Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. The diagnostic incidence of Cavernous Venous Thrombosis is increasing to 7 per 1,000, 000 as newer and more advanced imaging modalities emerge off late and hence every oral & maxillofacial surgeon must be aware of its occurrence and appropriate immediate management protocol. This article would throw light on anatomy, pathophysiology, clinical features, radiodiagnosis and management of Cavernous Sinus Thrombosis
Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. The diagnostic incidence of Cavernous Venous Thrombosis is increasing to 7 per 1,000, 000 as newer and more advanced imaging modalities emerge off late and hence every oral & maxillofacial surgeon must be aware of its occurrence and appropriate immediate management protocol. This article would throw light on anatomy, pathophysiology, clinical features, radiodiagnosis and management of Cavernous Sinus Thrombosis
Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. The diagnostic incidence of Cavernous Venous Thrombosis is increasing to 7 per 1,000, 000 as newer and more advanced imaging modalities emerge off late and hence every oral & maxillofacial surgeon must be aware of its occurrence and appropriate immediate management protocol. This article would throw light on anatomy, pathophysiology, clinical features, radiodiagnosis and management of Cavernous Sinus Thrombosis
Official Publication of Orofacial Chronicle , India
www.jhnps.weebly.com
REVIEW ARTICLE
Cavernous Sinus Thrombosis A succinct outlook
Maliha Saman BDS 1 , Akheel Mohammad MDS 2 , S.P. Singh MCh 3
1- Consultant dental surgeon 2- Oral & Maxillofacial Surgeon, Chennai India 3- Neuro and spine surgeon, Bhopal, India
ABSTRACT: Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. The diagnostic incidence of Cavernous Venous Thrombosis is increasing to 7 per 1,000, 000 as newer and more advanced imaging modalities emerge off late and hence every oral & maxillofacial surgeon must be aware of its occurrence and appropriate immediate management protocol. This article would throw light on anatomy, pathophysiology, clinical features, radiodiagnosis and management of Cavernous Sinus Thrombosis. Key Words: Cavernous sinus , thrombosis , management
Cite this Article: Maliha S., Akheel M.D, S.P. Singh: Cavernous Sinus thrombosis - A succinct outlook : J ournal of Head & Neck physicians and surgeons Vol 2 Issue 1 2014 : Pg 67-72 INTRODUCTION:
Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. It was first described by Dease in 1778 as a rare,
68
potentially fatal complication of dental infections, orbital cellulitis, and sinusitis. Intracranial complications of dental abscess are very rare, but could be fatal 1 . Later the striking syndrome of swollen orbit , limited ocular mobility , impaired vision was first pathologically recognized by Duncan in 1821 and later clinically defined by Bright in 1831 as a complication of epidural and subdural infections and eye findings by Knapp in 1868 2,3 . This article would throw light on anatomy, pathophysiology, clinical features, radiodiagnosis and management of Cavernous Sinus Thrombosis.
PATHOPHYSIOLOGY: Aseptic thrombosis occurs with trauma, tumor invasion, aneurysmal expansion and hypercoaguable states whereas septic thrombosis is more common and occurs due to the intimate juxtaposition of veins, arteries, nerves, meninges, and paranasal sinuses accounting for the characteristic etiology and presentation. CST is more commonly seen with sphenoid and ethmoid and to a lesser degree with frontal sinusitis. Due to its complex neurovascular anatomic relationship, cavernous sinus thrombosis is the most important of any intracranial septic thrombosis 4, 5 . Staphylococcus aureus accounts for approximately 70% of all infections. Streptococcus pneumoniae, gram-negative bacilli, and anaerobes can also be seen. Fungi are a less common pathogen and may include Aspergillus and Rhizopus species 6, 7, 8 . Another reason for the pathogenesis can be due to mycotic embolism where following a trauma to middle third of face could lead to an emoboli which could get lodged into the cavernous sinus producing CST symptomology. Another pathophysiology behind CST could be explained due to phelbothrombosis occurring in cavernous sinus or any of the connecting vein channels 8 .
The general symptoms include fever present along with the Ocular signs following a thrombosis of cavernous sinus include proptosis and edema of lips and conjunctiva and paresis of nerve supplied by Occulomotor, Trochlear and Abducent nerves when involved. Chemosis, Papilledema, Periorbital sensory loss, Decreased corneal reflex, nuchal rigidity are other associating features presentable.
69
In conditions of oculomotor nerve involvement parasympathetic and sympathetic denervation leads the pupils to become small and immobile. Bilateral symptomology can be explained due to the involvement of intercavenous sinus as a result of free communication that presents on either side 7, 8,9,10 .
DISCUSSION:
In 1732 Winslow coined the term cavernous sinus and later Dwight Parkisnson referred it as the anatomic jewel box 1, 9, and 10 . The Brains venous channels include the dural venous sinuses and are valveless located between the inner and outer layers of dura extending extradurally from the superior orbital fissure backward to apex of petrous part of temporal bone. The cavernous sinuses lie on either side of pituitary fossa and are interconnected by intercavernous sinus presenting the primary venous reservoir for outflow of superior and inferior ophthalmic veins, cerebral veins and sphenoparietal sinus. It communicates to transverse sinus via superior petrosal sinus. The important structures that surround the cavernous sinus include Occulomotor, Trochlear, Ophthalmic and Maxillary nerves laterally; along with Internal carotid artery and the sympathetic plexus and Abducent nerve medially 11, 12, and 13 . The diagnostic incidence of Cavernous Venous Thrombosis is increasing to 7 per 1 000 000 as newer and more advanced imaging modalities emerge off late. Females are more commonly affected than males, with a ratio of 1.29:1 3, 14 . It presents more commonly among women in the 2035 year age group. There is no race predilection, and the associated mortality is reported to be 7%. Prospective studies have reported an independent survival rate of approximately 80%. Prior to the advent of effective antimicrobial agents, the mortality rate from CST was effectively 100%. With aggressive management, the mortality rate is now less than 30%. Morbidity, however, remains high, and complete recovery is rare 14 . In 1926 Eagleton suggested 6 criteria which are now considered as the guidelines for diagnosis 1) a known site of infection 2) septicemia 3) early signs of venous congestion 4) ocular, maxillary, abducent nerve defecits 5) abscess or phlebitis contagious to cavernous sinus & 6) signs of intracranial infection though all these
70
features need not be sought but definite findings are sufficient to conclude a diagnosis. The most suspected differential diagnosis should include toxemia as an intravascular bacterial infection can present with aforesaid symptoms. Orbital vary, Orbital apex syndrome, Superior orbital fissure Syndrome, pseudotumour of orbit , mucormycosis , orbital cellultis and acute ethmoiditis also present with overlapping symptoms and should be kept in overview when treatment doesnt seem to resolve the symptoms 13,15,16,17 . Imaging studies remain the cornerstone of diagnosis. The diagnosis of cerebral venous sinus thrombosis is made on the appearance of the delta sign, a feature which is frequently absent on CT scans unlike scleral thickening, swollen ocular muscles and retrobulbar densities which are classically appreciated. The imaging modality of choice is magnetic resonance venography as it allows direct visualisation of the dural venous sinuses and the large cerebral veins. It is an invasive procedure with catheterisation of the jugular vein 15, 16 . Treatment can be broadly classified into either being aggressive or emergency management. The primary choice of medicine should be penicillin or a combination of synthetic penicillin which should be administered intravenously in the highest recommended dosage. Treatment options for cerebral venous sinus thrombosis also include anticoagulation, thrombolytic therapy, and, in some cases, surgical thrombectomy. Anti coagulant therapy is a bit controversial due to risk of intracranial bleeding but doesnt outweigh the benefit of recannulization and dissolution of thrombus thus is emerging as a promising treatment modality 15,16,17 .
CONCLUSION: In summary CST is still with us, though patients now have better survival rates. It is a disease primarily diagnosed with physical signs and symptoms, which requires prompt treatment. In our modern age of Computerization and laboratory based medical care CST demands the diagnostic skill of the physician whose prompt intervention can yield a favourable result.
71
REFERENCES:
1. Zahller, M., et al. "Cavernous sinus thrombosis." Western Journal of Medicine 133.1 (1980): 44. 2. Seltzer, Albert P. "Cavernous Sinus Thrombus with Antral Infection." Journal of the National Medical Association 54.6 (1962): 673. 3. Rael, Jesse R., et al. "Direct thrombolysis of superior sagittal sinus thrombosis with coexisting intracranial hemorrhage." American journal of neuroradiology 18.7 (1997): 1238-1242. 4. Clifford-Jones, R. E., et al. "Cavernous sinus thrombosis." Journal of Neurology, Neurosurgery & Psychiatry 45.12 (1982): 1092-1097. 5. Stam, Jan. "Thrombosis of the cerebral veins and sinuses." New England Journal of Medicine 352.17 (2005): 1791-1798. 6. Acheson, J., and A. Malik. "Cerebral venous sinus thrombosis presenting in the puerperium." Emergency medicine journal: EMJ 23.7 (2006): e44. 7. Karlin, Ronald J., and William A. Robinson. "Septic cavernous sinus thrombosis." Annals of emergency medicine 13.6 (1984): 449-455. 8. Fink, J. N., and D. L. McAuley. "Cerebral venous sinus thrombosis: a diagnostic challenge." Internal medicine journal 31.7 (2001): 384-390. 9. Sekhar, Laligam N., Manuel Dujovny, and Gutti R. Rao. "Carotid-cavernous sinus thrombosis caused by Aspergillus fumigatus: case report." Journal of neurosurgery 52.1 (1980): 120-125. 10. Bentley, J. Nicole, Ramn E. Figueroa, and John R. Vender. "From presentation to follow-up: diagnosis and treatment of cerebral venous thrombosis." Neurosurgical focus 27.5 (2009): E4. 11. Yarington Jr, C. Thomas. "Cavernous sinus thrombosis revisited." Proceedings of the Royal Society of Medicine 70.7 (1977): 456. 12. Levine, Steven R., Roy E. Twyman, and Sid Gilman. "The role of anticoagulation in cavernous sinus thrombosis." Neurology 38.4 (1988): 517-517. 13. Bousser, M-G. "Cerebral venous thrombosis: diagnosis and management." Journal of neurology 247.4 (2000): 252-258. 14. Masuhr, F., and S. Mehraein. "Cerebral venous and sinus thrombosis." Journal of neurology 251.1 (2004): 11-23. 15. Deshmukh, Vinayak, Bhavana Lakhkar, and Jayant Wagha. "CAVERNOUS SINUS THROMBOSIS." (2008). 16. Levine, Steven R., Roy E. Twyman, and Sid Gilman. "The role of anticoagulation in cavernous sinus thrombosis." Neurology 38.4 (1988): 517-517. 17. Bhatia, K., and N. S. Jones. "Septic cavernous sinus thrombosis secondary to sinusitis: are anticoagulants indicated? A review of the literature." The Journal of Laryngology & Otology 116.09 (2002): 667-676.
Acknowledgement- None
72
Source of Funding- Nil
Conflict of Interest- None Declared
Ethical Approval- Not Required
Correspondence Addresses : Maliha Saman Consultant Dental Surgeon Chennai, India Email Id - drmalihasaman@gmail.com Contact 091- 08056259725