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case records of themassachusetts general hospital

T h e n e w e n g l a n d j o u r n a l o f medicine

n engl j med 357;19 www.nejm.org november 8, 2007 1957

Founded byRichard C. CabotNancy Lee Harris, m.d., Editor Eric S. Rosenberg, m.d.,Associate EditorJo-Anne O. Shepard, m.d.,Associate Editor Alice M. Cort, m.d.,Associate EditorSally H. Ebeling,Assistant Editor Christine C. Peters,Assistant Editor

From the Department of Neurology,Brigham and Womens Hospital (M.A.S.);the Departments of Radiology (R.G.G.),Infectious Diseases (A.Y.K.), and Pathol-ogy (A.S.-R.), Massachusetts General Hos-pital; and the Departments of Neurology(M.A.S.), Radiology (R.G.G.), Medicine(A.Y.K.), and Pathology (A.S-R.), HarvardMedical School.

N Engl J Med 2007;357:1957-65.Copyright 2007 Massachusetts Medical Society.

Presentation of Case

A 77-year-old right-handed man was admitted to the hospital because of the recentonset of pain in the ear, difficulty speaking, and altered mental status. The patienthad been well until the day before admission, when he awoke in the morning withnasal congestion and pain on the right side of his face. That evening, pain, accom-panied by drainage, developed in the right ear; his wife administered ciprofloxacineardrops. The next morning, the temperature was 37.8C. At about 9 a.m., the pa-tients wife noted that his speech was slurred. The patient said he was tired andretired to nap. Ninety minutes later, his wife found him on the floor, unresponsive,and she called emergency medical services.

When the emergency medical technicians arrived, the patient was conscious, hadincomprehensible speech, and could not walk. The blood pressure was 140/94 mm Hg,the pulse 160 beats per minute, and the oxygen saturation 100% while the patientwas receiving supplemental oxygen; the respiratory rate was 20 breaths per minute.Dried blood was present in the nares and mouth. The pupils were equal and reactiveto light, the facial expression was symmetrical, the right-hand grip was weak, andthe torso leaned to the right. The patient did not move his feet when requested to doso. He was transported by ambulance to the emergency department of this hospital,arriving at 12:30 p.m.

Several days before admission, the patient had slipped on an icy sidewalk and

struck his head. He did not lose consciousness and did not seek medical attention.He had hypertension, adenomatous colonic polyps, and a torn left medial meniscus;the baseline creatinine level was 1.3 mg per deciliter (115 mol per liter). Lip swell-ing suggestive of angioedema had occurred after he consumed shellfish; therewere no allergies to medications. Medications included omeprazole, diphenoxylate,lisinopril, chlorpheniramine, hydrochlorothiazide, and triamterene. The patient hadbeen born in China and had immigrated to the United States in his third decade.He was a retired university professor who lived with his wife and traveled toMarthas Vineyard, Massachusetts, and China frequently. He drank wine daily, didnot smoke, and had no recent exposure to animals. His father had died from acerebral hemorrhage, and his mother had died from complications of diabetes.

Case 34-2007: A 77-Year-Old Manwith Ear Pain, Difficulty Speaking,

and Altered Mental Status

Martin A. Samuels, M.D., R. Gilberto Gonzalez, M.D., Ph.D., Arthur Y. Kim, M.D.,

and Anat Stemmer-Rachamimov, M.D.

The New England Journal of Medicine

Downloaded from nejm.org by BRAVE RIKAZ on January 11, 2014. For personal use only. No other uses without permission.

Copyright 2007 Massachusetts Medical Society. All rights reserved.

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n engl j med 357;19 www.nejm.org november 8, 20071958

In the emergency department, the blood pres-sure was 95/77 mm Hg, rising to 163/94 mm Hgwithin 5 minutes after arrival; the pulse was 147beats per minute, the respiratory rate was 20breaths per minute, and the oxygen saturation was96% while the patient was breathing 5 liters ofoxygen per minute by means of a nasal cannula.

The temperature was 37.4C. On examination by aneurologist, the patient could be roused with mildstimulation; he had aphasia and did not followcommands. The gaze was midline without de-viation; the pupils were equal and each 4 mm indiameter, decreasing to 2 mm on direct illumina-tion. There was no ptosis or facial droop. Driedblood was present in the right external ear canal,both nares, and the oropharynx. The neck wassupple, and rhonchi were heard in both lungs. Theheart sounds were normal, and the abdomen wasdistended and tender in the right upper quadrant,

without bowel sounds. The patient moved botharms and legs purposefully in response to noxious

stimuli. The reflexes were 1+ in the arms, trace atthe patellar tendons, and absent at the Achillestendons; the plantar responses were flexor.

An electrocardiogram showed sinus tachycar-dia with first-degree atrioventricular block butwas otherwise normal. Laboratory-test results areshown in Table 1. Urinalysis revealed few bacteria

and three to five granular casts per high-powerfield. Thiamine and glucose were administeredintravenously, followed by lorazepam (4 mg).

Computed tomography (CT) of the head per-formed 1 hour after the patients arrival in theemergency department, without the adminis-tration of contrast material, revealed pneumo-cephalus, opacified right mastoid air cells, andage-related parenchymal changes. The initial in-terpretation suggested the presence of a longitu-dinal fracture of the right temporal bone. A chestradiograph was normal.

Ninety minutes after arrival, the temperaturerose to 38.6C, and blood specimens were sent

Table 1.Results of Hematology and Serum Chemistry Tests.*

Variable Adult Reference Values Values on Admission

Hematocrit (%) Males, 41.053.0 45.7

Hemoglobin (g/dl) 13.517.5 16.0

White-cell count (per mm3) 4,50011,000 8,600

Neutrophils (%) 4070 74

Band forms (%) 010 24

Myelocytes (%) 0 1

Reactive lymphocytes (%) 0 1

Platelet count (per mm3) 150,000350,000 99,000

Mean corpuscular volume (m3) 80100 98

Prothrombin time (sec) 11.113.1 13.9

Prothrombin time (international normalizedratio)

1.3

Partial-thromboplastin time (sec) 22.135.1 28.6

Antithrombin III, functional (%) 80130 74

Protein C, functional (%) 70140 75

Activated protein C resistance (>2.0) 2.5Protein S, functional (%) 70140 95

Fibrinogen Elevated

Glucose (mg/dl) 70110 202

Sodium (mmol/liter) 135145 137

Potassium (mmol/liter) 3.44.8 3.1

Chloride (mmol/liter) 100108 102

Carbon dioxide (mmol/liter) 2430 24.5




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case records of the massachusetts general hospital


for culture. Acetaminophen, ceftriaxone (2 g),metronidazole (500 mg), and vancomycin (1 g)were administered. Three hours after arrival,a lumbar puncture was performed; the open-ing pressure was 270 mm of water. The cerebro-spinal fluid was xanthochromic; the resultsof laboratory tests are shown in Table 2. Speci-

mens were sent for fungal, bacterial, and viralcultures; Grams staining; and testing for cryp-tococcal antigen and for herpes simplex virusDNA. The closing pressure was 170 mm ofwater.

Four hours after arrival, CT of the temporalbones, performed without the administration ofcontrast material, revealed pneumocephalus inthe right middle and anterior cranial fossae, fluidwithin the middle ear and mastoid air cells, andloss of the bony integrity of the tegmen tympani.There was no evidence of a fracture of the tem-

poral bone.The results of a diagnostic test were received.

Differential Diagnosis

Dr. Martin A. Samuels:Dr. Gonzalez, may we seethe images?

Dr. R. Gilberto Gonzalez:CT of the head showedpneumocephalus (Fig. 1A) and opacification ofthe right middle ear and mastoid air cells. There

was a question of a longitudinal temporal-bonefracture, and a dedicated temporal-bone CT scanwas obtained, which showed opacification of theright middle ear (Fig. 1B). Sagittal images dem-onstrated loss of integrity of the tegmen tympani(Fig. 1C). There was no evidence of a fracture.

Dr. Samuels:Was the air in the epidural, subdu-ral, or subarachnoid space?

Dr. Gonzalez:It appears to be subarachnoid. Theair pocket in the middle cranial fossa is round,with an airliquid level. If it were in the subduralor the epidural space, it would conform to the

shape of the skull.Dr. Samuels:Although this is clearly a case of

Table 1.(Continued.)

Variable Adult Reference Values Values on Admission

Urea nitrogen (mg/dl) 825 20

Creatinine (mg/dl) 0.61.5 1.8

Total bilirubin (mg/dl) 0.01.0 1.3

Conjugated bilirubin (mg/dl) 0.00.4 0.5

Total protein (g/dl) 6.08.0 6.9

Albumin (g/dl) 3.14.3 3.2

Globulin (g/dl) 2.64.1 3.7

Phosphorus (mg/dl) 2.64.5 0.9, slight hemolysis

Magnesium (mmol/liter) 0.71.0 0.6

Calcium (mg/dl) 8.510.5 9.1

Alkaline phosphatase (U/liter) 45115 93

Aspartate aminotransferase (U/liter) 1040 56

Alanine aminotransferase (U/liter) 1055 24

Creatine kinase (U/liter) 60400 139

Creatine kinase, MB fraction (ng/ml) 0.06.9 0.7

Troponin T (ng/ml) 0.000.09 0.02

Toxic screen panels 15 Diphenhydramine and quininepresent

* To convert the values for glucose to millimoles per liter, multiply by 0.05551. To convert the values for urea nitrogen tomillimoles per liter, multiply by 0.357. To convert the values for creatinine to micromoles per liter, multiply by 88.4. Toconvert the values for total and conjugated bilirubin to micromoles per liter, multiply by 17.1. To convert the values forphosphorus to millimoles per liter, multiply by 0.3229. To convert the values for magnesium to milliequivalents per li-ter, divide by 0.500. To convert the values for calcium to millimoles per liter, multiply by 0.250.

The reference values are affected by many variables, including the population of patients and the laboratory methods used.The ranges used at Massachusetts General Hospital are for adults who are not pregnant and do not have medical con-ditions that could affect the results. They may therefore not be appropriate for all patients.




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otitic meningitis, it raises several important ques-tions: the cause of the otorrhea, the meaning ofthe pneumocephalus, the risks of lumbar punc-ture, the cause of the aphasia, the likely causalorganism, and the cause of the defect in the teg-men tympani.

Otorrhea

This patient had drainage from his ear that wasvariously described as a discharge and as driedblood. Was this an infectious discharge from theexternal ear, or was it cerebrospinal fluid otor-rhea? Cerebrospinal fluid otorrhea refers to thepresence of cerebrospinal fluid in the externalauditory canal due to an abnormal connectionbetween the sub-arachnoid space and the tympa-nomastoid space. A rent in the tympanic mem-brane is required for the cerebrospinal fluid toenter the external ear. Otherwise, f luid accumu-lating in the middle ear is drained via the eusta-chian tube into the nasopharynx and often goesunrecognized.

An important clinical challenge is to recognize

when f luid emanating from the ear is, in fact,cerebrospinal f luid. Cerebrospinal f luid otorrheamay be serosanguineous and mistaken for blood,as was probably the case in this patient. Otorrheaand rhinorrhea may be recognized as containingcerebrospinal fluid when a handkerchief soakedin the fluid does not stiffen when dry, becauseof the fluids relatively low protein level (i.e.,

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fects in 2%.4Rarely, pneumocephalus may becaused by brain abscess involving air-formingorganisms,5but there is no evidence for such aninfection in this case. In this patient, the presenceof pneumocephalus is evidence of a cerebrospinalfluid fistula, which allowed cerebrospinal fluidto exit through the ear and air to enter from the

mastoid air cells of pneumatized bone or fromthe external auditory canal.

Pros and Cons of Lumbar Puncture

The chance of increased intracranial pressure issubstantial in the presence of otic infection. In theera before antibiotics, hydrocephalus in the pres-ence of otic infection was termed otitic hydro-cephalus; this was a misnomer in most cases,since it was usually increased levels of interstitialbrain water (pseudotumor) related to poor venousdrainage from the failure of one or more of the

dural sinuses. However, in the presence of lepto-meningitis, an authentic hydrocephalus may de-velop because of the slowing of cerebrospinalfluid flow and blockage of the resorption of cere-brospinal fluid into the venous system at thearachnoid granulations. The two processes (hydro-cephalus and pseudotumor) could therefore co-exist in this patient, producing increased intra-cranial pressure while leaving ventricular sizerelatively normal.

Fortunately, the neurologists caring for thispatient were not afraid to perform a lumbarpuncture, despite the risk of increased intracra-nial pressure. The risks of the procedure, thoughreal, are generally overrated, and I believe it islikely that many more patients have had a deterio-rating condition from the failure to perform theprocedure than have had a complication or deathresulting from the procedure. The presence of amass, particularly near the midline or in theposterior fossa, probably increases the risks. Ifthe clinician is concerned about performing theprocedure in a patient in whom it is indicated be-

cause of the real threat of infection, rapid imag-ing of the brain should be performed before theprocedure is undertaken.6

The cerebrospinal fluid in this patient was, in-deed, under increased pressure (270 mm of water)and showed a neutrophilic pleocytosis, an elevat-ed protein level, and a glucose level that wasabout 45% of the blood glucose level. All thesefindings strongly suggests a bacterial leptomen-ingitis. It is likely that the lumbar subarachnoidspace, accessible with the use of the spinal needle,

l

A

B

C

Figure 1.Radiologic Images of the Head.

CT of the head performed in the emergency department

shows pneumocephalus, with air adjacent to the rightfrontal lobe (Panel A, arrow). Subsequently, dedicated

temporal-bone CT, reformatted in the coronal plane,

showed opacification of the right middle ear (Panel B,arrow). The sagittal image shows loss of integrity of the

tegmen tympani (Panel C, arrow). There was no evidenceof a fracture.




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did not fully reflect the vigorousness of the in-flammatory response around the brain, becausethe fluid was not flowing freely. The elevatedcerebrospinal fluid protein level of 322 mg perdeciliter may, in part, reflect stagnation of cere-brospinal fluid, known as Froins syndrome.

Aphasia

One of the more interesting and cryptic aspects ofthis case is the aphasia. Disorders of speech andlanguage are complex and often difficult to char-acterize accurately in the presence of generalizedencephalopathy. I shall assume that the neurolo-gist was correct in characterizing this patientsproblem as aphasia, a disorder of language. Forvirtually all right-handed people and most left-handed people, the major systems for languageare strongly lateralized to the left hemisphere. Ingeneral, aphasias are produced by disorders that

affect the cerebrum, its subcortical connections,and the thalamus. It is uncommon, for example,to see aphasia with a subdural hematoma, a lesionon the surface of the brain, until the patient is sodrowsy that the language problem is diff icult todistinguish from a disorder of consciousness.

What disorder of the left hemisphere couldhave occurred in this patient? Septic dural sinusthrombosis is a common complication of infec-tion of the tympanomastoid space,7,8 but thatshould have affected the right transverse sinus,which should not produce aphasia. Dural sinusseptic thrombophlebitis only rarely spreads to theopposite transverse sinus. Cerebritis or brain ab-scess in the left hemisphere could have occurred byhematogenous spread of infection in the right ear,but the imaging studies showed no such lesion.

The most likely explanation is cerebral vaso-spasm in reaction to the pus in the subarachnoidspace. To produce aphasia, the middle cerebralarteries should be affected. Prolonged, severe vaso-spasm can lead to cerebral infarction, which maybe the major sequela in survivors of bacterial,

fungal, and tuberculous meningitis.

The Organism

What organism or organisms are responsible forthis otitic meningitis? The most common bacteriaare Streptococcus pneumoniae(about half of cases),Neisseria meningitidis(about one fifth of cases), Lis-teria monocytogenes(about one tenth of cases), andHaemophilus influenzae(about one tenth of cases).9-11If one hypothesizes that the infection in the earactually caused the bony erosion that led to the

cerebrospinal fluid fistula, one might favor moreaggressive organisms such as Staphylococcus aureus,gram-negative organisms, and group A strepto-coccus. However, the relationship of the tegmendefects to the course of the ear infection is notknown, so there is no way to predict the identityof the organism. The decision to treat the patient

with broad-spectrum antibiotics, including cover-age for anaerobic organisms, was well founded.The only additional intervention might have beenintravenous high-dose corticosteroids, but the datasupporting this approach are equivocal.6

Defects of the Tegmen Tympani

The final issue revolves around the defects of thetegmen tympani found on the temporal-bone CT.The tegmen tympani is the portion of the tempo-ral bone that overlies the tympanic and mastoidcavities, forming the floor of the middle fossa.

A few (less than five) defects in the tegmen arecommon and have been found in 15 to 34% ofcarefully examined temporal bones; however, fiveor more defects are rare (found in

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disrupted the fragile tegmen and, together withthe chronic otitis media, produced a new rent inthe tympanic membrane. Cerebrospinal fluid otor-rhea, pneumocephalus, and bacterial meningitisensued. The organism was aggressive, further erod-ing the tegmen tympani. Pus in the subarachnoidspace caused cerebral vasospasm, producing apha-

sia. The dural sinuses, particularly the right trans-verse sinus, became incompetent, leading to in-creased intracranial pressure. The diagnostic testswere probably the blood culture and cerebrospi-nal f luid culture, as well as magnetic resonanceimaging (MRI), angiography, and venography.

Dr. Nancy Lee Harris(Pathology): Dr. Caviness,you cared for this patient on the Neurology Ser-vice; can you comment on your thinking?

Dr. Verne S. Caviness, Jr. (Neurology): Dr. AlirezaAtri was the neurologist called to see the patientin the emergency department. Aphasia was pres-

ent before the patients mental status deteriorat-ed; we considered in retrospect that the patientmight have had a seizure and that the aphasiaand transient right hemiparesis might have beenpostictal. Dr. Atri immediately recognized thatthis was meningitis, instituted three-drug therapy,and performed the lumbar puncture. At that time,a temporal-bone fracture was considered andsearched for but could not be identified. We con-sidered a diastatic suture in the medial temporalbone. A defect in the tegmen tympani was notreported at the time.

Dr. Harris:Dr. Kim, what was the opinion of theconsultants from the Department of InfectiousDisease?

Dr. Arthur Y. Kim:We suspected bacterial menin-gitis from an otitic or a mastoid source or both.

Clinical Diagnosis

Bacterial meningitis due to otitis or mastoiditisor both.

Dr. Mart in A. SamuelssDiagnosis

Otitic bacterial leptomeningitis, secondary to teg-men tympani defects caused by arachnoid granula-tions, possibly aggravated by minor head trauma.

Pathological Discussion

Dr. Kim:The diagnostic test was Grams stainingof the cerebrospinal fluid specimen, which re-

vealed moderate numbers of gram-positive cocciin pairs and chains, suggesting streptococcal spe-cies. Although S. pneumoniaeremained a primaryconsideration, we also considered other organ-isms, including group A streptococci and entero-cocci. We recommended broad-spectrum antibi-otics to cover these possibilities. Within hours,

group A streptococci were grown on blood cultureand cerebrospinal f luid culture.

Group A streptococci are a rare cause of bac-terial meningitis, accounting for 0.5 to 1.5% ofcommunity-acquired cases10,11,14; the mortalityrate (27%) is similar to that for pneumococcalmeningitis (30%).6Otitis media due to group Astreptococci is associated with high rates of localinvasion, including tympanic perforation andmastoiditis, as was seen in this case,15and it isthe most important risk factor for group A strep-tococcal meningitis among adult patients.16Most

patients with group A streptococcal meningitisdo not have the clinical features of septic shockassociated with invasive group A streptococcaldisease, and the incidence of the meningitis hasnot increased despite an increasing incidence ofother forms of invasive disease.16,17After the cul-ture results were received, additional imagingstudies were performed.

Dr. Gonzalez:Brain MRI was performed beforeand after the administration of contrast material,as was magnetic resonance angiography and venog-raphy. In addition to the pneumocephalus, subtleareas of increased signal involved the cortex ofthe right temporal, parietal, and frontal lobes.Diffusion MRI did not show evidence of an acuteischemic event. The magnetic resonance veno-gram showed flow within all the major veinsand sinuses. The angiogram was limited by theartifact of the technique, but it did not showgood flow distal to the internal carotid arteriesor distal to the basilar arteries. This can some-times be seen in normal persons as an artifact,but we cannot rule out a process such as vaso-

spasm.Dr. Kim:Persistent hypotension and multiorganfailure ensued; vasopressor support was with-drawn, and death occurred 19 hours after admis-sion to the emergency department. Permissionfor an autopsy was obtained.

Dr. Anat Stemmer-Rachamimov:At autopsy, multi-ple petechial hemorrhages were noted in the duraoverlying the right middle fossa, and the under-lying right mastoid bone was swollen, soft, andhemorrhagic. The venous sinuses were free of




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thrombi. The leptomeninges appeared cloudy,with small collections of white, thick f luid sur-rounding small meningeal vessels that were mostprominent in the leptomeninges overlying thecerebral hemispheres (Fig. 2A).

Microscopical examination showed a dense in-flammatory infiltrate in the subarachnoid space,which was composed of neutrophils and imma-ture mononuclear cells (Fig. 2B). Fibrinoid necro-sis and thrombosis were noted in some of the

meningeal arterioles. In the brain parenchyma,inflammatory cells were clustered around corti-cal arterioles and scattered in the neuropil. Theinf lammation involved the left temporal lobe aswell as other areas of the brain.

Sections of the mastoid bone were reviewedwith Dr. Saumil Merchant (Massachusetts Eye andEar Infirmary). There was no evidence of fracture,a preexisting chronic inflammatory condition(such as a cholesteatoma) in the middle ear, orlabyrinthitis in the semicircular canals. In con-

trast, the mastoid mucosal lining was thickenedby means of vascular engorgement, edema, andinflammatory-cell infiltrates (Fig. 2C). Largeinflamed and necrotic arachnoid granulations(>3 mm in diameter) were noted in sections of themastoid bone (Fig. 2D), and aggregates of gram-positive cocci were present in the subarachnoidspace and in the mastoid air cells.

Arachnoid granulations may increase in sizewith age, and intermediate and large granula-

tions (3.0 to 9.5 mm in diameter) may herniatethrough dural defects and erode bone (aberrantgranulations).12,13,18,19The presence of large arach-noid granulations and the absence of fracture,preexisting middle-ear disease, and labyrinthitissuggest that a dural defect and bone erosioncaused by aberrant arachnoid granulations are themost probable route for intracranial extension ofthe suppurative mastoiditis in this case, whichthen led to acute meningoencephalitis.

Dr. Harris:Would either of the patients sons,

A B

DC

l

Figure 2.Pathological Examination of the Brain at Autopsy.

On gross examination, the leptomeninges were opaque and perivascular white exudate was present (Panel A, ar-

rows). Microscopical examination of the subarachnoid space showed an inflammatory infiltrate (Panel B) composedof neutrophils and some immature myeloid cells (inset) (hematoxylin and eosin). Examination of the right mastoid

bone showed an inflammatory infiltrate in the mastoid mucosa and mastoid air cells (Panel C). Aberrant arachnoidgranulations (Panel D, arrows) are large, necrotic, and inflamed.




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Dr. Thomas Lee or Dr. Richard Lee, like tocomment?

Dr. Thomas H. Lee, Jr. (Internal Medicine,Brigham and Womens Hospital): We learnedfrom this case that the care of patients doescontinue after they die. The performance of theautopsy and the careful review of all aspects of

this case for this conference provided us withtwo opportunities that I believe every familywho loses a loved one would appreciate. Thefirst was the opportunity to know what causedhis death. During hospitalization, we knew thatthere was a suspicion of a fracture on the CTscan; after my fathers death, we left the hospitalbelieving that his fall on the ice had caused thefracture and therefore his death. After the au-topsy, which showed no fracture, we realizedthat perhaps the fall had not caused his death.After the discussion at this conference, we now

have a final answer.

The second opportunity is to have somethinggood arise from tragedy. My brother and I knowthat our father, as a professor at the Massachu-setts Institute of Technology, would have beencompletely in favor of having his death contrib-ute to the education of physicians who will carefor patients in the future. He would have joked

that this was his final publication, and I wouldhave said to him, It is your first in a journalworth reading.

Anatomical Diagnosis

Acute bacterial meningoencephalitis, acute rightotitis media and mastoiditis, and aberrant arach-noid granulations with erosion of the tempor-al bone.

Dr. Samuels reports receiving consulting fees from M/C Com-munications. No other potential conflict of interest relevant tothis article was reported.

References

Oberascher G. Cerebrospinal fluidotorrhea new trends in diagnosis. AmJ Otol 1988;9:102-8.

Brodie HA, Thompson TC. Manage-ment of complications from 820 temporalbone fractures. Am J Otol 1997;18:188-97.

Brodie HA. Prophylactic antibiotics forposttraumatic cerebrospinal fluid f istulae:a meta-analysis. Arch Otolaryngol HeadNeck Surg 1997;123:749-52.

Andrews JC, Canalis RF. Otogenic

pneumocephalus. Laryngoscope 1986;96:521-8.

Parmar MS. Pneumocephalus associ-ated with Bacteroides fragilis meningitis.J Postgrad Med 2004;50:272-3.

van de Beek D, de Gans J, Tunkel AR,Wijdicks EFM. Community-acquired bac-terial meningitis in adults. N Engl J Med2006;354:44-53.

Southwick FS, Richardson EP Jr, SwartzMN. Septic thrombosis of the dural venoussinuses. Medicine (Baltimore) 1986;65:82-106.

Stam J. Thrombosis of the cerebralveins and sinuses. N Engl J Med 2005;352:1791-8.

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Schuchat A, Robinson K, Wenger JD,et al. Bacterial meningitis in the UnitedStates in 1995. N Engl J Med 1997;337:970-6.

Durand ML, Calderwood SB, WeberDJ, et al. Acute bacterial meningitis inadults: a review of 493 episodes. N Engl JMed 1993;328:21-8.

van de Beek D, de Gans J, Spanjaard L,Weisfelt M, Reitsma JB, Vermeulen M. Clin-ical features and prognostic factors in

adults with bacterial meningitis. N Engl JMed 2004;351:1849-59. [Erratum, N EnglJ Med 2005;352:950.]

Merchant SN, McKenna MJ. Neuroto-logic manifestations and treatment of mul-tiple spontaneous tegmental defects. AmJ Otol 2000;21:234-9.

Gacek RR. Arachnoid granulation cere-brospinal fluid otorrhea. Ann Otol RhinolLaryngol 1990;99:854-62.

Swartz MN, Dodge PR. Bacterial men-ingitis a review of selected aspects:general clinical features, special problems,and unusual meningeal reactions mim-icking bacterial meningitis. N Engl J Med1965;272:725-31.

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Segal N, Givon-Lavi N, Leibovitz E,Yagupsky P, Lieberman A, Dagan R. Acuteotitis media caused by Streptococcus pyo-genes in children. Clin Infect Dis 2005;41:35-41.

van de Beek D, de Gans J, Spanjaard L,Sela S, Vermeulen M, Dankert J. Group Astreptococcal meningitis in adults: reportof 41 cases and a review of the literature.Clin Infect Dis 2002;34(9):e32-e36.

Sommer R, Rohner P, Garbino J, et al.

Group A beta-hemolytic streptococcusmeningitis: clinical and microbiologicalfeatures of nine cases. Clin Infect Dis1999;29:929-31.

Gacek RR. Evaluation and manage-ment of temporal bone arachnoid granu-lations. Arch Otolar yngol Head Neck Surg1992;118:327-32.

Rosenberg AE, OConnell JX, OjemannRG, Plata MJ, Palmer WE. Giant cysticarachnoid granulations: a rare cause oflytic skull lesions. Hum Pathol 1993;24:438-41.Copyright 2007 Massachusetts Medical Society.

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