Rhinogenic brain abscesses: causes, symptoms, diagnosis, treatment

The most common cause of the occurrence of rhinogenic brain abscesses are frontal and etmoiditis, less often the inflammation of the maxillary sinus and the sphenoid sinus, and as a rule, abscesses of the frontal lobe arise, which is primarily due to its proximity to the paranasal sinuses. Abscesses of the anterior cranial fossa, as well as otgegenye abscesses of the temporal and occipital lobes, are subdivided into EDA, SDA and intramedullary abscesses.

With chronic frontitis, the infection is most often spread per continuitatem, through pathoanatomical defects of the posterior wall of the frontal sinus or through the upper wall bordering the orbit. In the latter case, there may be a double complication - phlegmon of the orbit and one of the above-named rhinogenic intracranial complications. Involvement of lacrimal canals in the inflammatory process can lead to the third combination with the first two complications - purulent dacryocystitis.

With chronic etmoiditis, the infection spreads through a broken lattice plate with the formation of an epidural abscess above it. Hyperergic nature of inflammation leads to the formation of a fistula, which at the front is localized in the region of the posterior frontal sinus wall, with etmoiditis above the trellis plate, with sphenoiditis in the region of the wedge bone. In the fistula area, 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 infection is most often spread by hematogenous way. In this case, an abscess can occur in the substance of the frontal lobe without damaging the dura mater. In case of infection spreading inside the skull, EDA first develops, then necrosis and defect of the solid meninges and then - either generalized basilar meningitis or limited encephalitis with the formation of an abscess. The localization of the abscess in the frontal lobe is not substantially dependent on the side of LI lesion and can occur both on the side of the affected sinus and on the opposite side. This feature of localization of the abscesses of the frontal lobe VT Palchun and co-workers. (1977) is explained by the hematogenous spread of the infection, and in some cases by the asymmetric arrangement of the LI, in which one of them may simultaneously border on both frontal lobes of the brain. In addition, as noted by the authors mentioned, the occurrence of secondary rhinogenic intracranial complications in the osteomyelitis of the bones of the skull of different localization is possible. In this case, abscesses of the brain can occur at a distance and more often in the parietal-temporal and even occipital lobes. This is due to the fact that phlebitis of the upper longitudinal sinus first arises, from which the infection spreads by the hematogenous pathway. The same way, the infection can spread directly from the osteomyelitis focus.

Pathogenesis and pathological anatomy of cerebral abscesses. Under the abscess of the brain we mean a solitary accumulation of pus in the substance of the brain, delineated from the surrounding tissues by a demarcation barrier. The initial stage of the abscess is limited purulent encephalitis. With low virulence of microorganisms, with high immunity and nonspecific resistance of the organism and effective antibiotic therapy, encephalitis ceases development, and lysed brain tissue is replaced by a scar. In the reverse picture, the purulent fusion of the brain tissue progresses, and a pus-filled cavity is formed in white matter, the dimensions of which vary. An abscess the size of a chicken egg can form within 5-6 days, but more often under the influence of nonoperative treatment its development slows down, resulting in a capsule from the glia and connective tissue around the abscess, delimiting it from the surrounding brain substance. To form a more or less strong capsule, it takes 4-6 weeks. This concludes the final morphological formulation of the abscess. The capsule blocks the further spread of the infection, it forms an autonomous inflammatory system that has little effect on surrounding tissues and on the body as a whole. Therefore, the general and local symptoms of cerebral abscess are gradually reduced to almost an imaginary picture of complete recovery. A small abscess can be transformed into scar tissue, and then a true recovery comes, but with the involvement of the cerebral cortex in the scar process, epileptiform seizures may develop.

Under the influence of a skull injury, superinfection (influenza, angina, pneumonia, etc.) and other unfavorable factors, the slumbering infection in the abscess can activate, while the capsule undergoes purulent melting and diffuse spread of infection with the formation of new foci of purulent fusion of the brain.

A well developed capsule is formed usually with streptococcal infection; its thickness can reach 4 mm. Abscesses kolibacillary and caused by anaerobes are surrounded by an underdeveloped capsule, which is easily lysed or torn by surgical removal of the abscess. In some cases, with this infection, the capsule is not formed at all, and then purulent inflammation acquires external features of phlegmon with a rapid spread of purulent process in surrounding tissues, often with perforation of the walls of the ventricles of the brain. This kurtosis leads to a quick death.

Symptoms and clinical course of rhinogenic brain abscesses are determined by its localization, the activity of the inflammatory process (virulence and microbiota form), the state of the macroorganism and the effectiveness of the therapeutic measures. They, like otgenennye abscesses of the brain, are divided into three types: general infectious, 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, sharp decrease in efficiency and rapid mental fatigue, bradycardia up to 40 beats / min.

General cerebral symptoms: headache, increasing in the morning, with physical exertion, coughing, sneezing, straining and shaking your head. Increased headache is often accompanied by a sudden vomiting, a sign characteristic of increased intraocular pressure and intracerebral (ventricular) pressure. Changes on the fundus occur in 50-60%, more often than with an otogenic abscess of the temporal lobe, with signs of neuritis of the optic nerve discs over stagnant phenomena predominating. With chronic abscesses of the brain of any localization, epileptic seizures are often observed. With superficial localization and the absence of a capsule, envelope symptoms are observed. The pressure of the cerebrospinal fluid is increased, sometimes significantly, which leads to an increase in headaches. Sudden vomiting, dizziness, photopsy and other manifestations. When localizing cerebral abscess close to the cerebral cortex or ventricles in the spinal cord fluid, moderate cytosis with a predominance of neutrophils and a slight increase in the protein content (0.5-1.2 g / l) are noted.

After the formation of the capsule, especially when the abscess is deep, the cerebrospinal fluid acquires a normal or almost normal appearance (a sign of a false recovery). However, a sudden increase in the number of neutrophils in it and a sharp increase in the protein content against a background of acute worsening of the patient's condition and expressed shell symptoms indicate the 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 in the anterior horns of the lateral ventricles and in the central part of them.

Focal symptoms are diverse and depend on the functional specialization of the affected structures of the brain. Most often, abscesses of the frontal lobe are localized in the white matter of the upper or middle frontal gyrus, i.e., in the part of the brain that is attached to the posterior wall of the frontal sinus. However, the abscess can spread and posteriorly toward the inner capsule, in which the pyramidal pathways and axons of the second neurons of the cranial nerves pass, which, in effect, determines the focal symptomatology with the fallout of certain functions of the pyramidal system and cranial nerves.

With frontal localization of cerebral abscess, which occurs as a complication of acute or exacerbation of chronic purulent frontalitis, usually symptoms such as edema of the upper eyelid and hyperemia of the conjunctiva on the side of the lesion, exophthalmos with the shift of the eyeball downwards and diplopia, are most noteworthy. From the general cerebral symptoms, the forms of behavioral reactions that appeared atypical for the individual (euphoria, disinhibition in behavior, kakolalia, etc.) appeared. Focal symptoms include convulsions of mimic muscles on the side opposite to the localization of the abscess, paresis and papillary disorders. In far-reaching cases, convulsions can encompass limbs or acquire a generalized character. In the future convulsive syndrome, the central and then flaccid paralysis of the facial nerve and nerves of the extremities come to replace.

In complications of purulent diseases of the posterior (deep) paranasal sinuses (middle and posterior cells of the latticed labyrinth and sphenoid sinus), along with brain abscesses of various localizations, ophthalmic complications, as well as rhinogenic lesions of the venous system of the brain, are often dominated by separate sections of the present chapter. Here we touch on some issues of brain abscess.

The duration of the abscess of the brain varies from several days (with lightning-fast forms) to many months and even years. In chronic forms, a small well-encapsulated abscess can be asymptomatic and can be detected either with a planned X-ray (CT, MRI) brain examination or accidentally at autopsy. When lesions are especially virulent microorganisms, reduced immunity, delayed formation of a protective capsule, the abscess rapidly increases and can lead to death within a few days. Sudden loss of consciousness, the emergence of a co-morbid and then comatose state, as a rule, indicate a breakthrough of pus in the ventricles of the brain. The most well-suited are well encapsulated abscesses in the cerebral hemispheres, which are accessible to surgical removal without breaking the capsule, and which give only temporary mild exacerbations under the influence of intercurrent infections, head bruises, and sometimes without obvious causes. Often, such outbreaks do not pay attention to the patients and explain the headache, weakness, nausea caused by the provoking cause or for some other reasons, for example, arterial hypertension.

Diagnosis of cerebral abscesses is often very difficult, even with a thorough X-ray examination. In modern conditions, an accurate diagnosis can be established only by CT or MRI. The presence of cerebral abscess should be suspected when a qualitatively new cephalalgia differs from typical (habitual) pain in persons suffering not only chronic purulent diseases of the paranasal sinuses and the ear, but also purulent processes in any remote part of the body (bronchiectasis, gangrene of the lung , septic endocarditis, etc.).

Differentiate the brain abscess from infectious encephalitis of various etiologies, tumors, aneurysms and cysticercles of the brain, slowly accruing vascular disorders of a localized nature, the consequences of CMT with the formation of hematomas and cysts, etc.

The prognosis for cerebral abscess is ambiguous and is determined by many factors: early or late diagnosis, localization of the focus (the most anxious prognosis for stem and paraventricular abscesses), the general condition of the body and its immunological status, virulence of the microbiota, etc. In general, the forecast can be defined as optimistic-cautious and favorable for superficial well encapsulated abscesses. With metastatic abscesses of the brain, which are often multiple, the prognosis is usually unfavorable. Usually patients die from a complicated abscess of purulent spilled meningitis or when a pus breaks into the ventricles of the brain from a purulent ventriculitis. In the pre-sulfonamide and preantibiotics, the mortality rate from brain abscesses after the operation reached 50%. At present, according to the data of different authors, this indicator, by the end of the 20th century, amounted to 7-10%.

Treatment is certainly surgical, and it is carried out according to vital indications even with a complicated abscess of the brain purulent meningitis and stay of the patient in a co-morbid or comatose state.

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