eMedicine Specialties > Emergency Medicine > Neurology

Cavernous Sinus Thrombosis

Author: Rahul Sharma, MD, MBA, Instructor in Medicine, Weill Medical College of Cornell University; Consulting Staff, Department of Emergency Medicine, New York Presbyterian Hospital-Weill Cornell Medical Center
Coauthor(s): Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Contributor Information and Disclosures

Updated: Jul 18, 2008

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

United States

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.

Clinical

History

The early signs and symptoms of cavernous sinus thrombosis (CST) may not be specific. A patient who presents with headache and any cranial nerve findings should be potentially evaluated for CST. The most common signs of CST are related to the anatomical structures affected within the cavernous sinus (see Image 1).

• Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days. In as many as 25% of cases in which a furuncle is the precipitant, it will have been manipulated in some fashion (eg, squeezing, surgical incision).
• Headache is the most common presentation symptom and usually precedes fevers, periorbital edema, and cranial nerve signs. The headache is usually sharp, increases progressively, and is usually localized to the regions innervated by the ophthalmic and maxillary branches of the fifth cranial nerve.
• In some patients, periorbital findings do not develop early on, and the clinical picture is subtle.
• As the infection tracts posteriorly, patients complain of orbital pain and fullness accompanied by periorbital edema and visual disturbances.
• Without effective therapy, signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. Eye swelling begins as a unilateral process and spreads to the other eye within 24-48 hours via the intercavernous sinuses. This is pathognomonic for CST.
• The patient rapidly develops mental status changes including confusion, drowsiness, and coma from CNS involvement and/or sepsis. Death follows shortly thereafter.

Physical

Other than the findings associated with the primary infection, the following signs are typical:

• Periorbital edema may be the earliest physical finding.
  • Chemosis results from occlusion of the ophthalmic veins.
  • Lateral gaze palsy (isolated cranial nerve VI) is usually seen first since CN VI lies freely within the sinus in contrast to CN III and IV, which lie within the lateral walls of the sinus.
  • Ptosis, mydriasis, and eye muscle weakness from cranial nerve III dysfunction
• Manifestations of increased retrobulbar pressure follow.
  • Exophthalmos
  • Ophthalmoplegia
• Signs of increased intraocular pressure (IOP) may be observed.
  • Pupillary responses are sluggish.
  • Decreased visual acuity is common owing to increased IOP and traction on the optic nerve and central retinal artery.
• Hypoesthesia or hyperesthesia in dermatomes supplied by the V1 and V2 branches of the fifth cranial nerve
• Appearance of signs and symptoms in the contralateral eye is diagnostic of CST, although the process may remain confined to one eye.
• Meningeal signs, including nuchal rigidity and Kernig and Brudzinski signs, may be noted.
• Systemic signs indicative of sepsis are late findings. They include chills, fever, shock, delirium, and coma.

Causes

• Most cases of septic CST are due to an acute infection in an otherwise healthy individual. However, patients with chronic sinusitis or diabetes mellitus may be at a slightly higher risk.
• The causative agent is generally Staphylococcus aureus, although streptococci, pneumococci, and fungi may be implicated in rare cases.

• Search for CME/CE on This Topic »

• Sinusitis, Frontal, Acute, Surgical Treatment (Otolaryngology and Facial Plastic Surgery)
• Cerebral Venous Thrombosis (Neurology)
• Drainage, Nasal Septal Hematoma (Clinical Procedures)
• Hyponatremia (Pediatrics: Cardiac Disease and Critical Care Medicine)

• Multiple Cranial Neuropathies
• Diagnosing Ophthalmoplegic Migraine
• Common Ophthalmic Emergencies