Otogenic intracranial complications and otogenic sepsis

Otogennye intracranial complications are complications resulting from the penetration of infection into the cavity of the skull with purulent inflammation of the middle and inner ear.

Diseases of the middle and inner ear that cause intracranial complications: acute purulent otitis media, mastoiditis, chronic purulent meso- and epitimpanitis, purulent labyrinthitis. In their unfavorable course, limited purulent processes in the neighboring anatomical regions (abscesses) can lead to spilled inflammation of the meninges (meningitis) and brain substances (encephalitis), as well as sepsis.

Common features of the refined intracranial complications:

• Similar complications arise in purulent diseases of both the middle and inner ear;
• features of the anatomical structure of the temporal bone and various parts of the ear determine the interrelation of inflammatory processes in the middle and inner ear;
• all complications pose a danger to the life of the patient;
• processes have similar patterns of development:
• the causes and peculiarities of the course of these complications are common to all purulent processes in the body.

ICD-10 code

• G03.9 Meningitis
• G04.9 Encephalitis

Epidemiology of otogenic intracranial complications and otogenic sepsis

In the 20-ies of the last century, patients with otogennymi intracranial complications accounted for more than 20% of the total number of patients who underwent surgical intervention in the ear.

In the first place among intracranial otognenny complications is meningitis, on the second - abscesses of the temporal lobe of the brain and cerebellum, on the third - sinustromboz. Sepsis develops less often. The most common complication in childhood is spillage of meningoencephalitis.

Ottozhennye intracranial complications occupy the first place in the structure of detail in the otorhinolaryngology clinics. According to the otorhinolaryngological clinic, located in Winston-Salem (USA), during the years 1963-1982, mortality of patients with otogenic intracranial complications was 10%. According to modern domestic and foreign authors, this figure varies from 5 to 58%.

Despite the availability of new antimicrobials, mortality in purulent meningitis continues to be high and is 25% among adult patients. Especially high mortality rates in patients with meningitis caused by gram-negative flora and Staphylococcus aureus.

Prophylaxis of refractory intracranial complications and otogenous sepsis

Prevention of otogenic intracranial complications is the timely diagnosis of acute and chronic ear diseases. Effective measures to prevent otogenic complications are: performance of the paracentesis of the tympanic membrane with acute purulent otitis media, as well as dispensary observation of patients with chronic purulent otitis media and preventive sanitation of the ear.

Screening

Traditional methods of diagnosis (collection of anamnesis, laboratory studies, specialist advice) in combination with the latest modern research methods (zoeencephalography, angiography, CT and MRI) allow timely detection of the refractory intracranial complications.

Classification

Currently, the following forms of otogenic intracranial complications are distinguished:

• extradural abscess.
• subdural abscess;
• purulent meningitis.
• abscesses of the brain and cerebellum;
• sinus syndrome;
• otogenic sepsis.

Sometimes one form of complications passes into another, in some cases there can be a combination of several forms simultaneously. All this creates difficulties in the diagnosis and treatment of these complications.

Causes of otogenous intracranial complications and otogennogo sepsis

Microflora, sown from the primary source of infection, is mostly mixed and unstable. Most often the cocci flora predominates: staphylococci, streptococci, less often - pneumococci and diplococci, even more rarely Proteus and Pseudomonas aeruginosa. The occurrence of complications and the variant of the development of the inflammatory reaction depend on the virulence of the pathogen.

Pathogenesis of otogenous intracranial complications and otogenic sepsis

The pathogenesis of the repaired intracranial complications is complicated. In addition to the virulence of microflora, the state of general resistance of the organism is of great importance. Ultimately, it is their ratio that determines the direction and severity of the inflammatory reaction. On the one hand, the more virulent the flora, the more severe the inflammatory process and the organism is more difficult to withstand its spread. On the other hand, rapid progression of inflammation can be a consequence of the incompleteness of the formation of immunological reactions in childhood, as well as the pronounced reactivity of the child's organism. Sluggish flow of inflammatory reactions can be observed in elderly people as a result of a decrease in both general resistance and reactivity of the organism. Resistance and reactivity of the body are determined genetically, but they can change due to overfatigue, hypovitaminosis, alimentary dystrophy, systemic diseases, intoxications, zdokdinnyh disorders and allergic reactions.

The spread of infection into the subshell and brain is now recognized as the main and most significant way of development of intracranial otogenic complications. An important obstacle in this way is the natural protective barriers of the human body. In the central nervous system this protection is represented by: 1) anatomical and 2) immunological barriers.

The anatomical barrier serves as a mechanical barrier to the penetration of microbes and includes the bones of the skull and the meninges. If these anatomical structures are broken as a result of the spread of the purulent process from the ear, the risk of development of the otogenic intracranial complications increases significantly.

The development of refined intracranial complications is facilitated by:

• features of the structure of the temporal bone and the structures of the middle and inner ear located in it (the abundance of folds and pockets of the mucous membrane of the attic and the cellular structure of the mastoid process, ventilation and drainage of which are significantly hampered by inflammation):
• remnants of myxoid tissue in the tympanum in neonates;
• persistence in the walls of the tympanum;
• the stony-scaly cleft (fissura petrosqumosa), not clotted in small children;
• bony canals of the neurovascular anastomoses;
• labyrinth windows;
• aqueducts of the vestibule and snails.

Complications of acute purulent otitis media are mastoiditis and labyrinthitis. Labyrinthitis can develop with chronic purulent otitis media. Progressively destroying the temporal bone, pus from the mastoid process can fall under the periosteum - subperiosteal abscess, through the apex of the appendage under the muscles of the neck and further into the mediastinum - apical mastoiditis, and from the attic and the labyrinth into the cavity of the skull - the extradural abscess. If a purulent process develops in the region of the sigmoid sinus, then a perisinus abscess will occur. On the way of spreading the infection into the cranial cavity there is a dura mater, which along with the haematogenous barrier is a serious obstacle for the development of intracranial complications. Nevertheless, inflammation of the dura mater increases the permeability of the vascular walls and facilitates the penetration of the infection.

The blood-brain barrier separates the cerebrospinal fluid and the brain from intravascular contents and limits the penetration of various substances (including drugs) and microorganisms from the blood into the cerebrospinal fluid. The blood-brain barrier is usually divided into blood-brain and hematopoietic barriers. Anatomically the main components of these barriers are the endothelium of the capillaries of the brain, the epithelium of the choroid plexus and the arachnoid membrane. Compared to other capillaries, the endothelium of the capillaries of the brain has tight contacts between cells that prevent intercellular transport. In addition, the capillaries of the brain have a low density of pinocytic vesicles, an abundant amount of mitochondria and unique enzymes and transport systems.

Against the backdrop of the inflammatory process, the permeability of the blood-brain barrier increases due to rupture of tight connections between endothelial cells and an increase in the number of pinocytic vesicles. As a result, it is easier to overcome the hematoenzialphic barrier with microbes. It should be noted that most antibiotics do not penetrate badly through the blood-brain barrier, however, in the inflammatory process, their content in the cerebrospinal fluid increases significantly.

The organism resists the spread of infection, therefore purulent foci may be limited and located in close proximity to the brain or the cerebellum at a depth of 2-4 cm. The described process of infection spreading has been termed "continuation" (percontinuctatum).

The response of the immune system in response to microbial invasion includes three components: 1) the humoral response. 2) phagocytic cellular response and 3) otpet system complement. Under normal conditions, these protective reactions in the cerebrospinal fluid do not flow. In fact, the CNS is in an immunological vacuum, which is disturbed by intracranial penetration of microorganisms.

Tabular defects in the human immune system can predispose to the spread of infection in the central nervous system. These defects include hypogammagodobulinemia, aspension, leukopenia, complement deficiency, acquired immunodeficiency syndrome, and other T cell defects. Patients with Ig and complement defects constitute a risk group for infections caused by encapsulated microorganisms (Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae). Patients with neutropenia are at risk for developing bacterial infections (Pseudomonas aeruginosa, Staphylococcus aureus) and infections caused by pathogenic fungi. Finally, defects in cellular immunity may be the cause of infections caused by intracellular obligate microorganisms (listeria monocytogenes, Mycobacterium tuberculosis, Toxoplasma gondii, Nocardia asteroides, Cryptococcus neoformans and Aspergillus species).

When the process is generalized due to reduced resistance and altered reactivity of the body, more menacing meningitis, meningoencephalitis or sepsis may develop more severe otgenic intracranial complications. The septic state in acute purulent otitis in children develops when bacteria and their toxins enter the bloodstream from the tympanic cavity. Contributing factors: hyperreactivity and weakness of protective immunological reactions of the child's organism, as well as the difficulty of the outflow of pus from the tympanic cavity. The septic reaction develops violently, but it is comparatively easily reversible. This form of sepsis is characterized mainly by septicemia and toxemia. With chronic otitis, generalization of infection most often develops after thrombophlebitis of sigmoid sinus (rarely affects the bulb of the vomiting vein, transverse, upper and lower stony sinuses). The stages of this process are periphlebitis, endophlebitis, parietal thrombosis, complete thrombosis, infection and decomposition of thrombus, septicemia and septicopyemia. However, thrombosis of the sinuses does not always lead to sepsis. Even in case of infection, thrombus can be organized.

Each purulent ear disease has its own way of spreading the infection, which can consist of one or several mechanisms (contact, hematogenous, lymphogenous, lympholibrinogenic).

In acute purulent otitis media, the most frequent way of spreading the infection into the cranial cavity is through the roof of the tympanic cavity (mainly hematogenous). In second place is the path to the labyrinth through the window of the cochlea and the annular bundle of the window of the vestibule. It is possible hematogenous spread of the infection into the carotid plexus and from there to the cavernous sinus, and also through the lower wall of the tympanum into the bulb of the vomiting vein.

When mastoid pus, melting the bone, can break through the mastoid appendix (planum mastoideum) into the BTE, through the apex of the mastoid under the neck muscles and through the anterior wall of the mastoid process into the external auditory canal. In addition, it is possible to spread the process into the cranial cavity to the membranes of the brain, the sigmoid sinus and the cerebellum, and through the antrum's roof to the temporal lobe of the brain.

With chronic purulent epitimpanitis, in addition to intracranial complications, a fistula of the lateral semicircular canal can form and a labyrinthitis may occur.

With a purulent diffuse maze, the infection spreads along the water pipeline of the vestibule to the subarachnoid space of the bridge bridge, to the endolymphatic sac, to the posterior surface of the temporal bone pyramid to the brain and cerebellum shells, and also along the perineural pathways into the internal auditory canal and from there to the membranes and brain substance in the region of the cerebellar angle.

Sometimes there are associated complications. They most often are sinustroboz and abscess of the cerebellum, as well as meningitis and brain abscess. In this case, it is appropriate to talk about the stage of the spread of infection in the cranial cavity.

The spread of infection beyond the structures of the middle and inner ear is mainly due to the difficulty of the outflow of the purulent discharge from the tympanic cavity and the cells of the mastoid process into the external auditory canal. \ This occurs when the auditory tube does not cope with the drainage of a large amount of pathological separable with an acute purulent otitis media, and spontaneous perforation of the tympanic membrane is difficult. In mastoiditis, the block of cave entrance plays a decisive role. Chronic epithepanitis leads to a restriction of outflow from the upper floor of the tympanum to mesotimbanum. The spread of pus along the aqueducts of the cochlea and the vestibule into the cranial cavity with a purulent labyrinthitis also occurs on the ground of inflammation in the middle ear, associated with a disturbance in the outflow of the pathologic discharge or the formation of a cholesteatoma.

Extradural and subdural abscesses are often an accidental finding but the time of sanitizing operations in mastoiditis or chronic epitymitis.