbs
the area ahead of the needle tip makes sense. Then
the critical safety steps asprit pull back gently on the plunger,
do it in at least two planes, meaning rotate the
bevel slightly, and aspirate again. This confirms you're not inside
(10:42):
a blood vessel. Essential, especially with those larger gauge needles
in vascular areas.
Speaker 1 (10:47):
Absolutely critical. And the final.
Speaker 2 (10:49):
Step deposit the solutions slowly. A milliter per minute is
a good benchmark. Too fast causes pain, can tear tissues,
leading to soreness later, and drastically increases the risk of
a toxic reaction if you did happen to be intravascular
despite aspiration. Slow injection is paramount.
Speaker 1 (11:07):
Okay, excellent breakdown of the technique. Now let's shift focus
from the needle to the person holding it, the patient evaluation,
medical history dialogue. This is an optional right.
Speaker 2 (11:17):
It's a moral and legal necessity. You have to know
who you're treating. Using comprehensive medical history forms like the
standard UOP or met life ones and actually talking to
the patient about their health is fundamental and a key.
Speaker 1 (11:29):
Part of that assessment is using the ASA Physical Status classification.
Can you quickly recap that?
Speaker 4 (11:34):
For us?
Speaker 2 (11:34):
Sure, it's a scale from one to six, but clinically
we mainly focus on one through four. ASAS one is
a normal, healthy patient, ASA two has mild systemic disease,
maybe well controlled diabetes or hypertension, or perhaps extreme anxiety
about dentistry.
Speaker 1 (11:49):
Okay, ASA two is mild disease or significant anxiety. What
about three?
Speaker 2 (11:54):
ASA three means severe systemic disease that limits their activity,
but isn't incapacitating stable angina, a heart attack more than
six months ago, maybe poorly controlled hypertension COPD.
Speaker 1 (12:05):
So definite limitations. Yeah, An ASA.
Speaker 2 (12:08):
Four that's severe systemic disease that's a constant threat to life,
maybe unstable angina, recent heart attack or stroke, severe heart failure,
and stage renal disease. These patients often need treatment in
a hospital setting. Knowing the ASA class directly impacts our
treatment plan, especially our vasoconstrictor use.
Speaker 1 (12:24):
Right. Tying back to those dose limits, let's revisit a
couple of specific conditions you mentioned ASA two or three.
Heart failure patients often need good pain control, and VPS
used carefully can help achieve that. What about lung conditions.
Speaker 2 (12:35):
Patients with significant emphysema maybe ASA three or four rely
on what's called a hypoxic drive to breathe. Giving them
too much supplemental oxygen, say more than three liters per minute,
can actually knock out that drive and potentially cause respiratory arrest.
So caution with oxygen is needed.
Speaker 1 (12:53):
Good point. And while we're on patient factors allergies, how
common is a true allergy to a mid local anesthetic
like latyicane or articane.
Speaker 2 (13:02):
Virtually nil? It's incredibly rare. Most reported novocane allergies remember
novocane was an ester different class or even allergies to
modern amides turn out to be something else like way.
Often it's a psychogenic reaction, feinting due to fear or
perhaps mild ob of symptoms that were misinterpreted as allergy.
True IgE mediated anaphylaxis to an amid la is almost
(13:24):
unheard of.
Speaker 1 (13:25):
Okay, that's crucial context. Let's hammer down the most important
drug interactions we need to worry about, specifically with vasoconstrictors.
Speaker 2 (13:31):
Top of the list has to be tricyclic antidepressants TCAs,
things like amatrypto line. They can seriously potentiate the effects
of vasoconstrictors with levinordifrin or neropaneffern it could be a
five to ten fold enhancement of press to effects with
epanephrine maybe about twofold. The clinical advice is clear avoid
levenordifran and norpinifrin completely. Impatients on TCAs limit up an
(13:55):
effort strictly, maybe to that point zero four or point
zero five milligram dose range.
Speaker 1 (14:00):
TCAs are a big one.
Speaker 2 (14:01):
What else non selective beta blockers like propranolol. If you
give a patient on propranolol a vasoconstrictor like epinephrine, the
beta blocker prevents the vasodilation effect beta too, leaving the
alpha receptor vasoconstriction unopposed, resulting in potentially a sharp rise
in blood pressure and then a reflex slowing of the
heart rate bradycardia. It can be dangerous. Careful dose limitation
(14:23):
of epinephrine is needed here too.
Speaker 1 (14:25):
What about MAO inhibitors used to be a big contraindication.
Speaker 2 (14:28):
Yeah, that's changed. More recent evidence suggests that the typical
vasoconstrictors used in dentistry Epinepherne, levener de friend nor panfrin
don't actually cause a hypertensive crisis in patients taking MAOIs.
So that's less of a concern now than previously thought.
Speaker 1 (14:41):
Good update. How about malignant hyperthermia MH. They used to
be an absolute no for a my DA.
Speaker 3 (14:47):
LA's also updated.
Speaker 2 (14:49):
It's now generally considered a relative contraindication. Importantly, MH has
never actually been triggered when an amid local anesthetic was
the only drug given. The consensus is that 'ides are
likely safe, but consultation with the patient's physician is still wise.
Speaker 1 (15:04):
Okay. One more specific toxicity methemoglobinemia. What causes that?
Speaker 2 (15:09):
This one is primarily associated with prelocaine and also sometimes
benzicane topical It's caused by a metabolite called orthotoluidine.
Speaker 1 (15:18):
It's dose related and the signs are quite distinctive.
Speaker 2 (15:20):
Yes, it usually shows up maybe three to four hours
after the drug was given, the patient becomes lethargic, might
have trouble breathing, looks cyanotic, kind of bluish, But crucially,
the cyanosis doesn't improve much with oxygen. If you drew
arterial blood, it would look chocolate brown.
Speaker 1 (15:35):
And the treatment is specific too.
Speaker 2 (15:36):
Very specific. Slow intravenous administration of methylene blue is the antidote.
You need to recognize it and know the treatment protocol.
Speaker 1 (15:44):
Moving from risks to actual practice, choosing the right drug
and technique duration is key. Liticane two percent with one
point one hundred zer an epi gives about sixty minutes
of pople anesthesia.
Speaker 2 (15:55):
Roughly yes, and maybe three to five hours of soft
tissue numbness. Compare that to boop of a cane zero
point five percent with one point two hundred thousand epi
that gives you ninety minutes, maybe even up to one
hundred and eighty minutes of polple and soft tissue anthesia
for four to nine hours, much longer acting.
Speaker 1 (16:14):
So using that long acting boop of a gane for
just say a single filling that takes twenty minutes probably overkill.
Speaker 2 (16:21):
Absolutely, you're leaving the patient profoundly numb for hours longer
than needed, increasing that risk. We talked about self inflicted
injury to the lipper tongue, especially in kids or patients
who might not understand. Choose the drug that fits the
procedures required.
Speaker 1 (16:34):
Duration makes sense. Let's talk specific injection techniques. Maxillary first
infiltration the superperio steel injection is common, but maybe not
for multiple teeth.
Speaker 2 (16:44):
Right, it's great for one or two teeth. For molars,
we often use the posterior superior alveolar block, the PSA,
but it's got that well known quirt miss.
Speaker 1 (16:51):
Is the mesiobucle route of the first molar in a.
Speaker 3 (16:53):
Fair number of people, about twenty eight percent of the time.
Speaker 2 (16:55):
Yeah, the nerve supply sometimes comes from a different branch.
That's where supplemental infiltration might be needed.
Speaker 1 (17:00):
Are there other maxillary options, maybe for anterior teeth without
numbing the face.
Speaker 2 (17:05):
Yes, the more advanced palatal approaches, the AMSA anterior and
middle superior alveolar and the pasa palatal approach anterior superior
alveolar blocks.
Speaker 3 (17:15):
They can numb in.
Speaker 2 (17:16):
Sizors, canines, premolars, and the associated palatal tissue all from
a palatal injection site. Great for esthetic work where you
don't want lipdroop.
Speaker 1 (17:24):
And the nesicipalatine block for the anterior palet, known for
being a bit spicy.
Speaker 2 (17:28):
Can be uncomfortable, yes, but slow injection is key and
you only need a tiny amount like zero point three
milli mile usually does the trick for broad bilateral anesthesia
of the anterior palette.
Speaker 1 (17:39):
Okay, let's tackle the mandible. The big one is the
inferior alveolar nerve block, the IAANB, but it's notoriously unreliable.
Speaker 2 (17:47):
Sometimes it has the highest failure rate of any common block. Unfortunately,
success rates vary in the literature, but missing isn't uncommon. Plus,
it has that high positive aspiration rate maybe ten fifteen percent,
meaning you hit a blood vessel farly often.
Speaker 1 (18:00):
Which is why alternatives are so important.
Speaker 2 (18:02):
The Gaugates technique the Gugate's mandibular nerve block. Yes, it's
a true V three block, aiming higher up, closer to
the mendibular foreman. It anesthetizes almost all the branches of
mendibular nerve, inferior alveolar, lingual buckle, mylohyoid, auricular, temporal, and
the benefits much higher success rate. Often cited above ninety
(18:22):
five percent and a significantly lower positive aspiration rate maybe
around two percent. Because your higher up away from the
main vessels accompanying the.
Speaker 1 (18:31):
Ann so higher success, lower risk seems like a strong contender.
What about numbing just one tooth without widespread numbness.
Speaker 2 (18:38):
That's where supplemental technique shine. The periodontal ligament injection or
PDL injection, also intriossious IO injection directly into the cancellus
bone and intraceptal injection into the interdental septum.
Speaker 1 (18:50):
These give very localized anesthesia exactly.
Speaker 2 (18:53):
Single tooth may be adjacent soft tissue, but minimal lip
or tongue numbness. Great for isolated procedures or when bilateral.
Speaker 1 (18:59):
Blocks are and technology helps here too.
Speaker 2 (19:01):
Definitely, the c clad systems like the STA are really
advantageous for PDL and IO injections. They control the pressure
and flow rate very precisely. The SDA system even has
dynamic pressure sensing technology that helps guide the operator to
the optimal injection site in the PDL space, improving success
and comfort.
Speaker 1 (19:21):
What about that last resort, the intrapulple injection when nothing else.
Speaker 2 (19:25):
Works, usually for the hot tooth often a mandibular molar.
You drill into the pulp chamber and deposit directly. It
works partly by the drug action, but also significantly by
the applied pressure. It causes brief intense pain, followed almost
immediately by profound anesthesia. It's effective, but definitely a last resort.
Speaker 1 (19:45):
Okay, let's round this out by discussing complications. What can
go wrong? Parasgia seems to be a big concern.
Speaker 2 (19:50):
Parasesia persistent numbness or altered sensation lasting beyond the expected
duration of the anesthetic. It's distressing for patients. The lingual
nerve is involved in the vast majority of reporting cases,
maybe ninety percent.
Speaker 1 (20:01):
Is there an association with certain drugs.
Speaker 2 (20:04):
There's a statistically higher incidence reported with the four percent
local anesthetics, specifically arcticane and prelocane, compared to lower concentrations
like two percent lytocine. The thinking is it might relate
to the higher concentration itself potentially being neurotoxic to the
nerve fibers, especially if injected directly into the nerve bundle.
Speaker 1 (20:24):
That's a really important point for drug selection, especially for iambs.
What other common complications trismus.
Speaker 2 (20:30):
That's muscle soreness or limited opening. Basically a spasm of
the jaw muscles, usually mild after an imb maybe from
muscle trauma by the needle, managed with heat, gentle stretching,
maybe some anti inflammatories.
Speaker 3 (20:43):
Usually resolves in a few days.
Speaker 2 (20:44):
Ebaituma bruising happens when a blood vessel is nicked, most
common after the PSA block because of the vascular plexus
back there. Best management is immediate pressure applied to the
area for several minutes. It can look dramatic, but usually
resolves on its.
Speaker 1 (20:57):
Own overtime and fatal paralysis for the patient.
Speaker 2 (21:01):
Transient facial nerve paralysis hitting CMBF. This happens if you
inject anesthetic into the parotid gland, usually by inserting the
needle too far posteriorly during an IAANB or maybe a
vasiraniaknosi block. Its temporary lasts as long as the anesthetic,
but very alarming, preventable by adhering strictly to anatomical landmarks
and depth limits.
Speaker 1 (21:21):
Okay, last critical area managing emergencies. Let's reemphasize the difference
between overdose.
Speaker 2 (21:26):
And allergy, absolutely crucial distinction overdose is dose related. It
happens because the blood level of the drug gets too
high too fast. Allergy is not dose related, it's an
immune response. Even a minuscule amount can trigger a reaction
in a sensitized individual.
Speaker 1 (21:41):
How do we manage a mild to moderate overdose that
develops slowly?
Speaker 2 (21:45):
Basic life support is key. Position the patient comfortably administer oxygen,
provide reassurance, monitor vital signs. Most reactions are self limiting
as the drug redistributes and is metabolized. If seizures occur
in are prolonged, say four or five minutes, then an
anticondulcant like mitazolum might be needed, but only if you're
trained in its administration and advanced airway management.
Speaker 1 (22:07):
And allergy management. Especially the worst case anaphylaxis.
Speaker 3 (22:11):
Speed is everything.
Speaker 2 (22:12):
If you see signs of a severe, rapidly progressing allergic reaction,
difficulty breathing, hive spreading, drop in blood pressure, the primary
treatment is immediate epinephrine.
Speaker 1 (22:22):
What dosin root usually zero.
Speaker 2 (22:24):
Point three milligrams of one point one zero zero zero epinephrine,
given intramuscularly or subcutaneously for an adult, repeat every five
to fifteen minutes as needed, then basic life support, oxygen
call for emergency medical services. You might administer histamine, walkers
and corticosteroids later, but epinephrine is the first line life
(22:44):
saving drug.
Speaker 1 (22:45):
And just to be absolutely clear, is there any absolute
contraindication to using epinefin in a true anaphylactic emergency.
Speaker 2 (22:52):
Now, in the context of anaphylaxis, the benefits of epinephrine
far outweigh any potential risks. It's the drug of choice, period,
powerful reminder.
Speaker 1 (23:00):
Okay, looking ahead briefly, what are some key trends or
advancements changing practice?
Speaker 2 (23:04):
Well, two things stand out recently. One is the increasing
acceptance and evidence supporting the use of articane, that four
percent drug for simple infiltration anesthesia for mandibular posterior teeth
and adults potentially avoiding the IAANB for some procedures.
Speaker 1 (23:19):
Interesting infiltration instead of a block in the mandible.
Speaker 3 (23:23):
Yeah.
Speaker 2 (23:24):
And the other the development of a local anesthetic reversal
agent phantolamine mesylate brand name or VERSE. It's an alpha
adrinergic blocker.
Speaker 1 (23:33):
So it counteracts the vasoconstrictor.
Speaker 2 (23:34):
Exactly, it counteracts the epi or levo, allowing blood flow
to return to the area more quickly, which washes the
anesthetic away faster. It significantly speeds up the return of
normal soft tissue sensation, lip tongue numbness goes away much quicker.
Speaker 1 (23:48):
That seems huge for patient comfort and reducing that risk
of accidental biting, especially in kids.
Speaker 2 (23:53):
It's a major benefit, particularly in pediatric dentistry or for
patients having procedures before needing to speak or eat soon after.
Speaker 1 (24:00):
Fantastic. So we've really got an end to end here
from the axon level drug chemistry pH all the way
through equipment techniques, patient safety, ASA complications, emergencies, and even
future trends.
Speaker 2 (24:12):
It's a complex field. Administering local anesthetic is probably the
most common invasive procedure and dentistry, but it's never truly benign.
There are always risks, but.
Speaker 1 (24:22):
Adherence to the principles we've discussed, thorough patient evaluation, understanding
the drugs, meticulous technique like slow injection and aspiration, maybe
utilizing technology like c key lad it all draftically minimizes
those risks.
Speaker 2 (24:36):
That's the goal, predictable, profound and safe pain control.
Speaker 4 (24:39):
Okay, here's a final thought for everyone listening, particularly related
to that parastgia discussion. We know four percent local anesthetics
are widely used, but they carried that statistically higher risk
of nerve issues, especially with blocks. So the practical question
is what step can you take in your practice, maybe
even tomorrow, to ensure you're balancing the need for effective
anesthesia with the standard of care for protecting peripheral nerves.
(25:01):
Is it always about choosing a different drug or could
it be about refining your technique? Something to consider and
to wrap up, here's a quick review exercise based on
today's deep dive. You're treating an ASA three patient with
a history of stable cardiovascular disease. They need about sixty
minutes of pople anesthesia for a crown prep on a
lower molar. Which of these anesthetic options would likely be
the most suitable keeping in mind both efficacy and the
(25:23):
VP limits one point two percent lightocane plane NOVP two
point three percent mepvicane plan NOVP three point two percent
lightokane with one point one hundred thousand epifrine using maybe
one two cartridges, staying under the forty annoining limit. Four
point five percent pupvcane with one point two hundred thousand epinephrine.
Speaker 1 (25:39):
Again respecting the forty r ing gooing limit four per
one point five percent PVV came with one one think
about the need for profound anesthesia to minimize stress, versus
the duration needed versus the strict VP limit for this patient.
We'll let you ponder that one. Thanks for joining us
on the deep dive.
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