CAVERNOUS SINUS

Surgical anatomy and Cavernous Sinus Thrombosis

Dr. Mukhallat Qazi

1st Year Postgraduate
Department of OMFS
 OVERVIEW
• Introduction • Cavernous Sinus
• Development Thrombosis
o Clinical Presentation
• Anatomy o Danger Area of the Face
o Structures within o Investigations

o Structures around o Neuroradiology

o Tributaries o Complications

o Treatment

2
 INTRODUCTION
• “The space or compartment commonly called ‘the
cavernous sinus’ is a veritable anatomical jewel box
containing more significant structures than any other
comparable space outside the brain itself.” (Parkinson
1990)

• Cavernous+ Sinus
Cavernous- Cavern: “A large cave or chamber in a cave”
“specific type of cave, naturally formed in soluble rock with the ability
to grow speleothems”
3
Sinus- Medieval Latin: “A hollow curve or cavity in the body”
• Called “Circular sinus" by Ridley (1695)
• Wilson(1732)
Named this structure “ CAVERNOUS SINUS”  Due to it’s spongious structure
which seemed to be formed by numerous fibres and connective tissue septae

4
Dural Sinuses
• Lie between the endosteal and meningeal layers of dura
mater
• Are lined by endothelium, firm collagenous tissue
• Have no valves
• Walls are devoid of muscular tissue
• Numerous lacunes and trabeculae

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 DEVELOPMENT

• Padget (1956)
Cavernous sinus Plexiform extension of prootic sinus and
ventral myelencephalic vein
Superior ophthalmic v Primitive maxillary v as it drains into
the prootic sinus, and develops into the superior ophthalmic
vein which drains directly into the cavernous sinus.

7
 • Plexiform extension of prootic sinus
• Ventral portion of myelencephalic vein
40 mm

• Cavernous sinus which receives only ophthalmic veins

• Drains into the Inf. Petrosal sinus, ultimately the IJV
60 mm

• Cavernous sinus and Inf petrosal Sinus do not receive Cerebral Venous drainage

3rd month

• Cavernous Sinus receives SMCV, Sphenoparietal Sinus

• Drains into the IPS, SPS, Pterygoid Plexus
Adult
8
• Knosp (1987)
20% of fetal skull bases- SMCV drains into the Cavernous
Sinus
60% of fetal skull bases- SPS and Cavernous Sinus show a
connection
Hence developmental basis for varied pattern of venous
tributaries and drainage

9
 Schematic drawings of the developmental anatomy of cavernous and
para-cavernous venous structures in the embryonic stage.

S. Tanoue et al. AJNR Am J Neuroradiol 2006;27:1083-1089

©2006 by American Society of Neuroradiology

ANATOMY
• Number
2, Paired
• Dimensions
Length 20mm
Width 09mm
• Location
Middle Cranial Fossa
Either side of body of sphenoid
• Extent
From Superior Orbital Fissure to the
Petrous apex of Temporal bone
• Shape
Triangular in cross section, Boat
shaped 11
12
STRUCTURES WITHIN.. CONTENTS

13
14
Anatomical Relations

15
16
Osseous Relations
MEDIAL LATERAL POSTERIOR
ANTERIOR

Carotico- Greater Posterior

Optic strut clinoid wing of Cliniod
foramen sphenoid Process

Anterior Middle Dorsum

clinoid clinoid Foramina
(rotundum, Sella
process process
ovale,
Lesser wing Pituitary spinosum)
Petrous
of fossa Apex
sphenoid

Body of Trigeminal
sphenoid Impression
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Carotid
sulcus
18
 Ant Clin Process

Carotid sulcus- Course of ICA

Optic Strut- Lateral and inferior wall

of the optic canal
These three structures almost
encircle the ICA

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CLINICAL SIGNIFICANCE OF
OSSEOUS RELATIONS

• In surgically exploring cavernous sinus, an initial step is to

“unlock” the contents of the sinus from the bony confines.
• This step includes unroofing and mobilizing the optic nerve,
and then removing anterior clinoid process.
• This phase can be performed in an extradural or intradural
fashion.
DURAL RELATIONS
Superior Inferior
• Dura Mater • Periosteum
• Tentorium floor
Cerebelli

Medial Lateral
• Endosteum of • Dura Propria
Sella turcica’s of uncus of
Lateral wall temporal lobe
 ROOF
Anterior extension of the
Tentorium Cerebelli
Lateral extension of
Diaphragma Sella

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Posterior Wall
• Lower margin
shared with
basilar sinus,
pierced by
Abducens n
• Upper edge-
posterior
petroclinoidal
fold

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Medial Wall
• Dura covering
the lateral
aspect of the
Sella turcica
and the lateral
surface of body
of Sphenoid
bone
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Lateral
wall
Dura propria
of Uncus of
the
temporal
lobe

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26
Upper and lower dural rings

Upper • Upper margin

of anterior
dural clinoid
ring process

Lower • Lower margin

of anterior
dural clinoid
ring process

The segment of the internal carotid artery located between the upper and lower dural 27
rings, which is exposed by removing the anterior clinoid process, is referred to as the
clinoid segment.
NEURAL RELATIONS
• Cranial nerves III to VI are closely related to cavernous sinus.
 Oculomotor Nerve

CN III Courses Exits through

lateral to PCP SOF

Enters Cavernous
Passes along
sinus on
inferolateral
superolateral
surface of ACP
surface

Here its
Passes lateral to
epineurium
the cavernous
interweaves with
sinus
that of CN IV
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 After exiting through SOF,
between the heads of the lateral
rectus muscle

Inferior
Superior Division
division

Levator
Superior Medial and Inferior
Palpebrae
Rectus inferior recti Oblique 30
Superioris
Trochlear Nerve
Trochlear nerve enters the roof of the
sinus posterolateral to the oculomotor
nerve
Courses below the oculomotor nerve
in the posterior part of the lateral wall.

Anteriorly, below the base of the

anterior clinoid process, it passes
upward along the lateral surface of the
oculomotor nerve.

Passes medially between the

oculomotor nerve and anterior clinoid
and optic strut

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Reaches the medial part of the orbit
and the superior oblique muscle.
Ophthalmic Nerve

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33
Abducens Nerve
The abducens nerve pierces the dura
Forms lower part of the posterior wall of the sinus

At the upper border of the petrous apex, enters Dorello’s

canal

Passes below the petrosphenoid ligament (Gruber’s

ligament)

Bends laterally around the intercavernous carotid

Exit through the SOF and 34

Passes forward, medial to the ophthalmic nerve, on the supplies the Superior
lateral side of the internal carotid artery. Oblique m
Clinical Significance
• Cranial nerve palsy is the most common manifestation of pathologic
processes involving the cavernous sinus.

• Diplopia, Sixth nerve palsy with Horner’s Syndrome, impaired visual

acuity may suggest cavernous sinus lesions.

• Most cavernous sinus explorations are for benign disease with the
goal of preserving and improving cranial nerve function.

• Exploration of cavernous sinus usually follows mobilization of lateral

wall and entry through one or more of the various triangles formed
by these cranial nerves and dural folds. 35
Anatomic Triangles
Vascular Relations
• Arterial Relations • Venous Relations
• Internal Carotid Artery • Afferent Tributaries
and its anatomically
divided course- • Efferent Drainage
• Petrous
• Cavernous
• Intracranial

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Internal carotid artery

38
 Initially runs
vertically, becomes Crosses For. Ascends towards
horizontal in the
• Petrous part Lacerum under Cavernous Sinus
petrous temporal Trigeminal (C3)
bone (C2) ganglion LATERAL LOOP
POSTERIOR LOOP

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 Reaches
towards
Enters lateral
Becomes After aspect of Anterior
cavernous Horizontal horizontal
sinus Ascends ACP loop is
towards (C4) course oriented at
through the through Exits from
posterior Posterior MEDIAL 30 degrees
Clinoid sinus, it sinus (C5) to the
aspect LOOP
Process reverses its ANTERIOR horizontal
course LOOP plane

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41
 Inferior
hypopheseal

Meningohypophyseal
Tentorial
trunk from C5

Clival (Dorsal
Intracranial ICA Meningeal
In the cavernous Inferolateral
segment Trunk (Inf Cav Sin Artery to CN 3,4,6
Br.) from C4

Mc Connell’s Capsular Sella turcica, roof

Artery from C4 and floor

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Veinous relations
Tributaries (afferent veins):
 Superior ophthalmic vein
(SOV)
 Inferior ophthalmic vein
(IOV)
Central retinal vein
 Superficial middle cerebral
vein (SMCV)
 Uncal vein (UV)
 Sphenoparietal sinus (SPPS)
 Meningeal veins 43
Drainage (efferent
veins):
• Foramen ovale plexus (FOP)
• Vein of the foramen
rotundum
• Pterygoid plexus (PP)
• Internal jugular vein (IJV)
• Facial vein (FV)
• Angular vein (AV)
• Retromandibular vein
• Supraorbital vein
• Frontal vein (FrV) 44
• Basilar plexus (BP)
• Sphenoparietal sinus
(SPPS)
• Sigmoid sinus (SS)
• Superior petrosal sinus
(SPS)
• Inferior petrosal sinus
(IPS)
• Intercavernous sinus (ICS)
• Jugular bulb (JB)
• Middle temporal vein 45

(MTV)
46
 COMMUNICATIONS OF CAVERNOUS
SINUS

• Venous blood from the brain flows via the superficial( cortical) and the deep
cerebral veins into the venous (dural) sinuses.

• There are numerous connections between the cortical veins and dural sinuses.

• This facilitates the spread of thrombus infection between these vessels.

• Also allows opening of collateral draining vessels in the event of an occlusion.

Summary of communication
• The cavernous sinuses receive blood from
• cerebral veins
• the ophthalmic veins (from the orbit)
• emissary veins (from the pterygoid plexus of veins in the infratemporal fossa).

• These connections provide pathways for infections to pass from

extracranial sites into intracranial locations. In addition, because
structures pass through the cavernous sinuses and are located in the
walls of these sinuses, they are vulnerable to injury due to
inflammation.
49
Clinical significance of Vascular
Relations

• Lesion of surgical importance affecting ICA range from aneurysm to carotid-

cavernous fistulae.
• After removal of anterior clinoid process, mobilization of anterior loop of
ICA can be done for clipping of aneurysm.
• Treatment of aneurysm ranges from simple observation to balloon
occlusion and trapping of the lesion with or without bypass.
Conditions affecting Cavernous sinus
and its contents

• Midbrain Infection
• Cavernous Sinus Thrombosis
• Orbital Fracture
• Petrous Bone Fracture (Temporal bone Fracture )
• Internal Carotid Artery Aneurysm
• Mastoiditis
• Increased Intracranial Pressure
Clinical and applied aspects
• It is the only anatomic location in the body in which an artery travels
completely through a venous structure. If the internal carotid artery
ruptures within the cavernous sinus, an atriovenous fistula is
created.
• Cavernous sinus syndrome may result from mass effect from a
tumour or CST and cause opthalmoplegia from compression of the
oculomotor nerve, trochlear nerve, and abducens nerve, ophthalmic
sensory loss from compression of the ophthalmic nerve, and
maxillary sensory loss from compression of the maxillary nerve.
• Cavernous sinus thrombosis is the formation of a blood clot within
the cavernous sinus.
Emissary Veins
Emissary – Syn. ambassador
From skull veins to external veins
Importance- to maintain
intracranial and extracranial
venous pressure at an
equilibrium, valve-less to ensure
the same.
May carry Infected thrombus
from extracranial to intracranial
circulation
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CAVERNOUS SINUS THROMBOSIS
• Thrombosis of the cavernous sinus is one of the most dramatic of
neuro-ophthalmic conditions.

• Within a short period, a swollen orbit, limited ocular motility and

impaired vision develop, and may progress to a life threatening
condition

• Rapid diagnosis and therapeutic action are required.

• Morbidity is high, and outcome cannot be certain.

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Epidemiology
• Frequency:
In the US occurrence of CST has always been low, with only a few
hundred case reports in the medical literature. The majority of these date from
before the modern antibiotic era. One review of the English language found
only 88 cases from 1940 -1988.
• Mortality/ morbidity:
Prior to the advent of affective antimicrobial agents, the mortality
rate from CST was effectively 100%. Typically death is due to sepsis or central
nervous system infection. With aggressive management the mortality rate is
now less than 30%. Morbidity however remains high and complete recovery is
rare. Roughly one sixth of patients are left with some degree of visual
impairment and one half have cranial nerve deficits.
• Race : no predilection
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• Sex: no predilection
• Age : all ages are affected with a mean of 22 years
Causes of cavernous sinus
thrombosis

Mid face infection/ cellulitis

PNS infection (Ethmoid or Sphenoid Sinuses)

Odontogenic infections

Orbital Cellulitis

Septicemia
Danger area of the face

The cavernous sinus

communicates with
dangerous area of
face through 2 routes

Deep facial veins,

Angular vein
pterygoid plexus
Superior
of veins, emissary
ophthalmic vein
vein.

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Odontogenic origin of CVT
• CST is one of the major complications resulting from infection of teeth
or surrounding structures in the upper and lower jaws.
• Extraction of mandibular molars (Buccal Space) and maxillary anterior
teeth (Infraorbital Space) in the presence of acute infection, usually
staphylococcal, can cause this condition.
• The infection can spread by
• Direct
• Hematogenous(metastatic )
 Direct Spread Heamatogenous Spread
• Spread by direct extension via the
infratemporal space through the
cranial wall • More often from lower teeth
• By way of pterygoid plexus and than upper teeth
emissary veins, against the usual
flow.
• Reverse of direct spread.
• This is possible because of the • Streptococcus (haemolytic,
anatomic anomaly of the absence non-hemolytic, or viridans)
of valves in the angular, facial usually associated
and ophthalmic veins.
• Staphylococcus aureus
• More often from upper teeth
than lower teeth. 59
Method of spread into cranial cavity
• spread by way of the angular, supraorbital and
Infection of the upper lip, supratrochlear veins to the ophthalmic veins.
vestibule of the nose and eyelids Commonest route of infection.

Intranasal operations on the • through the ethmoidal veins.

septum, turbinates or ethmoid/
sphenoid sinus infection

Operations on the tonsil, • spread by pterygoid plexus or by direct extension

peritonsillar abscess, surgery or
to the internal jugular vein.
osteomyelitis of the maxilla, dental
extraction and deep cervical abscess

Involvement of the middle ear • retrograde spread through the petrosal sinuses to
and mastoid with lateral sinus the cavernous sinus.
phlebitis or thrombosis
Ptosis Proptosis Chemosis
62
Clinical history
• Patient generally have sinusitis or a midface infection (most
commonly a furuncle) for 5-10 days. In as many as 25% of cases in
which a furuncle is the precipitant, it will have been manipulated in
some fashion(eg: squeezing, surgical incision.)
• Headache, fever, and malaise typically precede the development of
ocular findings. As the infection tracts posteriorly, patient complains
of orbital pain and fullness accompanied by periorbital edema and
visual disturbances.
• In some patients, periorbital findings do not develop early on and the
clinical picture is subtle.
• Without effective therapy, signs appear in the contralateral eye by
spreading through the communicating veins to the contralateral
cavernous sinus. This is pathognomic for CST.
• The patient rapidly develops mental status changes from CNS
involvement and/or sepsis.
• If not treated promptly, death follows thereafter.
Other typical finding
• Initially signs of venous congestion may be present.
• Chemosis
• Eyelid edema
• Periorbital edema

• Manifestation of increased retrobulbar pressure

• Exophthalmos
• Opthalmoplegia
• Signs of increased intraocular pressure may be observed

• Pupillary responses are sluggish

• Decreased visual acuity is common owing to increased
iop and traction on the optic nerve and central retinal
artery.

• Cranial nerve palsies are found regularly

• Isolated sixth nerve dysfunction may be noted before

obvious orbital findings.
• Extraocular movements may be impaired.
• Depressed corneal reflex is possibly seen.
• Appearance of signs and symptoms in the contralateral eye
is diagnostic of CST, although the process may remain
confined to one eye.

• Meningeal signs may be noted, including nuchal rigidity and

Kernig and Brudzinski signs.

• Systemic signs indicative of sepsis are late findings. They

include chills, fever, shock, delirium, and coma.
68
Eagleton’s diagnostic criteria
In 1926 Eagleton suggested 6 criteria which are now
considered as the guidelines for diagnosis
1. A known site of infection
2. Septicemia
3. Early signs of venous congestion
4. Ocular, maxillary, abducent nerve deficits
5. Abscess or phlebitis contagious to cavernous sinus
6. Symptoms of complicated disease
Etiology
• Staphylococcus aureus is the most common infectious
microbe, found in 50% to 60% of the cases. Streptococcus
pneumoniae is the second leading cause.
• Gram-negative rods and anaerobes may also lead to
cavernous sinus thrombosis.
• Rarely, Aspergillus fumigatus, Mucormycosis, Haemophilus
influenzae cause CST.
BACTERIOLOGY
Children Adults

• Mixed infections
• H. influenzae • Aerobes
• Staph. aureus
• Anaerobes
• Strep. Pneumoniae
• Bacteroides
• Veillonella
• Peptostreptococci
• Strep. milleri
• Strep. constellatus
Complications

• Intracranial extension of infection may result in meningitis,

encephalitis, brain abscess, pituitary infection, and epidural
and subdural empyema.
• Cortical vein thrombosis can result in hemorrhagic
infarction.
• Extension of the thrombus to other sinuses can occur.
 CST

Increased venous
Systemic embolism Hypopituitarism
congestion

Increased venous Pulmonary

sinus &CSF embolism
pressure (10-20%)

Cerebral
haemorrhage & 73
infraction
Diagnosis and imaging
Cavernous sinus on MRI
Differential Diagnosis
• Orbital cellulitis
• Intraorbital abscess
• Intracavernous carotid artery aneurysm or Arteriovenous fistulae
• Idiopathic granulomatous inflammation of the superior orbital fissure
and cavernous sinus(Tolosa-Hunt syndrome)
• Periarteritis nodosa associated with cavernous sinus thrombosis
(Cogan’s syndrome)
• Nasopharyngeal tumor
• Meningeoma
• Trauma
MANAGEMENT OF CAVERNOUS SINUS THROMBOSIS

• The mainstay of therapy is early and aggressive antibiotic

administration.
• Although S aureus is the usual cause, broad-spectrum coverage for
gram-positive, gram-negative, and anaerobic organisms should be
instituted pending the outcome of cultures.
• Empiric antibiotic therapy should include a penicillinase-resistant
penicillin plus a third generation cephalosporin.
• Vancomycin may be added for MRSA.
• IV antibiotics are recommended for a minimum of 3-4 weeks.
Antibiotic therapy:
• Bactericidal antibiotic inhibiting cell wall synthesis
• Used in treatment of infections caused by penicillinase producing
Oxacillin staphylococci

• Alternate antimicrobial choice

• 3rd generation cephalosporin that has broad gram negative
Ceftriaxone spectrum, lower efficiency against gram positive organisms than
earlier generation cephalosporin.

• Additional anaerobic coverage

• Imidazole ring based antibiotic active against various anaerobic
Metronidazole bacteria and protozoa.
• Usually employed in combination with other antimicrobial agents

• Binds to 50s bacterial ribosomal subunits and inhibits bacterial

growth by inhibiting protein synthesis
Chloramphenicol • Effective against gram negative and gram positive bacteria
80
Anticoagulant therapy:
• Augments activity of antithrombin III and prevents conversion of fibrinogen
to fibrin.
• Does not actively lyse thrombus but inhibits further thrombogenesis.
• Prevents re-accumulation of clot after spontaneous fibrinolysis.
 Corticosteroid therapy:
• Corticosteroids may help to reduce inflammation and edema and should
be considered as an adjunctive therapy.
• These agents have anti inflammatory properties and cause profound and
varied metabolic effects. When the course of CST leads to pituitary
insufficiency, corticosteroids definitely are indicated to prevent adrenal
crisis.

82
• Mannitol: osmotic diuretic. Reduces elevated pressure in brain and
eye.
• Surgery on the cavernous sinus is technically difficult and has
never been shown to be helpful. The primary source of
infection should be drained, if feasible.
Prognosis
• Following the acute phase of infection, recovery is gradual
• Up to 50% of patients can have long-term neurological deficits in the
form of decreased visual acuity, diplopia, cranial nerve deficits,
hemiparesis, ataxia or epilepsy.
• The majority of reported cranial nerve deficits have involved the
occulomotor and abducens nerves. Long-term follow-up of these
patients is essential as relapses have been reported after apparent
clinical resolution.
• Recent studies have shown a mortality rate closer to 10%
CONCLUSION

85
REFERENCES
• Gray’s anatomy
• Cavernous Sinus- Developments and future perspectibes- Vinko Dolenc
• Neelima Malik 3rd edition
• Oral and Maxillofacial infections; Laskin
• Contemporary oral and maxillofacial surgery ; Peterson
• Operative neurosurgical techniques; Henry Schmidek
• Complications of head and neck surgery; Krespi and Ossoff
• Anatomy for surgeons: The head and Neck, vol 1; hollinshead
• Maxillofacial infections ; Topazian, 4th edition
• Brain’s diseases of nervous system 10th edition; John Walton
• Color atlas of clinical neurology 2nd edition; Malcom Parson
• Cavernous sinus thrombosis and blindness as complications of an odontogenic
infection; J Oral Maxillofac Surg 47 1317-1321,1989
• Ocular manifestations of cavernous sinus thrombosis- V Visvanathan, S Uppal, S
Prowse; BMJ Case Reports 2010 86
THANK YOU!!
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