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This study reviews clinical presentations, microbiological profiles, treatment outcomes, and prognostic factors. Methods A retrospective analysis was conducted at the Otorhinolaryngology Department of Mohammed VI University Hospital, Marrakech, including 39 patients hospitalized with necrotizing otitis externa between January 2020 and December 2024. Data included clinical assessments, laboratory markers (erythrocyte sedimentation rate), microbiological cultures, and high-resolution computed tomography imaging. All patients received systemic antimicrobial therapy and were followed for at least 6 months. Results The cohort (mean age 61.1 years; male-to-female ratio 2.25:1) had diabetes mellitus in 63.3% of cases, with 55.6% showing poor glycemic control (hemoglobin A1c greater than 7%). Common symptoms were severe otalgia (89.7%) and otorrhea (30.7%). Facial nerve palsy occurred in 18%. Microbiological analysis revealed Pseudomonas aeruginosa in 30% of cases and fungal pathogens in 23%. Erythrocyte sedimentation rate was elevated in 92%, with significantly higher values in fungal infections. Computed tomography imaging showed temporal bone erosion in 56.4%. Treatment involved combined intravenous ceftazidime and ciprofloxacin for 6–8 weeks, with systemic antifungals added for fungal infections. Complete resolution was achieved in 69.2% of patients; 30.8% had persistent disease requiring prolonged therapy. Conclusion Necrotizing otitis externa management requires long-term, targeted antimicrobial treatment guided by culture results and inflammatory markers. The emerging prevalence of fungal pathogens and rising antibiotic resistance necessitate updated treatment protocols. Necrotizing otitis externa Skull base osteomyelitis Pseudomonas aeruginosa treatment protocols Figures Figure 1 Figure 2 Introduction Necrotising otitis externa (NOE), also known as malignant external otitis or skull base osteomyelitis, is a severe infection of the ear canal with frequent bone erosion and local complications [1]. It is considered a severe infection that typically affects the elderly, patients with diabetes, and immunocompromised patients. Its high morbidity is related to frequent bone erosion and potential local complications. Pseudomonas aeruginosa is the main causative organism, but other species of bacteria, including methicillin-resistant Staphylococcus Aureus (MRSA), as well as fungal species have been reported [2]. The clinical presentation is varied and the treatment is mainly medical, based on antimicrobial agents. However, we have witnessed a rise in antimicrobial resistance to both antifungal and antibacterial agents. Therefore, our management protocols should be re-evaluated and updated continuously. The primary goal of this study is to review our experience while describing the clinical, microbiological and radiological features of NOE as well as its management. Materials and Methods This is a retrospective study carried out in the ENT Department of Mohammed VI University Hospital of Marrakech. It included all the patients hospitalized, for the management of NOE, over a 5 years period between January 2020 and December 2024. Thirty- nine patients were included in the study. Diagnostic workup data consists of history and clinical assessment. Laboratory tests were collected from all the patients including, random blood sugar testing on admission, erythrocyte Sedimentation rate (ESR) and glycated hemoglobin level (HbA1C). Swabs of the external ear canal; for Gram/aerobic, fungal, BAAR/mycobacteria exam/culture; were conducted for each patient. Bacterial identification was established using the conventional morphological and biochemical methods. All patients underwent High Resolution CT of the temporal bone. All patients with NOE were hospitalized and appropriate investigation and treatment had been instituted. A follow-up investigation of the patients involved in this study was carried out for a minimum of 6 months to assess their response to the treatment and re-emergence of symptoms. All statistical analyses were carried out using Microsoft office Excel Statistics Data Editor, version 2010. Results 1. Epidemiology and Demographics Thirty-nine cases of NOE were identified with a sex ratio Male/Female of 2.25:1 (27 males, 12 females). The average age was 61.1 years, with a range of 43 to 74 years. Diabetes mellitus and chronic kidney disease represented 63,33% and 27% of our cases respectively. Interestingly, it has been found that 27.1% of NOE cases are comorbid with hypertension. Diabetes severity was assessed based on glycated hemoglobin (HbA1c) levels at diagnosis. Of those with diabetes (n=25), 40% (n=10) had HbA1c above 7.0%, reflecting poor glucose control prior to diagnosis of NOE. The macrovascular and microangiopathic effects of diabetes were present in a significant proportion: 63.2% (n = 12) had ischemic heart disease, 15.8% (n = 3) had peripheral vascular disease, and 26.3% (n = 5) had end-stage renal failure. Lastly, a history of either acute otitis externa or otitis media was present in 43% of the cases in our series. 2. Clinical presentation A total of 39 patients with NOE were recruited in this study. The predominant complaint, reported by 89.7% (n = 35) of patients, was primary otalgia along with otorrhea in 30.7% (n = 12). Facial nerve palsy presented as the primary symptom with moderate dysfunction (House–Brackmann grades II–III) in 18% (n = 7) of cases. Moreover, 3 patients experienced parotid swelling and pain over the temporomandibular joint (7.6%). The average timeframe before diagnosis of Necrotizing otitis externa (NOE) was 1 month (range, 1-12 weeks). Paralysis of the soft palate was observed in one patient because of the probable expansion of the infection to the skull base, affecting the glossopharyngeal nerve (cranial nerve IX). In addition to the seventh cranial nerve (grade II), the sixth and trigeminal nerve were affected in another patient (Gradenigo's syndrome). Patient characteristics are summarized below in Table 1. Table 1. Distribution of clinical signs and symptoms SIGN AND SYMPTOMS Number of CASES Severe otalgia 35 otorrhea 12 Facial nerve palsy 7 Parotid swelling 3 Petrous apicitis (GRADENIGO’S syndrome) 2 3. Inflammatory markers Regarding inflammatory markers, white blood cells (WBC) were within normal limits in most patients. ESR was significantly elevated in 92% of patients (median 85 mm/h, IQR 69-106). Patients with fungal infections demonstrated higher ESR values compared to bacterial cases (median 106 vs. 69 mm/h; p=0.032). Our series confirmed that ESR correlates with disease severity: patients with fungal‑dominant infections exhibited a markedly higher median ESR than those with bacterial isolates, suggesting that ESR may reflect more aggressive tissue invasion (Fig. 1). No relationship was observed between ESR and the degree of disease spread on the CT scan. Abnormal Blood glucose level was seen in 20 patients with the mean glycemic value of 10.1 mmol/L. 1. Imaging Erosion of temporal bone on CT scan was described in 22 patients, with 18% of them having cranial nerve involvement. CT scan was likely nonspecific and may showed soft tissue swelling around the External Auditory Canal in the remaining cases (n=17). In two cases, the infection extended anteriorly to the petrous apex, infratemporal region, pterygopalatine fossa, clivus, and sphenoid sinuses, with associated infiltration of the adjacent meninges. 2. Microbiology In our series of 39 patients, microbiological analysis revealed a predominance of Pseudomonas aeruginosa (30%), including seven cases where it was the only organism isolated. This finding is consistent with the classical microbiological profile of malignant external otitis. Other pathogens identified were Staphylococcus aureus (15.3%), Candida species (23%), Proteus mirabilis (12.8%), Escherichia coli (10%), Enterococcus species (5%), and Streptococcus pyogenes (2.5%). Normal swab results were obtained in 12.8% of patients (Table 2). Biopsy of granulation tissue from the external ear canal was obtained in 25 patients. Histopathological examination described non-specific granulation tissue and inflammation. Table 2. Microbiological findings from ear canal swabs (n=39)] Swab finding No of patients % of patients Pseudomonas Aeruginosa 12 30% Staphylococcus Aureus 6 15,3% Fungal otitis (Candida albicans, Candida parapsilosis, Candida auris) 9 23% Enterococcus 2 5% Escherichia coli 4 10% Proteus mirabilis 5 12,8% Streptococcus pyogenes 1 2,5% NORMAL FINDINGS 5 12,8% 3. Treatment Given the predominance of Pseudomonas aeruginosa, all patients received combination antibiotic therapy: intravenous ceftazidime (2 g every 8 hours) plus ciprofloxacin (500 mg three times daily). This regimen was selected for its favorable safety profile, excellent bone penetration, and demonstrated in-vitro activity against predominant isolate. The introduction of these agents has markedly improved outcomes, with cure rates approaching 90% and minimal adverse effects. Despite early symptomatic improvement, treatment was maintained for 6–8 weeks following osteomyelitis management principles. For patients with fungal infections; representing 23% of the cohort—systemic antifungal therapy was incorporated into the treatment plan. Voriconazole or fluconazole administered intravenously at 4 mg/kg every 12 hours was used depending on species sensitivity and clinical presentation. Empirical antifungal therapy proved effective in cases with no clinical improvement, even when fungal cultures were negative. These therapeutic compounds were administered alongside local care measures, using topical Fluoroquinolone antibiotic, frequent suction in order to ensure resolution of the otologic infection and preventing progression to deeper tissue involvement. For cases resistant to Ciprofloxacin or Ceftazidime, Amikacin, Cefoperazone-Sulbactam, and Piperacillin remain effective alternatives, with Amikacin reserved for cases with preserved renal function. Surgical management was applied for diagnostic purposes only. In accordance with current therapeutic standards, operative intervention was limited to obtaining biopsy tissue, when necessary, as quinolone and antifungal therapies provided adequate disease control in the vast majority of cases. 4. Evolution The clinical course showed a generally favorable response to medical therapy. 27 patients achieved full resolution of symptoms and inflammatory markers by the end of the 6-week treatment period, while a group of 12 cases demonstrated persistent disease requiring prolonged management. Persistence tended to be more frequent among older individuals, particularly those aged 65 years and above; representing 25% of the cohort. This category showed slower clinical improvement compared with younger subjects. Discharge criteria included clinical improvement, normalization of ESR, and adequate glycemic control, with continued oral ciprofloxacin for six weeks. Among the initially resolved cases, 4 patients (14.8%) experienced recurrence of symptoms or demonstrated radiologic progression on follow-up imaging and eventually were hospitalized for further evaluation. In these cases, treatment was intensified, typically involving extended courses of intravenous antibiotics and additional microbiological or imaging assessments to ensure adequate disease control. The first case of NOE was described by Toulmouche in 1838 [3], and the term “malignant otitis externa” was introduced by Chandler in 1968. Although its global incidence remains unknown, available series indicate that NOE is rare. Age‑related prognosis remains controversial. In our series, the under-50-year age group has the lowest annual incidence, whereas the over 65-year age group exhibits the highest incidence. Some studies show poorer outcomes in patients >70 years due to comorbidities such as diabetes and atherosclerosis, whereas others report no direct correlation between age and prognosis [4]. Diabetes mellitus is the strongest associated comorbidity, with reported prevalence between 65% and 95%. Microangiopathy and impaired immune defenses predispose diabetic patients to NOE. However, HbA1c levels do not consistently correlate with disease severity, likely due to long‑standing microvascular changes [5]. In our cohort, 25 patients had known diabetes; 5 of the remaining cases were newly diagnosed. Higher HbA1c values were associated with prolonged hospitalization. Early NOE symptoms mimic simple otitis externa, contributing to diagnostic delay (mean 6.79 weeks). Facial nerve palsy is a frequent and clinically significant complication of necrotizing (malignant) otitis externa, occurring in roughly one‑third of patients [6]. Pathophysiologically, the infection can spread from the external auditory canal to the stylomastoid foramen via the osteocartilaginous junction and fissures of Santorini, rendering the facial nerve susceptible to bony erosion and inflammation [7]. Fungal necrotizing otitis externa, particularly Aspergillus infections, carries a higher risk of facial nerve palsy (75 % vs. 34 % in bacterial cases), highlighting its aggressive nature. Facial paralysis is associated with more severe disease and higher recurrence, though not consistently with mortality. Its involvement is a hallmark complication, underscoring the importance of early imaging and timely antimicrobial or surgical intervention to prevent permanent deficits [8]. Inflammatory markers, especially ESR and CRP, are valuable predictors of necrotizing otitis externa, with ESR showing the strongest diagnostic value (area‑under‑curve 0.92 for ESR and 0.80 for CRP), while other clinical and radiologic parameters are less reliable [9]. Leukocytosis is generally absent and is therefore unreliable for follow up. Nevertheless, longitudinal monitoring of both ESR and WBC, together with CRP, is recommended because persistent elevation after 6–8 weeks of therapy reliably signals ongoing infection and guides treatment duration [10]. Imaging is essential for delineating the anatomic spread of necrotizing otitis externa (NOE) and for monitoring therapeutic response, yet no single modality captures every disease facet [11]. Computed tomography (CT) is universally regarded as CT is universally regarded as the rapid first-line imaging study it readily visualizes cortical bone erosion and trabecular demineralization, findings that are pathognomonic for established NOE and that guide urgent biopsy planning [11]. Its diagnostic sensitivity rises from ≈ 70 % when bone erosion alone is considered to ≈ 96 % when any associated soft‑tissue abnormality is included, underscoring the value of combined bone‑and‑soft‑tissue assessment [12]. CT can therefore confirm disease extension beyond the external auditory canal in virtually all cases, as demonstrated in a cohort of 39 patients where every individual showed erosive changes on initial CT [13]. Although CT is less sensitive to the earliest osteomyelitic changes and may remain abnormal long after clinical remission, it remains indispensable for detecting the bony involvement that underlies facial‑nerve palsy and skull‑base spread. Consequently, MRI and radionuclide studies complement it for soft‑tissue and metabolic evaluation [14]. Management of necrotizing otitis externa (NOE) is challenged by its aggressive course and the lack of randomized trials, forcing clinicians to rely on retrospective series and expert consensus [15]. Pseudomonas aeruginosa remains the predominant pathogen, especially in diabetic patients, and its persistence drives the widespread use of antipseudomonal agents [16]. While topical antibiotics have uncertain benefit, systemic therapy is essential; most studies favour a dual‑phase regimen that begins with intravenous ceftazidime—often combined with oral ciprofloxacin—to achieve rapid bacterial clearance, followed by oral ciprofloxacin for step‑down therapy [17]. The University College London dual-phase regimen protocol (three weeks IV ceftazidime + ciprofloxacin, then three weeks oral ciprofloxacin) reported an 86 % cure rate in a 37‑patient cohort, underscoring the practicality of a structured IV‑to‑oral pathway [18]. Ceftazidime’s favorable safety profile and lack of reported resistance make it a cornerstone for severe or complicated disease, outperforming older aminoglycoside‑penicillin combinations in cure rates and tolerability. Ciprofloxacin’s excellent tissue penetration and oral bioavailability support its role in both initial and maintenance phases, yet recent series document rising resistance rates (35–79 %) that mandate culture‑guided adjustments [19]. Concurrently, fungal aetiology is emerging as a major contributor. A systematic review of fungal malignant otitis externa found fungi in 54 % of cases, with Candida and Aspergillus equally represented [20]. Retrospective analyses of 43 patients and of 15 patients with fungal necrotising otitis externa likewise report Candida as the predominant pathogen and emphasize culture‑directed treatment. In our own cohort, the fungal‑dominant group showed markedly higher ESR values (median 106 mm/h, range 77–135 mm/h) than the bacterial group (median 69 mm/h, range 51–87 mm/h), reinforcing the clinical impact of fungal infection [21-22]. We propose a management algorithm tailored to local resistance patterns and supported by strict glycemic control and meticulous aural debridement (Fig. 2). Finally, lack of clinical improvement should prompt repeat cultures or biopsy to differentiate resistant bacterial from fungal disease. Our treatment duration of 6–7 weeks is consistent with published data and supports the safety of transitioning to oral therapy once clinical stability is achieved [10-23]. Conclusion Necrotizing Otitis Externa (NOE) has dramatically improved in prognosis, dropping from a 50% mortality rate in the 1960s to a manageable infection today [4]. However, challenges remain, including the lack of validated prognostic markers and standardized antibiotic protocols. Current evidence is limited by small, retrospective studies, highlighting the need for large, prospective, multicenter research to develop evidence-based guidelines for diagnosis, risk assessment, and treatment, ultimately improving patient outcomes. Declarations Acknowledgments The authors sincerely thank the entire medical and paramedical team involved in the care of the of the patient for their dedication and support. Funding This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Competing Interests The authors declare that they have no competing interests. Author Contributions All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Laila Liqali and Youssef Lakhdar. The first draft of the manuscript was written by Laila Liqali and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript. Data Availability The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request. Ethics Approval This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of the Faculty of Medicine and Pharmacy of Marrakech, Morocco (Approval No. TH N° 178/25, dated 09 November 2025), Consent to Participate Informed consent was obtained from all individual participants included in the study. References Hasnaoui M, Derbel L, Daldoul F, Khalfallah A, Belhaj S, Kharrat M, Cherif A. (2020). Necrotising otitis externa: A single centre experience. Journal of Otology , 15(4), 171-176. PMC7814081 Handzel, O., & Halperin, D. (2003). Necrotizing (Malignant) External Otitis. American Family Physician, 68(2), 309-312. Toulmouche MA. Observations on acute otitis externa, complicated by facial and masticatory muscle paralysis, and followed by death from meningitis. Arch Gen Med. 1838;18:337-346 Chandler JR. Malignant external otitis. Laryngoscope. 1968;78(8):1257-1294. doi:10.1288/00005537-196808000-00002 Teronpi, Mirbon; Bhattacharjee, Abhinandan; Senapati, Arup; Nath, Sudip Kumar. Clinico-microbiological Study on Otitis Externa (Necrotizing) in Patients with Diabetes Mellitus. Indian Journal of Otology 30(3):p 157-161, Jul–Sep 2024. DOI: 10.4103/indianjotol.indianjotol_30_24 Dabiri, S., Karrabi, N., Yazdani, N., Rahimian, A., Kheiltash, A., Hasibi, M., & Saedi, E. (2020). Facial nerve paralysis in malignant otitis externa: comparison of the clinical and paraclinical findings. Acta Oto-Laryngologica, 140(12), 1056–1060. https://doi.org/10.1080/00016489.2020.1808242 Sreepada GS, Kwartler JA. Skull base osteomyelitis secondary to malignant otitis externa. Curr Opin Otolaryngol Head Neck Surg. 2003;11(5):316-323. doi:10.1097/00020840-200310000-00005 Ali T, Meade K, Anari S, ElBadawey MR, Zammit-Maempel I. Malignant otitis externa: case series. J Laryngol Otol . 2010;124(8):846-851. doi:10.1017/S0022215110000560 Stern Shavit S, Soudry E, Hamzany Y, Nageris B. Malignant external otitis: factors predicting patient outcomes. Am J Otolaryngol . 2016 Sep-Oct;37(5):425-30. doi:10.1016/j.amjoto.2016.04.005. Rubin Grandis J, Branstetter BF 4th, Yu VL. The changing face of malignant (necrotising) external otitis: clinical, radiological, and anatomic correlations. Lancet Infect Dis . 2004;4(1):34-39. doi:10.1016/s1473-3099(03)00858-2 Adams A, Offiah C. Central skull base osteomyelitis as a complication of necrotizing otitis externa: Imaging findings, complications, and challenges of diagnosis. Clin Radiol . 2012;67(10):e7-e16. doi:10.1016/j.crad.2012.02.004. Sudhoff H, Rajagopal S, Mani N, et al. 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Ciprofloxacin: drug of choice in the treatment of malignant external otitis (MEO). Laryngoscope . 1991;101(8):821-824. doi:10.1288/00005537-199108000-00004 Omran AA, Aref ZF, Menaissy YM, Omran M. Initial intravenous ceftazidime and fluoroquinolones for malignant otitis externa: a retrospective cohort study. J Chemother . 2020;32(3):146-152. doi:10.1080/1120009X.2020.1721175. Lengyel A, Farkas Z, Csomor P, Kénessey I, Tiszlavicz L, Vörös A. Clinical observations in malignant otitis externa. Folia Microbiol (Praha) . 2021;66(4):645-651. doi:10.1007/s12223-021-00872-2 Chawdhary G, Pankhania R, Douglas S, Bottrill I. Fungal malignant otitis externa: systematic review and individual patient data meta-analysis. Otol Neurotol . 2022;43(5):e548-e555. doi:10.1097/MAO.0000000000003523 Cohen D, Friedman P. The diagnostic criteria of malignant external otitis. J Laryngol Otol . 1987;101(3):216-221. doi:10.1017/s0022215100101599. Soudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of malignant external otitis with facial paralysis. Arch Otolaryngol Head Neck Surg . 2007;133(10):1002-1004. doi:10.1001/archotol.133.10.1002. Arslan, I.B., Pekcevik, Y. & Cukurova, I. Management and long-term comorbidities of patients with necrotizing otitis externa. Eur Arch Otorhinolaryngol 280, 2755–2761 (2023). https://doi.org/10.1007/s00405-022-07784-y Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Revision Version 1 posted Editorial decision: Revision requested 21 Mar, 2026 Editor assigned by journal 03 Feb, 2026 Submission checks completed at journal 03 Feb, 2026 First submitted to journal 02 Feb, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8767938","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":585070390,"identity":"388363f0-8b58-4aaa-af79-ab56b68bfaf3","order_by":0,"name":"Laila Liqali¹","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA90lEQVRIie3RvWrDMBSG4U8InMW1VwcCvQV3ayAl12IydGn3jicE3MXNnEy9i8wSGrIEsgY0ee/gbKZ46FHaWcpYiN7JFnr0g4BY7B+WQSwV8JgCklTHI8koQBIIYlIwEaQ3bkQGCeAIHJGpGwqSkSHVo5hke700s+/dfSYhuvOLh6QV6YYPNj5UZF7X9qGWkOPtznewilTKpFSONFYwSeSdj+Qt6cGRY0tm2th5mBS8+GWXE3+gt9UVhBeflHyXE2/3QXZRS7Hy3iXPn9v26202z44L0/WDffp8X+nu7CG/lbi8DkTt/gSF5v/lCIYrJ8disdhN9QPpmVLFmqawCgAAAABJRU5ErkJggg==","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":true,"prefix":"","firstName":"Laila","middleName":"","lastName":"Liqali¹","suffix":""},{"id":585070391,"identity":"2c35a9be-9cd6-4546-8050-666e837ddc06","order_by":1,"name":"Youssef Lakhdar¹","email":"","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":false,"prefix":"","firstName":"Youssef","middleName":"","lastName":"Lakhdar¹","suffix":""},{"id":585070393,"identity":"19b66c8a-73d6-4712-aa61-80f55be7dd9f","order_by":2,"name":"Omar Oulghoul¹","email":"","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":false,"prefix":"","firstName":"Omar","middleName":"","lastName":"Oulghoul¹","suffix":""},{"id":585070395,"identity":"1955075a-eaff-4019-98d6-d4e93850ddaf","order_by":3,"name":"Mohamed CHEHBOUNI¹","email":"","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":false,"prefix":"","firstName":"Mohamed","middleName":"","lastName":"CHEHBOUNI¹","suffix":""},{"id":585070396,"identity":"473d1558-6aeb-4f59-ade1-1b4c7481d67c","order_by":4,"name":"Othmane Benhoummad²","email":"","orcid":"","institution":"University Hospital Center Mohammed VI of Agadir","correspondingAuthor":false,"prefix":"","firstName":"Othmane","middleName":"","lastName":"Benhoummad²","suffix":""},{"id":585070397,"identity":"f5f77bee-8e51-447f-b37f-ec874bfd5989","order_by":5,"name":"Youssef Rochdi¹","email":"","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":false,"prefix":"","firstName":"Youssef","middleName":"","lastName":"Rochdi¹","suffix":""},{"id":585070399,"identity":"45c7bd5d-228b-47d5-b061-d6294301ea03","order_by":6,"name":"Abdelaziz Raji¹","email":"","orcid":"","institution":"University Hospital Center Mohammed VI","correspondingAuthor":false,"prefix":"","firstName":"Abdelaziz","middleName":"","lastName":"Raji¹","suffix":""}],"badges":[],"createdAt":"2026-02-02 17:53:48","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8767938/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8767938/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":102310643,"identity":"885fd75b-67fa-4cbc-ab7c-eba0e8f6f25b","added_by":"auto","created_at":"2026-02-10 11:55:39","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":22711,"visible":true,"origin":"","legend":"\u003cp\u003eESR correlations with infection type in necrotizing otitis externa\u003c/p\u003e\n\u003cp\u003eNo relationship was observed between ESR and the degree of disease spread on the CT scan. Abnormal Blood glucose level was seen in 20 patients with the mean glycemic value of 10.1 mmol/L.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-8767938/v1/6b19016bb8c5c050dbd56640.png"},{"id":102310791,"identity":"dd743b45-5a9b-4d6c-bdea-157a1dd1617a","added_by":"auto","created_at":"2026-02-10 11:56:14","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":236374,"visible":true,"origin":"","legend":"\u003cp\u003eSuggested treatment algorithm for NOE based on a case series of 39 patients from Head and Neck Surgery Department, University Hospital Center Mohammed VI, Marrakech (EAC = External Auditory Canal/ BAAR = Bacilli Alcool-Acido Resistenti)\u003c/p\u003e","description":"","filename":"floatimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8767938/v1/6f265807178459d09d2e6a98.jpeg"},{"id":102311828,"identity":"fbba05dd-074e-4515-a64f-ccb44647dcdc","added_by":"auto","created_at":"2026-02-10 11:59:05","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":850490,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8767938/v1/f3608cd5-be80-4d5c-a99d-34643d6a38af.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Necrotizing Otitis Externa: A 5 years perspective on Treatment Outcomes and Prognostic Factors","fulltext":[{"header":"Introduction","content":"\u003cp\u003eNecrotising otitis externa (NOE), also known as malignant external otitis or skull base osteomyelitis, is a severe infection of the ear canal with frequent bone erosion and local complications [1].\u003c/p\u003e\n\u003cp\u003eIt is considered a severe infection that typically affects the elderly, patients with diabetes, and immunocompromised patients. Its high morbidity is related to frequent bone erosion and potential local complications. Pseudomonas aeruginosa is the main causative organism, but other species of bacteria, including methicillin-resistant Staphylococcus Aureus (MRSA), as well as fungal species have been reported [2].\u003c/p\u003e\n\u003cp\u003eThe clinical presentation is varied and the treatment is mainly medical, based on antimicrobial agents. However, we have witnessed a rise in antimicrobial resistance to both antifungal and antibacterial agents. Therefore, our management protocols should be re-evaluated and updated continuously.\u003c/p\u003e\n\u003cp\u003eThe primary goal of this study is to review our experience while describing the clinical, microbiological and radiological features of NOE as well as its management.\u0026nbsp;\u003c/p\u003e"},{"header":"Materials and Methods","content":"\u003cp\u003eThis is a retrospective study carried out in the ENT Department of Mohammed VI University Hospital of Marrakech. It included all the patients hospitalized, for the management of NOE, over a 5 years period between January 2020 and December 2024.\u003c/p\u003e\n\u003cp\u003eThirty- nine patients were included in the study. Diagnostic workup data consists of history and clinical assessment. Laboratory tests were collected from all the patients including, random blood sugar testing on admission, erythrocyte Sedimentation rate (ESR) and glycated hemoglobin level (HbA1C). Swabs of the external ear canal; for Gram/aerobic, fungal, BAAR/mycobacteria exam/culture; were conducted for each patient. Bacterial identification was established using the conventional morphological and biochemical methods.\u003c/p\u003e\n\u003cp\u003eAll patients underwent High Resolution CT of the temporal bone. All patients with NOE were hospitalized and appropriate investigation and treatment had been instituted.\u003c/p\u003e\n\u003cp\u003eA follow-up investigation of the patients involved in this study was carried out for a minimum of 6 months to assess their response to the treatment and re-emergence of symptoms.\u003c/p\u003e\n\u003cp\u003eAll statistical analyses were carried out using Microsoft office Excel Statistics Data Editor, version 2010.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003e\u003cstrong\u003e1. Epidemiology and Demographics\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThirty-nine cases of NOE were identified with a sex ratio Male/Female of 2.25:1 (27 males, 12 females). \u0026nbsp;The average age was 61.1 years, with a range of 43 to 74 years. \u0026nbsp;\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eDiabetes mellitus and chronic kidney disease represented 63,33% and 27% of our cases respectively. \u0026nbsp; Interestingly, it has been found that 27.1% of NOE cases are comorbid with hypertension. Diabetes severity was assessed based on glycated hemoglobin (HbA1c) levels at diagnosis. Of those with diabetes (n=25), 40% (n=10) had HbA1c above 7.0%, reflecting poor glucose control prior to diagnosis of NOE.\u003c/p\u003e\n\u003cp\u003eThe macrovascular and microangiopathic effects of diabetes were present in a significant proportion: 63.2% (n = 12) had ischemic heart disease, 15.8% (n = 3) had peripheral vascular disease, and 26.3% (n = 5) had end-stage renal failure.\u003c/p\u003e\n\u003cp\u003eLastly, a history of either acute otitis externa or otitis media was present in 43% of the cases in our series.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e2. Clinical presentation\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA total of 39 patients with NOE were recruited in this study.\u003c/p\u003e\n\u003cp\u003eThe predominant complaint, reported by 89.7% (n = 35) of patients, was primary otalgia along with otorrhea in 30.7% (n = 12). Facial nerve palsy presented as the primary symptom with moderate dysfunction (House\u0026ndash;Brackmann grades II\u0026ndash;III) in 18% (n = 7) of cases. Moreover, 3 patients experienced parotid swelling and pain over the temporomandibular joint (7.6%).\u003c/p\u003e\n\u003cp\u003eThe average timeframe before diagnosis of Necrotizing otitis externa (NOE) was 1 month (range, 1-12 weeks).\u003c/p\u003e\n\u003cp\u003eParalysis of the soft palate was observed in one patient because of the probable expansion of the infection to the skull base, affecting the glossopharyngeal nerve (cranial nerve IX). In addition to the seventh cranial nerve (grade II), the sixth and trigeminal nerve were affected in another patient (Gradenigo\u0026apos;s syndrome).\u003c/p\u003e\n\u003cp\u003ePatient characteristics are summarized below in Table 1.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1.\u0026nbsp;\u003c/strong\u003eDistribution of clinical signs and symptoms\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"481\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSIGN AND SYMPTOMS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNumber of CASES\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003eSevere otalgia\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e35\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003eotorrhea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e12\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003eFacial nerve palsy\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003eParotid swelling\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 329px;\"\u003e\n \u003cp\u003ePetrous apicitis (GRADENIGO\u0026rsquo;S syndrome)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 151px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003e3. Inflammatory markers\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eRegarding inflammatory markers, white blood cells (WBC) were within normal limits in most patients.\u003c/p\u003e\n\u003cp\u003eESR was significantly elevated in 92% of patients (median 85 mm/h, IQR 69-106). Patients with fungal infections demonstrated higher ESR values compared to bacterial cases (median 106 vs. 69 mm/h; p=0.032).\u003c/p\u003e\n\u003cp\u003eOur series confirmed that ESR correlates with disease severity: patients with fungal‑dominant infections exhibited a markedly higher median ESR than those with bacterial isolates, suggesting that ESR may reflect more aggressive tissue invasion (Fig. 1).\u003c/p\u003e\n\u003cp\u003eNo relationship was observed between ESR and the degree of disease spread on the CT scan. Abnormal Blood glucose level was seen in 20 patients with the mean glycemic value of 10.1 mmol/L.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e1. Imaging\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eErosion of temporal bone on CT scan was described in 22 patients, with 18% of them having cranial nerve involvement.\u003c/p\u003e\n\u003cp\u003eCT scan was likely nonspecific and may showed soft tissue swelling around the External Auditory Canal in the remaining cases (n=17). In two cases, the infection extended anteriorly to the petrous apex, infratemporal region, pterygopalatine fossa, clivus, and sphenoid sinuses, with associated infiltration of the adjacent meninges.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e2. Microbiology\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn our series of 39 patients, microbiological analysis revealed a predominance of Pseudomonas aeruginosa (30%), including seven cases where it was the only organism isolated. This finding is consistent with the classical microbiological profile of malignant external otitis. Other pathogens identified were Staphylococcus aureus (15.3%), Candida species (23%), Proteus mirabilis (12.8%), Escherichia coli (10%), Enterococcus species (5%), and Streptococcus pyogenes (2.5%). Normal swab results were obtained in 12.8% of patients (Table 2).\u003c/p\u003e\n\u003cp\u003eBiopsy of granulation tissue from the external ear canal was obtained in 25 patients. Histopathological examination described non-specific granulation tissue and inflammation.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2.\u0026nbsp;\u003c/strong\u003eMicrobiological findings from ear canal swabs (n=39)]\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"620\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSwab finding\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNo of patients\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e% of patients\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePseudomonas Aeruginosa\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e12\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e30%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eStaphylococcus Aureus\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e15,3%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFungal otitis (Candida albicans, Candida parapsilosis, Candida auris)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e23%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEnterococcus\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e5%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEscherichia coli\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e10%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eProteus mirabilis\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e12,8%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eStreptococcus pyogenes\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e2,5%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNORMAL FINDINGS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 207px;\"\u003e\n \u003cp\u003e12,8%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003e3. Treatment\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eGiven the predominance of Pseudomonas aeruginosa, all patients received combination antibiotic therapy: intravenous ceftazidime (2 g every 8 hours) plus ciprofloxacin (500 mg three times daily). This regimen was selected for its favorable safety profile, excellent\u003c/p\u003e\n\u003cp\u003ebone penetration, and demonstrated in-vitro activity against predominant isolate.\u003c/p\u003e\n\u003cp\u003eThe introduction of these agents has markedly improved outcomes, with cure rates approaching 90% and minimal adverse effects. Despite early symptomatic improvement, treatment was maintained for 6\u0026ndash;8 weeks following osteomyelitis management principles.\u003c/p\u003e\n\u003cp\u003eFor patients with fungal infections; representing 23% of the cohort\u0026mdash;systemic antifungal therapy was incorporated into the treatment plan. Voriconazole or fluconazole administered intravenously at 4 mg/kg every 12 hours was used depending on species sensitivity and clinical presentation. Empirical antifungal therapy proved effective in cases with no clinical improvement, even when fungal cultures were negative.\u003c/p\u003e\n\u003cp\u003eThese therapeutic compounds were administered alongside local care measures, using topical Fluoroquinolone antibiotic, frequent suction in order to ensure resolution of the otologic infection and preventing progression to deeper tissue involvement.\u003c/p\u003e\n\u003cp\u003eFor cases resistant to Ciprofloxacin or Ceftazidime, Amikacin, Cefoperazone-Sulbactam, and Piperacillin remain effective alternatives, with Amikacin reserved for cases with preserved renal function.\u003c/p\u003e\n\u003cp\u003eSurgical management was applied for diagnostic purposes only. In accordance with current therapeutic standards, operative intervention was limited to obtaining biopsy tissue, when necessary, as quinolone and antifungal therapies provided adequate disease control in the vast majority of cases.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e4. Evolution\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe clinical course showed a generally favorable response to medical therapy. 27 patients achieved full resolution of symptoms and inflammatory markers by the end of the 6-week treatment period, while a group of 12 cases demonstrated persistent disease requiring prolonged management. Persistence tended to be more frequent among older individuals, particularly those aged 65 years and above; representing 25% of the cohort. This category showed slower clinical improvement compared with younger subjects.\u003c/p\u003e\n\u003cp\u003eDischarge criteria included clinical improvement, normalization of ESR, and adequate glycemic control, with continued oral ciprofloxacin for six weeks.\u003c/p\u003e\n\u003cp\u003eAmong the initially resolved cases, 4 patients (14.8%) experienced recurrence of symptoms or demonstrated radiologic progression on follow-up imaging and eventually were hospitalized for further evaluation. In these cases, treatment was intensified, typically involving extended courses of intravenous antibiotics and additional microbiological or imaging assessments to ensure adequate disease control.\u003c/p\u003e\n\u003cp\u003eThe first case of NOE was described by Toulmouche in 1838 [3], and the term \u0026ldquo;malignant otitis externa\u0026rdquo; was introduced by Chandler in 1968. Although its global incidence remains unknown, available series indicate that NOE is rare.\u003c/p\u003e\n\u003cp\u003eAge‑related prognosis remains controversial. In our series, the under-50-year age group has the lowest annual incidence, whereas the over 65-year age group exhibits the highest incidence. Some studies show poorer outcomes in patients \u0026gt;70 years due to comorbidities such as diabetes and atherosclerosis, whereas others report no direct correlation between age and prognosis [4].\u003c/p\u003e\n\u003cp\u003eDiabetes mellitus is the strongest associated comorbidity, with reported prevalence between 65% and 95%. Microangiopathy and impaired immune defenses predispose diabetic patients to NOE. However, HbA1c levels do not consistently correlate with disease severity, likely due to long‑standing microvascular changes [5].\u003c/p\u003e\n\u003cp\u003eIn our cohort, 25 patients had known diabetes; 5 of the remaining cases were newly diagnosed. Higher HbA1c values were associated with prolonged hospitalization.\u003c/p\u003e\n\u003cp\u003eEarly NOE symptoms mimic simple otitis externa, contributing to diagnostic delay (mean 6.79 weeks). Facial nerve palsy is a frequent and clinically significant complication of necrotizing (malignant) otitis externa, occurring in roughly one‑third of patients [6]. Pathophysiologically, the infection can spread from the external auditory canal to the stylomastoid foramen via the osteocartilaginous junction and fissures of Santorini, rendering the facial nerve susceptible to bony erosion and inflammation [7]. Fungal necrotizing otitis externa, particularly Aspergillus infections, carries a higher risk of facial nerve palsy (75 % vs. 34 % in bacterial cases), highlighting its aggressive nature. Facial paralysis is associated with more severe disease and higher recurrence, though not consistently with mortality. Its involvement is a hallmark complication, underscoring the importance of early imaging and timely antimicrobial or surgical intervention to prevent permanent deficits [8].\u003c/p\u003e\n\u003cp\u003eInflammatory markers, especially ESR and CRP, are valuable predictors of necrotizing otitis externa, with ESR showing the strongest diagnostic value (area‑under‑curve 0.92 for ESR and 0.80 for CRP), while other clinical and radiologic parameters are less reliable [9]. Leukocytosis is generally absent and is therefore unreliable for follow up. Nevertheless, longitudinal monitoring of both ESR and WBC, together with CRP, is recommended because persistent elevation after 6\u0026ndash;8 weeks of therapy reliably signals ongoing infection and guides treatment duration [10].\u003c/p\u003e\n\u003cp\u003eImaging is essential for delineating the anatomic spread of necrotizing otitis externa (NOE) and for monitoring therapeutic response, yet no single modality captures every disease facet [11]. Computed tomography (CT) is universally regarded as CT is universally regarded as the rapid first-line imaging study it readily visualizes cortical bone erosion and trabecular demineralization, findings that are pathognomonic for established NOE and that guide urgent biopsy planning [11]. Its diagnostic sensitivity rises from \u0026asymp; 70 % when bone erosion alone is considered to \u0026asymp; 96 % when any associated soft‑tissue abnormality is included, underscoring the value of combined bone‑and‑soft‑tissue assessment [12]. CT can therefore confirm disease extension beyond the external auditory canal in virtually all cases, as demonstrated in a cohort of 39 patients where every individual showed erosive changes on initial CT [13]. Although CT is less sensitive to the earliest osteomyelitic changes and may remain abnormal long after clinical remission, it remains indispensable for detecting the bony involvement that underlies facial‑nerve palsy and skull‑base spread. Consequently, MRI and radionuclide studies complement it for soft‑tissue and metabolic evaluation [14].\u003c/p\u003e\n\u003cp\u003eManagement of necrotizing otitis externa (NOE) is challenged by its aggressive course and the lack of randomized trials, forcing clinicians to rely on retrospective series and expert consensus [15]. Pseudomonas aeruginosa remains the predominant pathogen, especially in diabetic patients, and its persistence drives the widespread use of antipseudomonal agents [16]. While topical antibiotics have uncertain benefit, systemic therapy is essential; most studies favour a dual‑phase regimen that begins with intravenous ceftazidime\u0026mdash;often combined with oral ciprofloxacin\u0026mdash;to achieve rapid bacterial clearance, followed by oral ciprofloxacin for step‑down therapy [17]. The University College London dual-phase regimen protocol (three weeks IV ceftazidime + ciprofloxacin, then three weeks oral ciprofloxacin) reported an 86 % cure rate in a 37‑patient cohort, underscoring the practicality of a structured IV‑to‑oral pathway [18]. Ceftazidime\u0026rsquo;s favorable safety profile and lack of reported resistance make it a cornerstone for severe or complicated disease, outperforming older aminoglycoside‑penicillin combinations in cure rates and tolerability. Ciprofloxacin\u0026rsquo;s excellent tissue penetration and oral bioavailability support its role in both initial and maintenance phases, yet recent series document rising resistance rates (35\u0026ndash;79 %) that mandate culture‑guided adjustments [19].\u003c/p\u003e\n\u003cp\u003eConcurrently, fungal aetiology is emerging as a major contributor. A systematic review of fungal malignant otitis externa found fungi in 54 % of cases, with Candida and Aspergillus equally represented [20]. Retrospective analyses of 43 patients and of 15 patients with fungal necrotising otitis externa likewise report Candida as the predominant pathogen and emphasize culture‑directed treatment. In our own cohort, the fungal‑dominant group showed markedly higher ESR values (median 106 mm/h, range 77\u0026ndash;135 mm/h) than the bacterial group (median 69 mm/h, range 51\u0026ndash;87 mm/h), reinforcing the clinical impact of fungal infection [21-22].\u003c/p\u003e\n\u003cp\u003eWe propose a management algorithm tailored to local resistance patterns and supported by strict glycemic control and meticulous aural debridement (Fig. 2).\u003c/p\u003e\n\u003cp\u003eFinally, lack of clinical improvement should prompt repeat cultures or biopsy to differentiate resistant bacterial from fungal disease. Our treatment duration of 6\u0026ndash;7 weeks is consistent with published data and supports the safety of transitioning to oral therapy once clinical stability is achieved [10-23].\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eNecrotizing Otitis Externa (NOE) has dramatically improved in prognosis, dropping from a 50% mortality rate in the 1960s to a manageable infection today [4]. However, challenges remain, including the lack of validated prognostic markers and standardized antibiotic protocols. Current evidence is limited by small, retrospective studies, highlighting the need for large, prospective, multicenter research to develop evidence-based guidelines for diagnosis, risk assessment, and treatment, ultimately improving patient outcomes.\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eAcknowledgments\u003c/h2\u003e\n\u003cp\u003eThe authors sincerely thank the entire medical and paramedical team involved in the care of the of the patient for their dedication and support.\u003c/p\u003e\n\u003ch3\u003eFunding\u003c/h3\u003e\n\u003cp\u003eThis research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003ch3\u003eCompeting Interests\u003c/h3\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003ch3\u003eAuthor\u0026nbsp;Contributions\u003c/h3\u003e\n\u003cp\u003eAll authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Laila Liqali and Youssef Lakhdar. The first draft of the manuscript was written by Laila Liqali and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003ch3\u003eData\u0026nbsp;Availability\u003c/h3\u003e\n\u003cp\u003eThe datasets generated during and/or analysed during the current study are available from the corresponding\u0026nbsp;author\u0026nbsp;on\u0026nbsp;reasonable\u0026nbsp;request.\u003c/p\u003e\n\u003ch3\u003eEthics\u0026nbsp;Approval\u003c/h3\u003e\n\u003cp\u003eThis study was performed in line with the principles of the Declaration of Helsinki.\u0026nbsp;Approval was granted by the Ethics Committee of the Faculty of Medicine and Pharmacy of Marrakech, Morocco (Approval No. TH N° 178/25, dated 09 November 2025),\u003c/p\u003e\n\u003ch3\u003eConsent to Participate\u003c/h3\u003e\n\u003cp\u003eInformed consent was obtained from all individual participants included in the study.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eHasnaoui M, Derbel L, Daldoul F, Khalfallah A, Belhaj S, Kharrat M, Cherif A. (2020). Necrotising otitis externa: A single centre experience. \u003cem\u003eJournal of Otology\u003c/em\u003e, 15(4), 171-176. PMC7814081\u003c/li\u003e\n\u003cli\u003eHandzel, O., \u0026amp; Halperin, D. (2003). Necrotizing (Malignant) External Otitis. American Family Physician, 68(2), 309-312.\u003c/li\u003e\n\u003cli\u003eToulmouche MA. Observations on acute otitis externa, complicated by facial and masticatory muscle paralysis, and followed by death from meningitis. Arch Gen Med. 1838;18:337-346\u003c/li\u003e\n\u003cli\u003eChandler JR. Malignant external otitis. Laryngoscope. 1968;78(8):1257-1294. doi:10.1288/00005537-196808000-00002\u003c/li\u003e\n\u003cli\u003eTeronpi, Mirbon; Bhattacharjee, Abhinandan; Senapati, Arup; Nath, Sudip Kumar. Clinico-microbiological Study on Otitis Externa (Necrotizing) in Patients with Diabetes Mellitus. Indian Journal of Otology 30(3):p 157-161, Jul\u0026ndash;Sep 2024. DOI: 10.4103/indianjotol.indianjotol_30_24\u003c/li\u003e\n\u003cli\u003eDabiri, S., Karrabi, N., Yazdani, N., Rahimian, A., Kheiltash, A., Hasibi, M., \u0026amp; Saedi, E. (2020). Facial nerve paralysis in malignant otitis externa: comparison of the clinical and paraclinical findings. Acta Oto-Laryngologica, 140(12), 1056\u0026ndash;1060. https://doi.org/10.1080/00016489.2020.1808242 \u003c/li\u003e\n\u003cli\u003eSreepada GS, Kwartler JA. Skull base osteomyelitis secondary to malignant otitis externa. Curr Opin Otolaryngol Head Neck Surg. 2003;11(5):316-323. doi:10.1097/00020840-200310000-00005\u003c/li\u003e\n\u003cli\u003eAli T, Meade K, Anari S, ElBadawey MR, Zammit-Maempel I. Malignant otitis externa: case series. \u003cem\u003eJ Laryngol Otol\u003c/em\u003e. 2010;124(8):846-851. doi:10.1017/S0022215110000560\u003c/li\u003e\n\u003cli\u003eStern Shavit S, Soudry E, Hamzany Y, Nageris B. Malignant external otitis: factors predicting patient outcomes. \u003cem\u003eAm J Otolaryngol\u003c/em\u003e. 2016 Sep-Oct;37(5):425-30. doi:10.1016/j.amjoto.2016.04.005.\u003c/li\u003e\n\u003cli\u003eRubin Grandis J, Branstetter BF 4th, Yu VL. The changing face of malignant (necrotising) external otitis: clinical, radiological, and anatomic correlations. \u003cem\u003eLancet Infect Dis\u003c/em\u003e. 2004;4(1):34-39. doi:10.1016/s1473-3099(03)00858-2\u003c/li\u003e\n\u003cli\u003eAdams A, Offiah C. Central skull base osteomyelitis as a complication of necrotizing otitis externa: Imaging findings, complications, and challenges of diagnosis. \u003cem\u003eClin Radiol\u003c/em\u003e. 2012;67(10):e7-e16. doi:10.1016/j.crad.2012.02.004.\u003c/li\u003e\n\u003cli\u003eSudhoff H, Rajagopal S, Mani N, et al. Usefulness of CT scans in malignant external otitis: effective tool for the diagnosis, but of limited value in predicting outcome. \u003cem\u003eEur Arch Otorhinolaryngol\u003c/em\u003e. 2008;265(1):53-56. doi:10.1007/s00405-007-0413-y\u003c/li\u003e\n\u003cli\u003eRapoport Y, Redleaf MI, Hughes GB. Diagnosis of skull base osteomyelitis. \u003cem\u003eOtolaryngol Head Neck Surg\u003c/em\u003e. 1991;104(4):553-556. doi:10.1177/019459989110400419\u003c/li\u003e\n\u003cli\u003eChang PC, Fischbein NJ, Holliday RA. Central skull base osteomyelitis in patients without otitis externa: imaging findings. \u003cem\u003eAJNR Am J Neuroradiol\u003c/em\u003e. 2003;24(7):1310-1316\u003c/li\u003e\n\u003cli\u003eCarfrae MJ, Kesser BW. Malignant otitis externa. \u003cem\u003eOtolaryngol Clin North Am\u003c/em\u003e. 2008;41(3):537-549. doi:10.1016/j.otc.2008.01.004.\u003c/li\u003e\n\u003cli\u003eRubin Grandis J, Branstetter BF 4th, Yu VL. The changing face of malignant (necrotising) external otitis: clinical, radiological, and anatomic correlations. \u003cem\u003eLancet Infect Dis\u003c/em\u003e. 2004;4(1):34-39. doi:10.1016/s1473-3099(03)00858-2\u003c/li\u003e\n\u003cli\u003eLevenson MJ, Parisier SC, Dolitsky J, Bindra G. Ciprofloxacin: drug of choice in the treatment of malignant external otitis (MEO). \u003cem\u003eLaryngoscope\u003c/em\u003e. 1991;101(8):821-824. doi:10.1288/00005537-199108000-00004\u003c/li\u003e\n\u003cli\u003eOmran AA, Aref ZF, Menaissy YM, Omran M. Initial intravenous ceftazidime and fluoroquinolones for malignant otitis externa: a retrospective cohort study. \u003cem\u003eJ Chemother\u003c/em\u003e. 2020;32(3):146-152. doi:10.1080/1120009X.2020.1721175.\u003c/li\u003e\n\u003cli\u003eLengyel A, Farkas Z, Csomor P, K\u0026eacute;nessey I, Tiszlavicz L, V\u0026ouml;r\u0026ouml;s A. Clinical observations in malignant otitis externa. \u003cem\u003eFolia Microbiol (Praha)\u003c/em\u003e. 2021;66(4):645-651. doi:10.1007/s12223-021-00872-2\u003c/li\u003e\n\u003cli\u003eChawdhary G, Pankhania R, Douglas S, Bottrill I. Fungal malignant otitis externa: systematic review and individual patient data meta-analysis. \u003cem\u003eOtol Neurotol\u003c/em\u003e. 2022;43(5):e548-e555. doi:10.1097/MAO.0000000000003523\u003c/li\u003e\n\u003cli\u003eCohen D, Friedman P. The diagnostic criteria of malignant external otitis. \u003cem\u003eJ Laryngol Otol\u003c/em\u003e. 1987;101(3):216-221. doi:10.1017/s0022215100101599. \u003c/li\u003e\n\u003cli\u003eSoudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of malignant external otitis with facial paralysis. \u003cem\u003eArch Otolaryngol Head Neck Surg\u003c/em\u003e. 2007;133(10):1002-1004. doi:10.1001/archotol.133.10.1002.\u003c/li\u003e\n\u003cli\u003eArslan, I.B., Pekcevik, Y. \u0026amp; Cukurova, I. Management and long-term comorbidities of patients with necrotizing otitis externa. Eur Arch Otorhinolaryngol 280, 2755\u0026ndash;2761 (2023). https://doi.org/10.1007/s00405-022-07784-y\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"
[email protected]","identity":"the-egyptian-journal-of-otolaryngology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [The Egyptian Journal of Otolaryngology](https://ejo.springeropen.com/)","snPcode":"43163","submissionUrl":"https://submission.springernature.com/new-submission/43163/3","title":"The Egyptian Journal of Otolaryngology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Necrotizing otitis externa, Skull base osteomyelitis, Pseudomonas aeruginosa, treatment protocols","lastPublishedDoi":"10.21203/rs.3.rs-8767938/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8767938/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003ePurpose\u003c/h2\u003e \u003cp\u003eNecrotizing otitis externa is a life-threatening infection of the external ear and skull base, primarily affecting elderly, diabetic, and immunocompromised patients. This study reviews clinical presentations, microbiological profiles, treatment outcomes, and prognostic factors.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eA retrospective analysis was conducted at the Otorhinolaryngology Department of Mohammed VI University Hospital, Marrakech, including 39 patients hospitalized with necrotizing otitis externa between January 2020 and December 2024. Data included clinical assessments, laboratory markers (erythrocyte sedimentation rate), microbiological cultures, and high-resolution computed tomography imaging. All patients received systemic antimicrobial therapy and were followed for at least 6 months.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eThe cohort (mean age 61.1 years; male-to-female ratio 2.25:1) had diabetes mellitus in 63.3% of cases, with 55.6% showing poor glycemic control (hemoglobin A1c greater than 7%). Common symptoms were severe otalgia (89.7%) and otorrhea (30.7%). Facial nerve palsy occurred in 18%. Microbiological analysis revealed Pseudomonas aeruginosa in 30% of cases and fungal pathogens in 23%. Erythrocyte sedimentation rate was elevated in 92%, with significantly higher values in fungal infections. Computed tomography imaging showed temporal bone erosion in 56.4%. Treatment involved combined intravenous ceftazidime and ciprofloxacin for 6\u0026ndash;8 weeks, with systemic antifungals added for fungal infections. Complete resolution was achieved in 69.2% of patients; 30.8% had persistent disease requiring prolonged therapy.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eNecrotizing otitis externa management requires long-term, targeted antimicrobial treatment guided by culture results and inflammatory markers. The emerging prevalence of fungal pathogens and rising antibiotic resistance necessitate updated treatment protocols.\u003c/p\u003e","manuscriptTitle":"Necrotizing Otitis Externa: A 5 years perspective on Treatment Outcomes and Prognostic Factors","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-10 11:46:16","doi":"10.21203/rs.3.rs-8767938/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-22T03:54:13+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-02-03T13:15:06+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-02-03T13:12:05+00:00","index":"","fulltext":""},{"type":"submitted","content":"The Egyptian Journal of Otolaryngology","date":"2026-02-02T17:35:25+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
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