CAVERNOUS SINUS  THROMBOSIS

PRESENTED BY DR.NANDANI

Contents…

Anatomy Tributaries and communications Clinical features Etiology Treatment Reference

Introduction

Introduction

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart.

It forms a rout of communication between the veins of the face , cheek and brain

and internal jugular vein.

In 1831 by bright As a complication of epidural and

subdural infection.

ANATOMY

POSITION…

Extend from the medial end of the superior orbital fissure to the apex of the petrous temporal bone.

TributariesFrom orbit Superior and inferior ophthalmic vein.Central vein of ratina

From the brain

Superficial middle cerebral vein Inferior cerebral vein from temporal

lobe

From the meninges Spheno perital sinus Frontal trunk of the middle

meningeal vein via pterigoid plexus or in to sphenoperital or in to cavernus sinus.

Communication…

1) In to transverse sinus through the superior

Petrosal sinus. 2) In to internal jugular vein through

inferior Petrosal sinus and through plexus

around Internal carotid artery. 3) Pterygoid plexus. 4) Into the facial vein. 5) Intercavernus communication.

Drainage of Cavernous Sinus

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Eagleton criteria1926 A known site of infection. Evidence of the bloodstream infection. Early signs of venous obstruction in

retina, conjunctiva or eyelid. Paresis of 3rd , 4th and 6th cranial nerve

resulting from inflammatory edema. Abscess formation in the neighboring

soft tissue. Evidence of meningeal irritation.

Classic presentations are an abrupt onset of unilateral periorbital edema, headache,and proptosis.

Other common signs and symptoms include:

Ptosis, chemosis, cranial nerve palsies (III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common.

 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. The pupil may be dilated. Infection can spread to the contralateral cavernous sinus within 24–48 hours of initial presentation.

Clinical features:

Generalized constitutional symptoms, high fluctuating fever, chills, rapid pulse and sweating.

Initial sign and symptoms: The earliest clinical sign is congestion

of the eye on the unaffected side Headache.

The earliest eye manifestations are caused by venous congestion and include:

Chemosis (conjunctival oedema) Peri-orbital oedema Proptosis.

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Subsequently, the following signs may follow rapidly, as a result of cranial nerve involvement:

Painful ophthalmoplegia

Ptosis

Mydriasis.

Swelling of face (edematous involvement of the eyelids).Pain in the eye and tenderness to pressure.

Edema of the conjunctiva due to impaired venous return.

Pulsating exopthalmosCranial nerve involvement. Papilledema with multiple retinal hemorrhages, chemosis,epistaxis.

Late symptoms: Spreads to other side and B/L signs

can be seen.

Advanced stage: Advanced toxemia and meningitis,

producing stiffness of the neck.

 Menigeal involvement signs: Kernig’s sign: is positive when the

thigh is bent at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance). This may indicate subarachnoid hemorrhage or meningitis.

Brudzinski’s sign: patient lie in supine position:

The symphyseal sign, in which pressure on the pubic symphysis leads to abduction of the leg and reflexive hip and knee flexion

The cheek sign, in which pressure on the cheek below the zygoma leads to rising and flexion in the forearm.

 Brudzinski's reflex, in which passive flexion of one knee into the abdomen leads to involuntary flexion in the opposite leg, and stretching of a limb that was flexed leads to contralateral extension

The Brudziński neck sign or Brudziński's symptom is a clinical sign in which forced flexion of the neck elicits a reflex flexion of the hips. It is found in patients with meningitis,subarachnoid haemorrhage and possibly encephalitis.

Etiology

 facial, ear, oral, and dental infections Most commonly from contiguous spread of infection

from the  sphenoidal or ethmoidal sinuses and dental infections

 Less common primary sites of infection include tonsils, soft palate, middle ear, or orbit (orbital cellulitis)

 mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were available, the mortality was 80–100%

Morbidity rates also dropped from 70% to 22% due to earlier diagnosis and treatment.

Patients with the aseptic form of the disease have a similar but more subtle presentation and do not demonstrate signs and symptoms of sepsis, meningitis, or primary infection. Risk factors associated strongly with the development of aseptic CST include a genetic prothrombotic condition or acquired prothrombotic state.

Treatment of aseptic cavernous sinus thrombosis

Because it is often difficult to distinguish septic and non-septic causes of CST, the initial management is the same. Only when aseptic aetiology is ruled out definitively can antibiotics be withdrawn. In practice, therefore, the treatments are the same for both aseptic and septic disease.

Treatment of septic cavernous sinus thrombosis (CST)

Staphylococcus aureus

Drug of choice

Initial drug of choice

chloramphenical…1g/6h

Anticoagulant Heparin

manitol

most aetiologies, empiric therapy should include:

Vancomycin to cover for potential methicillin-resistant Staphylococcus aureus (MRSA) until the actual culture results are available,

A third-generation cephalosporin, such as ceftriaxone (to be used only in patients with no history of true allergy to penicillin).

In patients with documented true allergy to penicillin, quinolones should be used instead.

Intravenous metronidazole should be added if dental or sinus infection is suspected.

Cefotaxime 1.5 to 2 g IV q4h

High doses of intravenous antibiotics are required because thrombus may limit penetration of antibiotics. Bacteria, sequestered within the thrombus, may not be killed until the dural sinuses have started to re-canalise. Antibiotics also need to be administered over an extended period, for at least 2 weeks beyond the time of clinical resolution.

This aims to insure complete sterilisation and prevent relapses. Supportive therapy is necessary and includes resuscitation, oxygen support, and local eye care.

Based on limited observation, anticoagulation may be beneficial after exclusion of haemorrhagic complications by CT scan. Anticoagulation is thought by some to be dangerous in patients with bilateral CST and/or concurrent intracranial haemorrhage.

Adjunctive therapy: corticosteroids

The role of corticosteroids is controversial in many cases of CST.

Reducing intra-orbital congestion in patients with orbital oedema

Reducing cranial nerve inflammation in patients with cranial nerve dysfunction.

Further therapy post-stabilisationFinally, as soon as the patient's condition permits, prompt drainage of the primary site of infection (such as the para-nasal sinusitis, dental abscess) or other concurrent closed-space infection is advisable.

References cunningham’s ;MANUAL OF PRACTICAL

ANATOMY. 4TH edition ; pg. 48. Oral and maxillofacial infections;Topazian;4th

edition;pg 211 Textbook of oral medicine; Anil ghom; 2nd

edition; Pg-481. Oral and maxillofacial surgery; fonseca; vol-5; pg-108. Website

Thank

you

Thank

you