“CAVERNOUS SINUS”“CAVERNOUS SINUS”
• Venous sinuses of Dura Mater.
• Cavernous sinus.
 Structure.
 Location.
 Boundarie...
VENOUS SINUS OF DURA MATER:- These are venous spaces the
walls of which are formed by the duramater. They have an inner li...
5. Anterior intercavernous sinus.
6. Posterior intercavernous sinus.
7. Basilar plexus of veins.
CAVERNOUS SINUSES:-
Where...
What are its Boundaries?
The floor of the sinus is formed by endosteal dura mater. The lateral
wall, roof and median wall ...
• Trochlear nerve:- In the anterior part of the sinus it crosses
superficial to the 3rd
nerve, and enters the orbit throug...
• Inferior cerebral vein from the temporal lobe.
C. From the meninges:-
• Sphenoparietal sinus
• Frontal trunk of the midd...
The importance of cavernous sinus arises because of the structures
which lie in and around it. They may be involved with i...
Source Disease Route
Nose & Danger area
of the face
Furuncle, Septal abscess Pharyngeal Plexus.
Ethmoid sinus Orbital cell...
complain of orbital pain and fullness accompanied by
periorbital edema and visual disturbances.
• In some patients, perior...
• Exophthalmos and ophthalmoplegia.
3) Systemic signs indicative of sepsis:-
• Chills, Fever, Shock, Delirium and coma app...
ophthalmoplegia.
Laterality Often involves eyes. Involves both eyes.
• Lab Studies:-
CST is a clinical diagnosis and lab s...
Blood culture should be taken prior to starting
antibiotic therapy.
• Surgery of the cavernous sinus is technically diffic...
 Loss/difficulty in vision
 Bulging of the eyeball or drooping of eyelids.
 Difficulty in moving the eye in a certain d...
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Cavernous sinus

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Transcript of "Cavernous sinus"

  1. 1. “CAVERNOUS SINUS”“CAVERNOUS SINUS” • Venous sinuses of Dura Mater. • Cavernous sinus.  Structure.  Location.  Boundaries.  Relations.  Tributaries (Incoming Channels).  Draining Channels (Communications).  Applied Anatomy & Complications.  Cavernous Sinus Thrombosis.  Introduction  Etiology  Mortality/Morbidity rate  History of the patient  Clinical signs & symptoms -Venous -Cranial -Systemic  Differential Diagnosis  Lab Studies  Imaging/Radiographic aids  Treatment protocol -Emergency department care -Do’s & Don’ts -Right time to call the doctor  Damage to the Internal Carotid Artery.  Conclusion.  References. “CAVERNOUS SINUS”
  2. 2. VENOUS SINUS OF DURA MATER:- These are venous spaces the walls of which are formed by the duramater. They have an inner lining of endothelium. There is no muscle in their walls. They have no valves. Venous sinuses receive venous blood from the brain, meninges, and bones of the skull. Cerebrospinal fluid is poured into some of them. Cranial venous sinuses communicate with veins outside the skull through emissary veins. These communications help to keep the pressure of the blood in the sinuses constant. There are about 15 venous sinuses, of which some are paired and others are unpaired. Paired Venous Sinuses:- There is one sinus on each side (right or left). 1. Cavernous sinus. 2. Superior petrosal sinus. 3. Inferior petrosal sinus. 4. Transverse sinus. 5. Sigmoid sinus. 6. Sphenoparietal sinus. 7. Petrosquamous sinus. 8. Middle meningeal sinus. Unpaired venous Sinuses:- These are median in position. 1. Superior sagittal sinus. 2. Inferior sagittal sinus. 3. Straight sinus. 4. Occipital sinus.
  3. 3. 5. Anterior intercavernous sinus. 6. Posterior intercavernous sinus. 7. Basilar plexus of veins. CAVERNOUS SINUSES:- Where is it Located? Each Cavernous sinus (right or left) is a large venous space situated in the middle cranial fossa, on either side of the body of sphenoid bone. Its interior is divided into a number of spaces (caverns) by trabeculae. The trabeculae are much less conspicuous in the living than in the dead. Structure of cavernous sinus:- BUTLER (1957):- asserted that a distended adult sinus contains a few trabeculae, mostly in its periphery near the entry of its tributaries. When the sinus is collapsed, as in cadavers, its cavity is encroached upon by nerves and arachnoid granulations in its wall, creating a spurious resemblance to cavernous tissue; hence called as the Cavernous Sinus. PARKINSON (1963) & PERNKOPF (1973):- depicted the sinus as a “venous plexus”. BROWDER & KAPLAN (1976):- described the sinus as “reticulated”. It was not clear whether they meant plexiform or cavernous.
  4. 4. What are its Boundaries? The floor of the sinus is formed by endosteal dura mater. The lateral wall, roof and median wall are formed by the meningeal dura mater. Anteriorly, the sinus extends up to the medial end of the superior orbital fissure and posteriorly, up to the apex of the petrous temporal bone. It is about 2cm long and 1 cm wide. Relations:- A. Structures outside the sinus: • Superiorly: a) Optic Tract, b) Internal carotid artery and anterior perforated substance. • Inferiorly: a) Foramen lacerum and the junction of the body and greater wing of sphenoid bone. • Medially: a) Hypophysis cerebri and sphenoidal air sinus. • Laterally: a) Temporal bone with uncus. • Anteriorly: a) Superior orbital fissure and the apex of the orbit. B. Structures in the lateral wall of the sinus, form above downwards: • Occulomotor nerve:- In the anterior part of the sinus it divides in to superior and inferior divisions which leave the sinus by passing through the superior orbital fissure.
  5. 5. • Trochlear nerve:- In the anterior part of the sinus it crosses superficial to the 3rd nerve, and enters the orbit through the superior orbital fissure. • Ophthalmic nerve:- In the anterior part of the sinus it divide into the lacrimal, frontal and nasociliary nerves • Maxillary nerve:- It leaves the sinus by passing through the foramen rotundum on its way to the pterygopalatine fossa. • Trigeminal ganglion:- The ganglion (and its dural cave) project Ainto the posterior part of the lateral wall of the sinus. C. Structures passing through the centre of the sinus:- • Internal carotid artery:- with the venous and sympathetic plexuses around it. • Abducent nerve:- inferolateral to the internal carotid artery. These structures in the lateral wall and in the centre of the sinus are separated from blood by endothelial lining. Tributaries (incoming channels):- A. From the orbit:- • The superior ophthalmic vein. • A branch of inferior ophthalmic vein (sometimes the vein itself) • The central vein of retina:- may drain either into the superior ophthalmic vein or into the superior ophthalmic vein or into the cavernous sinus. B. From the brain:- • Superficial middle cerebral vein
  6. 6. • Inferior cerebral vein from the temporal lobe. C. From the meninges:- • Sphenoparietal sinus • Frontal trunk of the middle meningeal vein:- may drain either into the pterygoid plexus (through the foramen ovale) or into the Sphenoparietal or cavernous sinus. Draining channels (communications):- The cavernous sinus drains:- • Into the transverse sinus through the superior sinus, • Into the internal jugular vein through the inferior petrosal sinus and through a plexus around the internal carotid artery, • Into the pterygoid plexus of veins through the emissary veins passing through the foramen ovale, foramen lacerum and the emissary sphenoidal foramen, • Into the facial vein through the superior ophthalmic vein. • The right and the left cavernous sinuses communicate with each other through the anterior and posterior intercavernous sinuses and through the basilar plexus of veins. All these communications are valve less and blood can flow in either direction. Applied Anatomy and Complications of infections of cavernous sinus:-
  7. 7. The importance of cavernous sinus arises because of the structures which lie in and around it. They may be involved with infections which can spread to it along the many tributaries. Through its communications, it forms a route of communication between the face, cheek, brain and the internal jugular vein. Following are the complications arising from the infection of the cavernous sinus:- A). Cavernous sinus thrombosis:- Cavernous Sinus Thrombosis, as the name states, is the formation of blood clot (thrombus) in the cavernous sinus. It is important to know that CST affects cranial nerves III, IV and VI, which are necessary for eye movement, and cranial nerve V, which gives sensation to the top and middle portion of the face. Therefore, it is a serious, life-threatening infection that requires aggressive medical and surgical intervention. • Etiology:- It is not contagious neither infectious. The cause is usually infections starting in the face, sinuses (esp. sphenoid and ethmoid) or the ears; as the bloodstream drains back into the cavernous sinus in the skull, the infection spreads to this area and results in the disease. The causative agent is generally Staphylococcus aureus, although streptococci, pneumococci and fungi may be implicated in rare cases. Other sources of infection are:-
  8. 8. Source Disease Route Nose & Danger area of the face Furuncle, Septal abscess Pharyngeal Plexus. Ethmoid sinus Orbital cellilitis or abscess. Ophthalmic veins. Sphenoid sinus Sinusitis Direct. Frontal sinus Sinusitis and osteomylitis of frontal bone Supraorbital and ophthalmic veins Orbit Cellulitis and abscess Ophthalmic veins Upper eye lid Abscess Angular and ophthalmic veins Pharynx Acute tonsillitis or peritonsillar abscess Pharyngeal plexus Ear Petrositis Petrosal venous sinuses. • Mortality / Morbidity rates:- Prior to the advent of effective antimicrobial agents, the mortality rate from CST was effectively between 80-100%. With aggressive management, the mortality rate has come down to 20- 30%. Morbidity, however, remains high, and complete recovery is rare. Roughly, one-sixth of patients are left with some degree of visual impairment, and one half has cranial defects. • History of the patient:- • Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-19 days. • Headache, fever and malaise typically precede the development of ocular findings. As the infection tracts posteriorly, patients
  9. 9. complain of orbital pain and fullness accompanied by periorbital edema and visual disturbances. • In some patients, periorbital findings do not develop early on, and the clinical picture is subtle. • Without effective therapy, signs appear in the contra lateral eye by spreading through the communicating veins to the contra lateral cavernous sinus. This is pathognomonic of CST. The patient rapidly develops mental status changes from CNS involvement and/or sepsis. Death follows shortly thereafter. • Clinical featres:- Clinical picture presents the following systemic,venous and nervous symptoms: 1) Nervous symptoms:- • Severe pain in the eye and forehead in the area of distribution of Ophthalmic nerve. • Involvement of the third, fourth and sixth cranial nerves individually and sequentially resulting in the paralysis of the muscles supplied and eventually total ophthalmoplegia. Paralysis of the V cranial nerve results in the loss of sensation in the top and the middle portion of the face. 2) Venous symptoms:- • Eyelids get swollen with chemosis and proptosis of the eyeball. • Pupils become dilated and fixed. • Optic disc shows congestion and oedema with diminution of vision.
  10. 10. • Exophthalmos and ophthalmoplegia. 3) Systemic signs indicative of sepsis:- • Chills, Fever, Shock, Delirium and coma appear as late findings. • Differential Diagnosis:- CST needs to be differentiated from… • Cellulitis • Epidural Hematoma • Epidural and subdural infections • Glaucoma, Acute angle closure cases • Orbital infections • Periorbital infections • Sinusitis • Subarachnoid hemorrhage • Subdural hematoma • Orbital cellulites (most difficult to distuinguish). Distinguishing between CST and Orbital Cellulitis:- Orbital Cellulitis Cavernous Sinus Thrombosis Source Commonly ethmoid sinus Nose, sinus, orbit, ear or pharynx Onset Slow Abrupt Cranial nerve involvement Involved concurrently with complete Involved individually and sequentially.
  11. 11. ophthalmoplegia. Laterality Often involves eyes. Involves both eyes. • Lab Studies:- CST is a clinical diagnosis and lab studies are seldom specific. Most patients exhibit a PMN leucocytosis often marked with shift towards immature form. Blood cultures are generally positive for the offending organism. • Imaging studies:- Historically, a number of techniques have been used like:- • Plain Sinus radiography, • Carotid angiography • Orbital venography. In current practice the techniques being used are:- • CT scan • MRI • MR angiography • Lumber puncture • Neuroradiology • Treatment:- • I.V. broad spectrum antibiotic coverage and attention to the focus of infection. Eg:- Penicillin, Sulfadiazine, Chlomphenicol and metrinidazole.
  12. 12. Blood culture should be taken prior to starting antibiotic therapy. • Surgery of the cavernous sinus is technically difficult and never been shown to be helpful. The primary source of infection should be drained if possible (infected Ethmoid or Sphenoid sinus or facial abscess). • Corticosteroids may help to reduce inflammation and edema and should be considered as an adjunctive therapy Role of anticoagulants like heparin is not clear but is supported by recent studies. • Do’s:- a) Best treatment is prevention. Recognise the primary source of infection and treating this primary source expeditiously is the best way to prevent CST b) Understand that CST can be a life threatening, rapidly progressing disease with high mortality rates despite antibiotic use • Don’t s:- a) Don’t forget that CST is a medical emergency and depending on the location of the primary infection, the appropriate specialist should be involved. For Example: an ophthalmologist should be consulted if the infection is in the eye. • Right time to call the Doctor:- • Eye problems:-  Eye pain
  13. 13.  Loss/difficulty in vision  Bulging of the eyeball or drooping of eyelids.  Difficulty in moving the eye in a certain direction. • Ear problems:-  Ear pain  Hearing loss  Drainage from ear. • Fever, headache, nausea, vomiting, stiff neck • Drainage from the sinus. B) Damage to the Internal Carotid Artery:- The Internal Carotid Artery can be damaged by injuries to the base of the skull, leading to the leakage of the arterial blood into the sinus. This increases the pressure in the sinus and the veins entering it, so that the eyeball may protrude and produce a pulsating exophthalmos. CONCLUSION:- In our routine practice, we as dentists, would encounter many patients who would seem to be suffering from otherwise non-threatening and common infections of the eye, ear and nose. It is of paramount importance on our part that we assume the patient as a suspected case if he presents with a clinical picture suggesting that of CST. Though the occurrence of CST is very rare due to Operative procedures, the possibility still remains and it is called for that we employ sterilization procedures properly and consistently; reduce chances of cross-infection; to keep the threat of CST at bay.

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