orbital complications of rhino sinusitis,intra cranial complications of rhino sinusitis,classification of complications,diagnosis and treatment of complications
2. DEFINITION
A complication of rhinosinusitis may be defined as any
adverse progression of chronic or acute bacterial
infection beyond the paranasal sinuses, or compromise
in function of any part of the body due to local or distant
effects of the condition
3. DIVISIONS:
These are divided into
1. Acute
2. Chronic
1.Acute:
Acute complications of rhinosinusitis can be divided
into those that are due to local progression of the
disease, and systemic, presumed haematogenous
spread.
These are :
A. Local
B. Distant
4. LOCAL COMPLICATIONS
Local progression is via areas where the surrounding
bone is thin, such as the lamina papyracea, or where
there is a direct anatomical connection by way of a
nerve or bloodvessel, such as the infraorbital canal, or
the diploeic veins of the frontal and sphenoid bones.
The absence of valves in the veins between the orbit
and the sinuses facilitates retrograde venous spread
of infection.
The second premolar and first molar dental root
canals also provide a direct route of spread.
5. 1.Frontal sinus
A subperiosteal abscess may result from an acute
episode of frontal rhinosinusitis if the local
progression of the disease is through the outer
table of the skull.
This condition is still frequently referred to as Pott’s
puffy tumour, following its description by Sir
Percival Pott in 1760.
If the progress is inward, there may be an acute
intracranial complication, such as intracranial
abscess or meningitis.
6. 2.Ethmoid
The most important and
frequent acute complication
of ethmoid rhinosinusitis is
orbital cellulitis,
These stages are:
1. Preseptal cellulitis.
Inflammation does not
extend beyond the orbital
septum (the site at which
the medial orbital periosteal
reflection attaches to the
medial eyelid at the tarsal
plate).
2. Postseptal cellulitis or
orbital cellulitis without
abscess.
Inflammation extends into
the tissues of the orbit.
7. 3. Subperiosteal abscess.
There is abscess formation
deep to the periosteum of
the orbital bones, usually
the lamina papyracea.
4. Orbital abscess.
There is abscess formation
within the orbit which has
breached the periosteum.
5. Cavernous sinus
thrombosis/abscess.
The inflammatory process
has extended through the
optic foramen into the
cavernous sinus which
thromboses and possibly
progresses to abscess
formation.
8. 3.Maxillary sinus:
Isolated maxillary rhinosinusitis rarely gives rise to
acute local complications.
Patients with acute swelling of the cheek are almost
invariably suffering from a complication of primary
dental disease rather than sinus infection, although
there might be an associated maxillary
rhinosinusitis secondary to the dental disease.
9. 4.Sphenoid sinus
Acute local complications of sphenoid rhinosinusitis are
rare, but can result in cavernous sinus thrombosis by
direct spread.
Additionally, intracranial complications can occur as a
result of a base of skull fracture through the sphenoid
sinus
11. 2.CHRONIC COMPLICATIONS:
Mucocoeles are chronic, slowly expanding lesions in
any of the sinuses that may result in bony erosion and
subsequent extension beyond the sinus.
If the mucocoele becomes secondarily infected and the
contents purulent, it is described as a pyocoele
In the maxillary sinus due to the proximity of the dental
roots, the teeth may be affected by maxillary
rhinosinusitis.
12. ORBITAL COMPLICATIONS OF SINUSITIS
Orbital complications of sinusitis are most often
attributable to the ethmoid sinuses, though 84 % of
cases have radiographic evidence of disease
involving two or more sinuses
some series establish a minimum pattern of
concomitant maxillary, ethmoid, and frontal sinusitis
in 79 % of cases
Orbital infections arising from a sinonasal source
can arise by two mechanisms:
1. Direct extension
2. Retrograde thrombophlebitis
13. RELEVANT ORBITAL AND SINUS ANATOMY
The orbit is separated from the ethmoid sinuses
medially by a thin and often dehiscent lamina
papyracea, from the maxillary sinus by a similarly
thin orbital floor, and from the frontal sinus by a
portion of the orbital roof.
The bony orbit is vulnerable to spread of infection,
directly or by thrombophlebitic spread, via the
numerous fissures and foramina that transmit
vessels and nerves through the sinuses, orbit, and
intracranial space
14. The periosteal lining of the orbital bones, the
periorbita, is an additional layer of separation
between the orbital contents and the sinuses.
This fibrous tissue is firmly adherent to underlying
bone at the orbital rims, suture lines, orbital fissures
and lacrimal crest but loosely adherent elsewhere,
allowing infection to dissect into these potential
subperiosteal spaces
15. The orbital septum, a key feature of the classification of
orbital infections, arises from the union of the periorbita
with the periosteum of the forehead and cheekbones at
the orbital rim (the arcus marginalis) .
The orbital septa of the upper and lower eyelids form an
anatomic barrier to infection and define the preseptal
and postseptal spaces
The valveless veins of the orbit play a key role in
propagation of orbital infections, as they allow free
communication between the facial, sinus, orbital, and
intracranial venous network .
16. The superior ophthalmic vein is a well-defined vessel
formed by the union of the angular and supraorbital
veins, which receives multiple tributaries as it travels
posterolaterally through the orbit to exit via the superior
orbital fissure to enter the cavernous sinus .
The inferior ophthalmic vein originating near the
anterior orbital floor and terminating by sending one
branch to the pterygoid plexus via the inferior orbital
fissure and a second, larger contribution to the superior
ophthalmic vein; both will ultimately drain into the
cavernous sinus
17. Venous drainage from the frontal sinus begins in
diploic veins which pass through the multiple
anterior and posterior table foramina (Breschet’s
canals), coalescing in sequentially larger diploic
veins, developing into the frontal diploic vein that
joins at the supraorbital notch with the supraorbital
vein to create the superior ophthalmic vein.
The diploic veins of Breschet contribute significantly
to frontal bone osteomyelitis and intracranial
complications of sinusitis via their communications
with dural sinuses and the marrow cavity of the
frontal bone
20. BACTERIOLOGY
The most commonly cultured organisms in orbital infections
are :
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Streptococcus pyogenes
Anaerobic bacteria (Prevotella, Porphyromonas.
Fusobacterium and Peptostreptococcus spp.)
Previous analysis of patients found H. influenzae and S.
pneumoniae to be the most commonly isolated organisms.
However, in the post-vaccination era,,the incidence of H.
influenza , S. pneumonia and Streptococcus viridans is
decreased
An increase in S. aureus was noted recently
21. DIAGNOSTIC EVALUATION
Patients with preseptal cellulitis typically present with:
1. History of recent upper respiratory infection or symptoms of acute
bacterial rhinosinusitis
2. Edematous eyelids
3. Conjunctival injection
4. Varying degrees of discomfort
Preseptal infections do not routinely require imaging studies
Signs of postseptal involvement include:
1. Proptosis
2. Gaze restriction
3. Decreased visual acuity
4. Color vision changes
5. Afferent pupillary defect
22. Ophthalmologic examination is critical in measuring
proptosis, evaluating extraocular motility and, if
necessary, determining intraocular pressure.
To clarify the utility of diagnostic imaging in this setting,
Eustis and colleagues suggested the following
parameters:
(1) visual acuity changes;
(2) proptosis;
(3) limitation of motility;
(4) uncertainty of diagnosis; and
(5) deterioration of overall condition despite treatment
23. Contrast-enhanced CT
scans of the sinuses in
axial and coronal planes
are essential to
distinguishes between
cellulitis and abscesses
and identifies which
sinuses will need surgical
drainage
Magnetic resonance
imaging offers superior
soft-tissue resolution and
is most appropriate in the
context of intracranial
complications,
24. MEDICAL THERAPY FOR ORBITAL
COMPLICATIONS
Preseptal cellulitis, is treated empirically with broad-
spectrum intravenous antibiotics , having meaningful
CSF penetration, and possesses activity against beta-
lactamase producing strains.
Adjunctive topical and parenteral decongestants are
often added, though steroids are not thought to be
helpful.
Progression of symptoms or failure to respond to
antibiotics within 48 h of treatment necessitates a CT
scan and may constitute an indication for surgical
Therapy
25. Oxford identified five criteria for medical management .
These include:
(1) normal vision, pupil and retina;
(2) no ophthalmoplegia in one or more directions of gaze;
(3) intraocular pressure less than 20 mmHg;
(4) proptosis of 5 mm or less; and
(5)abscess width of 4 mm or less on CT.
26. SURGICAL THERAPY FOR ORBITAL
INFECTIONS
surgical intervention in postseptal disease is required in 12–66 % of
orbital complications of acute sinusitis .
Surgery is recommended for one of the following four indications:
1. CT evidence of abscess formation
2. Decreased visual acuity on presentation (20/60 or worse)
3. Severe orbital complications on initial presentation with ipsilateral
sinusitis (blindness, afferent papillary reflex, ophthalmoplegia)
4. Progression of symptoms or failure to improve during the first 48 h
of appropriate medical treatment
Immunocompromised patients (diabetes, chemotherapy, HIV)
should be approached with a lower threshold for surgical
intervention
27. SURGICAL TECHNIQUES
Chandler groups II (orbital cellulitis) and III
(subperiosteal abscess) are treated endoscopically.
The procedure is performed under general anesthesia.
The eye should be left visible to the operating surgeon
with adequate corneal protection.
The nose should be decongested with 1 %
oxymetazoline hydrochloride on cotton pledgets, placed
carefully in the nasal cavity.
The mucosa of the lateral nasal wall is then injected with
local anesthesia. The authors typically use 1 % lidocaine
with 1:100,000 epinephrine.
28. If any purulence is visualized in the middle meatus, it should be collected using
sterile technique and sent for culture and sensitivity.
Utilizing 0 and 30-degree telescopes, a maxillary antrostomy is performed.
Once the maxillary antrostomy is complete, the bulla ethmoidalis is entered and
removed with through-cutting instruments and a microdebrider.
Posterior ethmoidectomy may be needed depending on the extent of disease.
The lamina papyracea is skeletonized with through-cutting instruments.
At this point, the surgeon may see pus emanating from the orbit.
This should also be collected and sent for culture and sensitivity.
If no drainage is seen, the lamina papyracea is then fractured with a Cottle
elevator.
Bone from the lamina papyracea is then elevated and removed to achieve
adequate drainage of the abscess.
Subsequent antibiotic therapy is guided by intraoperative cultures.
29. Chandler group IV may also be managed
endoscopically.
Complete ethmoidectomy, medial orbital wall
decompression and incision of the periorbita usually
affords adequate drainage of most extraconal
abscesses .
Drainage of intraconal abscesses is best achieved
through a combined open and endoscopic approach
30. Chandler group V, is increasingly considered an
intracranial complication of sinusitis, and as such, its
management should include neurosurgical consultation.
Intravenous antibiotic are the primary therapeutic
measure, though endoscopic surgery directed toward
the involved sinuses
Use of adjunctive steroids and heparin and systemic
anticoagulation remains controversial,
31. CNS COMPLICATIONS
The frontal sinus is the most common source of intracranial complications of
sinusitis, followed by the ethmoid, sphenoid, and maxillary sinuses .
Suppurative complications may develop either via a direct or indirect pathway.
Direct spread can occur though infection of the frontal bone (osteitis,
osteomyelitis) or along preformed routes (encephaloceles, fractures, CSF fistula,
tumors) .
An indirect pathway, which is more commonly seen, involves hematogenous
spread through a communicating venous system.
CNS Complications of Sinusitis :
Meningitis
Epidural abscess
Subdural empyema
Brain abscess
Cavernous sinus thrombosis
Superior sagittal sinus thrombosis
Frontal bone osteomyelitis
32. SIGNS AND SYMPTOMS
The typical presentation of CNS complications of frontal
sinusitis is characterized by:
1. Acute or progressive headache
2. Fever
The process may be silent until serious neurological
symptoms and signs develop such as:
1. Focal neurological deficits
2. Change in mental status
3. Lethargy
4. Seizure
5. Coma
33. In a small number of cases, there may be osteomyelitis
of the anterior frontal sinus table, causing overlying
edema of the forehead (Pott’s Puffy Tumor)
Up to 40 % of these patients present with intracranial
complications .
Pott’s Puffy Tumor is often an indicator of intracranial
complication because the infection may spread to the
intracranial cavity through bony erosions, preformed
pathways, or septic thrombosis
34. CLINICAL FEATURES AND DIAGNOSTIC
EVALUATION
Patients with sinusitis and the following signs should
be presumed to have meningitis until proven
otherwise:
1. Persistent high fever
2. Severe headache
3. Meningismus-triad of neck rigidity,head
ache,photophobia
4. Photophobia
5. Irritability
6. Altered mental status
35. Epidural abscesses most commonly occur directly
behind an intact posterior table of the frontal sinus.
The dura is loosely attached in this region, allowing
pus to collect and expand.
Symptoms may be very mild until the collection
becomes large enough to increase intracranial
pressure.
Because of the proximity to the orbit, orbital
swelling is common, together with forehead edema
and tenderness.
36. Subdural empyema usually presents with:
1. Increasing headache
2. Fever
3. Elevated white blood cell count
4. Meningeal signs
As the process progresses, cortical signs and symptoms develop such as:
1) Hemiparesis
2) Hemiplegia
3) Cranial neuropathies
4) Seizure
Ultimately, the increase in intracranial pressure causes:
1. Nausea
2. Vomiting
3. Slowed heart rate
4. Hypertension
5. Decreased level of consciousness
37. In cavernous sinus thrombosis, the key findings are:
1. Proptosis
2. Chemosis
3. Ophthalmoplegia
4. Cranial nerves II and III palsies
5. Visual loss develops as the disease process worsens
38. Brain abscesses due to frontal sinusitis most commonly
derive from septic emboli that travel to the frontal lobe via
retrograde venous communications.
Typically, there will be liquefaction necrosis of the brain
surrounding the infected vein, with surrounding edema
The initial symptoms of brain abscess may be very mild or
nonexistent.
Only with significant edema can focal neurologic signs or
signs of increased intracranial pressure be seen.
Unfortunately, brain abscesses may not be apparent until
they rupture into the ventricular system causing rapid
death.
39. High resolution computed tomography (CT) with and without
contrast as the primary diagnostic test .
Magnetic resonance imaging (MRI) is an useful adjunctive
study when suspicion for intracranial exam is high based on
history of CT findings .
Input from otolaryngology, neurosurgery, ophthalmology, and
infectious diseases services are important in creating a
multidisciplinary approach to the care of the patient .
The need for lumbar puncture to rule out meningitis must be
weighed against the risk of precipitating brain herniation,
If elevated intracranial pressure has been excluded, lumbar
puncture should be performed, with cytological,
microbiological, and laboratory analysis of the cerebrospinal
fluid