Rhinogenic brain abscesses: causes, symptoms, diagnosis, treatment

The most common causes of rhinogenic brain abscesses are frontal sinusitis and ethmoiditis, less often inflammation of the maxillary sinus and sphenoid sinus, while, as a rule, abscesses of the frontal lobe occur, which is primarily due to its proximity to the paranasal sinuses. Abscesses of the anterior cranial fossa, like otogenic abscesses of the temporal and occipital lobes, are divided into EDA, SDA and intramedullary abscesses.

In chronic frontal sinusitis, the infection most often spreads per continuitatem, through pathological defects of the posterior wall of the frontal sinus or through the upper wall bordering the orbit. In the latter case, a double complication may occur - orbital phlegmon and one of the above-mentioned rhinogenic intracranial complications. Involvement of the lacrimal ducts in the inflammatory process may also lead to a third complication combined with the first two - purulent dacryocystitis.

In chronic ethmoiditis, the infection spreads through the destroyed cribriform plate with the formation of an epidural abscess above it. The hyperergic nature of the inflammation leads to the formation of a fistula, which in frontal sinusitis is localized in the area of the posterior wall of the frontal sinus, in ethmoiditis - above the cribriform plate, in sphenoiditis - in the area of the sphenoid bone platform. In the area of the fistula, an erosive defect of the dura mater is formed with the formation of SDA and its possible spread into the depth of the brain tissue.

In acute sinusitis, the infection most often spreads hematogenously. In this case, an abscess can occur in the substance of the frontal lobe without damaging the dura mater. If the infection spreads into the skull by contact, EDA first develops, then necrosis and a defect of the dura mater, and then either generalized basilar meningitis or limited encephalitis with abscess formation. The localization of an abscess in the frontal lobe does not significantly depend on the side of the lesion of the LI and can occur both on the side of the affected sinus and on the opposite side. V. T. Palchun et al. (1977) explain this feature of the localization of frontal lobe abscesses by the hematogenous spread of infection, and in some cases by the asymmetric location of the LI, in which one of them can simultaneously border on both frontal lobes of the brain. In addition, as the above-mentioned authors note, secondary rhinogenic intracranial complications may also occur with osteomyelitis of the skull bones of various localizations. In this case, brain abscesses may occur at a distance and most often in the parietal-temporal and even occipital lobes. This is explained by the fact that phlebitis of the superior longitudinal sinus occurs first, from which the infection spreads hematogenously. The infection can also spread directly from the osteomyelitic focus in this way.

Pathogenesis and pathological anatomy of brain abscesses. A brain abscess is a solitary accumulation of pus in the brain tissue, separated from the surrounding tissues by a demarcation barrier. The initial stage of an abscess is limited purulent encephalitis. With low virulence of microorganisms, high immune and nonspecific resistance of the body and effective antibiotic therapy, the development of encephalitis stops, and the lysed brain tissue is replaced by a scar. With the opposite picture, purulent melting of brain tissue progresses, and a cavity filled with pus is formed in the white matter, the size of which varies. An abscess the size of a chicken egg can form within 5-6 days, but more often, under the influence of non-surgical treatment, its development slows down, as a result of which a capsule is formed from glia and connective tissue around the abscess, separating it from the surrounding brain tissue. It takes 4-6 weeks for a more or less strong capsule to form. This completes the final morphological formation of the abscess. The capsule blocks further spread of infection, it forms a kind of autonomous inflammatory system that has little effect on the surrounding tissues and the body as a whole. Therefore, general and local symptoms of a brain abscess are gradually reduced to an almost imaginary picture of complete recovery. A small abscess can transform into scar tissue, and then true recovery occurs, however, if the meninges are involved in the scar process, epileptiform seizures can develop.

Under the influence of cranial trauma, superinfection (flu, tonsillitis, pneumonia, etc.) and other unfavorable factors, the infection dormant in the abscess cavity can become active, and the capsule undergoes purulent melting and diffuse spread of infection with the formation of new foci of purulent melting of the brain.

A well-developed capsule is usually formed with streptococcal infection; its thickness can reach 4 mm. Colibacillary abscesses and those caused by anaerobes are surrounded by a poorly developed capsule, which is easily lysed or ruptured during surgical removal of the abscess. In some cases, with this infection, the capsule does not form at all, and then the purulent inflammation acquires the external features of phlegmon with rapid spread of the purulent process into the surrounding tissues, often with perforation of the walls of the ventricles of the brain. This excess leads to rapid death.

The symptoms and clinical course of rhinogenic brain abscesses are determined by its localization, the activity of the inflammatory process (virulence and form of microbiota), the state of the macroorganism and the effectiveness of treatment measures. They, like otogenic brain abscesses, are divided into three types: general infectious, general cerebral and focal.

General infectious symptoms: increased body temperature within 37.5-38.5°C, moderate leukocytosis with a shift in the formula to the left, increased ESR (40-60 mm/h), weakness, insomnia with drowsiness, poor health, decreased appetite, a sharp decrease in performance and rapid mental fatigue, bradycardia up to 40 beats/min.

General cerebral symptoms: headache, increasing towards morning, with physical exertion, coughing, sneezing, straining and shaking the head. Increased headache is often accompanied by sudden vomiting, a symptom characteristic of increased intracranial pressure and intracerebral (ventricular) pressure. Changes in the fundus occur in 50-60%, more often than with otogenic abscess of the temporal lobe, with signs of optic disc neuritis prevailing over congestion. Chronic brain abscesses of any localization are often accompanied by epileptic seizures. With superficial localization and the absence of a capsule, meningeal symptoms are observed. Cerebrospinal fluid pressure is increased, sometimes significantly, which leads to increased headaches, sudden vomiting, dizziness, photopsies and other manifestations. When a brain abscess is localized close to the cortex or ventricles of the brain, moderate cytosis with a predominance of neutrophils and a slight increase in protein content (0.5-1.2 g/l) are observed in the cerebrospinal fluid.

After the capsule has formed, especially if the abscess is deep, the cerebrospinal fluid takes on a normal or almost normal appearance (a sign of false recovery). However, a sudden increase in the number of neutrophils and a sharp increase in protein content against the background of an acute deterioration in the patient's condition and pronounced meningeal symptoms indicate a breakthrough of the abscess into the subdural space or into the ventricles of the brain. With deep abscesses of the frontal lobes, a breakthrough of pus occurs most often into the anterior horns of the lateral ventricles and into their central part.

Focal symptoms are varied and depend on the functional specialization of the affected brain structures. Most often, frontal lobe abscesses are localized in the white matter of the superior or middle frontal gyri, i.e. in the part of the brain that is adjacent to the posterior wall of the frontal sinus. However, the abscess can also spread posteriorly toward the internal capsule, in which the pyramidal tracts and axons of the second neurons of the cranial nerves pass, which, in essence, determines focal symptoms with the loss of certain functions of the pyramidal system and cranial nerves.

In case of frontal localization of a brain abscess, arising as a complication of acute or exacerbation of chronic purulent frontal sinusitis, symptoms such as edema of the upper eyelid and hyperemia of the conjunctiva on the affected side, exophthalmos with downward and outward displacement of the eyeball, diplopia usually attract attention. Of the general cerebral symptoms, behavioral reactions that are atypical for this individual (euphoria, behavioral disinhibition, cacolalia, etc.) are noted. Focal symptoms include convulsions of the facial muscles on the side opposite to the localization of the abscess, paresis and pupillary disorders. In advanced cases, convulsions may involve the limbs or become generalized. Later, the convulsive syndrome is replaced by central and then flaccid paralysis of the facial nerve and nerves of the limbs.

In complications of purulent diseases of the posterior (deep) paranasal sinuses (middle and posterior cells of the ethmoid labyrinth and sphenoid sinus), along with brain abscesses of various localizations, ophthalmologic complications often dominate, as well as rhinogenic lesions of the venous system of the brain, to which separate sections of this chapter are devoted. Here we will touch upon some issues of brain abscess.

The duration of a brain abscess varies from several days (in fulminant forms) to many months and even years. In chronic forms, a small well-encapsulated abscess may be asymptomatic and be detected either during a routine X-ray (CT, MRI) examination of the brain or accidentally at autopsy. When affected by particularly virulent microorganisms, with reduced immunity, or a slow process of formation of a protective capsule, the abscess quickly increases and can lead to death within a few days. Sudden loss of consciousness, the onset of a soporous and then comatose state usually indicate a breakthrough of pus into the ventricles of the brain. Well-encapsulated abscesses in the cerebral hemispheres, which are accessible to surgical removal without rupturing the capsule, and which give only temporary mild exacerbations under the influence of intercurrent infections, head injuries, and sometimes without obvious causes, have the most favorable course. Often, patients do not pay attention to such outbreaks and explain the headache, weakness, nausea that has arisen as a result of the action of a provoking cause or some other reasons, such as arterial hypertension.

Diagnosis of brain abscesses is often very difficult, even with careful X-ray examination. In modern conditions, an accurate diagnosis can only be established by CT or MRI. The presence of a brain abscess should be suspected when a qualitatively new cephalgia appears, different from typical (habitual) pains in people suffering not only from chronic purulent diseases of the paranasal sinuses and ear, but also from purulent processes in some remote part of the body (bronchiectatic disease, pulmonary gangrene, septic endocarditis, etc.).

Brain abscess is differentiated from infectious encephalitis of various etiologies, tumors, aneurysms and cysticerci of the brain, slowly increasing vascular disorders of a localized nature, consequences of TBI with the formation of hematomas and cysts, etc.

The prognosis for brain abscess is ambiguous and is determined by many factors: early or late diagnosis, localization of the lesion (the prognosis is most alarming for brainstem and paraventricular abscesses), the general condition of the body and its immunological status, the virulence of the microbiota, etc. In general, the prognosis can be defined as optimistic-cautious and favorable for superficial well-encapsulated abscesses. In metastatic brain abscesses, which are often multiple, the prognosis is usually unfavorable. Patients usually die from purulent diffuse meningitis that complicates the abscess or from a breakthrough of pus into the ventricles of the brain from purulent ventriculitis. In the pre-sulfanilamide and pre-antibiotic period, the mortality rate from brain abscesses after surgery reached 50%. Currently, this figure, according to various authors, by the end of the 20th century was 7-10%.

Treatment is certainly surgical, and it is carried out according to vital indications, even in cases where purulent meningitis has complicated the brain abscess and the patient is in a soporous or comatose state.

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