Otogenic brain abscess is a localized collection of pus within the white matter of the brain, caused by complications of suppurative otitis media and mastoiditis. Otogenic brain abscesses account for 80% of all brain abscesses, and nearly all cerebellar abscesses are otogenic in origin. The abscesses are mostly located in the temporal lobe of the cerebrum, followed by the cerebellum, and are typically solitary. The predominant pathogens are bacilli (e.g., Proteus mirabilis, Pseudomonas aeruginosa), with fewer cases caused by Staphylococcus aureus and Streptococcus hemolyticus. Mixed infections are also observed.
Pathology
The formation of a brain abscess generally progresses through three stages:
- Localized encephalitis stage
- Suppuration stage
- Capsule formation stage
Localized encephalitis stage
In the early stage, blood vessels in the affected area of the brain's white matter dilate, inflammatory cells infiltrate, and the central brain tissue undergoes necrosis and liquefaction, surrounded by edema in the adjacent brain tissue.
Suppuration stage
The lesion is localized, and necrotic and liquefied tissue coalesces to form an abscess. The abscess is surrounded by a thin layer of inflammatory granulation tissue, newly formed blood vessels, and edematous brain tissue. At this stage, there is no clear boundary between the abscess and the surrounding brain tissue.
Capsule formation stage
As the abscess matures, fibroblasts from the meninges and blood vessel walls, along with granulation tissue and surrounding glial cells, form a capsule around the abscess. As the abscess enlarges, it causes increased intracranial pressure and focal neurological deficits. Severe intracranial hypertension may lead to brain tissue displacement, resulting in brain herniation, which can cause sudden death due to respiratory and cardiac arrest. Large abscesses may rupture into nearby ventricles or the subarachnoid space, leading to severe ventriculitis and meningitis.
Clinical manifestations
The clinical course of typical otogenic brain abscess can be divided into initial stage, latent stage, symptomatic stage, and terminal stage.
Initial stage
This stage lasts for several days and is characterized by mild meningeal irritation signs. Cerebrospinal fluid (CSF) analysis shows a mild to moderate increase in cell count and protein levels. Blood tests reveal neutrophilia with a left shift. This stage may be misdiagnosed as an acute exacerbation of chronic suppurative otitis media, presenting with sudden rigors, high fever, headache, nausea, emesis, and mild neck stiffness.
Latent stage
This stage lasts for 10 days to several weeks, corresponding to the pathological stage of localized suppuration. Symptoms are variable and may include mild headache, fatigue, lethargy, anorexia, low-grade fever, depression, hypologia, drowsiness, and irritability.
Symptomatic stage
The duration of this stage varies. It corresponds to the expansion of the brain abscess, with accompanying increased intracranial pressure and the following symptoms.
The initial symptoms often include apathy, sluggish responses, lethargy, and even somnolence. Afternoon low-grade fever or high fever may occur. Some patients experience reduced or increased appetite and constipation.
Headache, often starting on the affected side, may spread to the entire head, with the frontal and occipital regions being most prominent. It is typically persistent and worsens at night.
Projectile vomiting, unrelated to food intake, may occur. Varying severity of consciousness impairment may be present. Bradycardia is inconsistent with changes in body temperature. Papilledema may be observed.
Other symptoms include frequent unconscious actions (e.g., yawning, nose picking, handling the genitals), and personality and behavior changes.
The timing and severity of focal symptoms vary.
Temporal lobe abscess
In right-handed individuals, the speech sensory center is in the posterior part of the left temporal lobe. If affected, it may result in nominal aphasia, where the patient can describe the use of an object but cannot name it correctly. Involvement of the motor cortex may cause contralateral paralysis of the lower 2/3 of the face and the upper and lower limbs. Lesions involving the optic radiation may cause homonymous hemianopia, and involvement of the oculomotor nerve on the affected side may result in pupil dilation.
Figure 1 CT image of temporal lobe brain abscess
Cerebellar abscess
This condition primarily presents with space-occupying signs, such as ipsilateral hypotonia, ataxia, unsteady stance, and a staggering gait with a tendency to fall toward the affected side. Dysdiadochokinesia and abnormal finger-to-nose tests may be observed. Central nystagmus may worsen as the abscess enlarges, but the severity of nystagmus may not correlate with vertigo. Nystagmus may be irregular and multidirectional or mimic peripheral nystagmus. Symptoms of increased intracranial pressure, such as papilledema, may also occur.
Terminal stage
Patients may suddenly or gradually fall into a deep coma, with respiratory and cardiac arrest leading to death. Brain abscesses may rupture into the subarachnoid space, causing diffuse meningitis, or into the ventricles, resulting in fulminant meningitis and ventriculitis. Temporal lobe abscesses may cause transtentorial herniation, while cerebellar abscesses may lead to foramen magnum herniation. Both can damage the brainstem's vital centers, causing deepening coma, elevated blood pressure, weakened pulse, contralateral limb paralysis, and pupil dilation.
Diagnosis
A prior history of suppurative otitis media or middle ear cholesteatoma is an important diagnostic clue.
There are typical symptoms associated with brain abscess, such as headache, fever, neurological deficits, and signs of increased intracranial pressure.
Imaging studies can reveal the size, location, number of abscesses, and the severity of ventricular compression.
Papilledema may be observed upon fundoscopic evaluation.
Differential diagnosis
It is essential to distinguish otogenic brain abscess from conditions such as hydrocephalus and brain tumors.
Otogenic hydrocephalus can be either communicating or obstructive, with the former being more common. The primary symptom of hydrocephalus is increased intracranial pressure, but systemic symptoms are generally mild, and focal neurological signs are absent. CT or MRI scans can help differentiate hydrocephalus from brain abscess.
Brain tumors typically have a slow progression and lack a history of suppurative otitis media or intracranial infection. Imaging studies and clinical history are key to differentiation.
Treatment
Early administration of broad-spectrum antibiotics
Intravenous antibiotics targeting Gram-negative and anaerobic bacteria should be initiated. The antibiotic regimen can be adjusted based on bacteriological findings.
Mastoid exploration and abscess aspiration
During surgery, if destruction of the tegmen tympani, tegmen mastoideum, or sigmoid plate is observed, the exposure should be extended to normal boundaries. If the tegmen is intact, it should be drilled to expose the dura mater. Signs suggestive of a brain abscess include congested, thickened dura mater with granulation tissue, increased tension, and absent brain pulsation. For patients with severe intracranial hypertension or impending brain herniation, neurosurgical consultation is essential. In these cases, burr-hole aspiration or lateral ventricular drainage may be performed to reduce intracranial pressure before mastoid surgery.
Abscess management
Pus can be aspirated via a puncture through the mastoid cavity under strict aseptic conditions. To facilitate postoperative drainage, the puncture site should be located at the lower or basal wall of the abscess. Once the needle enters the intracranial space, the direction of the needle must not be altered. If redirection is necessary, the needle should be withdrawn and reinserted.
Incision and drainage are suitable for superficial abscesses or abscesses that have formed in the dura mater.
Abscess excision is indicated for thick-walled abscesses, abscesses resistant to repeated aspirations, or multilocular/multiple abscesses. Craniotomy is required for excision.
Supportive therapy and electrolyte balance
Frequent emesis may lead to dehydration and electrolyte disturbances. Long-term intravenous administration of glucose and dehydration therapy may be necessary. Electrolyte levels should be monitored, and fluids should be adjusted accordingly to correct acidosis, alkalosis, or prevent hypokalemia or hyponatremia.
Management of increased intracranial pressure
Dehydration therapy, such as intravenous administration of 50% glucose and 20% mannitol in alternating doses, can help reduce intracranial pressure. Glucocorticoids may be administered intravenously in appropriate doses to alleviate cerebral edema.
Management of brain herniation
If brain herniation or pre-herniation symptoms occur, intravenous 20% mannitol can be administered immediately. Endotracheal intubation can be performed, and oxygen therapy and mechanical ventilation can be initiated. Emergency aspiration of the brain abscess should be performed to drain pus. If necessary, lateral ventricular drainage can be performed to reduce intracranial pressure prior to abscess aspiration.