- Anatomical Structures Related to the External Auditory Canal (EAC) and Possible Extension Patterns for Malignant Otitis Externa (MOE) (Fig. 1)

Radiologists should be familiar with the anatomical structures related to the external auditory canal (EAC) and the possible extension patterns for MOE, as shown in Figure 1. In MOE, the invasive infection of the external auditory canal and periauricular soft tissue tends to spread anteromedially to the retrocondylar space and then to deeper cervical spaces, such as the parapharyngeal and masticator spaces. In imaging, the presence of fat in these spaces is very helpful, and a mirrored comparison with fat on the opposite side clearly shows inflammatory changes. Other areas of adjacent involvement include the retroauricular area and the mastoid. Additionally, the skull base may become involved, including the petrous apex, clivus, and occipital condyles. The proximity of vital intracranial structures includes cranial nerves, the inner ear, transverse and sigmoid venous sinuses, dura mater, brain parenchyma, and the internal carotid artery.

Based on the predictable spread of inflammation and the importance of examining adjacent vital structures, following a checklist and conducting a step-by-step review of imaging will be very helpful for accurate diagnosis and prevention of misdiagnosis.

- In a Temporal CT Scan, What Step-by-Step Items Should be Paid Attention to Diagnose MOE?       

     1. Soft Tissue Window:

• • EAC: The first step in examining the external auditory canal is to check for inflammation and increased thickness of the EAC. In a normal CT scan, there is no increase in the thickness of the external auditory canal, and air density is visible alongside the bony wall.
  • Neck Spaces Related to the EAC: After observing any inflammation and increased thickness in the external auditory canal, the next step is to examine the soft tissue window. In the soft tissue window, fat in the spaces related to the external auditory canal should be compared based on the described pattern of spread. The periauricular soft tissue, retrocondylar, parapharyngeal, masticator spaces, and retroauricular area should be compared accurately and sensitively with the opposite side spaces. Fat infiltration in the retrocondylar area is a key finding and is very helpful. Any changes in fat density on the affected side can indicate inflammation and suggest the presence of MOE (Fig. 2).
  • Intracranial Structures: The next step is intracranial evaluation. Pay attention to the brain and cerebellar parenchyma for changes in density as signs of inflammation, ischemic changes, or abscess formation. Monitoring for abnormal signals in the venous sinuses and conducting a thorough examination of the inner ear are also very important. When MOE is suspected based on the CT scan, especially in severe and complicated cases, MRI with contrast and diffusion-weighted imaging (DWI) should be recommended.

     2. Bone Window:

• • EAC: The next step is to examine the bony window. First, evaluate the external auditory canal for signs of bony erosion. Subtle bone erosion in the EAC can be an early sign of MOE (Figs 3 and 5).
  • Middle ear: Usually, due to inflammation in the Eustachian tube and dysfunction of it, opacity is observed in the mastoid air cells and tympanic cavity.
  • Adjacent Bones and the Base of the Skull: Based on the pattern of involvement, the condyle of the mandible and mastoid may also be affected. Assess the skull base, including the petrous apex, clivus, and occipital condyle. Erosion of the cortex or alterations in bone density should be noted (Fig. 4). When MOE is suspected based on the CT scan, especially in severe and complicated cases, MRI with contrast and DWI should be recommended.

- In a Temporal MRI, What Step-by-Step Items Should be Paid Attention to Diagnose MOE?

1. T1 Non-Fat Saturation Sequence (Fig. 6):
   • Soft Tissue Infiltration: The T1 Non-Fat Saturation sequence is key for assessing inflammation in the periauricular soft tissue and the adjacent deep neck spaces related to the external auditory canal. Compare the fat signal in the spaces associated with the external ear in a mirrored fashion with the opposite side. Any change in the signal may indicate MOE (Fig. 7). A signal drop in the retrocondylar fat is a key finding and very helpful.
   • Evaluation of Bone Marrow Signal: In the T1 Non-Fat Saturation sequence, the bone marrow signal is typically high. A reduction in signal in the bones adjacent to the external auditory canal, such as the mandibular condyle and mastoid, as well as in the skull base, suggests osteomyelitis (Fig. 8).
   • Intracranial Complications: In the T1 sequence, signs of intracranial complications may also be observed. Pay close attention to the signal from the venous sinus; loss of signal void may indicate venous thrombosis. Assess the course of the internal carotid artery for involvement, indicated by increased wall thickness and reduced luminal diameter suggesting vasculitis, or complete loss of arterial signal void, indicating arterial thrombosis. In cases involving the internal carotid artery, the likelihood of a watershed infarction exists, and the DWI sequence must be checked.
2. T2 Sequence (Fig. 9):
   • Fluid Accumulation: In the T2 sequence, preferably a heavily T2-weighted sequence, look for fluid accumulation and abscess formation. If fluid accumulation is observed with suspicion of an abscess, check post-contrast sequences to visualize enhancing structures, and evaluate DWI and ADC sequences for restriction.
   • Tympanomastoid Effusion: In the T2 sequence, look for effusion in the air cells of the mastoid, which is often secondary to inflammation and dysfunction in the Eustachian tube pathway (Fig. 10).
   • Inner Ear Structures: Examine the internal auditory canal and the structures of the inner ear, including the vestibule, cochlea, and semicircular canals. Abnormal signals in these structures may indicate labyrinthitis (Fig. 11).
3. T1 Post-Contrast Images (Fig. 12):
   • EAC and Related Spaces: In post-contrast images, inflammatory changes and fat infiltration observed in the T1 sequence without saturation will show increased enhancement.
   • Abscess Formation: Fluid collections with enhancing walls suggest the formation of an abscess, as indicated by the DWI sequence showing restriction (Fig. 13).
   • Osteomyelitis: Increased enhancement in the bone marrow of the adjacent bony structures of the external auditory canal (EAC) and the skull base, which corresponds with areas of decreased signal on the T1 sequence, suggests osteomyelitis.
   • Inner Ear: Examine the structures of the inner ear; increased enhancement may indicate labyrinthitis (Fig. 14).
   • Cranial Nerves: Assess the intracranial nerves for the extent of increased enhancement (Fig. 14); the most commonly involved nerve is the facial nerve (cranial nerve VII).
   • Other Intracranial Structures: Assess adjacent intracranial structures for complications, including epidural abscess, venous sinus thrombosis, intraparenchymal abscess, and vasculitis or thrombosis of the internal carotid artery (Figs 13 and 15).

 Axial brain FLAIR sequence is necessary for a more detailed examination of the brain parenchyma, as well as a DWI sequence to assess for acute infarction and evaluate abscesses in patients with suspected MOE.