Management of Common ENT Emergencies

transcript

Paul Paddle M.D. Laryngology Clinical Fellow

Ear – Petrous Temporal Bone Fracture

•  Classifica(on – Anatomical: Longitudinal vs Transverse (vs Oblique) –  Func(onal: OFc Sparing vs OFc DisrupFng

•  Epidemiology –  > 70% b/w 20-‐40 years of age –  Bilateral: 8-‐29%; Compound: 60% open #’s

•  Pathophysiology –  Blunt trauma –  Fracture takes path of least resistance

Ear – Petrous Temporal Bone Fracture Longitudinal #

•  80% TB Fractures •  Mechanism: Lateral forces

over the mastoid or squamous bone

•  # Parallels long axis of Petrous Pyramid

•  ComplicaFons: i)  15-‐20% CN VII n. involvement ii)  Ossicular disrupFon iii)  EAC laceraFon

Fracture Line

Ear – Petrous Temporal Bone Fracture Transverse #

•  20% TB Fractures •  Mechanism: Forces in the AP

DirecFon •  # Runs perpendicular to long

axis of petrous pyramid •  ComplicaFons:

i)  SNHL -‐ high rate ii)  VII n. involvement – 50% iii)  EAC intact

Fracture Line

Ear – Petrous Temporal Bone Fracture O(c Capsule Disrup(ng

•  2.5-‐5.8% of fractures •  # line traverses O(c

Capsule, but spares Ossicular Chain

•  Complica(ons: i)  Facial Nerve ii)  CSF Fistula iii)  Intra-‐cranial Injuries –

Greater risk iv)  Hearing Loss: Almost always

result in SNHL

O(c Capsule Sparing

•  # line involves squamous •  Complica(ons:

i)  Facial Nerve: paralysis in 6-‐14%

ii)  Hearing Loss: Tend to have CHL or Mixed HL

Ear – Temporal Bone Fracture

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transverse.8-14 In two large series using the newer classification scheme, only 2.5% to 5.8% of fractures disrupted the otic capsule,3,15 suggesting that many fractures that are oriented perpendicular to the petrous ridge do not actually cross the otic capsule. Many of the otic capsule– disrupting fractures are actually oriented in the longitudinal plane.15

The rationale for changing the classification scheme is to focus on the functional sequelae and complications of temporal bone fractures as opposed to merely describing the anatomic orientation of the frac-ture. Fractures that disrupt the otic capsule almost always result in a sensorineural hearing loss, although there are reported exceptions.16 Otic capsule–sparing fractures tend to have conductive or mixed hearing loss,3 whereas otic capsule–disrupting fractures have a much higher incidence of facial nerve paralysis (30% to 50% vs. 6% to 14%).3,15 In addition, Fisch17 reported a much higher incidence of nerve disruption in fractures involving the otic capsule. There is a twofold to fourfold increase in CSF fistula in otic capsule–disrupting fractures as

way to a new scheme that classifies fractures by whether they disrupt or spare the otic capsule (the bone that houses the cochlea and the semicircular canals) (Figs. 145-2 through 145-4).3,9

Fractures that spare the otic capsule typically involve the squa-mosal portion of the temporal bone and the posterosuperior wall of the external auditory canal. The fracture passes through the mastoid air cells and the middle ear and then fractures the tegmen mastoideum and tegmen tympani. The fracture proceeds anterolateral to the otic capsule, typically fracturing the tegmen in the region of the facial hiatus. Otic capsule–sparing fractures typically result from a blow to the temporopa-rietal region.

Otic capsule–disrupting fractures pass through the otic capsule, generally proceeding from the foramen magnum across the petrous pyramid and the otic capsule. The fracture often passes through the jugular foramen, the internal auditory canal, and the foramen lacerum; these fractures do not typically affect the ossicular chain or the external auditory canal.10 Otic capsule–disrupting fractures generally result from blows to the occipital region.

Longitudinal fractures reportedly make up 70% to 90% of tem-poral bone fractures, with the remaining 10% to 30% categorized as

Automob

ltFall

Motorcy

Bicycle

otMisc

Figure 145-1. Type of injury. (Data from Brodie HA, Thompson TC, Manage-ment of complications from 820 temporal bone fractures. Am J Otol. 1997;18:188.)

Figure 145-2. Axial-cut high-resolution computed tomography scan that demonstrates a longitudinally oriented fracture that is sparing the otic capsule. Black arrows point along the fracture line.

Figure 145-3. Axial-cut high-resolution computed tomography scan that demonstrates a transverse-oriented fracture resulting from a gunshot injury and disrupting the otic capsule. The black arrow points to the fracture line.

Figure 145-4. Axial-cut high-resolution computed tomography scan that demonstrates a mixed-oriented fracture that spares the otic capsule. The white arrows point to the fracture lines.

•  History: Mechanism of Injury •  Examina(on:

i)  Ear Exam – Scalp, face, pinna, EAC inspecFon ii)  Neurological Exam – CN VII, VesFbular, Bedside

hearing iii)  Bedside Hearing Assessment – Free Field, Forks

•  Audiometry

•  Treatment 1.   Manage Head Injury / ABCs 2.   Auricle – repair laceraFons, drain haematomas 3.   EAC -‐

Ear – Petrous Temporal Bone Fracture •  Treatment

4.   Facial Nerve Injury •  7% of facial nerve paralysis •  Onset:

a.  27% immediate b.  73% delayed, ranging

from 1-‐16 days c.  ? “Un-‐established”

•  Controversial i)  Conserva(ve: MOST

resolve spontaneously ii)  Surgical Explora(on/

Repair: only warranted in paFents with: a.   Complete (severity) b.   Immediate (onset) in

whom c.   Electrical S(mulability is

cular canal and the floor of the middle cranial fossa. The canal may have very little bone coverage, it may be seen as a blue line after simple dural elevation, or there may be a large number of air cells between the canal and the surface of the tegmen.

If the superior semicircular canal cannot be located by drilling over the arcuate eminence, two other methods may be considered. First, the tegmen tympani may be opened, thus exposing the ossicles. The location of the superior semicircular canal can be established by the spatial relationships. Second, the greater superficial petrosal nerve can be followed retrograde back through the facial hiatus to the geniculate ganglion. The intralabyrinthine portion of the facial nerve passes between the cochlea and the ampulla of the superior semicircular canal. The bone over the superior semicircular canal is removed using suction irrigation and diamond burrs.

A light medial to lateral stroke is used until the blue line of the superior canal is identified. After the superior canal has been identified, dissection proceeds along the meatal plane, which is the bone within a 60-degree angle from the blue line of the superior canal. Drilling within the confines of this plane will reduce the risk of inadvertent injury to the cochlea. Note that much wider drilling may be performed medially, whereas, at the lateral extent of the IAC, there is very little space between the cochlea and the ampulla of the superior semicircular canal.

Immediate onset paralysis Observation and systemicsteroids

Observation and systemicsteroids

Yes Unknown

Translabyrinthine totalfacial nerve decompression

Great auricular nerve cable graftor direct facial anastamosis

Combined transmastoid middlecranial fossa total facialnerve decompression

Complete paralysis

Adequate exposure

Procedure completed

Otic sparing fracture

Facial nerve severed

Facial nerve exploration

Loss of stimulability or95% degeneration onEnoG within 14 days

Well-aerated mastoidair cells or ossicular

discontinuity

Transmastoid/supralabyrinthinetotal facial nerve decompression

Total facial nervedecompression achieved

Great auricular nerve cablegraft or direct anastamosis

Severed facial nerveencountered

Figure 145-11. Management of traumatic facial paralysis.

Figure 145-12. Supralabyrinthine exposure of the geniculate ganglion and the intralabyrinthine portion of the facial nerve. I, Incus; M, malleus; G, geniculate ganglion.

Ear – Petrous Temporal Bone Fracture •  Treatment

5.   Hearing Loss i)  SNHL -‐ O"c Capsule Disrup"ng

–  Numerous AeFologies –  50% have at least 10dB SNHL (2000-‐4000 Hz)

ii)  CHL – O"c Capsule Sparing a.   Nil – 80% resolve spontaneously b.   Surgery – exploratory tymopanotomy and OCR

6.   CSF Leak

first month after injury. Clearly these confounding variables must be controlled in a prospective, multi-institutional study to adequately address the question of the efficacy of prophylactic antibiotics.

The most common infecting organisms in meningitis that occur in the presence of a CSF fistula are Streptococcus pneumoniae and Hae-mophilus influenzae.62,77,78 Fifty-seven percent to 85% of post-traumatic fistulas that are treated conservatively cease leaking within 1 week.49,61 Because acute posttraumatic CSF fistulas are associated with a high probability of early spontaneous closure and a low incidence of men-ingitis, they can be treated conservatively for 7 to 10 days; this treat-ment includes total bed rest with elevation of the head of the bed; stool softeners; instructions to avoid nose blowing, sneezing, and straining; and repeat lumbar punctures or lumbar drain if the leak persists. These measures are directed at maintaining the CSF pressure gradient below the healing tensile strength of the healing barrier. Because of the increased risk of meningitis after persistent CSF fistulas, the closure of fistulas that persist for more than 7 to 10 days is recommended.

Closure of CSF FistulasThe treatment algorithm for CSF fistulas is presented in Fig. 145-13. In a patient with a fracture of the otic capsule that results in profound sensorineural hearing loss, obliteration of the mastoid and middle ear is recommended.79,80 The ear canal, the tympanic membrane, the incus and malleus, and the middle ear mucosa are all excised. The external auditory meatus is closed in a two-layer closure, and a complete mas-toidectomy is performed. The mucosa of the eustachian tube is inverted, and a muscle plug is inserted. The incus is then inserted as well, wedging the muscle into place. The eustachian tube and the fracture

antibiotics in patients with CSF fistula was demonstrated. Three hundred and twenty patients were included in the analysis.74 The inci-dence of meningitis in patients with posttraumatic CSF fistulas treated with prophylactic antibiotics was 2.1%. In patients who did not receive prophylactic antibiotics, the incidence of meningitis was significantly higher, at 8.7% (P < .02). Individually, however, none of the studies included in the metaanalysis demonstrated a statistically significant effect of prophylactic antibiotics, which points out the pitfall of statis-tical analysis with inadequate numbers of patients. In a second study, no statistically significant effect of antibiotic prophylaxis was demon-strated.75 The problem with this second analysis is the inclusion of one study that reported on patients whose fistulas persisted for weeks to months.76 In the meta-analysis,75 20 of 29 patients in whom meningi-tis developed while on prophylactic antibiotics were in this one study,76 which permitted this very long duration of leakage.

In addition to the inadequate numbers of patients in these prior studies, there are significant problems inherent in this type of retrospec-tive study. How do we define adequate prophylaxis? Do 3 days of perioperative antibiotics for the repair of a concomitant open femur fracture constitute adequate prophylaxis for a CSF fistula that persists for 5 days? Do therapeutic antibiotics for a concurrent infection con-stitute adequate prophylaxis for a CSF fistula? One very important risk factor that increases the risk of meningitis in patients with CSF fistulas is the presence of a concurrent infection. Brodie and Thompson3 found a 20% incidence of meningitis in patients with concurrent infection and a 3% incidence of meningitis in the absence of concurrent infec-tion. In that study, in the absence of concurrent infection, meningitis did not develop in any patient receiving prophylactic antibiotics the

Elevate head of bedBedrestStool softenersProphylactic antibiotics

CSF fistula

Suspected leak

Surgical intervention

!2 transferrin

Adequatefluidsampleobtainable

Negative andlow suspicion

Negative

Positive

Leakresolves

Leak resolves

Positive

Persistentleak

Negative andhigh suspicion

Leak persistsfor 7−10 days

Fistula through cribriform plateor forea ethmoidalis

Otic capsule−sparingtemporal bone fracture

Otic capsule−disruptivetemporal bonefracture

Inadequatefluid

sampleobtainable

Obvious leak

Observe

Omnipaque CT of temporalbone/paranasal sinuses

Intranasalmucoperichondrial flap

Resect EAC, TM and obliteratemiddle ear and eustachian tube

Mastoidectomy with minimiddle cranial fossa craniotomy

Intrathecalfluorescein

Lumbar drain

Figure 145-13. Management of traumatic cerebrospinal fluid (CSF) fistula. EAC, external auditory canal; TM, tympanic membrane.

Petrous Temporal Bone Fracture

7.   Cholesteatoma 8.   Caro(d Artery Injury – Obtain Angiography if: i)  Neurological Exam not consistent with CT ii)  Lateralising Neurological defects iii)  Horner’s Syndrome iv)  Cervical Bruit v)  Displaced # through the CaroFd Canal

Ear – Acute Facial Paralysis

Category Specifics

Polyneuri(s Bells Palsy Herpes Zoster Guillain Barre Autoimmune Disease Lyme Disease HIV Kawasaki’s Disease XRT

Trauma Temporal Bone # Barotrauma Birth Trauma

O((s Media Bacterial – Acute / Chronic Cholesteatoma

Sarcoidosis

Neurologic Disorders CVA – central or peripheral MS

Melkersson-‐Rosenthal Syndrome

“All that Palsies are NOT Bell’s

Ear – Bell’s Palsy

•  Defini(on: Spontaneous, Idiopathic Lower Motor Neuron Facial Paralysis

•  Epidemiology: Common, Adults > 65, M=F •  Ae(opathogenesis: HSV-‐1

•  History: Onset / Trauma / Recent Illness / Pain / Other Neuropathies

•  Examina(on: 1.   Facial nerve exam: Side / Bilateral (2%) / Complete (70%) 2.   Full ENT Exam – esp.

i)  Ear Exam ii)  Other Cranial Nerves: weaknesses found in >50% of Bell’s Palsy

•  Inves(ga(on: 1.   Audiogram 2.   Electrophysiologic Tes(ng 3.   Imaging – MRI with gad

Ear – Bell’s Palsy •  Treatment

1.   Eye Care: i)  Ophthal Review ii)  Sunglasses during day iii)  Close eyelid @ night – e.g. Tape iv)  Ar(ficial Tears v)  +/-‐ Eye Chamber

2.   Speech / Diete(cs: 3.   Steroids:

•  STRONG evidence for Benefit •  Onset of Treatment: ideally within 3 days of Symptom onset; up to 14 days •  No consensus on Dose & Dura(on •  Prednisolone 1mg/Kg Body Weight/o/daily reducing over 10-‐14 days

4.   An(-‐virals

•  Prognosis/Recovery: – Complete Recovery in 80-‐90%; up to 12 months – Poor Outcome Prognos(c Factors:

a.   Complete paralysis b.   Age > 60 c.   Diabetes d.   Hyper-‐acusis e.   Severe Pain

•  Recurrence: 10% of cases

Ear – Ramsay Hunt Syndrome

•  Defini(on: VZV Related NeuriEs involving CN VII & CN VIII, and a vesicular rash.

•  Epidemiology: •  Ae(opathogenesis: – ReacFvaFon of Latent VZV within the Geniculate Ganglion.

– Due to intercurrent stress or illness –  Inflammatory/Oedema PLUS direct cytopathic effect

Ear – Ramsay Hunt Syndrome •  History:

–  Past History Chicken Pox / VZV –  More likely Severe pain than with Bell’s Palsy

•  Examina(on: 1.   Facial Nerve Weakness 2.   Vesicles: -‐  Onset:

-‐  Mostly concurrent with Paralysis -‐  25% of cases – precede the Paralysis

-‐  Distribu(on: Pinna / Post-‐auricular / EAC / Face / Mucous Membrane / Palate.

3.   Ocular Complica(ons: Herpes Zoster Ophthalmicus 4.   Hearing Loss / Ves(bular Disturbance -‐  25% of paFents

Right Trigeminal VZV Right Trigeminal VZV

•  Inves(ga(ons: 1.   Audiology: SNHL 2.   Serology: Rising AnE-‐VZV AnEbody Titres

•  Treatment:

1.   Cor(costeroids 2.   An(-‐Virals – Lessens Pain, Promotes resoluFon of Vesicles – Dose:

•  Prognosis: i)  Facial nerve

• Worse than Bell’s Palsy •  30-‐50% incomplete recovery

ii)  Ves(bulo-‐cochelar •  Complete Recovery: 68% of children, 38% of adults

Nose -‐ Fracture •  History:

i)  Mechanism of Injury ii)  Time since injury iii)  Deformity – Cosme"c? Func"onal? iv)  Associated Injuries v)  Prior Nasal Disease

•  Examina(on: i)  Nasal External ii)  Nasal Internal

a.   Septal Haematoma b.   CSF Rhinorrhoea c.   Septal #

iii)  Rest of Face a.  Orbital Rim # b.  Head Injury c.  C Spine

“Most Common Facial Bone Fracture”

Nose -‐ Fracture

•  Inves(ga(ons: –  Nasal Fracture is a clinical diagnosis

i)  Plain Films? NO ii)  CT? Rarely

•  MulF-‐Trauma •  Evidence adjacent

injuries

“Most Common Facial Bone Fracture”

Nose -‐ Fracture

•  Treatment: 1.   Acute Interven(on:

i)  Primary Survey ii)  Manage Epistaxis iii)  Manage Septal

Haematoma – Incision & Drainage

Nose -‐ Fracture

•  Treatment: 2.   Defini(ve Interven(on: –  Timing:

•  Within 1-‐2 hours of injury •  B/w 3 – 14 days

–  Children within 4 days •  Not ater 14 days

-‐  LA vs GA -‐  Open vs Closed ReducFon -‐  +/-‐ Acute Septoplasty

Nose – Fracture •  Late Nasal

Complica(ons: –  CosmeFc Deformity –  FuncFonal Deformity –  SinusiFs –  Septal PerforaFon –  Synechiae

•  Other: –  CSF Leak, –  Ophtalmologic

Nose -‐ Epistaxis •  Epidemiology: USA, AUS,

UK –  Commonest ENT emergency –  60% of popula(on in their

life(mes –  6% of cases requiring medical

amen(on –  Peaks in incidence: < 10

years & > 40 years –  Seasonality: Peak in Winter

•  Classifica(on: i)  Anterior (90%) ii)  Posterior (10%)

Nose -‐ Epistaxis

Anterior Epistaxis Posterior Epistaxis

Nose -‐ Epistaxis

•  Pathogenesis: •  Numerous Anastomoses •  Between ICA & ECA

Terminal Branches •  Both Ipsilateral and

Contralateral •  2 Key Watershed areas: i)  Anterior: Kisselbach’s

Plexus a.   Superior Labial a (Facial) b.   Greater PalaEne a.

(IMAX) c.   Anterior Ethmoidal a.

(Ophthalmic a.) d.   SphenopalaEne a. (IMAX)

ii)  Posterior: Woodruff’s Plexus a.   Posterior-‐lateral &

Posterior-‐medial br. Of SphenopalaEne (IMAX)

b.   Pharyngeal a. (IMAX)

Nose -‐ Epistaxis Local Factors

Factor Examples

Idiopathic (80%)

Trauma Nasal Fracture, Nose picking

Inflammatory / Infec(ous

Viral, Allergic, Bacterial, Granulomatous

Post-‐opera(ve Nasal Surgery

Primary Neoplasm Haemangioma, Papilloma, Pyogenic Granuloma, Carcinoma

Structural Septal Spur

Drugs Topical Steroids, Cocaine

Systemic Factors

Factor Examples

Hypertension Controversial,

Arteriosclerosis

Blood Dyscrasias VWF, Haemophilia,

Drugs Aspirin, Warfarin, Clopidogrel

Organ Failure Liver, kidney

Haematologic Malignancies

Leukaemia

Nose -‐ Epistaxis Local Factors Systemic Factors

Nose – Epistaxis -‐ Treatment

1.  Correct 1st Aid: –  Lean Forward –  Head Flexion –  ConFnuous Alar pressure 10-‐20mins

–  +/-‐ Ice to Suck

depends on whether it’s a ‘Trickle’ or a ‘Torrent’

2.  EMST Principles: –  ABCs i)  A

a.  Siwng Forward b.  SucFon

ii)  B iii)  C

a.  EsFmated Blood Loss b.  IV Access c.  CBC, BGH d.  IV Fluids, Blood as

necessary

3.  ‘Secondary Survey’ i)  Local:

•  Equipment: ProtecFve Eyewear, mask, Headlight, sucFon

•  Remove Clots •  Decongestant/AnaestheFc •  Establish Site:

–  Anterior Rhinoscopy –  Nasendoscopy

ii)  Systemic: •  Correct Systemic Causes –

e.g. Vitamin K, AnE-‐hypertensives, Prothrombinex®, Factor VIII

Nose -‐ Epistaxis

4.  Topical Treatment i)  Cautery: •  AgNO3 -‐ precauFons

ii)  Cream/Ointment •  Emollient – e.g. Vaseline ®

•  AnFsepFc – e.g. Nasalate® Mupirocin (Bactroban®), Chloromyce"n (Chlorsig®)

iii)  Dressing – Surgicel®

5.  Nasal Packing: – For 24-‐72 hours – Monitor Closely:AnFbioFc Prophylaxis: S Aureus TSST

– Anterior vs Posterior

Nose – Epistaxis

i) Anterior Packing – TradiEonal

Nose -‐ Epistaxis i)  Anterior Packing – Newer

–  Rapid Rhino ® –  Merocel ® –  Kaltostat ® –  Nasopore ®

Nose – Epistaxis

ii)  Posterior Packing – TradiFonal

Nose -‐ Epistaxis

ii)  Posterior Packing -‐ Newer –  Double Balloon Nasal Catheter – e.g. Brighton Balloon®, Simpson Plug®, Epistat Nasal Catheter ®

–  Foley catheter method

Nose – Epistaxis 5.   Packing – ComplicaFons:

i)  Immediate: a.  Naso-‐vagal Reflex – Hypotension & Bradycardia b.  Naso-‐pulmonary Reflex – Respiratory Depression

ii)  Early a.  Failure to cease bleeding / bleeding on removal b.  ObstrucFon:

i.  Nasolacrimal Duct: Epiphora ii.  OMC: sinusiF iii.  Nasal Airway: Hypoxia, OSA

c.  Displacement into oropharynx, acute airway obstrucFon d.  Toxic Shock Syndrome

iii)  Late a.  Pressure Necrosis of Alar

Nose – Epistaxis 6.   Surgery –  General IndicaFons: i)  Uncontrollable Bleeding -‐ failure of 1-‐2 properly placed

packs Op(ons: i)  EUA and Electrocautery

-‐  Bipolar preferred -‐  OpFc and Oculomotor n injuries reported

ii)  Septal Surgery – e.g. Septoplasty -‐  Access -‐  Raising mucoperiosteal flap may reduce bleeding -‐  Correct spur or deviaFon – turbulence & trauma -‐  (septal dermoplasty for HHT)

Nose – Epistaxis

6.   Surgery i)  SphenopalaEne Artery

LigaFon -‐  Mucosal flap raised posterior to membranous fontanelle

-‐  SPA clipped or diathermied (or both)

-‐  80-‐90% success

Nose – Epistaxis

6.   Surgery ii)  Anterior / Posterior

Ethmoidal Artery LigaFon

-‐  TradiFonally via an external ethmoidectomy approach (Lynch Incision)

-‐  Endoscopic and endoscopic-‐assisted approached

-‐  Improved outcomes when combined with SPA ligaFon

Nose -‐ Epistaxis

AEA Liga(on -‐ Artery AEA liga(on – Artery post clip

Nose – Epistaxis

6.   Surgery iii) Maxillary Artery LigaEon -‐  Rarely performed -‐  Modified Caldwell-‐luc Approach -‐  Vessel Clipped or diathermied -‐  87% effecFve iv)  External CaroEd Artery LigaFon -‐  Method of last resort in profound uncontrollable haemorrhage

-‐  Long-‐term failure rate 45% due to contralateral supply @ watershed areas

Nose – Epistaxis 7.   Selec(ve Embolisa(on –  Indica(ons: intractable

epistaxis where surgery failed or paFent unfit for surgery

–  ParFcles used: metal coils, latex, gelaFn Sponge

–  Angiography: via Femoral artery

–  Arteries Embolised: ECA supply, 2mm diameter vessels, bilateral super-‐selecFve approach

–  Success Rate: 87% effecFve –  Complica(on Rate: 2-‐6%

•  False Aneurysm •  CVA, Hemiplegia •  Ophthalmoplegia, Blindness.

Nose – Epistaxis

8.   Secondary Preven(on & Advice

Nose – Periorbital CelluliFs

•  Defini(on: ComplicaFon of Acute or Acute on Chronic RhinoSinusiFs where infecFon has spread beyond anatomic boundaries of sinus

•  @ Risk Groups: i)  Children ii)  Adolescent Males iii)  Immunosuppressed

•  Classifica(on

CHANDLER (1970) (+/-‐ Mechanism)

STAMMBERGER (1993)

MORTIMORE/WORMALD (1997)

I 36.7-‐70%

o  Pre-‐septal Celluli(s §  Venous congesFon in Superior

Ophthalmic Veins secondary to obstruc(on of Ethmoidal Vessels by pressure.

o  Pre-‐septal Celluli(s o  Pre-‐septal i)  Celluli(s ii)  Abscess

II 0-‐6.2%

o  Post-‐septal Celluli(s: InfiltraFon of orbital adipose Fssue with

inflammatory cells and bacteria No discrete Abscess

o  Sub-‐periosteal Celluli(s (peri-‐osEEs)

o  Post-‐Septal (Sub-‐periosteal) i)  Celluli(s ii)  Abscess

III 8-‐15%

o  Sub-‐periosteal Abscess: Abscess formaFon deep to the

Periosteum/peri-‐orbita of the orbital bones (usually Lamina Papyracea)

o  Sub-‐periosteal Abscess o  Post-‐septal (Intra-‐conal) i)  Celluli(s

a.   Localised – i.e. Orbital Apex Syndrome

b.   Diffuse

IV 0-‐6.2%

o  Orbital Abscess

o  Orbital Celluli(s/Abscess

ii)  Abscess

V o  Cavernous Sinus Thrombosis/Abscess (Considered an Intra-‐cranial ComplicaFon)

o  (Considered an Intra-‐cranial ComplicaFon)

Nose – Periorbital Sinus Cx

Pre-‐septal Celluli(s Sub-‐periosteal abscess

Orbital celluli(s Orbital Abscess

Nose -‐ Periorbital Sinus Cx

Cavernous sinus thrombosis Ae(opathology •  Sinus of origin: Ethmoid >>>

Frontal > Sphenoid > Maxillary •  Microbiology: Strep.

Pneumonia > Other strep > S.aureus > Anaerobes > G –’ve Rods

•  Anatomical: i)  Ostei(s èresorpFon ii)  Thrombophlebi(s of

communicaFng veins iii)  Bony Defects: congenital or

acquired

Nose – Periorbital Sinus Cx •  History: •  Examina(on:

•  Hx: – Mild URTI, followed by swelling around the eye. – +/-‐ Visual Symptoms (occur mostly within 2-‐2.5 days of onset of Fever/URTI!)

– +/-‐ Headache, meningism, Trigeminal Paraesthesia §  N.B. in children: pain & sepsis NOT always found

•  ExaminaFon: i)  Full ENT – esp. nasendoscopy ii)  Ocular exam – including formal ophthal consult:

Nose – Periorbital Sinus Cx STAGE On Examina(on

Pre-‐septal Celluli(s

-‐  Pre-‐septal NON-‐tender Oedema -‐  NO EOM impairment -‐  NO Δ Visual Acuity

Post-‐septal Celluli(s

-‐  As above -‐  +/-‐ Δ VA (6-‐15% of cases) -‐  +/-‐ EOM Impairment

Sub-‐periosteal Abscess:

-‐  As above -‐  + Proptosis (usually downward/lateral) -‐  +/-‐ EOM impairment -‐  +/-‐ Δ Visual Acuity (N.B. Subtle loss of colour vision (red) first) -‐  N.B. Abscess may rupture through orbital septum and present in the eyleids

Orbital Abscess

-‐  As above -‐  + Ophthalmoplegia -‐  + Chemosis -‐  + Severe Δ VA

Cavernous Sinus Thrombosis:

-‐  As above -‐  + Rapid extension to the Contralateral eye -‐  + Headache

+ Trigeminal Paraesthesia

•  Inves(ga(ons & Consults: i)  Pathology:

a.  SepFc Work Up – FBE, ESR, CRP b.  Meatal Swab – MC&S including Fungal c.  Risk Factors – e.g. HbA1c

ii)  Imaging: CT / MRI iii)  Consulta(on:

a.  Ophthalmology Consult, b.  Endocrine

Nose – Periorbital/Orbital CelluliFs

•  Treatment – General Principles: i)  Guided by the severity of the Eye Signs •  > 100 mins ReFnal Ischaemic Time: Irreversible Loss of Vision

ii)  Treat the ComplicaFon iii)  Treat the underlying Sinus

•  Treatment –  Specifics: i)  Medical

a.   An(-‐microbials: –  Against: Strep. Pneumoniae, Moraxella, Haemophilus Influenza, Staph

Aureus, Anaerobes –  Drug: e.g. Flucloxacillin + Ceeriaxone +/-‐ Metronidazole –  Route: IV; convert to oral –  Dura(on: ? 7-‐14 days

b.   Nasal Deconges(on -‐  No evidence for/against

c.   ? Steroids – Topical or Systemic -‐  No evidence for/against -‐  Risk/Benefit – medical decompression vs unwanted immunosuppression

Nose – Periorbital/Orbital CelluliFs •  Treatment –  Specifics Cont’d: ii)  Surgical

•  Indica(ons: a.   Disease Factors:

i.  Orbital Abscess ii.  Orbital CelluliFs – Decreased VA iii.  Sub-‐periosteal Abscess (SPA): controversial in Children iv.  Pre-‐septal CelluliFs: No improvement ater 24-‐48/24 of

Medical Mx b.   Pa(ent Factors

i.  Immuno-‐compromised ii.  ? Previous Sinus Surgery

•  Treatment – Specifics Cont’d: ii)  Surgical

•  Endoscopic vs Open a.   Disease Factors – Extent (e.g. Diffuse vs Focal), PosiFon,

(e.g. Medial vs Lateral) AddiFonal ComplicaFon (e.g. Intra-‐cranial,

b.   Pa(ent Factors -‐ ? Anatomy c.   Surgeon Factors – preference and experience

•  Treatment – Specifics Cont’d: ii)  Surgical

•  Nature of Surgery a.   General:

i.   Treat Complica(on: Decompression orbit, Drain abscess

ii.   Treat Sinusi(s: e.g. Fronto-‐ethmoidectomy b.   Specific:

i.   Endoscopic ii.   Open

Throat – Peritonsillar CelluliFs/Abscess

•  Defini(on: i)  Celluli(s: an inflammatory reacFon of the Fssue b/w Capsule of the

pala(ne tonsil and the Pharyngeal muscles; No pus. ii)  Abscess: a collecFon of pus located b/w capsule of pala(ne tonsil and

the Pharyngeal Muscles •  Epidemiology:

–  MOST common deep neck infecFon in children and adolescents –  30/100,000 persons aged 5-‐59

•  Microbiology: Polymicrobial –  GABHS –  S. Aureus (incl. MRSA) –  Respiratory Anaerobes – Fusobacteria, Prevotella, Veillonella

•  Risk Factors: i)  Smoking ii)  Recurrent Tonsilli(s

•  AeFopathogenesis: i)  Tonsilli(s è Spread of infecFon Usually Begins in @

Superior pole •  N.B. PTA can occur without preceding infecFon: such cases thought to be caused by obstruc(on of the Weber Glands

ii)  CelluliEs è iii)  Phlegmon è iv)  Abscess formaFon b/w tonsil bed and capsule

•  upper pole -‐ most commonly •  Mid pole or Lower pole – occasionally •  Dispersed with Mul(ple Locula(ons – rarely

•  History: ≥ 48/24 history –  Sore throat –  Fevers –  Dysphagia –  Altered speech

•  Examina(on: –  Swinging fever –  Trismus –  Palatal fullness –  Hot potato speech –  Tonsillar displacement

•  Inves(ga(ons: –  NOT generally indicated unless atypical

i)  Laboratory: a.  FBE, U&E b.  EBV Serology

ii)  Imaging: a.  CT Neck with Contrast

•  Treatment: i)  Suppor(ve:

a.  HydraFon b.  Analgaesia

ii)  Medical: a.   An(bio(cs: -‐  Target: Strep. Pnuemoniae, Staph Aureus, Resp. Anaerobes -‐  Drug and Dose: Benzylpenicillin 1.2g IV qid PLUS Metronidazole

500mg IV tds -‐  Dura(on: follow with oral course to complete 14 days a.   Cor(costeroids:

-‐  Evidence: limited -‐  Indica(on: severe Trismus, pain, dysphagia -‐  Drug and Dose: Dexamethasone 4mg IV bd for 3 doses

•  Treatment: iii)  Surgical

-‐  2 awake techniques: -‐  RCTs show similar succss rates

(≥ 92%) -‐  Repeat aspiraFon/drainage:

4-‐10% a.   3 point aspira(on

i.   LA: Lidocaine spray, Submucosal Lignocaine with Adrenaline 2% with 1:100,000

ii.   < 18g needle on 5ml leur-‐lock syringe

iii.   1st amempt: juncFon horizontal line through base of uvula and verFcal line through anterior pillar

iv.  2nd and 3rd amempts: along curvilinear arc

Throat – Peritonsillar CelluliFs/Abscess •  Treatment:

iii)  Surgical b.   Incision and Drainage

i.   LA: as before ii.   Guarded 11 blade iii.   Stab-‐incision iv.  Curvilinear extension v.  Break-‐down loculaFons with

curved haemostat c.   ‘Hot’ Tonsillectomy -‐  Generally avoid; increased risk

haemorrhage -‐  Indica(ons:

i.   Airway ii.   Non-‐resolu(on iii.   Severe Sepsis /

Immunosuppression

•  Treatment: iii)  Surgical

d.   ‘Cold’ Tonsillectomy -‐  Timing: 6-‐12/52 post last

tonsilliFs -‐  Indica(ons:

-‐  2nd abscess -‐  ParFcularly severe episode -‐  Other addiFonal indicaFons

for tonsillectomy

•  Outcomes: –  Resolu(on: 90% –  Complica(ons: i)  Local:

a.   Infec(ous: i.  Parapharyngeal Space abscess ii.  Retropharyngeal Space abscess

b.   Obstruc(ve

ii)  Systemic: a.  Sepsis

–  Recurrence: 33% post 1st quinsy, 85% post 2nd quinsy

Throat -‐ Post-‐tonsillectomy haemorrhage •  Classifica(on

i)  Primary •  At Fme of surgery i.e. sEll in OR

ii)  ReacFonary •  Following surgery, usually within 6 hours

iii)  Secondary •  During recovery period, usually

•  Children – 

Throat -‐ Post-‐tonsillectomy haemorrhage

•  Management: i)  Preven(on:

•  Cold steel vs diathermy (O’Leary & Vorrath 2005) •  Bleed rate 1.85% vs 2.35% (p<0.05) •  More reacFonary bleeds in cold steel group, more secondary bleeds in dissecFon group (Day 4-‐7) •  Bleeds > 500mL more common in diathermy group •  MeFculous Haemostasis

Throat -‐ Post-‐tonsillectomy haemorrhage •  Management:

ii)  Bedside Management a.   ABCs – aggressive resuscitaFon

-‐  Easy to underesFmate blood loss in children -‐  Assess degree of blood loss: Gd I (<15%), Gd II (15-‐30%), Gd III (30-‐40%),

Gd IV (> 40%) b.  Remove clot c.  Apply cophenylcaine® (Lignocaine 1%, phenylephrine ) soaked swab

+/-‐ pressure d.  Hydrogen peroxide 3% gargles (adults) e.  Tranexamic Acid Mouthwash f.  Silver Nitrate cautery +/-‐ pressure

•  Bleeding stops ð bed rest, IV anFbioFcs, NBM •  Bleeding conFnues ð OT

•  Management cont’d: iii)  OR Management

a.   GA: Rapid Sequence inducFon (supine vs let lateral) b.   Equipment:

i.  2x working suckers ii.   IV access x 2

c.   Resuscita(on i.   Request FBE, U&E, Coags, XM4 ii.   Replace with Crystalloid

» 20 ml/Kg Bolus Isotonic Crystalloid over 5-‐10 mins » Repeat boluses to a total of 60 mL / Kg, within 30-‐60 mins » 2/3 of Crystalloid equilibrates into intersFFum

iii. +/-‐ PRBCs +/-‐ Platelets/FFP via warming coil »  10 mL/Kg boluses of PRBCS

•  Management cont’d: iii)  OR Management

d.  Technique: i.  Cautery ii.  +/-‐ Suture ligaFon iii.  +/-‐ Suture Pillars together iv.  +/-‐ HaemostaFc Agent: e.g. Flo-‐Seal ® (topical

thrombin with gelaEn granules) » N.B. whilst Fibrin sealants like Tisseal®(concentrated fibrinogen + Factor XII) have significantly higher rates of haemostaEc control, they are more expensive

v.   +/-‐ ECA liga(on through Trans-‐cervical approach:

Throat -‐ CaroFd blowout

•  Defini(on: Rupture of the extra-‐cranial caroFd arteries or their major branches

•  Epidemiology: –  Incidence following neck dissecFon: 3% – Historically associated with 40% mortality, 60% severe neurologic morbidity

– Recent advances in management have reduced this to <8% mortality, 0% neurological deficit

Throat -‐ CaroFd blowout •  Classifica(on

1.  Threatened •  ExaminaFon/radiology suggesFve of inevitable haemorrhage – neoplasFc invasion, pseudoaneurysm

2.  Impending •  Episode of senFnel haemorrhage (transcervical or transoral) – resolves spontaneously or with pressure/packing

3.  Acute •  Haemorrhage which cannot be controlled with pressure or packing

4.  Recurrent: ipsi-‐ or contralateral side, 1 day – 6 yrs ater

Throat -‐ CaroFd blowout •  History:

–  ExisFng Malignancy –  PHx: Neck Surgery, Radiotherapy

•  Examina(on: –  ExtravasaFon of blood into Fssues (venous erosion usually causes thrombosis)

–  SenFnel bleeds – recurrent small haemorrhages from nose, mouth or ear

– Massive haemorrhage – Onset of shock –  Ipsilateral Horners syndrome – Unexplained IX to XII cranial neuropathies

Throat -‐ CaroFd blowout •  Management:

i)  Preven(ve: •  Minimise handling and diathermy of major vessels • Well-‐vascularised covering (flaps) •  Avoid pre-‐operaFve radiaFon where possible •  Avoid trifurcate incisions, esp. over caroEd

Throat -‐ CaroFd blowout

ii)  Acute Management: a.   ABCs b.   Direct Pressure c.   Foley Catheter trans wound placed endovascular

iii)  Cura(ve Management: a.   OR: ExploraFon of the neck and ligaFon of vessels

-‐  High morbidity and mortality -‐  Q. Why? A. Unstable paFent, wound may be infected +/-‐ residual tumour è friability of Fssues/vessels

b.   Angiography -‐  IdenFfies bleeding site or aneurysmal dilataFon -‐  Assess completeness of cerebral circulaFon i.  Endovascular occlusion ii.  Endovascular stents

Throat -‐ CaroFd blowout – curaFve management

iii)  Cura(ve Management Cont’d:

i.   Endovascular occlusion -‐  Suitable for bleeding from external caroFd system or IJV, or tumour

ii.   Endovascular stents

-‐  Suitable for internal or common caroFd systems -‐  Following balloon occlusion test

Throat -‐ CaroFd blowout – curaFve management

•  Complica(ons i)  Intra-‐opera(ve

a.  TIA, CVA b.  Failure ð ongoing haemorrhage

ii)  Postopera(ve a.  Early -‐  Delayed cerebral ischaemia -‐  Permanent Horner’s syndrome (8% with embolisaFon)

a.  Late -‐  Stent infecFon / occlusion -‐  Re-‐haemorrhage

Thank You

Management of Common ENT Emergencies

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