Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2763_Библиотеки_им_академика_М_И_Перельмана
.pdf
Vertigo
https://t.me/med1917
DEFINITION
Abnormal sensation of movement / ‘room spinning’ → usually with nausea &
vomiting
CAUSES
Chapter 8: Ear, nose and throat 257
Central causes
= brainstem
• Space-occupying lesion
• Head injury
• Alcohol/drugs
• Degenerative disease e.g. MS
• Vascular ischaemia
Peripheral causes
= ears, eyes, somatosensors
• Labyrinthitis
• Vestibular neuronitis
• BPPV
• Ménière’s
• Ototoxic drugs
• Vestibular migraine
Non-vertigo causes of dizziness
• Postural hypotension/vasovagal
• Arrhythmias
• Presbystasis = age-related dysfunction of
vestibular system
DIFFERENTIALS OF VERTIGO SUMMARY
Labyrinthitis Vestibular
neuronitis
Pathophysiology Inflammation of
inner ear
Aetiology
Onset Sudden Sudden Sudden & episodic
Duration Hours – days Hours – days Secs – mins 30–40min Constant
Symptoms
Investigations
Management Supportive:
• URTI
• AOM
• N&V
• Nystagmus
± SNHL
1. ENT exam
2. PTA
• Vestibular
sedatives*
• Antiemetics
• Bed rest
Inflammation of
vestibular nerve
Viral infection • Spontaneous
• N&V
• Nystagmus
• No ear Sx
1. ENT exam
2. PTA
Supportive:
• Vestibular
sedatives*
• Antiemetics
• Bed rest
*
Prochlorperazine
BPPV Ménière’s disease Acoustic neuroma
Displaced semi-circular
calculi
• Head injury
(if head moved)
• N&V
• No ear Sx
1. ENT exam
2. PTA
3. Dix–Hallpike
manoeuvre
• Eply manoeuvre
• Cawthorne–Cooksey
exercises
Reassure: spontaneously
resolves in 12–18m
Vestibular sedative:
Excess endolymph Compression of vestibular
Unknown Schwannoma of vestibular
Sudden, recurrent,
progressive
(stress may trigger)
• N&V
• Nystagmus
• Low freq SNHL
• Aural fullness
1. ENT exam
2. PTA
3. Romberg test +ve
+ CT/MRI: r/o neuroma
Supportive:
• Vestibular sedatives*
• Antiemetics
• Bed rest
Medical:
• Steroids
• Intratympanic
gentamycin
Prevention:
• Low salt/caffeine
nerve
nerve
Progressive
• Facial palsies
• Headache
• Ataxia
• SNHL
• Tinnitus
CT/ MRI head
Medical:
Radiotherapy
Surgical excision
Monitoring
Advise patients NOT TO DRIVE while experiencing vertigo
258 Chapter 8: Ear, nose and throat
https://t.me/med1917
Hearing assessment
Assessment involves: history +
otoscope + audiometric tests
CHL: outer/mid ear problem BC normal, AC
SNHL: inner ear problem AC = BC
Mixed: CHL + SNHL AC > BC
Tuning fork tests
→ use 512Hz tuning fork
1. Weber’s test: vibrating tuning fork placed in middle of forehead
2. Rinne’s test: vibrating tuning fork placed on mastoid → when it can no longer
be heard, it is moved next to the ear canal
Interpreting the results:
Normal SNHL CHL
Weber’s Central/no
lateralisation
Lateralises to opposite side to loss
Cochlear damage means no sound
detection on that side
Lateralises to same side as loss
Distracting external sounds not
heard so fork seems louder
Rinne’s AC>BC Positive: AC>BC Negative: BC>AC
Pure tone audiometry (PTA)
How is it performed?
→ Uses electrical equipment to control frequency & intensity of sound
→ Produces audiograms
Interpreting the results:
→ Quantify HL for diagnosis, monitoring & rehab
Normal threshold
CONDUCTIVE HL: BC normal, AC
Normal threshold
SENSORINEURAL HL: AC = BC
Normal threshold
→
Gap >15dB
→
Gap <5–10dB
Key to symbols most commonly used
on audiograms
14
RIGHT LEFT
AC
AC masked
BC
BC masked [[ ]]
Indications for masking other ear:
1. AC between ears >40dB different
2. BC >10dB more than AC in same ear
MIXED HL: AC > BC
→Gap >15dB
14
ASHA (1974) Guidelines for audiometric symbols. 16(5): 260–4
Fig. 8.13
Tympanometry
Compliance
https://t.me/med1917
How is it performed?
Measures 3 components:
1. canal volume
2. middle ear pressure
3. compliance
Interpreting the results:
Type C
Type Ad
Type A
Type B
Chapter 8: Ear, nose and throat 259
TYPE A: normal
TYPE Ad: compliance
• healed TM perforation
• retraction pocket
• ossicle disarticulation
TYPE As: compliance
• TM scarring
• fluid in middle ear
0
Type As
0
Air pressure (mm H2O)
Fig. 8.14
Paediatric hearing assessment
NEWBORN HEARING SCREENING PROGRAMME
Who for? All babies within 5w of birth
How is it done?
1. Automated otoacoustic emission (AOE) = play sound in ear & measure
reflected vibrations – if fail AOE twice then:
2. Automate auditory brainstem response (AABR) = play sound in ear &
measure brain waves – if high risk/fail both:
3. AUDIOLOGY REFERRAL
OLDER CHILDREN
Who for? Based on developmental age
How is it done?
1. Visual reinforcement audiometry: 6–36m
→ condition to look at toy when sound heard
2. Play audiometry / performance test: ≥30m
→ ask child to perform action when sound heard
3. Pure tone audiometry: >5y
TYPE B: no peak compliance
• middle ear effusion / tumour
• TM perforation
• grommet
TYPE C: peak compliance at low frequency
• Eustachian tube dysfunction
High risk babies that automatically have
AABR:
• Neonatal sepsis
• NICU stay
• FHx congenital deafness
260 Chapter 8: Ear, nose and throat
https://t.me/med1917
Rhinosinusitis
Risk factors for rhinosinusitis
• polyps
• deviated septum
• dental infections
• smoking
Acute: <4w
Subacute: 4–12w
Chronic: >12w
Inflammation of nasal & sinus mucosa causing URTI Sx for >10d
↳ Common cold usually <10d
Acute rhinosinusitis
PATHOPHYSIOLOGY
→ Viral URTI causes hyperaemia & oedema of mucosa & secretions
→ Stagnant secretions become infected by bacteria (H. influenza,
Strep. pneumoniae)
SYMPTOMS
• Mucopurulent rhinorrhoea
• Nasal obstruction/congestion
• Smell/taste
• Facial pain – over infected sinus, worse bending forward
• Malaise/pyrexia
INVESTIGATIONS
• Anterior rhinoscopy – inflamed mucosa
• FNE/endoscopy – mucopus in oropharynx
→ CT would show sinus opacification
Complications of acute rhinosinusitis
• Chronic sinusitis
• Osteomyelitis
• Intracranial* (meningitis, brain abscess)
• Mucoceles
• Facial cellulitis
• Periorbital cellulitis
NB Facial pain without nasal symptoms =
unlikely sinusitis
Sources
• Orbital cellulitis
• Sinusitis
• Osteomyelitis
MUCOCELE
= collection of sterile mucus in obstructed sinus
→ over years pressure causes sinus expansion
Symptoms:
• Eye displacement
• Visual problems
• Facial swelling
Management: surgical sinus drainage
• 2° infection of mucocele
*need CT
MANAGEMENT
1. Conservative
• Simple analgesia
• Steam inhalations / nasal rinses
• Nasal decongestants (pseudoephedrine)
2. Medical
• Steroid nasal spray e.g. Beconase
• Antibiotics (penicillin V or co-amoxiclav) – ONLY if severe pain/high fever/
persistent Sx
3. Surgical (ENT referral)
• Maxillary sinus washout – ONLY if progressive pain/complications
• Functional endoscopic sinus surgery (FESS) if complications
15
Facial cellulitis
AETIOLOGY: infection spreads to skin
SYMPTOMS: red, warm, painful skin
MANAGEMENT: high dose ABX + sinus drainage
Periorbital cellulitis
AETIOLOGY: infection spreads into orbit (usually ethmoid sinus through thin
ethmoid bone)
SYMPTOMS
• Unilateral eyelid swelling, pain, redness
• Proptosis/ophthalmoplegia
• Blurred vision / loss of colour vision
• Fever, headaches, meningism, septicaemia
CT indicated in periorbital cellulitis if:
bilateral; unable to assess eye; proptosis; reduced
vision; failure to improve after 48h
MANAGEMENT: urgent ENT referral
• High dose IV ABX
• Nasal decongestant
• Careful eye obs (signs of abscess pressing on optic nerve)
15
EPOS (2020) European Position Paper on Rhinosinusitis and Nasal Polyps
• Colour vision
• Acuity
• Eye movements
Chronic rhinosinusitis (>3m)
https://t.me/med1917
Chapter 8: Ear, nose and throat 261
PATHOPHYSIOLOGY
→ Infection: viral/bacterial (anaerobes, Staph. aureus, Gram –ve)
→ Allergens: dust mites, pollen, animal hair
SYMPTOMS
• Nasal obstruction/congestion
• POST-NASAL DRIP – worse at night, morning cough to clear
• Smell/taste or unpleasant smell
• Intermittent facial pain – only with acute exacerbations
• Crusting/bleeding – careful monitoring for vasculitis/septal perforation/
neoplasm
INVESTIGATIONS: diagnosis based on history
• Anterior rhinoscopy and FNE/endoscopy
→ show inflammation, mucopus ± polyps
MANAGEMENT
• Consider macrolide treatment for 3–6w
• Topical nasal steroids (6–8w) e.g. betamethasone or fluticasone drops
• Steroid nasal spray (after finishing drops)
• Nasal douching
16
apply with head
upside down over
edge of bed
→
Nasal polyps
Specific form known as ALLERGIC RHINITIS:
→ sneezing
→ itchy eyes
→ rhinorrhoea
Mx: antihistamines, PO steroids, avoid allergens
If no improvement in 8w:
→ ENT referral
→ Confirm Dx with nasal endoscopy
→ CT & surgery to clear drainage pathways
Nasal douching: ½ tsp salt + ½ tsp sugar
+ ½ tsp bicarb dissolved in boiled water
→ draw up some with syringe
→ block one nostril with finger & sniff up mix
with other nostril
→ let it run out after
* should do before using nasal sprays/drops
→ grey/white, soft & mobile pedunculated swelling in nose/sinuses
SYMPTOMS
• Nasal obstruction
• Anosmia
• Rhinorrhoea
Unilateral or bleeding polyp = red flag
→ ENT referral
ASSOCIATIONS/RISK FACTORS
• Cystic fibrosis
• Infective sinusitis
• Samter’s triad: polyp + asthmas + aspirin sensitivity
INVESTIGATIONS
• Anterior rhinoscopy → biopsy if suspicious
MANAGEMENT
Medical: antihistamines, steroids (oral or drops/spray), decongestants → reduce
size in 80%
Surgical: polypectomy → if significant blockage / red flag features
Nasopharyngeal carcinoma
→ squamous cell carcinoma
SYMPTOMS
• Cervical lymphadenopathy
• Unilateral otalgia (CN IX)
• Unilateral OME
• Nasal obstruction ± discharge
± epistaxis
• CN palsies (CN III–VI)
16
ENT UK (2016) Commissioning Guide: Chronic Rhinosinusitis
MANAGEMENT
• CT & MRI
• Radiotherapy
• Surgery
Risk factors for carcinoma
• Southern Chinese origin
• EBV
262 Chapter 8: Ear, nose and throat
https://t.me/med1917
Emergency presentations
Epistaxis
CAUSES
• Idiopathic
• Nose-picking
• Trauma
• Infection
• Tumours
PREDISPOSING FACTORS
• Hypertension
• Anticoagulants, NSAIDs, aspirin
• Coagulopathies
• Hereditary haemorrhagic telangiectasia
most common
Unilateral epistaxis in adolescent boys
consider juvenile angiofibroma
(nasopharyngeal vascular tumour) → needs CT
& excision
*need prophylactic ABX if packing for >48h
Features suggesting posterior bleed:
• Profuse
• Bilateral
• Failed anterior packing
MANAGEMENT17 → Examine with thudicum to find source of bleed
1. First aid
• Lean forward, pinch fleshy part → for 10min
• Apply ice to bridge of nose
• Avoid swallowing blood
2. Resuscitation (if severe)
• Estimate blood loss, measure pulse/BP
• FBC, coag screen, G&S
• IV fluids if needed
3. Cauterisation – if bleeding from Little’s area (anterior bleed)
• Silver nitrate or bipolar diathermy
4. Packing* – if cannot visualise or cauterise bleed
• First-line: anterior packing (RapidRhino/Merocel)
• Second-line: posterior packing
6. Surgery/theatre – if cannot stop bleed
• Sphenopalatine artery (SPA) ligation
• Anterior ethmoid ligation (if trauma or SPA fails)
90% of bleeds are from ‘Little’s area’
Nose fracture
→ must rule out serious complications
MANAGEMENT
1. Manage epistaxis / acute problems
2. Rule out serious complications
• Zygomatic/facial fracture – diplopia, face numbness, trismus
• Head injury – LOC, N&V, amnesia, pupils
• CSF leak – unilateral clear nasal discharge
• Obstructed airways
• Chest/abdo injuries
• Septal haematoma
3. Clinic 7–10d later
→ Assess bony nose injury once swelling has subsided
4. Manipulation of bony deformity
→ Must be done within 14d of injury
17
NICE (2020) CKS Management Scenario: Acute epistaxis
Septal haematoma
https://t.me/med1917
AETIOLOGY: bleed between septum & perichondrium
ON EXAMINATION: bilateral red/purple bulge
COMPLICATIONS
→ Blocks nose & gets infected
→ Necrosis & septal perforation or saddle nose deformity
MANAGEMENT
→ Immediate ENT referral
→ Surgical drainage & IV ABX
Septal perforation
CAUSES
• TRAUMA/SURGERY
• Avascular necrosis – septal haematoma / cocaine
• Granulomatous infection – syphilis, TB, granulomatosis with polyangiitis
Chapter 8: Ear, nose and throat 263
SYMPTOMS
• Sense of nasal obstruction
• Whistling
• Crusting/bleeding
MANAGEMENT
• Douching & Vaseline
• Surgery (septal button or flap repair)
Foreign body
SYMPTOMS
• Unilateral offensive discharge
• ± epistaxis
COMPLICATIONS
• Inhaled foreign body
• Vestibulitis
MANAGEMENT
→ Removal: forceps/Johnson probe/suction
Be suspicious if child presents with these symptoms
264 Chapter 8: Ear, nose and throat
https://t.me/med1917
Facial palsies
→ ALL NEED THOROUGH ENT & NEURO EXAMINATION
Frontalis spared: UMN problem
Entire facial palsy: LMN problem
Investigations
• Hx, ENT exam, neuro exam
• PTA
• Electroneuronography = electrical stimulation of FN
• MRI/CT – if suspicious case
General management
Eye care: artificial tears, eye patch at night
Differentials of facial palsy
BELL’S PALSY (55%)
Aetiology: viral infection of FN
( risk in diabetes & pregnancy)
Symptoms: sudden onset (hours)
• Ipsilateral facial palsy (inc. frontalis)
• ± Pain
→ No ear/CNS pathology
Management: 80% fully recover in 2m
• High dose PO steroids
• Eye care + analgesia
Causes of facial palsy in kids
• Congenital
• Forceps delivery
• Chickenpox (VZV)
• Acute OM
RAMSAY HUNT (7%)
Aetiology: HZV infection of facial nerve
Symptoms
• Ipsilateral facial palsy (inc. frontalis)
• Ear pain / vesicles
• Vesicular rash
± SNHL, vertigo, tinnitus
Management: palsy = irreversible
• Aciclovir + corticosteroids
• Eye care + analgesia
Fig. 8.15 Left facial palsy, frontalis
notspared.
MIDDLE EAR DISEASE = AOM, cholesteatoma, mastoiditis
TRAUMA = temporal bone fracture, penetrating injury
TUMOUR = glomus jugular tumour, vestibular schwannoma, parotid gland
OTHER = CVA, multiple sclerosis, Guillain–Barré
Red flags of facial palsy
• Associated ear infection / foul otorrhoea → cholesteatoma / complicated otitis media
• Progressive palsy / parotid mass → neoplasm
• Associated neuro symptoms → cerebrovascular accident
265
https://t.me/med1917
OPHTHALMOLOGY
Acute painless vision loss .............................................. 266
Neuro-ophthalmology
Acute red eye
Miscellaneous acute ocular problems
Diabetic eye disease
Age-related macular degeneration
.......................................................................... 268
..................................................... 267
.................. 270
.......................................................... 271
........................ 272
ABBREVIATIONS
AION – Anterior ischaemic optic
neuropathy
AMD – Age-related macular degeneration
AV – Arterio-venous
BB – Beta-blocker
CAI – Carbonic anhydrase inhibitors
CN – Cranial nerve
CPEO – Chronic progressive external
ophthalmoplegia
CRA – Central retinal artery
CRAO – Central retinal artery occlusion
CRVO – Central retinal vein occlusion
CTD – Connective tissue disorder
EOM – Extraocular muscles
GCA – Giant cell arteritis
HSV – Herpes simplex virus
HZV – Herpes zoster virus
ICP – Intracranial pressure
IOL – Intraocular lens
IOP – Intraocular pressure
IRMA – Intraretinal microvascular
abnormality
MS – Multiple sclerosis
NAAION – Non-arteritic anterior ischaemic
optic neuropathy
NFT2 – Neurofibromatosis type 2
Cataracts
Glaucoma................................................................................... 274
Refractive errors
Orthoptics
Visual fields
09
.................................................................................... 273
................................................................... 275
................................................................................. 276
.............................................................................. 278
NPDR – Non-proliferative diabetic
retinopathy
PCA – Posterior cerebral artery
PDR – Proliferative diabetic retinopathy
PG – Prostaglandin
RA – Rheumatoid arthritis
RAPD – Relative afferent pupillary defect
RPE – Retinal pigment epithelium
SLE – Systemic lupus erythematosus
VEGF – Vascular endothelial growth factor
VF – Visual field
266 Chapter 9: Ophthalmology
https://t.me/med1917
Acute painless vision loss
Retinal detachment
Monocular causes Binocular causes
• Vitreous haemorrhage
• Ischaemic optic
neuropathy (GCA)
• Non-ischaemic optic
neuropathy
• Retinal vessel occlusion
• Retinal detachment
• Pituitary
tumour
• Optic neuritis
• Severe
papilloedema
• CVA
• Dry eyes
(± pain)
CAUSES
• Age
• Post-op/trauma
• Diabetic retinopathy
RISK FACTORS
• Myopia
• Stickler’s syndrome (in children)
Vitreous haemorrhage
TREATMENT: refer for urgent
surgery = vitrectomy & reattachment
SYMPTOMS
Floaters
Flashes
Field loss
Fall in acuity
+ absent red reflex
Floaters
= small black dots
in vision; patients may
describe “blobs” or “ink
splodge”
CAUSES
• Proliferative diabetic
retinopathy
• Retinal vein occlusion with
neovascularisation
• Retinal tear
• Retinal detachment
Fig. 9.1 Retinal tear.
INVESTIGATION: B-scan (USS of the
eye used when blood blocks view
of the retina)
Retinal vessel occlusion
• Retinal artery occlusions: caused by CVD
→ cardiovascular assessment for cause &
Cherry red spot
Fig. 9.2 CRAO.
Symptoms Signs Investigations Management
CRAO Sudden, profound,
entire vision loss
BRAO Sudden central or
sectoral vision loss
CRVO Blurred,
widespread vision
loss
BRVO Blurred, central or
sectoral vision loss
• RAPD
• Retinal oedema
• Pale retina (ischaemic)
• Cherry red spot
± carotid bruits
• Field defect
• Signs of hypertensive retinopathy
± carotid bruits
• RAPD
• Flame haemorrhages (widespread)
• Oedema
• Disc swelling
• Tortuous veins
± cotton wool spots
Flame haemorrhages (focal)
long-term Mx of diet/exercise/smoking
• Retinal vein occlusion: 2° to
atherosclerotic thickening of CRA,
compressing veins, or thick blood
→ HTN = major RF
• BP
• FBC, ESR, glucose
• Carotid USS
• Cardiac echo
To r/o causes of:
• HTN, DM
• Heart problems
• GCA (CRAO only)
• BP
• FBC, ESR, glucose
• IOP
To r/o causes of:
• HTN, DM
• Glaucoma
• Blood problems
Refer to EYE CASUALTY & TIA CLINIC
• Rebreathe into paper bag = CO2 dilates vessels
• Ocular massage
• Acetazolamide IOP
• Paracentesis IOP
NB Little evidence for these, as once vision lost = often irreversible
Refer to EYE CASUALTY & TIA CLINIC
1. Refer to EYE CASUALTY
2. Manage cardiovascular risk factors
3. Manage complications of retinal vein occlusion
(neovascularisation / macular oedema)
SYMPTOMS
• Floaters – many small or one large
• Absent red reflex – if large bleed
TREATMENT
• Proliferative/neovascular cause:
observation then pan-retinal laser
once bleed settles
• Tear/detachment: vitrectomy
Widespread
haemorrhages
Fig. 9.3 CRVO.
1
1
RCOphth (2015) Retinal Vein Occlusion (RVO) Guidelines
Соседние файлы в папке Библиотека им академика М.И. Перельмана