Chapter 13: Ears & Nose

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Welcome back to the Deep Dive.

Today we are opening the medical bag and pulling out something that, you know, it looks a bit like a flashlight but is actually a window into the brain, the system in the senses.

It really is.

We are tackling chapter 13, a Bates guide to physical examination and history taking.

Specifically, we are zooming in on the ears and the nose, and I know listeners might be thinking, okay, ears and noses, I have them, I see them, how hard can this possibly be?

That was exactly my first thought.

I mean, I really thought this was going to be a quick skim, but as we went through this text and I really combed through it, I realized this isn't just about, you know, looking for earwax or handing out tissues for a runny nose.

Not at all.

This is about mastering the machinery of how we sense the world.

It really is.

The level of, like, engineering in the ear alone is mind -blowing, and the mission for this deep dive is very specific.

We are imagining that you, the listener, are stepping into the white coat.

Maybe you're a medical student prepping for boards, a nursing student about to touch your first patient, or just someone fascinated by how clinical reasoning actually works.

We aren't just listing facts here.

We are going to walk through the text exactly as Bates presents it.

We're going to build the anatomy, then learn the detective work of the history, then master the physical skills, and finally learn how to write it all down so you don't look like an amateur in the medical chart.

Precisely.

It's a walkthrough of how to think like a clinician.

We want to get you to the point where you aren't just looking at an ear, you're looking into the physiology and the history of the patient.

So here is our roadmap for the hour.

We're going to start with the hardware, the anatomy, and physiology, because you don't know how the machine is built.

You can't fix it.

Makes sense.

Then we move to the health history.

That's the interview.

And that is where you ask the questions that differentiate a simple cold from something, you know, much more serious.

A brain tumor, even.

It's high stakes.

Then the otoscope, the tuning forks, and the specific techniques.

Like why pulling the ear a certain way makes all the difference between seeing the eardrum and staring at a wall of skin.

And we will wrap up with recording findings and health promotion, because if you didn't write it down, it didn't happen.

And we need to talk about the vital importance of screening for hearing loss.

All right, let's dive right in.

Section one, the anatomy and physiology of the ear.

Now, Bates breaks this down into three compartments.

The external ear, the middle ear, and the inner ear.

Let's start with what we can see.

The external ear.

So the visible part that we usually just call the ear is technically the auricle or pinna.

It's mostly cartilage covered by skin.

It should feel firm and elastic.

And you really need to know the landscape here, right?

Just to document where a lesion is or something.

Absolutely.

You can't just say a bump on the ear.

So you have the helix.

That's the curved outer ridge.

The rim, basically.

The part you'd get pierced at the top.

Exactly.

And then running parallel to that, curving inside it is the antihelix.

And down at the bottom, the fleshy part we're all familiar with, the lobule or earlobe.

The lobule is interesting because it's the only part of the auricle that has no cartilage, right?

It's just soft tissue.

Correct.

It's just skin and fat.

But there is one little landmark that is absolutely crucial for the exam later.

The tragus.

The tragus.

Okay, describe this for us because this becomes a button we push later, doesn't it?

It absolutely does.

The tragus is that little nodular protrusion that points backward, sort of protecting the entrance to the ear canal.

It's right in front of the hole.

Remember that name because pressing on the tragus is a key diagnostic test for infection.

Got it.

Okay.

So from there,

let's travel inward.

We enter the ear canal itself.

Bates notes it's about 24 millimeters long,

but it's not a straight shot, is it?

No.

And this is so vital for the physical exam.

The canal has an S shape.

It curves inward, downward, and anteriorly.

If you just look straight in with a light, you're going to hit the wall of the canal.

You won't see anything.

You'll see nothing.

You have to mechanically straighten it out to see the end.

There was a detail here about the texture of the canal that I found really practical.

I mean, the canal isn't made of the same stuff all the way down.

This is the don't hurt your patient rule.

The outer one third of the canal is cartilage.

It's basically an extension of the auricle.

That's where the hair is.

That's where the cerumen glands are that produce earwax.

So the outer part is hairy and waxy.

Got it.

Right.

And the skin there is relatively thick, but the inner two thirds, that is bone.

It's actually a tunnel through the temporal bone of the skull.

And it is lined by very, very thin skin.

There are no hair follicles or wax glands there.

So why does this matter so much for the clinician?

Because the skin on that bone is incredibly sensitive.

If you jam a hard plastic speculum into that bony intersection, or if you scrape it while trying to remove wax, you are going to cause your patient significant pain.

It can even trigger a cough reflex sometimes, or just sharp, intense pain.

Okay.

So the rule is be really, really gentle in the deep end.

Got it.

So at the end of this canal, we hit the wall, the tympanic membrane, the eardrum.

Correct.

The eardrum marks the border.

It separates the external ear from the next section, the middle ear.

And this brings us to our second compartment, the middle ear.

This isn't fluid filled, right?

It's an air -filled cavity.

Ideally, yes, it is an air -filled cavity in the temporal bone.

And inside we have those famous tiny bones, the ossicles.

The malleus, the incus, and the I remember these from biology class.

The hammer, the anvil, and the stirrup.

Exactly.

And their job is mechanical transformation.

They take the sound vibrations hitting the eardrum and turn them into mechanical waves.

They act as a lever system to amplify the force so it can push into the inner ear.

Now, when we are looking through the otoscope, we aren't seeing the sapes usually.

It's tucked away.

But we are definitely looking for the malleus.

Oh, absolutely.

The malleus attaches directly to the center of the eardrum.

When you look at a healthy eardrum, you see the handle of the malleus.

And at the tip of that handle is the umbo.

That's the center point where the drum is pulled inward.

And from that umbo, we look for a specific reflection, the cone of light.

The cone of light is a key landmark.

It's just a reflection of your otoscope bulb.

But it fans downward and anteriorly from the umbo.

If the eardrum is in the correct position, that light is crisp.

If the eardrum is bulging out or sucked in, that light gets scattered or moves.

It's a huge clue that something is wrong with the pressure in there.

Bates also mentions the pars flaccida and pars tensa.

What's that about?

Right.

The pars flaccida is a small portion of the eardrum above the short process of the malleus.

As the name suggests, it's a bit lax, a bit floppy.

The pars tensa is the rest of the drum, which is, well, tense.

And it's the part that vibrates for hearing.

Okay.

Before we leave the middle ear, we have to talk about the plumbing, the eustachian tube.

Critical structure.

It connects the middle ear to the back of the throat, the nasopharynx.

Its job is to equalize pressure.

You know when your ears pop on a plane?

Yeah, of course.

That's your eustachian tube opening to let air in or out to match the cabin pressure.

And it drains mucus too, right?

It does.

But if that tube gets blocked, say, from a cold or allergies,

the air in the middle ear gets absorbed by the body,

a vacuum forms, and fluid gets pulled out of the surrounding tissue.

That's how you get fluid behind the ear.

Which is the setup for an ear infection.

Exactly.

It's a drainage problem.

Okay.

Moving deeper.

The inner ear.

The command center.

This is buried deep in the bone.

It is.

It's the labyrinth.

And it houses two distinct systems.

You have the cochlea, which is snail -shaped and dedicated to hearing.

And you have the semicircular canals and otolith organs, which are all about balance and equilibrium.

And this is where the physics gets cool.

The steve's bone vibrates the oval window, which sets the liquid that the perilymph inside the cochlea into motion.

Right.

And that moving liquid bends microscopic hair cells.

Those hair cells are the transducers.

They turn that mechanical bending into an electrical spark.

And that electricity travels via cranial nerve eight.

The vestibulocochlear nerve.

It takes that signal to the brain, which then interprets it as music or speech or, you know, car horn.

Now Bates makes a big distinction here that sets up everything we do in the physical exam later.

The difference between the conductive phase and the sensor neural phase.

We really need to unpack this.

This is fundamental.

Think of hearing as a relay race.

The first leg is the conductive phase.

That involves the external ear catching the sound, the canal funneling it, the eardrum vibrating and the ossicles pushing.

It's all mechanical.

It's moving parts.

So if I have a glob of wax blocking my canal or a hole in my eardrum or fluid stopping the bones from moving.

That is a conductive hearing loss.

The mechanism is broken or blocked.

The sound isn't getting conducted to the nerve.

Okay.

And the second leg of the race.

The sensor neural phase.

This involves the cochlea sensing the wave, the nerve carrying the signal and the brain interpreting it.

If you have damage to the hair cells from loud noise or aging or a tumor pressing on the nerve.

That is sensor neural loss.

The nerve or the sensor is the problem.

Precisely.

And we also need to understand the two pathways sound can take.

Air conduction versus bone conduction.

Air conduction seems obvious.

Sound traveling through the air.

Right.

It goes through the canal and the middle ear.

This is the normal most sensitive way we hear.

But sound can also vibrate the skull itself and bypass the middle ear entirely stimulating the cochlea directly.

That's bone conduction.

Which explains why my voice sounds deeper to me than it does on a recording.

I'm hearing the bone vibrations in my own head.

Exactly.

You're hearing a mix of both.

In a normal exam, air conduction should always be much more efficient, much better than bone conduction.

We write that as ACBC.

If that flips or if the balance changes, it tells us exactly where the problem is.

And we will get to testing that with the tuning forks later.

But for now, let's shimmy over to the nose and sinuses.

Section two of our anatomy.

Okay.

The nose.

Structurally, it's a mix of materials.

The upper third is bone.

If you grab the bridge of your nose, that hard part, that's bone.

The lower two thirds, that's cartilage.

It's flexible.

And inside, we have the vestibule, that widened area just inside the narrus.

Bates points out that this is lined with hair bearing skin, unlike the rest of the nasal cavity, which is mucous membrane.

Right.

And then you hit the perbinates.

I love the engineering of the turbinates.

They're just so elegant.

These are the bony shelves, right?

The little curved things on the side.

Yes.

You have three on each side,

superior, middle and inferior.

They curve out from the lateral walls.

They're covered in a very vascular mucous membrane, meaning they have a ton of blood flow.

What is their actual function?

Why are they there?

Think of them as the radiator or the HVAC system of the face.

They increase the surface area dramatically.

As air rushes in, it hits these shelves and gets tumbled around.

The turbinates clean the air, humidify it, and warm it up to body temperature before it hits your delicate lungs.

That makes perfect sense.

And below each turbinate is a groove called a metis.

And the metis is all about drainage.

The nasolacrimal duct, which drains tears from your eyes, empties into the inferior metis.

So that's why your nose runs when you cry.

That's exactly why.

You're literally crying into your nose.

And the sinuses, where do they drain?

The paranasal sinuses drain into the middle metis.

And this is a huge clinical point.

If that metis gets swollen shut, say, from a cold, the sinuses can't drain, and you get sinusitis, it's a plumbing problem again.

Speaking of sinuses, these are air -filled cavities in the skull.

We have four pairs,

maxillary, ethmoid, frontal, and sphenoid.

But clinically, we can't really touch all of them, can we?

No, not at all.

In a routine physical exam, only the frontal sinuses, which are above the eyebrows, and the maxillary sinuses, which are in the cheekbones, are accessible.

The ethmoid and sphenoid are deep inside the skull.

We can't palpate them directly.

All right, we've built the machine.

We know the parts.

Now let's talk about the detective work.

Section 3, the health history of the ear.

As with everything in Bates, it starts with the opening question.

You don't just jump to, do your ears hurt?

You start broad.

How is your hearing?

Or have you had any trouble with your Simple but effective.

Bates lists the big symptoms we need to track.

Hearing loss, tinnitus, otorhea, otalgia, and vertigo.

Let's break these down, starting with hearing loss.

If a patient says they have hearing loss, your antenna needs to go way up.

You need to clarify.

Is it in one ear or both?

And maybe more importantly, was it sudden or gradual?

Why is the timing sudden versus gradual so critical?

Because sudden sensor neural loss in one ear is a medical emergency.

It could be a viral attack on the nerve or a vascular clot cutting off blood supply.

If you treat it with high dose steroids immediately, you might save the hearing.

If you wait, it's often permanent.

That's a huge red flag then.

Massive.

And we can actually get clues about the type of loss just from the history.

This part was really interesting to me.

It is.

Ask the patient about their environment.

If a patient has sensor neural loss nerve damage, they often have trouble understanding speech, they'll say people are mumbling, and interestingly, noisy environments make it worse.

Right, the cocktail party effects.

They can't filter out the background noise to hear the voice they want to focus on.

Exactly.

Now contrast that with conductive loss, like a wax plug or fluid.

If you have a conductive blockage, background noise might actually help them hear.

Wait, how does noise help?

That seems so backwards.

Well, think about it.

If the room is noisy, people tend to talk louder, right?

The blockage in the patient's ear acts like a natural ear plug, dampening the background chaos, but the louder speech punches through.

So paradoxically, they might hear better in a noisy room than someone with nerve damage.

That's a great clinical pearl.

We also need to ask about medications.

I didn't realize how many common drugs are ototoxic damaging to the ear.

Oh, absolutely.

You need to review the med list.

Aminoglycosides like gentamisin are famous for this.

Chemotherapeutic agents like cisplatin can cause permanent damage, but even common things like aspirin or NSAIDs like ibuprofen can cause temporary hearing loss or tinnitus if taken in high doses.

Let's talk about ERAC.

The medical term is otalgia and discharge or otorrhea.

If there is pain, you have to cast a wide net.

Ask about associated symptoms, fever, sore throat, cough.

If those are present, it's likely an upper respiratory infection that's spreading to the ear.

We also try to differentiate the location of the pain.

How do we do that with just questions?

You can ask where it hurts.

If it hurts in the external canal when they touch it, it's likely otitis externa swimmer's ear.

If it's a deep throbbing pain inside their head, it's more likely otitis media, a middle ear infection.

And the discharge.

Look at the color and consistency.

Yellow -green usually signals infection.

It could be from the canal itself, or it could be a perforated eardrum where the pus from the middle ear is finally leaking out.

Now on to tinnitus and vertigo.

Tinnitus is that ringing, rushing, or roaring sound with no external source.

It's incredibly common, especially as we age.

But you have to ask about the pattern.

If tinnitus is accompanied by fluctuating hearing loss and vertigo, you have to suspect Meniere disease.

That's a classic triad of symptoms.

Vertigo.

Okay, this is a term that gets thrown around loosely in casual conversation, but Bates is very, very strict about the definition.

Very strict.

And this is a huge stumbling block for students.

Patients will say, I'm dizzy.

You cannot just write down dizziness.

You have to ask, what do you mean by dizzy?

So what are the options?

What are they really feeling?

What you need to find out?

Do they feel like the room is spinning around them or like they are spinning?

That is vertigo.

True rotational spinning.

That points to a problem in the vestibular system, the inner ear, or the brainstem.

As opposed to what?

As opposed to presyncope, feeling like you're going to faint or pass out lightheaded.

That's usually a heart or blood pressure issue, an arrhythmia or orthostatic hypotension.

Okay, so spinning versus fainting.

What else?

Or disequilibrium, feeling unsteady on your feet like you might fall over.

That's a balance or gait issue, maybe from the legs or the cerebellum.

You have to separate these three things.

Vertigo, presyncope, and disequilibrium.

Table 13 -1 in the book is essential for this.

So if we establish its true vertigo, the spinning sensation, we then have to figure out if it's peripheral or central.

Right, and that's the next big step.

Peripheral causes originate in the inner ear.

Things like benign positional vertigo or BPPV, which is sudden, lasts seconds, and is triggered by specific head movements, like rolling over in bed, or labyrinthitis, an inflammation which can last for hours or even days.

And central causes.

That means the brain.

The brainstem or cerebellum.

This is the scary stuff.

Stroke, tumor.

Central vertigo often comes with other neurological signs.

Double vision, which is diplopia, slurred speech, or clumsiness, which is ataxia.

If you see vertigo, PLUS, a cranial nerve deficit, you need imaging, and you need it now.

Let's move to the nose history.

Section 4, rhinorrhea and congestion.

Rhinorrhea is drainage, a runny nose.

Congestion is stuffiness.

The big fork in the road here is determining if it's viral or allergic.

How do we tell the difference just by asking?

Viral, like the common cold, usually runs its course in less than seven days.

It might have muscle aches, maybe a low grade fever.

Allergic lignitis is often seasonal and triggered by environmental stuff like cats or dust.

And the key symptom for allergy is itching.

Itching.

If the eyes are witchy, the nose is icky, the palate, the throat is scratchy, that screams allergy.

Hyruses don't usually cause that intense itching.

And what about the drugs again?

We mentioned it with ears, but it applies here too.

If someone overuses topical decongestants like aphrine, it can cause a rebound effect.

The nose becomes dependent on the spray to stay open.

That's called rhinitis medicamentosa.

Or, you know, you have to ask about cocaine use if the history is suspicious.

Let's talk about the dreaded sinus infection.

Acute bacterial sinusitis.

Everyone who gets a cold thinks they have a sinus infection that needs antibiotics.

They do, but clinical guidelines are strict to prevent antibiotic resistance.

Bates notes that it is unlikely to be bacterial until viral symptoms have persisted for more than seven days.

So if I've been sick for three days with a stuffy nose, it's probably viral.

Almost certainly.

We look for the double sickening.

Patients get a cold, they start to get a little better, and then boom, they get worse again with high fever and facial pain.

You really need purulent, thick -colored drainage A and D facial pain to make that diagnosis confidently.

Finally, epistaxis.

Nose bleeds.

First, you need to pinpoint the source.

Is it coming from the nose?

Or is the patient coughing up blood from the lungs, which is hemoptysis?

Or vomiting blood from the stomach, which is emidivisus?

That can be confusing.

Assuming it's the nose, what causes it?

Most nose bleeds are local trauma, nose picking, especially in kids, dryness from winter air, or inflammation.

But if they are recurrent or huge volume, you have to ask about anticoagulants like warfarin or bleeding disorders.

Okay, we've asked the questions, we've built the rapport, now we get physical.

Section five, the physical exam of the ear.

We start with inspection of the auricle.

Look for deformities, lumps, or lesions.

Bates has a great table on this, table 13 -2.

Yeah, let's hit a few of those common lumps you might find.

Well, you might see kiloids, those thick scar tissue masses, common after ear piercings, especially in patients with darker skin.

You might see TOFA, which are hard, chalky nodules on the helix.

If you see those, you have to ask about gout.

Gout in the ear, really?

Yes, uric acid crystals deposit in the cooler areas of the body, like the ear rim.

It's a classic sign.

You might also see basal cell carcinoma, a shiny, slow growing nodule with rolled borders,

or rheumatoid nodules in patients with rheumatoid arthritis.

Then comes the tug test.

This sounds like a wrestling move, but it's diagnostic.

It's diagnostic gold, it's so simple.

You gently move the oracle up and down, and then you press firmly on the tragus.

And what are we looking for?

Pain.

If moving the ear hurts or pressing the tragus hurts, it is almost certainly acute otitis externa, or swimmer's ear.

The skin of the canal is inflamed, so pulling on the cartilage around it causes pain.

And if it's otitis media, the deep infection.

Usually the tug test is painless.

The infection is behind the drum, so wiggling the outer ear doesn't bother it much.

It's a great way to distinguish the two before you even put the otoscope in.

Also, check the mastoid bone behind the ear.

Yes.

Palpate it firmly.

Tenderness there can signal mastoiditis, which is a serious infection of the bone itself that can spread to the brain.

It's a complication of untreated otitis media.

Now, the moment of truth.

The otoscope.

Bates is very specific about the technique in Box 13 -1.

This is where beginners fail.

First, you need to select the largest speculum that will fit comfortably.

Then you need to straighten the canal.

For adults, you pull the oracle upward, backward, and away.

Up, back, and away.

That aligns the S shape so you can see down the barrel.

In kids, it's more down and back because their canals are shaped differently.

And the hand position.

This seemed weird when I first read it, but it makes so much sense.

It is absolutely crucial.

You hold the handle between your thumb fingers, but you must brace your hand against the patient's cheek.

You rest your pinky or the side of your hand on their face.

Why the brace?

Why is that so important?

Because if the patient sneezes or flinches or jerks their head, which happens all the time when you stick things in people's ears, and your hand is floating in the air, the otoscope stays still while their head moves toward it.

You're going to drive that hard plastic speculum right into their tender, bony ear canal.

If you brace, your hand moves with their head.

It's a safety mechanism.

You must do it every single time.

Smart.

So we are looking in the canal.

We might see wax or swelling.

If the canal is swollen, narrowed, and moist, that's acute otitis externa.

Sometimes it's so swollen you can't even see the drum.

You might also see exostoses, little nonmalignant bony bumps.

Those are common in surfers or swimmers who spend a lot of time in cold water.

And finally, the tympanic membrane itself.

We're looking for those landmarks we discussed.

Look for the handle of the malleus and the cone of light.

A normal drum is pinkish gray and translucent.

You should be able to see through it a little bit.

And abnormalities.

Bates has a whole table.

Table 13 -3.

Let's walk through the big ones.

Okay.

If it's red bulging outward toward you and you can't see the bony landmarks because they're obscured, that's acute otitis media.

The pressure from pus is pushing the drum out.

What if we see bubbles behind it?

If you see amber colored fluid with air bubbles behind the drum, that's serous effusion.

It's fluid without infection, often from a viral cold or barotrauma, like from flying or scuba diving.

What about holes?

Perforations.

You might see a literal hole in the drum.

It can be central or marginal, or you might see tympanosclerosis.

That's a big word.

It just means scarring.

It looks like chalky white patches on the drum.

Usually those white patches don't affect hearing much, but they tell you the patient has had tubes or a lot of infections in the past.

It's a sign of old inflammation.

There's one scary sounding one, bulismarangitis.

That is extremely painful.

You see hemorrhagic vesicles, blood blisters right on the eardrum itself.

It's usually caused by mycoplasma or certain viral infections.

Moving on to section six, auditory acuity and tuning fork tests.

We've looked at the ear.

Now we test how it works.

We start with the whisper test.

This is your quick screen.

It's outlined in box 13 -2.

You stand two feet behind the patient so they can't lip read.

Have them include the non -test ear.

And they should rub the tragus of the other ear to create some white noise and block sound.

Right.

Exactly.

Then you whisper a combination of three numbers and letters, like 4K2.

If they get three out of six correct after a couple of tries, they pass.

It's surprisingly good at detecting loss greater than 30 decibels.

But if they fail, we break out the tuning forks.

The Weber and the RIN tests.

Bates suggests a 512 hertz fork.

Right.

Because that frequency is in the range of conversational speech.

These tests help us distinguish between conductive and sensor neural loss.

This is the logic puzzle part of the exam.

Let's start with the Weber test.

This tests for lateralization.

You get the fork vibrating and place the base firmly on top of the head or mid -forehead.

You ask the patient, where do you hear the sound?

An oral result is hearing the sound equally in both ears.

Midline.

But what if I have hearing loss in my right ear?

What happens then?

That depends on the type of loss.

This is where it gets really interesting and a little non -intuitive.

If you have conductive loss in your right ear, say a wax plug, the sound will lateralize to the BA ear.

You will hear it louder in the right ear.

That seems so counterintuitive.

Why do I hear it louder in the blocked ear?

Because the blockage blocks out the ambient room noise.

It's like plugging your ear and humming.

The background noise is gone.

So the bone conduction sound from the fork becomes dominant and undistracted.

The inner ear on that side is perfectly fine.

Ah, okay.

That makes sense now.

And if I have sensor neural loss nerve damage in the right ear, then the sound lateralizes to the good ear, the left ear.

Because the nerve in the right ear just can't pick up the signal even when it's delivered directly through the bone.

Okay, that's Weber.

It tells us there is a difference and points us in a direction.

Now, rim.

This compares air to bone conduction.

You place the vibrating fork on the mastoid bone behind the ear.

That's bone conduction.

Ask them to tell you when the sound stops.

The second they say now, you quickly move the tines of the fork to just outside the ear canal without touching them.

That's air conduction.

And normally.

Normally, air conduction is more efficient.

They should still hear the sound vibrating in the air even after the bone sound stopped.

We write that as ACBC.

That's a normal or positive rim.

Now, what happens in conductive loss?

In conductive loss, the air pathway is blocked.

So, they hear it on the bone, but when you move it to the air, silence.

Or it's very faint.

So, bone conduction is equal to or longer than air conduction.

BCOAC.

And sensor neural.

The pattern stays normal, ACBC, because the mechanics are fine.

But the total time they hear it in either position might be much shorter because the nerve is just weak overall.

It really is a matrix.

You have to put Weber and Wren results together to solve the case.

Bates has a summary table, table 13 to 4, that lays this all out beautifully.

Conductive causes are things like foreign bodies, perforation, otitis media, or otosclerosis.

Sensor neural causes are aging, which is called presbycusis, noise exposure, or ototoxic drugs.

Okay, section 7, physical examination of the nose and sinuses.

You start with the surface.

Inspect for any asymmetry.

Is the nose crooked?

Then test for obstruction.

Press on each alenace, the wing of the nose, and ask the patient to breathe in.

See if one side collapses.

Then we go inside.

Can we use the otoscope here too?

Yes.

Put a large speculum on.

Tilt the patient's head back.

But be really careful.

The nasal septum is extremely sensitive.

Right.

Do not touch the septum.

Direct the speculum laterally, away from the septum, toward the ear to view the turbinates.

You should be able to see the inferior and middle turbinates.

What are we looking for on the turbinates?

Color and swelling.

In viral rhinitis, a common cold, the mucosa will be reddened and swollen.

But in allergic rhinitis, it looks distinctive.

It is often pale, bluish, or red.

Beats uses the word boggy.

Yes, boggy, like it's waterlogged and swollen.

That pale, boggy look is a classic sign of allergies.

And we also have to check the septum.

Look for deviation.

A little bit of deviation is very common.

Look for perforation a hole.

This can happen from cocaine use, trauma, or surgery.

In polyps, what do they look like?

Polyps are pale, sac -like growths of inflamed tissue.

They look like peeled grapes.

They're usually associated with asthma, aspirin sensitivity, or chronic allergies.

And finally, palpating the paranasal sinuses.

We check for tenderness.

Press up from under the bony brows for the frontal sinuses.

Press up on the cheeks for the maxillary sinuses.

What does tenderness mean, clinically?

Tenderness suggests inflammation.

If you have tenderness, plus purulent discharge from the nose, plus symptoms lasting more than seven days, that strongly suggests acute bacterial rhinosinusitis.

We've gathered all this data.

Section 8, recording findings.

We have to translate ear looks red into professional language.

Occupation is key.

We move from sentences to concise phrases.

A normal exam, often documented under heat for head, eyes, ears, nose, throat might read.

Ears, acuity, good to whispered voice.

TM's pearly gray, intact.

Landmarks visualized.

Weber midline.

Rhin, AC, BC.

Nose.

Mucosa, pink.

Septum, midline.

No sinus tenderness.

Crisp, professional.

And if it's abnormal?

You detail the positive findings.

Ears, acuity diminished on right.

Right, external canal swollen with erythema and purulent discharge.

TM obscured.

Weber laterizes to right.

Wind, BC, AC on right.

Nose.

Mucosa swollen and erythematous.

Tender to palpation over maxillary sinuses.

That synthesis tells a story.

Just by reading that, I know the patient likely has otitis externa on the right with a conductive hearing loss and also sinusitis.

Exactly.

The note should paint a picture and lead you to the diagnosis.

This brings us to section 9, health promotion and counseling.

The big topic here is screening for hearing loss.

This is a huge public health issue.

Bates highlights presbycusis, that's the age -related degeneration of hair cells in the cochlea, usually starts with loss of high -frequency sounds.

The stats are wild.

One -third of adults over 50 have some hearing loss, 80 % of those over 80.

It's incredibly pervasive and because it happens so gradually, people often don't notice it.

Their family notices it first because the TV is so loud.

So logically, we should screen everyone over 50, right?

Just run a quick whisper test at their annual physical.

Well, here is the dilemma.

The USPSTS, the US Preventive Assurances Task Force, cites insufficient evidence to recommend for or against widespread screening in asymptomatic adults over 50.

That feels wrong.

Why?

If it's so common, why not look for it?

It's not that we can't find it.

We can.

The issue is the so -what factor.

The evidence shows that even when hearing loss is detected,

hearing aid usage rates remain very low.

Why is that?

It's a mix of things.

Cost, comfort, and stigma.

People don't want to wear them.

So the task force argues that screening the whole population doesn't necessarily lead to improved quality of life outcomes if nobody ends up using the treatment.

That is a fascinating, if frustrating, public health paradox.

It is.

But as a clinician seeing an individual patient, you should still be vigilant and prevention is key.

Counseling on noise reduction, industrial health standards, and protecting your ears at concerts.

Okay, let's wrap this up.

We've covered the anatomy, the why, the ear and nose work.

We've covered the history, the what to ask.

We've covered the exam, the how to look, and we've covered the documentation.

If you take one thing away, remember the connection between the structure and the exam.

You pull the ear up and back because the canal is S -shaped.

You brace your hand because the inner canal is bony and painful.

Every move you make should be dictated by the anatomy.

And here is a final thought to chew on.

We talk about hearing loss as a mechanical failure, a broken bone, a dead nerve,

a decibel on a chart.

But think about the isolation.

That's the real tragedy of it.

Hearing is how we connect.

It's how we hear a joke, how we follow a story at the dinner table.

When someone stops hearing well, they stop engaging.

They stop going to the dinner party because it's just too much work to filter the noise.

They withdraw, they smile and nod, but they're not really there.

It's true.

Hearing loss is strongly linked to social isolation, depression, and even an increased risk of cognitive decline and dementia.

As a clinician, you aren't just checking a cranial nerve.

You are checking that patient's connection to their family and their world.

That's the mission.

Detect the deficit, not just for the chart, but for the person.

Well said.

Beautifully said.

That's it for this deep dive into Bates Chapter 13.

Go practice your tug test gently, and we will see you next time.

Thank you from the Last Minute Lecture team.

Keep listening.