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Cavernous Sinus Thrombosis

Cavernous sinus thrombosis (CST) is an uncommon clinical condition caused by blood clot formation that obstructs the cavernous cavity. It is mostly caused by an infection with high morbidity and mortality rate. Imaging techniques and laboratory tests are used for diagnosing this condition.


Presentation

The presentation of CST may be acute or sub-acute. Most patients show symptoms of fever, headache, exophthalmia, periorbital edema and sometimes with chemosis. Most of the patients usually have external ophthalmoplegia, which results from the venous congestion of eye tissues, inflammation of body organ including extra-ocular muscle and/or cranial nerves III, IV and VI [7]. Also, the patient may present with eyelid erythema, autonomic nervous system dysfunction, papilledema (optic nerve swelling) pupillary defects and changes in sensory nerve distribution particularly in the ophthalmic or maxillary trigeminal region [7] [8]. Although vision loss may be rare since the orbital nerve is located externally to cavernous sinus, it can develop through other pathophysiological mechanisms such as internal carotid artery occlusion (ICA), ophthalmic (central) retinal arteries obstructions, orbital congestion and arteritis [7]. If not diagnosed early , CST which affects one eye may spread to the other within 24-48 hours [9].

Fever
  • Following this, she developed a fever and a protruding right eye, and septic cavernous sinus thrombosis was diagnosed. This complication had never been reported in a patient with systemic lupus erythematosus, and related literature is reviewed.[ncbi.nlm.nih.gov]
  • A 56-year-old woman was admitted because of a high fever, right ptosis, chemosis, proptosis and ocular muscle palsy. Cranial MRI revealed a cavernous sinus thrombosis and a subarachnoid abscess.[ncbi.nlm.nih.gov]
  • The diagnosis of SCST was suspected and rapidly confirmed based on high fever, dramatic and typical signs of left cranial nerve paralysis and the result of digital subtraction angiography after the onset of the disease.[ncbi.nlm.nih.gov]
  • Then following an upper respiratory tract infection, headache, bilateral periorbital pain and swelling, spiking fever, neck stiffness, bilateral chemosis and ophthalmoplegy developed.[ncbi.nlm.nih.gov]
  • A previously healthy 14-year-old boy developed headache, stiff neck, fever, diplopia, right proptosis, and right complete sixth and partial third cranial nerve palsies. Orbital CT showed features of pansinusitis and orbital fat stranding.[ncbi.nlm.nih.gov]
Chills
  • .  Pyrexia  Rapid, weak, thready pulse  Chills and sweats  Delirium - meningitis supervenes terminally  Septic emboli to various other parts of body. 15.  Proptosis (first oedema & chemosis)  Oedema of eyelids and bridge of nose  Dilatation and[slideshare.net]
  • A day after, he started having high-grade fever, not associated with chills or rigors. This was followed by progressive swelling of the upper and lower lids of the left eye for 3 days.[ijo.in]
  • These complications can include: meningitis – an infection of the outer protective layer of the brain that can cause symptoms such as a stiff neck, mental confusion and sensitivity to light sepsis or blood poisoning – this can cause symptoms such as chills[beaconmedicalgroup.nhs.uk]
  • They include chills, fever, shock, delirium, and coma. Causes Most cases of septic cavernous sinus thrombosis (CST) are due to an acute infection in an otherwise healthy individual.[emedicine.medscape.com]
Rigor
  • A day after, he started having high-grade fever, not associated with chills or rigors. This was followed by progressive swelling of the upper and lower lids of the left eye for 3 days.[ijo.in]
  • Less common symptoms may include rigors, stiff neck, facial numbness, confusion, seizures, stroke symptoms, or coma.[ncbi.nlm.nih.gov]
  • A day after, she started having high-grade fever associated with chills or rigors. This was followed by progressive swelling and redness of both eyelids in the right eye with proptosis and opthalmoplegia developing subsequently.[ispub.com]
Nausea
  • In cyclophosphamide therapy, there can be some side effects such as nausea, vomiting, and infection. We report on a case receiving a combination of high dose steroid and intravenous cyclophosphamide.[ncbi.nlm.nih.gov]
  • She presented with fever, nausea without vomiting, frontal headache, bilateral ptosis and swelling, double vision, a partial loss of visual acuity in the left eye, and restricted lateral ocular movements.[ncbi.nlm.nih.gov]
  • The headaches are sharp shooting and severe in nature accompanied by fever and nausea. As the sinus lies proximal to few cranial nerves, neurological disturbances may be experienced.[healthtipsandguides.net]
  • These are generally mild and can include diarrhoea, nausea and a skin rash. Anticoagulants You may also be given a medication called heparin to help dissolve the clot and prevent further clots.[nhs.uk]
  • Patients may present with fever, headache, nausea and vomiting, proptosis, chemosis, ophthalmoplegia, papilledema, diplopia, and mental status changes.[neurologyindia.com]
Vomiting
  • In cyclophosphamide therapy, there can be some side effects such as nausea, vomiting, and infection. We report on a case receiving a combination of high dose steroid and intravenous cyclophosphamide.[ncbi.nlm.nih.gov]
  • She presented with fever, nausea without vomiting, frontal headache, bilateral ptosis and swelling, double vision, a partial loss of visual acuity in the left eye, and restricted lateral ocular movements.[ncbi.nlm.nih.gov]
  • Other signs/symptoms include evidence of intracranial hypertension (vomiting, papilledema, visual disturbances), neurologic deficits, seizures, and coma.[shmabstracts.com]
  • Patients may present with fever, headache, nausea and vomiting, proptosis, chemosis, ophthalmoplegia, papilledema, diplopia, and mental status changes.[neurologyindia.com]
  • , Neonatal Vomiting , Nephrology Renal , Nerve Block , Neurologic , Newborn Rashes , Nonoperative Management , Non Purulent Infection , nose , nosebleeds , Nuchal Rigidity , Nursemaids Elbow , Omphalitis , oncology , Oral , Osteoarthritis , Otitis Externa[hippoed.com]
Chemosis
  • A 56-year-old woman was admitted because of a high fever, right ptosis, chemosis, proptosis and ocular muscle palsy. Cranial MRI revealed a cavernous sinus thrombosis and a subarachnoid abscess.[ncbi.nlm.nih.gov]
  • Then following an upper respiratory tract infection, headache, bilateral periorbital pain and swelling, spiking fever, neck stiffness, bilateral chemosis and ophthalmoplegy developed.[ncbi.nlm.nih.gov]
  • A 46-year-old white woman presented to our emergency room with proptosis, ophthalmoplegia, and conjunctival chemosis of her left eye. An ophthalmologist, having diagnosed orbital cellulitis in her left eye, suspected a cavernous sinus thrombosis.[ncbi.nlm.nih.gov]
  • A 33-year-old female visited our hospital for severe, right-sided, temporal headache, chemosis, periorbital edema, and proptosis.[ncbi.nlm.nih.gov]
  • A 25-year-old male with a history of a nasal furuncle presents with an acute onset of fixed and dilated pupils, bilateral exophthalmos, hemorrhagic chemosis, elevated intraocular pressures, restricted extraocular motility, and unresponsiveness.[ncbi.nlm.nih.gov]
Eye Pain
  • When to see your GP Contact your GP if you experience a persistent and severe headache you haven't had before, or if you develop eye pain or swelling of one or both eyes.[nhs.uk]
  • Calling your health care provider Call your doctor right away if you have: Bulging of your eyes Drooping eyelids Eye pain Inability to move your eye in any particular direction Vision loss[coordinatedhealth.com]
  • Call your health care provider right away if you have: Bulging of your eyes Drooping eyelids Eye pain Inability to move your eye in any particular direction Vision loss Durand ML. Periocular infections. In: Bennett JE, Dolin R, Blaser MJ, eds.[medlineplus.gov]
Periorbital Edema
  • A 33-year-old female visited our hospital for severe, right-sided, temporal headache, chemosis, periorbital edema, and proptosis.[ncbi.nlm.nih.gov]
  • Headache is the most common presentation symptom and usually precedes fevers, periorbital edema, and cranial nerve signs.[emedicine.medscape.com]
  • Most patients show symptoms of fever, headache, exophthalmia, periorbital edema and sometimes with chemosis.[symptoma.com]
  • Case report A 33-year-old female visited our hospital for severe, right-sided, temporal headache, chemosis, periorbital edema, and proptosis.[head-face-med.biomedcentral.com]
  • His exam was significant for profound bilateral periorbital edema with significant chemosis, drainage, and overlying erythema. (Figure 1.) The right eye was impossible to examine because of significant swelling.[journals.lww.com]
Diplopia
  • An allograft recipient is described who presented with diplopia and developed CST in the early post-transplant period likely caused by a filamentous fungus.[ncbi.nlm.nih.gov]
  • A previously healthy 14-year-old boy developed headache, stiff neck, fever, diplopia, right proptosis, and right complete sixth and partial third cranial nerve palsies. Orbital CT showed features of pansinusitis and orbital fat stranding.[ncbi.nlm.nih.gov]
  • The patient had experienced in the past 6 months intermittent diplopia and an irreducible conjunctival hyperemia. Hemodilution was dismissed. Soon after initiation of anticoagulation therapy, the patient's clinical signs and symptoms improved.[ncbi.nlm.nih.gov]
  • The most frequent initial symptom was headache (66.7%), followed by ophthalmic complaints (diplopia or ophthalmoplegia, 55.6%; blurred vision or blindness, 55.6%), and ptosis (44.4%). Initial cranial images failed to identify CTS in all patients.[ncbi.nlm.nih.gov]
  • Patients may present with fever, headache, nausea and vomiting, proptosis, chemosis, ophthalmoplegia, papilledema, diplopia, and mental status changes.[neurologyindia.com]
Retinal Hemorrhage
  • Papilledema , retinal hemorrhages , and decreased visual acuity and blindness may occur from venous congestion within the retina. Fever , tachycardia and sepsis may be present. Headache with nuchal rigidity may occur.[en.wikipedia.org]
  • .  Proptosis (first oedema & chemosis)  Oedema of eyelids and bridge of nose  Dilatation and tortuosity of retinal veins  Retinal hemorrhages  Involvement of the contralateral eye – (48 hours)  When pterygoid plexus is occluded along with sinus,[slideshare.net]
  • These include periorbital edema (initially unilateral but typically bilateral), lid erythema, chemosis, ptosis, proptosis (due to impaired venous drainage of orbit), restricted or painful eye movement, and less commonly papilledema, retinal hemorrhages[ncbi.nlm.nih.gov]
  • Bilateral papilloedema with retinal hemorrhages in association with cerebral venous sinus thrombosis and paroxysmal nocturnal hemoglobinuria.[academic.oup.com]
Epistaxis
  • Elderly , Emergency Care , Emergency Department , Emergency Department Recidivism , Emergency Department Visit , Emergent Surgical Conditions , Employment , EM/Surgery , endocrine , endometriosis , ENT (systems based) , Envenomation , Epidemiology , epistaxis[hippoed.com]
Headache
  • We report a case of cavernous sinus thrombosis in a 55-year-old Chinese man who presented with headache, ophthalmoplegia and ptosis. Campylobacter rectus was eventually isolated from the blood cultures.[ncbi.nlm.nih.gov]
  • The patient developed headache, rapidly progressive ophthalmoplegia, and signs of orbital congestion. After 2 days of ineffective broad spectrum antibiotic therapy he underwent a second transsphenoidal craniotomy for abscess drainage.[ncbi.nlm.nih.gov]
  • Then following an upper respiratory tract infection, headache, bilateral periorbital pain and swelling, spiking fever, neck stiffness, bilateral chemosis and ophthalmoplegy developed.[ncbi.nlm.nih.gov]
  • A 55-year-old man reported a severe headache of 3 days' duration, left ptosis and left lid swelling before examination.[ncbi.nlm.nih.gov]
  • Clinical symptoms of headache and retro-orbital pain out of proportion to clinical signs on presentation prompted a suspicion of something beyond sinusitis and raised the clinical suspicion of cavernous sinus involvement.[ncbi.nlm.nih.gov]
Meningism
  • Although Staphylococcus aureus (S aureus) is the most common bacterial pathogen causing CST, it is infrequent as a cause of meningitis.[ncbi.nlm.nih.gov]
  • A case of cavernous sinus thrombosis is usually a complication of severe orbital cellulitis and meningitis. The authors reported a retrograde cavernous sinus thrombosis and orbital cellulitis in an immunocompetence child, due to meningitis.[ncbi.nlm.nih.gov]
  • Although Staphylococcus aureus is the most common pathogen causing septic cavernous sinus thrombosis [CST], it is an uncommon cause of meningitis.[ncbi.nlm.nih.gov]
  • We describe our experience in the management of this case of anaerobic meningitis and the unusual complication of ischemic stroke; this case suggests that more aggressive therapy in addition to empirical antibiotics may be warranted.[ncbi.nlm.nih.gov]
  • He had fulminant staph bacteraemia (as evidenced by persistently positive blood cultures) with meningitis and cerebral abscess. Extensive search was made to find the source of infection, but it was inconclusive.[ncbi.nlm.nih.gov]
Seizure
  • Altered mental status that can range from confusion to coma Bouble vision and seizures are rare.[webmd.com]
  • Other signs/symptoms include evidence of intracranial hypertension (vomiting, papilledema, visual disturbances), neurologic deficits, seizures, and coma.[shmabstracts.com]
  • A few complications associated with Cavernous Sinus Thrombosis include: Seizures Permanent loss of vision Meningitis: Infection that occurs in the outer protective layers of the brain Sepsis: Systemic spread of infection Death may occur if the condition[dovemed.com]
  • Focal neurological signs and/or seizures may also occur 5 . Isolated CN III palsy is thought to be an early manifestation.[radiopaedia.org]
  • […] and irritation in and around both eyes Drooping eyelids Bulging of eyes Photophobia (discomfort or pain in eyes from exposure to light) Inability to move the eye or eyes High fever Pain or numbness in the face or eyes Loss of vision, or double vision Seizures[parashospitals.com]
Confusion
  • Despite the use of the term sinus the cavernous sinuses should not be confused with the maxillary or frontal sinuses, which can be affected by sinusitis.[irishhealth.com]
  • […] by tearing Swelling, redness, or irritation around one or both eyes Drooping eyelids Inability to move the eye High fever Pain or numbness around the face or eyes Fatigue Vision loss or double vision Seizures Altered mental status that can range from confusion[webmd.com]
  • Dizziness, confusion and delirium are experienced in advanced stages and if left untreated it can lead to coma and eventual death. Cavernous Sinus Thrombosis Causes The main cause of cavernous thrombosis is spread of infection form facial region.[healthtipsandguides.net]
  • Decreased level of consciousness, confusion, seizures, and focal neurologic deficits are signs of CNS spread.[merckmanuals.com]
  • […] blurred vision difficulty moving the eyes drooping of the eyelids Other symptoms Other symptoms of cavernous sinus thrombosis include: a high temperature of 38C (100.4F) or above vomiting seizures (fits) changes in mental state, such as feeling very confused[beaconmedicalgroup.nhs.uk]
Papilledema
  • Patients with severe papilledema may develop permanent vision deficits without treatment. Importantly, head CT is normal in up to 30% of cases.[shmabstracts.com]
  • Symptoms and signs include pain, proptosis, ophthalmoplegia, vision loss, papilledema, and fever. Diagnosis is confirmed by CT or MRI. Treatment is with IV antibiotics. Complications are common, and prognosis is poor.[merckmanuals.com]
  • Also, the patient may present with eyelid erythema, autonomic nervous system dysfunction, papilledema (optic nerve swelling) pupillary defects and changes in sensory nerve distribution particularly in the ophthalmic or maxillary trigeminal region.[symptoma.com]
  • Papilledema , retinal hemorrhages , and decreased visual acuity and blindness may occur from venous congestion within the retina. Fever , tachycardia and sepsis may be present. Headache with nuchal rigidity may occur.[en.wikipedia.org]
  • Patients may present with fever, headache, nausea and vomiting, proptosis, chemosis, ophthalmoplegia, papilledema, diplopia, and mental status changes.[neurologyindia.com]

Workup

In patients with septic CST, most clinical signs and symptoms develop rapidly and may assist in establishing the diagnosis of the condition. The onset of the disease condition may present with nonspecific features which may require optical and neurological investigations to establish the diagnosis. However, some of the common symptoms seen early in CST patient include, fever, conjunctival edema, periorbital edema, exophthalmos. These observable changes are due to venous congestion or occlusion of the sinus related to the cavernous sinus. The involvement of the cranial nerves may result into painful, external ophthalmoplegia and ptosis. Also, a mid-size mydriasis may be observed due to the relatedness of the sympathetic nervous system with the cavernous sinus resulting into internal ophthalmoplegia which causes blunted pupillary response of the patient to light. Cranial nerve (CN) VI is covered by a fibrous membrane laterally to the wall of cavernous causing CN IV to be prone to intra-cavernous pathological effect. Therefore, lateral gaze palsy development may precede ophthalmoplegia with a decrease in corneal reflex due to the position of the cranial nerve VI.

The sequential spread of the disease to both eyes usually indicates CST although, previously observed signs and symptoms may assist in establishing the diagnosis. These include identification of the primary route of infection, sepsis, visual defect, pupillary dysfunction and features of meningismus (photophobia and nuchal rigidity). The ophthalmoscopy examination may reveal papilloedema, retinal vein dilatation, hyperesthesia or hypoaesthesia in the arrangement of ophthalmic nerve including the maxillary. Most often, these features are not common in periorbital and orbital cellulitis, which are often misdiagnosed as CST. 50% of the affected population develop visual loss due to corneal ulceration resulting from proptosis, papilloedema, and corneal reflex loss. Also, occlusion or obstruction of the internal carotid artery, ophthalmic artery, central retinal artery, orbit cavity congestion or embolism may cause impaired vision. The seizure usually occurs as a complication of septic CST due to intracranial suppuration. Rarely, patients with septic CST can manifest milder symptoms, with gradual cranial nerve dysfunction and reduced clinical manifestation of sepsis or ocular defects. A unilateral isolated form of lateral gaze palsy is usually the initial sign of subacute septic CST which may later transform into the bilateral form. The mechanism behind these presentation shows that a slow progressive destruction of the cavernous sinus results in an increased compensation during rapid venous occlusion. The previous study postulated this phenomenon when there is an infection spread into the cavernous sinus through retrograde pathway such as otogenic infection which is commonly seen before the development of antibiotics [9].The pattern of disease development in aseptic CST is similar to the acute septic form but may be slower and less complex. Although, it may sometimes be difficult to differentiate between septic and subacute, aseptic CST, however, the most clinical feature of sepsis and primary infection are not commonly seen. Most often, aseptic CST is usually related to known predisposing factors which include, hypercoagulability syndrome, sinus surgery history, and neoplasms.

Septic CST may be diagnosed adequately with clinical findings, however, when there is co-existence of other diseases such as meningitis or orbital infections, the clinical details may not be appropriately analyzed [9]. Therefore, the patient with sepsis and manifestations of focal neurological dysfunction or orbital symptoms urgently needs an immediate contrast computed tomography (CT scan) and/or magnetic resonance imaging (MRI) to identify the location of the infection. Both CT scan and skull MRI techniques are the primary radiological technique used to establish the diagnosis of CST. Also, they may be used in assessing the etiological cause and the disease pathology. However, both techniques are not totally sensitive and specific for septic CST. MRI technique particularly MRV (venography) is usually adapted for CST diagnosis and can be used to detect all the stages in thrombus formation. There are contradicting views in the early detection of clot development in dural (cerebral or cranial) sinuses. Some studies reported CT scan has higher sensitivity compared to MRI in the early detection of clot formation in the cavernous sinuses [10], while MRI is better in other types of the cranial sinuses. MRI may also be useful for diagnosing CST in cases where CT scan is not efficient, analyzing complications that involve pituitary gland or spread of infection to the brain. Angiography may also be required. In the recent diagnosis of septic CST, conventional imaging methods such as venography and cerebral angiography are limited in use with a report of severe complications in their choice. Also, use of normal x-ray method (mastoid and sinus plain films, sinus tomograms) has reduced following the use of CT scan and MRI.

Routine laboratory investigations may be done as part of the diagnostic plan. A marked leukocytosis is usually observed in complete blood cell count (CBC) during septic disease. Also, the result of CBC may help to evaluate the factors that may influence the disease condition. These include polycythemia, thrombocytopenia, (which may be indicative of thrombotic thrombocytopenic purpura). Leukocytosis could assist in differentiating septic CST from the aseptic form. The causative bacteria establishing infection may be isolated from the primary infective site including exudate samples and blood culture method. Cerebrospinal fluid (CSF) samples may be collected by lumbar puncture (LP) to differentiate between peri-orbital cellulitis and septic CST. The increase in inflammatory cells are commonly seen in about 75% cases of affected patient with septic CST and sometimes, CSF culture may help to identify the infecting microorganism.

Clinical assessment of hypercoagulable syndrome may include antiphospholipid syndrome test, quantify the level of antiphospholipid or anticardiolipin antibodies in the blood. Other tests may also be done to determine the cause of the hypercoagulable states. These include factor V protein, antithrombin III, protein C and S estimation. Hemoglobin electrophoresis may be useful to identify patients blood genotype in order to rule out sickle cell disease.

Treatment

The main therapeutic approach for managing cavernous sinus thrombosis is by prompt and adequate antibiotic administration. Although the common bacteria causing infection in CST is usually S aureus, broad-spectrum antibiotics which are effective for both gram-positive and gram-negative including anaerobes should be administered before the culture result. Treatment with empiric antibiotic drugs includes penicillin (penicillinase-resistant type) with cephalosporin (3rd and 4th generation preferably). In the case of suspected anaerobic infection of the teeth, selected antibiotics may be administered against the anaerobes. Intravenously administered antibiotics for about 3-4 weeks is usually recommended. There are contradicting views on the use of anticoagulation for cavernous sinus thrombosis treatment. Because of the low prevalence of this condition, there are no current drug trials for the use of anticoagulation in CST. Previous studies revealed a reduction in the mortality rate and clot development by anticoagulation. Few shreds of evidence showed that anticoagulant used as drugs in treating coagulopathy disorder is safe and also effective in treating the patient with sinus thrombosis [11]. It is therefore recommended that anti coagulopathy is treated with heparin in other to prevent thrombosis development and subsequent increase in the septic emboli incidence.

A study review reported that a low-molecular-weight type of heparin (LMWH) are more effective than unfractionated heparin (UFH) in the treatment of the condition [12]. There is contraindication in the use of heparin for CST patient with other diseases. These include intracerebral hemorrhage and another hemorrhagic diathesis. Thrombolytics may be experimentally administered to treat CST patients locally particularly for severe refractory cases. Also, adjunct therapy of corticosteroids may be used to subside inflammation, edema and in CST cases which may result in pituitary insufficiency so as to prevent adrenal complication. This should be administered after antibiotic therapy. Also, drugs such as dexamethasone or hydrocortisone may be recommended. Most often, the effectiveness of surgical technique involving the cavernous sinus is unknown. The primary route of infection can be superficially drained in cases such as sphenoid sinusitis and facial abscess. Early identification of infected sphenoid sinus is usually important in order to inhibit the transmission of infection to the cavernous sinus. Adequate provision and medical care must be provided for CST patient requiring drainage including appropriate antibiotic regimen particularly if surgery is required.

Prognosis

The mortality rate is 30% in affected patients and about 50% among those having an underlying sphenoid sinusitis. Also, more than 30% of the affected individual may develop severe sequelae [6], such as ophthalmoplegia, sight loss, pituitary incapability and physical disability resulting in stroke, which sometimes may be permanent.

Etiology

Cavernous sinuses are thick-walled sinuses, situated at the base of the skull draining venous blood directly from the facial veins. CST condition is a very rare complication commonly associated with facial infections [2], including the nasal furuncles which are responsible for 50% of all cases. Other causes include sphenoidal (ethmoidal) sinusitis and dental infections which account for 30% and 10% cases respectively. Most frequently, the main pathogens are bacteria such as staphylococcus aureus, and streptococcus spp. Also, in cases where the underlying infection results from infected tooth or sinusitis, anaerobic bacteria may be the causative agent. Other types of intracranial septic thromboses may develop but are rarer than CST. These include thrombosis of the lateral sinus (associated with mastoiditis) and superior sagittal sinus. Sagittal sinus thromboses are usually caused by bacterial meningitis.

Epidemiology

The incidence of cavernous sinus thrombosis is generally low, with only a few reported cases in the medical publications. There is no age difference among the affected patients. The majority of the mentioned cases are not recent, mostly before the development of newly effective therapeutic agent. CST rarely occurs, with an approximate value of 4.5 cases in 1,000,000 population per year [3]. Among the types of dural venous sinus thrombosis, it is responsible for <1.5% of known cases. The mortality rate associated with this condition was close to 100% before the development of newly, effective antibiotics. However, following the development of improved or better approach, the mortality rate has reduced below 30%. Most often, patient death caused by CST is usually due to sepsis and infection of the central nervous system (CNS). Also, the morbidity is still high and full recovery is uncommon. About 18% of the affected patients permanently develop varying degree of visual defect, while 50% have cranial nerve abnormalities. The mortality or morbidity rates may partially be due to delay in establishing diagnosis thereby hindering prompt surgical drainage and proper drug administration.

Sex distribution
Age distribution

Pathophysiology

As previously stated, cavernous sinuses are thick-walled venous pathways with the anterior end extending from the superior orbital fissure. The posterior end is attached to the petrous part of the temporal bone. Cavernous sinuses are covered in the dura between the layers of the meninges and the periosteum. Each side of the cavernous sinuses has an extension of internal carotid artery, cranial nerves III, IV, and VI. Cranial nerve IV is situated laterally to the sinus wall. The dural layers release a trabeculae support which projects the sinuses with a reticular pattern, thereby assisting in trapping foreign objects such as bacteria, thrombi, and emboli. Infections with bacteria can also stimulate thrombogenesis through released toxins or tissue damage. Thrombus growth is suggested to be a barrier preventing antibiotic penetration into the cavernous sinuses. In this situation, administration of antibiotics may not be effective in treating the patient because the thrombus clot will hinder the drug penetration from reaching the site of infection [4]. Cerebral emissary veins and the dural sinuses are usually valveless, allowing blood flow in dual directions depending on the pressure gradient of the vascular system. Therefore, infections spread into the cavernous sinuses from the nasal region, sinuses, or middle third of the face moves in an anterograde direction while dental or lateral venous sinuses, otogenic infections spread to the sinuses through retrograde direction. Generally, the mechanism of disease development can be divided into three [5]. These include thrombophlebitis caused by inflammation of the vein inflammation associated with a thrombus which spread into the cavernous sinuses. Also, it may be due to an embolization of infectious substance, which may occur following trauma, injury, abscess, or infection. Phlebothrombosis (aseptic type) resulting from thrombosis of a vein usually without inflammatory reaction is another mechanism. It is different from other types because of the absence of sepsis or a primary source of infection.

Prevention

Most of the preventive approaches involve a lifestyle change. Furuncles in faces should not be forcefully removed and proper antibiotics must be administered at the appropriate regimen plan in order to avoid development of the septic form of cavernous sinus thrombosis.

Summary

Cavernous sinus thrombosis (CST) was first reported in the year 1831 by Bright as a complication resulting from infections in the epidural and subdural region. Dural sinuses are classified into three types, which include sagittal sinuses, cavernous sinuses and lateral sinuses. Lateral sinuses can be further differentiated into transverse, sigmoid or petrosal sinuses. Due to its complexity and the extensive neurovascular involvement, CST is the most severe among the classes of intracranial septic thrombosis [1]. CST usually results lately from the complications of the central facial infections or paranasal sinusitis. Other possible causes of CST may include septicemia, trauma, otitis and maxillary teeth infection. Most often, cavernous sinus thrombosis is sudden and severe in nature with high incidence of morbidity and mortality. However, recent development of new, potent antimicrobial drugs have assisted in reducing reported cases of cavernous sinus thrombosis.

Patient Information

Cavernous sinus thrombosis (CST) is an uncommon clinical condition caused by clot formation in cavernous sinuses. This condition may be due to bacterial infections such as those caused by S. aureus and streptococcus spp, contagious transmission of bacterial and fungal from the sinus, nasal or dental region. An immune response to the infection may result in the formation of blood clot in the sinus which if undiagnosed early or untreated may be severe. Factors such as age, gender and blood clotting disorder predispose individuals to cavernous sinus thrombosis. Pregnant women and those on contraceptives are at risk of developing the disease because of the blood clotting. Also, the disease is commonly seen among children and adolescents. Therefore, it is important to discuss various health issues with healthcare provider.

The symptoms of CST vary ranging from a severe headache, fever to either localized or unilateral facial pain, involving retro-orbital or frontal regions. Affected patient may develop a condition called ophthalmoplegia (a blunted eye papillary response to light), proptosis, and conjunctival edema. Also, the patient may have a seizure, neurologic complications (due to cranial nerve involvement), reduced facial sensation or consciousness. Optical effect may result in anisocoria, vision impairment, mydriasis, and papilledema. Following careful clinical examination of the suspected patient by the physician, the diagnosis is established after proper and adequate investigations. Various investigations may be required. These include CT scan, MRI ( sometimes venogram) and X-ray of the sinus. Patient medical history may also be requested. Other laboratory investigations such as complete blood count, bacteriological culture and blood clotting test may also assist the clinicians in establishing the right diagnosis.

The choice of treatment depends on the discretion of the physician. It is, therefore, important to discuss health challenges and self-medication is not encouraged. However, in most cases of CST, antibiotics are recommended in managing the condition. Antibiotics such as nafcillin, oxacillin, cephalosporin, metronidazole are usually administered. Also, drugs such as corticosteroids may be used to manage the patient if there are neurological involvement. Depending on the condition of the patient, surgery may be needed to effectively treat the condition.

References

Article

  1. Laupland KB. Vascular and parameningeal infections of the head and neck. Infect Dis Clin North Am. 2007. 21(2):577-90, viii.
  2. Southwick FS, Richardson EP Jr, Swartz MN. Septic thrombosis of the dural venous sinuses. Medicine. 1986; 65:82-106.
  3. Leach J, Fortuna R, Jones B, et al. Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic Pitfalls1. Radiographics. 2006; 26 (suppl1):S19-S41.
  4. Karlin RJ, Robinson WA. Septic cavernous sinus thrombosis. Ann Emerg Med. 1984; 13:449-455.
  5. Yarington CT. Cavernous sinus thrombosis revisited. Proc R Soc Med. 1977; 70:456-459.
  6. Southwick FS, Richardson EP Jr, Swartz MN. Septic thrombosis of the dural venous sinuses. Medicine. 1986; 65:82-106.
  7. DiNubile MJ. Septic thrombosis of the cavernous sinuses. Arch Neurol. 1988;45: 567-572.
  8. Southwick FS, Richardson EP Jr, Swartz MN. Septic thrombosis of the dural venous sinuses. Medicine. 1986;65:82-10
  9. Bhatia K, Jones NS. Septic cavernous sinus thrombosis secondary to sinusitis: are anticoagulants indicated? A review of the literature. J Laryngol Otol. 2002; 116:667-676.
  10. Schuknecht B, Simmen D, Yuksel C, et al. Tributary venosinus occlusion and septic cavernous sinus thrombosis: CT and MR findings. AJNR Am J Neuroradiol. 1998; 19:617-626.
  11. Coutinho J, de Bruijn SF, Deveber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Cochrane Database Syst Rev. 2011. Aug 10. CD002005.
  12. Coutinho JM, Ferro JM, Canhão P, Barinagarrementeria F, Bousser MG, Stam J. Unfractionated or low-molecular weight heparin for the treatment of cerebral venous thrombosis. Stroke. 2010;41(11): 2575-80.

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Last updated: 2018-06-21 21:05