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Cavernous Sinus Thrombosis

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Cavernous sinus thrombosis is a very rare, typically septic, thrombosis of the cavernous sinus, usually caused by bacterial sinusitis. Symptoms and signs include pain, proptosis, ophthalmoplegia, vision loss, papilledema, and fever. Diagnosis is confirmed by CT or MRI. Treatment is with IV antibiotics. Complications are common, and prognosis is poor.

Etiology

The cavernous sinuses are trabeculated sinuses located at the base of the skull that drain venous blood from facial veins. Cavernous sinus thrombosis (CST) is an extremely rare complication of common facial infections, most notably nasal furuncles (50%), sphenoidal or ethmoidal sinusitis (30%), and dental infections (10%). Most common pathogens are Staphylococcus aureus (70%), followed by Streptococcus sp; anaerobes are more common when the underlying cause is dental or sinus infection.

Thrombosis of the lateral sinus (related to mastoiditis) and thrombosis of the superior sagittal sinus (related to bacterial meningitis) occur but are rarer than CST.

Pathophysiology

The 3rd, 4th, and 6th cranial nerves and the ophthalmic and maxillary branches of the 5th cranial nerve are adjacent to the cavernous sinus and are commonly affected. Complications include meningoencephalitis, brain abscess, stroke, blindness, and pituitary insufficiency.

Symptoms and Signs

Initial symptoms are progressively severe headache or facial pain, usually unilateral and localized to retro-orbital and frontal regions. High fever is common. Later, ophthalmoplegia (initially the 6th cranial nerve, lateral gaze), proptosis, and lid edema develop and often become bilateral. Facial sensation may be diminished or absent. Decreased level of consciousness, confusion, seizures, and focal neurologic deficits are signs of CNS spread. Patients may also have anisocoria or mydriasis (3rd cranial nerve dysfunction), papilledema, and vision loss.

Diagnosis

  • MRI or CT

CST is often misdiagnosed because it is rare. It should be considered in patients who have signs consistent with orbital cellulitis. Features that distinguish CST from orbital cellulitis include cranial nerve dysfunction, bilateral eye involvement, and mental status changes.

Diagnosis is based on neuroimaging. MRI is the better study, but CT is also helpful. Useful adjunct testing may include blood cultures and lumbar puncture. Lumbar puncture may show inflammatory cells (PMNs, lymphocytes, monocytes); other possible abnormalities include low glucose, high protein, and positive CSF cultures. Cultures of any suspected source infections also are done.

Prognosis

Mortality is 30% in all patients and 50% in those with underlying sphenoid sinusitis. An additional 30% develop serious sequelae (eg, ophthalmoplegia, blindness, disability due to stroke, pituitary insufficiency), which may be permanent.

Treatment

  • IV high-dose antibiotics
  • Sometimes corticosteroids

Initial antibiotics can include nafcillin Some Trade Names
UNIPEN
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or oxacillin Some Trade Names
BACTOCILL
PROSTAPHLIN
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1 to 2 g q 4 to 6 h combined with a 3rd-generation cephalosporin (eg, ceftriaxone Some Trade Names
ROCEPHIN
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1 g q 12 h). In areas where methicillin-resistant S. aureus is prevalent, vancomycin Some Trade Names
VANCOCIN
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1 g IV q 12 h should be substituted for nafcillin Some Trade Names
UNIPEN
Click for Drug Monograph
or oxacillin Some Trade Names
BACTOCILL
PROSTAPHLIN
Click for Drug Monograph
. A drug for anaerobes (eg, metronidazole Some Trade Names
FLAGYL
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500 mg q 8 h) should be added if an underlying sinusitis or dental infection is present.

In cases with underlying sphenoid sinusitis, surgical sinus drainage is indicated, especially if there is no clinical response to antibiotics within 24 h.

Secondary treatment may include corticosteroids (eg, dexamethasone Some Trade Names
DECADRON
DEXASONE
HEXADROL
Click for Drug Monograph
10 mg po q 6 h) for cranial nerve dysfunction; anticoagulation is controversial because most patients respond to antibiotics, and adverse effects may exceed benefits.

Last full review/revision September 2008 by James Garrity, MD

Content last modified September 2008

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