CAVERNOUS SINUS THROMBOSIS

1. Cavernous Sinus Thrombosis
PRESENTED BY –
Dr.ANKITA RAJ (MDS Reader)
Oral & Maxillofacial Surgery Department
Rama Dental College, Kanpur

2. Anatomy of cavernous sinus

3. • Paired venous sinus, on
either side of body of
sphenoid.
• 2cm in length
height of 1cm
• Traversed by numerous
trabeculae, dividing it into
several caverns (spaces)
hence cavernous.

4. • Relations:
– Medial – pituitary above, sphenoidal air cell below
– Lateral – temporal lobe, uncus
– Anterior - superior orbital fissure
– Posterior - petrous apex
– Superior – optic chiasm

6. • Tributaries:
– Superior and inferior opthalmic veins
– Sphenoparietal sinus
– Inferior cerebral veins
– Superficial middle cerebral veins
– Central vein of retina
• Drainage:
– Superior petrosal sinus---> transverse sinus
– Inferior petrosal sinus --->internal jugular vein

7. • Tributaries:
– Superior and inferior opthalmic veins
– Sphenoparietal sinus
– Inferior cerebral veins
– Superficial middle cerebral veins
– Central vein of retina
• Drainage:
– Superior petrosal sinus---> transverse sinus
– Inferior petrosal sinus --->internal jugular vein

8. • Communication:
– Intercavernous sinuses – communication between the two
– Pterygoid plexus – via emissary veins passing through
foramen ovale, emissary sphenoidal foramen and foramen
lacerum.
– Pharyngeal plexus – via a vein passing through carotid canal.
– Facial vein – via superior opthalmic vein.

9. Contents of cavernous sinus
• - Internal Carotid artery with sympathetic plexus
• - CN 3
• - CN 4
• - CN 5 (1st and 2nd divisions)
• - CN 6

10. Cavernous sinus thrombosis

11. • Includes cases of phlebitis, thrombo-phlebitis
and aseptic thrombosis
• Septic type (most common) - coagulase
positive staphylococcus
• Aseptic types may follow trauma, local stasis
or a failing circulation.

12. Causes
Septic CST
• Infectious
Aseptic CST
• Trauma
• Post surgery
Rhinoplasty
Base of skull
Tooth extraction
• Hematologic
• Malignancy
Nasopharyngeal Ca.
• Dehydration

13. • More commonly seen with sphenoid and
ethmoid and to a lesser degree with frontal
sinusitis
• Staphylococcus aureus -70% of all infections.
Streptococcus pneumoniae, gram-negative
bacilli, and anaerobes can also be seen.
• Fungi are a less common pathogen and may
include Aspergillus and Rhizopus species(more
common in diabetics)

14. Spread of infection
• No valves in dural sinuses, cerebral and
emissary veins
• Infection of upper lip, vestibule of nose and
eyelids-> spread by way of angular,
supraorbital, supratrochlear veins to
ophthalmic veins=commonest route
• Intranasal operation of septum, turbinates,
ethmoid/sphenoid sinus infection->through
ethmoidal veins

16. • Operation of tonsil, peritonsillar abcess,
maxillary osteomyelitis/surgery, dental
extraction->spread by pterygoid plexus or
direct extension in internal jugular vein
• Involvement of middle ear/mastoid ->
retrograde spread through petrosal sinus to
cavernous sinus

18. Sources:
• Nose – Paranasal 40%
• Orbit- Face 35%
• Mouth – Teeth 13%
• Ear 9%
• Other – tonsil, soft palate, pharynx, posterior
portions of the superior and inferior alveolar
arches 3%

20. Clinical features
1. Sepsis
2. Venous obstruction
3. Involvement of cranial nerves

21. Sepsis
• Pyrexia
• Rapid, weak, thready pulse
• Chills and sweats
• Delirium - meningitis supervenes terminally
• Septic emboli to various other parts of body.

22. Venous obstruction
• Proptosis (first oedema & chemosis)
• Oedema of eyelids and bridge of nose
• Dilatation and tortuosity of retinal veins
• Retinal hemorrhages
• Involvement of the contralateral eye – (48
hours)
• When pterygoid plexus is occluded along with
sinus, - oedema of the pharynx or tonsil

23. Involvement of cranial nerves
• First CN involved is VI
• Ptosis - paralysis of oculomotor nerve
• Dilatation of pupil- third nerve and stimulation of
sympathetic plexus
• Decreased abduction (paralysis of abducens
nerve)
• Complete opthalmoplegia
• Loss of vision
• Retro-orbital pain and supra-orbital headache->V

25. Diagnosis
• Strong clinical suspicion
1)Orbital venography
• Not recommended
• Difficult to puncture facial veins in odema
• May help in dissemination of infection

26. 2) Contrast enhanced CT
• Slice thickness 3mm or less
• Shows enlargement and expansion of cavernous
sinus cavity with flattening or convexity of lateral
wall
• Multiple or single filling defect with enhancing
CS.
• Exopthalmos, soft tissue edema
• Dilation of superior ophthalmic vein

28. 3) MRI:
• – A sensitive, noninvasive
• Can be combined with venography to
demonstrate lack of blood flow in the
cavernous sinus
• Show associated meningitis, involvement of
pituitary gland

30. 4) CSF examination
• Elevated protein
• Normal sugar
• Mild pleocytosis
5) Complete blood count
• Elevated TLC
• Leucocytosis
6) Blood culture
7) Local tissue culture

31. Complications
• Intracranial extension of infection->
meningitis, encephalitis, brain abcess,
pituitary infection,epidural, subdural
empyema
• Cortical vein thrombosis->hemorrhagic
infarction
• Extension to other sinuses

32. Differential Diagnoses
• Orbital cellulitis–differentiated from CST by B/L
involvement, papillodema, dilated pupil, decreased
periocular sensation, abnormal spinal fluid in latter
• Preseptal cellulitis- no proptosis
• Orbital apex syndrome- more visual loss,
opthalmoplegia, less proptosis, periorbital odema
• Sinusitis
• Orbital malignancy
• Facial Cellulitis
• Glaucoma-angle closure

33. Treatment

34. Antibiotics
• Immediate empiric antibiotic coverage must
include gram-positive, gram-negative and
anaerobic bacteria.
• Later treatment can be narrowed, adjusted to
cultures and sensitivities
• Third generation cephalosporin + vancomycin
with metronidazole
• Duration- 3-4 weeks

35. Antifungals
• Used in setting of fungal sinusitis
• More common in diabetics
• Aspergillus more common
• Parentral amphotericin B for 3 weeks followed
by posaconazole(400mg BD) prophylaxis
• Dose-0.5-1.5mg/kg/day(deoxycholate), 5-
10mg/kg/day(liposomal)

36. Anticoagulation
• Intravenous heparin (maintaining the partial
thromboplastin time or thrombin clot time at
1.5 to 2 times that of the control)->24,000-
30,000 U/day.
• Warfarin sodium (maintaining the
prothrombin time at 1.3±1.5 times the
control) -continued for 4 to 6 weeks to allow
adequate collateral channels to develop

37. • Mortality was lower among patients who
received heparin treatment, 14% vs. 36%
• Early administration of heparin may serve to
prevent spread of thrombosis to the other
cavernous sinus as well as to the inferior and
superior petrosal sinuses.

38. Steroids
• Not influence mortality
• May prevent residual cranial nerve
dysfunction caused by inflammation.
• Dexamethasone used most commonly

39. Surgical treatment
• Surgical drainage of affected sinuses
• Endoscopic sinus surgery
• Surgical debridement in fungal sinusitis
• Surgical drainage of any collection

40. Prognosis
• 100% mortality prior to antibiotics
• 30% mortality despite aggressive treatment
• 44% of survivors remain with chronic sequelae,
• Roughly one sixth of patients are left with some
degree of visual impairment
• One half have cranial nerve deficits
• Hypopituitarism- rare, can occur before or after 1
year.

41. References
• Septic cavernous sinus thrombosis-Neurology
and Neurosciences;2014;4:117-118
• Treatment of Cavernous Sinus Thrombosis;
IMAJ 2002;4:468±469
• Septic thrombosis of cavernous sinus-Arch
Intern Med;2001;161:2671-2676

42. Thank You