Brain and spinal cord abscesses - Causes and pathogenesis

Causes of Brain and Spinal Cord Abscesses

It is not always possible to isolate the infectious agent from the contents of a brain abscess. In approximately 25% of cases, abscess contents cultures are sterile. Among the isolated pathogens of hematogenous abscesses, streptococci (aerobic and anaerobic) predominate, often in association with bacteroides (Bacteroides spp.). In hematogenous abscesses due to lung abscess, Enterobacteriaceae (in particular, Proteus vulgaris) are often encountered. The same pathogens are characteristic of otogenic abscesses.

In penetrating craniocerebral trauma, staphylococci (primarily St. aureus) predominate in the pathogenesis of brain abscesses. Pathogens of the genus Enterobacteriaceae are also found.

In patients with various immunodeficiency states (taking immunosuppressants after organ transplantation, HIV infection), Aspergillus fumigatus predominates among pathogens.

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Pathogenesis of brain and spinal cord abscesses

The main routes of infection penetration into the cranial cavity and spinal canal are the following:

• hematogenous;
• open penetrating craniocerebral trauma or spinal trauma;
• purulent-inflammatory processes in the paranasal sinuses;
• wound infection after neurosurgical interventions.

The conditions for the formation of an abscess when an infection penetrates are the nature of the pathogen (virulence of the pathogen) and a decrease in the patient's immunity. In developed countries, hematogenous abscesses are most typical. In developing countries, brain abscesses most often form against the background of chronic inflammatory processes in adjacent tissues, which is associated with inadequate treatment of the latter. In approximately 25% of cases, it is not possible to establish the source that led to the formation of a brain abscess.

In hematogenous abscesses, the source of bacterial emboli is most often inflammatory processes in the lungs (lung abscess, bronchiectasis, pleural empyema, chronic pneumonia). A bacterial embolus is a fragment of an infected thrombus from a vessel on the periphery of the inflammatory focus. The thrombus enters the systemic circulation and is carried by the blood flow to the vessels of the brain, where it is fixed in small-diameter vessels (arteriole, precapillary or capillary). Acute bacterial endocarditis, chronic bacterial endocarditis, sepsis and gastrointestinal infections are of lesser importance in the pathogenesis of abscesses.

The cause of brain abscess in children is often "blue" heart defects, primarily tetralogy of Fallot, as well as pulmonary arteriovenous shunts (50% of them are associated with Rendu-Osler syndrome - multiple hereditary telangiectasias). The risk of developing a brain abscess in such patients is about 6%.

In purulent-inflammatory processes in the paranasal sinuses, middle and inner ear, the infection can spread either retrogradely through the sinuses of the dura mater and cerebral veins, or with direct penetration of the infection through the dura mater (in this case, a limited focus of inflammation is first formed in the meninges and then in the adjacent part of the brain). Odontogenic abscesses are less common.

In penetrating and open craniocerebral trauma, brain abscesses may develop as a result of direct infection into the cranial cavity. In peacetime, the proportion of such abscesses does not exceed 15%. In combat conditions, it increases significantly (gunshot and mine-explosive wounds).

Brain abscesses can also form against the background of intracranial infectious complications after neurosurgical interventions (meningitis, ventriculitis). As a rule, they occur in severe, weakened patients.

Pathomorphology

The formation of a brain abscess goes through several stages. Initially, a limited inflammation of the brain tissue develops - encephalitis ("early cerebritis", in modern English terminology). The duration of this stage is up to 3 days. At this stage, the inflammatory process is reversible and can resolve either spontaneously or against the background of antibacterial therapy. If the protective mechanisms are insufficient and in case of inadequate treatment, the inflammatory process progresses, and by the 4th-9th day, a cavity filled with pus appears in its center, capable of increasing. By the 10th-13th day, a protective connective tissue capsule begins to form around the purulent focus, preventing further spread of the purulent process. By the beginning of the 3rd week, the capsule becomes denser, a gliosis zone forms around it. The further course of a brain abscess is determined by the virulence of the flora, the reactivity of the body and the adequacy of treatment and diagnostic measures. Sometimes the abscess undergoes reverse development, but more often there is either an increase in its internal volume or the formation of new inflammatory foci along the periphery of the capsule.

Brain abscesses can be single or multiple.

Abscesses in the subdural or epidural space are less common than intracerebral abscesses. Such abscesses are usually caused by local spread of infection from adjacent purulent foci in the paranasal sinuses, and also occur with open craniocerebral trauma, osteomyelitis of the skull bones. As with intracerebral abscesses, a dense connective tissue capsule can form with subdural and epidural abscesses. If this does not happen, diffuse purulent inflammation develops in the corresponding space. This process, as in general surgery, is called subdural or epidural empyema.