Cavernous sinus thrombosis (CST) is a rare, life-threatening disorder that can complicate facial infection, sinusitis, orbital cellulitis, pharyngitis, or otitis or following traumatic injury or surgery, especially in the setting of a thrombophilic disorder. Early recognition of cavernous sinus thrombosis which, often presents with fever, headache, eye findings such as periorbital swelling, and ophthalmoplegia, is critical for a good outcome. Despite modern treatment with antibiotics and anticoagulation, the risk of long-term sequelae, such as vision, diplopia, and stroke, remains significant. This activity examines when cavernous sinus thrombosis should be considered, how to properly evaluate this condition and the role of the interprofessional team in caring for patients with this condition.

1. Cavernous Sinus
Thrombosis
Gholam Dastagir Barakzay
Roshana Eye Hospital
16th August 2022

2. Contents
• Anatomy Cavernous Sinus
• Cavernous Sinus
Thrombosis
• Risk Factors
• Epidemiology
• Etiology
• The mechanism of Septic
CST
• Septic CST Complications
• Symptoms
• Physical Exam
• Diagnostic Methods
• Treatment / Management
• Differential Diagnosis

3. Anatomy of Cavernous Sinus
• Sinus: means a cavity, space or channel in the body
• Dural venous sinuses : are venous channel found between the
endsteal and meningeal layers of dura mater in the brain.
• There are 13 dural venous sinuses
• Cavernous sinus is one of the dural venous sinuses

4. Anatomy Cavernous Sinus

5. Venous Drainage of the Brain
• Networks of small venous channels
• Cerebral veins and brainsteam veins
• Diploic veins and emissary veins
• All empty to dural venous sinusis
• CS empties to S/I pertrosal sinuses
• Leads to internal jugular vein

6. Anatomy Cavernous Sinus

7. Anatomy Cavernous Sinus

8. Cavernous Sinuses
• Receive blood from
1. Cerebral veins
2. Ophthalmic veins
3. Emissary veins
4. Sphenoparietal sinus
• These connections provide pathways for infection
1. From extracranial sites to intracranial locations
2. Other structures close to CS are vulnerable to
injury and infections

9. Structures passing through CS
1. The internal carotid arteries
2. The abducent nerve [VI]
• Structures in the latera wall of each
CS
1. The oculomotor nerve [III]
2. The trochlear nerve [IV]
3. The ophthalmic nerve [V1]
4. The maxillary nerve [V]
• Intercavernous sinuses connect R/L CS

10. The cavernous sinuses
• One on each side of the
sella turcica
• above and lateral to the
sphenoid sinuses
• Anteriorly superior orbital
fissure
• Posteriorly petrous part of
the temporal lobe

11. Cavernous Sinus Thrombosis
• Thrombosis occur when blood clots block vein or artery
• CST is a rare, life-threatening disorder
• Can be complication of facial infection, sinusitis, orbital cellulitis,
pharyngitis
• Otitis or following traumatic injury or surgery, especially in the
setting of a thrombophilic disorder

12. Cavernous Sinus Thrombosis

13. Risk Factors
• The biggest risk factors are:
• Facial infections, acute sinusitis, and periorbital infections.
• Thrombophilia is a significant risk factor for cavernous sinus
thrombosis.
• Women who are pregnant, post-partum, or receiving oral
contraceptives or hormone replacement therapy

14. Risk Factors
• A variety of thrombophilic genetic
• Factor V Leiden mutation, prothrombin G20210A mutation, antithrombin III, protein
C or S deficiency, or increased factor VIII.
• Acquired disorders
• Antiphospholipid antibody syndrome, hyperhomocysteinemia, heparin-induced
thrombocytopenia, and obesity
• Severe dehydration
• Hyperosmolar non-ketotic state, nephrotic syndrome, and sickle cell disease

15. Epidemiology
• CST comprises approximately 1% to 4% of cerebral venous and sinus
thrombosis (CVST)
• CVST incidence is approximately two to four per million people per
year
• with a higher incidence in children
• The annual incidence of CST approximately 0.2 to 1.6 per 100,000 per
year.
• A male or female predominance in cavernous sinus thrombosis is
uncertain.

16. Etiology
• Usually septic, but can also be aseptic
• Septic
• Central facial infection
• Abscess, Cellulitis, sinusitis, dental infection and otitis media.
• Aseptic
• Less common
• Trauma, surgery and pregnancy.

17. Etiology
• Staphylococcus aureus may account for two-thirds of cases
• Streptococcus species (approximately 20% of cases
• Pneumococcus (5%)
• Proteus, Hemophilus, Pseudomonas, Fusobacterium, Bacteroides
• Corynebacterium and Actinomyces
• Fungal infection
• Aspergillosis (most common), Zygomycosis (such as Mucormycosis) or
Coccidiomycosis

18. Etiology
• Parasites
• Toxoplasmosis, malaria, and trichinosis
• Viral
• Herpes simplex, cytomegalovirus, measles, hepatitis, and human
immunodeficiency virus (HIV).

19. Etiology of Septic CST
• Local spread, often from valveless
facial and ophthalmic veins
• Adjacent infections, such as
sinusitis (sphenoiditis and
ethmoiditis)
• Facial cellulitis or abscess
• Periorbital and orbital cellulitis
• Pharyngitis
• Tonsillitis
• Otitis media
• Mastoiditis
• Dental infections

20. The mechanism of Septic CST
• 1. Embolization: 1. bacteria 2. infectious organisms
thrombosis
cavernous sinus
1. Decreased drainage from the facial vein
2. Decreased drainage from superior and inferior ophthalmic veins

21. The mechanism of Septic CST
1. facial and periorbital edema
2. Ptosis
3. Proptosis
4. Chemosis
5. Discomfort and pain with eye muscle movement
6. Papilledema
7. Retinal venous distention
8. Loss of vision

22. The mechanism of Septic CST
Local compression and inflammation of cranial nerves
Several partial or complete cranial neuropathies
Diplopia and Ophthalmoplegia

23. The mechanism of Septic CST
1. Internal ophthalmoplegia (non-reactive pupil) occurs from loss of
sympathetic fibers from the short ciliary nerves (resulting in miosis)
2. Loss of parasympathetic fibers from cranial nerve III (resulting in
mydriasis)
3. Numbness (around the eyes, nose, forehead)
4. Loss of corneal blink reflex from the ophthalmic nerve, a branch of
the trigeminal nerve (V)
5. Facial pain, paresthesias from compression of the maxillary branch
of the trigeminal nerve.

24. The mechanism of Septic CST

25. Septic CST Complications
• central nervous system
• Meningitis
• Dural empyema
• Brain abscess
• Pulmonary
• Septic emboli
• Abscess
• Pneumonia
• Empyema
• Vascular
• Stroke
• Vasculitis
• Cortical vein thrombosis.
• Hypopituitarism
• due to ischemia or the direct
spread of infection.

26. Symptoms
• Fever
• Headache (50% to 90%)
• Periorbital swelling and pain
• Vision changes, such as photophobia, diplopia, loss of vision.
• Usually, it starts with one eye and then progresses to another eye.
• Less common symptoms
• Rigors, stiff neck, facial numbness, confusion, seizures, stroke symptoms, or
coma

27. Physical Exam
• Vital signs: fever, tachycardia and hypotension.
• Neurologic finding:
• altered mentation, lethargy, or obtundation
• Seizures or stroke syndromes (such as hemiparesis)
• Eye findings are nearly universal (90%).
• Periorbital edema (initially unilateral but typically bilateral)
• Lid erythema, chemosis, ptosis, proptosis
• Restricted or painful eye movement
• Papilledema, retinal hemorrhages, decreased visual acuity (7% to 22%)
• Photophobia, diminished pupillary reflex
• Pulsating conjunctiva
• Blindness can result in 8% to 15% of cases.

28. Physical Exam
• Eye findings are nearly universal (90%).
• Periorbital edema (initially unilateral but typically bilateral)
• Lid erythema, chemosis, ptosis, proptosis
• Restricted or painful eye movement
• Papilledema, retinal hemorrhages, decreased visual acuity (7% to 22%)
• Photophobia, diminished pupillary reflex
• Pulsating conjunctiva
• Blindness can result in 8% to 15% of cases.

29. Physical Exam
• External ophthalmoplegia
• Sixth, third and fourth cranial
neuropathy
• Internal ophthalmoplegia
• Nonreactive pupil
• Miosis
• Mydriasis
• Horner syndrome
• Ptosis, miosis, and anhidrosis
• The sensory exam might
• Diminished sensation to face
• Impaired corneal reflex.

30. Diagnostic Methods
• Contrast-enhanced computed tomography (CT)
• Magnetic resonance imaging (MRI)
• CT venogram (CTV)
• Contrast-enhanced MR venogram (MRV)

31. CTV and enhanced-MRV
• Dilation of the cavernous sinus, enhancement,
• Convexity of the lateral wall (which is normally concave)
• On coronal views
• Heterogeneous and asymmetric filling defects after contrast
• Increased density of orbital fat
• Thrombosis in the superior ophthalmic vein
• Tributaries leading to the cavernous sinus
• Carotid artery narrowing, carotid arterial wall enhancement
• Cerebral infarcts, intraparenchymal hemorrhages
• Empyema, meningitis, cerebritis or abscess

32. Blood studies
• white blood cell count (WBC)
• C-reactive protein (CRP)
• Erythrocyte sedimentation rate (ESR,) and D-dimer.
• Blood cultures should be obtained routinely and are frequently positive.
• Lumbar puncture is important to exclude meningitis
• Elevated opening pressure
• Pleocytosis
• Screening for thrombophilia may give false results during anticoagulation
therapy and should be delayed until after treatment is completed.

33. Treatment / Management
• Antimicrobial therapy
• Anti-staphylococcal agent (vancomycin if methicillin resistance is high, or
nafcillin),
• Third-generation cephalosporin, and metronidazole (for anaerobic coverage)
• Antifungal therapy with amphotericin B.
• A prolonged duration of parenteral therapy, typically three to four
weeks or at least two weeks beyond clinical resolution is suggested.

34. Treatment / Management
• Anticoagulation
• Unfractionated heparin (UFH)
• Low molecular weight heparin (LMWH) for several weeks to several months.
1. decrease in mortality from 40% to 14% with UFH
2. Reduction in neurologic morbidity, from 61% to 31%
3. The Cochrane Collaboration (Coutinho) suggests that anticoagulation for
cerebral venous and sinus thrombosis appears safe
4. The (EFNS) recommends three months of anticoagulation in secondary
cerebral venous and sinus thrombosis with a transient risk factor
5. Six to 12 months for idiopathic cerebral venous and sinus thrombosis and
those with mild thrombophilia

35. Treatment / Management
• Corticosteroids are often given but without demonstrated efficacy.
• The potential benefit would be decreased inflammation
• Vasogenic edema surrounding cranial nerves and orbital structures.
• Steroids are necessary, however, for cases of hypopituitarism.
• The (ISCVT) reported steroid use in 24% of cerebral thrombosis with no evidence
of improvement.
• No surgical interventions are recommended for the cavernous sinuses
themselves.
• However, some patients might require
• sphenoidectomy, ethmoidectomy, maxillary antrostomy, mastoidectomy, abscess drainage,
craniotomy (subdural empyema), orbital decompression, or ventricular shunt placement.
• Patients should be followed closely even after the discontinuation of the
antibiotics.

36. Differential Diagnosis
• Local compression of the cavernous sinus
• from noninfectious and non-thrombotic lesions, 30% of which are tumors:
• Carotid cavernous fistula, with enhanced CT or MRI showing
• proptosis, enlarged superior ophthalmic vein, “dirty” appearance of retro-
orbital fat, and enlarged extraocular muscles.
• Lytic bone lesions near the sphenoid sinus or sella turcica, tumors
• metastatic cancer, meningioma, schwannoma, plexiform neurofibroma,
pituitary adenoma, chordoma, chondrosarcoma, melanocytoma or
nasopharyngeal carcinoma, the most common primary malignant tumor),
• cavernous hemangioma

37. Differential Diagnosis
• Meningioma
• Sino-orbital aspergillosis
• Superior orbital fissure syndrome
• Tolosa-Hunt syndrome
• Involving a retro-orbital granulomatous pseudotumor into the cavernous
sinus, manifesting as retro-orbital pain, ophthalmoplegia, cranial nerve palsy,
and clinical response to systemic steroids

38. Differential Diagnosis
• Orbital apex syndrome
• (inflammation of the posterior orbit, including the superior orbital fissure
through which cranial nerves III, IV, V, and VI and the superior ophthalmic vein
traverse, as well as the optic canal involving the ophthalmic artery and optic
nerve and characterized by less edema and proptosis but more vision loss
than cavernous sinus thrombosis)
• Orbital cellulitis
• Sarcoidosis
• Syphilis
• Tuberculosis

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