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Radiology and Treatment of Skull Base Osteomyelitis

Radiology and treatment of SBO

Skull base osteomyelitis (SBO) is a debilitating progressive disorder occurring in immunocompromised individuals. It commonly affects the bony external auditory canal with extension to involve the neighbouring bony and soft tissue structures. In this blog, we aim to discuss the radiology and treatment aspects of Skull base osteomyelitis.


Skull base Osteomyelitis(SBO) presents with diverse manifestations with involvement of bone and soft tissue. Extension into the intracranial compartment producing debilitating complications in uncontrolled SBO is not uncommon. Various inflammatory pathologies and malignancies mimic SBO, hence, it is paramount that an appropriate radiological investigation is chosen in the diagnosis and prognosis of SBO.

High-Resolution CT Imaging

The primary purpose of doing a high-resolution CT scan with contrast administration is to determine the erosion of bone. Subtle cortical erosions, thickening of external auditory canal skin, and fat plane effacement in the stylomastoid foramen and infratemporal fossa regions are the early manifestations, however, these findings are not specific to SBO. CT scan can pick up bony erosion only if there is a minimum of 30% bony demineralization due to osteolysis caused by the underlying pathology. Hence, a CT scan even with its exceptional anatomic resolution exhibits poor sensitivity and specificity in early diagnosis of SBO, however, the sensitivity improves when there is a locally advanced SBO i.e SBO. The advantage of a CT scan is that it is widely available and inexpensive when compared to other radiological investigations used in the diagnosis of SBO.

MRI With Gadolinium Contrast

Soft tissue assessment is superior to MRI when compared to a CT scan. T1-weighted images demonstrate a hypointense signal in the external auditory canal and subtemporal region soft tissues and an isointense to minimal hyperintense signal on T2-weighted images. Most of the inflammatory conditions exhibit hyperintense signals on T2-weighted MRI due to hyperemia and edema, unlike SBO which exhibits isointense or mild hyperintense signals due to the compromised vascular supply primarily due to diabetic microangiopathy and necrotizing pathology. Gadolinium contrast administration may demonstrate diffuse or focal rim-enhancing fluid collection due to inflammation. Fat suppression following contrast administration accurately determines skull base enhancement. Dural enhancement and bony medullary space involvement is also a feature of MRI which makes it superior to CT scan. The advantage of MRI is there is no radiation burden to the patient. MRI is also superior to CT imaging in detecting the anatomical site of involvement. Diffusion-weighted imaging(DWI) on MRI has an additional advantage in bacterial SBO wherein, an enhanced apparent diffusion coefficient helps it to differentiate from lymphoma and malignancy.

Both MRI and CT are poor in therapeutic prognostication of SBO as the bone and soft tissue changes remain for a period of 6 months to 1 year after the disease has resolved.

Nuclear Imaging

Beta-emitting tracers and gamma tracers have been used in SBO to aid in early diagnosis and follow-up. These tracers form an important component of scintigraphy, SPECT, and PET. The inherent disadvantage of this imaging modality is the poor anatomical detail and spatial resolution.

(a) Gamma tracers

Technitium 99m-methylene diphosphonate detects osteoblastic activity. Any condition with an increased bone turnover is detected by this radiotracer. It detects even a 10% enhancement of activity, thereby making it beneficial in the early stages of SBO. It cannot be used effectively in the detection of treatment response as osteoblastic activity persists post-therapy. Technitium-labeled leukocytes detect infectious foci. However, the disadvantage of using it is the expense involved and its inability to detect low-grade infections. Gallium-67-citrate binds to vigorously dividing leukocytes in SBO. It is extremely useful in detecting the therapeutic response. However, it delivers a high radiation dose and is expensive.

(b) Beta tracers

FDG (2-Fluoro-2-desoxy-glucose) detects enhanced metabolism and is not a specific infection tracer as it is highly sensitive and detects any pathology with increased metabolic activity.

Meta-analysis of nuclear imaging in SBO revealed a sensitivity of 82%, 61%, 78%, 84% and specificity of 25%, 77%, 84%, and 60% for bone scintigraphy, leukocyte scintigraphy, combined bone-leukocyte scintigraphy, and MRI respectively. 18F-FDG PET/CT was considered a reliable diagnostic and prognostic imaging indicator until the advent of hybrid imaging. A gallium-67-citrate scan is a good indicator for the resolution of SBO. Recently 99m Tc‐HMPAO‐leukocyte scintigraphy has been found to be promising in the assessment of healing with a sensitivity and specificity of 86% and 75% respectively.

Hybrid Imaging

Hybrid imaging has emerged as the workhorse in the combined anatomical and functional detection of SBO. Technitium 99m-MDP SPECT/CT scan has reported a sensitivity of 100% and a specificity of 78%. This imaging modality can detect bony changes 24-48 hours after disease onset. FDG-PET/CT has reported a sensitivity and specificity of 96% and 91% making it a reliable imaging technique in the early detection of SBO.


Antibacterial Therapy

Multiple studies have debated the role of monotherapy vs combination antibacterial therapy in the treatment of SBO. Resistance of Pseudomonas aeruginosa to ciprofloxacin, however, has warranted the role of combination therapy in SBO. Second, there is increasing evidence of polymicrobial infection in SBO which include S.aureus, MRSA, and anaerobic bacteria. In addition, Aspergillus, Candida, and Mycobacteria have been evident in immunocompromised patients in the 20th century.

6-week-course of culture-directed antibacterial combination therapy is the norm for SBO/SBOM which includes the 4 weeks required for bone revascularisation. Fluoroquinolone(Ciprofloxacin) and a 3rd generation cephalosporin(Ceftazidime) is the first line of treatment for SBO. Piperacillin/Tazobactam as monotherapy has shown an equally good therapeutic response. The role of additional antibiotics is limited to the presence of MRSA and anaerobic bacterial culture which may include vancomycin or metronidazole respectively. The role of gentamicin as long-term therapy is limited because of its toxicity in spite of its capability of augmenting the action of penicillin agents although it has been recommended with a prescription limited to one week. Individuals who are sensitive to the penicillin group can be safely substituted with 3rd generation cephalosporins as there is evidence of only 10% cross-sensitivity between the groups. Topical fluoroquinolones in SBO is controversial and avoided due to its ability to change the ph drastically in an already altered environment in the external auditory canal. Burow’s solution(ph 3.2) in 1:4 dilution is beneficial due to its antibacterial nature (acidic environment + aluminium acetate action). 1:4 dilution ascertains minimal discomfort in an acutely inflamed environment. Re-assessment of therapy is done by imaging at 6 weeks with repeat culture to ascertain the future course of treatment.

Avoidance of Ciprofloxacin Monotherapy as First-Line Therapy

Drug resistance is the most important cause for monotherapy avoidance. Mutation of topoisomerase IV and DNA gyrase enzymes which are primarily responsible for quinolone activity has been the dominant cause of ciprofloxacin-resistant pseudomonas. Other reasons for quinolone resistance are the prescription of improper oral and topical drug regimes for the treatment of systemic/otological conditions and the development of pseudomonas biofilms. There is also evidence of enhanced risk of C.difficile infection in an already immunocompromised patient which may have drastic consequences in long-term monotherapy.

Antifungal Therapy

Increased evidence of invasive Aspergillus species has been reported with SBO in immunocompromised individuals. Voriconazole has been proposed as the first-line antifungal therapy in the treatment of Aspergillus SBO. It has demonstrated satisfactory bone, tissue, and blood-brain barrier penetrability and superior innate anti-Aspergillus action when administered orally or intravenously. It has a better safety profile and efficacy compared to Amphotericin B(conventional or liposomal). However, it has potential hepatic adverse effects and drug interactions that mandate therapeutic drug monitoring in immunocompromised individuals. The presence of candida in SBO warrants the use of fluconazole as therapy. Long-term use of fluconazole has gastrointestinal adverse effects. Hence, Itraconazole is a viable second-line option in Candida SBO.

Antifungal therapy should be initiated under the following circumstances (1) No response to culture-directed antibacterial therapy after 6 weeks (2) Emergence of complications (nerve palsies, features of SBOM) (3) Positive fungal culture.

Antitubercular Therapy

Role of Mycobacteria in SBO can be suspected under three circumstances: (1) No response to antibacterial or antifungal therapy after 6 months as evidenced by imaging (2) Endemic mycobacterial geographical distribution (3) Positive gen expert tissue MTB assay. Literature review on mycobacterial involvement in SBO is sparse and one case report from a mycobacterial endemic zone reported remission of SBO following intensive therapy for 2 months with isoniazid, rifampicin, pyrazinamanide and ethambutol and continuation therapy with isoniazid and rifampicin for 4 months when antibacterial and antifungal therapy had failed.

Surgical Treatment

The role of surgical therapy in SBO is minimal considering the advancement in antimicrobial therapy and there are isolated case reports in literature which suggest minimal debridement to radical surgery. Peled et al in their series have suggested specific indications for surgical intervention. They are (1) Non-response to antibiotic therapy. (2) Advanced disease (nerve palsies, TMJ involvement, infratemporal fossa or nasopharyngeal involvement) or bilateral disease (3) Isolated facial paralysis (4) Deep tissue sterile culture. The surgical debridement should be able to achieve complete removal of osteomyelitic bone.

Hyperbaric Oxygen Therapy (HBOT)

Hyperbaric oxygen therapy has been proposed as an adjunct in the treatment of MOE/SBOM. Although there is no concrete evidence in the literature for the application of HBOT in MOE/SBOM, it has shown promise in advanced stages with single/multiple cranial nerve palsies, intracranial extension, or fungal MOE/SBOM. 100% oxygen is delivered at approximately 2-2.5 absolute atmosphere(ATA) once/twice daily over one to two hours for a duration ranging from 20 to 40 days in conjunction with antibiotic/antifungal therapy as per HBOT protocol. The hypoxic state produced by inflammation and osteomyelitis is retracted by 100% oxygen administration which enhances vasoconstriction and oxygen carrying capacity of the blood. It also increases the antibacterial leukocyte activity and osteal activity with a reduction in tissue edema. Sustained administration improves angiogenesis and collagen deposition thereby promoting tissue healing. The documented side effects of HBOT are acute pulmonary edema, oxygen-toxic seizures, claustrophobia, and tympanic membrane perforation.


Radiology forms an integral part of the treatment of skull base osteomyelitis. Impetus lies on the extension of the disease which commonly involves the cranial nerve and causes severe debility. Surgery along with medical therapy forms the prime treatment of choice in skull base osteomyelitis.

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