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Cavernous Sinus ThrombosisA Case Report

Candy T. Cahilog, MD 1st year Internal Medicine Resident

ABSTRACT Cavernous sinus thrombosis is usually a late complication of an infection of the central face or paranasal sinuses. Other causes include bacteremia, trauma, and infections of the ear or maxillary teeth. Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. Occurrence of cavernous sinus thrombosis (CST) has always been low, with only a few hundred case reports in the medical literature.(1) This paper presents a case of cavernous sinus thrombosis following a folliculitis on right axilla on a 32-year old female who was then diagnosed with diabetes mellitus. Patient presented with on and off headache for one month which became very severe three days prior to admission. The condition was associated with somnolence and with progressive blindness on both eyes for three days. This condition has mortality rate as high as 30% and the majority of survivors suffer permanent sequelae. (1)

CASE REPORT A 32-year old female and housewife was admitted on May 20, 2013 in Northern Mindanao Medical Center due to headache and blindness. Patient was a known hypertensive with good compliance to her maintenance medication. Condition started one month prior to admission with onset of recurrent generalized headache which was tolerable in intensity. She denied fever, vomiting and other symptoms. Three days prior to admission, headache was noted to be persistent, 10/10 in intensity and was associated with episodes of vomiting and blurring of vision. On the day of admission, patient was noted to be sleeping most of the time hence brought to the hospital and was subsequently admitted. On physical examination, patient was hypertensive at 150/120. She was drowsy but able to wake up with name-calling and was coherent. She was afebrile and not in respiratory distress. Pertinent skin finding was presence of pustular lesions on right axilla. She was noted to have plethora. Left eyeball was noted to be fixed and with both proptosis and ptosis. There was no light perception on both eyes. On funduscopic examination, there was no papilledema, hemorrhage, nor exudate. Patient was referred to Ophthalmology Department for evaluation. Pupils were anisocoric, both nonreactive to light. There was flattening of left nasolabial fold. Motor strength on all extremities were intact. There was a note of Babinski reflex on right foot. No nuchal rigidity was noted. The rest of the physical examination was within normal limits.

Blood tests were done on admission. Complete blood count revealed leucocytosis at 18, 000 with predominance of neutrophils. ESR was elevated at 23 mm/hr. Ramdom Blood sugar was elevated at 245 mg/dL. Plain cranial CT scan revealed acute haemorrhage centered in the midbrain with subarachnoid extension and left sphenoid sinusitis. Patient was referred and seen by a Neurologist. High dose antibiotics were started. Ceftriaxone 2 grams IV every 12 hours and Oxacillin 2 grams IV every 6 hours were given. Nimodipine, antihypertensive, and analgesic were also started. Blood glucose was monitored and controlled by giving Metformin and stat doses of regular insulin. MRA/MRV was ordered to rule out vascular malformation that may have caused bleeding. The test revealed negative. On 6th hospital day, fever was noted to lyse. Patient had no complaint of headache. Plethora was resolving. Neurologic deficits were persistent. After 2 weeks on intravenous antibiotics, vision on right eye was noted to improve. Patient that time was able to count fingers. Left eye remained to be blind. Discharge plans were made. Patients vision on right eye continued to improve after another two weeks. On follow up, patient was able to ambulate in the clinic without assistance. Facial asymmetry was resolved. However, blindness on left eye was persistent. Although patient needed assistance in crossing streets and unfamiliar environment, she was able to do activities of daily living as well as household chores without assistance.

Discussion Cavernous sinus thrombosis was first described as a pathological entity in 1821 by Duncan.* Bright in 1831 reported the proptosis and ocular changes associated with the disease. The development of septic cavernous sinus thrombosis occurs as a result of bacteria or fungi entering the cerebral venous system and spreading to the cavernous sinus. Knowledge of the neuroanatomy of this region is helpful in understanding how septic cavernous sinus thrombosis may develop with its unique clinical presentation. The paired cavernous sinuses are trabeculated structures, lying between the two layers of dura mater, on either side of the pituitary fossa and body of the sphenoid bone. Laterally each extends to the maxillary nerve and trigeminal ganglion, anteriorly to the superior orbital fissure and posteriorly to the apex of the petrous temporal bone.4 The cavernous sinuses are connected by the intercavernous sinus around and below the hypophysis cerebri. 177 Afferent veins of the cavernous sinus include superior ophthalmic vein, inferior ophthalmic vein, superficial middle cerebral vein and spheno-parietal sinus. Blood drains from the cavernous sinus into the superior petrosal sinus, inferior petrosal sinus and pterygoid plex~s.~ The superior petrosal sinus drains into the sigmoid sinus as does the mastoid emissary vein and veins from the endolymphatic sac and du~t.~,~ As the sigmoid sinus ends in the jugular bulb it is joined by the inferior petrosal sinus. At this point the internal jugular vein is formed and begins its vertical descent. The cavernous sinus also drains into the pterygoid plexus which in turn connects with the deep facial vein5 A number of important structures either

pass through the cavernous sinus or run a course forward in its lateral wall. The internal carotid artery, with its accompanying sympathetic plexus and the sixth cranial nerve lie within the cavernous sinus. The sixth nerve runs forward on the lateral side of the internal carotid artery. The third and fourth cranial nerves enter the roof of the cavernous sinus and run forward in its lateral wall. The third nerve initially lies above the fourth nerve during its course within the lateral wall passing down medial to the fourth nerve, to reach the superior orbital fissure. The ganglion of the fifth cranial nerve with its ophthalmic and maxillary divisions lie within the lower part of the lateral wall of the cavernous sinus.6 As there are no valves in the ophthalmic veins the blood by reverse flow can pass from cavernous sinuses to supraorbital, facial and other veins; can flow to the pterygoid plexus and also to the pharyngeal plexus. Similarly, the dural venous sinuses and cerebral veins have no valves, with flow depending on pressure gradients. Hence there is relatively easy spread of infection or thrombi through the cerebral venous system.' The disease process may occur several ways.8 An infected focus leads to localised thrombophlebitis of the veins draining the area. Propagation of phlebitis and/or thrombophlebitis eventually reaches the cavernous sinus. Alternatively, spread of infected emboli which lodge in the trabeculated structure of the cavernous sinus then gives rise to thrombophlebitis. Infections of the face, especially the medial third of the face, are most frequently reported as the site of primary infection, especially in the pre-antibiotic Bacteria may enter the cavernous sinus from the venous drainage of these, sites, via the facial veins or pterygoid plexus and then through the ophthalmic veins.'* Since the advent of antibiotics, sinusitis has increasingly been noted as a site of primary infection, particularly infection of the sphenoid and ethmoid sinuses. '',I3 Sphenoid sinus infection may be difficult to diagnose both clinically and radiologically, which may lead to delays in treatment. The sphenoid sinus may be thin walled, allowing infection to spread to adjacent structures such as cortical venous sinus, meninges and cranial nerves.I4 Other sites of primary infection less frequently reported include otic infections, odontogenic infections and extraction, styes, tonsillitis, facial erysipelas and facial The range of organisms which have been implicated in septic cavernous sinus thrombosis reflects the type and site of the primary infection. Staphylococcus aureus is the most frequently reported causative organism, being reported in nearly 70% of cases.8.10 This is to be expected in view of the high incidence of predisposing skin infections. Streptococcus pneumoniae and other streptococcal species occur in a further 20% of cases." These organisms have been reported as the most commonly cultured in both sphenoid and maxillary sinu~itis.'~ Gram-negative bacilli, anaerobes and fungi have also been identified as causing cavernous sinus thrombosis.8.10

Clinical presentation Classically, cavernous sinus thrombosis is described as having a dramatic onset and running a fulminant course.2o In acute septic cavernous sinus thrombosis there is a latent period of about one week between the primary infection and onset of symptoms.12 This type of presentation is associated with spread to the cavernous sinus through the afferent veins, principally via the

ophthalmic veins.*I A slower, more indolent form of cavernous sinus thrombosis has been described with milder signs and symptoms. These tend to occur following middle ear or mastoid infections with spread via the superior petrosal sinus." Post mortem evidence of low-grade thrombosis without clinical signs has been reported.' Headache occurs in just over 50% of patients developing cavernous sinus thrombosis.10 Pain was distributed over the sensory distribution of the ophthalmic and maxillary branches of the trigeminal nerve. Fever and generalised toxicity occurred in over 90% of cases. Ptosis, proptosis and chemosis are the most frequently reported ocular changes, occurring in % of reported cases. Extraocular muscle palsies, including third, fourth and sixth nerves also occur frequently. Sensory deficits in ophthalmic and maxillary nerve distribution, including corneal anaesthesia, are also described. Pupillary abnormality may also be present, occurring as a sign of third nerve deficit, involvement of the sympathetic plexus or in association with visual failure. Reduced visual acuity occurs less commonly (about 20%). Fundal changes, either venous engorgement or papilloedema, have been reported as occurring in 65% of cases. Over half of the patients exhibited mental changes ranging from drowsiness and lethargy to coma. Signs of meningism may also be present. Septic emboli have been found in lungs, brain and orbit and kidney at post mortem examination. In a review of patients with orbital cellulitis or cavernous sinus thrombosis those with cavernous sinus thrombosis were found to be more likely to be extremely unwell with slower recovery. They were also more likely to have visual, pupillary abnormalities, retinal changes and Laboratory tests and radiologic imaging may be helpful in the diagnosis and management of cavernous sinus thrombosis. Full blood count shows a raised ESR, increased polymorphonuclear leukocytes and anaemia. Blood cultures, especially if the patient has not been receiving antibiotics, are frequently positive. Culture of the primary site of infection may grow the causative CSF findings are reported as abnormal in a high proportion of cases.O CSF findings reported include raised polymorphonuclear leukocytes, low glucose and elevated protein consistent with parameningeal infection. A positive culture of CSF is rare. Radiologic imaging depends on the availability of the particular investigation. X-rays of sinuses, including sphenoid sinuses, may reveal the possible site of origin of infection. However, some difficulty in demonstrating pathology with the sphenoid sinus has been reported.I0 CT findings within the cavernous sinus include multiple irregular filling defects (low attenuation values) within the enhantcing cavernous sinus. These are considered to represent thr~mbi.~-~ The lateral boundary of the cavernous sinus shows diffuse b~lging.~ There is normal enhancement of he intracavernous portion of the internal carotid artery and pituitary gland, both of which are identified by density difference compared with the thrombosed cavernous sinus.25 Orbital abnormal- ities included tortuous dilated superior ophthalmic veins, thickening of extraocular muscles, bulbar thickening, periorbital swelling and increased soft tissue strands in the retrobulbar fat.

The mainstay of treatment is early high-dose antibiotic therapy which should especially cover Gram-positive cocci. This can be modified later according to the results of microbiological examinations and the clinical response to treatment. The role of anticoagulants in the treatment of cavernous sinus thrombosis is not yet well established. Levine et al found no reduction in mortality with the use of anticoagulants in cavernous sinus. However, early anticoagulant therapy reduced morbidity. A retrospective review of patients treated with heparin suggested mortality may be reduced if heparin is administered. Possible hazards of heparin therapy include bleeding from haemorrhagic sites of cortical infarction or from necrotic areas of carotid artery within the cavernous sinus. Corticosteroids have been used with beneficial effect on the ophthalmoplegia in addition to antibotic and anticoagulant treatment.~' They may be necessary as replacement therapy if pituitary necrosis and insufficiency occurs.2' Local ocular treatment may be required to protect the cornea as exposure may result from inability to close the eyelids. Frequent lubricant drops or ointment are required to prevent corneal ulceration and conjunctival dessication. If intraocular pressures are raised, then hypotensive agents should also be considered.~~ Surgery for the direct removal of venous thrombi is no longer an accepted treatment. Several authors suggest that drainage of closed infected spaces is vital to recovery. Prompt drainage of an infected sphenoid sinus or orbital abscess is recommended by Southwick'O and Lew.14 Surgical drainage of infected mastoid air cells in addition to antibiotic therapy is considered optimal therapy by Venezio et al.I5 In the pre-antibiotic era cavernous sinus thrombosis was usually fatal. Grove reviewed 400 cases reported before 1936, finding a mortality rate of nearly Clune reviewed 36 cases in the literature from 1948 to 1963. Of these, 26 patients recovered, giving a survival rate of 72%. Over 50% of those who survived had no residual morbidity.~ Yarington reviewed 878 cases reported in the liter- ature between 1821 and 1960.32 In this he found a mortality rate of 80% and morbidity rate of 75%. In 1977 he reported a further review of 28 cases reported from 1965 to 1977, finding a considerable improvement in both mortality, 13.6%, and morbidity, 22.770.~ Blindness in at least one eye has been reported in at least 8% of cases. Partial visual impairment remains in a further 7%.33 Reported causes of blindness include occlusion of central retinal artery by pressure at the orbital apex, by emboli, by internal carotid arteritis, by ischaemic optic neuropathy without central retinal artery occlusion or by corneal ulceration secondary to loss of ability to close the eyelids and loss of corneal sensation. Slightly less than 20% of survivors have residual oculomotor nerve palsies. The third and sixth nerves are most commonly involved but the fourth and upper two divisions of the fifth nerve can also be involved.~ Less common sequelae include hemiparesis, cerebral atrophy, and pituitary insufficiency following pituitary necrosis With aggressive and early antibiotic treatment the outlook for patients with this disorder has considerably improved.

REFERENCES Rahul Sharma, MD, MBA, FACEP; Chief Editor: Barry E Brenner, MD, PhD, FACEP, et.al, Cavernous Sinus Thrombosis Follow-up. March 7, 2013. Nov 20, 2013. Medscape. http://emedicine.medscape.com/article/791704-followup#a2650

Heather T. Mackintosh, FRACO, FRACS, Septic cavernous sinus thrombosis - A case report. Nov 7, 2007. Nov 20, 2007. Australian and New Zealand Journal of Ophthalmology. http://onlinelibrary.wiley.com/doi/10.1111/j.1442-9071.1991.tb00656.x/pdf