Otogenic intracranial complications and otogenic sepsis

Otogenic intracranial complications are complications that arise as a result of infection penetrating into the cranial cavity during purulent inflammation of the middle and inner ear.

Diseases of the middle and inner ear causing intracranial complications: acute purulent otitis media, mastoiditis, chronic purulent meso- and epitympanitis, purulent labyrinthitis. If they progress unfavorably, limited purulent processes may develop in adjacent anatomical areas (abscesses), diffuse inflammation of the meninges (meningitis) and brain matter (encephalitis), as well as sepsis.

Common features of otogenic intracranial complications:

• similar complications arise in purulent diseases of both the middle and inner ear;
• the peculiarities of the anatomical structure of the temporal bone and various parts of the ear determine the relationship between inflammatory processes in the middle and inner ear;
• all complications pose a danger to the patient's life;
• The processes have similar development patterns:
• The causes of occurrence and features 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 1920s, patients with otogenic intracranial complications accounted for more than 20% of the total number of patients who underwent ear surgery.

Meningitis is the most common intracranial otogenic complication, followed by abscesses of the temporal lobe of the brain and cerebellum, and sinus thrombosis. Sepsis develops less frequently. The most common complication in childhood is diffuse meningoencephalitis.

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

Despite the availability of new antimicrobial drugs, mortality from purulent meningitis remains high and amounts to 25% among adult patients. Mortality rates are especially high in patients with meningitis caused by gram-negative flora and Staphylococcus aureus.

Prevention of otogenic intracranial complications and otogenic sepsis

Prevention of otogenic intracranial complications also includes timely diagnostics of acute and chronic ear diseases. Effective measures for preventing otogenic complications include: performing paracentesis of the eardrum in acute purulent otitis media, as well as dispensary observation of patients with chronic purulent otitis media and preventive ear sanitation.

Screening

Traditional diagnostic methods (anamnesis, laboratory tests, specialist consultations) in combination with the latest modern research methods (echoencephalography, angiography, CT and MRI) allow timely detection of otogenic 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;
• sinusorrhombosis;
• otogenic sepsis.

Sometimes one form of complications turns into another, in some cases there may be a combination of several forms at the same time. All this creates difficulties in the diagnosis and treatment of the above complications.

Causes of otogenic intracranial complications and otogenic sepsis

Microflora isolated from the primary source of infection is mostly mixed and variable. Most often, coccal flora predominates: staphylococci, streptococci, less often pneumococci and diplococci, even less often proteus and pseudomonas aeruginosa. The occurrence of complications and the variant of development of the inflammatory reaction depend on the virulence of the pathogen.

Pathogenesis of otogenic intracranial complications and otogenic sepsis

The pathogenesis of otogenic intracranial complications is complex. In addition to the virulence of the microflora, the state of the general resistance of the body 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 more difficult it is for the body to resist its spread. On the other hand, rapid progression of inflammation can be a consequence of the incomplete formation of immunological reactions in childhood, as well as the pronounced reactivity of the child's body. Sluggish inflammatory reactions can be observed in elderly people as a result of a decrease in both general resistance and reactivity of the body. Resistance and reactivity of the body are determined genetically, but they can change due to overwork, hypovitaminosis, alimentary dystrophy, systemic diseases, intoxications, endocrine disorders and allergic reactions.

The spread of infection into the subarachnoid space and into the brain is now recognized as the main and most significant path of development of intracranial otogenic complications. An important obstacle on this path are the natural protective barriers of the human body. In the CNS, this protection is represented by: 1) anatomical and 2) immunological barriers.

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

The development of otogenic 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 (abundance of folds and pockets of the mucous membrane of the attic and the cellular structure of the mastoid process, the ventilation and drainage of which are significantly hampered by inflammation):
• remnants of myxoid tissue in the tympanic cavity of newborns;
• persistence in the walls of the tympanic cavity;
• unhealed petrosquamous fissure (fissura petrosqumosa) in young children;
• bone canals of vascular-nerve anastomoses;
• labyrinth windows;
• aqueducts of the vestibule and cochlea.

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

The blood-brain barrier separates the cerebrospinal fluid and brain from the 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 the blood-brain barrier and the blood-cerebrospinal fluid barrier. Anatomically, the main components of these barriers are the endothelium of the cerebral capillaries, the epithelium of the choroid plexus, and the arachnoid membrane. Compared to other capillaries, the endothelium of the cerebral capillaries has tight junctions between cells, which prevent intercellular transport. Additionally, cerebral capillaries have a low density of pinocytic vesicles, an abundant number of mitochondria, and unique enzymes and transport systems.

Against the background of the inflammatory process, the permeability of the blood-brain barrier increases due to the rupture of tight junctions between endothelial cells and an increase in the number of pinocytic vesicles. As a result, it is easier for microbes to overcome the blood-brain barrier. It should be noted that most antibiotics poorly penetrate the blood-brain barrier, but during the inflammatory process, their content in the cerebrospinal fluid increases significantly.

The body resists the spread of infection, so purulent foci can be limited and located in close proximity to the brain or cerebellum at a depth of 2-4 cm. The described process of infection spread is called "continuation" (percontinuctatum).

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

Tabular defects in the human immune system may predispose to dissemination of infection to the CNS. These defects include hypogammaglobulinemia, asplenia, leukopenia, complement deficiency, acquired immunodeficiency syndrome, and other T-cell defects. Patients with Ig and complement defects are at risk for infections caused by encapsulated microorganisms (Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae). Patients with neutropenia are at risk for 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).

With generalization of the process due to decreased resistance and altered reactivity of the body, more formidable otogenic intracranial complications may develop: purulent meningitis, meningoencephalitis or sepsis. A septic condition in acute purulent otitis in children develops when bacteria and their toxins enter the blood from the tympanic cavity. Contributing factors: hyperreactivity and weakness of the protective immunological reactions of the child's body, as well as difficulty in the outflow of pus from the tympanic cavity. The septic reaction develops rapidly, but it is relatively easily reversible. This form of sepsis is characterized mainly by septicemia and toxemia. In chronic otitis, generalization of the infection most often develops after thrombophlebitis of the sigmoid sinus (less often the bulb of the jugular vein, transverse, superior and inferior petrosal sinuses are affected). The stages of this process are periphlebitis, endophlebitis, parietal thrombosis, complete thrombosis, infection and thrombus disintegration, septicemia and septicopyemia. However, sinus thrombosis does not always lead to sepsis. Even in case of infection, thrombus organization is possible.

Each purulent ear disease is characterized by its own route of infection, which may consist of one or several mechanisms (contact, hematogenous, lymphogenous, lympholabyrinthogenic).

In acute purulent otitis media, the most common route of infection spread into the cranial cavity is through the roof of the tympanic cavity (mainly hematogenously). The second route is into the labyrinth through the cochlear window and the annular ligament of the vestibular window. Hematogenous spread of infection into the pericarotid plexus and from there into the cavernous sinus is possible, as well as through the lower wall of the tympanic cavity into the bulb of the jugular vein.

In mastoiditis, pus, melting the bone, can break through the mastoid process (planum mastoideum) into the parotid region, through the apex of the mastoid process under the neck muscles and through the anterior wall of the mastoid process into the external auditory canal. In addition, the process can spread into the cranial cavity to the membranes of the brain, sigmoid sinus and cerebellum, and through the roof of the antrum - to the temporal lobe of the brain.

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

In purulent diffuse labyrinthitis, the infection spreads through the vestibular aqueduct into the subarachnoid space of the cerebellopontine pons, into the endolymphatic sac, onto the posterior surface of the pyramid of the temporal bone to the meninges and cerebellum, and also along the perineural pathways into the internal auditory canal and from there to the meninges and brain matter in the region of the cerebellopontine angle.

Sometimes combined complications occur. These are most often sinus thrombosis and cerebellar abscess, as well as meningitis and brain abscess. In this case, it is appropriate to talk about the stages of infection spreading into the cranial cavity.

The spread of infection beyond the structures of the middle and inner ear occurs mainly due to the difficulty of drainage of purulent discharge from the tympanic cavity and mastoid cells into the external auditory canal. This occurs when the auditory tube cannot cope with the drainage of a large amount of pathological discharge in acute purulent otitis media, and spontaneous perforation of the eardrum is difficult. In mastoiditis, the block of the entrance to the cave plays a decisive role. Chronic epitympanitis leads to a limitation of the outflow from the upper floor of the tympanic cavity to the mesotympanum. The spread of pus through the aqueducts of the cochlea and vestibule into the cranial cavity in purulent labyrinthitis also occurs due to inflammation in the middle ear associated with a violation of the outflow of pathological discharge or the formation of cholesteatoma.

Extradural and subdural abscesses are often an incidental finding during sanitizing operations for mastoiditis or chronic epitympanitis.