Cavernous Sinus Thrombosis: A Comprehensive Review

Introduction

Cavernous sinus thrombosis (CST) is a rare but life-threatening condition characterised by the formation of a blood clot within the cavernous sinus, a large venous channel located at the base of the skull. This disease, often resulting from the spread of infection from adjacent facial or paranasal structures, can have devastating neurological and systemic consequences. Historically, CST was almost universally fatal before the advent of antibiotics, but advances in diagnosis and management have significantly improved outcomes. Nevertheless, prompt recognition and intervention remain critical to reducing morbidity and mortality.

The epidemiology of CST has evolved over time, with a notable decline in incidence due to improved hygiene, widespread use of antibiotics, and better management of sinus and facial infections. However, CST continues to be a significant concern in medical practice because of its rapid progression, complex clinical presentation, and potential for severe complications.

Anatomy and Physiology

Cavernous Sinus: Location and Structure

The cavernous sinus is a paired dural venous sinus located on either side of the sella turcica, flanking the body of the sphenoid bone. It extends from the superior orbital fissure anteriorly to the apex of the petrous part of the temporal bone posteriorly. Each cavernous sinus measures approximately 2 cm in length and 1 cm in width.

Structurally, the cavernous sinus is a trabeculated venous space, traversed by numerous fibrous septa. It is unique among dural sinuses because it contains several vital neurovascular structures within its lateral wall and through its centre. The internal carotid artery and the abducens nerve (cranial nerve VI) pass through the sinus itself, while the oculomotor (III), trochlear (IV), ophthalmic (V1), and maxillary (V2) nerves are embedded in its lateral wall.

Venous Drainage and Communications

The cavernous sinus receives blood from multiple sources, including:

• Superior and inferior ophthalmic veins
• Superficial middle cerebral vein
• Sphenoparietal sinus
• Emissary veins from the pterygoid plexus

It drains posteriorly via the superior and inferior petrosal sinuses into the internal jugular vein. Notably, the facial veins communicate with the cavernous sinus via the angular and superior ophthalmic veins, creating a potential route for the spread of facial infections.

Relevance to Disease

The anatomical complexity and rich venous communications of the cavernous sinus make it particularly susceptible to the spread of infection and thrombosis. The close proximity to cranial nerves and the internal carotid artery also means that CST can produce a wide range of neurological deficits and vascular complications.

Etiology and Risk Factors

Infectious Causes

The vast majority of CST cases are secondary to infection, most commonly originating from:

• Paranasal sinuses (especially the sphenoid and ethmoid sinuses)
• Facial skin and soft tissue infections (such as furuncles of the upper lip, nose, or periorbital region)
• Dental abscesses
• Orbital cellulitis

The “danger triangle” of the face (bounded by the corners of the mouth and the bridge of the nose) is particularly significant, as infections in this area can easily spread via venous channels to the cavernous sinus.

Non-Infectious Causes

Although less common, CST can also arise from non-infectious causes, including:

• Trauma (skull base fractures, surgical interventions)
• Neoplastic invasion (tumours involving the sinus or skull base)
• Hypercoagulable states (inherited or acquired thrombophilias, pregnancy, oral contraceptive use)
• Inflammatory diseases (systemic lupus erythematosus, Behçet’s disease)

Common Pathogens

The most frequently implicated organisms in infectious CST are:

• Staphylococcus aureus (most common, including methicillin-resistant strains)
• Streptococcus species (especially Streptococcus pneumoniae)
• Gram-negative bacilli (such as Escherichia coli and Klebsiella)
• Anaerobic bacteria (especially in dental or sinus infections)
• Fungal pathogens (such as Aspergillus and Mucor species, particularly in immunocompromised individuals)

Mixed infections are not uncommon, especially in cases with dental or sinus involvement.

Predisposing Factors

Predisposing factors for CST include:

• Uncontrolled diabetes mellitus
• Immunosuppression (HIV/AIDS, immunosuppressive therapy)
• Malnutrition
• Poor dental hygiene
• Recent facial or sinus surgery
• Chronic sinusitis

Pathophysiology

Mechanisms of Thrombosis

CST develops when infection or other prothrombotic stimuli lead to inflammation and endothelial injury within the cavernous sinus. This triggers the coagulation cascade, resulting in the formation of a thrombus. The thrombus may partially or completely occlude the venous sinus, impeding blood flow and increasing intracranial pressure.

Spread of Infection

Infections can spread to the cavernous sinus via:

• Direct extension through bone or soft tissue
• Retrograde venous flow through valveless facial and ophthalmic veins
• Lymphatic spread (less common)

Once within the cavernous sinus, bacteria or fungi can proliferate, causing septic thrombophlebitis and further propagation of the thrombus.

Impact on Cranial Nerves and Adjacent Structures

The anatomical proximity of the cavernous sinus to multiple cranial nerves means that thrombosis and inflammation can rapidly involve these structures, leading to ophthalmoplegia, sensory disturbances, and other neurological deficits. The involvement of the internal carotid artery can result in vascular complications such as carotid-cavernous fistula or stroke.

Clinical Presentation

Signs and Symptoms

CST typically presents with an acute, rapidly progressive clinical picture. The classic features include:

• Severe headache, often retro-orbital or frontal
• Periorbital oedema and chemosis (conjunctival swelling)
• Proptosis (bulging of the eyeball)
• Ophthalmoplegia (paralysis of extraocular muscles), resulting in diplopia (double vision)
• Ptosis (drooping of the upper eyelid)
• Decreased visual acuity and, in severe cases, complete vision loss
• Facial pain or numbness, particularly in the distribution of the ophthalmic (V1) and maxillary (V2) divisions of the trigeminal nerve
• Fever and systemic signs of sepsis (tachycardia, hypotension)

Progression and Bilaterality

Symptoms often begin unilaterally but may rapidly become bilateral due to the inter-cavernous sinuses connecting the two sides. The progression from mild periorbital swelling to full-blown ophthalmoplegia and altered consciousness can occur within hours to days.

Differential Diagnosis

Conditions that can mimic CST include:

• Orbital cellulitis
• Superior ophthalmic vein thrombosis
• Carotid-cavernous fistula
• Meningitis
• Intracranial tumours involving the cavernous sinus

Careful clinical and radiological evaluation is essential for accurate diagnosis.

Diagnostic Approach

Clinical Assessment

A high index of suspicion is essential in any patient presenting with acute periorbital oedema, ophthalmoplegia, and signs of infection. A detailed neurological examination should assess cranial nerve function, visual acuity, and mental status.

Laboratory Investigations

• Complete blood count (CBC) may reveal leukocytosis.
• Blood cultures are crucial for identifying the causative organism.
• Inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are typically elevated.
• Coagulation profile to assess for underlying hypercoagulable states.

Imaging Modalities

Imaging is indispensable for confirming the diagnosis and delineating the extent of the disease.

• Contrast-enhanced computed tomography (CT): May show enlargement of the cavernous sinus, filling defects (suggestive of thrombus), and adjacent sinus or orbital infection.
• Magnetic resonance imaging (MRI): Superior soft tissue resolution; MR venography can directly visualise thrombus within the cavernous sinus and assess for venous congestion or infarction.
• CT/MR angiography: Useful for evaluating the patency of the internal carotid artery and identifying vascular complications.

Diagnostic Criteria

The diagnosis of CST is based on a combination of clinical features and radiological evidence of thrombosis within the cavernous sinus. Microbiological confirmation strengthens the diagnosis, especially in infectious cases.

Management and Treatment

Medical Therapy

Antibiotic Therapy

Empirical broad-spectrum intravenous antibiotics should be initiated immediately, targeting the most likely pathogens. The regimen is then tailored based on culture and sensitivity results. Common choices include:

• Vancomycin (for MRSA coverage)
• Third-generation cephalosporins (such as ceftriaxone)
• Metronidazole (for anaerobic coverage)

Duration of therapy is typically 3-4 weeks, depending on clinical and radiological response.

Anticoagulation

The use of anticoagulants in CST remains controversial. Some studies suggest that anticoagulation with heparin may prevent thrombus propagation and improve outcomes, especially in cases without active bleeding or contraindications. However, risks and benefits must be weighed carefully on a case-by-case basis.

Adjunctive Therapies

Corticosteroids may be considered in selected cases to reduce inflammation and oedema, particularly when there is significant cranial nerve involvement or impending vision loss. Supportive care includes management of sepsis, fluid and electrolyte balance, and monitoring for complications.

Surgical Interventions

Surgical intervention may be necessary in certain scenarios:

• Drainage of septic foci (such as paranasal sinus abscess or orbital abscess)
• Decompression of the orbit in cases of severe proptosis or vision threat
• Neurosurgical intervention in cases with intracranial extension or abscess formation

Surgery is always combined with aggressive medical management.

Supportive Care

Patients with CST often require intensive care support, especially those with altered consciousness, systemic sepsis, or respiratory compromise. Close monitoring of neurological status and prompt recognition of complications are essential.

Complications

Neurological Deficits

CST can lead to permanent neurological sequelae, including:

• Persistent ophthalmoplegia
• Visual impairment or blindness
• Trigeminal neuralgia or sensory loss
• Facial palsy

Vision Loss

Impaired venous drainage, increased intraocular pressure, and direct involvement of the optic nerve can result in irreversible vision loss in the affected eye(s).

Systemic Complications

Sepsis, septic shock, disseminated intravascular coagulation (DIC), and multi-organ failure are potential life-threatening complications of CST. Intracranial extension can lead to:

• Meningitis
• Brain abscess
• Cerebral infarction or haemorrhage

Mortality

Despite advances in treatment, the mortality rate for CST remains significant, ranging from 10% to 30% in various studies. Morbidity is even higher, with many survivors experiencing permanent deficits.

Prognosis

Outcomes

Prompt diagnosis and aggressive treatment have improved outcomes in CST, but the prognosis remains guarded. Early intervention is associated with better visual and neurological recovery. Delayed treatment, severe sepsis, bilateral involvement, and underlying immunosuppression are associated with poorer outcomes.

Factors Affecting Prognosis

• Time to initiation of appropriate therapy
• Extent of neurological involvement at presentation
• Type of infecting organism (fungal infections have worse prognosis)
• Patient’s immune status and comorbidities

Recovery and Rehabilitation

Rehabilitation may be necessary for patients with persistent neurological deficits, including physiotherapy, occupational therapy, and vision rehabilitation. Psychosocial support is also important for patients and families coping with long-term sequelae.

Prevention

Preventive Strategies

Preventing CST involves both primary and secondary measures:

• Prompt and effective treatment of facial, dental, and sinus infections
• Education of healthcare workers and the public regarding the risks of manipulating facial lesions in the danger triangle
• Good dental hygiene and regular dental check-ups
• Early recognition and management of predisposing conditions (diabetes, immunosuppression)

Early Recognition

A high index of suspicion and early imaging in patients with suggestive symptoms can facilitate timely diagnosis and treatment, thereby reducing morbidity and mortality.

Management of Risk Factors

Optimising control of chronic illnesses, minimising unnecessary use of immunosuppressive agents, and appropriate use of prophylactic antibiotics in high-risk surgical procedures can reduce the risk of CST.

Nursing Care of Patients with Cavernous Sinus Thrombosis

Nursing care plays a crucial role in the early recognition, management, and rehabilitation of patients with CST.

Nursing Assessment

A comprehensive and continuous assessment is vital for patients with CST. Nursing assessment should include:

• Neurological checks: Monitor Glasgow Coma Scale (GCS), pupil size/reactivity, extraocular movements, and cranial nerve function regularly.
• Vital signs: Monitor for fever, tachycardia, respiratory status, and blood pressure changes.
• Ocular assessment: Document the presence and progression of proptosis, chemosis, vision changes, or pain.
• Pain assessment: Utilize appropriate pain scales and evaluate the need for analgesia.
• Infection surveillance: Observe for signs of systemic infection or sepsis, including chills, rigors, and hemodynamic instability.
• Skin and mucous membranes: Inspect for breakdown or infection at facial entry points (nose, teeth, sinuses).

Nursing Diagnoses

Potential nursing diagnoses for patients with CST may include:

• Impaired cerebral tissue perfusion related to venous thrombosis
• Acute pain related to inflammation and increased intracranial pressure
• Risk for infection related to underlying or ongoing sepsis
• Impaired physical mobility related to cranial nerve dysfunction
• Risk for sensory/perceptual alteration (visual impairment)
• Anxiety and fear related to sudden illness and potential complications
• Self-care deficit related to neurological impairment

Nursing Interventions

• Monitor and maintain airway, breathing, and circulation (ABCs):
• Ensure airway patency, especially in patients with altered mental status or decreased GCS.
• Position head of bed at 30 degrees to promote venous drainage and reduce intracranial pressure.
• Provide supplemental oxygen as prescribed.

Neurological and visual assessment:

• Perform frequent neurological checks to detect early signs of deterioration.
• Monitor visual acuity and report any changes immediately to the medical team.

Infection control and antimicrobial therapy:

• Administer intravenous antibiotics as prescribed; early, broad-spectrum coverage is critical.
• Monitor for adverse reactions to antibiotics.
• Practice strict aseptic technique during all invasive procedures.

Pain management:

• Administer prescribed analgesics and monitor their effectiveness.
• Apply cold compresses to the periorbital area if not contraindicated to relieve discomfort.

Prevention and management of complications:

• Monitor for signs of increased intracranial pressure: headache, vomiting, decreased consciousness, papilledema.
• Observe for seizures and maintain safety precautions; administer anticonvulsants if prescribed.
• Be vigilant for signs of sepsis and disseminated intravascular coagulation (DIC).

Supportive care and rehabilitation:

• Assist with activities of daily living (ADLs) as needed, promoting patient independence within limits of safety.
• Encourage passive and active range-of-motion exercises to prevent contractures and maintain muscle tone.
• Collaborate with physiotherapists and occupational therapists for rehabilitation planning.

Patient and family education:

• Educate patient and family about CST, the importance of early treatment, and warning signs of complications.
• Offer emotional support and address concerns regarding prognosis, vision loss, or neurological deficits.
• Provide instruction on medication administration and infection prevention for home care post-discharge.

Psychosocial support:

• Offer counseling services or spiritual support as needed.
• Encourage open communication about fears and anxieties related to illness and possible long-term effects.

Collaborative Management

Nursing interventions are undertaken in collaboration with the multidisciplinary team, including physicians, infectious disease specialists, neurosurgeons, ophthalmologists, physiotherapists, and social workers. Key collaborative measures involve:

• Timely laboratory tests (blood cultures, coagulation profiles, inflammatory markers)
• Neuroimaging (MRI, CT scan) to confirm the diagnosis and monitor disease progression
• Possible surgical intervention for abscess drainage or sinus surgery, if indicated
• Anticoagulation therapy in select cases, as prescribed by the medical team
• Adjustment of medications based on culture sensitivities

Evaluation of Nursing Care

The effectiveness of nursing interventions is evaluated through:

• Regular monitoring of neurological status and visual function
• Stabilization or improvement of vital signs
• Resolution of infection as evidenced by normalization of white blood cell counts, temperature, and clinical symptoms
• Reduced pain and discomfort
• Prevention of secondary complications such as pressure injuries, contractures, or hospital-acquired infections
• Enhanced patient and family understanding of disease and care needs
• Facilitation of transition to rehabilitation or home care, as appropriate

Discharge Planning and Patient Education

Effective discharge planning is essential for CST patients, as they may have ongoing needs related to neurological recovery, medication adherence, and infection prevention. Discharge instructions should address:

• Signs and symptoms warranting immediate medical attention (e.g., sudden visual changes, recurrent fever, new neurological symptoms)
• Antibiotic regimen and importance of completing the course
• Home care for any surgical wounds or intravenous lines
• Follow-up appointments with neurology, infectious disease, ophthalmology, and rehabilitation services
• Community resources and support groups

REFERENCES

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3. Ali S. Cavernous Sinus Thrombosis: Efficiently Recognizing and Treating a Life-Threatening Condition. Cureus. 2021 Aug 20;13(8):e17339.
4. Plewa MC, Hall WA. Cavernous Sinus Thrombosis. 2025 Jun 16. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 28846357.
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6. Raj A, Kaur N, Kaur N. Cavernous sinus thrombosis with central retinal artery occlusion in COVID-19: A case report and review of literature.. https://pubmed.ncbi.nlm.nih.gov/33913893/)Indian J Ophthalmol. 2021;69(5):1327-1329.
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