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Table of Contents    
LETTER TO EDITOR
Year : 2020  |  Volume : 68  |  Issue : 3  |  Page : 694-695

Bacterial Meningitis in Patient with Sigmoid Sinus Diverticulum


1 Department of Ophthalmology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas, USA
2 Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave. Box 673, Rochester NY, 14642, USA

Date of Web Publication6-Jul-2020

Correspondence Address:
Dr. Menachem Weiss
Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.288978

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How to cite this article:
Weiss M, Risco J. Bacterial Meningitis in Patient with Sigmoid Sinus Diverticulum. Neurol India 2020;68:694-5

How to cite this URL:
Weiss M, Risco J. Bacterial Meningitis in Patient with Sigmoid Sinus Diverticulum. Neurol India [serial online] 2020 [cited 2020 Aug 12];68:694-5. Available from: http://www.neurologyindia.com/text.asp?2020/68/3/694/288978




Sir,

A sigmoid sinus diverticulum (SSD) is an aneurysmal dilatation of the brain's dural venous sinus into the adjacent mastoid bone. Turbulent blood within the diverticulum reverberates against the nearby cochlea producing pulsatile tinnitus. This malformation is present in nearly a quarter of pulsatile tinnitus cases.[1] Newly diagnosed patients are predominantly middle-aged women.[2] Surgical correction of SSD, via transmastoid or endovascular approaches, can resolve tinnitus.[2],[3] This vascular malformation has no other established clinical repercussions.

We describe a patient who, on anticoagulation, developed right bloody otorrhea followed by bacterial meningitis. Imaging revealed a right-sided sigmoid sinus diverticulum (SSD), mastoid, and middle ear effusion. The patient's clinical course suggests that the SSD bled into the mastoid and ear, providing a route for infection.

A 75-year-old woman with a past medical history of hypertension and atrial fibrillation on anticoagulation presented to the emergency department after two days of right-sided bloody otorrhea and otalgia. On the morning of presentation, she awoke with headache and emesis, prompting the visit. On arrival, the patient's daughter noted new onset word-finding difficulty. This triggered a neurology stroke consultation. The patient's daughter denied preceding altered mental status, history of recurrent headaches, fever, purulent otorrhea, or injury.

On arrival, the blood pressure was 170/78 mmHg, heart rate was 83/min and irregular, temperature was 37.2°C, respiratory rate was 24/min, and SpO2 was 92%. Dried blood covered her right ear canal and tympanic membrane. There was no evidence of trauma, polyps, tumors, foreign body, infection, or ruptured tympanic membrane. The patient was somnolent, had decreased attention, and was intermittently agitated. She had nonfluent speech with frequent paraphasic errors. Her neck was supple.

Within an hour of arrival, the patient's vitals changed. She became tachycardic and febrile with a heart rate of 120/min and temperature of 39.3°C. Blood cultures were drawn. Otolaryngology was consulted and advised that there was no component of mastoiditis. She was empirically started on meningitic doses of ceftriaxone, vancomycin, acyclovir, ampicillin, and metronidazole. Dexamethasone was administered for suspected pneumococcal meningitis. Lab work revealed a white blood cell count of 11,500/μL on arrival which increased to 18,900/μL (75% neutrophils) and 22,500/μL (76.2% neutrophils) eight and 12 hours later, respectively. C-reactive protein was 118 mg/L, lactate was 3.6 mmol/L, and INR was 2.9.

The lumbar puncture was delayed, given her anticoagulation with warfarin, until her INR normalized following administration of Kcentra/Vitamin K. Lumbar puncture revealed an opening pressure >55 cm of H2O and cloudy CSF. There was pleocytosis (nucleated cells 11,972/μL, with 98% polymorphonuclear cells), elevated red blood cells (1139/μL), decreased glucose (<2 mg/dL), and elevated protein (>600 mg/dL). Her blood glucose at the time of lumbar puncture was 142 mg/dL. CSF stain revealed Gram-positive cocci in pairs though no organism was isolated on culture. Blood cultures obtained prior to starting antibiotics revealed growth at 9 hours and Streptococcus pneumoniae was eventually isolated.

CT and CT angiography showed right-sided sigmoid sinus diverticulum, mastoid, and middle-ear opacification [Figure 1]. MRI revealed a fluid level within the ventricles, consistent with pus, without pneumocephally. The remainder of her workup was unremarkable—chest x-ray, abdominal and pelvic CT, urinalysis.
Figure 1: CT venogram of the head. The white arrow indicates the right sigmoid sinus diverticulum (a). Noncontrasted axial CT of the temporal bone, displaying both for comparison. There is opacification of the right mastoid air cells. The white arrow indicates bone erosion of the right temporal bone at the site of the sigmoid sinus diverticulum. The black arrow indicates the corresponding area of the normal left sigmoid sinus (b). Noncontrasted CT of the right temporal bone. The white arrow indicates opacification of the middle ear cavity (c)

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The patient was diagnosed with bacterial meningitis complicated by septic shock. On the day of admission, her mental status continued to decline, requiring intubation. She required an external ventricular drain and hypertonic saline for raised intracranial pressure. After six days, the patient was extubated. With organism susceptibility, antibiotics were narrowed to ceftriaxone followed by levofloxacin. There was no further ear bleeding during her hospitalization. Anticoagulation was restarted. After ten days, she was discharged to an acute rehab facility, where she remained for 11 days. Upon discharge to home, she had mild executive dysfunction and mobility impairment.

The patient's clinical course suggests that the sigmoid sinus diverticulum (SSD) bled into the mastoid and ear, providing a route for infection and, subsequently, meningitis. To the best of our knowledge, this is the first description of a vascular malformation presumed to predispose a CNS infection.

Bacterial meningitis is a deadly infectious disease of the leptomeninges. The organisms responsible for meningitis access the CNS through different routes. Infection can occur via hematogenous dissemination or direct invasion from a contiguous source. The latter occurs with disruption of the meninges from trauma, surgery, medical devices (shunts, intracranial pressure monitors), or contiguous infection (mastoiditis, sinusitis). Persistent meningeal disruption can lead to recurrent meningitis.

Our patient's presentation began with bloody otorrhea, raising concerns for infection through direct invasion. Bloody otorrhea can result from trauma, polyps, tumors, foreign body, or bullous myringitis. Inspection of our patient's ear canal ruled out these causes. The patient's bloody discharge was not cultured, which may have yielded additional information. Instead, imaging revealed a mastoid and middle ear effusion. Mastoiditis and associated otitis media would present with purulent discharge, which our patient did not have. However, an ipsilateral SSD was present. In the absence of an alternate explanation, it is likely that the SSD was the source of the hemorrhage.

This patient's presentation progressed from otorrhea to meningitis. Rapidly changing vitals, mental status, and inflammatory markers indicate that meningitis developed quickly on the morning of admission. This suggests that the SSD bled, providing a route for infection.

The need to repair her SSD is unclear. She does not have pulsatile tinnitus, the only known indication for surgery. She may be at risk of recurrent hemorrhage and meningitis. We adopted a watchful and waiting approach. Her otorrhea spontaneously resolved and the risks and benefits of restarting anticoagulation were also considered. Her CHA2 DS2-VASc score was 4 and it was decided to restart her anticoagulation.

SSD is a known cause of pulsatile tinnitus. Our case suggests that it can also cause bloody otorrhea and potentially meningitis. Patients with bloody otorrhea or recurrent meningitis of undetermined etiology may require vascular imaging as part of their workup. To the best of our knowledge, this is the first description of a vascular malformation presumably predisposing a CNS infection.[4]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Schoeff S, Nicholas B, Mukherjee S, Kesser BW. Imaging prevalence of sigmoid sinus dehiscence among patients with and without pulsatile tinnitus. Otolaryngol Head Neck Surg 2014;150:841-6.  Back to cited text no. 1
    
2.
Wang GP, Zeng R, Liu ZH, Liang XH, Xian JF, Wang ZC, et al. Clinical characteristics of pulsatile tinnitus caused by sigmoid sinus diverticulum and wall dehiscence: A study of 54 patients. Acta Otolaryngol 134;2014:7-13.  Back to cited text no. 2
    
3.
Houdart E, Chapot R, Merland JJ. Aneurysm of a dural sigmoid sinus: A novel vascular cause of pulsatile tinnitus. Ann Neurol 2000;48:669-71.  Back to cited text no. 3
    
4.
Srivastava AK, Khanna N, Sardana V, Gaekwad S, Prasad K, Behari M. Cerebral venous thrombosis in ulcerative colitis. Neurol India. 2002;50:215-7.  Back to cited text no. 4
    


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