Chapter 25: Epistaxis

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When a patient walks into the clinic with a nosebleed, the universal instinct is to

just hand them tissue.

Oh, absolutely.

Hand them a tissue, tell them to pinch their nose, and just treat it like a minor nuisance.

Yeah, exactly.

It's visible, it's messy, and the immediate goal is really just to make it stop.

Right, because we see the blood and our brain immediately focuses purely on fixing the plumbing leak.

But for an advanced practice nurse,

stopping at the plumbing actually skips, well, it skips the most critical step in clinical reasoning.

It really does.

Because here is the fundamental concept you have to lock in before you do anything else.

A nosebleed or epistaxis, as we'll be referring to it today, is a physical symptom.

Right.

It is not a disease in itself.

Exactly.

It's a blinking check engine light.

And while, yes, you absolutely have to clean up the oil spill, your real job is to pop the hood and figure out exactly why that vessel ruptured in the first place.

It's all about moving past that superficial presentation to uncover the underlying systemic or anatomical cause.

Because if you don't find the why, the patient is just going to bounce right back into your exam room a week later.

Which nobody wants.

So if you are an advanced practice nursing student listening right now, consider this, your one -on -one clinical prep session.

Welcome in.

We know you are getting ready for clinicals and exams.

And absorbing all this material can feel honestly like drinking from a fire hose.

Oh, for sure.

So today, just take a deep breath.

We are going to do a comprehensive deep dive into epistaxis, pulling directly from Chapter 25 of your text.

We're going to build your clinical understanding logically, starting with the underlying pathophysiology.

Right.

The systemic causes and then moving right through to what you'll actually see in the exam room and finishing up with evidence -based management.

Sounds like a solid plan.

Let's start with the who and the why.

Statistically speaking, who is actually getting these nosebleeds?

Well, almost everyone.

Roughly 60 % of the general population will experience at least one significant nosebleed in their lifetime.

Wow.

60%.

Yeah.

But when we look at the demographics, we see a very distinct bimodal age distribution.

Meaning it peaks at two specific times.

Exactly.

The frequency peaks heavily in children under 10 years old, and then it peaks again in adults over 50 years old.

And is there a gender difference?

Actually no.

It affects males and females equally across the board.

Okay.

So we have our two main demographics.

Let's look at the systemic causes that make those populations vulnerable.

I like to think of the nasal mucosa as this incredibly fragile little ecosystem.

That's a great way to picture it.

It requires the perfect balance of moisture, physical integrity, and blood flow.

Just like a real ecosystem, it can be easily thrown off balance by systemic weather changes, if you will, happening elsewhere in the body.

And chronic allergies or sinusitis are perfect examples of that systemic weather.

Because of the inflammation.

Right.

They cause chronic inflammation, which draws excess blood flow to the area, while simultaneously making the tissue boggy and friable.

Friable meaning it just tears easily.

Exactly.

That fundamentally alters the ecosystem, making the capillaries much more prone to spontaneous rupture.

Now, the textbook also brings up hypertension.

But looking closely at the text, it specifically notes that hypertension is significantly associated with epistaxis, but it does not have a proven causal relationship.

Right.

That's a key distinction.

So if high blood pressure doesn't actually cause the initial bleed, why is it such a massive red flag in our clinical assessment?

Think of the physics involved.

Hypertension might not be the match that starts the fire, but it absolutely acts like gasoline once a vessel does rupture.

Oh, that makes sense.

Yeah.

The elevated hydrostatic pressure inside those tiny fragile vessels turns a slow, easily clotted capillary leak into a high pressure spray.

So the bleeding is faster.

Faster, the volume of blood loss is higher, and it is significantly harder to control with standard pressure.

Meaning the vessel breaks for an unrelated reason, maybe a sneeze or a dry room, but the high pressure dictates the severity.

Spot on.

And speaking of severity, you have to be vigilant about coagulopathies when formulating your inferential diagnosis.

So patients who physically can't clot.

Right.

A patient with chronic liver disease, like cirrhosis or chronic renal disease, is at a really high risk.

The liver is essentially the primary factory for synthesizing clotting factors.

So if liver is failing.

The body physically lacks the proteins required to form a stable clot.

The text also flags cancer, specifically Hodgkin's disease, as a systemic driver.

And then we have the genetic disorders, you know, the familial blood dyscrasias.

And you really need to know these for your clinicals.

You've got hemophilia A, which is a factor eight deficiency, and hemophilia B, which is a factor nine deficiency, also known as Christmas disease.

Got it.

You also need to watch for von Willebrand disease, which is the most common genetic bleeding disorder, and hereditary hemorrhagic telangiectasia, or HHT.

HHT, right.

Yeah, HHT is particularly tricky because it causes abnormal connections between arteries and veins, these arteriovenous malformations, right in the mucosal lining.

So those are the internal systemic factors.

But we also have to account for the local toxins and medications that patients are, you know, voluntarily introducing into that nasal ecosystem.

Oh, absolutely.

Prolonged use of intranasal corticosteroids is incredibly common.

Like over -the -counter allergy sprays.

Yes.

While they reduce inflammation, over time, they physically atrophy and thin the lining of the nasal mucosa, exposing the underlying vessels.

Making them sitting ducks?

Pretty much.

And then you have oral medications like anticoagulants, NSAIT, and salicylates, which intentionally block the body's natural clotting cascade.

Illicit drugs play a major role here, too, right?

They do.

Snorting powdered drugs like cocaine or heroin causes intense immediate vasoconstriction.

Which cuts off the blood supply to the septum.

Exactly.

That leads to ischemia and eventual tissue necrosis.

The dead tissue slews off, creating a septal perforation and severe recurrent bleeding.

Your text also highlights nutritional deficiencies, like scurvy, which is a vitamin C deficiency.

Which you don't see every day, but it's important.

Right, because vitamin C is an essential building block for collagen synthesis.

Without it, the structural scaffolding of the capillaries literally dissolves.

Making them just leak blood into the surrounding tissue.

And febrile infections like rheumatic, scarlet, or typhoid fevers.

They can also trigger epistaxis through extreme systemic stress and vascular inflammation.

Right.

So we've established how systemic issues like high blood pressure or clotting disorders turn a small leak into a flood.

Let's shift a bit.

How does age change this physical landscape?

When we look at our geriatric patients, it seems like their baseline risk is significantly

Older adults are facing a compounding set of risks.

Instead of healthy elastic vessels, geriatric blood vessels are more like a parchment paper trying to wrap a high pressure line.

Oh wow.

Arteriosclerosis makes the vessels stiff, meaning they can't effectively constrict to clamp down on a bleed.

And combine that with a nasal mucosa that is naturally drier as we age.

Exactly.

Plus a higher prevalence of vascular disease and the likelihood that they are taking daily blood thinners.

It is just a perfect storm.

And the actual location of the bleed changes in older adults too.

They are much more likely to present with bleeding from the posterior nasal septum.

And posterior bleeds completely change the clinical scenario.

Oh so?

The vessels in the posterior septum are much larger and sit deeper in the nasal cavity.

When they rupture, the volume of blood is massive, you can't easily visualize the source, and it is incredibly hard to stop with simple interventions.

Which explains why older patients with epistaxis have a much higher rate of ED visits and hospital admissions.

Exactly.

It's a whole different ballgame.

So we have older, stiffer vessels and drier mucosa.

That brings up an environmental factor that tech specifically calls out, which is CPAP therapy.

Continuous positive airway pressure, right?

Now CPAP machines are prescribed to help patients breathe better at night.

How does a machine designed to support the airway end up causing respiratory irritation and bleeding?

Isn't that counterintuitive?

It sounds like it, yeah, but it comes down to the physical mechanism of the machine.

A CPAP forces continuous, high -velocity air pressure through the upper airway.

Like a wind tunnel.

Literally.

That constant wind tunnel effect completely overwhelms the goblet cells in the nose, which are responsible for producing mucus and humidifying the air.

So the mucosa dries out faster than the body can rehydrate it.

Exactly.

The tissue cracks like dry winter skin, leading to congestion, sneezing, and eventually the exposure and rupture of those brittle capillaries.

Okay, so let's zoom in on the anatomy and the direct physical trauma that causes those initial ruptures.

We know the environment dries things out, but what actually breaks the vessel?

The most common direct cause is, perhaps unsurprisingly, digital manipulation.

Meaning nose picking.

Yes, clinically termed epistaxis digitorum.

Gotta love the clinical terms.

Beyond that, you have facial and septal fractures, forceful nose blowing, or iatrogenic causes.

Like a nurse inserting an NG tube or a nizendotracheal tube, and accidentally scraping the mucosa.

Structurally, a deviated septum can cause chronic epistaxis too, right?

It can, because it disproportionately funnels all the airflow onto one side of the nasal cavity, dramatically drying out that specific localized area.

But we also have to talk about nasopharyngeal cancer, or NPC, which is a critical red flag in your differential.

Yes.

NPC is particularly prominent in populations of Asian descent, especially from Southeast Asia.

And why is that?

It's due to a complex mix of dietary habits, viral exposures like Epstein -Barr, and environmental factors.

The textbook emphasizes something really sobering about NPC, which is that epistaxis might be the sole manifestation of this cancer.

Which is terrifying.

The tumor outgrows its blood supply or erodes into surrounding vascular beds, causing a bleed.

And it has a poor prognosis, specifically because the diagnosis is so often delayed.

Patients and providers just write it off as a stubborn nosebleed.

This is exactly why understanding the anatomical origin of the bleed is so crucial.

You need to know exactly where the blood is coming from to rule out these serious pathologies.

So let's map out that anatomy for the students.

When we talk about anterior bleeds, which make up roughly 90 % of all epistaxis cases, we are talking about Kieselbach's plexus.

Right.

I always picture it as a watershed area.

A spot where three busy, high -speed arterial highways all crash together right at the superficial front of the nose.

That's a perfect visual.

Kieselbach's plexus is located in Little's area on the anterior portion of the nasal septum.

And those three highways converging.

They are the septal branch of the anterior ethmoid artery, the septal portion of the superior labial branch of the facial artery, and the lateral nasal branch of the sphenopilatine artery.

That is a lot of arterial traffic in one spot.

It really is.

All that high -pressure blood is converging in one superficial spot that is constantly exposed to dry air and, well, wandering fingers.

But from a management perspective, anterior bleeds are usually handled effectively in primary care because they are physically accessible.

Exactly.

You can easily apply direct pressure or quickly reach the site with chemical cautery.

Now the posterior bleeds, the other 5 to 10%, those are a different story entirely.

Those occur deep in the nasal cavity in an area known as Woodruff's plexus.

Woodruff's plexus.

Okay.

And this bleeding most commonly originates from the rupture of the posterior wall and colonal branches of the sphenopilatine artery.

Because it is so deep, you cannot just pinch the nose and hold pressure.

No, you can't.

The blood flows heavily down the back of the throat, it's terrifying for the patient, and it frequently requires hospital admission and specialist intervention.

Knowing those anatomical differences is going to be vital when we move to management.

But we need to pause and look at our pediatric and adolescent populations because the text highlights some very specific red flags here.

Pediatrics will be your most common epistaxis patients.

Nearly 3 out of 4 kids will get a nosebleed.

And they're usually anterior.

Almost exclusively anterior, located right in Kieselbach's plexus, and usually benign.

They resolve quickly with compression and are almost always caused by dryness, aggressive picking, or kids lodging foreign bodies in their nears.

But the text presents a massive red flag that genuinely shocked me when I first read it.

Epistaxis is extremely rare in children under 2 years old.

It is.

So if a parent brings an infant into the clinic with a nosebleed, how are you supposed to handle that?

With an unwavering focus on patient safety, if you see epistaxis in an infant under 2, your clinical reasoning must immediately pivot.

Pivot to what?

You must have a high index of suspicion for either physical abuse or a severe undiagnosed coagulopathy.

Why is it such an absolute red flag?

Because of the anatomical protection and the lack of digital dexterity in an infant.

Finding a nosebleed in a baby isn't just a minor issue, it's practically a structural impossibility without blunt force trauma or a profound systemic failure.

Right, and infants' vessels don't just spontaneously rupture from dry air.

Exactly.

It mandates immediate, careful, and thorough investigation.

You cannot dismiss it.

For adolescents, specifically males between the ages of 10 and 20, the clinical red flag shifts to juvenile nasopharyngeal angiofibroma, or JNA.

JNA is a rare, benign, but highly aggressive, locally invasive vascular tumor.

What are the early symptoms?

Early symptoms present as epistaxis, nasal obstruction, and chronic sinus infections.

But because it's benign, it doesn't metastasize.

Right, it doesn't spread to other organs, but the late symptoms occur because the tumor physically expands locally.

It grows into the sinuses, the eye sockets, and the cranial vault.

Which causes some severe issues.

Yeah, that causes headaches, facial numbness, cheek swelling, droopy or protruding eyes, and even vision or hearing loss.

It's a stark reminder that a nosebleed is never just a nosebleed.

Wow.

Okay, let's bring all of this into the exam room.

Your patient is sitting in front of you.

How are we assessing them, and what tests are actually necessary?

Well, you start subjectively with a detailed history.

Box 25 .2 in the text gives you the roadmap.

So you are asking about the duration of the bleed, what interventions they've tried at and all medications, both prescribed and illicit.

Exactly.

Recurrent minor anterior bleeds usually have a history spanning several weeks.

But the subjective history gets complicated when a patient with a posterior bleed presents with hemoptysis, which is coughing up blood, or hematomasis, vomiting bloodstream stomach contents.

They might even report melena, which is black, terry stools from blood that has been swallowed and digested.

Wait, if someone walks into the clinic vomiting blood or coughing it up, my brain immediately screams massive GI bleed or a pulmonary emergency.

How can an advanced practice nurse confidently dial that back to just a nosebleed?

It is a terrifying presentation, but this is where your objective visual assessment saves you.

You have to find the source of the river.

Look upstream.

Exactly.

In the absence of other respiratory or gastrointestinal findings, you grab your light source and look inside the nose and throat.

And what are we looking for?

If you look into the nasopharynx and see clotted blood or prominent brown to red throat discoloration actively draining down the posterior pharyngeal wall, you have locked in your diagnosis of posterior epistaxis.

For an anterior bleed, the visual is much easier, right?

You use a speculum or an otoscope and you'll typically see bright red blood or prominent engorged traversing vessels right on the anterior septum.

Yes, but if you look inside and see diffuse oozing from multiple mucosal sites simultaneously, that is a strong indicator of an underlying systemic bleeding disorder rather than a single ruptured vessel.

You should also palpate the sinuses for tenderness, which could point your differential toward an active infection or a malignancy.

Absolutely.

Let's talk diagnostics.

We aren't ordering labs for every kid with a bloody nose, right?

Routine diagnostics are rarely needed unless the bleeding is recurrent, unusually severe, or you suspect a systemic issue.

So when do we pull labs?

If you suspect a clotting disorder, you order coagulation studies and you really must know the mechanism behind them to interpret the results.

The text mentions both PTT and PT.

Right, so PTT, or partial thromboplastin time, measures the integrity of the intrinsic clotting pathway.

Think factors inside the blood itself.

A prolonged PTT indicates disorders like hemophilia A or B.

PT, or proslombin time, measures the extrinsic pathway.

Think tissue factors outside the vessel.

A prolonged PT points to an issue like a factor 7 deficiency.

You might also order a CBC to check hemoglobin and hematocrit for evidence of chronic slow blood loss.

Yes.

And an x -ray or CT scan of the sinuses is useful to detect soft tissue masses or rule out severe sinusitis.

Once your assessment is complete, your differential diagnosis should naturally fall into place.

Table 25 .1 categorizes everything we've discussed.

Trauma, NPC, medications, structural deformities, J &A, allergies, and bleeding disorders.

With the differential in mind, we transition into evidence -based management to stop the act of bleeding.

The initial treatment for uncomplicated anterior pustaxis is straightforward, but incredibly commonly done incorrectly.

You apply firm, continuous pressure to the lower third of the nose for five minutes or longer.

Yes, the lower third.

I always picture pinching a leaky garden hose.

You don't pinch the hard metal spigot at the top.

You pinch the soft rubber hose where the water is actually flowing.

You pinch the soft lower cartilage of the nose.

That's a great analogy.

But we have to call out the biggest myth out there, which is tilting the head back.

Why do we see so many people tilt their heads back when they get a nosebleed?

It's an old wives' tale, and the pathophysiology behind it makes it quite dangerous.

How so?

If you tilt the head back or hyperextend the neck, you are using gravity to funnel that blood directly down into the posterior pharynx and the airway.

Which means they swallow it.

This guarantees the patient will swallow blood, which aggressively irritates the stomach lining and causes severe nausea and vomiting.

Worse, it increases the risk of aspirating blood directly into the lungs.

So sit upright and bend the head forward, let the blood drain out where you can see it and manage it.

Exactly.

Sit upright, head forward, continuous pressure on the soft tissue.

If that fails.

If that fails, the algorithm moves to pharmacological agents.

You soak a small cotton pledge in a topical vasoconstrictor.

Like 0 .25 % phenylephrine or 1 .1000 epinephrine.

Right.

Or 0 .1 % silylmethazaline or a 4 % cocaine solution and press it against the site for 5 -10 minutes.

Over -the -counter oxymethazine, which is afferent, is also very effective for this step.

But we have some major safety alerts attached to these medications.

You absolutely must not use epinephrine in patients with hypertension or coronary artery disease.

Because it's a vasoconstrictor.

Exactly.

Epinephrine causes profound systemic vasoconstriction.

In a patient with baseline hypertension, this can trigger a dangerous hypertensive crisis.

And similarly, cocaine solutions should never be used in pediatric patients due to systemic toxicity risks.

Right.

Now, if pressure and topical meds fail, the next step is chemical cauterization.

So burning it closed?

Essentially, yes.

You must thoroughly anesthetize the area first, usually with 4 % lidocaine or cocaine on a cotton ball or a 2 % lidocaine jelly.

And once it's numb?

Once numb, you apply a bead of chromic acid, 25 % to 50 % trichloroacetic acid, or a silver nitrate stick directly onto the bleeding vessel.

You hold firm pressure for exactly 30 seconds.

The chemical literally burns and coagulates the proteins in the blood and tissue, sealing the leak.

That's it.

But if caudery fails, or if it's a diffuse ooze that you can't pinpoint,

the final primary care step is nasal packing to physically tamponade the entire nasal fossa.

You have resorbable and non -resorbable packing.

Resorbable packing melts away on its own.

And this is your absolute go -to for patients with bleeding disorders, those on anticoagulants or young children.

Why is that?

Because pulling out non -resorbable packing a few days later tears the newly formed clot and restarts the whole bleeding process.

Non -resorbable packing, like gauze or inflatable balloons, has to be manually removed.

And there's a vital physiological monitoring point here during the packing procedure itself, right?

The vasovagal response.

Yes.

Shoving packing deep into the nasal cavity can stimulate the vagus nerve.

This triggers a sudden, massive parasympathetic surge.

What does that look like in the patient?

The patient's heart rate drops, their blood vessels dilate, their blood pressure tanks, and they can experience syncope, meaning fainting right there in the chair.

You must monitor their vital signs continuously during packing.

Packing is also incredibly uncomfortable once the anesthetic wears off, so pain management is required.

Acetaminophen is preferred.

You must explicitly tell them to avoid NSAIDs and aspirin.

Right, because those medications impair platelet function and will encourage more bleeding.

You also need to re -evaluate any daily blood thinners they are on and consult with their prescribing physician.

And to be crystal clear, if it is a posterior bleed, they need an immediate ENT consult.

Absolutely.

Primary care does not pack posterior bleeds.

Those patients often require specialized balloon packing, nerve blocks, or surgical ligation of the artery.

Know your scope of practice.

So the bleeding has finally stopped, and we are prepping for discharge.

Minor anterior bleeds usually need no follow -up.

But recurrent anterior bleeds or any posterior bleed require an ENT referral.

And hypovolemic or anemic patients need a physician referral for a possible blood transfusion.

If you use non -reservable packing, they must follow up for timely removal.

Leaving packing in too long creates immense pressure on the delicate septal cartilage.

This can cause pressure necrosis or a septal hematoma, where blood pools between the cartilage and the paracondrium, physically destroying the cartilage.

There's also the risk of airway obstruction if an inflatable balloon breaks and migrates down the throat.

Which is obviously a medical emergency.

So if you only have two minutes before discharge, you need to deliver a rock -solid patient education speech to prevent a bounce -back visit.

The tech synthesizes this into two main pillars,

hydration and peace,

and quiet for the nose.

For hydration, the mucosa must stay moist.

Instruct them to use a home humidifier, frequent intranasal saline sprays, and apply petroleum jelly inside the nerves.

Prevent the tissue from cracking.

And the peace and quiet.

They need to protect that fragile blood clot.

No blowing the nose, no sneezing through the nose if they can help it, no rubbing, and absolutely no picking.

Have them cut their fingernails short if they are prone to probing in their sleep.

Can they use OTC affrin at home if it starts oozing again?

They can, but here is your major medication warning to pass along.

Limit oxymethasoline to three consecutive days.

Only three days.

If they use it longer, the receptors down -regulate and they will develop rhinitis medicamentosa.

Which is what exactly?

This is a severe rebound vasodilation and congestion that actually makes the nasal lining thicker and more prone to bleeding than before.

You also need to give them immediate post -attack rules.

If it starts bleeding again, spit the blood into a container, don't swallow it.

Don't talk during active bleeding as it moves the facial muscles and disrupts the clot.

And avoid alcohol and hot liquids right after an attack, because both cause systemic vasodilation, which can reopen the sealed vessel.

Those simple, mechanism -based educational points will absolutely save your patients a trip back to the ED.

We've covered a massive amount of clinical ground today.

We've traced the anatomical origins of epistaxis and quesivax and Woodruff's plexuses,

mapped out how systemic weather and dry environments cause those fragile vessels to rupture, and walked step -by -step through clinical assessment and safe pharmacological management.

You know how to differentiate a minor bleed from a major red flag, and exactly what to teach your patients.

You are treating the symptom, but you are diagnosing the cause.

And that is the absolute essence of advanced practice nursing.

Before we wrap up, I want to leave you with a final clinical thought to mull over.

Considering our rapidly aging population, meaning more patients with arteriosclerosis and daily anticoagulants, combined with the massive rise in at -home CPAP therapy for sleep apnea,

how might the baseline presentation and frequency of severe, environmentally -triggered

epistaxis shift in your primary care clinics over the next decade?

It's a changing landscape.

And you are going to be on the front lines of it.

Thank you for studying with us.

You got this.

From all of us here on the Last Minute Lecture team.