When an Ear Infection Reaches the Brain: A Case of Sinus Thrombosis, Abscess and Hydrocephalus

A routine ear infection is something most people shrug off, but a newly published case report shows how, in rare circumstances, the same infection can march silently inward toward the brain and set off a cascade of life-threatening complications. Writing in Clinical Case Reports, a team of Romanian physicians describes a 44-year-old man who arrived at the hospital with a cerebellar abscess, obstructive hydrocephalus and extensive thrombosis of the major venous sinuses draining his brain, all traced back to a severe suppurative infection of the mastoid bone behind his left ear. The report, published open access in October 2026, offers a detailed look at how modern multidisciplinary teams untangle such emergencies, and it highlights several questions that still divide the field, including how aggressively surgeons should operate on a thrombosed venous sinus and whether anticoagulant drugs help or harm these patients.

The condition at the center of the case is otogenic sigmoid sinus thrombosis, an uncommon but feared intracranial complication of otomastoid infection, meaning infection of the middle ear and mastoid air cells. In this disease, infected material and inflammation extend from the temporal bone to the sigmoid sinus, one of the large venous channels that carry blood away from the brain, and a clot forms inside the vessel. The authors note that the older term lateral sinus thrombosis can be imprecise, because the lateral sinus encompasses both the transverse and sigmoid segments, and they argue that clinicians should describe the exact venous segments involved whenever possible. Contemporary literature, they add, generally supports combining medical and surgical treatment, while the extent of direct surgery on the sinus itself and the role of anticoagulation remain actively debated topics without randomized trial evidence to settle them.

The patient’s story began on 20 November 2024, when he was admitted to the neurosurgical service with no documented major comorbidities but with neuroimaging showing a left cerebellar abscess, obstructive hydrocephalus, and multiple intracranial venous sinus thromboses. The posterior fossa, the compartment housing the cerebellum and brainstem, is an unforgiving location for a growing abscess, because swelling there can compress the fourth ventricle and block the circulation of cerebrospinal fluid, driving pressure upward throughout the skull. Surgeons therefore moved on the day of admission, placing an external ventricular drain through a right frontal approach to divert cerebrospinal fluid and evacuating the cerebellar abscess through an occipital craniectomy. The referral documentation did not specify how long his symptoms had lasted or whether he had received antibiotics before arriving at the hospital, a gap that would later complicate the microbiological picture.

Once the immediate neurosurgical emergency was controlled, the patient was transferred intubated and mechanically ventilated to the ear, nose and throat service, whose task was to find and eradicate the source of the infection. High-resolution computed tomography of the temporal bone showed opacification of the left mastoid air cells and middle ear cavity, consistent with otomastoiditis and pointing to an otogenic origin for the intracranial disaster. Otomicroscopy revealed a polypoid lesion in the left external auditory canal, mainly in the anteroinferior quadrant, with bulging of the medial canal wall, while the visible portions of the tympanic membrane appeared intact. Formal audiometry was impossible in the acute setting because the patient was on a ventilator, and no quantitative hearing test from earlier evaluations was available to the team.

On 22 November 2024, surgeons performed a left canal-wall-down radical mastoidectomy, an operation that removes the infected bone and creates an open, drainable cavity. What they found inside was striking. The mastoid cavity was packed with chronically inflamed polypoid mucosa, the ossicular chain of the middle ear was partially eroded, the intratympanic segment of the facial nerve was dehiscent, meaning its bony covering was missing, and the plate of bone over the sigmoid sinus had been destroyed by disease. Through that dehiscent plate, the team could see an actual thrombus sitting inside the sigmoid sinus, a direct visual confirmation of the clot that imaging had suggested. Purulent secretion was collected for bacteriological analysis, tissue fragments went to histopathology, and hemostasis was secured before the cavity was packed with sterile gauze.

Here the case takes on its most instructive dimension: what the surgeons chose not to do. Despite directly visualizing the intrasigmoid thrombus, they did not incise the sinus, did not attempt thrombectomy, and did not ligate the internal jugular vein. Historically, management of otogenic sigmoid sinus thrombosis often included exactly those maneuvers, but contemporary practice tends to reserve direct sinus procedures for selected situations such as persistent septicemia, septic embolization, progressive thrombosis despite treatment, or failure of source control. The team weighed the extensive venous thrombosis, the very recent posterior fossa surgery, the substantial postoperative bleeding risk, and the absence of documented persistent septicemia, and concluded that otologic source control without opening the sinus was a reasonable, risk-balanced strategy. Histopathology showed severe suppurative polypoid otomastoiditis with destructive inflammatory changes; cholesteatoma, a keratin-producing destructive lesion that was clinically suspected, was not confirmed under the microscope.

The recovery was not linear. Early after mastoidectomy, otorrhea and vertigo improved, but on 6 December 2024 a follow-up cranial CT revealed recurrence or enlargement of the left cerebellar abscess, now measuring roughly 12 by 48 millimeters with surrounding edema and mass effect. The patient was transferred back to neurosurgery on 9 December but discharged himself the same day against medical advice, returning on 11 December, when repeat posterior fossa surgery was performed; the procedural record from 13 December documented drainage of the intracranial infection and posterior fossa decompression. The authors caution that the recurrence cannot be pinned on a single cause. Plausible contributors include advanced disease at presentation, a residual infected collection, impaired venous drainage, and the culture-negative microbiology that prevented therapy from being narrowed to a specific pathogen.

That microbiological silence is itself a central lesson of the report. Purulent mastoid secretion tested after 48 hours grew no pathogenic bacteria and no Candida species; cerebrospinal fluid obtained on 18 December was culture-negative with no organisms on Gram staining and no acid-fast bacilli on Ziehl-Neelsen staining; and otic and fungal cultures from 20 December were also negative. Blood cultures and cultures from the initial abscess drainage were unavailable in the reviewed records. With no isolate, susceptibility testing could not guide treatment, so the team relied on broad empirical coverage: piperacillin-tazobactam 4.5 grams every eight hours combined with amikacin 500 milligrams every twelve hours, reconstructible from the medication chart as approximately 18 treatment days of the former and 9 of the latter. Anticoagulation was similarly fragmented rather than protocolized, with unfractionated heparin listed around the second neurosurgical intervention, a single recorded enoxaparin syringe in intensive care, and additional heparin entries during the ENT admission lacking route, dose, frequency and duration. No anti-Xa monitoring, thrombophilia work-up or outpatient anticoagulation plan was documented.

By 17 December 2024, postoperative CT showed that the cerebellar abscess cavity had disappeared, with reduced edema and mass effect, yet the left internal jugular vein, sigmoid sinus and transverse sinus still failed to opacify with contrast, and no spontaneous recanalization was seen. The authors emphasize the distinction this reveals between clinical recovery and venous outcome: the patient improved even though his venous system had not. They note that MRI with magnetic resonance venography is generally preferred for characterizing thrombus and tracking venous follow-up, and they are careful not to claim that recanalization occurred. After intensive care from 13 to 15 December, during which he was weaned from sedation and successfully extubated, he returned to the ENT ward, where serohematic secretion interpreted as otoliquorrhea, a leak of fluid suggestive of cerebrospinal fluid, progressively diminished and remitted by discharge on 30 December 2024, afebrile and without documented neurological deficit.

The authors are candid about the limits of what this single case can prove. Retrospective documentation, the patient’s failure to attend the planned three-month outpatient reassessment, and missing blood-culture, audiological and venographic data all restrict conclusions about optimal antimicrobial duration, anticoagulation strategy and long-term outcome. Yet the report’s practical value survives those limitations. It demonstrates that otogenic sigmoid sinus thrombosis can present first as a neurological emergency, with posterior fossa abscess, hydrocephalus and widespread venous thrombosis overshadowing the ear disease that caused them; that staged neurosurgical and otologic source control remains the backbone of treatment; that conservative management of a thrombosed sinus can be defensible even when clot is visible at the operating table; and that favorable early outcomes are possible even when cultures stay negative and venous recanalization is not yet demonstrated, provided urgent source control, careful imaging surveillance and individualized, risk-balanced anticoagulant decisions are prioritized.

Subject of Research: Otogenic sigmoid sinus thrombosis complicated by cerebellar abscess and hydrocephalus

Article Title: Otogenic Sigmoid Sinus Thrombosis Complicated by Cerebellar Abscess and Hydrocephalus: A Case Report

Article References: Bizdu‐Branovici, A. M., Gherasie, L., Ionița, I. G., Zica, M. D., Rusescu, A., Hainaroșie, R., & Zainea, V. (2026). Otogenic Sigmoid Sinus Thrombosis Complicated by Cerebellar Abscess and Hydrocephalus: A Case Report. Clinical Case Reports, 14(10), Article e73589. https://doi.org/10.1002/ccr3.73589

Image Credits: AI Generated

DOI: 10.1002/ccr3.73589

Keywords: sigmoid sinus thrombosis, otogenic infection, cerebellar abscess, hydrocephalus, mastoidectomy, otomastoiditis, cerebral venous sinus thrombosis, anticoagulation, neurosurgery, ear infection, case report, posterior fossa