Cavernous Sinus Thrombosis
- Jan 18th, 2015
- Jennifer Robertson
Cavernous Sinus Thrombosis
Author: Jennifer Robertson, MD (EM Attending Physician, Cleveland Clinic) // Editor: Alex Koyfman, MD
Cavernous sinus thrombosis (CST) is a rare condition, defined as a septic thrombophlebitis of the cavernous sinus. It is caused by a bacterial infection that typically originates in the face, sinuses, ears, or orbits (1). Prior to the discovery of antibiotics, mortality was nearly 100% (2). It still causes significant morbidity and mortality today, even with treatment (3,4,5). Due to the rarity of CST, data is limited as randomized control trials will likely never be conducted (4). Thus, some proposed treatments, such as anticoagulation and steroids, remain controversial (1,4,6). Antimicrobial therapy, however, is paramount and due to the potentially severe complications from CST, physicians should have a low threshold for initiating antibiotics as early as possible (1,7).
The two cavernous sinuses are located on both sides of the sella turcica. Important structures are located in, or run through, the cavernous sinus, including the pituitary gland, cranial nerves III, IV, V and VI, and the internal carotid arteries (ICA) (6,8). The cavernous sinuses receive blood from the superior ophthalmic and cerebral veins, the sphenoparietal sinuses, and emissary veins. The cavernous sinuses also communicate with the deep facial and inferior ophthalmic veins. Many of these veins have no valves and blood can flow in either direction, depending on pressure gradients. It is hypothesized that this is the reason why infection spreads and thromboses form (2,6). In addition, the thrombus itself is a good growth medium for bacteria and the bacteria, in turn, stimulate thrombosis by releasing substances that cause tissue damage (1,9).
Sphenoid and ethmoid sinusitis are the most common causes of CST (3,4,5,6). Other risk factors include dental infections, facial cutaneous infections, otitis media, maxillofacial surgery, and trauma (1,3,4, 5,6,10). Even bacterial seeding from a distant site of infection has been a reported cause of CST (11). Staphylococcus aureus is the primary organism that causes CST, but many other bacteria can be involved (4,10).
CST can present acutely or sub-acutely. Most patients will have fever, headache, proptosis, periorbital edema and/or chemosis. Most will also have external ophthalmoplegia, due to venous congestion of orbital tissues, extra-ocular muscle inflammation and/or inflammation of cranial nerves III, IV and VI (1,5,6,12). Other symptoms include eyelid erythema, autonomic dysfunction, sensory changes in the ophthalmic and maxillary trigeminal nerve distributions, pupillary abnormalities, and papilledema (1, 3, 4, 6). Vision loss is rare as the orbital nerve lies outside the cavernous sinus but it can occur via other mechanisms such as occlusion of the ICA, ophthalmic or central retinal arteries, orbital congestion, or arteritis (1,13). CST commonly spreads from one eye to both within 24 to 48 hours (4,6).
Physicians should keep a wide differential, especially in patients with pain with extra-ocular movements and ophthalmoplegia. Differential diagnoses include orbital cellulitis, orbital apex syndrome, ICA aneurysm, malignancy of the CS, trauma, carotid-cavernous fistula (CCF), Tolosa-Hunt Syndrome, and ischemic stroke (6,14)
If CST is suspected, imaging should be ordered. Either computed tomography (CT) or magnetic resonance imaging (MRI) may be obtained, but CT tends to be the initial test of choice, as it is better than MRI in detecting thrombus directly in the cavernous sinus (1, 15,16). MRI, however, is better at detecting dural venous sinus thromboses (1,16). On CT, various direct and indirect findings of CST may be found. Direct signs include enlargement of the cavernous sinuses, convex bowing of the lateral wall of the cavernous sinus and/or abnormal filling defects. Indirect signs include dilation of the superior ophthalmic vein, exophthalmos, and/or increased dural enhancement along the lateral wall of the sinus (1,6,15,16).
Antibiotics are primary in the treatment of CST (1,3,7). Empiric therapy should consist of a third generation cephalosporin, nafcillin, and metronidazole. Vancomycin can be substituted for nafcillin if methicillin-resistant Staphylococcus aureus (MRSA) is a concern (4,6). Along with antibiotics, surgery may be necessary; it is rarely needed for drainage of the primary infection (1,4,5,6,17).
The use of anticoagulation and corticosteroids remains controversial (1,4). Some studies have found improved cranial nerve function with steroid use, but there is currently no data to support its routine use (1,4,6).
Regarding anticoagulation, data is also limited given the rarity of CST and the lack of prospective trials (1,6). It is theorized that anticoagulation may prevent the spread of the thrombus to other sinuses (1,5) as well as help dissolve the clot, allowing the antibiotic to reach the infected thrombus more readily (13,17). On the other hand, there is a risk of systemic and intracranial bleeding and some authors state it may result in dissemination of septic emboli (4,5,13). Most authors recommend considering anticoagulation only if there is no evidence of severe bleeding risk or current hemorrhage by history, exam, and imaging (1,4,5). It is always best to consult with specialists regarding treatment regimens.
Even with appropriate treatment, the complications of CST can be devastating and mortality still remains high at 20-30% (6,7). In addition, nearly half of patients have residual sequelae including cranial nerve lesions, weakness of extraocular muscles, impaired vision, hemiparesis, or hypopituitarism (5,6,13,18). Because of the high mortality and devastating consequences of CST, physicians need to keep a high level of suspicion for the condition, image liberally, and administer antibiotics as soon as possible.
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