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Complications of

Rhinosinusitis

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specified. All images used without permission.

Viet Pham, M.D.

Faculty Advisor: Patricia Maeso, M.D. The University of Texas Medical Branch (UTMB Health)

Department of Otolaryngology

Grand Rounds Presentation

April 22, 2010

Synopsis of Critical Sequelae

Outline

Sta

ndring S

, ed. G

ray'

s A

nato

my,

40th

Ed

.

Spain

: C

hurc

hill

Liv

ingsto

ne,

2008.

Anatomy

Rhinosinusitis

Acute

Chronic

Complications

Orbital

Intracranial

Bony

Conclusion

Anatomy Maxillary Sinus

Largest and first sinus to develop

At 3 months gestation

Volume 6-8cm3 at birth

Volume 15cm3 by adulthood

Biphasic periods of rapid growth

First 3 years and between 7-18 years

Coincides with dental development

Natural ostium drains into ethmoidal infundibulum

Accessory ostia in 15-40%

Haller cell can impair drainage

Kennedy

DW

, B

olg

er

WE

, Z

inre

ich S

J, eds.

Dis

eases o

f th

e S

inuses –

Dia

gnosis

and

Managem

ent.

Ham

ilton: B

C D

ecker,

2001.

Notes: The anterior wall forms the facial surface of the maxilla,

the posterior wall borders the infratemporal fossa, the medial

wall constitutes the lateral wall of the nasal cavity, the floor of

the sinus is the alveolar process, and the superior wall serves

as the orbital floor.

Anatomy Maxillary Sinus

Bailey, et al. 2006. pp 10.

Innervation via V2 distribution

Infraorbital nerve

Dehiscent intraorbital canal

in 14%

Vasculature

Maxillary artery and vein

Facial artery

First and second

molar roots dehiscent

in 2%

NOTES: Haller cell is an ethmoidal cell that

pneumatizes between maxillary sinus and

orbital floor.

Anatomy Ethmoid Sinus

First seen at 5 months gestation

Five ethmoid turbinals

Agger nasi

Uncinate

Ethmoid bulla

Ground/basal lamella

Posterior wall of most posterior ethmoid cell

Between 3-4 cells at birth

Adult size by 12-15 years

Between 10-15 cells

Volume 2-3cm3 by adulthood

Hansen JT, ed. Netter’s Clinical

Anatomy, 2nd Ed. Philadelphia:

Saunders, 2010.

Kennedy,

et al. 2

001

Nasolacrimal

Duct

Infundibulum

Uncinate Process

Hiatus Semilunaris

Ethmoid Bulla

Basal Lamella

Retrobulbar Recess

NOTES: The lateral portions form the medial walls of the orbits, the sphenoid

establishes the posterior face, the superior surface is formed by the skull base of

the anterior cranial fossa, and many of the key structures of the lateral nasal wall,

derived from basal lamellas, extend posteroinferiorly from the skull base. The

lateral wall of the ethmoid sinus, or lamina papyracea, forms the paper-thin medial

wall of the orbit. The midline vertical plate of the ethmoid bone is composed of a

superior portion in the anterior cranial fossa called the crista galli and an inferior

portion in the nasal cavity called the perpendicular plate of the ethmoid bone that

contributes to the nasal septum. The anterior cranial fossa is separated from the

ethmoid air cells superiorly by the horizontal plate of the ethmoid bone, which is

composed of the thin medial cribriform plate and the thicker, more lateral ethmoid

roof. The ethmoid roof articulates with the cribriform plate at the lateral lamella of

the cribriform plate, which is the thinnest bone in the entire skull base.

The ethmoid sinuses are separated by a series of recesses demarcated by five

bony partitions or lamellae. These lamellae are named from the most anterior to

posterior: first (uncinate process), second (bulla ethmoidalis), third (ground or

basal lamella), fourth (superior turbinate), and fifth (supreme turbinate).

Anatomy

Ethmoid Sinus

Anatomy Ethmoid Sinus

Drainage

Anterior cells via ethmoid infundibulum

Posterior cells via sphenoethmoid recess


Branches from nasociliary nerve

Anterior and posterior ethmoids

Vasculature

Ophthalmic artery

Maxillary and ethmoid veins

Nasociliary Nerve

Anterior Ethmoidal Artery

Posterior Ethmoidal Artery

Ophthalmic

Nerve

Ophthalmic

artery

Posterior cells drain into superior meatus

Ophthalmic artery provides anterior and posterior

ethmoidal arteries

Cavernous sinus gives off maxillary and

ethmoidal veins

Anatomy Frontal Sinus

Not present at birth

Starts developing at 4 years

Radiographically visualized at 5-6 years

Development not complete until 12-

20 years

Volume 4-7cm3 by adulthood

No or poor pneumatization in 5-10%

Drainage via frontal recess

Anterior: posterior agger nasi

Lateral: lamina papyracea

Medial: middle turbinate

Tolle

fson T

T, S

trong E

B. F

ronta

l S

inus F

ractu

res.

eM

edic

ine 1

3 J

ul 2009.

Kennedy,

et al. 2

001

Frontal Sinus

Frontal

Recess

Basal

Lamella

Infundibulum

Posterior

Ethmoid Uncinate

Process

NOTES:The anterior table of the frontal sinus is twice as thick

as the posterior table, which separates the sinus from the

anterior cranial fossa. The floor of the sinus also functions as

the supraorbital roof, and the drainage ostium is located in the

posteromedial portion of the sinus floor

A markedly pneumatized agger nasi cell or ethmoidal bulla can

obstruct frontal sinus drainage by narrowing the frontal recess.

Drainage of the frontal sinus also depends on the attachment of

the superior portion of the uncinate process

Anatomy Frontal Cell Types

Type 1: single cell superior to agger nasi

Type 2: > 2 cells superior to agger nasi

Type 3: single cell from agger nasi into sinus

Type 4: isolated cell within sinus

Type 1 Type 2 Type 3 Type 4

Sold arrow – Frontal cell type

Dashed arrow – Agger nasi cell DelGaudio JM, et al. Multiplanar computed tomography analysis of

frontal recess cells. Arch Otolaryngol Head Neck Surg 2005; 131:230-5.

NOTES:Type 3 cell

attaches to anterior

table.

Anatomy Frontal Sinus

Vasculature

Supraorbital artery and vein

Supratrochlear artery

Ophthalmic vein

Foramina of Breschet


Supraorbital

Supratrochlear

Supratrochlear

Nerve

Supraorbital

Nerve

Supratrochlear

Artery

Supraorbital

Artery

NOTES:Foramina of Breschet: small

venules that drain the sinus mucosa

into the dural veins

Anatomy Sphenoid Sinus

Evagination of nasal mucosa into sphenoid bone

First seen at 4 months gestation

Pneumatization begins in middle childhood

Minimal volume at birth

Volume 0.5-8cm3 by adult

Reaches adult size by 12-18 years

Sellar type (86%)

Presellar (11%)

Conchal (3%)

NOTES: Approximately 25% of bony capsules separating the

internal carotid artery from the sphenoid sinus are partially

dehiscent. An optic nerve prominence is present in 40% of

individuals with dehiscence in 6%.

In most cases, the posteroinferior end of the superior

turbinate was located in the same horizontal plane as the

floor of the sphenoid sinus. The ostium was located medial to

the superior turbinate in 83% of cases and lateral to it in 17%.

Anatomy Sphenoid Sinus

Innervation via sphenopalatine nerve

V2 distribution

Parasympathetics

Vasculature via maxillary artery and vein

Sphenopalatine artery

Pterygoid plexus

Acute Rhinosinusitis (ARS)

Inflammation of the nasal mucosa and lining of the

paranasal sinuses

Obstruction of sinus ostia

Impaired ciliary transport

Viral etiology in majority of cases

Superimposed bacterial infection in 0.5-2%

Symptoms for at least 7-10 days or worsening

after 5-7 days

Symptoms present for < 4 weeks

“Recurrent ARS” with > 4 episodes, lasting > 7-10

days

NOTES: Most viral upper respiratory tract infections are

caused by rhinovirus, but coronavirus, influenza A and B,

parainfluenza, respiratory syncytial virus, adenovirus, and

enterovirus are also causative agents.

http://emedicine.medscape.com/article/227820-overview






Acute Rhinosinusitis (ARS)

Major symptoms

Facial pain/pressure

Facial congestion/fullness

Nasal obstruction

Nasal discharge/purulence

Minor symptoms

Headache

Fever (non-ARS)

Halitosis

Fatigue

Diagnosis with two major or one major and two minor

factors

Hyposmia/anosmia

Purulence on exam

Fever (ARS only)

Dental pain

Cough

Ear pain/pressure/fullness

Acute Rhinosinusitis (ARS) Microbiology

Children Adults

Streptococcus pneumoniae (30-43%)

Haemophilus influenzae (20-28%)

Moraxella catarrhalis (20-28%)

Other Streptococcus species

Anaerobes

Streptococcus pneumoniae (20-45%)

Haemophilus influenzae (22-35%)


Anaerobes

Moraxella catarrhalis

Staphylococcus aureus

Chronic Rhinosinusitis (CRS)

Symptoms present for > 12 consecutive weeks

“Subacute” for symptoms between 4-12 weeks

Chronic inflammation

Bacterial, fungal, and viral

Allergic and immunologic

Anatomic

Genetic predisposition

No clear consensus on pathophysiology

NOTES: One of the major problems with identifying the pathogenesis of CRS is that neither symptoms, findings, nor

radiographs, taken independently, are sufficient basis for the diagnosis. One study showed that current symptom-based

criteria had only a 47% correlation with a positive CT scan result.

Stankiewicz JA, Chow JM: A diagnostic dilemma for chronic rhinosinusitis: definition accuracy and validity. Am J

Rhinol 2002; 16:199-202.

Chronic Rhinosinusitis (CRS) Microbiology

Children Adults

Anaerobes



Streptococcus pneumoniae

Haemophilus influenzae

Pseudomonas aeruginosa

Anaerobes


Haemophilus influenzae




Complications of Sinusitis

Incidence has decreased with antibiotic use

Three main categories

Orbital (60-75%)

Intracranial (15-20%)

Bony (5-10%)

Radiography

Computed tomography (CT) best for orbit

Magnetic resonance imaging (MRI) best for intracranium

Siedek et al, 2010

Complications of Sinusitis Orbital

Most commonly involved complication site

Proximity to ethmoid sinuses

Periorbita/orbital septum is the only soft-tissue barrier

Valveless superior and inferior ophthalmic veins

Continuum of inflammatory/infectious changes

Direct extension through lamina papyracea

Impaired venous drainage from thrombophlebitis

Progression within 2 days

Children more susceptible

< 7 years – isolated orbital (subperiosteal abscess)

> 7 years – orbital and intracranial complications

NOTES:

-- close proximity of the orbit to the paranasal sinuses, particularly the ethmoids, make it the most commonly

involved structure in sinusitis complications; rarely from frontal or maxillary sinuses

-- pediatric population difference likely related to age-related sinus development

* pain and deterioration is not necessarily always present

* increase in WBC only found in 50%

Orbital Complications Microbiology

Children Adults

Streptococcus species


Anaerobes (Bacteroides and

Fusobacterium species)

Gram-negative bacilli

Staphylococcus epidermidis


Hemophilus influenzae



Anaerobes

Orbital Complications Chandler Criteria

Five classifications

Preseptal cellulitis

Orbital cellulitis

Subperiosteal abscess

Orbital abscess

Cavernous sinus thrombosis

Not exclusive, can occur concurrently

Bailey, et al. 2006.

Orbital Complications Preseptal Cellulitis

Symptomatology

Eyelid edema and erythema

Extraocular movement intact

Normal vision

May have eyelid abscess

CT reveals diffuse thickening of lid and

conjunctiva

Baile

y, e

t al. 2

006.

Orbital Complications Preseptal Cellulitis

Medical therapy typically sufficient

Intravenous antibiotics

Head of bed elevation

Warm compresses

Facilitate sinus drainage

Nasal decongestants

Mucolytics

Saline irrigations

Ram

adan e

t al, 2

009

Orbital Complications Orbital Cellulitis

Symptomatology

Post-septal infection

Eyelid edema and erythema

Proptosis and chemosis

Limited or no extraocular movement limitation

No visual impairment

No discrete abscess

Low-attenuation adjacent to lamina

papyracea on CT

Baile

y, e

t al. 2

006.

Ram

adan e

t al, 2

009

NOTES: Patients may complain

of pain and diplopia and a

history of recent orbital trauma

or dental surgery.:

Orbital Complications Orbital Cellulitis

Facilitate sinus drainage

Nasal decongestants

Mucolytics

Saline irrigations

Medical therapy typically sufficient


Head of bed elevation

Warm compresses

May need surgical drainage

Visual acuity 20/60 or worse

No improvement or progression

within 48 hours

Harr

ingto

n J

N. O

rbital cellu

litis

.

eM

edic

ine

, 25 O

ct 2010.

Orbital Complications Subperiosteal Abscess

Symptomatology

Pus formation between periorbita and lamina papyracea

Displace orbital contents downward and laterally

Proptosis, chemosis, ophthalmoplegia

Risk for residual visual sequelae

May rupture through septum and present in eyelids

Rim-enhancing hypodensity with mass effect

Adjacent to lamina papyracea

Superior location with frontal

sinusitis etiology

Diagnostically accurate 86-

91%

Ramadan et al, 2009

NOTES: Patients will complain of diplopia,

ophthalmoplegia, exophthalmos, or reduced

visual acuity. The patient has limited ocular

motility or pain on globe movement toward

the abscess.; may have normal movement

early on. Orbital signs include proptosis,

chemosis, and visual impairment.


Surgical drainage

Worsening visual acuity or extraocular

movement

Lack of improvement after 48 hours

May be treated medically in 50-67%

Meta-analysis cure rate 26-93% (Coenraad 2009)

Combined treatment 95-100%


Open ethmoids and remove lamina

papyracea

Approaches

External ethmoidectomy (Lynch incision)

is most preferred

Endoscopic ideal for medial abscesses

Transcaruncular approach

Transconjunctival incision

Extend medially around lacrimal caruncle

Baile

y, e

t al. 2

006.

Orbital Complications Orbital Abscess

Symptomatology

Pus formation within orbital tissues

Severe exophthalmos and chemosis

Ophthalmoplegia

Visual impairment

Risk for irreversible blindness

Can spontaneously drain through eyelid

Drain abscess and sinuses

Baile

y, e

t al. 2

006.

Kirsch C

FE

, T

urb

in R

, G

or

D. O

rbital

infe

ction im

agin

g.

eM

edic

ine,

24 M

ar

2010.

Lafferty KA. Orbital infections. eMedicine, 22 Sep 2009.

Orbital Complications Orbital Abscess

Incise periorbita and drain intraconal abscess

Similar approaches as with subperiosteal

abscess

Lynch incision

Endoscopic

NOTES:Transcaruncular approach allegedly does not utilize a

facial incision.

Orbital Complications Cavernous Sinus Thrombosis

Symptomatology

Orbital pain

Proptosis and chemosis

Ophthalmoplegia

Symptoms in contralateral eye

Associated with sepsis and meningismus

Radiology

Poor venous enhancement on CT

Better visualized on MRI

Contralateral involvement is distinguishing

feature of cavernous sinus thrombosis

MRI findings of heterogeneity and increased size

suggest the diagnosis

Orbital Complications Cavernous Sinus Thrombosis

Mortality rate up to 30%

Surgical drainage


High-dose

Cross blood-brain barrier

Anticoagulant use is

controversial

Prevent thrombus propagation

Risk intracranial or intraorbital

bleeding

Agayev A, Yilmaz S. Cavernous sinus thrombosis.

N Engl J Med 2008; 359:2266.

MRI better especially if suspecting intracranial involvement, too.

Cavernous Sinus Thrombosis Anticoagulation

Beneficial

Southwick et al (1986)

Reduction in mortality

Not recommended for other dural sinus thrombosis

Levine et al (1988)

No change in mortality

Mortality reduction with added early

Bhatia et al (2002)

PTT ratio 1.5-2.5

INR 2-3

Anticoagulate for 3 months

Harmful

Bhatia et al (2002)

Fatal hemorrhagic cerebral

infarction

Subarachnoid hemorrhage

reversed with protamine

NOTES: 1980s were retrospective reviews

Bhatia was a literature review

Complications of Sinusitis Intracranial

Occurs more commonly in CRS

Mucosal scarring, polypoid changes

Hidden infectious foci with poor antibiotic penetration

Male teenagers affected more than children

Direct extension

Sinus wall erosion

Traumatic fracture lines

Neurovascular foramina (optic and olfactory nerves)

Hematogenous spread

Diploic skull veins

Ethmoid bone NOTES: Teenagers affected more because of developed frontal and sphenoid sinuses, and because they

are more prone to URI’s than adults.

Thrombophlebitis originating in the mucosal veins progressively involves the emissary veins of the

skull, the dural venous sinuses, the subdural veins, and, finally, the cerebral veins. By this mode, the

subdural space may be selectively infected without contamination of the intermediary structure; a

subdural empyema can exist without evidence of extradural infection or osteomyelitis.

Intracranial Complications Types

Seizure (31%)

Hemiparesis (23%)

Visual disturbance (23%)

Meningismus (23%)

Five types (not exclusive)

Meningitis

Epidural abscess

Subdural abscess

Intracerebral abscess

Cavernous sinus, venous sinus thrombosis

Common signs and symptoms

Fever (92%)

Headache (85%)

Nausea, vomiting (62%)

Altered consciousness (31%)

NOTES: Not exclusive, can occur concurrently. Percentages in children (Hicks et al, 2011)

Intracranial Complications Meningitis

Most common intracranial complication of sinusitis

Symptomatology

Headache

Meningismus

Fever, septic

Cranial nerve palsies

Sinusitis is unusual cause of meningitis

Sphenoiditis

Ethmoiditis

Usually amenable with medical treatment

Drain sinuses if no improvement after 48 hours

Hearing loss and seizure sequelae

NOTES: Also incidence of neurologic sequelae such as hearing loss and seizure disorder.

Meningitis Microbiology

Children Adults




Anaerobes (Bacteroides and

Fusobacterium species)

Gram-negative rods

Streptococcus pnuemoniae

Hemophilus influenzae

Intracranial Complications Epidural Abscess

Ram

achandra

n T

S, et al, 2

009.

Papilledema

Hemiparesis

Seizure (4-63%)

Second-most common intracranial complication

Generally a complication of frontal sinusitis

Symptomatology

Fever (>50%)

Headache (50-73%)

Nausea, vomiting

Crescent-shaped hypodensity on CT

Intracranial Complications Epidural Abscess

Lumbar puncture contraindicated

Prophylactic seizure therapy not necessary

Antibiotics Good intracerebral penetration

Typically for 4-8 weeks

Drain sinuses and abscess

Frontal sinus trephination

Frontal sinus cranialization

Stereotactic-guided drainage

NOTES: Will likely need antibiotics for 4-8

weeks; usually vancomycin and 3rd or 4th

generation cephalosporin

Prophylactic seizure therapy not necessary

unless there’s an associated subdural

abscess.

Intracranial Complications Subdural Abscess

Generally from frontal or ethmoid sinusitis

Symptomatology

Headaches

Fever

Nausea, vomiting

Hemiparesis

Lethargy, coma

Third-most common intracranial

complication, rapid deterioration

Mortality in 25-35%

Residual neurologic sequelae in 35-55%

Accompanies 10% of epidural abscesses

Intracranial Complications Subdural Abscess

Lumbar puncture potentially fatal

Aggressive medical therapy

Antibiotics

Anticonvulsants

Hyperventilation, mannitol

Steroids


Medical therapy possible if < 1.5cm

Craniotomy or stereotactic burr hole

Endoscopic or external sinus drainage

NOTES:Need antibiotics with good intracerebral penetration, typically

3-6 weeks

Craniotomy is favored over burr hole placement due to better exposure

Intracranial Complications Intracerebral Abscess

Uncommon, frontal and frontoparietal lobes

Generally from frontal sinusitis Sphenoid

Ethmoids

Symptomatology Headache (70%)

Mental status change (65%)

Focal neurological deficit (65%)

Fever (50%)

Mortality 20-30%

Neurologic sequelae 60%

Nausea, vomiting (40%)

Seizure (25-35%)

Meningismus (25%)

Papilledema (25%)

NOTES: May have mood swings

and behavioral changes with

frontal lobe involvement

Worsening headache with

meningismus suggests possible

rupture of the abscess.

Intracranial Complications Intracerebral Abscess

Lumbar puncture potentially fatal


Antibiotics

Anticonvulsants

Hyperventilation, mannitol

Steroids


Medical therapy possible if abscess < 2.5cm

Excision or aspiration

Diagnostic aspiration if < 2.5cm or cerebritis

Stereotactic-guided aspiration

Endoscopic or external sinus drainage

NOTES: Antibiotic regimen is typically 6-8 weeks; typically ceftriaxone, vancomycin or nafcillin, and metronidazole

Corticosteroid use is controversial. Steroids can retard the encapsulation process, increase necrosis, reduce antibiotic penetration into the

abscess, increase the risk of ventricular rupture, and alter the appearance on CT scans. Steroid therapy can also produce a rebound effect

when discontinued. If used to reduce cerebral edema, therapy should be of short duration. The appropriate dosage, the proper timing, and

any effect of steroid therapy on the course of the disease are unknown. The procedures used are aspiration through a bur hole and complete

excision after craniotomy. Aspiration is the most common procedure and is often performed using a stereotactic procedure with the guidance

of CT scanning or MRI.

Intracranial Abscesses Microbiology

Children Adults

Anaerobes (anaerobic Streptococcus, Bacteroides, Fusobacterium species)


Other Streptococcus species (Streptococcus milleri)

Gram-negative bacilli (Hemophilus influenzae)

Staphylococcus epidermidis

Eikenella corrodens

Polymicrobial

NOTES: Incidence of anaerobes in suppurative

intracranial complications range from 60-100%

Intracranial Complications Venous Sinus Thrombosis

Sagittal sinus most common

Retrograde thrombophlebitis from

frontal sinusitis

Extremely ill

Subdural abscess

Epidural abscess

Intracerebral abscess

Decreased cavernous carotid

artery flow void on MRI

Elevated mortality rate

Intracranial Complications Venous Sinus Thrombosis


Antibiotics

Steroids

Anticonvulsants

Anticoagulation controversial

Heparin inpatient, warfarin outpatient

Thrombus resolution by 6 weeks (Gallagher 1998)

Increased intracranial pressure

outweighs bleeding risk (Gallagher 1998)

Drain sinuses

External

Endoscopic

Complications of Sinusitis Bony

Pott’s puffy tumor

Frontal sinusitis with acute osteomyelitis

Subperiosteal pus collection leads to “puffy” fluctuance

Rare complication

Only 20-25 cases reported in post-antibiotic era (Raja 2007)

Less than 50 pediatric cases in past 10 years (Blumfield 2010)

Symptomatology

Headache

Fever

Neurologic findings

Periorbital or frontal swelling

Nasal congestion, rhinorrhea

Sab

ati

ello

M, et

al.

Th

e P

ott

s p

uff

y t

um

or:

an

un

usu

al co

mp

licati

on

of

fro

nta

l sin

usit

is, m

eth

od

s f

or

its d

ete

cti

on

. P

ed

iatr

Derm

ato

l 2010;

27:4

06

-8.

NOTES: Sir Percivall Pott described Pott's Puffy tumor in

1768 as a local subperiosteal abscess due to frontal bone

suppuration resulting from trauma. Pott reported another

case due to frontal sinusitis.


Associated with other abscesses in 60%

Pericranial

Periorbital

Epidural

Subdural

Intracranial

Cortical vein thrombosis

Frontocutaneous fistula

Upadhya

y S

. R

ecurr

ent P

ott's

puff

y t

um

or,

a r

are

clin

ical entity

. N

euro

l In

dia

2010; 58:8

15

-7.

Baile

y, e

t al. 2

006.

Blu

mfield

, et al. 2

010.

NOTES: Sir Percivall Pott described Pott's Puffy

tumor in 1768 as a local subperiosteal abscess due

to frontal bone suppuration resulting from trauma.

Pott reported another case due to frontal sinusitis.

Pott’s Puffy Tumor Microbiology

Children Adults

Streptococcus species (Streptococcus milleri)


Anaerobes (Bacteroides species)

Gram-negative bacilli (Proteus species)

Polymicrobial


Cooperative effort

Otolaryngology

Neurosurgery

Infectious disease

Surgical and medical therapy

Drain abscess and remove infected bone

Intravenous antibiotics for six weeks

May obliterate frontal sinus to prevent

recurrence

Dia

z P

M, et al. T

um

or

hin

chado d

e P

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Conclusions

Complications are less common

with antibiotics

Orbital

Intracranial

Bony

Can result in drastic sequelae

Drain abscess and open involved

sinuses

Surgical involvement

Ophthalmology

Neurosurgery

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