Acute and chronic otitis media with mastoiditis can easily spread to adjacent or distant areas, leading to various complications collectively referred to as otogenic complications. These complications are categorized into intracranial and extracranial complications. Among them, intracranial complications are the most dangerous and can be life-threatening.
Etiology
Bone destruction in the middle ear and mastoid is most seen in cases of middle ear cholesteatoma, which can lead to infections in adjacent structures and subsequent complications. Suppurative otitis media is a less common cause.
Individuals with compromised immunity, such as those with diabetes, tuberculosis, severe chronic systemic diseases, or prolonged malnutrition, older adults, frail individuals, and children, are more prone to the spread of middle ear infections and the development of complications.
The primary pathogens are Gram-negative bacilli, including Proteus, Pseudomonas aeruginosa, Escherichia coli, Klebsiella, and Clostridium perfringens. In some cases, cocci or mixed infections involving two or more pathogens are observed. Antibiotic-resistant bacteria increase the risk of otitis media complications.
Pathways of spread
The pathways for the spread of infections leading to otogenic complications include:
- Spread through bony defects
- Spread through anatomical pathways or unclosed sutures
- Hematogenous spread
Figure 1 Diagram of the pathways of spread in otogenic complications
1, Postauricular subperiosteal abscess
2, Epidural abscess
3, Deep cervical abscess (lateral to the digastric muscle)
4, Perisinus abscess (around the sigmoid sinus)
5, Sigmoid sinus thrombophlebitis
6, Brain abscess
7, Cerebellar abscess
8, Dura mater of the temporal lobe
9, Periosteum
10, Deep cervical abscess (medial to the digastric muscle)
Spread through bony defects
When the bony walls of the tympanic cavity, mastoid air cells, sigmoid sinus, or sinodural angle are destroyed, infections can spread intracranially. Perforation of the outer or inner bony walls of the mastoid can result in subperiosteal abscesses behind the ear or deep cervical abscesses. Destruction of the semicircular canals or promontory allows bacteria and toxins to spread into the inner ear, causing various forms of labyrinthitis. Destruction of the facial nerve canal can lead to otogenic facial paralysis. Additionally, trauma or surgically created pathways can serve as routes for infection.
Spread through anatomical pathways or unclosed sutures
Bacteria and toxins can spread intracranially through unclosed sutures in children or via normal anatomical pathways such as the cochlear aqueduct, vestibular aqueduct, and internal auditory canal. Congenital inner ear anomalies, such as communication between the internal auditory canal and inner ear and congenital cerebrospinal fluid otorrhea, may also provide routes for infections to enter the inner ear and intracranial structures, leading to profound hearing loss and cochlear ossification.
Hematogenous spread
Small blood vessels in the mucosa of the middle ear, mastoid emissary veins, and small veins in the bony canals communicate with meningeal and cerebral surface vessels, allowing middle ear infections to spread intracranially. Septicemia associated with suppurative otitis media can result in distant purulent infections in organs such as the lungs (pneumonia, lung abscess) and liver (hepatic abscess).
Classification
Complications of otitis media are divided into intracranial complications and extracranial complications. Clinically, complications inside and outside the temporal bone are often classified as extracranial complications.
Intracranial complications include:
Extracranial complications include:
Diagnosis
Due to the widespread use of antibiotics, the symptoms of otogenic intracranial complications are often atypical. Diagnosis requires a comprehensive analysis based on medical history, symptoms, physical examination, and imaging studies.
In patients with otitis media, lethargy or especially apathy should raise suspicion of complications.
In otitis media patients, a sudden decrease or increase in otorrhea, accompanied by ear pain, persistent headache, general malaise, and fever, as well as redness, swelling, and tenderness in the mastoid area or hard line in the neck, should be noted.
The presence of meningeal irritation signs, increased intracranial pressure, cranial nerve palsy, or central focal neurological signs should prompt further investigation. Changes in the fundus of the eye, abnormalities in cerebrospinal fluid analysis obtained via lumbar puncture, and bacterial culture results can assist in diagnosis.
CT scans may reveal bone destruction in the mastoid or tegmen tympani. Contrast-enhanced CT and MRI scans can help determine the extent and type of complications.
Treatment
Mastoidectomy can be performed to explore and carefully examine the tegmen tympani, tegmen mastoideum, and sigmoid plate, and necrotic bone should be removed. Local abscesses should be managed with aspiration, irrigation, drainage, or excision as necessary.
Based on bacterial culture results, adequate antibiotics capable of penetrating the blood-brain barrier can be selected, and combination therapy can be considered if needed.
Supportive care, including fluid replacement, blood transfusion, or administration of plasma, compound amino acids, and albumin, can be provided according to the patient's condition.
For patients with increased intracranial pressure, treatments to reduce intracranial pressure are required. For example, 20% mannitol (1-2 g/kg) can be given via rapid intravenous infusion, or 50% glucose (40-60 mL) can be injected. Glucocorticoids, such as dexamethasone (10-20 mg/day), can be administered via intravenous infusion.