What Is Cavernous Sinus Thrombosis?

Cavernous sinus is a complex anatomical structure that can cause diverse and changeable symptoms and signs clinically. In order to better understand the clinical characteristics and differential diagnosis of this disease, the anatomy of cavernous sinus is briefly introduced first. The cavernous sinus is located on both sides of the sphenoidal saddle and is composed of a multi-spaced epidural space called the cavernous sinus venous plexus. The two sides communicate with each other, and communicate with the intracranial dural sinus and the facial deep vein plexus. The cavernous sinus contains many important structures. The inside is the S-shaped internal carotid artery siphon, and the outside is the III, IV, 1, 2, and pairs of cerebral nerves. The cavernous sinus receives blood from the superior eye vein, inferior eye vein, and sphenopalatine sinus, and is introduced into the superior or inferior petrosal sinus.

Cavernous sinus thrombosis

Cavernous sinus thrombosis (CST) was first described by Duncan as early as 1821. It is a rare and fatal infectious disease of the central nervous system (CNS). The mortality rate can reach 80% before the application of antibiotics. Delays, etc., still cause 13.6% of patients to die. Therefore, early diagnosis and intensive treatment are very important.

Anatomy of cavernous sinus thrombosis

Cavernous sinus thrombosis etiology and pathogenesis

Cavernous sinus thrombosis is often caused by otogenic, sinus and orbital facial purulent infections (such as otitis media, mastoiditis, sinusitis) and systemic infections, rarely due to non-infectious diseases such as tumors, trauma, and arteriovenous malformation. Cause. CST on one or both sides can also spread from other dural sinus infections. Suppurative thrombosis often involves the cavernous sinus on one side at the beginning of the disease, which can quickly spread to the contralateral side through the ring sinus.

Clinical manifestations of cavernous sinus thrombosis

Cavernous sinus suppurative thrombosis usually develops rapidly, with high fever, orbital pain, and orbital tenderness, often with severe headaches, nausea, and vomiting, and can cause disturbances of consciousness. Obstruction of venous return of the eye causes bulbar conjunctival edema, protruding eyeballs on the affected side, inability to close the eyelids, and redness and swelling of the soft tissue around the eye. Eye movements are often affected simultaneously with the first branch of the trigeminal nerve, sometimes the second branch of the trigeminal nerve; drooping eyelids, restricted eye movements, eyeball fixation and diplopia, etc., and sometimes eyelids can make the eyelids droop. obvious.

Patients may be complicated by meningitis and brain abscess. If the internal carotid artery cavernous sinus segment has inflammatory changes and thrombosis, there may be carotid tenderness, contralateral central hemiplegia, and hemiplegia. Such as spreading to the pituitary can cause abscesses and necrosis, resulting in disturbances of water and electrolyte metabolism. Cerebrospinal fluid (CSF) examination showed increased white blood cells.

If the thrombus progresses rapidly due to the suppurative emboli and the deep cerebral veins or cerebellar veins are involved, the patient may be in a coma.

Fungi are the most common pathogen (55.6%). If the patient is too old or the child is too young, the prognosis is poor, and the mortality rate in hospitalized cases can be as high as 44.4% [6]. If thrombosis revascularizes, the condition may ease. CST has a high mortality rate and a low blood culture positive rate. Therefore, the possibility of fungal CST should be considered in immunocompromised patients with eyes complaining from one eye to the other. Magnetic resonance imaging (MRI) or coronal thin-layer contrast-enhanced CT (CECT) can confirm the diagnosis.

Diagnosis and differential diagnosis of cavernous sinus thrombosis

Cavernous sinus thrombosis diagnosis

Purulent or septic CST is a life-threatening disease that requires immediate diagnosis and evaluation, but its early clinical manifestations are often non-specific and the sensitivity of conventional axial thick slice CT scans (layer thickness 10 mm) on the head is low. . Therefore, the doctor's high alertness to this disease is important for clinical diagnosis. First, cavernous sinus disease should be determined based on the patient's typical clinical symptoms and signs: Patients often show numbness in the first branch of the trigeminal nerve with diplopia or periorbital pain. Cavernous sinus syndrome can be diagnosed if there is also exophthalmos, bulbar conjunctival edema, headache, and fever. Second, combined with pyogenic infections such as otitis media, mastoiditis, and sinusitis, other dural sinus infections or a history of systemic infections, clinical symptoms such as headache, vomiting, ophthalmoplegia, diplopia and disturbance of consciousness, and MRI or CECT Neuroimaging findings can diagnose cavernous sinus thrombosis.

CST ocular muscle palsy is characterized by oculomotor nerve palsy which can be painful or painless, mostly partial dysfunction, pupils can be affected or uninvolved, pupil dilation can occur, photoreaction disappears, with or without IV, 1, Cerebral nerve palsy, Horner sign can also occur. Optic nerves are less affected, vision is normal or moderately reduced, occasional oedema of the optic papillae, and bleeding may occur around the fundus.

Outer rectus paralysis should be distinguished from other possible causes. Abductive neuropathy in elderly patients is often idiopathic or caused by vascular disease or diabetes, but the rate of red blood cell sedimentation should be tested to rule out rare giant cell arteritis. Skull base radiology can exclude nasopharyngeal carcinoma or other tumors. Patients with painless abduction nerve paralysis, if the above examination is normal, without other systemic and neurological symptoms, and intracranial pressure does not increase, conservative treatment can be followed up. Try prednisone (60 mg / d orally for 5 consecutive days). If the symptoms of painful abductive nerve palsy are significantly reduced, supraorbital fissure (superior orbital fissure syndrome) or idiopathic cavernous sinus inflammation (Tolosa- Hunt syndrome); if the pain persists after steroid treatment, cavernous sinus should be examined by MRI or CECT, and digital subtraction angiography (DSA) should be performed if necessary.

Differential diagnosis of cavernous sinus thrombosis

Attention should be paid to the identification of arteriovenous fistula, tumor, cavernous sinus infection, diabetic ophthalmoplegia, painful ophthalmoplegia and malignant exophthalmos.

2.1 Cavernous sinus thrombosis 2.1

Internal carotid cavernous sinus fistula Carotid-cavernous fistula (CCF) is the direct communication between the internal carotid cavernous sinus and the venous cavernous sinus. It is the most common traumatic arteriovenous fistula and can occur. After closed head trauma or skull base fracture. Clinical manifestations are pulsatile exophthalmos, ophthalmoplegia, and conjunctival congestion, orbital murmurs can be heard, and carotid exophthalmos can be relieved. A MRI of the head often confirms the diagnosis, and carotid angiography is an optional test. The internal carotid artery siphon aneurysm can cause oculomotor nerve palsy and rupture can cause carotid cavernous sinus fistula.

2.2 Cavernous sinus thrombosis 2.2

Tumors such as cavernous sinus meningiomas, schwannomas (most commonly trigeminal schwannomas), and pituitary adenomas (usually painless, non-invasive lesions that slowly expand and erode the bony saddle can expand into the cavernous sinus), in addition It also includes orbital tumors, other tumors in the sphenoid region, and metastases. For example, chordomas are usually benign and grow slowly, but there are also invasive types, which easily erode the skull base and cavernous sinus. Oculomotor nerve palsy is common, followed by cerebral nerve palsy of , , and ; MRI examination of T2WI is common. The signal can be slightly enhanced, often accompanied by calcification. If the pain is severe, it may indicate an aneurysm dilatation, such as progressive oculomotor nerve palsy, especially causing dilation of the pupil, which may be signs of dilatation of a posterior communication aneurysm, or may reflect increased intracranial pressure and early cerebral hernia.

2.3 Cavernous sinus thrombosis 2.3

Cavernous sinus infections and inflammatory osteomyelitis can be fatal complications of immunocompromised states, diabetes, mastoiditis, and paranasal sinus infections. Patients with diabetes and other immune system deficiencies can present painless infections involving the cavernous and sagittal sinus areas. Nonspecific diplopia and headache in diabetic patients should be considered fungal or other types of infection. Fungal infections such as Candida albicans and Cryptococcus neoformans in immunocompromised patients often cause cavernous sinus thrombosis. Cavernous sinus can also be affected by retrobulbar cellulitis or abscess spread. These patients usually have signs of infection and severe pain during eye movements, and are at high risk of involving the optic nerve.

2.4 Cavernous sinus thrombosis 2.4

Diabetic ophthalmoplegia is usually isolated with saccades, tackles, or abduction nerves. CT or MRI examinations are usually normal. Ocular neuropathy is characterized by pupil avoidance, with or without pain. Uninvolved pupils are often caused by infarction of the contractile fibers surrounding the pupil due to a central infarct.

2.5 Cavernous sinus thrombosis 2.5

Painful ophthalmoplegia can occur in CST, but it must be distinguished from other lesions of cavernous sinus such as Tolosa-Hunt syndrome, primary or metastatic tumor, carotid-cavernous sinus fistula, and aneurysm. Tolosa-Hunt syndrome is idiopathic granulomatous inflammation that affects cavernous sinus, which is mainly manifested as ophthalmoplegia, diplopia with postocular pain [3]. CST must also be distinguished from orbital lesions such as orbital pseudotumor, sinusitis, tumors (primary or metastatic), and infections (bacteria or fungi). Unlike cavernous sinus disease, orbital diseases involving the oculomotor nerve are often associated with optic nerve involvement and exophthalmos. Orbital lesions and cavernous sinus lesions are sometimes difficult to distinguish clinically, with the help of MRI or CECT [2]. Attention should be paid to the inspection and palpation of the exophthalmos (to help determine the orbital or anterior cavernous sinus lesions), auscultation of the eyeball murmur (to determine the carotid- cavernous sinus fistula), and evaluation of diabetes. Tolosa-Hunt syndrome responds well to oral corticosteroids such as prednisone 60-100 mg / d.

2.6 Cavernous sinus thrombosis 2.6

Diplopia Differential CST can occur with diplopia. Common eye movement, tackle, abduction, and trigeminal nerve are common in the first branch, and sometimes the second branch is affected at the same time. There are many causes of diplopia, and the following signs can help locate the disease and determine the cause.

Possible diagnostic features

Anterior cavernous sinus disease, supraorbital fissure syndrome, ophthalmoplegia, Horner syndrome, impaired V1 sensation

Posterior cavernous sinus lesions Ophthalmoplegia, Horner syndrome, V1, V2, and / or V3 impaired sensation

Duane retraction syndrome (Duane retraction syndrome) narrowing of blepharoplasty during adduction and abduction

Myasthenia gravis, eyelid or extraocular muscle fatigue, cervical flexor and bulbar muscle weakness

Cavernous sinus thrombosis treatment

Special treatment for cavernous sinus thrombosis

Because CST is a fatal disease, early diagnosis and timely treatment are very important. Unlike cerebral venous sinus thrombosis, which is usually treated with anticoagulation, thrombolysis and antiplatelet aggregation, CST is an infectious disease and should be used in combination at an early stage. If the results of pathogen culture and drug sensitivity tests can be obtained, the original protocol can be optimized ; But because the blood culture positive rate is very low, large doses of broad-spectrum antibiotics can usually be used. Some third-generation cephalosporins, nafcillin, methicillin, and vancomycin are more penetrating, while aminoglycosides are less effective. Many foreign CST case reports have confirmed that the infection is Streptococcus pneumoniae, which is effective in the penicillin family. Three generations of cephalosporins such as cefotaxime sodium (6 g / d for adults) or ceftriaxone sodium (2 to 4 g / d for adults) are available. The course of antibiotic application can be determined according to the clinical response and dynamic changes of neuroimaging of the patient, and generally should not be less than 4 weeks.

In a recent case report of 9 cases of septic CST, 5 (55.6%) were confirmed to be fungal infections, and the primary infections were sinusitis, of which 3 were Zygomycete and Aspergillus One case and one case of undetermined fungus were confirmed by sinus biopsy [6]. Despite a clear etiology and antifungal treatment, 3 of the 5 died.

Anticoagulation therapy should be applied with caution. A recently reported case of CST-induced non-aneurysmal subarachnoid hemorrhage in the mesencephalic cistern, due to the application of low-molecular-weight heparin (2 mg / kg · d) to treat cavernous sinus thrombosis, a large amount of intracranial hemorrhage occurred after 1 week .

Symptoms of cavernous sinus thrombosis

For the increase of intracranial pressure and cerebral edema, dehydration and intracranial pressure can be applied. Attention should also be paid to maintaining the balance of water, electrolytes and acid-base.