Cavernous Sinus Thrombosis

INTRODUCTION

Background: Cavernous sinus thrombosis (CST) was initially described by Bright in 1831 as a complication of epidural and subdural infections. CST is usually a late complication of an infection of the central face or paranasal sinuses. Other causes include bacteremia, trauma, and infections of the ear or maxillary teeth. CST is generally a fulminant process with high rates of morbidity and mortality. Fortunately, the incidence of CST has been decreased greatly with the advent of effective antimicrobial agents.

Pathophysiology: The cavernous sinuses are irregularly shaped, trabeculated cavities located at the base of the skull. The cavernous sinuses are the most centrally located of the dural sinuses and lie on either side of the sella turcica. These sinuses are just lateral and superior to the sphenoid sinus and are immediately posterior to the optic chiasm (see Image 1). Each cavernous sinus is formed between layers of the dura mater, and multiple connections exist between the 2 sinuses.

The cavernous sinuses receive venous blood from the facial veins (via the superior and inferior ophthalmic veins) as well as the sphenoid and middle cerebral veins. They, in turn, empty into the inferior petrosal sinuses, then into the internal jugular veins and the sigmoid sinuses via the superior petrosal sinuses. This complex web of veins contains no valves; blood can flow in any direction depending on the prevailing pressure gradients. Since the cavernous sinuses receive blood via this distribution, infections of the face including the nose, tonsils, and orbits can spread easily by this route.

The internal carotid artery with its surrounding sympathetic plexus passes through the cavernous sinus. The third, fourth, and sixth cranial nerves are attached to the lateral wall of the sinus. The ophthalmic and maxillary divisions of the fifth cranial nerve are embedded in the wall (see Image 1).

This intimate juxtaposition of veins, arteries, nerves, meninges, and paranasal sinuses accounts for the characteristic etiology and presentation of CST.

Staphylococcus aureus accounts for approximately 70% of all infections. Streptococcus pneumoniae, gram-negative bacilli, and anaerobes can also be seen. Fungi are a less common pathogen and may include Aspergillus and Rhizopus species.

Frequency:

• In the US: Occurrence of CST has always been low, with only a few hundred case reports in the medical literature. The majority of these date from before the modern antibiotic era. One review of the English-language literature found only 88 cases from 1940-1988.

Mortality/Morbidity: Prior to the advent of effective antimicrobial agents, the mortality rate from CST was effectively 100%. Typically, death is due to sepsis or central nervous system (CNS) infection. With aggressive management, the mortality rate is now less than 30%. Morbidity, however, remains high, and complete recovery is rare. Roughly one sixth of patients are left with some degree of visual impairment, and one half have cranial nerve deficits.

Race: No predilection

Sex: No predilection

Age: All ages are affected, with a mean of 22 years.