1) Cavernous sinus thrombosis is a blood clot that forms within the cavernous sinus, which is a venous channel within the skull. 2) It can be aseptic (caused by trauma, tumors, or hypercoagulable states) or septic (caused by bacterial infection spreading from nearby areas like the face, sinuses, or ears). 3) The most common symptoms are headaches, signs of sepsis, and ocular issues like proptosis, ophthalmoplegia, ptosis, and blurred vision. Complications can include orbital abscesses, meningitis, or extensions of the clot or infection.

1. CARVENOUS SINUS
THROMBOSIS

2. What is cavernous sinus ?
intracranial Venous channels
It is formed by the splitting of the Dura matter.
• The 2 cavernous sinus are interconnected by small
anterior and posterior inter cavernous channels
• The lateral wall of cavernous sinus is composed
of 2 layers
1. Superficial layer of dura – dura matter on the medial
side of middle cranial fossa
2. Deep layer of dura – formed by sheath of :
Oculomotor 3
Trochlea 4
Trigeminal(Ophthalmic and Maxillary). 5

4. Cavernous sinus receives blood from the following:
• Face, eyes and maxilla
superior and inferior ophthalmic veins
Pterigoid plexus via emissary veins
• Anteriorly
Sphenoparietal vein
Superficial middle cerebral vein
• Posteriorly
Superior petrosal sinus
Inferior petrosal sinus • It drains into
1. Transverse sinuses
2. Internal jugular vein

7. What is CST ?
 Formation of blood clot within the cavernous sinus
What are the types of CST ?
Pathology of CST can be divided in to two types:
1. Aseptic thrombosis
2. Septic thrombosis
Aseptic thrombosis occurs with:
1) Trauma
2) Tumor invasion
3) Aneurysmal expansion
4) Hypercoagulable states
septic thrombosis occurs with:
• It is the commonest type .
• 2ry to the spread of infection by veins and by direct
extension..

8. Septic CST occurs via infection through
1. Danger area of the face (angular &ophthalmic
vein).
2. Tooth extraction
3. Nasal sinuses ( maxillary , spheroidal )
4. Otitis media .
5. Extension from infected internal jugular vein,
lateral sinus or petrosal sinus
What is The most commonly isolated organisms
causing CST ?
1) Staphylococcus aurous (about 70%)
2) Streptococcus species (about 20%)..

11. General syptoms :--
• Headache (50% to 90% of cases) generally
unilateral, fronto temporal, or retro bulbar in
location.
• Signs of sepsis,
1) FAHM.
2) Tachycardia
3) Hypotension.
4) Confusion.
5) coma.
6) Pyrexia is seen usually with a “picket fence”

12. Ocular symptoms :-
1) Periorbital edema.
2) Eye pain
3) Ptosis
4) Proptosis
5) Conjunctival Chemosis
6) Ophthalmoplegia . Why ??
Orbital congestion – stasis sec to thrombosis
Infection of EOM.
NB : -
Impaired EOM starting with a LR..

13. • Blurred vision due to:-
Arterial insufficiency
Venous stasis with engorged retinal vessels
Retinal hemorrhage
Papilledema
Keratitis due to loss of corneal sensation
• Diplopia

15. What are the complications of CST ??
• Orbital abscess .
• Septicemia
• Intracranial extension of infection may result in:-
 Meningitis,
 Encephalitis,
 Brain abscess
• Extension of the thrombus to other sinuses
• Cortical vein thrombosis can result in:-
 Hemorrhagic infarction
 hemiplegia

16. Differential Diagnosis
1) THS ( painful Ophthalmoplegia ) , no affect on ON.
2) OAS (cranial nerve palsy +optic nerve dysfunction).
3) Myositis .
4) Orbital cellulitis
5) Orbital tumor
6) Orbital pseudo tumor .

17. Investigations
1) FBP & ESR
2) Blood culture and sensitivity
3) Lumber puncture
1) mixed pleocytosis and polymophonuclear cells
2) Raised proteins
3) Normal/low glucose
4) CT Brain and orbit

18. MRI brain

20. Management of CST

21. Medical Management
ANTIBIOTICS
• Broad spectrum iv antibiotics – 3 to 4 weeks but if
evidence of intracranial suppuration then 6 to 8 weeks.
i.e.
1. Ceftriaxone IV
2. Metronidazole IV
ANTICOAGULANTS .(ASAP )
• The proposed benefit is to dissolve the clot E.g. heparin .
STEROID THERAPY
• Helps reduce level of inflammation

22. Surgical Management
SURGICAL MANAGEMENT
• Surgical intervention should be directed at the
primary source of the infection and the
surrounding areas of involvement.
• Incision and drainage should be done ASAP.

23. Septic CST

24. Aseptic CST

25. SUPERIOR ORBITAL FISSURE
Left orbit

26. SUPERIOR ORBITAL FISSURE
• 22 mm long
• It communicate ( ) the orbit & the middle cranial
fossa
• Lateral superior part of the fissure is narrower
than the medial inferior part.

27. SOFS
• Causes :-
1) Idiopathic
2) Trauma ( craniofacial fractures) (most commonly)
3) Tumor
4) hematoma of the cavernous sinus .
5) Infections
6) Narrowing, aneurysm of ICA.

28. Clinical picture :- DOPPE ( diplopia , Ophthalmoplegia , ptosis , Proptosis ).
It occurs as a result of inflammation & Compression of
adjacent nervous tissue
• Diplopia
• Orbital pain .
• Lid ptosis
– Sympathetic fibers in CS – Mullers muscle
– Efferent fibers Superior Oculomotor Nerve – Levetor
palpebrae superioris muscle
• Ophthalmoplegia
– Impairment of cranial nerves III, IV, and VI.
• Anesthesia of the forehead and upper eyelid.
• Proptosis
– loss of tone of EOM muscles ..

31. Investigations
1) FBP & ESR
2) Blood culture and sensitivity
3) CT/MRI Brain and orbit
4) Angiogram

32. Maxillofacial CT scan

33. Angiogram SOFS
Left carotid angiogram showing narrowing with
aneurysm

34. CT Brian – Axial view for SOFS

35. Treatment
1. Exploration .
2. Treatment of the cause
3. Steroids
4. Antibiotics
5. surgical intervention .
a) Orbitotomy.
b) Orbital decompression .

36. Surgical Treatment of SOFS

37. SOFS