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 cavernous Sinus Thrombosis

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مُساهمةموضوع: cavernous Sinus Thrombosis   الإثنين يناير 03, 2011 10:05 am

Cavernous sinus thrombosis

Cavernous sinus thrombosis (CST) was initially described by Bright in 1831 as a complication of epidural and subdural infections. The dural sinuses are grouped into the sagittal, lateral (including the transverse, sigmoid, and petrosal sinuses), and cavernous sinuses. Because of its complex neurovascular anatomic relationship, cavernous sinus thrombosis is the most important of any intracranial septic thrombosis.1 Cavernous sinus thrombosis 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. Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. Fortunately, the incidence of cavernous sinus thrombosis has been decreased greatly with the advent of effective antimicrobial agents.


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, as depicted in the image below. Each cavernous sinus is formed between layers of the dura mater, and multiple connections exist between the 2 sinuses.
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Anatomy of cross section of cavernous sinus showing close proximity to cranial nerves and sphenoid sinus.

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, as depicted in the image above.

This intimate juxtaposition of veins, arteries, nerves, meninges, and paranasal sinuses accounts for the characteristic etiology and presentation of cavernous sinus thrombosis (CST). CST is more commonly seen with sphenoid and ethmoid and to a lesser degree with frontal sinusitis.

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.


United States

Occurrence of cavernous sinus thrombosis (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.


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. These mortality and morbidity rates may be due to delayed diagnosis without prompt surgical drainage and antibiotic administration.


No predilection


No predilection


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



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, as depicted in the image below.

[ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذا الرابط]

Anatomy of cross section of cavernous sinus showing close proximity to cranial nerves and sphenoid sinus.

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).
The clinical presentation is usually due to the venous obstruction as well as impairment of the cranial nerves that are near the cavernous sinus.
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.
Some cases of CST may present with focal cranial nerve abnormalities possibly presenting similar to an ischemic stroke.2
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.

Other than the findings associated with the primary infection, the following signs are typical for cavernous sinus thrombosis:

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.3
Ptosis, mydriasis, and eye muscle weakness from cranial nerve III dysfunction
Manifestations of increased retrobulbar pressure follow.
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.

Most cases of septic cavernous sinus thrombosis (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.

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مُساهمةموضوع: رد: cavernous Sinus Thrombosis   الأحد يناير 09, 2011 10:33 pm

An interesting topic !


Thank you so so much


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مُساهمةموضوع: رد: cavernous Sinus Thrombosis   السبت فبراير 26, 2011 9:22 pm

زهرة البفسج

Thank you for these precious information

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cavernous Sinus Thrombosis
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