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
3.
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
5.
6.
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%)..
9.
10.
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”
13. • Blurred vision due to:-
Arterial insufficiency
Venous stasis with engorged retinal vessels
Retinal hemorrhage
Papilledema
Keratitis due to loss of corneal sensation
• Diplopia
14.
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 .
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.
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 ..
29.
30.
31. Investigations
1) FBP & ESR
2) Blood culture and sensitivity
3) CT/MRI Brain and orbit
4) Angiogram
35. Treatment
1. Exploration .
2. Treatment of the cause
3. Steroids
4. Antibiotics
5. surgical intervention .
a) Orbitotomy.
b) Orbital decompression .