The external ear is subject to a wide variety of injuries. All trauma patients require appropriate stabilization and triage of associated injuries based on their severity. Adherence to basic surgical principles and wound care prevents complications and improves the likelihood of a successful outcome.
- History of auricular trauma
- Edematous, fluctuant, and ecchymotic pinna with loss of normal cartilaginous landmarks
- Early diagnosis and treatment necessary to minimize cosmetic deformity.
Auricular hematoma refers to the accumulation of blood in the subperichondrial space, usually secondary to blunt trauma.
Cartilage lacks its own blood supply and instead relies on the vascularity of the perichondrium via diffusion. Shearing forces secondary to blunt trauma to the pinna lead to an accumulation of blood in the subperichondrial space. This creates a barrier for diffusion between the cartilage and the perichondrial vascularity, leading to necrosis of the cartilage and predisposing it to infection and further injury.
A patient with an auricular hematoma usually presents with an edematous, fluctuant, and ecchymotic pinna, with loss of the normal cartilaginous landmarks. Failure to evacuate the hematoma may lead to infection and/or cartilage necrosis and permanent disfigurement known as “cauliflower ear.”
The evacuation of hematomas can be performed using a skin incision parallel with the natural auricular skin folds. The irrigation of evacuated hematomas with topical antibiotics reduces the likelihood of infection. Splinting after drainage prevents the reaccumulation of hematomas, and options include cotton bolsters, plaster molds, silicon putty, and water-resistant thermoplastic splints. Through-and-through whip-type absorbable mattress sutures without a bolster have also been described.
Sharp or severe blunt trauma may lead to laceration or avulsion of the auricle. The expeditious repair and prevention of infection are essential. Auricular lacerations should be cleansed and débrided prior to repair. Simple lacerations can be closed primarily, whereas extensive injuries with tissue loss may require undermining, flap reconstruction, or tissue grafts. In the case of a near-total ear avulsion still attached to the helical root, the ear can be successfully reattached as the supply of the upper auricular-helical artery seems to be sufficient for the entire ear. Leech therapy may be required to support venous outflow until neovascularization occurs. Repairs should be covered with pressure dressings to prevent edema and hematoma formation, and cartilage-penetrating antibiotics such as quinolones should be prescribed. Excellent cosmetic results can be achieved, even with extensive lacerations.
Pham TV, Early SV, Park SS. Surgery of the auricle. Facial Plast Surg.
(A thorough review of external ear anatomy and embryology, as well as the surgical management of auricular deformities and trauma.)
- Otalgia, otorrhea, pruritus, hearing loss, history of water exposure
- In severe cases in which edema occludes ear canal, wick is critical to maintain EAC and permit antibiotic drops to reach infected tissues
- Cases in which erythema and tenderness extend outside of EAC require oral antibiotics with antipseudomonal activity.
Otitis externa is an inflammatory and infectious process of the EAC. Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated organisms. Less commonly isolated organisms include Proteus species, Staphylococcus epidermidis, diphtheroids, and Escherichiacoli. Fungal otitis externa is discussed in the next section.
In the preinflammatory stage, the ear is exposed to predisposing factors, including heat, humidity, maceration, the absence of cerumen, and an alkaline pH. Loss of acidity has been shown to be proportionate to the degree of infection. This can cause edema of the stratum corneum and occlusion of the apopilosebaceous units. In the inflammatory stage, bacterial overgrowth ensues, with progressive edema and intensified pain. Incomplete resolution or persistent inflammation for more than 3 months refers to the chronic inflammatory stage.
Symptoms of otitis externa may vary, depending on the stage and extent of disease. The clinical diagnosis is suggested by the presence of otalgia, otorrhea, aural fullness, pruritus, tenderness to palpation, and varying degrees of occlusion of the EAC. The patient may also present with hearing loss, which results from occlusion of the EAC by edema and debris. Signs of otitis externa include pain on distraction of the pinna, EAC erythema, edema, otorrhea, crusting, and, in more advanced disease, lymphadenopathy of the periauricular and anterior cervical lymph nodes. Skin changes of cellulitis may be present as well. In the chronic stage, the skin of the EAC may be thickened. A culture may be helpful for infections that are refractory to treatment.
Treatment for otitis externa involves meticulous atraumatic debridement of the EAC with the help of a microscope. Analgesia can be achieved with nonsteroidal antiinflammatory drugs (NSAIDs), opioids, or topical steroid preparations. After cleansing is complete, otic drop preparations that are antiseptic, acidifying, or antibiotic (or any combination of these) should be used. These have been shown to be equally effective in the management of uncomplicated otitis externa in a recent Cochrane review. If the degree of stenosis of the canal is severe, a wick must be placed in an effort to stent open the EAC and permit delivery of drops to the medial portion of the canal.
Available antiseptic preparations include acetic and boric acids, ichthammol, phenol, aluminum acetate, gentian violet, thymol, thimerosal (eg, Merthiolate), cresylate, and alcohol. Available antibiotic preparations include ofloxacin, ciprofloxacin, colistin, polymyxin B, neomycin, chloramphenicol, gentamicin, and tobramycin. Polymyxin B and neomycin preparations are often used in combination for the treatment of Saureus and P aeruginosa infections. Ofloxacin and ciprofloxacin are single-agent antibiotics with an excellent spectrum of coverage for pathogens encountered in otitis externa. Preparations with steroids help to reduce edema and otalgia. Systemic antibiotics are indicated for infections that spread beyond the EAC. For chronic otitis externa, a canalplasty may be indicated for thickened skin that has caused canal obstruction. Patients must be instructed to avoid EAC manipulation and water exposure if they have a history of recurrent otitis externa (Figure 47–6).
High-resolution coronal CT scan demonstrating soft tissue edema of the left external auditory canal consistent with otitis externa.
- Pruritus, otalgia, otorrhea, fullness, hearing loss, no response to topical antibiotics
- Fungal elements on physical examination
- Positive KOH preparation or fungal culture.
Otomycosis is an inflammatory process of the external ear canal due to infection with fungi and is responsible for more than 9% of the diagnoses of otitis externa. In 80% of cases, the etiologic agent is Aspergillus, whereas Candida is the next most frequently isolated fungus. Other more rare fungal pathogens include Phycomycetes, Rhizopus, Actinomyces, and Penicillium.
Otomycosis has similar predisposing factors to bacterial otitis externa. Patients with diabetes mellitus or an immunocompromised state are particularly susceptible to otomycosis. Patients with a mastoid bowl after a canal wall down procedure are predisposed to development of otomycosis as well.
Patients with otomycosis most frequently present with pruritus, aural fullness, and otorrhea, and may also complain of otalgia and hearing loss. The hearing loss associated with otomycosis usually results from the accumulation of mycotic debris.
Otoscopy often reveals mycelia, establishing the diagnosis. The EAC may be erythematous and fungal debris may appear white, gray, or black. Patients have typically been tried on topical antibacterial agents with no significant response. The diagnosis can be confirmed by identifying fungal elements on a KOH preparation or by a positive fungal culture.
The treatment of otomycosis includes cleansing and debriding the EAC, acidifying the canal, and administering antifungal agents. Nonspecific antifungal agents include thimerosal (eg, Merthiolate) and gentian violet. Commonly used specific antifungals include clotrimazole, Nystatin (otic drops or powder), and ketoconazole. Topical ketoconazole, cresylate otic drops, and aluminum acetate otic drops were all relatively effective with >80% resolution rate on initial application. CSF powder (chloramphenicol, sulfamethoximazole, and fungizone) is also an excellent option.
- Immunosuppressed patients with intense otalgia, otorrhea, hearing loss, fullness, and pruritus
- Edema and erythema of the EAC, granulation tissue at the bony–cartilaginous junction, cranial neuropathies in advanced stages
- Elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). Culture of EAC. CT and/or technetium scan diagnostic; gallium scan to follow resolution of disease
- Biopsy is necessary to rule out carcinoma.
Skull base osteomyelitis, also known as malignant otitis externa or necrotizing otitis externa (NOE), is a bacterial infection of the EAC and skull base. This disease process is most frequently seen in elderly diabetics and immunocompromised patients. It most commonly begins as an external otitis that progresses to involve the temporal bone, and may progress to fatal meningitis, sepsis, and death if unrecognized or untreated.
Skull base osteomyelitis commonly begins as an external otitis that progresses to cellulitis, chondritis, osteitis, and, ultimately, osteomyelitis. Unlike otitis media, which spreads through the pneumatized portion of the temporal bone, NOE disseminates through the haversian canals and vascularized spaces of the skull base. As this progresses along the base of the skull, the facial nerve (stylomastoid foramen), hypoglossal nerve (hypoglossal canal), the abducens and trigeminal nerves (petrous apex), the glossopharyngeal, vagus, and spinal accessory nerves (jugular foramen) may be involved. Cranial neuropathy has classically been considered to portend a poor prognosis, although recent data has not supported a difference in mortality.
The most frequently isolated causative organism is P aeruginosa, which may exhibit high levels of antibiotic resistance. Aspergillus may also be an etiologic organism and is thought to originate from the middle ear or mastoid. Elderly diabetics are thought to be particularly susceptible because of the microangiopathic changes that blunt an already attenuated immune response. The cerumen of diabetic patients has also been described to be more acidic in nature, further contributing to their susceptibility.
Patients may present with intense otalgia, otorrhea, aural fullness, pruritus, and hearing loss. As the disease advances to involve the temporal bone, granulation tissue is seen on the floor of the EAC at the osteocartilaginous junction. Bony sequestra can also be found in the EAC. Edema, periaural lymphadenopathy, and trismus may be present. Cranial neuropathies occur in more advanced presentations of disease, and the facial nerve is the most frequently affected cranial nerve. Further progression may lead to sigmoid sinus thrombosis, meningitis, sepsis, and death.
Inflammatory markers such as ESR and CRP may be elevated. Cultures and sensitivity should be obtained to help in selecting appropriate antibiotics.
CT and MRI are useful in the initial evaluation to determine the extent of disease. Bone scans are sensitive for assessing bony involvement but are not specific (Figures 47–7, 47–8, and 47–9). Gallium scans are used to track the resolution of the infection, since bone scans often remain positive long after the infection has resolved (Figure 47–10).
Axial high-resolution CT scan demonstrating skull base osteomyelitis with evidence of petroclival bone erosion.
Axial T1-weighted MRI depicting the replacement of bone marrow in the clivus with inflammatory tissue.
Axial T1-weighted MRI, with gadolinium enhancement, with evidence of petroclival bone erosion and enhancement of inflammatory tissue secondary to skull base osteomyelitis.
Sagittal image of a bone scan in a patient with skull base osteomyelitis revealing focal enhancement of the skull base.
Carcinomas of the EAC, chronic granulomatous disease, Paget disease, fibrous dysplasia, and nasopharyngeal carcinomas must be considered in the differential diagnosis. As carinoma of the EAC mimics many features of NOE, a biopsy is requisite to rule out carcinoma.
Long-term parenteral antibiotics are the treatment of choice. Aminoglycosides (eg, tobramycin) and antipseudomonal β-lactam antibiotics, including piperacillin, ticarcillin, or ceftazidime, may be used. Some physicians recommend the use of outpatient fluoroquinolones such as ciprofloxacin or ofloxacin; however, this is appropriate only for patients with early presentations who can be followed up closely. Control of hyperglycemia and immunosuppression is necessary to maximize treatment. Surgical debridement may be necessary to remove necrotic tissue. Circumferential petrosectomy has been described as a method for surgical debridement with hearing and facial nerve function preservation. The use of hyperbaric oxygen has been described in cases refractory to antibiotics, with variable results. In an effort to prevent skull base osteomyelitis, all diabetic and immunocompromised patients must be followed up closely and treated aggressively if they present with symptoms suggestive of external otitis.
Rubin Grandis J, Branstetter BF IV, Yu VL. The changing face of malignant (necrotizing) external otitis: Clinical, radiological, and anatomic correlations. Lancet Infect Dis.
(An overview of the diagnosis and management of skull base osteomyelitis.)