Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Lateral Sinus Thrombosis Although seldom encountered in the practice of modern otology, lateral sinus thrombosis (LST) and other intracranial complications of otitis media still occur. The classic picture of this disease is often modified by prior antibiotic treatment, making the diagnosis and management difficult. Infective thrombosis of the lateral sinus was first described in 1826 by Hooper. This disease was universally fatal until surgical intervention was established in 1888 by Lane. Despite later advances in surgical techniques mortality remained at nearly 50% until the introduction of antibiotics. Prior to the advent of antibiotic therapy, the mortality of all intracranial complications was extraordinarily high. 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. 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. 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. The Toby-Ayer test is measured by monitoring the CSF pressure during a lumbar puncture. No increase in CSF pressure during external compression of the internal jugular vein on the affected side, and an exaggerated response on the patent side, is suggestive of LST. Since the introduction of antibiotics, some authors have noted that a high percentage of cases are due to chronic rather than acute cases of otitis media; however this finding has not been consistent in all reports. Teenagers and young adults are more commonly affected in modern reports whereas younger children were reported in higher numbers in earlier series. In the pre-antibiotic era streptococcus and staphylococcus were reported as causing the majority of cases of LST, recent reports have included anaerobic and gram negative organisms as well. The diagnostic procedure of choice is MRI with MR angiography. 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. Treatment is always surgical removal of the infected thrombosis in addition to broad spectrum antibiotic coverage. Once a highly controversial issue, ligation of the internal jugular vein is seldom necessary. In the majority of recent cases, anticoagulation has not been found to be necessary. However, it has been advocated by Shambaugh and may be indicated in selected cases. Case Presentation A 6-year-old Hispanic male presentedwith no prior history of systemic illness or otologic disease. He was seen at Ben Taub General Hospital with a five day history of upper respiratory infection, headache, and bilateral otorrhea. Two days earlier swelling and tenderness had developed along the left sternocleidomastoid muscle. On arrival, his temperature was 101°F and white blood cell count was 18,300; he was alert and appropriate, but irritable and uncooperative. A CT scan was obtained that showed bilateral opacification of the mastoid air cells, and an abscess in the left upper neck. That night he was taken to the OR for incision and drainage of the neck abscess and complete otologic examination. There was marked swelling of the left external auditory canal which precluded visualization of the left tympanic membrane. The right external auditory canal was also swollen, but the tympanic membrane could be visualized. The tympanic membrane was found to be thickened, a myringotomy was performed, purulent fluid was aspirated from the middle ear cleft and a ventilating tube was left in place. He was initially treated with Ceftriaxone (Rocephin) and Cortisporin otic drops. Cultures obtained from the right tympanic aspiration and the left neck abscess grew Streptococcus pneumonia and a Pseudomonas grew from the left external canal specimen. Antibiotic therapy was changed to ticarcillin and clavulanate (Timentin). However, despite this, he continued to spike fevers to 101 and 102° F. On April 2, 1992 a second CT scan with thin cuts through the temporal bones was then obtained. This study suggested thrombosis of the left lateral sinus. While arrangements were being made for surgical decompression, an MR angiogram was performed. This confirmed vascular flow through the right sigmoid sinus and jugular vein, but no flow through the left lateral sinus or jugular vein. A few hours later, he underwent a left complete mastoidectomy with incision of the lateral sinus and removal of an obstructing thrombus. Postoperatively, his antibiotics were changed to Ceftazidime (Fortaz), Amikacin and Penicillin G. Anticoagulation therapy was instituted for two weeks following surgical decompression. Subsequent MRA studies showed the development of collateral flow around the left sigmoid sinus and internal jugular vein. Additionally, reduced flow in the right system persisted. On April 21, 1992, he underwent right mastoidectomy. An MRA obtained on April 30, 1992 demonstrated unobstructed flow through the right venous system and no evidence of recanalization through the left sigmoid sinus or jugular vein. Bibliography Albert DM, Williams SR. Clinical and anatomical considerations of the TobeyAyer test in lateral sinus thrombosis. J Laryngol Otol 1986;100:13111313. Alford BR, Pratt FE. Intracranial complications for otitis media. Texas Med 1966;62:66-70. 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