Malignant Otitis Externa Presenting With Nasopharyngeal Hematoma: A Case Report of an Unusual Complication

ABSTRACT

Objective

Malignant otitis externa (MOE) is a potentially life‐threatening infection of the external auditory canal (EAC), often with skull base extension. Vascular complications are exceptionally rare, with only six reports of petrous internal carotid artery (ICA) pseudoaneurysm following MOE.

Methods

We present the first reported case of a nasopharyngeal hematoma as a complication of MOE.

Results

An 82‐year‐old male with poorly controlled diabetes presented with 2 months of recurrent left ear otalgia, purulent otorrhea, and facial nerve palsy. He was commenced on 6 weeks of antimicrobial therapy following diagnosis of MOE on imaging. One month post‐treatment, an interval scan found a new collection in the left pharyngeal submucosal region expanding into the torus tubarius. Endoscopic examination revealed a left torus tubarius mass effacing the eustachian tube orifice with some blood‐stained mucous. The patient was otherwise afebrile and reported only mild trismus with rust‐colored sputum. Subsequent computed tomography (CT) imaging revealed that the mass was likely a subacute or evolving nasopharyngeal hematoma, in close proximity to the left petrous and caudal lacerum ICA, with mild luminal irregularities. An angiogram showed no active contrast extravasation or pseudoaneurysm. He was managed conservatively given the absence of active bleeding and a stable airway. A repeat nasoendoscopy 2 weeks later revealed interval decrease in size of the mass, with resolution of symptoms.

Conclusion

The pathophysiology of nasopharyngeal hematoma as a complication of MOE may involve direct infection‐mediated and inflammatory‐induced erosion of arterial walls. Though rare, nasopharyngeal hematomas should be considered in MOE patients with unexplained nasopharyngeal masses. These hematomas, especially when associated with luminal ICA irregularities, may represent a sentinel finding preceding the eventual formation of a carotid pseudoaneurysm. Thus, the presence of nasopharyngeal hematomas warrants vigilant surveillance, with escalation to urgent endovascular intervention in the event of vascular instability.

1. Introduction

Malignant otitis externa (MOE) is an aggressive infection of the external auditory canal (EAC) with potentially severe and life‐threatening complications if not promptly diagnosed and treated [1]. Its incidence is estimated at 0.221–1.19 cases per 100,000 individuals, with elderly and immunocompromised patients being particularly vulnerable [2]. Untreated, MOE can progress to skull base osteomyelitis, cranial neuropathies, and intracranial extension. This can be through contiguous spread from the external ear to the temporal bone, skull base, eventually extending into the intracranial space [2, 3].

Vascular complications from MOE are exceptionally rare. To date, only six cases of petrous internal carotid artery (ICA) pseudoaneurysm secondary to MOE have been reported in literature [4, 5]. We describe, to our knowledge, the first reported case of a nasopharyngeal hematoma arising as a complication of MOE. This case highlights a rare and diagnostically challenging presentation of the disease, underscores the importance of considering vascular pathology in atypical nasopharyngeal masses, and reviews the possible pathophysiology, diagnostic pitfalls, and management strategies. While nasopharyngeal masses in this setting often suggest abscess formation or a concurrent malignancy [6], recognition of occult vascular sequelae is equally as critical to prevent catastrophic outcomes.

2. Case Report

An 82‐year‐old man with poorly controlled Type 2 diabetes mellitus and chronic renal failure presented with recurrent left ear otalgia and otorrhea over 2 months. Despite multiple courses of oral ciprofloxacin and ototopic ofloxacin, his condition deteriorated, culminating in MOE complicated by a House‐Brackmann grade IV facial nerve palsy.

Otoscopic examination revealed purulent debris in the left EAC. Ear swab cultures grew Pseudomonas aeruginosa . Contrast‐enhanced computed tomography (CT) of the temporal bone demonstrated extensive bony and soft tissue involvement of the left EAC, middle ear, and mastoid air cells, consistent with acute mastoiditis superimposed on MOE. There was also involvement of the left intra‐temporal and post‐styloid spaces, with concerns of extension into the left middle cranial fossa.

The patient was subsequently treated with a total of 6 weeks of antimicrobial therapy, including 2 weeks of intravenous cefepime. This resulted in gradual clinical improvement. However, interval magnetic resonance imaging (MRI) of the temporal bone performed 1 month after completion of antibiotics revealed a new submucosal collection in the left nasopharynx, expanding into the torus tubarius. (Figure 1) This was initially suspected to represent an abscess. Clinically, the patient reported mild trismus, reduced oral intake, and intermittent expectoration of brown‐tinged sputum. Nasoendoscopy found a left torus tubarius mass obstructing the ipsilateral eustachian tube orifice, with overlying blood‐stained mucous, but no purulent drainage. (Figure 2) Inflammatory markers were unremarkable, and the patient remained afebrile. Epstein–Barr virus DNA was undetectable.

FIGURE 1.

MRI of nasopharynx. (A) Coronal T2W sequence showing 3.3 × 2.7 cm well circumscribed heterogeneous lesion in the left pharyngeal submucosal region expanding the left torus tubarius. (B) Axial T1W sequence showing left nasopharyngeal mass with areas of T1W hyperintensity. (C) Axial ADC (apparent diffusion coefficient) sequence showing left nasopharyngeal mass with focus of restricted diffusion inferiorly.

FIGURE 2.

Nasoendoscopy showing left nasopharyngeal mass over the torus tubarius, effacing the left eustachian tube orifice.

Subsequent contrasted CT demonstrated heterogeneous attenuation within the left nasopharyngeal mass, without rim‐enhancement or focal arterial enhancement. (Figure 3) The lesion was closely related to the left petrous and caudal lacerum segments of the ICA, which showed mild luminal irregularities but no discrete saccular outpouching or aneurysm. (Figure 3) The imaging findings favored a diagnosis of subacute or evolving nasopharyngeal hematoma, rather than an abscess.

FIGURE 3.

CT angiogram of the head. (A) CT angiogram delayed phase showing lesion in the left nasopharynx expanding the torus tubarius with heterogeneous attenuation, with no convincing arterial enhancing focus or rim‐enhancement at delayed phase. It is in close relationship to the left petrous ICA and caudal lacerum ICA. (B) CT angiogram showing mild luminal irregularity of the left petrous ICA. Mild luminal irregularity of the petrous and caudal lacerum segments of the left ICA is seen. (C) CT angiogram showing short segment of mild narrowing of the left petrous ICA.

Digital subtraction angiography (DSA) confirmed the absence of active contrast extravasation, pseudoaneurysm, or aneurysms involving the left ICA, external carotid artery (ECA), or vertebral artery (VA). The patient was managed conservatively, receiving 1 week of intravenous cefepime. Repeat nasoendoscopy 2 weeks post‐discharge demonstrated interval reduction in the size of the nasopharyngeal mass. The patient's trismus and blood‐stained sputum had also resolved completely. Follow‐up MRI of the nasopharynx at 6 weeks showed resolution of the hematoma.

In the context of MOE, some differential diagnoses initially considered were an abscess or malignancy, particularly nasopharyngeal carcinoma or a lymphoma. On imaging, a nasopharyngeal abscess typically demonstrates rim enhancement and may be accompanied clinically by systemic features of sepsis. In this patient, there was no convincing arterial enhancing focus or rim enhancement on the delayed phase. Furthermore, there was no clinical deterioration or raised inflammatory markers to suggest a deep neck space infection.

Malignancy, on the other hand, is usually characterized by an infiltrative soft tissue mass with aggressive bone destruction, nodal disease, or progressive enlargement despite antimicrobial therapy. The lesion in question was well‐circumscribed with no adjacent invasion, showed no pathologic lymphadenopathy, and demonstrated interval shrinkage without features of invasive neoplasia. Taking into consideration CT angiography findings of ICA irregularities, this futher supports the diagnosis of a hematoma.

3. Discussion

MOE is a destructive, invasive infection capable of extending from the EAC to the temporal bone, skull base, and surrounding neurovascular structures. Extension beyond the temporal bone produces a spectrum of well‐described complications such as skull base osteomyelitis, cranial nerve palsies, and intracranial sepsis [2]. However, vascular complications are uncommon and often underrecognized. To date only a small number of case reports have documented vascular sequelae of MOE, including petrous ICA pseudoaneurysms [4, 5] and internal maxillary artery pseudoaneurysms presenting with massive epistaxis [7].

Vascular complications in MOE include venous or submucosal bleeding and arterial pseudoaneurysm formation. Although both sequelae most commonly arise from contiguous infectious spread with secondary arterial wall involvement [8], subtle but important differences exist in the underlying pathophysiology.

In MOE, venous and submucosal bleeding are thought to result from infection‐driven inflammation and tissue necrosis, leading to erosion of low‐pressure submucosal veins and capillaries in the EAC, particularly in diabetic or immunocompromised patients. This can lead to slow, low‐volume hemorrhage rather than brisk arterial bleeding [9]. In this case, local tissue necrosis of adjacent soft tissue infection may have disrupted the integrity of small submucosal venules or capillaries, resulting in submucosal hemorrhage and contributing to the formation of the nasopharyngeal hematoma [10].

Arterial complications arise from direct infectious and inflammatory involvement of the arterial wall. Progressive spread of infection to the skull base and parapharyngeal spaces can result in infectious arteritis, with enzymatic degradation and necrosis of the adventitia and media, leading to progressive weakening of the vessel wall, permitting blood to dissect into adjacent soft tissues [11]. Ongoing hemodynamic stress on this structurally compromised artery may culminate in focal wall rupture and pseudoaneurysm formation, especially if the underlying infection is not well controlled. If the arterial defect is small or temporarily sealed by adjacent soft tissue and thrombus, submucosal hemorrhage and hematoma may occur in the absence of an angiographically detectable pseudoaneurysm [4].

Currently, diagnostic challenges arise when differentiating a nasopharyngeal hematoma from an abscess or neoplasm in the setting of diagnosed MOE. High‐resolution MRI and contrast‐enhanced CT scans can delineate lesion morphology, characterize soft tissue extent, and its relationship to vascular structures. However, they may not always reveal small pseudoaneurysms or active but slow arterial extravasation [12].

In equivocal cases or in situations where vascular involvement is suspected, timely DSA remains the gold standard for detecting the presence of an active arterial bleeding or a pseudoaneurysm, allowing for immediate therapeutic intervention if required [5]. In this case, DSA was quickly performed after MRI and CT imaging demonstrated a concerning vascular mass, in order to exclude an angiographically‐treatable lesion. We reinforce the need for timely multimodal imaging in evaluating vascular complications in a patient diagnosed with MOE.

Management of MOE‐related vascular sequelae must balance control of the primary infectious process, avoidance of iatrogenic hemorrhage, and timely intervention of underlying arterial lesions. Importantly, as evidenced in this case study, clinicians should not be quick to exclude vascular pathologies as a possible differential. In cases where the patient is hemodynamically stable, has no active bleed, no airway compromise, and negative angiography, conservative management with culture‐directed antimicrobial therapy, close endoscopic follow‐up, and interval imaging is reasonable [13]. While there are no existing standardized guidelines on when imaging should be repeated in the context of a pseudoaneurysm, existing literature states that repeat scans should be done within 6 months following treatment [14, 15]. Repeat scans are important to ensure resolution of the mass. In the event of active hemorrhage, expanding hematoma, or angiographic evidence of a pseudoaneurysm, urgent endovascular therapy would be warranted to prevent mortality [16].

4. Conclusion

This case study expands the recognized spectrum of MOE‐associated complications to include nasopharyngeal hematoma, a rare but clinically significant vascular manifestation. Even in the absence of angiographically demonstrable pseudoaneurysm, the presence of a nasopharyngeal mass in the context of MOE should prompt suspicion for occult vascular injury. Thus, vigilant surveillance and potential early involvement of interventional neuroradiology to enable rapid escalation to endovascular intervention if progression or bleeding occurs should be considered. Timely recognition, meticulous radiological evaluation, and multidisciplinary management are pivotal in preventing life‐threatening outcomes.

Funding

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Chen V. H. E., Chew N. S. M., and Ng L. S., “Malignant Otitis Externa Presenting With Nasopharyngeal Hematoma: A Case Report of an Unusual Complication,” Laryngoscope Investigative Otolaryngology 11, no. 1 (2026): e70348, 10.1002/lio2.70348.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.