All You Need To Know About Cavernous Sinus Thrombosis

The cavernous sinus is an important anatomical part. When thrombosis occurs in it, this is called cavernous sinus thrombosis. Read on to know about its anatomy, radiology, and tributaries in detail.

Cavernous sinus anatomy and its tributaries

cavernous sinus thrombosis radiology

The right and left cavernous sinuses are trabeculated dural venous sinuses situated on the lateral aspect of the sella turcica, extending from the superior orbital fissure to the petrous apex of the temporal bone. Each cavernous sinus is linked to its counterpart via anterior and posterior intercavernous sinuses that encircle the pituitary gland.

Blood enters the cavernous sinuses from the ophthalmic veins, the superficial middle cerebral veins, inferior cerebral veins and the sphenoparietal sinuses, as well as from the sphenoid sinuses via communicating veins in the intervening bone. The cavernous sinuses drain via emissary veins into the pterygoid venous plexus, and via the inferior and the superior petrosal sinuses draining into the internal jugular vein and the sigmoid sinus respectively. The cavernous sinuses and their connections are devoid of valves, consequently bidirectional spread of infection and thrombi can occur throughout this network.

Infection of the thrombus within the cavernous sinuses cannot be proven in the vast majority of antemortem cases of septic CST, but has been demonstrated in postmortem studies. This Infection could spread via a thrombophlebitis within the veins.

Infection may spread within veins from the primary source to the cavernous sinuses as a contiguous phlebitis/ thrombophlebitis which are trapped within the cavernous sinus.

Bacteria are potent stimulators of thrombosis by mechanisms that include release of coagulative substances or toxins causing tissue damage, and the thrombus itself is an excellent growth medium for bacterial. Bacteria within the deeper layers of the thrombus are shielded from antibiotic penetration by the outer layers of the thrombus that they can subsequently infect.

Etiology of CST

In the early antibiotic era, paranasal sinusitis was responsible for up to 30 per cent of cases of septic CST.1 Although septic CST is now infrequently documented, contemporary reports suggest that a greater proportion of CST is due to sinusitis, and it is possible that this has become the most prevalent aetiology as a result of a disproportionately greater reduction in complicated facial infections. This may be explained by the fact that facial

In sinogenic cases of septic CST, the sphenoid and/ or ethmoid sinuses are almost invariably involved.

This contrasts to an indirect pathway that is more frequently responsible for the intracranial spread of ethmoid sinusitis, notably infection reaching the cavernous sinus via ophthalmic veins after breaching the lamina papyracea. Secondly, sphenoid sinusitis produces very few localizing symptoms or external signs (headache felt in the vertex is uncommon 12 per cent, pain or altered sensation in the distribution of the ophthalmic or maxillary nerves occurs in one third of patients).Thirdly, sphenoid sinusitis is notoriously difficult to diagnose by routine clinical and radiological examination. Consequently, sphenoid sinusitis is frequently misdiagnosed on presentation, is referred initially to clinicians other than rhinologists, and is suspected only

Cavernous sinus thrombosis radiology

radiology of cavernous sinus thrombosis

Radiology CT and MRI are the primary radiological modalities used to confirm the diagnosis that should be suspected on clinical grounds. It should be noted that neither modality is absolutely sensitive or specific for CST, although both have improved with refinements in technology. The greatest advantage of CT and MRI over other more conventional techniques is their safety, particularly in septic patients. Furthermore, as CT and MRI become more sensitive they may be able to confirm the diagnosis unequivocally at an earlier stage than could be achieved on clinical grounds alone. Traditionally, the most sensitive investigation of intracavernous occlusive defects has been venography, either via the orbital or inferior petrosal veins.

Cerebral angiography had also been advocated as the primary confirmatory technique, since it frequently demonstrated abnormal findings such as narrowing or occlusion of the intracavernous segment of the internal carotid artery, and the venous phase images from angiography have shown poor filling of the cavernous sinuses or reversal of normal venous flow at the base of the skull.

However, conventional venography and angiography have several drawbacks; they require iodinated contrast material that can cause dissemination of infection and thrombus extension in patients with septic thrombophlebitis, they are invasive and technically difficult in patients with periorbital inflammation and sepsis, and they are not always reliable (the venous phase images from technically well-performed angiograms demonstrate the cavernous sinuses in only 42 per cent of normal subjects). As a result of these limitations, these older techniques have a limited role in the modern diagnosis of septic CST.

It is important to note that intracavernous filling defects may be observed using any imaging modality in pathologies other than thrombosis. These pathologies include thrombosed intracavernous carotid artery aneurysms, trigeminal neuromas, intracavernous metastases, and cartocio-cavernous fistulas.

Using either CT or MRI, both direct and indirect signs of thrombosis are sought to increase the accuracy for diagnosing CST. Direct signs include expansion of the cavernous sinuses, convex bowing of the lateral wall, abnormal filling defects and asymmetry between each side. Indirect signs relate to concomitant venous obstruction and include

Clinical features of CST

Person suffering from cavernous sinus

An abnormal ENT examination has been reported in 40 per cent, findings include a purulent nasal or posterior pharyngeal discharge, inflamed nasal mucosa and tenderness over the sinuses. However, this is likely to underestimate the incidence of ENT pathology since several cases of sinogenic septic CST have been misdiagnosed antemortem. Eye signs are caused initially by venous congestion within orbital veins as a result of impaired inflow to the thrombosed cavernous sinuses.

As the disease process becomes established, eye signs subsequently develop as a result of neural involvement, and this has been proven unequivocally by evidence of aberrant regeneration of the oculomotor nerve in one case that has survived. Typically, one eye is affected first and more severely in acute presentations of septic CST, and this is followed by signs in the other eye within 48 hours in most cases. Chemosis, periorbital oedema and proptosis are the most consistent (95 per cent) and visible features of septic CST.

Impaired ocular motility invariably occurs and has different mechanisms; mechanical restriction caused by venous congestion of orbital tissues, extraocular muscle inflammation and infection, and inflammatory involvement of the oculomotor, trochlea, and abducent nerves within the orbit and cavernous sinus.

Gaze paresis may develop sequentially, with lateral gaze being affected initially and most severely. This may be explained by the susceptibility of the abducent nerve to intracavernous pathology because of its intraluminal course. The trochlear nerve is affected least in septic CST, which may be explained by the fact that this nerve lies outside the muscle cone in the orbit, hence is spared from mechanical damage from muscle inflammation and orbital pressure.