Lateral Sinus Thrombosis

Hooper first described infective thrombosis of the lateral sinus in 1826. This disease was universally fatal until Lane established surgical intervention in 1888.

The thrombus can be identified by its signal intensity on MRI and the flow void in the affected sinus is clearly documented on MR angiography.

Classic symptoms of LST include a "picket fence" fever pattern; chills; progressive anemia (especially with beta-hemolytic strep); and, symptoms of septic emboli, headache and papilledema may indicate extension to involve the cavernous sinus.

Respiratory mucosa, intact boney walls and protective granulations provide natural defense barriers within the middle ear; complications occur when these are overcome. The spread of infection through the natural defenses can occur by osteothrombosis, bone erosion and when present along preformed pathways.

Before the advent of antibiotic therapy, the mortality of all intracranial complications was extraordinarily high. In spite of advances in surgical techniques mortality remained at nearly 50% until the introduction of antibiotics.

In a study of autopsy statistics at LA County Hospital, it was found that before the introduction of antibiotics approximately 25:1,000 deaths were due to an intracranial complication of otitis media. The death rate from these complications dropped 90% after the introduction of antibiotics.

The intracranial complications of otitis media include purulent meningitis, extradural or peridural abscess, LST, brain abscess and otitic hydrocephalus.

Treatment is always surgical removal of the infected thrombosis in addition to broad spectrum antibiotic coverage.

Lateral sinus thrombosis (LST) and other intracranial complications of otitis media still occur in the practice of otology. The disease is often modified by prior antibiotic treatment, making the diagnosis and management difficult.