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CAVERNOUS SINUS THROMBOSIS

Of all the dural venous sinuses, the cavernous sinuses are most often affected by thrombosis. The two cavernous sinuses are situated on either side of the sella turcica and are connected by the intercavernous sinuses cavernous sinus thrombosis. Within the lateral wall of the sinuses run cranial nerves (CN) III, IV, V1, and V2. The internal carotid artery and CN VI course through the center of the sinuses.

Septic thrombi of the cavernous sinuses most often result from infections of the midface, with Staphylococcus aureus being the predominant pathogen. Other primary foci of infection include paranasal sinusitis (primarily sphenoid) and otitis media. In approximately 10% of patients with cavernous sinus thrombosis (CST).

Sterile CST has been associated with polycythemia, sickle cell disease, paroxysmal nocturnal hemoglobinuria, contraceptive use, dehydration, compressive brain tumors or aneurysms, and pregnancy. Occasionally, no predisposing condition is evident.

Patients with CST often present with headache, unilateral retro-orbital pain, periorbital edema, fever, proptosis, chemosis, ptosis, mental status changes, and meningismus. An isolated sixth nerve palsy may be seen, since CN VI is the only CN that runs through the interior of the cavernous sinus. Bilateral signs occur as the thrombophlebitis.

Ludwig's angina is an infection of the submandibular region, manifested by swelling of the floor of the mouth, and elevation and posterior displacement of the tongue. A brawny edema and cellulitis of the suprahyoid region of the neck develops later in the disease course.

Deep neck abscesses such as Ludwig's angina are less common now than 50 years ago because of the development of effective antibiotics and improved dental care. Deep neck infections in the antibiotic era most commonly result from odontogenic infections and local trauma.

The most common predisposing factors for the development of Ludwig's angina are carious and abscessed teeth, periodontal disease, and extractions of the lower molars. Uncommon etiologies include upper respiratory infections, floor-of-mouth trauma, mandibular fractures, and sialadenitis. The second and third mandibular molars have roots which lie at the level of the mylohyoid muscle.

All age groups may be affected, but young adults have the highest prevalence rates. The disease is unusual in children. Comorbid conditions predisposing to Ludwig's angina have included diabetes mellitus, malnutrition, alcoholism, neutropenia, lupus erythematosus, aplastic anemia, and glomerulonephritis. Symptoms may persist for several days before the patient seeks medical attention.

The patency of the airway is the main concern with Ludwig's angina, and patients often will require a tracheotomy to prevent or correct airway obstruction. Intravenous antibiotic therapy and selective application of surgical drainage are the other two treatment measures. Although some authors advocate tracheotomy in all cases.

Although Ludwig's angina had been associated with mortality greater than 50% in the pre-antibiotic era, some recent series have reported no deaths associated with the disease. Broad-spectrum antibiotics may be chosen initially to combat the typically polymicrobial nature of the infection, but high-dose penicillin (12 million to 20 million U daily for adults, 300,000 U/kg/d for children) still remains a good agent.

In the pre-antibiotic era, surgical drainage of the submandibular space was the recommended treatment for all cases of Ludwig's angina. Incisions into the submandibular space were used to prevent airway compromise.

Infections of the submandibular space may spread to the lateral pharyngeal and retropharyngeal spaces.