Malignant Otitis ExternaMANAGEMENT

ENT AND MAXILLOFACIAL PRESENTATIONS · 12 SECTIONS

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702 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Acute laryngitis Acute pharyngitis Auricular hematoma Bezold's Abscess Cerumen impaction Dry socket Ear foreign body Epistaxis (anterior)Epistaxis (Posterior)Labyrinthitis Ludwig's Angina Malignant Otitis Externa Marcus Gunn Pupil Mastoiditis Meniere's Disease Nasal Bone Fracture Nasal foreign body Nasal Septal Hematoma Otitis externa Otitis Media Post-tonsillectomy hemorrhage Sialolithiasis and sialadenitis Sinusitis Sudden Sensorineural Hearing Loss TMJ dislocation Tympanic membrane perforation Vestibular Neuronitis

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp46

Immediate priorities

›Time-critical recognition

›Malignant otitis externa (MOE) is a life-threatening skull base osteomyelitis

›Historically mortality up to 33% overall

›Mortality up to 80% when cranial nerves involved

›Classic at-risk patient: elderly diabetic male with severe otalgia and otorrhea unresponsive to topical therapy

›Pain out of proportion to visible exam findings

›Symptoms progressing over weeks

›If cranial nerve deficit detected, escalate immediately to ENT and infectious disease

›Facial nerve palsy is most common and most urgent

›CN IX, X, XI involvement suggests advanced skull base extension

Stabilization and early actions

›Initial ED stabilization

›IV access and fluid resuscitation if septic physiology

›MAP target >= 65 mmHg

›Lactate >= 2 mmol/l triggers sepsis pathway

›Pain management early — otalgia in MOE is severe and often requires opioids

›IV morphine or hydromorphone titrated to comfort

›Inadequate analgesia is a common pitfall

›Obtain EAC culture swab before starting antibiotics

›Deep canal swab for aerobic and fungal culture

›Gram stain for immediate pathogen guidance

›Glucose check at bedside

›Hyperglycemia worsens outcomes and requires immediate correction

›HbA1c to quantify baseline control

Escalation triggers

›Triggers for immediate specialist activation

›Any cranial nerve deficit

02History/hx65

Presenting symptoms

›Core symptom complex

›Severe unrelenting otalgia

›Classically described as excruciating

›Worse at night

›Pain out of proportion to external appearance

›Purulent otorrhea

›Persistent despite topical therapy

›Duration >= 2 weeks unresponsive to standard drops

›Hearing loss

›Conductive from canal occlusion

›Sensorineural from cochlear involvement in advanced disease

›Alarm symptoms requiring urgent evaluation

›Facial weakness or asymmetry

›CN VII palsy — most common cranial nerve involvement

›Ask about difficulty smiling, closing eye, raised eyebrow

›Dysphagia or hoarseness

›CN IX or X involvement

›Suggests parapharyngeal or jugular foramen spread

›Shoulder weakness

›CN XI involvement

›Skull base extension

›Trismus or jaw pain

›TMJ or infratemporal fossa involvement

›Headache or confusion

›Intracranial extension concern

›Sigmoid sinus thrombosis or cerebral abscess

03Physical Exam/exam68

Vital signs and general

›Hemodynamic and systemic assessment

›Temperature

›Fever often absent in early MOE

›Absence of fever does not exclude serious infection

›Tachycardia

›Sepsis marker when present

›Pain-related tachycardia also common

›Blood pressure

›Hypotension rare but indicates systemic sepsis

›MAP < 65 mmHg triggers resuscitation

›General appearance

›Disproportionate distress relative to visible findings

›Ill appearance in advanced disease

Otoscopic exam

›EAC findings

›Granulation tissue at bony-cartilaginous junction

›Hallmark finding of MOE

›Not always present in early disease

›Edematous and erythematous canal wall

›Purulent debris

›Necrotic tissue

›Tympanic membrane integrity

›Perforation assessment

›Middle ear involvement evaluation

›Tragal tenderness

›Pinna tenderness

›Periauricular edema

04Differential Diagnosis/ddx58

Life-threatening mimics

›Critical diagnoses not to miss

›Squamous cell carcinoma of the EAC

›ICD-10 C44.20 malignant neoplasm EAC

›Most critical mimic — tissue biopsy required to exclude

›May present identically to MOE on exam and imaging

›Intracranial infection

›ICD-10 G00.9 bacterial meningitis

›Cerebral abscess ICD-10 G06.0

›Sigmoid sinus thrombosis ICD-10 G08

›Sepsis of otogenic origin

›ICD-10 A41.9

›Organ dysfunction from advanced MOE

Otologic differential

›Ear-focused differentials

›Malignant otitis externa (necrotizing otitis externa)

›ICD-10 H60.2 malignant otitis externa

›SNOMED CT necrotizing otitis externa disorder

›Uncomplicated acute otitis externa

›ICD-10 H60.319

›Responds to topical therapy within 1 to 2 weeks

›No granulation tissue or bony erosion

›Chronic otitis externa

›ICD-10 H60.31

›Pruritus predominant

›Duration > 3 months without osteomyelitis

›Ramsay Hunt syndrome

›ICD-10 B02.21

05Laboratory Tests/lt45

Inflammatory markers

›ESR and CRP — key diagnostic and monitoring markers

›ESR

›ESR > 26 mm/h has positive likelihood ratio of 10.15 for MOE

›AUC 0.92 in diagnostic studies

›Limitation: remains elevated after clinical resolution — not used alone to confirm cure

›CRP

›CRP > 10 mg/L has positive likelihood ratio of 8.25

›Serial CRP useful for treatment response monitoring

›If both ESR and CRP normal, alternative diagnosis should be actively sought

›Serial monitoring during treatment

›Trending downward is a favorable response indicator

›Rising markers despite antibiotics suggest treatment failure or extension

Microbiology

›Culture and sensitivity

›EAC swab culture — essential before antibiotics

›Deep canal swab for aerobic bacterial culture

›Fungal culture when otomycosis suspected or in immunocompromised

›Gram stain for immediate guidance

›Tissue biopsy of granulation tissue

›Performed by ENT for both culture and histopathology

›Histopathology to exclude squamous cell carcinoma

›Aerobic, anaerobic, and fungal cultures from tissue

›Blood cultures

›If febrile or hemodynamically unstable

›Bacteremia uncommon but possible in severe disease

Metabolic and renal labs

›Metabolic panel

06Diagnostic Tests/dt82

Scoring Systems

›Diagnostic criteria for MOE — combination required

›Classic clinical and laboratory criteria

›Severe otalgia in immunocompromised or diabetic host

›Purulent otorrhea unresponsive to topical therapy >= 2 weeks

›Granulation tissue at bony-cartilaginous junction

›Elevated ESR > 26 mm/h

›Positive EAC culture — Pseudomonas in > 90% of cases

›Radiographic evidence of soft tissue or bone involvement

›Severity staging for clinical decision making

›Early or localized: EAC inflammation with granulation tissue, no cranial nerve involvement, positive Tc-99m scan

›Advanced or extensive: skull base osteomyelitis, cranial nerve palsies, periauricular extension

›Intracranial: meningitis, cerebral abscess, sigmoid sinus thrombosis — highest mortality

›Clinical implications of staging

›Early disease: outpatient oral ciprofloxacin may be considered in selected cases

›Advanced disease: IV antipseudomonal combination therapy and admission

›Intracranial: ICU, neurosurgery, maximal antimicrobial therapy

MRI

›MRI of skull base with gadolinium

›Indications

›Suspected intracranial extension — meningitis, cerebritis, abscess

›Dural involvement evaluation

›Sigmoid sinus or jugular vein thrombosis assessment

›Soft tissue extent mapping for surgical planning

›Advantages over CT

›Superior soft tissue contrast

›Earlier detection of marrow edema and meningeal enhancement

›No ionizing radiation

›ACR Appropriateness Criteria

›MRI with gadolinium is usually appropriate for inflammatory ear disease with complications

›Preferred for intracranial extension evaluation over CT alone

›Limitations

›Less sensitive than CT for cortical bone erosion

›Motion artifact risk in distressed patients

›Availability and time constraints in acute setting

›Contraindicated with incompatible implants

›CT temporal bone — first-line imaging for MOE

›Indications

›All patients with suspected MOE

›Characterize extent of bony erosion at skull base

›Identify soft tissue extension to parapharyngeal space, infratemporal fossa, TMJ

›Protocol

›High-resolution CT temporal bone without contrast

›CT with contrast if abscess or vascular complication suspected

›Key CT findings

›Cortical bone erosion of EAC floor

›Soft tissue density filling EAC

›Mastoid air cell opacification

›Skull base cortical destruction

›Infratemporal fossa fat stranding

›Performance characteristics

›CT sensitive for cortical bone destruction

›May underestimate medullary bone and soft tissue involvement

›Negative CT does not exclude early MOE

›ACR Appropriateness Criteria

›CT temporal bone usually appropriate for suspected necrotizing otitis externa

›Preferred initial study for bony involvement

›CT chest or neck with contrast

›If deep space neck infection or mediastinal spread suspected

›Jugular foramen involvement assessment

Ultrasound

›Ultrasound role in MOE

›Limited primary role for deep skull base assessment

›CT and MRI are the primary imaging modalities

›Ultrasound cannot visualize temporal bone or skull base

›Adjunctive applications

›Preauricular or periauricular soft tissue abscess evaluation

›Lymph node assessment for regional spread

›Parotid gland assessment for parotitis or abscess

›Point-of-care applications

›Soft tissue swelling characterization at bedside

›Guidance for regional lymph node aspiration if needed

›Nuclear medicine imaging — critical for diagnosis and monitoring

›Technetium-99m bone scan

›High sensitivity for osteomyelitis including early MOE

›Positive scan supports diagnosis even when CT is negative

›Limitation: remains positive after clinical resolution — cannot confirm cure

›Gallium-67 scintigraphy

›Normalizes with infection resolution

›Preferred modality to guide antibiotic cessation

›Serial scanning at 6-week intervals

›FDG-PET/CT

›Emerging as alternative for diagnosis and treatment monitoring

›Higher resolution than nuclear medicine scans

›Correlates with metabolic activity of infection

07Disposition/dispo49

Admission criteria

›Indications for inpatient admission — most patients with MOE require admission

›Suspected or confirmed MOE

›All patients with classic presentation should be admitted

›IV antipseudomonal antibiotics required

›ENT and ID involvement for ongoing management

›Cranial nerve deficit

›Urgent admission and specialist assessment

›Advanced or intracranial staging

›Poorly controlled diabetes

›Inpatient glycemic optimization

›Endocrinology consultation

›Intracranial complications

›ICU level care

›Neurosurgery involvement

Level of care selection

›ICU indications

›Intracranial extension

›Cerebral abscess

›Meningitis

›Sigmoid sinus thrombosis

›Hemodynamic instability or septic shock

›Vasopressor requirement

›Rising lactate despite resuscitation

›Rapidly progressive cranial nerve palsies

›Airway compromise from parapharyngeal extension

Specialist consultations

›Mandatory consultation triggers

08Treatment/t97

Initial stabilization

›ED immediate interventions

›IV access and analgesia

›Morphine 0.1 mg/kg IV titrated

›Hydromorphone 0.015 mg/kg IV for opioid-sensitive patients

›Obtain EAC culture before antibiotics

›Deep swab for aerobic and fungal culture

›Priority before empiric therapy

›Glucose management

›Point-of-care glucose and HbA1c

›Insulin sliding scale or infusion for hyperglycemia

›Target glucose 6 to 10 mmol/l

Empiric antipseudomonal antibiotic therapy

›Start immediately upon clinical suspicion — do not delay for imaging

›First-line combination regimen for moderate to severe disease

›Ceftazidime IV 2 g every 8 hours

›Combine with ciprofloxacin for synergistic antipseudomonal activity

›Continue for 3 weeks then transition

›Ciprofloxacin IV 400 mg every 8 hours or oral 750 mg every 12 hours

›High bioavailability of oral formulation permits PO step-down

›Ciprofloxacin monotherapy after 3 weeks if cultures confirm susceptibility

›Total duration 6 weeks

›Alternative combination regimens

›Piperacillin-tazobactam IV 4.5 g every 6 hours

›Used for ciprofloxacin-resistant organisms or beta-lactam preference

›Extended infusion over 4 hours per local protocol

›Meropenem IV 1 g every 8 hours

›Reserved for multidrug-resistant Pseudomonas or ciprofloxacin failure

›ID guidance recommended

›Oral ciprofloxacin monotherapy — selected mild or susceptible cases

›Ciprofloxacin 750 mg orally every 12 hours

›Duration 6 to 8 weeks guided by culture and imaging response

›Only if susceptibility confirmed and no cranial nerve involvement

›Close ENT outpatient monitoring required

Antibiotic duration and de-escalation

›Duration of therapy

›Minimum 6 weeks of systemic antipseudomonal therapy

›Guided by culture and sensitivity results

›Clinical response, serial ESR/CRP, and imaging

›Antibiotic cessation guided by nuclear medicine imaging

›Gallium-67 scan normalization before stopping antibiotics

›FDG-PET/CT as emerging alternative endpoint

›Extended courses 8 to 12 weeks for cranial nerve involvement or slow response

Antibiotic selection for resistant organisms

›Ciprofloxacin-resistant Pseudomonas management

›Antibiogram-guided therapy essential

›Culture with susceptibility testing before selecting definitive agent

›ID consult mandatory for resistant organisms

›Options for resistant cases

›Meropenem IV 1 g every 8 hours

›Ceftazidime-avibactam IV 2.5 g every 8 hours for extended-spectrum resistance

›Colistin only as last resort with ID guidance

›Aminoglycosides avoided

›Ototoxicity risk is unacceptable in this patient population

›Cochlear and vestibular toxicity risk

Fungal MOE treatment

›Aspergillus or Candida MOE

›Systemic antifungal therapy required

›Voriconazole IV 6 mg/kg every 12 hours for two doses loading then 4 mg/kg every 12 hours

›Preferred for Aspergillus

›Duration guided by imaging and culture clearance

›Amphotericin B IV 0.7 to 1 mg/kg daily as alternative

›Reserved for voriconazole-intolerant or resistant cases

›Nephrotoxicity monitoring required

›Candida MOE: fluconazole 400 mg daily if susceptible

›Suspect fungal MOE when bacterial cultures negative or in profoundly immunocompromised

›HIV with CD4 < 200 cells/mm3

›Hematologic malignancy with neutropenia

Topical and local therapy

›Adjunctive topical treatments

›Antipseudomonal otic drops

›Ciprofloxacin otic solution after debridement

›Applied after ENT canal cleaning

›Acetic acid 2% otic drops

›Restores acidic EAC pH to inhibit Pseudomonas

›Adjunct to systemic therapy only

Surgical management

›ENT-directed surgical interventions

›Debridement of necrotic and granulation tissue

›Performed by ENT

›Essential for culture and to remove infected tissue

›Repeat debridement as needed during treatment

›Tissue biopsy — mandatory

›Histopathology to exclude SCC

›Aerobic, fungal, and tissue cultures

›Extensive surgery reserved for refractory cases

›Mastoidectomy or temporal bone resection in severe osteomyelitis

›Facial nerve decompression for acute palsy

Adjunctive therapies

›Glycemic optimization

›Endocrinology consultation for all diabetic patients

›Strict glycemic control directly impacts outcomes

›HbA1c reduction is a modifiable prognostic factor

›Inpatient insulin management

›Continuous glucose monitoring or frequent checks

›Target HbA1c < 7% for long-term recurrence prevention

›Hyperbaric oxygen therapy

›Considered in refractory or recurrent MOE

›Cochrane review found no RCTs supporting use

›Used as adjunct when standard therapy fails

›Availability limited to specialized centers

›Correction of immunosuppression when possible

›Reduction in corticosteroid dose when clinically feasible

›ART optimization in HIV patients

›Granulocyte-colony stimulating factor for neutropenic patients with ID guidance

09Special Populations/sp65

Pregnancy

›Pregnancy-specific considerations

›MOE in pregnancy is extremely rare

›Immunologic changes of pregnancy may modestly increase susceptibility

›Poorly controlled gestational diabetes is a risk factor

›Antibiotic safety in pregnancy

›Ciprofloxacin — category C; avoid if alternatives available

›Theoretical cartilage toxicity concern

›May be used if benefit clearly outweighs risk for life-threatening infection

›Piperacillin-tazobactam — category B; preferred antipseudomonal alternative in pregnancy

›3.375 g IV every 6 hours or 4.5 g IV every 6 hours for serious infection

›Aztreonam 2 g IV every 8 hours — beta-lactam monobactam alternative

›Aminoglycosides avoided — ototoxicity risk to fetus

›Antifungals: amphotericin B preferred over azoles in pregnancy

›Imaging in pregnancy

›CT temporal bone with abdominal shielding if urgent

›MRI without gadolinium preferred when feasible

›Fetal monitoring for viable gestation

›Multidisciplinary care

›Obstetrics co-management mandatory

›Glycemic targets adjusted for pregnancy

Geriatric

›Older adult-specific features

›MOE is predominantly a disease of the elderly

›Mean age 62 to 77 years

›Comorbidity burden increases complexity

›Atypical presentation

›Fever often absent

10Background/b67

Epidemiology

›Incidence and population burden

›Rare but life-threatening invasive infection

›Exact incidence not well established due to rarity

›Rising incidence attributed to aging diabetic population

›Demographic profile from published series

›Mean age 62 to 77 years

›Male sex 62 to 74% of cases

›Diabetes mellitus present in 65 to 90%

›Mortality data

›Historical overall mortality up to 33%

›Cranial nerve involvement mortality up to 80% historically

›Modern mortality reduced with early antipseudomonal antibiotics and CT/MRI

›Comorbidity profile

›Chronic kidney disease common in diabetic population

›Hypertension and ischemic heart disease as frequent comorbidities

›HIV/AIDS and immunosuppressive therapy as secondary risk groups

›Causative organism distribution

›Pseudomonas aeruginosa > 90% of bacterial MOE

›Aspergillus species in profoundly immunocompromised — especially HIV

›Candida and other organisms rare

Pathophysiology

›Mechanism of invasion and spread

›Entry point and initial infection

›External auditory canal is the primary site

›Pseudomonas colonizes alkalinized or traumatized EAC

›Diabetic microangiopathy reduces local tissue defense

›Ceruminous gland involvement early in course

›Invasion pathway

›Bacteria penetrate through fissures of Santorini at bony-cartilaginous junction

›Spread to periauricular soft tissue

›Osteomyelitis of temporal bone follows

›Skull base osteomyelitis — hallmark of advanced MOE

›Extension patterns

›Anterior spread to parotid gland and infratemporal fossa

›Posterior spread to mastoid and sigmoid sinus

›Superior spread to temporal bone and intracranial space

›Jugular foramen involvement — cranial nerves IX, X, XI

›Intracranial extension — meningitis, cerebral abscess, sinus thrombosis

›Cranial nerve involvement mechanism

›CN VII (stylomastoid foramen) — most commonly affected

›CN IX, X, XI (jugular foramen) — extension to skull base

›CN VI and XII involvement in most advanced cases

Therapeutic Considerations

›Antibiotic strategy principles

›Antipseudomonal coverage is the cornerstone

›Pseudomonas aeruginosa is the dominant pathogen (> 90%)

›Empiric antipseudomonal therapy must not be delayed

›Combination vs monotherapy debate

›Initial combination (beta-lactam plus fluoroquinolone) preferred for moderate to severe disease

›Monotherapy ciprofloxacin acceptable for mild susceptible disease

›Evidence base from case series — no RCTs available

›Duration is critical

›Minimum 6 weeks for bacterial MOE

›Premature discontinuation leads to relapse

›Nuclear medicine imaging guides cessation, not symptom resolution alone

›Resistance surveillance

›Ciprofloxacin resistance is emerging

›Always obtain baseline culture with antibiogram

›Repeat cultures if clinical failure at 4 to 6 weeks

›Glycemic control as core therapeutic intervention

›Poorly controlled DM independently worsens prognosis

›Microvascular disease impairs tissue perfusion and immune response

›Strict glycemic control reduces risk of treatment failure and recurrence

›Endocrinology partnership is standard of care

›Monitoring framework

›Serial ESR and CRP for treatment response

›Gallium-67 or FDG-PET/CT for antibiotic cessation decision

›ENT follow-up at 1 week intervals during acute phase

›Long-term follow-up for at least 1 year post-treatment for recurrence surveillance

11Patient Discharge Instructions/pdi38

copy discharge instructions

›Malignant otitis externa — what you need to know

›This is a serious ear bone infection that requires long-term antibiotic treatment

›Do not stop antibiotics early even if feeling better

›Full course is 6 to 8 weeks — stopping early causes relapse

›Take all medications exactly as prescribed

›Ciprofloxacin must be taken on an empty stomach for best absorption

›Do not take antacids, calcium, or iron within 2 hours of ciprofloxacin

›Ear care instructions

›Do not insert anything into the ear canal

›No cotton swabs

›No ear canal irrigation

›Keep the ear dry

›No swimming

›Use a cotton ball with petroleum jelly for showering

›Apply prescribed ear drops as directed by your ENT

›Diabetic control is critical

›Check blood sugar as prescribed

›Target fasting glucose as directed by your doctor

›Keep a glucose log to bring to follow-up appointments

›Take your diabetes medications without missing doses

›Insulin schedule as prescribed

›Poor sugar control worsens the infection and raises relapse risk

›Warning signs — return to the emergency room immediately for

›New weakness or drooping of the face

›Difficulty swallowing or hoarseness of voice

›New shoulder weakness

›Worsening ear pain despite antibiotics

12References/r22

Guidelines and key sources

›Primary clinical references

›Long DA, Koyfman A, Long B — Emergency Medicine-Focused Review of Malignant Otitis Externa, American Journal of Emergency Medicine 2020

›Rubin Grandis J, Branstetter BF, Yu VL — The Changing Face of Malignant (Necrotising) External Otitis, Lancet Infectious Diseases 2004

›Patel S, Owen GS, Vivas EX — Otitis Externa and Malignant Otitis Externa for the Hospitalist/Internist, Medical Clinics of North America 2026

›Treviño González JL, Reyes Suárez LL, Hernández de León JE — Malignant Otitis Externa: An Updated Review, American Journal of Otolaryngology 2021

Evidence and diagnostic studies

›Key diagnostic and treatment studies

›Stocker M, Hempel JM — Patient Cases with Malignant Otitis Externa at Ludwig Maximilians University Munich 2009 to 2020, Scientific Reports 2025 — ESR and CRP likelihood ratios

›Handzel O, Halperin D — Necrotizing (Malignant) External Otitis, American Family Physician 2003 — antibiotic regimen evidence

›Pulcini C et al — Antibiotic Therapy in Necrotising External Otitis: Case Series 32 Patients, European Journal of Clinical Microbiology 2012

›Sadé J et al — Ciprofloxacin Treatment of Malignant External Otitis, American Journal of Medicine 1989

›Phillips JS, Jones SE — Hyperbaric Oxygen as Adjuvant Treatment for MOE, Cochrane Database Systematic Reviews 2013

›Stern Shavit S et al — FDG-PET/CT for Diagnosis and Follow-Up of Necrotizing External Otitis, Laryngoscope 2019

›Agarwal M et al — ACR Appropriateness Criteria Inflammatory Ear Disease, Journal of the American College of Radiology 2025

›Krawiec E et al — Epidemiology and Risk Factors for Extension of Necrotizing Otitis Externa, European Archives of ORL 2024

›Tabashiri A et al — Clinical and Radiological Features of Patients with MOE, BMC Infectious Diseases 2025

›Haleem AH et al — Refining Necrotising Otitis Externa Management and Role of Nuclear Medicine Imaging, American Journal of Otolaryngology 2025

Coding reference

›Diagnostic coding

›ICD-10 H60.2 malignant otitis externa

›ICD-10 H60.319 acute otitis externa (simple)

›ICD-10 C44.20 squamous cell carcinoma EAC

›ICD-10 A41.9 sepsis unspecified organism

›SNOMED CT necrotizing otitis externa disorder

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Comprehensive Clinical Review

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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