Meningitis in Children - I.V. Bohadelnikov 2005

Primary purulent meningitis in children. General overview

Meningitis is a group of diseases caused by viral or bacterial pathogens, as well as Fungi and Protozoa, and is characterized by primary inflammation of the arachnoid and pia mater (the leptomeninges) of the Brain.

The urgency of this problem stems from the fact that, despite numerous studies on the Etiology, Pathogenesis, clinical manifestations, Diagnosis, and Treatment of Purulent meningitis, the mortality rate and the incidence of residual neurological sequelae among surviving children remain high.

Depending on The Nature of the meningeal inflammation and Changes in the CEREBROSPINAL FLUID (CSF), meningitis is classified into purulent (suppurative) and serous forms.

When meningitis occurs as an independent condition, it is referred to as primary meningitis. If it develops as a complication of a systemic or localized infectious process, it is classified as secondary.

The etiological spectrum of meningitis involves A wide variety of pathogens, including Bacteria, Viruses, fungi, and protozoa. Purulent meningitis is primarily caused by bacteria and fungi, whereas serous meningitis is usually caused by viruses and, less frequently, by bacteria (Mycobacterium tuberculosis, Brucella, Leptospira, Salmonella typhi, Treponema).

Bacteria represent the largest group of meningitis pathogens. Among Gram-negative microbes, meningitis is most commonly caused by meningococci and Haemophilus influenzae (Pfeiffer's bacillus), and less frequently by Escherichia coli, salmonellae, and other Enterobacteriaceae. Among Gram-positive bacteria, pneumococcus is the most frequent causative agent, while staphylococci, listeriae, spirochetes, and others are less common. Meningitis caused by fungi, protozoa, and helminths is relatively rare. Viral meningitis is most frequently caused by mumps virus, Coxsackie and ECHO viruses, polioviruses, tick-borne encephalitis virus, and lymphocytic choriomeningitis virus. The Classification of meningitis based on CSF changes and the etiological factor is presented in Table 1.

Table 1. Classification of meningitis According to the nature of cerebrospinal fluid changes and etiological factors

The most common primary purulent meningitides in children are of meningococcal and pneumococcal etiology. Haemophilus meningitis is less frequent. The only source of infection is a human—either a patient with a localized or generalized form of meningococcal infection or a meningococcal carrier, who poses a particular epidemiological hazard.

A significant role in The Development of the pathological process is played by the patient's baseline health status prior to the illness. This includes acute respiratory and bacterial infections, hypothermia, inadequate childcare, injuries, sudden climate changes, emotional stress, and physical overexertion. These factors presumably impair the body's immunological status, diminishing its defense mechanisms.

Despite the variety of etiological factors capable of causing meningitis and the different routes by which pathogens enter the Central Nervous system (CNS), the Clinical presentation of meningitis caused by various agents shares significant similarities, especially during the initial stages. This is due to the uniformity of early pathogenetic and morphological changes in the body during the development of purulent meningitis, which occur regardless of the underlying etiology.

The pathogenesis of purulent meningitis is driven by three key mechanisms: bacteremia, toxemia, and the host's physiological state. The primary port of entry in primary meningitis is the nasopharynx, respiratory tract, and occasionally the gastrointestinal tract. Pathogens spread throughout the body and reach the Meninges most frequently via the hematogenous route, while segmental-vascular and contact pathways are less common.

Bacteria circulating in the Blood partially break down, releasing endotoxins, which leads to toxemia and elevated levels of BIOLOGICALLY ACTIVE SUBSTANCES and Metabolic waste products. This increases the permeability of cellular and vascular membranes, including the blood-brain barrier (BBB), creating favorable conditions for bacteria and toxins to invade the CNS with preferential involvement of the pia mater. Despite the wide range of causative agents, the pathomorphological changes in purulent meningitis are similar. The pathological process is typically localized in the pia mater and arachnoid mater (leptomeningitis). The dura mater is rarely affected, usually showing only small purulent deposits and hemorrhages (pachymeningitis). To varying degrees, the pathological process also involves the Cranial Nerves, superficial brain structures, ependyma, and ventricular choroid plexuses. Exudate accumulates within the cerebral sulci. When present in large amounts, it infiltrates the meninges and collects at the Base of the brain or over the convex surface of the hemispheres, particularly in the frontal and parietal regions. The changes occurring in the CNS have been studied in greatest detail in Meningococcal meningitis:

Day 1: The meninges show minimal alteration; mild edema and hyperemia of the leptomeninges are observed, though they remain transparent. A significant amount of slightly turbid fluid accumulates in the subarachnoid space.

Day 2 (sometimes by the end of the first day): The entire subarachnoid space is filled with a fibrino-purulent exudate, and alterations are visible in the pia-arachnoid membranes and the brain tissue itself. They become turbid and covered with fibrino-purulent exudate. Pronounced changes occur on the hemispheric surfaces and the base of the brain, leading to cranial nerve involvement (optic, vestibulocochlear, and less commonly, facial nerves).

Day 3: With appropriate treatment, the fibrino-purulent exudate undergoes regression through the phagocytosis of fibrin and necrotic Cells by macrophages. Reparative processes take place over 2–4 weeks or longer (P.S. Gurevich, 1989).

If meningitis goes undiagnosed or is improperly treated, the pathological process progresses, leading to the Organization OF THE inflammatory exudate (by days 5–6) and The formation of a characteristic purulent "cap" covering both hemispheres. The organization of pus and the precipitation of fibrin strands result in adhesions between the Cerebral Cortex AND the meninges, forming so-called enclosed cysts. This obstructs the foramina of Magendie, blocks CSF dynamics, and creates conditions for increased intracranial pressure and the development of Hydrocephalus. In such cases, the pathological process may extend into the brain parenchyma, causing cerebral vascular thrombosis and hemorrhages, which further impairs neurological function.

Based on their clinical course, purulent meningitides are classified as acute or subacute.

Primary purulent meningitis and many secondary forms have an acute onset, characterized by a sharp spike in body Temperature, severe chills, and a rapid surge in general intoxication symptoms. Early signs of purulent meningitis include intense headache, dizziness, recurrent vomiting, and generalized hyperesthesia. Quite frequently, generalized seizures and impaired consciousness, progressing even to coma, develop within the first hours of the illness. Initial excitation is soon replaced by lethargy or loss of consciousness. General cerebral symptoms predominate at first, which may later be followed by various focal neurological deficits. If the focal symptoms are solely due to transient circulatory disturbances or cerebral edema, they regress early and rapidly. However, if meningoencephalitis develops, the resulting focal symptoms are more pronounced, regress slowly, and often persist for life.

Purulent meningitis can sometimes cause cranial nerve palsies, most frequently involving cranial nerves III, IV, VI, VII, and VIII. The inflammatory process manifests as toxic or infiltrative neuritis, followed by rapid or slow functional recovery.

Muscle tone in purulent meningitis is typically decreased, tendon Reflexes are hyperactive, and anisoreflexia may be present. In cases of severe intoxication, tendon reflexes are usually absent, which is attributed to the toxic effect on the reflex arc. FOOT clonus and pathological Babinski and Rossolimo reflexes are frequently observed. Changes in Internal Organs and other body systems may occasionally occur, such as hepatosplenomegaly, intestinal disorders, and myocardial damage.

The diagnosis of purulent meningitis is established based on epidemiological history, acute onset, the presence of infectious-toxic and meningeal syndromes, CSF abnormalities, peripheral blood findings, and bacteriological test results.