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ENT/Opth Flashcards

1
Q

what is a positive Rinne’s test and what does it imply?

A

when air conduction is louder than bone conduction.

either normal hearing or sensorineural hearing loss.

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2
Q

what is a negative Rinne’s test and what does it imply?

A

when bone conduction louder than air conduction - suggests conductive hearing loss.

(can get false +ve where the other ear is hearing the sound)

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3
Q

how do you interpret the findings of Weber’s test?

A

localises to contralateral ear in sensorineural hearing loss, but to the affected ear if conductive.

may localise to midline if bilateral sensorineural hearing loss!

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4
Q

what is otitis externa/how does it present?

A

severe pain, debris in ear canal ± swelling O/E

due to acute inflammation of skin of the meatus - diffuse infection (bacterial, viral or fungal) of skin of ear canal

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5
Q

what causes otitis externa?

A

excessive canal moisture

also - trauma (e.g. from fingernails), high humidity, absence of wax (from self-cleaning), narrow ear canal, hearing aids

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6
Q

what organisms commonly cause otitis externa?

A

pseudomonas most common
also - Staph aureus

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7
Q

explain the differences between mild, moderate and severe OE

A

mild - scaly skin, with some erythema. normal diameter of external auditory canal (EAC).
mod. - painful ear, narrowed EAC, smelly creamy discharge
severe - EAC occluded

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8
Q

how do you manage mild vs moderate vs severe OE?

A

mild - cleaning the EAC (e.g. gentle syringing, dry mopping, microsuction)
mod. - swab for micro, clean canal. topical abx ± steroid drops.
severe - insert thin ear wick with aluminium acetate, then after a few days meatus will open up enough for microsuction/cleaning

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9
Q

what should you be concerned about if a pt has OE resistant to treatment / persistent unilateral OE?

A

resistant to rx - could be SCC, do biopsy.
if persistent in diabetics/immunosuppressed/elderly - risk is of malignant/necrotizing OE

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10
Q

what is malignant/necrotizing OE? what causes it? management?

A

aggressive infection of external ear that can lead to temporal bone destruction and skull base osteomyelitis.
causes - 90% have diabetes. pseudomonus aeruginosa main cause (also Proteus, Klebsiella).
Rx - surgical debridement, systemic abx, specific immunoglobulins.

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11
Q

what is barotrauma, how does it present? management?

A

if Eustachian tube occluded, middle ear pressure can’t be equalised in diving/aircraft descent, causing damage.

Symps - severe pain, then secondary effusion (either transudate or haemotympanum).
Rx - supportive.

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12
Q

what is TMJ dysfunction? how does it present?

A

temperomandibular joint dysfunction.

symps - earache, facial pain, joint clicking/popping (on teeth grinding, join derangement, or stress)
signs - joint tenderness exacerbated by lateral movement of open jaw, or trigger points in pterygoid muscles.

can be a biopsychosocial thing and become a chronic pain syndrome!

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13
Q

how is TMJ dysfunction managed?

A

reassure/explain. simple analgesia.
specialist therapy - dental occlusion therapy, physio, CBT etc

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14
Q

name some causes of referred ear pain, classified by nerve affected

A

arises from diseases in areas around the nerves supplying the ear:
- V: auriculotemporal nerve (branch of trigeminal), can refer pain from dental disease, TMJ dysfunction
- VII: sensory brance of facial nerve refers pain in geniculate herpes (Ramsay Hunt)
- IX + X: tympanic branch of glossopharyngeal nerve + auricular branch of vagus can refer pain from posterior 1/3 tongue, pyriform fossa or larynx, or from the throat (e.g. tonsillitis, quinsy) - can cause otalgia post-tonsillectomy
- C2,3: great auricular nerve refers pain from soft tissue injury in neck + from cervical spondylosis/arthritis

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15
Q

briefly describe the physiology of hearing

A

1) sound waves are transmitted to the fluid filled cochlea via the external auditory canal, tympanic membrane and bony ossicles.
2) hair cells in basilar membrane of cochlea then detect vibrations and transduce them into nerve impulses
3) these impulses pass via the cochlear nerve (division of CNVIII) to the choclear nucleus in brainstem, then to the superior olivary nuclei

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16
Q

what is the function of the vestibular nerve?

A

carries information from the semicircular canals about balance

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17
Q

name the 3 bony ossicles of the ear

A

stapes
incus
malleus

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18
Q

briefly describe the anatomy of the middle ear

A

three bony ossicles are attached to tympanic membrane. the semicircular canals are filled with fluid, involved in balance sensation.
the tympanic cavity of the middle air is usually filled with air, communicating with mastoid air cells superiorly and the nasopharynx via the Eustachian tube

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19
Q

what is the function of the Eustachian tube?

A

it’s a pressure-equalizing valve for the middle ear, opens for a fraction of a second in response to swallowing or yawning

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20
Q

what is conductive hearing loss? what would Rinne’s/Weber’s show?

A

hearing loss due to problems with the outer or middle ear
Rinne negative
Weber - localises to affected side

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21
Q

what is sensorineural hearing loss? what would Rinne’s/Weber’s show?

A

hearing loss due to problems with the inner ear, cohclea or cochlear nerve
Rinne positive
Weber - localises to normal side

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22
Q

list some causes of conductive hearing loss

A
  • congenital: atresia
  • external auditory canal: wax, foreign body, otitis externa, chronic suppuration
  • ear drum: perforation/trauma
  • middle ear: otosclerosis, disorder of ossicles, otitis media
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23
Q

list some causes of sensorineural hearing loss

A
  • end organ: advancing age, occupation acoustic trauma, Meniere’s disease, drugs (gentamycin, furosemide)
  • CN VIII lesions: acoustic neuroma, cranial trauma, inflammatory lesions (e.g. TB meningitis, sarcoidosis, neurosyphilis, carcinomatous meningitis)
  • brainstem lesions (rare): MS, infarction
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24
Q

describe the structure/function of the “vestibular apparatus” of the inner ear

A

two components - semicircular canals (rotational movements) and the otoliths (urticle and saccule - sense linear acceleration)
provide info to brainstem (via vestibular division of CN VIII) and cerebellum re static head position + turning of head

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25
Q

what is vertigo? list some causes

A

illusion of movement - i.e. everything is spinning/moving
causes = BPPV, vestibular neuronitis, Meniere’s disease, central causes (e.g. vascular, drug-induced, MS)

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26
Q

what is BPPV?

A

benign paroxysmal positional vertigo - causes 50% of peripheral vestibular dysfunction
calcium debris in one of the semicircular canals leads to recurrent episodes of vertigo (lasting secs-mins)
eps provoked by specific head movements e.g. turning in bed
no serious underlying cause, may resolve spontaneously

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27
Q

what is vestibular neuronitis? what causes it? treatment?

A

due to a viral infection affecting labyrinth
sudden onset of severe vertigo, nystagmus and vomiting (but no deafness)
lasts days-weeks
Rx = symptomatic with vestibular sedatives (e.g. prochlorperazine)

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28
Q

what is Meniere’s disease? cause/treatment?

A

build up of endolymphatic fluid in the inner ear
recurrent eps of vertigo lasting 30mins-few hrs
associated ear fullness, sensorineural hearing loss, tinnitus, vomiting
Rx = vestibular sedatives in acute phase (e.g. cinnarizine), low-salt diet, betahistine, caffeine avoidance

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29
Q

what is acute otitis media? how does it present?

A

inflammation of middle ear, usually due to viral infection

rapid onset severe pain, conductive hearing loss, mucous discharge (if ear drum perforated), possible fever/irritability/anorexia
often occurs after viral URTI

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30
Q

list some common organisms causes acute OM

A

often viral

pneumococcus, haemophilus, moraxella, streps/staphs

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31
Q

how do you manage acute OM?

A

pain relief
often will resolve within 24h w/o abx
if systemically unwell or no improvement after 24hrs (can give ‘delayed’ abx prescription) - amoxicillin 40mg/kg/day in 3 divided doses for 5 days
erythromycin if penicillin allergy

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32
Q

what is mastoiditis?

A

destruction of air cells in mastoid bones ± abscess formation, due to middle ear inflammation (e.g. can be complication of acute OM)
consider if fever, tenderness, swelling and redness behind ear
do a CT, admit for IV abx, myringotomy ± definitive mastoidectomy

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33
Q

what is chronic OM?

A

chronic infectious/inflammatory condition of middle ear - ear drum perforation with recurrent/chronic infections
divided into:
- benign/inactive COM: “dry” tympanic membrane perforation, no active infection
- chronic serous OM: continuous serous drainage
- chronic suppurative OM: persistent purulent drainage through perforated tympanic membrane

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34
Q

how do you manage chronic OM?

A

topical/systemic abx, cleaning, advice on water precautions
may need myringoplastic/mastoidectomy

potential complication = cholesteatoma

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35
Q

what is a cholesteatoma, how does it develop? treatment?

A

as a complication from chronic OM - prolonged low middle ear pressure leads to development of retraction pocket of pars tensa/flaccida - as this enlarges, squamous epithelium builds up and gets stuck - leads to cholesteatoma

has serious but rare complications - meningitis, cerebral abscess, hearing loss, mastoiditis, facial nerve dysfunction
peak age = 5-15yrs

Rx = mastoid surgery to remove the disease, leaving a safe dry ear (secondary benefit is this can preserve hearing!)

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36
Q

what is a myringoplasty? what about mastoidectomy?

A

myringoplasty = surgery to repair tympanic membrane - patch up a perforation using a graft
mastoidectomy = often done with tympanoplasty (repair of tympanic membrane and ossicles) - used for mastoiditis or advance cholesteatoma

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37
Q

list some risk factors for otitis media

A

URTI
bottle feeding
passive smoking
dummy/pacifier use
presence of adenoids
asthma
malformations (e.g. cleft palate)
GORD/high BMI (for adults)

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38
Q

what is otitis media with effusion (OME)?

A

aka Glue ear - presents in childhood with parents noticing hearing impairment.
basically the middle ear is filled with fluid due to some combination of eustachian tube dysfunction, URTIs, oversized adenoids etc

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39
Q

list some childhood RFs for OME

A

boys
Downs’ synd.
cleft palate
winter
atopy
passive smoking

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40
Q

what are the features of OME on history and examination?

A

hx - poor listening/speech, language delay, poor behaviour, poor school performance
O/E - retracted or bulging drum, may be dull/grey/yellow, may see bubbles or fluid levels etc

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41
Q

how is OME managed?

A

usually mild/transient, resolves spontatneously.
1) active observation for 3/12 - repeat hearing tests, advise on minimising background noise, give short, simple instructions at child’s level etc
2) topical/systemic methods - NOT recommended by NICE
3) autoinflation of eustachian tube with Otovent may help
4) surgery - GROMMETS - mainstay of Rx, if treatment is needed
they will usually fall out after 3-12/12 - recheck hearing, consider need for re-insertion

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42
Q

what is tinnitus?

A

a perception of sound, in absence of auditory stimulation
can be unilateral, bilateral, pulsatile, non-pulsatile etc
ringing/hissing/buzzing = inner ear or central cause
popping/clicking = external/middle ear or palate issue

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43
Q

how is tinnitus classified?

A

objective vs subjective
objective = audible to examiner - often pulsatile and due to a weird vascular problem by the ear etc
subjective = much more common - often associated with disorders causing sensorineural hearing loss.

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44
Q

list the ototoxic drugs

A

can cause bilateral tinnitus w/associated hearing loss:
cisplatin, aminoglycosides - can cause permanent loss
aspirin
NSAIDs
quinine
macrolides
loop diuretics

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45
Q

how do you manage tinnitus?

A

treat any underlying cause (often isn’t one - although investigate more if unilateral, for acoustic neuroma)
psychosocial approach.
hearing aids if there’s loss
CBT

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46
Q

what are acoustic neuromas?

A

usually benign subarachnoid tumours that cause problems by local pressure, then act as SOLs.
arise from superior vestibular nerve schawnn cell layer (aka vestibular schwannoma)

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47
Q

how can acoustic neuromas present? Ix? management?

A

progressive ipsilateral tinnitus ± sensorineural deafness (due to chochlear nerve compression). other weird neuro symps.
tests - always do an MRI for unilateral tinnitus/deafness.
Rx - might do surgery if young and fit. quite fiddly!

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48
Q

how can duration of vertigo episodes help distinguish the cause?

A

seconds - minutres = BPPV
30mins - 30 hrs = Meniere’s disease or migraine
30hrs - a week = acute vestibular failure

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49
Q

briefly describe the anatomy of the nose/nasal cavity

A

nasal cavity is continuous with the nose in front, pharynx below, and is divided by midline septum (bone + cartilage)
walls of the cavity = maxilla, nasal bone, roof of the mouth
paranasal sinuses connect to nasal cavity via ostia
blood supply = branches of internal + external carotid arteries, anastomose in ant. nasal septum (Little’s area)

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50
Q

name the 4 para nasal sinuses

A

frontal
ethmoidal
sphenoid
maxillary

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51
Q

what are the two main functions of the nose?

A

1) smell - via olfactory epithelium in roof of nose + CN I
2) respiration - moistening, warming and filter inspired air

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52
Q

what is the most common site of bleeding in epistaxis?

A

Little’s area - anastomosis of blood vessels in the anterior nasal septum

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53
Q

list some causes/RFs for epistaxis

A

local factors - trauma, nasal fracture, surgery, intranasal steroids, tumours of the nose/paranasal sinuses/nasopharynx
systemic factors - anticoagulants, bleeding disorders, hypertension, familial hamorrhagic telangiectasia

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54
Q

outline management of epistaxis

A

1) ABCDE, resuscitate as needed - fluids, O2 etc
2) ask pt to lean forward, pinch lower part of nose for 20 mins, can place ice pack on nose as well
3) cotton ball soaked in adrenaline for 2 mins, or lidocaine spray - to vasoconstrict
4) locate bleeding points (on ant. septum), apply silver nitrate cautery - NEVER cauterise both sides of septum!!
5) Rapid Rhino pack (anterior nasal pack) for 24h
6) if continues - try foley catheter balloon back - woks better for posterior bleeds

ENT steps for serious posterior epistaxis can involve: EUA ± diathermy of bleeding/repacking, arterial ligation

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55
Q

what causes sinusitis?

A

usually strep pneumoniae or haemophilus influenzae

could also be - Staph aureus, moraxella catarrhalis, fungi

often complicates allergic rhinitis or an URTI - mucosal oedema and blockage of ostium draining the sinus

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56
Q

describe the symptoms and management of sinusitis

A

frontal headache (“worse on bending forwards”), facial pain + tenderness, discoloured nasal discharge. symptoms tend to have a unilateral predominance. fever.

clinical Dx.

Rx - most can avoid abx - anaglesia, saline irrigation, intranasal decongestants (e.g. ephedrine)
only give abx if supect bacterial e.g. duration >2 weeks

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57
Q

what are the possible (rare) complications of sinusitis? when would you consider imaging in sinusitis?

A

local/cerebral abscess formation, osteomyelitis, intracranial involvement (eg. meningitis, encephalitis), mucoceles, “Pott’s puffy tumour”

consider imaging with CT or MRI if - suspected abscess formation, recurrent acute (>4 eps/yr) or chronic sinusitis (ep lasts >3/12)

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58
Q

give some different causes of acute sinusitis (i.e. not just post viral URTI)

A

1) direct spread - diving/swimming in infected water, dental root infection
2) odd anatomy - septal deviation, polyps etc
3) ITU causes - mechanical ventilation, recumbency, NG tubes
4) systemic - Kartagener’s, immunodeficiency etc
5) Biofilms forming on sinus mucosa

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59
Q

outline management of nasal fractures

A

excluded signif. head/c-spine injury
treat epistaxis
analgesia, ice
close any skin injury
refer to ENT clinic for in 5-7/7 to reassess once swelling resolved
manipulation under anaesthetic (MUA) - 10-14/7 after injury - just pop it back into place!

(when examining, check for septal haematoma - boggy swelling of septum causing near-total nasal obstruction - required incision & drainage)

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60
Q

list some causes of nasal septal perforation, and explain management

A
  • trauma - foreign body, picking, laceration, septal haematoma
  • inhalants - nasal steroid/decongestants, cocaine
  • infection - TB, syphilis, HIV
  • inflammation/malignancies - SCC, Churg-Strauss, granulomatosis w/ polyangitis

Rx - saline nasal irrigation, petroleum jelly to edge of perforation. possible need for surgical closure, but often this is unsuccessful/intolerable

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61
Q

list some differential diagnoses for hoarseness (dysphonia)

A

*investigate any hoarseness lasting >3/weeks, esp if smoker, as it’s the chief presentation of laryngeal Ca**
- laryngeal cancer: progressive + persistent gruff voice
- vocal cord palsy: weak + breathy, often due to cancer (larynx, thyroid, oesophaus, hypopharynx, bronchus)
- reflux laryngitis: associated with GORD
- Reinke’s oedema: chronic cord irritation from smoking ± chronic voice abuse, causes build up of fluid under the epithelium of the cord
- vocal cord nodules: caused by voice overuse - singing, shout etc

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62
Q

list some causes of stridor

A

inhaled foreign body
infections - epiglottitis, diphtheria, tonsilitis
tumour of trachea or larynx
trauma

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63
Q

what is the most common bacterial cause of sore throat? Rx?

A

Group A beta haemolytic streptococcus
Rx = phenoymethylpenicillin 500mg every 6h for 10/7

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64
Q

what causes an acute sore throat?

A

acute pharyngitis or tonsillitis - usually viral, usually resolves within 3 days, almost all within 1 week.

viral - rhinovirus, coronovirus, parainfluenza virus. also influenza A dn aB, adenovirus, HSV, EBV.

bacterial - Group A beta-haemolytic strep (decide whether to treat using Centor criteria).

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65
Q

how do you investigate/manage an acute sore throat?

A

throat swabs should NOT be done routinely.
use Centor criteria to decide whether to give abx.

symptomatic relief - painkillers, Difflam spray if severe. rest + fluids.
abx - penicillin V 10 day course or clarithromycin/erythromycin 5 day course if oenicillin allergic.
AVOID AMOXICILLIN - gives a rash if EBV!

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66
Q

list the Centor criteria

A

want a score of 3 or 4 to consider abx:
- presence of tonsillar exudate
- tender anterior cervical lymphadenopathy
- fever
- absence of cough/coryzal symps

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67
Q

give some possible complications of tonsillitis

A
  • otitis media
  • sinusitis
  • peritonsillar abscess (quinsy)
  • parapharyngeal abscess - rare, diffuse neck swelling, I&D under GA
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68
Q

what is a quinsy? management?

A

peritonsillar abscess
sore throat, dysphagia, peritonsillar bulge (unilateral predominance) - uvular deviation, trismus (unable to fully open mouth), muffled “hot potato” voice
needs urgent abx and aspiration!!

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69
Q

give the criteria for tonisllectomy

A

7+ well documented + clinically significant sore throats in preceding year
OR
5+ in eps in each of last 2 years
OR
3+ eps in each of the last 3 years

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70
Q

outline acute airway management of stridor in adults

A
  • give O2
  • nebulised adrenaline (1ml of 1:1000, with 1ml saline)
  • note O2 sats, RR, HR, BP
  • call ENT and anaesthetics
  • take hx from relatives to establish cause of stridor

invasive management:
- ET intubation
- emergency needle cricothyroidotomy
- surgical cricothyroidotomy - often quicker and easier in an emergency!

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71
Q

explain what a laryngeal nerve palsy is, how it presents, management etc

A

recurrent laryngeal nerve supplies intrinsic muscles of larynx - in charge of movements of vocal cord. originates from vagus, has “tortuous” course so susceptible to damage.
symps - weak, ‘breathy’ voice + weak cough, repeated coughing, exertional dyspnoea
causes - cancer! (larynx, thyroid, oesophagus, hypopharynx, bronchus). iatrogenic (post surgery), CNS disease, TB, aortic aneurysm, idiopathic

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72
Q

list the malignant causes of dysphagia

A

oesophageal cancer
pharyngeal cancer
gastric cancer
extrinsic pressure e.g. from lung cancer or node enlargement

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73
Q

list some non-malignant causes of dysphagia

A

neurological - bulbar palsy, lateral medullary syndrome, myasthenia gravis, syringomyelia
other - benign strictures, pharyngeal puch, achalasia, systemic sclerosis, oesophagitis, iron deficient anaemia

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74
Q

list some symptoms that should prompt you to consider head and neck squamous cell carcinomas

A

neck pain/lump
hoarse voice >6 weeks
sore throat
mouth bleeding
mouth numbness
sore tongue
painless ulcers
patches in the mouth
earache/effusion
lip/mouth/gum lumps
speech change
dysphagia

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75
Q

list some risk factors for head and neck SCC

A

smoking
high alcohol consumption

vit A&C deficiency
nitrosamines in salted fish
HPV
GORD

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76
Q

how do oral cavity/tongue SCCs present? management?

A

persistent, painful ulcers; white/red patches on tongue/gums/mucosa; otalgia; odonophagia; lymphadenopathy

Rx - surgery/radiotherapy

> 80% 5yr survival if caught early
uncommon in UK

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77
Q

how do oropharyngeal SCCs present? management?

A

often advanced at presentation. more common in men - old bloke, smoker with sore throat, sensation of a lump and referred otalgia
do MRI.
Rx - surgery and radiotherapy.
5yr survival c.50% if stage I at presentation.

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78
Q

how do laryngeal cancers present? management?

A

older bloke, smoker, progressive hoarseness then stridor and either dysphagia or odynophagia ± haemoptysis ± ear pain.
if younger - will be HPV+ve
Ix - laryngoscopy + biopsy, MRI staging.
Rx - radical radiotherapy for small tumours, laryngectomy for larger tumours.
5yr survival 66%.

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79
Q

describe the course of the facial nerve

A

arises in medulla, travels between pons and medulla, through posterior fossa and middle ear, emerges at stylomastoid foramen to pass into the parotid
lesions can occur anywhere along this course

80
Q

what are the 5 major extracranial branches of the facial nerve?

A

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

81
Q

list some causes of facial nerve palsy

A

intracranial: brainstem tumours, strokes, polio, MS, cerebellopontine angle lesions (acoustic neuroma, meningitis)
intratemporal - otitis media, Ramsay Hunt, cholesteatoma
infratemporal - parotid tumours, trauma

others - Lyme disease, sarcoid, diabetes, Bells palsy

82
Q

describe the different signs seen in a facial nerve palsy due to upper vs lower motor lesions

A

if lower - paralysis of whole side of the face
upper = forehead and eyelid muscles spared, as they’re bilaterally innervated

83
Q

what is Bell’s palsy?

A

unilateral LMN facial palsy - causes 70% of facial palsies, is idiopathic.
features - abrupt onset facial nerve paralysis (eg. overnight, after a nap), complete weakness by 24-72hrs. more common in pregnancy.

84
Q

how do you manage Bell’s palsy?

A

prednisolone if they’ve presented within 72hrs of symptom onset.
5-10 day course.
protect the eye - lubricating drops, ointment and taping over night.

85
Q

what are the borders of the anterior triangle of the neck?

A

superior = inferior border of madible
lateral = medial border of sternocleidomastoid
medially = sagittal line down body

86
Q

what are the subdivisions of the anterior triangle of the neck? what does each subdivision contain?

A

carotid = common carotid, vagus, hypoglossal nerve
submental = submental lymph nodes
submandibular = submandibular gland + lymph nodes, facial artery/vein
muscular = pharynx, thyroid, parathyroid

87
Q

what are the borders of the posterior triangle of the neck? what does it contain?

A

ant. = posterior border sternocleidomastoid muscle
inf. = middler 1/3 clavicle
posterior = anterior border trapezius

contains = subclavian vein

88
Q

briefly describe the lymphatic drainage in the neck?

A

superficial + deep lymphatic vessels:
superficial = covers scalp, face + neck
deep = receive all lymph from head and neck, 6 main sections

89
Q

list the main locations of superficial lymph nodes in the head/neck, and where they drain

A
  • ring shape under chin round to posterior head
  • occipital = scalp
  • mastoid/post-auricular = post. neck, upper ear
  • pre-auricular = superficial face, temporal
  • parotid = nose, orbit, external ear
  • submental = lip, mouth, tongue
  • submandibular = upper lip, gums, tongue
  • facial = nose, cheeks, eyelids
  • superficial cervical = anterior + posterolateral superficial, drains superficial neck
90
Q

what are the 6 divisions of the deep head/neck lymph nodes?

A
  • submandibular + submental
  • superior jugular and jugulo digastric
  • midjugular
  • inf. jugular
  • lateral jugular
  • central compartment
91
Q

what is cervical lymphadenopathy?

A

abnormal size/consistency/number of cervical lymph nodes

can be localised, regional or generalised

92
Q

list some causes of cervical lymphadenopathy

A

CHICAGO:
Cancer - H/NH lymphoma, CLL
Hypersensitivity
Infection - rule out EBV if youngish, CMV, hep B/C, adeno, HSV, HIV, MMR, staph + strep pharyngitis, cat scratch disease, TB
Collagen vascular disease
Atypical lymphoproliferative disorders
Granulomatous disease
Other

93
Q

list the salivary glands

A

parotid
submandibular
sublingual

94
Q

describe the examination findings of parotid swelling

A
  • loss of jaw angle or lump ant. to ear
    if localised ?tumour, generalised = inflammation/obstruction
    can examine duct opening at second molar with cheek spatular to retract.
    check facial nerve - problem can suggest malignancy
95
Q

list some causes of parotid swelling

A
  • viral parotitis (mumps)
  • stone in salivary duct
  • benign/malignant tumours
  • Sjogrens
  • sarcoidosis
  • acute/chronic bacterial parotitis
  • Wegener’s
  • HIV
96
Q

how does parotitis present?

A

painful tender swelling
dry mouth
decreased mouth opening
pain on eating
foul taste (bacterial)
fever

97
Q

how does mumps present?

A

bilateral parotid swelling lasting one week
low grade fever

98
Q

list some possible Ix for parotitis

A

salivary antibody testing (salivary mumps IgM)
pus swab MC&S
FBC, ESR/CRP, UE, blood culture, viral serology
sialography for blockage
USS
CT/MRI to excl. neoplasm

99
Q

how should you manage parotitis?

A

mumps is self-limiting
if suspect bacterial (e.g. suppurative) - Abx ± I&D
warm compress aids salivary flow
oral hygiene

100
Q

what key diagnoses shouldn’t be missed for atypical facial pain?

A

urgent = temporal arteritis

early diagnosis opportunity for malignancy

101
Q

how do you manage atypical facial pain if all other causes have been excluded? what features of a hx suggest it might just be a weird facial pain?

A

worse with fatigue/stress, linked to depression or mood disturbance

first line = TCA (amitryptiline ± CBT)

102
Q

when would nasal polyps be a cause for concern?

A

unilateral - must rule out nasal tumour
in children - should consider testing for CF

103
Q

how might nasal polyps present? Rx?

A

obstruction, discharge (watery), dull headache, hyposmia, snoring
Ix - rigid/flexible rhinoscopy
first line = topical fluticasone or budesonide + saline douche
other = functional endoscopic sinus surgery is gold standard

104
Q

briefly describe the anatomy/layers of the eye

A

sclera - thick protective membrane forming outer coat of eyeball (white of the eye)
cornea - transparent dome on outer covering of eye, continuous with sclera. does most of the refracting.
conjunctiva - mucous membrane covering surface of sclera and continuous with insides of eyelids.
anterior chamber - contains aqueous humour, providing nutrients and oxygen to cornea.
iris - coloured bit of the eye, muscles control pupil size + thus amount of light entering the eye.
lens - transparent biconvex structure
retina - contains the rods/cones (photoreceptors), mostly in the macula in the centre (esp. cones). fovea is the spot in the middle of the macula.

105
Q

list some benign causes of a red eye i.e. no need for urgent referral

A

conjunctivitis - bacterial, viral, allergic, chlamydia
subconjunctival haemorrhage
episcleritis

106
Q

list the causes of a red eye requiring an urgent, same day referral to ophthamology

A
  • keratitis
  • acute glaucoma
  • anterior uveitis
  • scleritis
  • endopthalmitis
107
Q

what features of a history suggest conjunctivitis? describe the “site of redness”

A

bilateral, itchy, gritty eye
purulent discharge if bacterial

diffuse redness of ocular surface

108
Q

what features of a history suggest subconjunctival haemorrhage? describe the “site of redness”

A

lots of eye rubbing, severe coughing
(rarely) hypertension, blood clotting disorder
diffuse area of bright red blood under conjunctiva of one eye

109
Q

what features of a history suggest episcleritis? describe the “site of redness”

A

mild irritation and redness
diffuse or localized injection of conjunctiva

110
Q

what features of a history suggest keratitis? describe the site of redness/visual acuity/pupils/cornea

A

pain, foreign body sensation, blurred vision, photophobia
reduced visual acuity
ciliary injection (max. redness around edge of cornea)
normal pupil
corneal ulceration (use fluorescein drops + blue light)

111
Q

what features of a history suggest acute glaucoma? describe the site of redness/visual acuity/pupils/cornea

A

sudden onset of severe eye pain, blurred vision, rainbow “halos” around lights ± N&V
reduced visual acuity
diffuse redness
pupils fixed and semi-dilated
cloudy cornea

112
Q

what features of a history suggest anterior uveitis? describe the site of redness/visual acuity/pupils/cornea
causes?

A

painful eye, blurred vision, photophobia
normal/reduced acuity
ciliary injection (max. redness around edge of cornea)
small and fixed pupils
normal cornea

autoimmune diseases, sometimes infectious

113
Q

what features of a history suggest scleritis? describe the site of redness/visual acuity/pupils/cornea
what usually causes it?

A

mild to severe eye pain
normal/decreased acuity
diffuse or localised redness
normal pupil
normal cornea

often there’s an underlying vasculitis

114
Q

what features of a history suggest enophthalmitis? describe the site of redness/visual acuity/pupils/cornea

A

blurred vision, painful eye, photophobia, floaters
decreased acuity
diffuse or localised redness
small and fixed pupils
cloudy

115
Q

list some causes of keratitis

A

infections
autoimmune
exposure keratopathy
contact lens related

116
Q

what causes acute glaucoma?

A

sudden severe rise in intraocular pressure due to reduced aqueous fluid drainage

117
Q

what causes enophthalmitis?

A

infection of the eyeball after eye surgery, injury or spread via bloodstream

118
Q

when might you consider referring a patient with conjunctivitis?

A

symptoms continue >2 weeks
eye becomes painful
vision decreases

119
Q

how do you manage conjunctivitis?

A

bacterial = topical broad spec abx e.g. chloramphenicol
take conjunctival swabs for Gram stain if no response or suspect gonococcal conjunctivitis
viral = self-limiting, pt highly contagious when eye red, encourage strict hygiene and separate towels.

120
Q

what is amaurosis fugax?

A

cause of severe temporary visual loss - due to transient lack of blood supply to retina or visual cortex
usually a TIA or temporal arteritis

needs urgent assessment/treatment due to risk of impending blindness/stroke

121
Q

list some causes of sudden/rapidly progressive visual loss requiring urgent referral?

A

ALL OF THEM!
- central retinal artery occlusion = V. urgent referral (within 1h)
- acute uveitis, acute glaucoma, keratitis = also present with red eye
- acute retinal detachment
- retinal vein occlusion
- vitreous haemorrhage
- “wet” age-related macular degeneration

122
Q

list some causes of gradual visual loss

A
  • slowly progressive optic atrophy
  • chronic glaucoma
  • cataracts
  • diabetic retinopathy
  • macular degeneration
  • chronic retinal detachment
123
Q

describe the features of acute retinal detachment (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - flashing lights, floating spots, field loss (curtain from periphery)
Acuity - decreased w/field defect
Pupils - RAPD
Ophthal. - abnormal red reflex. grey + wrinkled detached retina.
NB - normal opthal. exam does NOT excl Dx.

124
Q

what is RAPD?

A

relative afferent pupillary defect
pupil in affected eye dilates in response to light rather than constrictin

125
Q

describe the features of retinal vein occlusion (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - sudden loss of vision in all (if central vein) or part (branch of retinal vein) of visual field
Acuity - decreased, w/visual field defect
Pupils - RAPD if severe
Ophthal. - retinal haemorrhages, tortuous dilated retinal veins, macular oedema, cotton wool spots

126
Q

describe the features of retinal artery occlusion (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - sudden painless loss of vision
Acuity - markedly reduced
Pupils - RAPD
Ophthal. -pale retina with central macular “cherry red spot”

127
Q

describe the features of acute optic neuropathy (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - rapidly progressive loss of vision, ?decreased colour vision, symps of an underlying disease (MS, nerve ischaemia due to atherosclerosis)
Acuity - decreased
Pupils - RAPD
Ophthal. - normal or swollen optic disc

128
Q

describe the features of vitreous haemorrhage (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - severe visual loss if major bleed, floating blobs/spots if mild/moderate
Acuity - normal or reduced
Pupils - NO RAPD
Ophthal. - decreased red reflex

129
Q

describe the features of “wet” age-related macular degeneraion (history/visual acuity/pupils/ophthalmoscopy)

A

Hx - elderly. sudden distortion, central blank patch, or just blurring of vision
Acuity - decreased w/ central scotoma (macula is in centre of retina so when diseased causes a central blank patch on field testing)
Pupils - usually no RAPD
Ophthal. - macular oedema and/or subretinal haemorrhages and hard exudates

130
Q

explain the function of different eye drops used in ophthalmoscopy

A

need a dilated pupil
- sympathomimetic drops stimulate radial muscles in the iris e.g. phenylephrine
- parasympatholytic agents relax the sphincter muscles (tropicamide, cyclopentolate, atropine)
all also paralyse the ciliary muscle, inhibiting accommodation - can’t drive till worn off

CI’ed if head injury (need the pupil reflex) or risk of closed angle glaucoma

131
Q

what can cause an absent red reflex?

A

cataract or a tumour

132
Q

LEARN VISUAL FIELDS DEFECTS

A

LEARN VISUAL FIELD DEFECTS

133
Q

what causes a central scotoma?

A

(central blindspot on visual field testing)
lesion in optic nerve between nerve head and chiasm
e.g. optic neuritis

134
Q

what visual field defect is seen in a pituitary tumour?

(1 of 2 most common cancers associated w/visual fields)

A

left sided central scotoma

135
Q

what visual field defect is seen in a meningioma?

(1 of 2 most common cancers associated w/visual fields)

A

contralateral superior temporal quadrantopia

136
Q

what is the macula? the fovea? cones and rods?

A

macula = central/thickest part of retina, high conc. of cones
fovea = small depression in centre of macula
cones = central retina, colour vision and acuity
rods = outer retina, night vision

137
Q

what causes gradual loss of vision?

A

usually chronic, degenerative conditions in elderly.
less common - inherited disorders of retina/optic nerve e.g. retinitis pigmentosa

  • cataracts
  • glaucoma
  • ARMD
138
Q

explain how visual acuity is tested with a Snellen chart

A

use at 6m
if can read top line = 6/60 (can read at 6m what normal can read at 60m).

if can only read top line at 2m = 2/60.
if can read middle line = 6/12.
etc.

139
Q

what is a cataract?

A

opacity/clouding of the lens, progressive over years and usually bilateral.

associated with ageing, Down synd.

140
Q

what is the function of the lens?

A

changes in shape to allow accommodation (loss of this = presbyopia)

141
Q

list some risk factors for cataracts

A

sunlight
age
smoking
alcohol
corticosteroids
DM

142
Q

describe the pathology of cataracts

A

protein denaturation (e.g. oxidation) due to metabolic disturbance (hyperglycamia) or toxins (smoking, alcohol) etc

143
Q

how do cataracts present?

A

gradual painless loss/blurring of vision - may be unnoticed in unilateral cataracts, although distance judgement will go.
± dazzle esp. in sunlight
± monocular diplopia

‘hard to drive at night, I see haloes around the street lights’

144
Q

how are cataracts treated?

A

mydriatic drops, sunglasses help a bit but if life impacted or unable to drive = surgery
quick, local anaesthetic day case, no sutures due to small incision.
often need distance glasses after.
2% get serious complications (enophthalmitis), + 20% get post-op posterior capsule thickening (“feels like cataracts are coming back”)
“phacoemulsion + intraocular lens implant”

145
Q

how soon should congenital cataracts be treated?

A

need the operation within 6 weeks of life - latent stage of visual development.
urgent referral as soon as it’s picked up, defs within 4 weeks of life.
do a TORCH screen as well.

146
Q

what is chronic open angle glaucoma?

A

optic neuropathy with death of many retinal ganglion cells and their optic nerve axons.

often have raised IOP but this is not part of the definition

147
Q

how does chronic glaucoma present?

A

progressive visual field loss –> tunnel vision. asymptomatic until the fields are badly impaired so needs to be screened for - at least annual (more frequent earlier on) screening if a raised IOP is found.

148
Q

give some risk factors of chronic open angle glaucoma

A

raised IOP
afro-caribbean
family history
steroid use
ageing
HTN/DM (?)

149
Q

how is chronic open angle glaucoma diagnosed?

A

requires:
- IOP measurement using tonometry
- central corneal thickness measurement
- peripheral anterior chamber configuration and depth assessments (gonioscopy)
- visual field measurement
- slit lamp and fundus examination of optic nerve

150
Q

how is chronic open angle glaucoma managed?

A

regular screening needed! can’t restore sight so really important to treat deteriorations as they appear!!

drug Rx aims to reduce IOP by 30% of baseline, surgery if drugs fail. compliance to drops is poor.

first line = prostaglandin analogue (latanoprost) or beta blocker (timolol) drops
other drops:
- alpha-adrenergic agonists (brimodine, apraclonidine)
- carbonic anhydrase inhibitors (dorzolamide, brinzolamide)
- miotics (pilocarpine)
- sympathomimetic (dipivefrine)
- can get fixed-dose combo drops.
laser therapy (trabeculoplasty) increased aqueous outflow to decrease IOP.
trabeculectomy = filtration surgery creating a valve thingy.

151
Q

what are the key features that should make you think of glaucoma? (“glaucoma triad”)

A
  • raised IOP (but not always present!)
  • “optic disc cupping” - cup:disc ratio increases beyond normal population values
  • visual field changes in 3 or more locations
152
Q

describe the visual field losses typically seen in chronic open angle glaucoma

A
  • scotomata = sausage-shaped defects near blind spot that can join up to form big defects
    central field intact - this is why people don’t present till too late.
153
Q

briefly outline the screening process for chronic open angle glaucoma

A

IOP = low specificity + high false positives (FP)
visual field test also high FP, same for fundoscopy (for optic disc cupping)

need to combine all 3.
pressure measured by tonometry.

154
Q

describe the features/progression of dry age-related macular degeneration (AMD)

A

ophthalmoscope = atrophy of retinal pigment epithelium (RPE) - visible choroidal arteries
visual fields = central scotoma with preserved peripheral vision

progression = frequent deterioration, eligible to register blind.

155
Q

what actually is the macula, what does it do?

A

area 5.5mm across, just lateral to optic disc.
fovea is a 1.5mm pit in the middle - full of densely packed cones, responsible for acuity.

visual acuity requires functional rods+cones, healthy retinal pigment epithelium (RPE) and perfusion of the choroid (capillary layer).

156
Q

describe the pathogenesis of ARMD

A

there’s pigment, drusen (a signifier of optic nerve-head degeneration) and sometimes bleeding at the macula.
progresses to retinal atrophy over time.
chief cause of registrable blindness + most common cause of irreversible vision loss in developed world!!

157
Q

give some risk factors for ARMD

A

increasing age
smoking
CVD
FHx
cataract surgery

158
Q

differentiate between wet and dry ARMD

A

Wet - choroidal neovascular membranes develop under retina - leak fluid/blood and cause the area to scar. Vision deteriorates rapidly (few months), distortion key feature. Fluid exudate seen on ophthalmoscopy.
Dry - much slower progression (decades). aetiology unknown, not much treatment (wet is treatable if act quickly!). vitamin A, E, zinc and lutein supplements recommended.

159
Q

how do you manage wet ARMD?

A
  • arrange fluorescein angiogram, plus 4-6 weekly reviews with photograph and optical coherence tomography (OCT)
  • intravitreal vascular endothelial growth factor (VEGF) inhibitors e.g. monthly bevacizumab and ranizumab injections for 1y.
  • laser photocoagulation
  • photodynamic therapy
  • intravitreal steroids

advise quit smoking, diet rich in green veg - consider zinc, vits C&E supplements

160
Q

list some causes of branch/central retinal artery occlusion? presentation?

A

pres = sudden total loss of vision (central) or only top/bottom half (branch). + RAPD.
Causes:
- emboli (atheroma, cholesterol, cardiac valve)
- GCA
- thrombophilic conditions

!! this is essentially a stroke and should be managed as such.

161
Q

how does retinal vein occlusion present? causes?

A

this is way more common than arterial occlusion.
pres = blurred vision, VF defect.

causes = vascular things - atherosclerosis, HTN, DM, smoking, thrombophilia. also assoc. w/glaucoma.

162
Q

what is seen on ophthalmoscopy of retinal vein occlusion?

A

flame haemorrhages
leaking veins
intact arteries.

163
Q

how is retinal vein occlusion managed?

A
  • refer to on call ophthalmologist.
  • intravitreal anti-VEGF is 1st line if visual loss. then dexamethsone implants or intrevitreal triamcinolone acetonide.
  • photocoagulation used if retinal neovascularisation present.
164
Q

what is optic neuritis? describe the natural history?

A

often first presentation of MS - painful loss of vision in one eye.
recovers in 6-8 wks, steroids may help speed this up.

165
Q

what is anterior ischaemic optic neuropathy (AION)? what’s it associated with?

A

sudden and profound loss of vission + RAPD. damage to optic nerve due to insufficient blood supply (ischaemia).

associated w/GCA (think - recent onset headache, PMR, jaw claudication)

166
Q

how do you manage a patient presenting with suspected anterior ischaemic optic neuropathy / GCA?

A

key Ix = ESR, CRP, FBC

give high dose steroids if GCA - can prevent vision loss

167
Q

what is retinal detachment?

A

it is what it sounds like really. potential space between photoreceptors and RPE fills with fluid, retina lifts/detaches –> field defect.
normally due to retinal tear.

168
Q

how does retinal detachment present? Rx?

A

flashes, floaters, field loss.

majority of flashes and floaters are due to benign vitreous detachment though.

requires surgery to prevent full detachment.

169
Q

list the four features of hypertensive retinopathy on ophthalmoscopy

A

microinfarcts
heightened reflex on artery - silver wiring
flame haemorrhages
arteriovenous crossing change - “nipping” - vein disappears under artery cos arterial wall is thickened.

± exudate

170
Q

list some possible complications of hypertensive retinopathy

A

1) retinal vein occlusion
2) retinal artery occlusion
3) AION
4) exacerbation of diabetic retinopathy
5) retinal macroaneurysms

171
Q

what is diabetic retinopathy?

A

effect of chronic and progressive diabetic microvascular leakage + occlusion on the retina.

25% of T2DM have retinopathy at Dx!

172
Q

list some RFs for diabetic retinopathy

A

poor glycaemic control
systemic HTN
carotid stenosis
pregnancy
renal disease
anaemia
hyperlipidaemia

173
Q

describe the structural changes that occur in the eye in someone with DM

A

ocular ichaemia –> new blood vessels forming on the iris (rubeosis) - if these block the drainage of aqueous fluid, can get glaucoma.
age-related cataract formation is accelerated.

174
Q

describe the pathogenesis of diabetic retinopathy

A

microangiopathy in capillaries causes:
1) vascular occlusion –> ischaemia –> new vessel formation - these then bleed (vitreous haemorrhage).
fibrous tissue with the new vessels –> increased risk of retinal detachment. occlusion = cotton wool spots too.
2) vascular leakage - capillaries bulge –> oedema and hard exudates. rupture of microaneurysms causes flame haemorrhages (supericial) or blot haemorrhages (deep)

175
Q

how is diabetic retinopathy classified?

A

non-proliferative vs proliferative - proliferative = when there’s new vessels on the retina (neovascularization).

Non-proliferative (NPDR) is rated mild/mod/severe depending on degree of ischaemia. Can progress to proliferativ (PDR).

Maculopathy = leakage from vessels close to macula cause oedema, sig. threat to vision

Urgent referral needed for maculopathy, severe NPDR or PDR.

176
Q

describe the role of screening in diabetic retinopathy

A
  • v important! enables timely laser photocoagulation.
  • T1 and T2DM should be screened at diagnosis and then at least annually. (if onset <30y then within 5y of Dx and then annually).
  • every trimester during pregnancy.
  • screening is by dilated fundus photography.
  • referred to surgeon if maculopathy, features of pre-proliferative retinopathy or any proliferative retinopthy.
177
Q

how is diabetic retinopathy managed?

A
  • target BP <140/80 (or <130/80 if end organ damage)
  • good glycaemic control is KEY to prevention
  • photocoagulation by laser is used to treat maculopathy + PDR.
  • intravitreal triamcinolone and anti-VEGF drugs used with laser for macular oedema.
178
Q

how does episcleritis present? Rx?

A

eye aches dully, tender over inflamed area.
sclera looks blue underneath focal area of engorged vessels. acuity ok.
Rx = symptomatic relief - artificial tears, topical/systemtic NSAIDs.

179
Q

how does scleritis present? Rx?

A

generalised inflammation of the sclera itself.
50% will have assoc. systemic disease (e.g. RA, granulomatosis with polyangitis).
constant severe dull ache, painful ocular movements.

Rx - URGENT REFERRAL. NSAIDs, oral high dose prednisolone, or more aggressive immunosuppression depending on type of scleritis.

180
Q

what red flags would make you worry about a red eye?

A

impaired vision/decreased acuity
pain/photophobia
lack of ocular discharge

181
Q

what is blepharitis, how does it present?

A

inflammation of eyelids
- gritty, irritable eyes
- watery discharge
- foreign body sensation under eyelid
- red, inflamed eyelids, loss of eyelashes, reduced closure.
- notched upper lid, poor tear film, ingrowing eyelash

182
Q

blepharitis Rx?

A
  • main point is lid hygiene - cotton bud and baby shampoo diluted 1:10 twice a day
183
Q

what is a stye? Rx?

A

inflammatory lid swelling, typically infection of lash follicle (hordeolum externum, mostly staph.)
Rx = warm compress for 5-10 mins several times per day until resolves.

184
Q

explain what eyelid entropion/ectropion means

A

entropion = lid inturning. usually bottom lid. lashes irritate eye - taping, botox injections or even surgery needed.
ectropion = lower lid eversion - irritated, watery eye ± exposure keratitis. assoc. w/ old age and facial palsies. may need surgical correction.

185
Q

how does anterior unveitis present?

A

working age adults. pain, blurred vision, photophobia. onset over hrs/days.
assoc systemic disease - ank. spon., sarcoid, Behcet’s, IBC, reactive arthritis, herpes, TB, syphilis, HIV.

186
Q

how is anterior uveitis diagnosed? Rx?

A

slit lamp w/dilated pupil to visualise inflammatory cells location.

Rx = URGENT EYE CLINIC. Rx guided by cause.
prednisolone drops, cyclopentolate drops relieves pupil spasm.

187
Q

what is a corneal abrasion? Ix/Rx?

A

scratch on the cornea - pain, photophobia ± reduced acuity.
e.g. accidental scratches from contact lenses, sharp objects, trauma.
use fluorescein drops and blue light on slit lamp to Dx - lesions stain green. invert eyelid to look for foreign bodies.

188
Q

what causes corneal ulcers? Rx?

A

can be bacterial (beware pseudomonas), fungal etc.
get help unless very simple abrasion (Rx chloramphenicol ointment ± cyloplegia).

anything else - REFER. remove contact lenses. alternative chloramphenical drops with ofloxacin drops (cover Gram+ve and -ve respectively) until cultures known. OR cefuroxime drops + gentamicin drops.

189
Q

how does acute angle-closure glaucoma present?

A

rare but serious. elderly, long-sighted or female.
VERY high IOP.
unilateral painful red eye, profound loss of vision, N&V.

190
Q

how do you manage acute angle-closure glaucoma?

A

1) Lower the pressure - topical carbonic anhydrase inhibitors/topical beta-blockers + oral acetazolamide (carbonic anhydrase inhibitor) and intravenous mannitol
2) Constrict the pupil - pilocarpine drops (topical cholinergic agonists)
3) Prevent recurrence - Laser ± surgery OR Laser iridotomy (hole in iris) stops a second attack by providing a bypass

191
Q

list 4 golden rules for managing red eye

A

1) bilateral red eye is less serious than unilateral (conjunctivitis, blepharitis)
2) most benign causes will resolve spontaneously (conjunctivitis, episcleritis)
3) pain + loss of vision = SERIOUS (acute glaucoma, keratitis, scleritis, iritis)
4) beware prescribing topical steroids (increase ocular pressure, cataracts, prolong viral conjunctivitis, propagate corneal ulcers you might not have noticed…)

192
Q

LEARN PUPILS, VF DEFECTS, SQUINTS

A

LEARN PUPILS, VF DEFECTS, SQUINTS

193
Q

list some causes of dry eyes

A
  • ageing
  • medications: diuretics, antidepressants, antihistamines, beta blockers
  • systemic illness: RA, SLE, Sjogrens
  • Blepharitis (decreased tear production)
  • allergic conjunctivitis
194
Q

how do you manage someone with dry eyes?

A

artificial tears (4-6x daily)
drops - hypromellose, sodium chloride (3-4x daily)
gels - cling to surface of the eye. carbomers e.g. Viscotears (3-4x daily).

195
Q

how would you manage a foreign body in the eye?

A

examine whole eye and be sure to evert the lids.
if suspect metal FB, XR orbit. consider orbital US if high-velocity FB.
use 1% tetracaine drops if needed (local anaesthetic)
removal with a triangle of clean card if possible, followed by chloramphenicol drops.

if concerned about corneal abrasions, examine after giving local anaesthetic drops. stain with fluorescein - send home with analgesics, re-examine after 24h if needed and again at 48h if no improvement. if not showing signs of healing at 48h then refer.

Finals (15 decks)

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