Sinus drains Superior petrosal sinus transverse sinus.Inferior petrosal sinus IJV and a plexus of vein on ICAVeins traversing the emissary Sphenoidal foramen, foramen ovale and foramen lacerum Pterygoid plexus.Superior ophthalmic vein Facial vein.
Pulsating exopthalmos because ( carotid pulse is transmitted trough the retrobulbar edema)
Cavernous sinus thombosis
CAVERNOUS SINUS THROMBOSIS
Tributaries and communications
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
Extend from the
medial end of the
fissure to the apex
of the petrous
Superior and inferior
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.
1) In to transverse sinus through the superior
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.
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
Evidence of meningeal irritation.
Classic presentations are an abrupt onset of
unilateral periorbital edema, headache,and
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
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
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
The earliest eye manifestations are caused by
venous congestion and include:
Chemosis (conjunctival oedema)
Subsequently, the following signs may follow rapidly, as a
result of cranial nerve involvement:
Swelling of face (edematous involvement of the eyelids).
Pain in the eye and tenderness to pressure.
Edema of the conjunctiva due to impaired venous
Cranial nerve involvement.
Papilledema with multiple retinal hemorrhages,
Spreads to other side and B/L signs can be
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
Brudzinski’s sign: patient lie in supine
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
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
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
haemorrhage and possibly encephalitis.
facial, ear, oral, and dental infections
from contiguous spread of infection from
the sphenoidal or ethmoidal sinuses and
Less common primary sites of infection include
tonsils, soft palate, middle ear, or orbit
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
Treatment of aseptic cavernous
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
Drug of choice
Initial drug of choice
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
Reducing cranial nerve inflammation in patients with
cranial nerve dysfunction.
Further therapy post-stabilisation
Finally, 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.
cunningham’s ;MANUAL OF PRACTICAL
ANATOMY. 4TH edition ; pg. 48.
Oral and maxillofacial infections;Topazian;4th
Textbook of oral medicine; Anil ghom; 2nd
Oral and maxillofacial surgery; fonseca; vol-5;