Complete ENT (Otorhinolaryngology) question bank — ear, nose, throat, larynx, airway & head-neck — in explanation-first exam-topper style, with 72 diagrams.
12chapters144questions77High-Yield
THE CONCEPT
Epistaxis is bleeding from the nose — a very common ENT emergency. Most (about 90%) are anterior, from Little's area on the antero-inferior septum, and are minor; a minority are posterior, from branches of the sphenopalatine artery, and are more severe (older, hypertensive/atherosclerotic patients).
CAUSES
Causes are local or systemic:
Local: trauma (nose-picking — the commonest in children, injury, foreign body, surgery), inflammation (rhinitis, sinusitis), a deviated septum/spur, tumours (juvenile nasopharyngeal angiofibroma in adolescent boys, carcinoma), atrophic rhinitis, dry air, and cocaine.
Assessment begins with ABC and resuscitation if severe, estimating blood loss and checking vital signs, then identifying the site (anterior rhinoscopy after decongestion/suction), taking a history (side, duration, cause, drugs, comorbidity), and investigating (FBC, coagulation, group-and-save/crossmatch if severe).
STEPWISE MANAGEMENT
First aid — sit up, lean forward, pinch the soft part of the nose over Little's area for 10–15 minutes, spit out blood, apply ice → Cautery (if a bleeding point is seen) — chemical (silver nitrate) or electrocautery → Anterior nasal packing (if cautery fails/no point seen) — ribbon gauze (BIPP), Merocel, tampon → Posterior packing / balloon (posterior bleeds) — postnasal pack, Foley catheter or epistaxis balloon; admit → Surgical/interventional (refractory) — endoscopic sphenopalatine artery ligation, anterior ethmoidal ligation, or embolization
Throughout, the underlying cause is treated (control blood pressure, correct coagulopathy, stop/reverse anticoagulants).
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CLINICAL PEARL: Epistaxis = nosebleed; 90% anterior (Little's area, children/young, minor) vs 10% posterior (sphenopalatine, older/hypertensive, severe). Causes are local (trauma/nose-picking commonest, DNS, tumour [JNA in an adolescent boy], atrophic rhinitis) or systemic (hypertension, bleeding disorders, anticoagulants, HHT). Stepwise: first aid (sit up, lean forward, pinch the nose 10–15 min) → cautery (silver nitrate) → anterior pack → posterior pack/balloon → SPA ligation/embolization; treat the underlying cause.
WHY THE ANTERIOR/POSTERIOR DISTINCTION MATTERS
The most useful way to think about epistaxis is to separate anterior from posterior bleeds, because they differ in almost every practical respect. Anterior bleeds — from Little's area on the front of the septum — make up the vast majority, occur in children and young adults, are usually minor, and can be seen and controlled easily at the front of the nose by pressure or cautery. Posterior bleeds — from the sphenopalatine system deep in the nose — are fewer but far more troublesome: they occur in older, hypertensive or atherosclerotic patients, are often profuse, and cannot be seen or pinched from the front, so the blood runs down the throat and the patient may swallow large amounts. This distinction determines the whole approach: an anterior bleed is usually managed simply in the clinic, whereas a posterior bleed often needs posterior packing, admission and sometimes surgery. Recognising which type one is dealing with is therefore the first and most important clinical judgement.
WHY FIRST AID IS DONE THE WAY IT IS
The simple first-aid manoeuvre for epistaxis is worth understanding mechanistically, because it is often done wrongly. The correct advice is to sit up and lean forward, and to pinch the soft (cartilaginous) part of the nose firmly for ten to fifteen minutes. Leaning forward (not tilting the head back) prevents blood running down the throat, which would otherwise be swallowed — causing nausea and vomiting — or aspirated, and it lets the amount of bleeding be seen. Pinching the soft part compresses Little's area against the septum, applying direct pressure to the commonest bleeding site, and holding it continuously for a full ten to fifteen minutes allows a clot to form (repeatedly releasing to check disrupts the clot and is a common reason first aid 'fails'). Understanding that the aim is direct, sustained pressure on Little's area — with the airway protected — explains each part of the standard advice and why it stops most nosebleeds.
THE BOTTOM LINE
Epistaxis is usually a minor anterior bleed from Little's area managed by first aid and cautery, but a posterior bleed in an older, hypertensive patient can be severe and needs packing, admission and sometimes surgery, alongside treatment of the underlying cause.
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KEY POINTS / NUMBERS (viva)
Epistaxis: 90% anterior (Little's area/Kiesselbach's plexus, antero-inferior septum; children/young; minor) vs 10% posterior (sphenopalatine; older/hypertensive; profuse, harder to control).
Assess ABC/resuscitate, identify site, history + FBC/coagulation/crossmatch if severe.
Stepwise: first aid (pinch nose 10–15 min) → cautery → anterior pack → posterior pack/balloon → SPA ligation/embolization; treat the cause.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
The nose has a rich blood supply from both the internal and external carotid systems, which anastomose at Little's area (Kiesselbach's plexus) on the antero-inferior septum — the commonest site of epistaxis. This dual supply and anastomosis explain bleeding patterns and guide arterial ligation.
Arterial supply of the nose
Internal carotid
External carotid
ophthalmic a.
anteriorethmoidal
posteriorethmoidal
maxillary a.
facial a.
sphenopalatine(main artery)
superior labial(septal branch)
Upper nose ← ICA (ethmoidals) · rest of nose ← ECA (sphenopalatine = main); all anastomose at Little's area
The nose is supplied by both carotid systems: the internal carotid (via the ophthalmic → anterior and posterior ethmoidal arteries) supplies the upper nose, while the external carotid (via the maxillary → sphenopalatine, the main nasal artery, and the facial → superior labial) supplies the rest. This dual supply and its anastomoses explain bleeding patterns and guide arterial ligation.
ARTERIAL SUPPLY
From the internal carotid (via the ophthalmic artery): the anterior and posterior ethmoidal arteries, supplying the upper/superior nose (roof, upper septum, upper lateral wall).
From the external carotid — maxillary artery → sphenopalatine artery (the main artery of the nose, supplying most of the lateral wall/septum posteriorly and the source of most posterior epistaxis) plus the greater palatine artery.
From the external carotid — facial artery → superior labial artery (septal branch), supplying the antero-inferior septum.
LITTLE'S AREA (Kiesselbach's plexus)
Little's area is the antero-inferior part of the nasal septum, where four arteries anastomose — the anterior ethmoidal, the sphenopalatine (septal branch), the greater palatine and the superior labial. This rich, superficial, exposed anastomosis is the commonest site of (anterior) epistaxis, especially in children. Posteriorly, Woodruff's plexus (beneath the posterior end of the inferior turbinate) is the source of posterior epistaxis.
Little's area (Kiesselbach's plexus)
nasal septum
Little's area (antero-inferior)
anterior ethmoidal (ICA)
sphenopalatine
greater palatine
superior labial (facial)
Little's area (Kiesselbach's plexus) on the antero-inferior nasal septum is where four arteries anastomose — the anterior ethmoidal (from the internal carotid), and the sphenopalatine, greater palatine and superior labial (from the external carotid). This rich, exposed junction is the commonest site of (anterior) epistaxis.
CLINICAL RELEVANCE
Clinically, Little's area gives anterior epistaxis (cauterised there), the sphenopalatine artery gives posterior epistaxis (treated by SPA ligation), and the anterior ethmoidal artery is ligated for superior/refractory bleeds.
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CLINICAL PEARL: Nasal blood supply = ICA (ophthalmic → anterior + posterior ethmoidal, supplying the upper nose) + ECA (maxillary → sphenopalatine [the main artery, posterior] + greater palatine; facial → superior labial). Little's area (Kiesselbach's plexus) = the antero-inferior septal anastomosis of the anterior ethmoidal + sphenopalatine + greater palatine + superior labial → the commonest epistaxis site (cautery here). Woodruff's plexus = the posterior source. SPA ligation for posterior, anterior ethmoidal ligation for superior bleeds.
WHY THE DUAL BLOOD SUPPLY MATTERS CLINICALLY
The clinical importance of the nose's dual blood supply, from both the internal and external carotid systems, cannot be overstated, because it explains both why the nose bleeds so readily and how bleeding is surgically controlled. The rich anastomosis of these two systems at Little's area means there is an abundant, superficial, exposed vascular bed at the front of the septum — ideal for the minor trauma of nose-picking or dry air to provoke bleeding. Surgically, knowing which system supplies which part of the nose tells the surgeon which artery to target: a posterior bleed comes from the external-carotid-derived sphenopalatine artery (clipped in SPA ligation), whereas a high, superior bleed comes from the internal-carotid-derived ethmoidal arteries (which must be ligated rather than embolized, since embolizing the internal carotid system risks stroke and blindness). The anatomy therefore directly dictates the safe surgical approach.
WHY LITTLE'S AREA IS SO PRONE TO BLEEDING
It is worth understanding precisely why Little's area is the commonest site of epistaxis, since it recurs throughout the topic. Several features conspire: it is the point where four arteries from two different arterial systems anastomose, creating a dense vascular network; this network lies superficially, just beneath a thin mucosa, on the most anterior part of the septum; and this location is the most exposed to drying air currents, digital trauma (nose-picking) and minor injury. The combination of a rich, superficial vascular plexus in the most exposed and easily traumatised part of the nose makes it uniquely liable to bleed, particularly in children who pick their noses and in dry environments. This is also why it is the site targeted by first-aid pressure and by cautery, and why understanding it underpins the whole practical management of the common anterior nosebleed.
THE BOTTOM LINE
The nose is supplied by both carotid systems anastomosing at Little's area, and this anatomy explains why the front of the septum bleeds so readily and dictates which artery is targeted — sphenopalatine for posterior, ethmoidal for superior bleeds.
External carotid → maxillary → sphenopalatine (the main nasal artery; posterior) + greater palatine; and facial → superior labial (antero-inferior septum).
Little's area (Kiesselbach's plexus) = antero-inferior septum anastomosis of anterior ethmoidal + sphenopalatine + greater palatine + superior labial; commonest epistaxis site.
Woodruff's plexus (posterior, below the posterior inferior turbinate) = source of posterior epistaxis.
Clinical: cautery at Little's area (anterior); sphenopalatine ligation (posterior); anterior ethmoidal ligation (superior bleeds).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Juvenile nasopharyngeal angiofibroma (JNA) is a benign but locally aggressive, highly vascular tumour of the nasopharynx, occurring almost exclusively in adolescent males (about 10–20 years). Although histologically benign, it is locally invasive and destructive, and is the classic cause of recurrent severe epistaxis in a teenage boy.
Juvenile nasopharyngeal angiofibroma
nasal cavity
nasopharynx
vascular mass at
sphenopalatine foramen
extends into nose
Adolescent male · recurrent profuse unilateral epistaxis + nasal obstruction · biopsy contraindicated
Juvenile nasopharyngeal angiofibroma: a benign but locally aggressive, highly vascular tumour arising near the sphenopalatine foramen in an adolescent male, extending into the nose and nasopharynx. Its hallmark is recurrent, profuse, unilateral epistaxis — and biopsy is contraindicated because of the bleeding risk.
ORIGIN & CLINICAL FEATURES
It arises near the sphenopalatine foramen (the posterolateral wall of the nose/roof of the nasopharynx) and is testosterone-dependent (hence adolescent boys). Its features are:
Recurrent, profuse, spontaneous, unilateral epistaxis — the hallmark.
Progressive unilateral nasal obstruction, with nasal discharge and a hyponasal voice.
Mass effect as it spreads: cheek swelling, proptosis, a 'frog-face' deformity, diplopia and cranial-nerve involvement (with intracranial extension).
Conductive hearing loss (Eustachian-tube block).
INVESTIGATION & MANAGEMENT
WHY BIOPSY IS ABSOLUTELY CONTRAINDICATED
One of the most important and frequently examined points about JNA is that biopsy in the clinic is absolutely contraindicated, and understanding why is essential. The tumour is extraordinarily vascular — essentially a mass of thin-walled vessels with poor contractile ability — so cutting into it to take a biopsy can provoke torrential, difficult-to-control haemorrhage. This is why the diagnosis is instead made on the characteristic clinical picture (a teenage boy with recurrent profuse unilateral epistaxis and nasal obstruction) together with imaging (CT and MRI), which are diagnostic enough to avoid the need for tissue. It is also why, when the tumour is removed, it is preceded by angiographic embolization of its feeding vessels to reduce its vascularity and make surgery safer. The rule 'never biopsy a nasopharyngeal mass in an adolescent boy' captures a genuinely dangerous pitfall and is a favourite of examiners.
WHY IT AFFECTS ADOLESCENT BOYS
A distinctive and memorable feature of JNA is its almost exclusive occurrence in adolescent males, which points to a hormonal basis. The tumour is testosterone-dependent, which is why it arises around puberty in boys as testosterone levels rise, and why it may regress after adolescence. This sex- and age-specificity is so characteristic that the clinical scenario itself — a boy of about 10 to 20 years with recurrent, spontaneous, profuse nosebleeds and a progressively blocked nose — should immediately bring JNA to mind. Recognising this typical demographic is important because it prompts the correct imaging-based work-up (and avoidance of biopsy) rather than treating the nosebleeds as ordinary epistaxis, and because missing the diagnosis allows a locally aggressive tumour to continue its destructive spread toward the orbit and skull base.
THE BOTTOM LINE
JNA is a benign but locally aggressive, highly vascular nasopharyngeal tumour of adolescent boys presenting with recurrent profuse unilateral epistaxis and nasal obstruction, diagnosed on imaging (never biopsied), and treated by pre-operative embolization and surgical excision.
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DANGER / REMEMBER: It spreads locally into the nose, pterygopalatine and infratemporal fossae, orbit, sphenoid and intracranially. Investigation is by CT (bony extent; anterior bowing of the posterior maxillary wall — the Holman-Miller sign), MRI (soft-tissue/intracranial extent) and angiography (feeding vessels, usually from the maxillary artery, with pre-operative embolization). Biopsy is contraindicated (the tumour is highly vascular — risk of torrential bleeding). Treatment is pre-operative embolization (to reduce vascularity) followed by surgical excision (endoscopic or open), with radiotherapy for intracranial/unresectable disease.
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CLINICAL PEARL: JNA = a benign but locally aggressive, highly vascular nasopharyngeal tumour of adolescent males, arising near the sphenopalatine foramen (testosterone-dependent). Hallmark: recurrent profuse unilateral epistaxis + progressive nasal obstruction in a teenage boy; it spreads to the pterygopalatine/infratemporal fossa, orbit and intracranially (Holman-Miller sign on CT). Biopsy is contraindicated (bleeding). Treat with pre-operative embolization + surgical excision; radiotherapy for unresectable disease.
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KEY POINTS / NUMBERS (viva)
JNA = benign, locally aggressive, highly vascular nasopharyngeal tumour; adolescent males (10–20 y); arises near the sphenopalatine foramen; testosterone-dependent.
JNA = benign but locally aggressive, highly vascular nasopharyngeal tumour of adolescent males; arises near the sphenopalatine foramen (testosterone-dependent).
Hallmark: recurrent, profuse, unilateral epistaxis + progressive unilateral nasal obstruction in a teenage boy.
Rx: pre-operative embolization + surgical excision; radiotherapy for intracranial/unresectable disease.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
The nasal bones are the most commonly fractured facial bones (they project prominently). Nasal trauma causes a fracture ± displacement, epistaxis, deformity and important associated injuries (a septal haematoma or a CSF leak).
Nasal bone fracture
fracture +deviation
Lateral blow → deviation; frontal blow → depression · always exclude septal haematoma & CSF leak
Nasal bone fracture: the prominent nasal bones are the most commonly fractured facial bones. A lateral blow deviates the nose and a frontal blow depresses it; the two associated injuries that must always be excluded are a septal haematoma and a CSF leak.
MECHANISM & FEATURES
A direct blow (assault, sports, road accident, fall) is usual: a lateral force deviates the nose, while a frontal force depresses/flattens it (a comminuted fracture). The features are epistaxis, pain, swelling, deformity (deviation/depression), crepitus, tenderness, periorbital bruising and nasal obstruction.
WHY THE TWO ASSOCIATED INJURIES MUST NEVER BE MISSED
In assessing any nasal fracture, the two associated injuries that must never be missed — a septal haematoma and a CSF leak — matter far more than the fracture itself, and understanding why explains the whole assessment. A septal haematoma, if overlooked, rapidly destroys the septal cartilage (which depends on the perichondrium for its blood supply) and can become a septal abscess, leaving a permanent saddle-nose deformity — so every injured nose must have the septum inspected and any bilateral swelling drained urgently. A CSF leak signals a fracture of the anterior skull base breaching the dura, opening a route for ascending meningitis — so a clear watery discharge after nasal trauma must be recognised and investigated. Because both are potentially serious yet easily overlooked in a swollen, bleeding nose, actively looking for them is the most important part of examining any nasal injury, ranking above concern for the cosmetic deformity.
WHY TIMING OF REDUCTION MATTERS
A practical point that often confuses students is the timing of nasal fracture reduction, which is governed by two competing considerations. On the one hand, immediate assessment is hampered by soft-tissue swelling that obscures the true deformity, so examination is best delayed a few days until the swelling settles. On the other hand, the fractured nasal bones begin to knit and set within about two weeks, after which they can no longer be moved by simple closed reduction. This creates a window — roughly from when the swelling subsides (day 3–5) to before the bones set (around 10–14 days) — during which closed reduction should be performed. Miss that window and the deformity becomes fixed, requiring a much larger corrective operation (septorhinoplasty) months later once healing is complete. Understanding this timing explains why patients are often reviewed a few days after injury and reduced shortly thereafter, rather than either immediately or late.
THE BOTTOM LINE
Nasal fractures are common and largely a clinical diagnosis reduced within a two-week window, but the priority in any nasal injury is to exclude and treat a septal haematoma and a CSF leak.
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DANGER / REMEMBER: It is essential to assess for a septal haematoma (a bilateral septal swelling that must be excluded and drained), CSF rhinorrhoea (from a cribriform/skull-base injury — a clear watery discharge with a halo sign, confirmed by beta-2 transferrin), associated facial fractures and eye injury.
MANAGEMENT
The patient is examined after the swelling settles (3–5 days) for deformity (X-ray is of little value — the diagnosis is clinical; CT is used for associated/complex injuries). Management is to control epistaxis, exclude and drain any septal haematoma (urgent) and rule out a CSF leak, then perform closed reduction of a displaced fracture under LA/GA within about 10–14 days (before the bones set); a late or persistent deformity needs a septorhinoplasty after healing. Simple measures are analgesia, ice and head elevation.
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CLINICAL PEARL: The nasal bones are the commonest fractured facial bone. Nasal trauma → epistaxis, deformity (lateral blow = deviation, frontal = depression), swelling and crepitus. Always exclude and drain a septal haematoma (bilateral swelling → abscess/saddle nose) and CSF rhinorrhoea (cribriform; halo sign, beta-2 transferrin). Examine after the swelling settles; perform closed reduction within ~2 weeks (before the bones set); a late deformity needs septorhinoplasty.
Examine after swelling settles (3–5 days; X-ray unhelpful, CT for complex injuries). Closed reduction (LA/GA) within ~10–14 days before bones set; late/persistent deformity → septorhinoplasty. Analgesia, ice, head elevation.
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KEY POINTS TO REMEMBER
Nasal bones are the most commonly fractured facial bones; lateral blow → deviation, frontal blow → depression.
Always exclude and drain a septal haematoma (bilateral swelling → abscess/saddle nose) and exclude CSF rhinorrhoea (halo sign, beta-2 transferrin).
Examine after swelling settles (3–5 days); X-ray unhelpful (clinical diagnosis); CT for complex/associated injuries.
Closed reduction within ~2 weeks (before bones set); late deformity → septorhinoplasty; analgesia/ice/head elevation.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
CSF rhinorrhoea is the leakage of cerebrospinal fluid from the nose, due to a defect in the skull base (the anterior cranial fossa floor — the cribriform plate/ethmoid roof) connecting the subarachnoid space to the nasal cavity. It carries a risk of ascending meningitis.
CAUSES
Traumatic (commonest): head injury with an anterior skull-base fracture (cribriform/frontal/ethmoid/sphenoid), or iatrogenic (a complication of endoscopic sinus/skull-base surgery).
Spontaneous: raised intracranial pressure (idiopathic intracranial hypertension), tumours eroding the skull base, and congenital defects.
CLINICAL FEATURES
There is a clear, watery, unilateral nasal discharge, increased on bending forward/straining/Valsalva, with a halo (double-ring) sign on tissue (CSF forms an outer clear ring around central blood), a salty taste (postnasal drip), and sometimes headache/anosmia. The key risk is recurrent meningitis (and pneumocephalus).
DIAGNOSIS & MANAGEMENT
Diagnosis is confirmed by beta-2 transferrin (or beta-trace protein) in the fluid — specific for CSF (fluid glucose is unreliable), with HRCT (bony defect), MRI cisternography and intrathecal fluorescein (to localise the defect at surgery). Management is conservative first — most traumatic leaks stop (bed rest, head elevation, avoiding straining/nose-blowing, stool softeners, ± a lumbar drain), with treatment of any raised ICP; endoscopic surgical repair (grafting the defect) is done for a persistent leak (>1–2 weeks), recurrent meningitis, or a spontaneous/large leak.
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CLINICAL PEARL: CSF rhinorrhoea = a CSF leak from the nose via a skull-base (cribriform/ethmoid-roof) defect → meningitis risk. Causes: traumatic (skull-base fracture, iatrogenic post-FESS) commonest; spontaneous (raised ICP, tumour). It gives a clear watery unilateral discharge increased on bending/straining, a halo sign and a salty taste. Confirm with beta-2 transferrin; localise with HRCT/MRI. Treat conservatively (bed rest, head up, avoid straining, lumbar drain) — most stop — with endoscopic repair if persistent/recurrent meningitis/spontaneous.
WHY BETA-2 TRANSFERRIN IS THE KEY TEST
The single most important investigation in suspected CSF rhinorrhoea is the detection of beta-2 transferrin in the nasal fluid, and understanding why clarifies the whole diagnostic approach. The difficulty is that a clear watery nasal discharge is common and usually benign (allergic or vasomotor rhinitis), so the crucial question is whether the fluid is actually CSF. Older tests — such as checking the fluid's glucose — are unreliable, because nasal secretions and contamination can give false results. Beta-2 transferrin (and beta-trace protein) are proteins found almost exclusively in CSF (and perilymph) and not in normal nasal secretions, making their presence in the fluid highly specific for a CSF leak. This is why a small sample of the discharge sent for beta-2 transferrin is the definitive way to confirm the diagnosis before proceeding to imaging to localise the defect — avoiding both missed leaks and unnecessary investigation of simple rhinorrhoea.
WHY MOST LEAKS ARE MANAGED CONSERVATIVELY FIRST
An important principle in CSF rhinorrhoea is that most traumatic leaks are managed conservatively at first because the majority close on their own. Following a skull-base fracture, the small dural tear frequently seals spontaneously within a week or two if the pressure across it is minimised — which is the rationale for bed rest, head elevation, avoiding nose-blowing, straining and heavy lifting, using stool softeners and sometimes a lumbar drain to lower CSF pressure. Rushing to surgery is therefore usually unnecessary and exposes the patient to operative risk for a leak that would have closed anyway. Surgical (endoscopic) repair is reserved for leaks that persist beyond this period, that recur, that are accompanied by meningitis, or that are spontaneous (associated with raised intracranial pressure, which will not resolve with rest). This stepwise approach — conservative first, surgery for the minority — balances the meningitis risk against the risks of operating.
THE BOTTOM LINE
CSF rhinorrhoea is a skull-base CSF leak risking meningitis, confirmed by beta-2 transferrin and localised by imaging, and managed conservatively first since most traumatic leaks close, with endoscopic repair for the persistent or spontaneous minority.
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KEY POINTS / NUMBERS (viva)
CSF rhinorrhoea = CSF leak from the nose via an anterior skull-base defect (cribriform plate/ethmoid roof) → ascending meningitis risk.
Clear watery unilateral discharge increased on bending/straining, halo (double-ring) sign, salty taste; risk of recurrent meningitis.
Confirm with beta-2 transferrin (specific); glucose unreliable; localise with HRCT/MRI cisternography/intrathecal fluorescein.
Treat conservatively first (bed rest, head elevation, avoid straining, lumbar drain) — most stop; endoscopic repair if persistent/recurrent meningitis/spontaneous.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Anterior nasal packing controls anterior epistaxis when first aid and cautery fail, or when no bleeding point is seen.
Anterior nasal packing
Ribbon gauze (BIPP) layered from the floor upward, or an expanding tampon (Merocel)
applies pressure to the bleeding mucosa · antibiotic cover · left 24–48 h
Anterior nasal packing controls anterior epistaxis when first aid and cautery fail: the cavity is packed firmly (ribbon gauze impregnated with BIPP, or an expanding tampon) to apply direct pressure to the bleeding mucosa, with antibiotic cover, and is left for 24–48 hours.
TECHNIQUE
The nasal cavity is packed firmly to apply pressure: ribbon gauze impregnated with BIPP (bismuth-iodoform-paraffin paste) or petroleum jelly, layered horizontally from the floor upward (an expanding tampon such as Merocel, or an inflatable device, is an alternative). It is left for 24–48 hours with antibiotic cover (to prevent toxic shock syndrome and sinusitis).
COMPLICATIONS
Complications include pressure necrosis, sinusitis, toxic shock syndrome (staphylococcal), hypoxia (a nasopulmonary reflex, especially in the elderly), dislodgement and discomfort. It is removed once the bleeding is controlled.
A NOTE ON ANTIBIOTIC COVER
An important practical point with anterior packing is the routine use of antibiotic cover while a pack is in place. A nasal pack is a foreign body sitting in a warm, moist cavity, which can become colonised by bacteria and, in particular, provides the conditions for staphylococci to produce the toxin causing toxic shock syndrome — a rare but potentially fatal complication. Packing also blocks the natural drainage of the sinuses and can precipitate sinusitis. For these reasons, patients with a pack in place are usually given prophylactic antibiotics and the pack is not left in longer than necessary (typically 24–48 hours), and they are warned to seek help if they develop fever, rash or feeling unwell — the warning signs of toxic shock.
THE BOTTOM LINE
Anterior nasal packing applies firm pressure to an anterior bleed with BIPP gauze or a tampon, left 24–48 hours under antibiotic cover to prevent sinusitis and toxic shock syndrome.
A further practical point is that packing is uncomfortable and not without risk even anteriorly, so it is used when simpler measures fail rather than as a first resort, and modern expanding tampons and inflatable packs have made the procedure quicker and better tolerated than traditional layered ribbon gauze, though the same principles of pressure, antibiotic cover and timely removal still apply.
It is also worth remembering that packing should be secured and documented, and that both nasal cavities are sometimes packed to provide counter-pressure across the septum for a stubborn septal bleed, with the patient reviewed for pack removal and any re-bleeding once the acute episode has settled.
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KEY POINTS TO REMEMBER
Anterior nasal packing controls anterior epistaxis when first aid/cautery fail or no bleeding point is seen.
Ribbon gauze with BIPP layered from the floor upward, or an expanding tampon (Merocel)/inflatable device; applies direct pressure.
Left 24–48 hours with antibiotic cover (prevent toxic shock syndrome/sinusitis).
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Posterior nasal packing is used for posterior epistaxis (from the sphenopalatine system) not controlled by an anterior pack.
Posterior packing / balloon tamponade
balloon innasopharynx
Balloon/Foley inflated posteriorly + anterior pack · for posterior bleeds · admit & monitor
Posterior packing/balloon tamponade controls posterior epistaxis (from the sphenopalatine system): a balloon (or Foley catheter) is inflated in the nasopharynx to plug the choana, combined with an anterior pack. It requires admission and monitoring because of the risk of hypoxia and discomfort.
TECHNIQUE
The traditional postnasal pack is a gauze pack placed in the nasopharynx (drawn into place via a catheter through the nose, tied with tapes over the anterior nares and through the mouth) to plug the posterior choana, combined with an anterior pack. The modern method uses an epistaxis balloon (a double-balloon device) or a Foley catheter, whose balloon is inflated in the nasopharynx and pulled forward to tamponade the bleed, again with an anterior pack.
CARE & COMPLICATIONS
A NOTE ON WHY ADMISSION IS NEEDED
The key point distinguishing posterior from anterior packing is that posterior packing requires hospital admission and monitoring, and understanding why is important. A posterior pack or balloon sits at the back of the nose against the soft palate and can, through a nasopulmonary (and nasocardiac) reflex, cause a fall in oxygen levels — particularly dangerous in the elderly patients who most often have posterior bleeds. It is also uncomfortable and may need sedation and analgesia, both of which can further depress breathing, and there is a risk of the pack dislodging and obstructing the airway. Because of these risks, a patient with a posterior pack is admitted for observation, with oxygen-saturation monitoring and cautious use of sedatives, rather than being sent home — in clear contrast to the simple anterior pack, which can often be managed as an outpatient.
THE BOTTOM LINE
Posterior packing or balloon tamponade controls posterior epistaxis but requires admission and monitoring because of the risk of hypoxia and airway problems.
A further point is that, because posterior packing is uncomfortable and carries these risks, its failure to control the bleed is now often followed relatively promptly by endoscopic sphenopalatine artery ligation rather than prolonged repacking, since definitive surgical control both stops the bleeding and spares the patient a distressing pack.
It is also worth noting that a Foley catheter, though improvised, is effective and widely used where a purpose-made epistaxis balloon is unavailable: its balloon is inflated in the nasopharynx, drawn forward to seat in the posterior choana, and secured at the nostril, taking care to pad the nasal alae to avoid pressure necrosis of the skin.
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DANGER / REMEMBER: It requires admission and monitoring (risk of hypoxia from a nasopulmonary/nasocardiac reflex, discomfort, and the need for analgesia/sedation). Complications include hypoxia/hypercapnia, dislodgement, pressure necrosis (soft palate/alae) and infection. If it fails, surgical ligation or embolization follows.
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KEY POINTS TO REMEMBER
Posterior packing is for posterior epistaxis (sphenopalatine) not controlled by an anterior pack.
Traditional postnasal gauze pack plugs the choana (via catheter, tied over nares + through mouth) + anterior pack.
Modern: epistaxis balloon or Foley catheter inflated in the nasopharynx + anterior pack.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Chemical cautery with silver nitrate is a first-line method to stop anterior epistaxis when a bleeding point is visible (especially in Little's area).
TECHNIQUE
After decongestion and local anaesthesia, a silver-nitrate stick is applied to the bleeding point/vessel to chemically cauterise (coagulate) it — applying to the periphery first, then the point. Crucially, only one side of the septum is cauterised (never both sides simultaneously — the risk of septal perforation from cartilage ischaemia). Electrocautery is an alternative, and a topical antiseptic/moisturiser cream is applied afterwards.
COMPLICATIONS & USE
Complications include septal perforation (especially with bilateral cautery), pain and mucosal damage. It is suitable for minor, visible anterior bleeds.
A NOTE ON THE ONE-SIDED CAUTERY RULE
The most important safety rule in cautery is that only one side of the septum should be cauterised at a single sitting, and the reason is worth understanding. The septal cartilage receives its blood supply from the mucosa (mucoperichondrium) on either side. If both sides are cauterised at the same point at the same time, the cartilage there is deprived of its blood supply from both surfaces and can necrose, leaving a septal perforation. This is why, if both sides need treatment, the cautery is staged — one side now and the other at a later visit — and why cautery is applied sparingly and precisely. The same principle underlies the caution against bilateral cautery for recurrent epistaxis, and it is a frequently-tested point because the resulting perforation is a preventable iatrogenic complication.
THE BOTTOM LINE
Silver-nitrate cautery is first-line for a visible anterior bleeding point, applied to one side of the septum only to avoid a perforation.
A further practical point is that cautery only works when a discrete bleeding point can actually be seen and the field is dry, so adequate decongestion, good illumination and suction are essential first; if the bleeding is too brisk to see the point, pressure or packing is used first and cautery reserved for once the field can be cleared.
It is also worth remembering that after cautery the patient is advised to keep the area moist and avoid nose-picking and forceful blowing, since a freshly cauterised spot can re-bleed, and that repeated bleeding despite adequate cautery should prompt a search for an underlying local or systemic cause rather than simply more cautery.
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KEY POINTS TO REMEMBER
Silver-nitrate chemical cautery: first-line for a visible anterior bleeding point (Little's area).
After decongestion + local anaesthesia, apply to the periphery then the point to coagulate the vessel.
Cauterise ONE side of the septum only (never both sides at once — risk of septal perforation from cartilage ischaemia).
Complications: septal perforation (esp bilateral cautery), pain, mucosal damage; electrocautery is an alternative.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Arterial ligation is the surgical control of refractory epistaxis by ligating/clipping the feeding artery when packing fails.
OPTIONS (by site of bleed)
Sphenopalatine artery ligation (endoscopic SPAL) — the main procedure for posterior epistaxis; the SPA is clipped at the sphenopalatine foramen.
Maxillary (internal maxillary) artery ligation — a transantral approach.
Anterior (± posterior) ethmoidal artery ligation — for superior/anterior bleeds from the ICA/ethmoidal system (via a medial orbital incision).
External carotid ligation — rarely.
PREFERENCE & ALTERNATIVE
Endoscopic SPA ligation is now preferred (effective and targeted). An alternative is angiographic embolization (of maxillary/ECA branches — but not the ethmoidal/ICA system, because of the risk of stroke/blindness).
A NOTE ON WHY EMBOLIZATION AVOIDS THE ETHMOIDALS
A crucial safety point in the interventional management of epistaxis is that embolization is used for the external-carotid (maxillary/sphenopalatine) supply but not for the ethmoidal arteries, and the reason is anatomical. The ethmoidal arteries arise from the ophthalmic artery, a branch of the internal carotid, which also supplies the retina and brain. Attempting to embolize this territory risks passing embolic material into the ophthalmic or cerebral circulation, causing blindness or stroke. The maxillary/sphenopalatine system, by contrast, arises from the external carotid and can be embolized relatively safely. This is why superior bleeds from the ethmoidal system are controlled by surgical ligation rather than embolization, and it is another example of how the nose's dual (internal and external carotid) blood supply dictates safe treatment choices.
THE BOTTOM LINE
Refractory epistaxis is controlled by ligating the feeding artery — endoscopic sphenopalatine ligation for posterior bleeds, ethmoidal ligation for superior ones — with embolization an option for the external-carotid supply only.
A further point is that the shift toward endoscopic sphenopalatine artery ligation reflects its high success rate and low morbidity: by targeting the vessel precisely at its foramen it controls the great majority of posterior bleeds, and it has largely replaced the older, blinder and more morbid maxillary-artery and external-carotid ligations.
It is also worth noting that arterial ligation is generally reserved for bleeds that have failed conservative measures and packing, and that in the acute setting resuscitation, correction of any coagulopathy and control of blood pressure proceed in parallel, since a definitive vascular procedure addresses the bleeding point but not an underlying bleeding tendency.
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KEY POINTS TO REMEMBER
Arterial ligation controls refractory epistaxis by clipping the feeding vessel when packing fails.
Sphenopalatine artery ligation (endoscopic SPAL) — main procedure for posterior epistaxis (clip at the sphenopalatine foramen).
Endoscopic SPA ligation now preferred; alternative — embolization of maxillary/ECA branches (NOT ethmoidal/ICA — stroke/blindness risk).
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu) is an autosomal dominant disorder of blood vessels characterised by multiple mucocutaneous telangiectasias and arteriovenous malformations.
FEATURES
Its features are recurrent epistaxis (the commonest presentation — from nasal telangiectasias), mucocutaneous telangiectasias (lips, tongue, face, fingers, GI tract), a family history (autosomal dominant), and visceral AVMs — pulmonary (risk of paradoxical embolism/stroke/brain abscess), hepatic and cerebral. Diagnosis uses the Curaçao criteria (epistaxis, telangiectasia, visceral AVM, family history).
MANAGEMENT
Management is to control the epistaxis (humidification, laser/coagulation of telangiectasias, septodermoplasty, or Young's procedure/nostril closure for severe cases; anti-angiogenics such as bevacizumab), give iron/transfusion for anaemia, and screen/treat visceral AVMs.
A NOTE ON THE SYSTEMIC IMPLICATIONS
Although recurrent epistaxis is what usually brings a patient with HHT to the ENT clinic, it is important to appreciate that HHT is a systemic disease with potentially serious visceral consequences. The same vascular malformations that bleed in the nose also occur in the lungs, liver and brain, and pulmonary arteriovenous malformations are particularly important because they allow blood to bypass the lung's filter, so clots or bacteria can pass directly to the brain, causing paradoxical strokes or brain abscesses. This is why a patient presenting with the tell-tale combination of recurrent nosebleeds, visible telangiectasias and a family history should be screened for visceral AVMs rather than having their nosebleeds treated in isolation. Recognising epistaxis as the visible tip of a systemic vascular disorder — and arranging appropriate screening — can prevent life-threatening complications, which is the key learning point.
THE BOTTOM LINE
HHT is an autosomal dominant vascular disorder presenting with recurrent epistaxis and telangiectasias, whose visceral AVMs (especially pulmonary) make systemic screening important.
A further practical point is that the epistaxis of HHT is often difficult to control and recurrent, so management aims to reduce its frequency and severity — through humidification, laser treatment of the telangiectasias and, in severe cases, procedures such as septodermoplasty or nostril closure — rather than expecting a single definitive cure, while iron replacement manages the chronic blood loss.
It is also worth being aware that the diagnosis is often first suspected in the ENT clinic by simply noticing the small red telangiectasias on the lips and tongue of a patient presenting with recurrent nosebleeds, so a careful look at the mucous membranes and a family history are simple but valuable clues to this systemic diagnosis.
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Nasal myiasis is infestation of the nose by maggots (fly larvae, e.g. Chrysomya bezziana/screwworm), common in tropical countries (including India) in patients with poor hygiene, atrophic rhinitis, foul nasal disease, leprosy, or who are debilitated/unconscious (flies lay eggs on the foul nasal discharge).
FEATURES
A NOTE ON WHY THE UNDERLYING CONDITION MATTERS
A key lesson from nasal myiasis is that it is almost always a disease of a compromised host or a foul nasal environment, so treatment must address the underlying condition, not just remove the maggots. Flies are attracted to lay their eggs by the foul-smelling discharge of atrophic rhinitis, chronic infection, malignancy, leprosy or neglected wounds, and infestation is commoner in the debilitated, the unconscious and those with poor hygiene. Simply extracting the maggots without treating the atrophic rhinitis or other predisposing condition and improving hygiene invites re-infestation. Recognising myiasis as a marker of neglect or underlying nasal disease therefore prompts a wider assessment, and its capacity for rapid, destructive tissue invasion reaching the sinuses, orbit and even the cranium is why it is treated urgently and thoroughly — a dramatic but genuinely important tropical ENT emergency.
THE BOTTOM LINE
Nasal myiasis is a destructive tropical maggot infestation of a compromised or foul nose that must be treated urgently by removing the larvae and addressing the underlying condition.
A further point is that prevention is as important as treatment: improving nasal hygiene, treating atrophic rhinitis and other predisposing conditions, and protecting debilitated or unconscious patients from flies all reduce the risk of infestation, which is why nasal myiasis is regarded as a largely preventable condition linked to neglect and poor living conditions.
It is also worth noting that instilling agents such as turpentine oil or chloroform water works by irritating and immobilising the maggots so that they emerge or can be removed, and that treatment usually requires several sittings over days because the larvae burrow deeply, with careful inspection to ensure none are left behind to continue destroying tissue.
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DANGER / REMEMBER: It causes a foul smell, nasal obstruction, blood-stained discharge, intense irritation, facial swelling/pain and a crawling sensation, with visible maggots. It can cause extensive tissue destruction (cartilage/bone) and spread to the sinuses, orbit and cranium — making it dangerous.
MANAGEMENT
Management is to remove the maggots (manually, plus instilling turpentine oil/chloroform water to kill/irritate them out over several days), with repeated cleaning, antibiotics, treatment of the underlying condition (e.g. atrophic rhinitis) and tetanus cover. It is treated as an emergency because of the tissue destruction.
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KEY POINTS TO REMEMBER
Nasal myiasis = maggot (fly larva, e.g. Chrysomya bezziana) infestation of the nose; tropical, in poor hygiene/atrophic rhinitis/leprosy/debilitated patients.
Can cause extensive tissue destruction (cartilage/bone) and spread to sinuses/orbit/cranium — dangerous.
Rx: remove maggots (manual + turpentine oil/chloroform water over days), repeated cleaning, antibiotics, treat underlying cause, tetanus cover.
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SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Woodruff's plexus is a venous (and arterial) plexus in the posterior part of the nasal cavity, on the lateral wall inferior/posterior to the posterior end of the inferior turbinate, near the posterior choana.
SIGNIFICANCE
Its importance is that it is the source of posterior epistaxis (just as Little's area is the source of anterior epistaxis). Posterior bleeds from Woodruff's plexus (and the sphenopalatine branches) occur in older/hypertensive patients, are more profuse and harder to control, and often need posterior packing or sphenopalatine artery ligation.
CONTRAST
It contrasts with Little's area (the antero-inferior septum, the site of anterior epistaxis) — Little's for anterior, Woodruff's for posterior.
A NOTE ON ITS PAIRING WITH LITTLE'S AREA
The value of knowing Woodruff's plexus is that it provides the posterior counterpart to Little's area, completing the picture of where nosebleeds arise. Just as Little's area explains the common, minor, easily-controlled anterior bleeds of the young, Woodruff's plexus (with the sphenopalatine branches) explains the less common but more dangerous posterior bleeds of older, hypertensive patients — bleeds that cannot be seen or pinched from the front, that run into the throat, and that often need posterior packing or sphenopalatine artery ligation. Remembering the pair — Little's area anteriorly, Woodruff's plexus posteriorly — gives a simple anatomical framework for understanding why anterior and posterior epistaxis behave so differently and are managed so differently, which is exactly why examiners like to ask about it.
THE BOTTOM LINE
Woodruff's plexus is the posterior lateral-wall source of the more dangerous posterior epistaxis, the counterpart to Little's area for anterior bleeds.
A further point is that identifying the bleed as posterior — arising from Woodruff's plexus or the sphenopalatine branches rather than the visible anterior septum — changes the whole management, prompting posterior packing or sphenopalatine ligation instead of the simple anterior measures that would be futile for a bleed arising deep in the back of the nose.
It is also worth appreciating that, historically, posterior bleeds attributed to Woodruff's plexus were difficult to manage precisely because the source lay out of easy reach at the back of the nose, and that modern endoscopic techniques have transformed this by allowing the sphenopalatine artery supplying the area to be identified and clipped directly under vision.
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KEY POINTS TO REMEMBER
Woodruff's plexus = a venous/arterial plexus in the posterior nasal cavity, on the lateral wall below/behind the posterior end of the inferior turbinate.
It is the source of posterior epistaxis (as Little's area is for anterior epistaxis).
Posterior bleeds (older/hypertensive patients) are more profuse and harder to control — often need posterior packing or SPA ligation.