| 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. Intracranial Complications of Otitis Media You can’t talk about complications of otitis media without briefly mentioning otitis media. It’s common among healthy individuals. With or without antibiotics the natural history is such that most cases will resolve. Otitis media remains the second most common reason for pediatric visits second only to well baby checks. It is the most common indication for antibiotic prescription in children. Approximately 9-18% of children have greater than three episodes during the first year of life and approximately 3% of adults have chronic otitis media. Complications occur once host defenses are overwhelmed and classically have been divided into intratemporal and intracranial. Historically, it was Batiste in 1790 who first described an operation to treat complications of otitis media, specifically mastoiditis. He used a trepan, pictured here, to drill out the mastoid and evacuate pus. This was done without anesthesia and of course, the patient was not prepped and draped in a sterile surgical fashion so you can imagine that the operation was quite morbid. Close to 100 years later, Schwartz reexamined the operation and said that it did have scientific validity and it could be used as a means to control an infection. Zoful first described an operation to create a common cavity between the mastoid, the external auditory canal and the antrum and further, Bundy modified that operation to preserve the ossicles in order to preserve hearing. In the pre-antibiotic era approximately 10% of cases of acute otitis media went on to develop intracranial complications and 25% of cases of chronic otitis media. Antibiotics have decreased the incidence of intracranial complications which was noted most recently by Friedman and Sulek. However, the natural history may not have changed that much once the intracranial complication has occurred. As I mentioned earlier, complications have been divided into intratemporal and intracranial, intratemporal being facial paralysis, petris apicitis , etc. Intracranial being meningitis, lateral sinus thrombosis, otitic hydrocephalus and intracranial abscess which can be intraparenchymal, extradural or subdural. The pathophysiology of intracranial spread occurs along three pathways. First and foremost, thrombophlebitis or paraphlebitis is the most common means of infection to spread from the middle ear space to the sub-arachnoid space, the brain parenchyma or the subdural space. This can occur directly along veins as an inflammatory process proceeds or it can occur in what’s called Virchow-Robin spaces which are spaces around the peri-arteriolar vessels. You can also have bony erosion. This occurs secondary to granulation tissue formation or osteoneogenesis. This is the most common way for infection to spread in a well-pneumatized mastoid. And last, you can have direct extension through preformed pathways such as the round window. You can also have dehiscence within the bony outline of the mastoid or you can acquire dehiscences from surgery or trauma. The anatomy of the temporal bone is complex enough so that I won’t dwell on it. Needless to say that within a few millimeters, critically important structures such as the middle cranial fossa, the posterior cranial fossa, the sigmoid sinus, the facial nerve, are separated by just millimeters of either soft tissue or eggshell thin bone. There are two important studies to keep in mind looking at the overall complication rate of intracranial extension of chronic or acute mastoiditis or otitis media. Kafka in 1935 looked at 3,200 patients. This is considered the pre-antibiotic era study. In his study, the intracranial complication rate was 6%. Meningitis occurred 48% of the time. Lateral sinus thrombosis occurred 22% of the time and brain abscess 16% of the time. The overall mortality rate was 76%. A 1995 study looked at 24,000 patients in the post-antibiotic era. His intracranial complication rate was 0.36% with meningitis still accounting for close to half of the cases, lateral sinus thrombosis 18% and brain abscess 33% with a mortality rate of 18% which is still of great significance although reduced. You can describe the symptoms of intracranial extension into early and late. Early symptoms include fever, purulent drainage, emesis, and blurred vision. Late signs include change in mental status such as seizures, cranial nerve palsies, nuchal rigidity, severe otologic complications such as suppurative labyrinthitis and MRI has consistently been shown to be the best means of evaluation. Dr. Roller last year eloquently described otogenic meningitis so I won’t belabor her point. Needless to say, acute otitis media is the most common etiology of meningitis. A second intra-temporal or intracranial complication is usually present. Intracranial spread occurs along one or a combination of the three pathways. Involvement of preformed pathways usually results in severe vertigo and/or deafness. The overall mortality is 18 to 31% with chronic otitis media being slightly more, having a slightly greater morbidity and mortality. Most cases involve persons younger than 20 years of age and as I have mentioned 86% of the time a second intratemporal or intracranial complication will be present. On physical examination the most important thing to remember is that neck stiffness is the most significant physical exam finding for meningitis. And leukocytosis with left shift is almost always present as a laboratory finding. Management includes ABCs, IV fluids, radiographic evaluation such as CT to rule out temporal bone complications, MRI to rule out intracranial complications, you want to perform a myringotomy and a lumbar puncture to obtain a gram stain and cultures, broad spectrum antibiotics. Most people would say that an ID consult is absolutely mandatory. Here is a picture of acute meningitis. The brain is here. This is a subarachnoid space and you can see it is completely filled with acute inflammatory cells. Lateral sinus thrombosis is another kind of intracranial complication. The lateral sinus or sigmoid sinus is a confluence of the superior petrosal sinus as well as the superior sagittal sinus and the infection usually starts as with thrombophlebitis, in the middle ear space and this spreads along the veins to involve the, to proceed to get a peri-sinus abscess which is an abscess around the sigmoid sinus resulting in thrombosis. As the thrombosis becomes organized you get impediment of blood flow as well as super infection and then you have extension or propagation of the clot which can lead to end stage sequelae such as bacteremia, sepsis, brain abscess and impaired venous drainage. Here is a picture depicting the pathophysiology - inflammation of the outer wall, the sinus, development of the neuro-thrombus, the thrombus completely occludes the canal and it propagates and breaks down to form an abscess. It’s the second most frequent complication according to Schambaugh in the pre-antibiotic era. It had a 35% mortality rate. A recent study in 1983 showed that the mortality rate was 17% so the overall incidence has decreased however, most authors would say that the overall mortality has not decreased that much. In the post-antibiotic era it is more commonly associated with chronic otitis media with effusion. The clinical presentation is difficult to diagnose: Fever, low grade or intermittent, neck tenderness, torticollis, otalgia. These are all common findings in patients with just an ear disease as opposed to lateral sinus thrombosis. Additionally, with each stage the symptoms change. Some further symptoms as the disease progresses include: Jugular foramen syndrome. If it propagates down into the internal jugular vein you can actually feel the clot or a palpable cord in the vein. The Tobey-Ayer-Queckenstedt's test is of historical significance. It is pictured here. Traditionally, when you perform the lumbar tap you measure the CSF pressure and as you measure the pressure you would compress the internal jugular vein on both sides. It would normally result in a rise in CSF pressure. However, if there was no rise in CSF pressure that is suggestive that a lateral sinus thrombosis existed on the ipsilateral side. Again, more late findings: Anemia, leukocytosis. Perhaps the best way to think about the presentation is to go back and think about the pathophysiology. Initially, you have the thrombus formation. You have infection with occlusion of the vessel and then propagation of the clot. And with each of those steps you can have specific symptoms such as fever, headaches. As the thrombus becomes infected you can have septic emboli leading to the classic picket fence fever pattern followed by symptom free intervals. If he has occlusion of the vessel you get increased intracranial pressure, papilledema and persistent headaches. As the thrombophlebitis propagates you can have the neck pain, jugular bulb syndrome, torticollis, etc. Your index of suspicion should be high in any patient who has acute otitis media with sepsis or chronic otitis media and intermittent fevers. CT may miss the diagnosis however, those are older studies and newer CTs have higher resolution so CT now can actually make the diagnosis. Subtraction angiography which is depicted here can make the diagnosis and most people would consider MRI, MRA the method of choice. Anticoagulation as a method of treatment is somewhat controversial. Some people would argue that anticoagulation should only be used if the clot is impending upon vital structures such as the cavernous sinus. Others say you should consider it no matter what and surgical exploration is the mainstay of therapy. You want to perform a prompt mastoidectomy, a complete exposure of the sigmoid and then sigmoid exploration. Internal jugular vein ligation is controversial. Arguments for internal jugular vein ligation include you have better control of disease. You prevent septic clots from entering the systemic circulation and that the morbidity of the procedure itself is not that much greater than the initial operation. Arguments against it are that any operation is associated with potential complications and there are numerous cases of asymptomatic lateral sinus thrombosis. So the course of the disease may not be as malignant as one thinks. Otitic hydrocephalus is another type of intracranial complication. It’s a rare complication. It was described first by Simmons in 1931. It can be secondary to acute or chronic otitis media and it is associated with lateral sinus thrombosis. At one point it was thought to be a form of pseudo-tumor cerebri in the sense that you have increased intracranial pressure with normal sized ventricles. However, now most would say that this is an indistinct entity. You have increased intracranial pressure with normal ventricles in the presence of acute or chronic otitis media. The signs are of increased intracranial pressure with normal ventricles in the presence of acute or chronic otitis media. The signs are of increased intracranial pressure: Nausea, vomiting, visual changes. On physical examination you can have otorrhea, papilledema, cranial nerve VI palsy and by definition you should have normal size ventricles. The pathophysiology of otitis hydrocephalus is often debated. There are two theories. One theory is that as the clot is formed and it begins to propagate eventually it will affect the sagittal sinus and once you have, once it affects the sagittal sinus you have disruption of arachnoid villi functioning and that will lead to a back flow of CSF causing increased intracranial pressure. Not all cases of otitis hydrocephalus however involve the sagittal sinus so there must be a second mechanism. That theory is that all you need is a thrombus in the dominant sinus and you block the dominant outflow valve if you will and that can cause increased venous pressure directly, transmit directly to the CSF causing increased intracranial pressure. Or because you block the dominant outflow valve we have by default impeded arachnoid villi functioning resulting in decreased transfer of CSF leading to increased intracranial pressure. The management is straight forward. The ear disease is treated on its own merit. The goal is to reduce intracranial pressure and prevent optic nerve atrophy. Steroids, diuretics, Mannitol, serial lumbar punctures are the mainstay of therapy. For worse cases you can perform a VP shunt and overall, the prognosis is excellent and the recurrence rate is rare. Intracranial abscess is perhaps the most challenging intracranial complication to deal with. It can be extradural, subdural, intercerebral or intracerebellar. Otogenic etiology is responsible for 25% of childhood cases and 50% of adult cases. The temporal lobe and the cerebellum are the most common sites. Direct spread plays only a minor role in that thrombophlebitis is the major route of spread. It occurs in three distinct clinical stages. It is the second most common intracranial complication in some studies and in terms of the pre-antibiotic era the mortality rate was 40%. In the post-antibiotic era I think the interesting thing is that one study said that any patient who has chronic otitis media has a 3% lifetime risk of developing a brain abscess. The presentation and the pathophysiology go hand in hand. First you have spread of peri-phlebitis. You have infection spreading along veins or in the Virchow-Robbins spaces and the body is now trying to fight that infection. You can have chills, moderate rise in temperature, headaches - extremely non-specific symptoms. If you can catch this at this point and treat it with antibiotics you can halt the further progression of disease. However, because of the most non-specific symptoms, it is often missed. The latent phase is the next phase. It is characterized by desmoplastic reaction as the body picks up its effort to wall off the infection and these patients are often asymptomatic or may just have irritability, poor appetite, etc. The final stage is when the abscess becomes well formed. You have edema, surrounding encephalitis, severe projectile vomiting, headaches, and disorientation. Eventually you will start having localizing signs as you have increased intracranial pressure and midline shift. MRI is the study of choice. Here you can see the classic presentation of a ring-enhancing lesion. The microbiology: 50% of cultures are sterile. It’s a polymicrobial infection as with most abscesses. Aerobic, microphilic and anaerobic streptococci account for most common organism cultures. Bacteroides is the most common anaerobe. Management is combined otologic and neurosurgical approaches and this can’t be emphasized enough that this is a surgical illness and that most patients who do not have prompt surgical attention will expire of their illness. You treat the most pressing first which is usually the neurosurgical aspect. Needle aspiration, open craniotomy, resection, whatever it takes to get the disease out. Needless to say, acute otitis media, wide myringotomy and chronic otitis media mastoidectomy, intravenous antibiotics, ceftriaxone and metronidazole is the current standard regimen. Epidural abscess is a type of brain abscess. It results not from peri-phlebitis but from direct spread with bony destruction and contact of pus with dura. Cholesteatoma is frequently involved. An abscess over the sigmoid sinus is called a peri-sinus abscess. It can be completely asymptomatic hence, the adage that any patient undergoing mastoidectomy for an acute infection should have the dura inspected to rule out a peri-sinus abscess. The classic presentation includes pulsatile otorrhea and throbbing otalgia. MRI is diagnostic and in surgery is the mainstay of therapy. Finally, subdural empyema. It’s not a true abscess hence the term empyema. It’s a collection of pus in the subarachnoid space. It’s very rare. It’s more common with frontal sinusitis. It can occur as a result of direct spread or peri-phlebitis. You can get subdural hematoma type symptoms, early signs include malaise and fever. Late signs include hemiplegia and CT or MRI can be diagnostic of this and surgical therapy is how this is dealt with. In conclusion, intracranial complications of otitis media remain important clinical entities in modern medicine. The signs and symptoms are often subtle until late in the course of the disease and a high index of suspicion may be the best way to prevent late complications of intracranial spread. Case presentation: Physical examination was consistent with cholesteatoma and chronic otitis media. An incidental R parotid mass was also found. An FNA of the lesion was suspicious for mucoepidermoid carcinoma. The management outlined to the patient consisted of surgical excision of the parotid mass to be followed by treatment of his ear disease. The patient underwent an uneventful R superficial parotidectomy and was discharged home with routine follow-up. At home the patient became lethargic and on post operative day 7 was found obtunded as well as having a L hemiparesis. He was transported immediately to Ben Taub. Upon arrival in the shock room, the patient was in extremis. His pupils were fixed and dilated. His breathing was agonal in nature and purulent drainage was present in the R EAC. He was intubated immediately. A head CT scan was ordered. The patient was transferred to the NICU for management. Unfortunately, a cerebral blood study was negative for blood flow. Support was withdrawn and the patient expired shortly thereafter. Bibliograhpy : Alford BR. Complications of chronic ear disease in children. Postgrad Med 1970;48:65-70. Alford BR, Pratt FE. Intracranial complications from otitis media. Texas Med 1966;62:66-71. Balance CA , Green CD. 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