CST is a relatively rare but life-threatening cause of cavernous sinus syndrome [6
]. The mortality rate remains high, and significant morbidity includes residual cranial nerve palsies and blindness. Thus, early diagnosis and medical intervention are crucial.
The primary source of sepsis may be a distant focus or neighboring region [7
]. CST may result from any infection of the tissue drained by the cavernous sinus. This includes the face, tonsils, soft palate, teeth, and ears. Once antibiotic therapy became widely available, however, the sphenoid sinus emerged as the most common primary source of infection predisposing to CST [7
]. The sphenoid sinus has important anatomical relationships with the cavernous sinus. As a midline structure, it can present with bilateral or contralateral intracranial complications. Isolated sphenoid sinusitis is rare, nevertheless, sphenoid sinusitis occurs in a significant proportion of cases of septic CST, either in isolation or in combination with involvement of other sinuses [4
]. The two cavernous sinuses are formed by the separation of the layers of the dura mater. In some areas, the cavernous sinus may be separated from the sphenoid air sinuses by only small amounts of soft tissue [8
]. Sphenoid sinusitis can cause CST through a combination of factors. Spread of infection from the sphenoid sinus proceeds mainly through the afferent veins to the unvalved cavernous sinus and results in a classic fulminant CST. Microorganisms can spread directly from an infected sphenoid sinus to the cavernous sinus via communicating veins, via osteomyelitis of the intervening diploic bone, or by breaching mucosa in the presence of bony defects [10
]. Sphenoid sinusitis produces very few localizing symptoms or external signs. Thus, sphenoid sinusitis is notoriously difficult to diagnose by routine clinical and radiological examination. Consequently, sphenoid sinusitis is frequently misdiagnosed on presentation; patients are referred initially to clinicians other than otolaryngologists, and the condition is suspected only after the development of complications. The resultant delays in instituting appropriate medical and surgical treatments for sphenoid sinusitis may explain why CST caused by this primary infection appears to have a poorer prognosis than CST caused by other etiologies [4
]. In our case, intra-operative remarks showed that no abnormality was seen in the left sphenoid sinus and the right sphenoid sinus contained pus and was lined with polypoid mucosa. CT showed that the right sphenoid sinus was the dominant sinus, extending posterior to the left sphenoid sinus and lying in contact with both cavernous sinuses. This could perhaps explain the reason for the spread of infection to the left cavernous sinus.
The diagnosis of CST is best established on clinical grounds and confirmed by appropriate radiographic studies. High-resolution contrast-enhanced CT or MRI is useful in the assessment of cases with clinical features of cavernous sinus thrombosis. Contrast-enhanced CT scan may reveal the primary source of infection, thickening of the superior ophthalmic vein, and irregular filling defects in the cavernous sinus [11
]. However, MRI is more sensitive than CT in the detection of septic CST because it can demonstrate details of the blood vessels and provide more multiplanar sections. Direct signs of CST on MRI include changes in signal intensity and in the size and contour of the cavernous sinuses; while indirect signs include dilatation of the tributary veins, exophthalmos, and increased dural enhancement along the lateral border of the cavernous sinuses [12
]. However, the CT and MRI findings may be normal, especially early in the disease course. The imaging evidence of bilateral CST is shown, even when clinical manifestations are limited to one side. In our patient, radiographic examination did not clearly show thrombosis of the cavernous sinus. However, inflammation of the cavernous sinus and dilation of the superior ophthalmic vein were noted by CT and MRI. Sphenoid sinusitis was observed contralaterally. Sphenoid sinusitis was regarded as the cause of CST, due to the predominance of the right sphenoid sinus and its location beneath the cavernous sinus.
The consensus on treatment of septic cavernous sinus thrombosis is that it should include high-dose intravenous antibiotics directed at the most common pathogens associated with the inflammation and surgical drainage of the source of infection in the paranasal sinuses [6
]. Appropriate selection of empirical antimicrobial therapy should also take into account the source of primary infection. Antibiotics should be administered for an extended period, at least two weeks beyond the time of clinical resolution, because bacteria sequestered within the thrombus may not be killed until the dural sinuses have started to recanalize [14
]. Surgery is indicated for drainage of the primary site of infection. Surgical intrusion into the cavernous sinus is difficult and not recommended. If sphenoid or ethmoid sinusitis is documented on CT scans, surgical drainage of these infected pockets should be performed promptly. Endonasal sinus surgery (ESS) is an essential step in the treatment of these patients. The procedure restores the sinuses to their normal physiologic state by providing adequate aeration and restoration of the normal mucociliary flow [15
]. ESS adequately drains the infected sinuses with little morbidity. If the patient cannot withstand general anesthesia, ESS can be performed under local anesthesia. In our case, rapid improvement occurred after ESS and intravenous antibiotics improved the clinical condition without any morbidity. We consider the combination of antibiotics and ESS optimal treatment strategy for CST caused by paranasal sinusitis. However, heparin was administered to the patient, although the use of anticoagulants remains controversial.