Thursday, January 12, 2012

What causes cavernous sinus thrombosis?

What causes cavernous sinus thrombosis?

Cavernous sinus thrombosis (CST), one of the infections-sinus-induced complications, affects cranial nerves passing through the cavernous sinus. This thrombophlebitis results in thrombosis and inflammation. Bilateral ocular findings are characteristic of CST, but unilateral ocular symptoms occurring simultaneously with meningitis symptoms may also indicate presence of the thrombosis. Bilateral CST is rare and fatal. The unilateral CST may affect the opposite eye within 48 hours of the onset of the thrombosis.

Generally, blood-borne infection travels from the paranasal sinuses, nasal cavity, ear or face to the cavernous sinus or the surrounding area via inferior and superior ophthalmic veins. The thrombosis, therefore, interrupts the venous flow, especially flow in the superior ophthalmic vein that is the main drainage channel of the orbit. Even untreated or poorly managed orbital infections may also cause CST. Staphylococcus aureus is the main cause of CST (up to 70% cases).

CST, a serious condition, can be of aseptic (non-infectious) or septic (infectious) origin. However, infections-sinus-induced CST, an ocular emergency, is septic. Although infections-sinus and orbital cellulites are principally responsible for CST, dental abscess, gingivitis and other odontogenic infections may lead to CST. If only one eye is affected, diagnosing CST is quite difficult. CST may also follow upper respiratory tract symptoms. CST may occur in immunity deficient host.  For instance, in diabetic patients, fungal sinusitis may cause CST.

The cavernous sinuses, located on the sides of the sphenoid, intercommunicate and feature a network of venous passages. The cerebral veins and superior ophthalmic vein supply blood to the cavernous sinuses. The cranial nerves passing through the cavernous sinus enters the orbit and performs many basic eye functions. For instance, cranial nerves III, IV and VI control eye movements. Except cranial nerve VI, all these nerves occupy cavernous sinus’s lateral wall. The cranial nerve VI is located near carotid artery and is affected by the cavernous sinus diseases fast due to its location.

CST could be dangerous. For instance, if phlebitis, inflammation of the veins, reaches the cortical veins and dural sinuses, abscesses, multiple cerebral thrombosis and meningitis may develop. If inflammation also affects the pituitary gland, pituitary insufficiency may occur. If contralateral ocular symptoms develop, loss of vision, paralysis of the eye muscles (ophthalmoplegia) and bulging of the eyeball (proptosis) may happen. However, blindness, ophthalmoplegia and pituitary insufficiency are non-fatal. The CST mortality rate is up to 30%, but untreated CST is fatal.


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  2. Hello Brian, Thank you for your interest in Nasodren blog.

    Cavernous sinus thrombosis (CST) represents a rare but devastating disease process that may be associated with significant long-term patient morbidity or mortality. The prompt recognition and management of this problem is critical.

    Cavernous sinus thrombosis may result from any infection of the tissue drained by the cavernous sinus. This includes the midface, orbit and sinonasal cavity. The mortality rate remains high at 30%, and significant morbidity includes residual cranial nerve palsies and blindness.

    Treatment for cavernous sinus thrombosis includes high-dose intravenous antibiotics directed at the most common causative organisms, coupled with surgical drainage of the primary source of infection.

    The role of anticoagulation is contentious because its efficacy is undetermined and it may cause or exacerbate concurrent intracranial haemorrhage in patients with septic CST. Moreover, prospective trials of anticoagulation may never be performed due to the rarity of this condition. Nevertheless, retrospective reviews of published reports indicate that haemorrhage caused by anticoagulation is rare, and that early adjunctive anticoagulation is beneficial in these patients if commenced after excluding the haemorrhagic sequelae of CST radiologically.
    After application of NASODREN®, a slight issuing of red blood cells in the nose was observed in some patients. Therefore, treatment with anticoagulants (e.g. coumarin derivatives, acetylsalicylic acid) should be suspended, taking account of the rate of elimination of the particular anticoagulant.

    Best Regards