Clinical Medicine and Surgery I · Exam 3 — Study Guide

Also tested

• Canal versus middle ear disease. Pain on moving the tragus or pinna localizes disease to the canal, because middle ear infection sits behind an intact drum and is unaffected by moving the external ear.
• Retained ear canal foreign body. A porous object obstructs drainage and acts as a nidus for infection; foul unilateral discharge without pain or fever in a young child should prompt a search for something in the canal.
• Vertigo after ear trauma. A simple perforation does not cause vertigo, so vertigo calls for urgent assessment for inner ear injury (ossicular disruption with perilymphatic fistula, or labyrinthine injury) as well as for a perforation.
• Embedded earring back. It should be removed because infection is the main risk; removal treats the source and prevents spread into the auricular cartilage, where perichondritis can deform the ear.
• Otitis externa with a swollen canal. When edema stops drops at the outer canal, place an ear wick. It is an absorbent strip that draws medication along the canal by capillary action, restoring delivery without changing the drug.
• Sudden pain relief in otitis media. In acute otitis media pain comes from pus under pressure stretching the drum. When the drum perforates, the pressure is released, pain stops abruptly and discharge appears.
• Removing a smooth round object from the canal. Forceps push it deeper. Instead, pass a hook or curette beyond it under direct vision and draw it outward, since the risk is pushing the object against or through the drum.
• Swimmer's otitis externa. Treatment must cover Pseudomonas and Staphylococcus. Water raises canal pH and macerates skin, favoring Pseudomonas; topical fluoroquinolones cover both, whereas oral amoxicillin would be inadequate.
• Necrotizing external otitis. It is confirmed by imaging (computed tomography or magnetic resonance imaging) showing infection in the bony structures.
• Facial palsy in necrotising otitis externa. It means the infection has reached the skull base and facial nerve, marking advanced disease and a worse prognosis.
• Preventing otitis externa. Dry the ears after swimming and avoid cotton buds: retained water raises the pH and macerates the skin, while cotton buds strip the protective wax and abrade the epithelium.
• Otitis externa frequency. About ten percent of people experience otitis externa in their lifetime.
• Fungal external ear infection. Treatment involves clearing the debris and topical antifungals; cleaning matters as much as the drops.
• Home care in otitis externa. Keep the ear dry and finish the full course, because the pain settles well before the infection does.
• Foreign body in the ear canal. A smooth, round, manufactured blue object in the canal is a foreign body in the ear canal, because its color and shape are ones no biological material has.
• Ear canal infection with water exposure. Pain on moving the pinna localizes disease to the canal; water macerates canal skin and raises its pH so Pseudomonas and Staphylococcus overgrow. Treat with topical ciprofloxacin-dexamethasone: the fluoroquinolone covers those organisms and the steroid shrinks the edema.
• Otitis externa with spreading infection. Topical therapy is first line because disease is confined to canal skin; once infection extends into surrounding soft tissue, with cellulitis, fever and regional nodes, it is beyond a topical agent and the next step is to add systemic antibiotics.
• Small traumatic tympanic membrane perforation. With clean edges and no vertigo or facial nerve deficit, keep the ear dry and review: the drum heals spontaneously, and keeping water out stops bacteria reaching the middle ear through the hole.
• Persistent tympanic membrane perforation. Most close within weeks to a few months; one still open at eight months with persistent conductive loss is unlikely to heal spontaneously, so refer for consideration of tympanoplasty, which restores hearing and closes the route for water.
• Tragus. The small projection immediately in front of the ear canal opening, which is why pressing it hurts in canal infection.
• Clinical divisions of the ear. The ear is separated into three: external, middle and inner.
• Otitis externa with significant pain. Adding a corticosteroid to the antibiotic drops addresses the pain directly, because it reduces pain and inflammation.

Also tested

• Suspected canal carcinoma. Otitis externa unresponsive to appropriate treatment, with bloody otorrhea and friable tissue, needs biopsy of the canal lesion, since only histology distinguishes malignancy from chronic inflammation.
• Diving barotrauma. Persistent vertigo and sensorineural loss after diving suggest inner ear barotrauma with possible perilymphatic fistula, from a ruptured round or oval window membrane; it needs prompt specialist assessment and avoidance of straining.
• Flying with a cold. Use a topical decongestant before descent and swallow or yawn frequently; the decongestant shrinks the mucosa around the eustachian tube opening so it can open and equalize pressure.
• Undrained auricular swelling. Left undrained, a swollen ear leads to permanent deformity, known as cauliflower ear.
• Avulsed auricle. Recovered detached tissue should be reattached; reattachment is often successful.
• Auricular hematoma. A tense, boggy swelling of the auricle with loss of the normal ridges should be drained now; early drainage is what prevents permanent deformity.
• Earlobe keloid. After excision the patient must be followed closely for recurrence, which is common.
• Auricular hematoma. Drain within seven days; after that, granulation tissue makes drainage much harder.
• Auricle blow that looks bruised but not swollen. Arrange re-examination in twelve to twenty-four hours, because the collection can appear hours after the injury.
• Perichondritis. A red, hot, exquisitely tender auricle that spares the lobule, which contains no cartilage, implicates the perichondrium. Pseudomonas is the usual organism after high piercings, so treatment needs antipseudomonal antibiotics or the cartilage necroses and the ear deforms.
• Swollen, tense, purple auricle. Blood collecting between the perichondrium and the cartilage strips the cartilage of its blood supply, which comes entirely from the perichondrium; untreated it necroses into cauliflower ear, so treat with drainage and a pressure dressing, which stops it reaccumulating.
• Keloid. Firm rounded overgrowths of scar tissue at a site of previous trauma, extending beyond the original wound.

Also tested

• Ear discharge character. Scanty discharge suggests the canal, which has no mucous glands; mucoid discharge suggests the middle ear, where mucous membrane exists, and profuse mucoid otorrhea comes through a perforation.
• Allergic rhinitis and the ear. Mucosal edema obstructs the eustachian tube, which is lined by the same respiratory mucosa as the nose; trapped middle ear air is absorbed, the drum retracts, and fullness with popping results.
• Eustachian tube dysfunction. When the tube cannot ventilate the middle ear, trapped air is absorbed, pressure falls below atmospheric and the drum retracts. Tympanometry shows a type C tympanogram, with the peak shifted to negative pressure.
• Normal tympanic membrane. The normal drum is pearly gray; loss of that appearance is the first sign something lies behind it.
• Pneumatic otoscopy. Puffing air against the drum through a bulb assesses whether the drum moves; reduced mobility signals fluid or pressure behind it.
• Normal drum. A normal tympanic membrane is pearly gray and mobile.
• Forceful exhalation against a pinched nose. With purulent nasal discharge it can force infected material into the middle ear, which risks acute otitis media.
• Diving ear pain with vertigo. Spinning vertigo, ringing, nausea and reduced hearing mean the inner ear has been involved; rupture of the round or oval window adds these features.
• Chronic otitis media. A perforation that has failed to heal, with recurrent painless discharge and conductive hearing loss over years, defines chronic suppurative otitis media; absence of pain separates it from acute infection, and absence of keratin debris or a retraction pocket separates it from cholesteatoma.
• Eustachian tube in young children. The child's tube is shorter, wider and flatter (nearly horizontal) than the adult tube, which runs downward at an angle, so nasopharyngeal secretions and organisms reach the middle ear easily and drain poorly; this is why young children get infections more often than adults.
• Barotrauma. Severe ear pain and muffled hearing beginning during the descent of a flight, with a dark blue-black drum that barely moves on insufflation, indicate barotrauma with hemotympanum (blood behind the eardrum).

Also tested

• Straightening the canal in a toddler. The infant and toddler canal runs upward from the drum, so pull the pinna downward and backward. In older children and adults the pinna is pulled up and back.
• Painless discharge in chronic suppurative otitis media. The perforation gives the middle ear a permanent outlet, so pressure never builds and infection appears as discharge rather than pain. Painlessness is the hallmark separating chronic from acute disease.
• Watchful waiting in acute otitis media. Observation is reasonable with a plan to treat if not improving, provided the child is older, disease is mild and follow-up is reliable. Start antibiotics if there is no improvement in 48 to 72 hours.
• Otitis media failing amoxicillin. Persisting fever and a bulging drum after 72 hours of adequate first-line therapy suggest a beta-lactamase producing organism, typically Haemophilus influenzae or Moraxella catarrhalis. Change to amoxicillin-clavulanate, which keeps pneumococcal coverage.
• Course of acute otitis media. Most episodes resolve spontaneously, which is why watchful waiting is reasonable.
• Diagnosing acute otitis media. With fever, ear pain and a red bulging drum, no confirmatory test is needed; the diagnosis is clinical.
• Unvaccinated child with acute otitis media. Haemophilus influenzae becomes a greater concern, because vaccination is why that organism has become less common.
• Mastoiditis. The mastoid air cells communicate directly with the middle ear, forming one continuous mucosa-lined space, so infection extends by direct continuity; mastoiditis is the classic suppurative complication of untreated otitis media.
• Conductive loss from middle ear fluid. Weber lateralizes toward the affected ear (here, to the right), and bone conduction exceeds air conduction in that ear.
• Recurrent otitis media with persistent effusion. Recurrent acute infections plus a persistent bilateral effusion (flat tympanograms) and hearing concern at the age of language acquisition justify referral for consideration of tympanostomy tubes, which ventilate the middle ear, restore hearing and reduce recurrence.
• Effusion after treated otitis media. Sterile fluid often takes weeks to months to clear as the eustachian tube recovers. An amber, non-bulging drum in an afebrile, painless child is a resolving effusion, so management is observation, with intervention reserved for persistence or developmental concern.
• Chronic otitis media in primary care. Management is referral to an ear, nose and throat specialist.
• Cause of acute otitis media. By far the commonest cause overall is a virus; most episodes are viral, which is why most resolve without antibiotics.
• Ear infection after a cold. Ear pain in a child a few days into a runny nose and cough is most likely acute otitis media caused by a virus; most acute otitis media is viral, so most resolves without antibiotics.
• Acute otitis media treatment. A bulging drum with reduced mobility and acute fever indicates bacterial acute otitis media, not a simple effusion. High-dose oral amoxicillin is first line in a child with no recent antibiotic exposure and no penicillin allergy.

Also tested

• Cholesteatoma complications. Vertigo with a same-sided facial palsy involving the forehead means the cholesteatoma is eroding into the labyrinth and facial nerve canal. Accumulating keratin releases enzymes that erode adjacent bone.
• Imaging cholesteatoma. Computed tomography defines the extent of a suspected cholesteatoma and is especially useful when the drum is opaque and extent cannot be judged by looking.
• Perforation after acute otitis media. A small perforation that follows discharge may close within days, in as little as forty-eight to seventy-two hours.

Also tested

• Wax impaction. Complete occlusion by wax causes a purely mechanical conductive loss; the drum, ossicles and cochlea are normal. Weber lateralizes to the blocked ear and hearing returns to baseline once the wax is removed.
• Non-healing external ear "infection". An external ear problem that fails repeated treatment and now bleeds on touch with an irregular growth needs a biopsy of the lesion, because canal carcinoma is often misdiagnosed as external otitis.
• Rinne test. It compares air conduction against bone conduction in one ear.
• Weber test. It compares bone conduction between the two ears: a tuning fork is placed on the midline and the patient says which side is louder.
• Otosclerosis. It causes gradual conductive hearing loss with a normal-looking drum, and hearing is better in noise than in a quiet room.

Also tested

• Wax removal with possible drum defect. Irrigation is contraindicated when the drum may not be intact, since water forced into the middle ear causes suppurative otitis media; use microsuction or a curette under direct vision.
• Mixed hearing loss. An air-bone gap indicates a conductive component, and elevated bone conduction thresholds indicate a sensorineural component. Both together define a mixed loss, so correcting the conductive part will not restore normal hearing.
• Shallow tympanogram peak at normal pressure. It indicates a stiff mechanism, as in ossicular fixation (type As), pointing to otosclerosis or tympanosclerosis.
• Weber lateralizing to one ear. A Weber that lateralizes to the left ear means a left conductive loss or a right sensorineural loss: it lateralizes toward a conductive loss and away from a sensorineural loss, so only Rinne separates the two.
• Keloid. An overgrowth of collagen in response to skin injury that extends beyond the boundaries of the original wound, unlike a hypertrophic scar, which stays within it; ear piercing is the classic auricular trigger, and keloids recur readily after excision.
• Tympanogram. Type A indicates a normal middle ear.

Also tested

• Otosclerosis counseling. It often runs in families and may worsen during pregnancy.
• Imaging in sudden hearing loss. Magnetic resonance imaging is done to exclude a retrocochlear lesion such as a schwannoma, because a proportion of sudden loss turns out to be vestibular schwannoma and clinical features cannot identify them.
• Ototoxic drug classes. Aminoglycosides destroy cochlear hair cells, usually permanently, starting at high frequencies; loop diuretics affect the stria vascularis and their effect is more often reversible.
• Childhood hearing loss urgency. Language acquisition depends on hearing during a limited early-childhood window. Reduced auditory input then produces delays that persist even after hearing is restored, so the threshold to intervene is lower than in adults.
• Aminoglycoside monitoring. Baseline and serial audiometry are used because aminoglycosides damage the outer hair cells at the cochlear base, which encode the highest frequencies. Early detection allows the drug to be changed, as the damage is usually permanent.
• Otosclerosis on tuning fork testing. Abnormal bone fixes the stapes footplate in the oval window, so bone conduction exceeds air conduction on the affected side (reversed Rinne). The cochlea is normal, so this is a conductive loss.
• Untreated presbycusis. Reduced auditory input contributes to social withdrawal, isolation, depression and accelerated cognitive decline. Framing hearing aids as protection against these is usually what persuades reluctant patients.
• Normal hearing range. Normal hearing is zero to twenty decibels, and the whole scale then runs in twenties.
• Hearing screening age. Hearing is screened routinely in primary care from age sixty-five.
• Profound hearing loss. Hearing loss is classified as profound above eighty decibels.
• Pure tone audiometry. This test presents single tones at set frequencies to find the softest audible level.
• Rinne in sensorineural loss. Air conduction remains greater than bone conduction bilaterally, because a sensorineural loss leaves the normal Rinne relationship intact.
• Ototoxicity. Loop diuretics are ototoxic; ototoxicity from the diuretic can explain a sensorineural hearing loss.
• Otosclerosis treatment. Stapedectomy and a hearing aid are both reasonable: surgery addresses the mechanism, an aid amplifies. Surgery carries a small chance of a sensorineural loss.
• High-frequency sensorineural loss. Consonants are high-frequency sounds and carry most of the meaning, whereas vowels are low-frequency and loud; losing high frequencies removes the information while leaving the sound.
• Weber in unilateral sensorineural loss. It lateralizes to the unaffected ear, away from the bad side.
• Age-related hearing loss. The characteristic audiogram is a curve sloping downward at high frequencies.
• Acoustic neuroma. It is a sensorineural cause of hearing loss: a tuning fork on the forehead is loudest in the unaffected ear, and in the affected ear air conduction exceeds bone conduction.
• Otosclerosis tuning fork findings. Otosclerosis is a conductive loss, so Weber lateralizes to the affected ear and bone conduction in that ear is at least equal to air.

Also tested

• Exostoses. These are multiple smooth bony swellings of the canal wall that narrow the lumen but are covered by normal skin.
• Temporary threshold shift. Intense sound temporarily fatigues cochlear hair cells, and hearing recovers within 24 to 48 hours; repeated temporary shifts eventually become permanent, so recovery is a warning rather than a reassurance.
• Exostoses (surfer's ear). Repeated exposure to cold water stimulates new bone formation in the canal walls, giving bilateral, symmetrical swellings that trap water and debris and cause recurrent otitis externa.
• Jugular foramen mass. A tumor at the jugular foramen compresses cranial nerves nine, ten and eleven (glossopharyngeal, vagus, spinal accessory), causing difficulty swallowing, hoarseness and shoulder weakness alongside pulsatile tinnitus and conductive loss.
• Bilateral non-pulsatile tinnitus. With symmetrical sensorineural loss it is generated centrally as the brain compensates for reduced input. Management is reassurance, hearing aids and sound therapy; amplification often reduces it, and sound therapy reduces the contrast between tinnitus and silence.
• Tinnitus. It is sound perceived with no external source, such as ringing, buzzing, humming or hissing.
• Glomus tumor. Paralysis of the ninth, tenth and eleventh cranial nerves may accompany it.
• Unilateral pulsatile tinnitus. Tinnitus in one ear that beats in time with the pulse needs further investigation, since unilateral and pulsatile tinnitus are both red flags.
• Exostoses. Hard, smooth, symmetric swellings of the canal wall that narrow both canals and trap debris are exostoses, bony growths from repeated cold water exposure.
• Tinnitus drug treatment. No drug has proved better than placebo; masking and biofeedback may help instead.
• Tinnitus red flag. Pulsatile unilateral tinnitus requires investigation for a vascular cause. Tinnitus that is unilateral or synchronous with the pulse suggests turbulent blood flow or a vascular middle ear lesion such as a glomus tumor.
• Noise-induced hearing loss. Cumulative noise exposure classically produces an audiogram notch centered around 4000 hertz with some recovery at higher frequencies, unlike presbycusis, which declines progressively as frequency rises and does not recover; the curve shape makes the diagnosis.

Also tested

• Autoimmune inner ear disease. Rapidly progressive bilateral sensorineural loss is managed with a trial of systemic corticosteroids, which is both therapy and a diagnostic test, as it is one of the few sensorineural losses that responds to treatment.
• Sudden sensorineural hearing loss. It is a syndrome rather than a disease, and a cause is often never found; because the differential includes treatable and dangerous entries, it prompts urgent referral and imaging.
• Suspected perilymphatic fistula. Initial management is bed rest with head elevation and avoidance of straining, since the leak is pressure-dependent; many fistulae close spontaneously before surgical repair is considered.
• Syphilis testing in hearing loss. When syphilis is suspected as a cause, order fluorescent treponemal antibody and microhemagglutination assays.
• Syphilis in sensorineural hearing loss. It is specifically sought because it is treatable and mimics another condition exactly; its presentation is often indistinguishable.
• Sudden one-sided hearing loss. It needs same-day assessment because treatment works only if started early.
• Sensorineural loss with sexual infection risk. Consider human immunodeficiency virus and syphilis in unexplained sensorineural hearing loss with multiple risk factors, since both can produce it.
• Temporary threshold shift. It is hearing loss recovering in twenty-four to forty-eight hours.
• Sudden sensorineural hearing loss. It demands prompt specialist referral, because the corticosteroid window is short.
• Sudden hearing loss and vertigo after a dive. With a popping sensation at onset, management is symptomatic treatment and specialist referral.
• Sudden hearing loss and vertigo after heavy lifting. With a pop at onset, the likely mechanism is an abnormal opening at the round or oval window.
• Waardenburg syndrome. Sensorineural deafness with a white forelock, widely spaced medial canthi and heterochromia of the irises defines Waardenburg syndrome, a neural crest disorder; neural crest gives rise to the melanocytes of skin, hair and iris and to the stria vascularis of the cochlea.
• Waardenburg syndrome. Sensorineural hearing loss with a white forelock and eyes of different colors suggests Waardenburg syndrome, one of the named hereditary causes.
• Syphilis and inner ear symptoms. In fluctuating hearing loss, tinnitus and vertigo with suspected syphilis, the Venereal Disease Research Laboratory test should not be relied on; it is specifically described as not helpful here.

Also tested

• Vestibular neuronitis counseling. It is benign and self-limiting and settles over days to weeks; patients should move about rather than lie still, since bed rest and vestibular suppressants delay central compensation.
• Otosyphilis. Syphilis can mimic Meniere disease exactly and is worth excluding serologically, because it has a specific curative treatment while Meniere does not.
• Meniere disease self-care. Restricting dietary salt, caffeine and alcohol is advised. The underlying abnormality is endolymphatic hydrops; less sodium lowers fluid retention and endolymph volume, and caffeine and alcohol are recognized triggers.
• Meniere disease. It is defined by episodic vertigo lasting minutes to hours, fluctuating sensorineural hearing loss, tinnitus and aural fullness, all in the same ear. Loss is low-frequency because the cochlear apex, which codes low frequencies, distends most from endolymphatic hydrops.
• Audiogram in Meniere disease. Loss confined to the low frequencies that improves between attacks suggests Meniere disease: a low-frequency, fluctuating sensorineural loss.
• Benign paroxysmal positional vertigo. Most cases are thought to be caused by debris in the posterior semicircular canal.
• Positional nystagmus on Dix-Hallpike. Nystagmus that begins after a brief delay, lasts under a minute and diminishes on repetition indicates a peripheral cause, consistent with positional vertigo; central positional nystagmus begins immediately, persists and does not fatigue.

Also tested

• Central versus peripheral vertigo. Headache, ataxia, or focal neurological signs raise concern for a central cause. Severe truncal ataxia, direction-changing nystagmus, diplopia, dysarthria or facial numbness point to the brainstem or cerebellum and require urgent imaging.
• Suspected non-organic hearing loss. Auditory brainstem response testing records electrical activity along the auditory pathway, giving a threshold estimate without the patient reporting anything. It resolves discrepancies between claimed and demonstrated hearing.
• Vertigo with crossed sensory findings. Acute vertigo with facial weakness, crossed loss of pain sensation and a drooping eyelid requires emergency evaluation for stroke, since crossed sensory findings mean a brainstem problem.
• Vestibular schwannoma and balance. Balance is only mildly affected because central compensation adjusts to a slowly growing lesion: vestibular input falls gradually over years and the brainstem and cerebellum recalibrate, so patients describe unsteadiness rather than the dramatic spinning of a sudden vestibular loss such as neuronitis.

Also tested

• Invasive fungal sinusitis. Black necrotic mucosa in a diabetic or immunocompromised patient indicates angioinvasive fungal disease; because the blood supply is destroyed, surgical debridement is needed alongside systemic therapy and control of the diabetes.
• Impaired mucociliary clearance. The cilia can no longer move the mucus blanket out of the sinus: chronic inflammation damages the cilia and thickens the mucus, so secretions stagnate and invite repeated infection.
• Orbital cellulitis from sinusitis. Periorbital swelling with painful restricted eye movement and diplopia means infection has crossed the paper-thin lamina papyracea from the ethmoid sinus; it needs urgent imaging and admission for intravenous antibiotics.
• Sinusitis with immunosuppression. Management needs earlier imaging and a lower threshold for invasive fungal disease, because Aspergillus and the mucormycetes can invade blood vessels and cause tissue infarction within days; inspect the nasal mucosa for necrotic tissue.
• Sinusitis pain on bending. Bending forward increases the hydrostatic pressure of the fluid within the obstructed sinus against inflamed mucosa; postural worsening is characteristic of sinusitis.
• Bacterial rhinosinusitis. Symptoms persisting ten days or more without improvement help identify the small bacterial minority of rhinosinusitis (90 to 98 percent is viral). Amoxicillin-clavulanate twice daily is first line, as clavulanate covers beta-lactamase producing Haemophilus influenzae and Moraxella catarrhalis plus pneumococcus.
• Ethmoid sinusitis and the orbit. The lamina papyracea, the medial orbital wall separating ethmoid from orbit, is paper-thin, the thinnest bone in the orbit. Ethmoid sinusitis is therefore the commonest sinus source of orbital cellulitis, particularly in children.
• Sinusitis in children. The same criteria apply as in adults, so ten days of purulent discharge without improvement indicates bacterial sinusitis. Children have maxillary and ethmoid sinuses from birth, and ethmoid proximity to the orbit makes recognition important.
• Fever in suspected bacterial sinusitis. Before accepting fever as a sign, confirm that the patient is not taking an antipyretic.
• Viral share of rhinosinusitis. Ninety to ninety-eight percent of acute rhinosinusitis is viral.
• Sinus tenderness. Absence of tenderness on pressing the maxillary and frontal areas argues against bacterial infection: that pain is reproducible on palpation, whereas a common cold's is not.
• Early, mild rhinosinusitis. With afebrile course, clear discharge and pressure not reproduced on palpation, use symptomatic treatment alone, since most acute rhinosinusitis is viral and improves without antibiotics.
• Fungus ball. In an immunocompetent patient with unilateral sinus disease and no bony erosion, surgery alone is the treatment. Antifungals are added only if bony erosion has occurred.
• Sinusitis with orbital signs. Diplopia and periorbital swelling are named urgent features, so the priority is urgent computed tomography.
• Rhinosinusitis duration. Acute is under four weeks and chronic is beyond twelve weeks, with subacute occupying the interval between four and twelve.
• Chronic rhinosinusitis. Continuous symptoms beyond 12 weeks define it; repeated antibiotic courses treat the flares without changing the underlying problem of impaired mucociliary clearance with persistent inflammation.
• Sinusitis in immunocompromised patients. Fungi are the organisms that cause it.
• Nasal discharge color. Yellow or green is the least helpful color for deciding on antibiotics; color barely helps, and only black, rust or pure clear carry any signal.
• Bacterial sinusitis. Double worsening, unilateral pain reproduced on palpation and fever together point to a bacterial cause; start amoxicillin with clavulanate.
• Sinusitis with altered mental status. Altered mental status, like diplopia and periorbital swelling, is an urgent feature; it indicates the infection may have crossed into the cranial cavity (meningitis, epidural or subdural collection, brain abscess), so urgent evaluation for intracranial extension with imaging and admission is needed.
• Imaging in chronic sinusitis. Sinus computed tomography contributes extent, anatomy and response.
• Acute sinusitis risk factors. Smoking is a named risk factor, alongside chronic allergies, immunocompromise and anatomical defects.
• Counseling a patient referred for persistent sinus disease. Tell the patient four elements: diagnosis, cause, treatment and referral.

Also tested

• Auricular laceration. A full-thickness break in the skin and cartilage, it is an open wound rather than a swelling.
• Septal perforation from topical agents. The anterior septum has thin mucosa over cartilage with no other blood supply, so chronic ischemia from prolonged intranasal steroid (especially sprayed at the septum) or cocaine can perforate it.
• Septal deviation. An asymptomatic deviation needs no treatment. It is treated only when it causes obstruction, recurrent epistaxis from the drier open side, obstructive sleep apnea, snoring or facial pain.
• Timing of nasal fracture reduction. A displaced fracture is straightened once swelling settles, within about two weeks. Swelling obscures bony position, and the bones begin to unite after roughly two weeks.
• Saddle nose deformity. Septal cartilage has no blood supply of its own and depends on perichondrium. A hematoma strips it away, causing avascular necrosis and collapse of the dorsum, which is why drainage is urgent rather than elective.
• Undrained septal hematoma. The concern is cartilage damage, because the collection separates cartilage from its blood supply.
• Septal perforation. Management is to treat the cause; otherwise, septoplasty.

Also tested

• Epistaxis on anticoagulation. Clotting studies are not routine in epistaxis but are indicated in anticoagulated patients; correct the anticoagulation as well as treating the nose, or the systemic reason for bleeding is left unaddressed.
• Brisk epistaxis with hemodynamic compromise. Dizziness and confusion mean an intravenous line and fluids come first, since resuscitation precedes control of the bleeding point. Bilateral bleeding with no visible source suggests a posterior (sphenopalatine artery) bleed.
• Epistaxis first aid. Pinch the soft part (alae) continuously for ten minutes, leaning forward. The bleeding point in 90 percent of cases is Kiesselbach plexus on the anterior septum; leaning forward stops blood tracking into the pharynx.
• Epistaxis with clots. Blow out clots first, since retained clot holds the vessel open; then spray a topical vasoconstrictor such as oxymetazoline and pinch the alae continuously for ten minutes.
• Childhood anterior epistaxis. Ninety percent of nosebleeds are anterior, from Kiesselbach plexus; digital trauma is the commonest cause and dry winter air worsens it. Short bleeds stopped by pressure in a well child are managed conservatively with humidification and behavior change.
• Epistaxis blood tests. Clotting studies (prothrombin time and international normalized ratio) are not routine for epistaxis. They are reserved for anticoagulated patients or those with other evidence of a bleeding tendency.
• After epistaxis is controlled. The patient must avoid blowing the nose.
• Positioning in epistaxis. The patient should sit up and lean forward so blood is not swallowed.
• Preventing recurrent epistaxis. A chronic dry nose is a named risk factor, so humidify and keep the nose moist.
• Epistaxis on anticoagulants. Prolonged heavy bleeding in an anticoagulated patient calls for a clotting study, crossmatch and count; the clotting study is indicated because of the anticoagulation.
• Recurrent nosebleeds in children. The commonest cause is trauma from the child's own finger, with a chronic dry nose as a risk factor.

Also tested

• Nasal foreign body in a calm child. The first attempt is a parent-delivered positive pressure blow: the parent seals the child's mouth with their own and blows while the unaffected nostril is occluded. It is atraumatic and needs no instruments.
• Minor nasal trauma. When tenderness is confined to the bony bridge, each nostril is patent, the nose is straight without septal deviation, and there is no septal hematoma, use ice and elevation without radiography. Treatment of an undisplaced fracture is symptomatic.
• Unilateral foul nasal discharge in a child. Unilateral, foul-smelling purulent discharge in a young child is a retained nasal foreign body until proven otherwise. Direct visualization of the nasal vestibule makes the diagnosis and allows removal.
• Nasal trauma imaging. Imaging can be omitted only when all four reassuring criteria are met. A deviated nose or a blocked nostril fails them, so radiography is indicated and the nose is assessed for reduction.
• Button battery in the nose. Urgent removal is required. The battery generates current across moist mucosa, producing hydroxide ions and liquefactive necrosis that can perforate the septum within hours, making it the one nasal foreign body treated as a true emergency.
• Nasal injury check. Before discharge, inspect and feel the septum for a boggy swelling. A septal hematoma is easy to miss because attention goes to the bridge, yet it destroys cartilage within days if not drained.
• Clear rhinorrhea after trauma. Clear nasal fluid after significant facial or head trauma, especially with bilateral periorbital bruising, suggests a cerebrospinal fluid leak from a skull base fracture through the cribriform plate. It is a neurosurgical problem with a risk of meningitis.
• Nasal foreign body diagnosis. Direct visualization establishes the diagnosis; imaging is rarely needed.
• Nasal fracture. The external nose is deviated and swollen with blood at the nares: deformity, not just bleeding.
• Nasal trauma imaging. When swelling and tenderness are confined to the bony bridge, breathing is free through each nostril, the nose is straight and there is no septal hematoma (all four criteria met), no imaging is required.

Also tested

• Adenoidal hypertrophy. Chronic mouth breathing, snoring and hyponasal speech with bilateral nasal obstruction and no discharge indicate it; the bilateral, discharge-free pattern distinguishes it from a foreign body or infection.
• Vasomotor rhinitis. Clear bilateral rhinorrhea triggered by cold air, strong smells and alcohol, with no itch and negative allergy testing, is driven by autonomic dysregulation rather than an immunoglobulin E response.
• Conductive anosmia. Polyps, chronic inflammation or marked mucosal swelling block airflow to the olfactory epithelium, so receptors are intact but never reached; treating the obstruction can restore smell.
• Allergic rhinitis treatment. About 80 percent of patients need two or more agents because different symptoms are driven by different mediators. A typical combination is an antihistamine with an intranasal corticosteroid, adding a leukotriene inhibitor at night, and immunotherapy if drugs are insufficient.
• Rebound congestion. Prolonged topical decongestant use worsens congestion: receptors downregulate and vessels dilate more each time the drug wears off, prompting more frequent use. These sprays carry a three-to-five-day limit.
• Nasal polyps after surgery. Recurrence is expected, because polyps arise from ongoing mucosal inflammation and surgery gives only temporary relief. Medical treatment of the underlying inflammation continues afterwards.
• Using an intranasal corticosteroid. Aim the spray laterally toward the turbinate, away from the septum. Repeated delivery to the thin mucosa over the septal cartilage, with chronic vasoconstriction there, is a named cause of septal perforation.

Also tested

• Nasopharyngeal carcinoma and sex. Incidence is two to threefold higher in males.

Also tested

• Nodal level in neck metastasis. The involved nodal level predicts where the primary is likely to be, because each region drains to a predictable group: jugulodigastric to the tonsil, juguloomohyoid to the tongue, submandibular to the face, sinuses and mouth.
• Jugulodigastric node. This deep cervical node drains the palatine tonsil, so tonsillitis produces a tender node high in the jugular chain just below the angle of the jaw; it is the node examined in a sore throat.
• Posterior triangle nerve injury. The spinal accessory nerve crosses the muscular floor of the occipital triangle before passing deep to trapezius, leaving it superficial and exposed; injury denervates trapezius and causes a painful drooping shoulder.

Also tested

• Imaging a suspected thyroid cancer. Use ultrasound, which characterizes nodules without radiation and guides aspiration. Avoid iodine-containing contrast computed tomography, because the iodine load saturates the thyroid and compromises subsequent radioiodine treatment.
• Neck mass features suggesting malignancy. These are no infectious origin, duration over two weeks, size greater than 1.5 centimeters, firm, non-cystic, non-tender with little or no mobility, age over 40, and tobacco and alcohol use. Size alone is not diagnostic.
• Malignant node features. An immobile, firm, non-tender cervical node raises concern for malignancy: immobility suggests tumor fixation to surrounding structures, firmness suggests solid tissue, and non-tenderness points away from inflammation.
• Laboratory workup of a persistent neck mass. It includes full blood count, HIV and Epstein-Barr serology, inflammatory markers and thyroid panels; the panel is broad because the differential is broad.
• Positron emission tomography. It measures metabolic uptake of tagged glucose, higher in cancer and inflammation, so a positive result cannot by itself establish cancer.
• Neck mass persisting after antibiotics. Failure of an antibiotic trial is the point to refer to a specialist now rather than prescribe another course, because early and aggressive treatment is needed in some neoplastic conditions.
• Fluctuance in a neck mass. A soft mass with a fluid wave transmits pressure as a fluid would, so it suggests a cystic lesion containing liquid rather than solid tissue. Other rules of thumb: pulsatility means vascular, years of stability means benign, rapid growth means infection or lymphoma.
• Rapidly growing neck mass. Rapid growth is usually infectious when other infective symptoms accompany it and lymphoma when they do not, as with night sweats and weight loss instead; lymphoma is also the noted exception to the rule that masses under 40 are usually inflammatory.
• Neck lump with an obvious infective context. Reactive adenopathy is expected in the first days of an infection and regresses in one to two weeks; duration over two weeks is what appears on the malignancy list, so treat the infection and reassess in two weeks.
• Painless enlarging node under age 40. Most neck masses under 40 are inflammatory, but a painless, firm, enlarging supraclavicular node with no infection suggests lymphoma, with Hodgkin lymphoma the named exception.

Also tested

• Infected branchial cleft cyst. Control the infection first, then excise the cyst and its tract; leaving the tract behind is what causes recurrence.
• Neonatal neck teratoma. A large firm neck mass with calcifications noted at birth is a teratoma, requiring surgical excision because large ones cause respiratory compromise or dysphagia.
• Thyroglossal duct cyst. Vertical movement with swallowing or tongue protrusion is pathognomonic: a persistent tract tethers the cyst to the hyoid, so protruding the tongue pulls the cyst upward.
• Infantile hemangioma. Observation is the default because about 90 percent involute, but airway compromise, skin ulceration, dysphagia, thrombocytopenia or cardiac failure call for intervention; start propranolol, first line for infants without a contraindication.
• Infected congenital neck cyst. Control the infection first, then excise the cyst and its tract; the tract must be removed too, because leaving it behind causes recurrence.
• Branchial cleft cyst. It arises from pharyngobranchial ducts that fail to obliterate during fetal development and presents laterally, at the anterior border of the sternocleidomastoid; that position is the first branch of the congenital differential, lateral against midline.

Also tested

• Neck mass by age. Under 40 most neck masses are inflammatory, except Hodgkin lymphoma; above 40 the probability shifts toward malignancy.
• Pulsatile neck mass. Pulsatility or a bruit means a vascular lesion, most likely a paraganglioma, which arises at the carotid body, the vagus or the jugulotympanic region. It must not be biopsied blindly and needs computed tomography angiography first.
• Persistent cervical node. A node over 1 centimeter is abnormal, and reactive nodes regress within one to two weeks. Persistence beyond four to six weeks, or continued enlargement, triggers investigation, with biopsy for fungal, granulomatous or neoplastic causes.
• Suppurative lymphadenitis. A hot, tender, fluctuant node with fever after sore throat is most often Staphylococcus aureus or group A beta-hemolytic streptococcus, in the submandibular or jugulodigastric regions. Empirical antibiotics come first, with aspiration or drainage if they fail.
• Persistent lymphadenopathy in an immunocompromised host. If bacterial cultures are negative and antibiotics fail, send fungal cultures and serology; fungal causes are most commonly Candida, Histoplasma and Aspergillus.
• Persistent generalized lymphadenopathy in HIV. It is defined by the absence of an identifiable infectious or neoplastic cause, and is treated by treating the HIV with antiretroviral therapy.
• Actinomycosis. It presents as a painless fluctuant mass in the submandibular or upper digastric region; painlessness with fluctuance separates it from an ordinary pyogenic abscess, which is exquisitely tender. Diagnosis is clinical and by biopsy, and penicillin is the treatment.
• Oropharyngeal tularemia. Exposure to rabbits, ticks or contaminated water points to Francisella tularensis; tonsillitis with painful adenopathy and systemic symptoms is the oropharyngeal form. Diagnosis is by serology and culture, and streptomycin is the treatment of choice.
• Kaposi sarcoma. One of the conditions to exclude in an HIV-positive patient with lymphadenopathy, alongside tuberculosis, Pneumocystis and lymphoma; its vascular nature gives a purple appearance, unlike the follicular hyperplasia behind most adenopathy in this group.
• Kawasaki disease. A non-infectious inflammatory cause of neck masses, alongside Sjogren syndrome, sarcoidosis and IgG4-related disease. The cervical node is one criterion among several, and untreated Kawasaki disease causes coronary artery aneurysms.
• Kawasaki disease. A non-infectious inflammatory cause of neck masses, alongside Sjogren syndrome, sarcoidosis and IgG4-related disease. Features are high fever for five days, red eyes without discharge, strawberry tongue, cracked lips, rash and one large cervical node. Untreated, it causes coronary artery aneurysms.

Also tested

• Squamous cell neck node. The neck disease is a metastasis, so the primary must be located; its site determines the extent of resection and the radiotherapy field. Every mucosal surface, the thyroid, the salivary glands and the skin are examined systematically.
• Examining a cervical mass. Also palpate the inguinal, axillary and supraclavicular nodes to distinguish regional disease from generalized lymphadenopathy, which points to a systemic cause such as lymphoma, mononucleosis or HIV. Examine the thyroid, liver and spleen, and auscultate any vascular abnormality.
• Neck mass history. Ask about recent travel and possible tuberculosis exposure, along with recent infection, exposure to pets and animals, malignancy risk factors, recent trauma and immunodeficiency.
• Exposure history for cervical adenopathy. Ask about tuberculosis contact and animal exposure; recent travel makes the tuberculosis and zoonotic causes considerably more relevant.
• General symptoms of a concerning neck mass. Fever, postnasal drip, rhinorrhea, sore throat, otalgia, night sweats, weight loss, malaise, dysphagia and hoarseness accompany it; hoarseness and dysphagia suggest upper aerodigestive tract involvement.
• Neck mass that swells at mealtimes. Swelling that varies with eating points to a salivary rather than a nodal cause, because eating stimulates salivary flow and an obstructed gland distends; lymph nodes and neoplasms do not change size over minutes.
• Size of hyperplastic lymph nodes. Reactive hyperplastic nodes are rarely larger than 2 centimeters, so exceeding that adds weight to the concern raised by the other features.

Also tested

• Surgery for papillary thyroid carcinoma. Almost all thyroid cancers require thyroidectomy. The exception is disease localized to one lobe, well differentiated and without metastasis, where lobectomy may be sufficient, preserving the contralateral gland and reducing risk to the recurrent laryngeal nerves and parathyroids.
• Thyroid mass on Hashimoto background. Primary thyroid lymphoma is usually a non-Hodgkin B cell tumor arising on Hashimoto thyroiditis. Aspiration cannot reliably separate a reactive from a monoclonal infiltrate, so proceed to open biopsy, then lymphoma staging.
• Incidental thyroid nodule. Nodules over 1 centimeter found incidentally warrant evaluation: ultrasound with fine needle aspiration plus thyroid-stimulating hormone and thyroid hormones, asking about recent growth, dysphagia or obstruction.
• Thyroid carcinoma prognosis. Papillary is best, then follicular, then medullary, with anaplastic worst. Papillary is commonest; follicular spreads hematogenously; medullary is insidious and most likely to metastasize; anaplastic is most aggressive, causing death in 6 to 36 months and resistant to all treatment.
• Medullary thyroid carcinoma surveillance. The tumor arises from parafollicular C cells, whose normal product is calcitonin, so it secretes calcitonin and the level tracks tumor burden, making it a specific marker for residual or recurrent disease.
• Anaplastic thyroid carcinoma operation. Almost all thyroid cancers require thyroidectomy; the two exceptions are well-differentiated disease localized to a single lobe with no metastasis, and anaplastic carcinoma, where isthmectomy is specified because it is not curable by resection.

Also tested

• Oral lichen planus. It carries a 1 to 4 percent risk of carcinoma (squamous cell), higher if ulcerative, which is why close follow-up is the point of the diagnosis.
• Minor aphthous ulcers. They are the commonest form, under 1 centimeter, preceded by burning and tingling, painful, and heal in 7 to 10 days without scarring.
• Oral lichen planus. 1 to 4 percent progress to squamous cell carcinoma, higher with ulcerative lesions, so close follow-up is the point of making the diagnosis.
• Mucous membrane involvement in systemic lupus. About 40 percent of patients have it, and oral lesions may be the first sign; the oral ulcers do not correlate with systemic activity.
• Oral ulcers in Behcet syndrome. They are the commonest feature, affecting up to 100 percent of patients, with genital ulcers in about 75 percent that look identical to oral aphthae.
• Causes of stomatitis. Listed causes include chemotherapy or radiation, ill-fitting dentures or braces, cheek and tongue biting, surgery, herpes or coxsackievirus, candidiasis, xerostomia, tobacco, zinc or iron deficiency, allergy, and idiopathic aphthous ulceration.

Also tested

• Chronic granulomatous sialadenitis. Chronic gland swelling with minimal pain is the picture; consider primary tuberculosis where risk factors exist. The wide differential (cat scratch disease, sarcoidosis, actinomycosis, granulomatosis with polyangiitis, syphilis) means fine needle aspiration biopsy is needed.
• Acute bacterial parotitis. Dehydration causes salivary stasis, letting bacteria ascend the duct; Staphylococcus aureus is commonest, and pus from Stensen duct confirms infection. Treat with rehydration and antistaphylococcal antibiotics, plus warm compresses, massage and sialogogues.
• No improvement at 48 hours. Failure to improve after 48 hours of rehydration, antibiotics, warm compresses, massage and sialogogues means an abscess should be presumed. The gland becomes doughy and indurated; ultrasound or computed tomography locates the loculation for drainage or guided aspiration.
• Sialolithiasis. It causes recurrent swelling and pain that worsens with eating, because eating stimulates salivary flow and the obstructing stone traps saliva behind it.
• Parotid gland duct. The parotid gland drains through Stensen duct, which crosses the masseter and opens opposite the upper second molar; pus is expressed from it in acute suppurative sialadenitis, characteristically a parotid disease.
• Salivary stones. 80 to 90 percent form in the submandibular gland because its duct (Wharton) is long and uphill, and its saliva is alkaline and mucin-rich with high calcium and phosphate, favoring precipitation of calcium phosphate and carbonate.

Also tested

• Recurrent respiratory papillomatosis. Avoid tracheostomy, because it creates another squamociliary junction, a site the papillomas favor, and spreads disease distally into the trachea.
• Laryngeal electromyography in vocal cord paralysis. It predicts whether function will return by showing whether the nerve is still in continuity, which decides between waiting and proceeding to medialization or thyroplasty.

Also tested

• Suspected epiglottitis. Avoid intraoral examination and venipuncture once it is suspected, because anxiety-provoking examinations may precipitate complete airway obstruction. Mirror or fiberoptic laryngoscopy in a controlled setting is the gold standard.
• Adult supraglottitis. Admit for observation, intravenous antibiotics and airway monitoring; it progresses more slowly than the pediatric form and often does not require immediate intubation, but intubation or tracheostomy becomes necessary if the airway obstructs.
• Declining epiglottitis. Haemophilus influenzae type B vaccination explains it: the commonest pediatric pathogen, with routine immunization reducing supraglottitis by over 90 percent. It still occurs in unimmunized children.
• Suspected supraglottitis in a child. Do not examine the throat; secure the airway with the appropriate team. Intraoral examination and venipuncture increase anxiety and may precipitate complete airway obstruction.

Also tested

• Pharyngitis, tonsillitis, pharyngotonsillitis. The terms name which structure is inflamed: tonsillitis if the tonsils, pharyngitis if the throat, pharyngotonsillitis if both. They are not different diseases and the same organisms cause all; tonsillar involvement raises the possibility of peritonsillar abscess.
• Monospot timing. The test can be falsely negative early in the illness, in the first week, because antibodies take time to appear; serology for Epstein-Barr antibodies is then used. A positive result needs no further testing.
• Negative rapid antigen test. In a child with high clinical probability, send a throat culture before deciding about antibiotics; rapid antigen tests are specific but not sufficiently sensitive, so a negative result is confirmed by culture.
• Rash after an aminopenicillin for sore throat. Infectious mononucleosis, with the aminopenicillin triggering a widespread exanthem; fever, tonsillar pharyngitis and cervical lymphadenopathy fit mononucleosis rather than streptococcus.
• Cause of pharyngitis. About 70 percent is viral; the remaining 30 percent is bacterial, chiefly group A beta-hemolytic streptococcus.
• Viral pharyngitis. Cough, hoarseness, rhinitis and conjunctivitis point to viral pharyngitis, about 70 percent of cases; with a minimal Centor score, management is supportive care with no further testing (hydration, antipyretics, analgesia), and antibiotics are not indicated.
• Infectious mononucleosis. Tonsils so enlarged that they nearly meet, under a thick gray-white membranous exudate.
• Epstein-Barr virus serology. A positive IgM indicates current infection, since IgM appears during acute infection, while a positive IgG means past infection, since IgG persists. Serology is particularly useful in patients under four years, with a negative heterophile test, or with atypical symptoms.

Also tested

• Cervical node features suggesting malignancy. Immobility (fixation to surrounding structures by tumor) and non-tenderness (inflamed nodes hurt) suggest malignancy. Persistence or continued enlargement triggers fine needle aspiration.
• Unilateral solitary anterior cervical node. Beta-hemolytic streptococcus accounts for about 70 percent, about 20 percent are staphylococcal including MRSA, and 10 percent are viral, atypical mycobacterial or Bartonella.
• Ludwig angina in diabetes. Klebsiella is more often involved in patients with diabetes, and those patients may have a more aggressive clinical course.
• Retropharyngeal abscess. The space extends to the posterior mediastinum, giving infection a direct route into the chest; mediastinitis carries a 50 percent mortality.
• Recurrent tonsillitis with peritonsillar abscesses. Tonsillectomy is indicated, usually after the acute infection resolves, because the tissue planes are cleaner and bleeding is less.
• Ludwig angina. This rapidly spreading cellulitis of the submental, sublingual and submandibular spaces swells the floor of the mouth and pushes the tongue up and back into the airway, so secure the airway, then antibiotics (penicillin and metronidazole, or ampicillin-sulbactam), with external drainage through bilateral submental incisions if needed.
• Peritonsillar abscess. Asymmetry is the finding: one side bulges medially and the uvula is displaced away from it.
• Retropharyngeal abscess complications. Mediastinitis carries a 50 percent mortality because the space extends from the base of the skull to the posterior mediastinum; other complications are respiratory distress, rupture with aspiration pneumonia, and spread into the danger space.
• Peritonsillar abscess. Limited mouth opening is called trismus, caused by pus tracking beside the medial pterygoid and irritating it into spasm; it is the most reliable of the triad of trismus, uvular deviation and dysphonia, and makes examination and drainage difficult.

Also tested

• Dental abscess in an unrestorable tooth. Extraction followed by curettage of the apical tissue, because leaving infected granulation tissue behind lets infection persist in the socket.
• Periodontal disease. It raises the risk of endocarditis and other systemic disease, including pneumonia and decreased bone density, and with caries is a primary cause of tooth loss.

Also tested

• Oral thrush in infants. Common because immune systems and oral flora are still establishing; topical antifungal therapy is the first step, using nystatin oral suspension, which acts locally with negligible systemic absorption.

Also tested

• Salivary tumors and gland size. The smaller the gland, the higher the proportion that are malignant: parotid tumors are 75 to 80 percent benign, submandibular 50 to 60 percent, and minor salivary gland tumors only about 35 percent.
• Glottic tumor. Hoarseness is the expected and usually earliest symptom, since a mass replacing the true vocal cord prevents normal vibration and apposition. Referred ear pain reflects shared vagal innervation between the larynx and the ear.
• Oral cancer risk factors. Risk factors are tobacco chewed and smoked, alcohol, betel nut chewing, poor oral hygiene and immunosuppression. Squamous cell carcinoma is the commonest malignancy of the oral cavity and oropharynx, and prevention rests on tobacco and alcohol cessation.
• Oral or oropharyngeal malignancy. Suspect possible oral or oropharyngeal malignancy when ill-fitting dentures accompany non-healing ulcers, bleeding, pain, vague discomfort or a foreign body sensation in the throat.
• Salivary gland tumor prognosis. A parotid mass with pain and facial nerve palsy suggests a malignant salivary tumor, with a poor prognosis. Prognosis is poor with pain, facial or other nerve involvement, high-grade histology, skin or tissue invasion, or recurrent disease; facial nerve palsy indicates invasion rather than compression.