Complications of meningitis

Inflammation of the soft membranes of the brain, especially in severe form, is fraught with long-term consequences and life-threatening, and many complications of meningitis are irreversible and lead to disability. [1]

Epidemiology

According to WHO research-based data, the majority of patients (70%) with bacterial meningitis have hydrocephalus, and the resulting serious disorders occur in almost 90% of patients.

It is also noted that the development of neurologic complications is more common in meningitis of bacterial etiology. When the brain membranes are affected by Streptococcus pneumonia bacteria and pneumococcal meningitis develops, the mortality rate reaches 20%, and complications such as brain damage, paralysis, learning disabilities are noted in 25-50% of surviving patients.

Hearing loss is a complication of pneumococcal meningitis in 14-32% of children. This complication occurs on average in 13.5% of patients with meningococcal inflammation of the cerebral membranes and in 20% of cases of meningitis caused by Haemophilus influenzae.

Causes of the complications of meningitis

Infectious disease specialists and neurologists link the causes of complications meningitis with dysfunctions of cells (including neurons) damaged by circulating toxins and antibodies of meningococci (Neisseria meningitidis), pneumococci (Streptococcus pneumoniae), Streptococcus agalactiae group B, Listeria monocytogenes, Haemophilus influenzae, Escherichia coli, enteroviruses of the Picornaviridae family, Coxsackie and ECHO viruses, Paramyxoviridae, Herpes simplex, Varicella zoster. [2]

Overcoming the blood-brain barrier, they can penetrate not only into the brain membranes and subarachnoid space, but also into its parenchyma.

In addition, a more aggressive response of immune cells of microglia and dura mater plays a role in neuronal alteration - during the invasion of infection and the inflammatory process it induces: antibodies (IgG and IgM) produced to destroy bacteria or viruses can enhance the humoral intrathecal (subglial) immune response, leading to cellular damage and the development of various neuropsychiatric sequelae. [3]

Risk factors

Key risk factors for developing serious complications of meningitis are noted such as:

• Older age and childhood (especially the first year of life);
• immunodeficiency conditions;
• A severe form of meningitis, particularly purulent meningitis;
• a transient clinical course of the disease;
• prolonged prodromal period of the inflammatory process;
• impaired consciousness at the first manifestations of the disease;
• late detection of the disease due to delay in seeking medical attention;
• untimely or inadequate treatment of febrile-intoxication syndrome and meningitis proper - with delayed start of antibiotic therapy.

Pathogenesis

The mechanism of cerebral structures and central nervous system damage, that is, the pathogenesis of the development of complications in inflammation of the soft membranes of the brain of bacterial and viral origin, is discussed in publications:

• Acute bacterial meningitis
• Tuberculosis of the cerebral membranes (tuberculous meningitis)
• Viral meningitis
• Enterovirus meningitis.
• Serous meningitis
• Purulent meningitis

For example, the mechanism of cerebrospinal fluid (liquor) accumulation in the brain ventricles (cerebral hydrocephalus or hydrocephalus) in bacterial (including tuberculous) meningitis is explained by the fact, that the outflow of liquor after its exit from the fourth cerebral ventricle is obstructed by the exudate blockage of the arachnoid (spider) villi in the medial and lateral foramen (Mazhandi's and Luschka's foramen) of the subarachnoid space.

And hydrocephalus, swelling and focal purulent infiltrates of brain tissue lead to their necrosis and cause headaches, vision and memory problems, seizures, coordination disorders, etc.

Symptoms of the complications of meningitis

In complications of meningitis, symptoms appear based on the nature, localization and extent of damage to the cells of the brain membranes and substance - after the acute inflammation and symptoms of meningeal syndrome have disappeared. Although the first signs that the disease will cause complications and long-term consequences may appear during the acute phase. These include heaviness in the head and poorly controlled cephalgia, as well as increased intracranial pressure (intracranial hypertension), which is manifested by nausea and vomiting, bouts of sweating, generalized weakness, diplopia (double vision), blurred consciousness, and can lead to brain herniation. [4]

One of the clinical manifestations of bacterial meningitis is seizures, and when they occur within the first three days and are difficult to suppress, it is likely that the patient will not be able to avoid persistent neurologic complications.

In addition to hydrocephalus, numerous systemic and neurologic complications of bacterial meningitis, including complications of meningococcal meningitis and pneumococcal meningitis, may manifest as:

• cerebral edema; [5]
• movement coordination and balance disorders - vestibulo-ataxic syndrome; [6]
• seizures and convulsions epilepsy; [7]
• partial or complete sensorineural hearing loss, associated with paralysis of the VIII pair of cranial nerves (n. Vestibulocochlearis); [8]
• deterioration or loss of vision due to inflammation of the optic nerve (II pair of cranial nerves - n. Opticus); [9]
• speech disorders - bulbar dysarthria; [10]
• memory and concentration problems indicative of cognitive impairment; [11]
• formation of an effusion between the spider web and dura mater - subdural empyema, [12] which can lead to brain abscess, [13] and in fungal cryptococcal meningitis - cryptococcoma; [14]
• spread of inflammation to brain tissue, leading to meningoencephalitis, which often causes irreversible cerebral damage;
• meningeal cerebral coma.

There are such complications of tuberculous meningitis as basal adhesive or opticochiasmal arachnoiditis with seizures and visual impairment due to damage to the optic nerve and its sheaths; formation of tumor-like granulomatous formation in the brain - meningeal tuberculoma; arteritis (inflammation of the walls) of small or large vessels. [15] As medics explain, extensive vascular complications in patients with mycobacterium tuberculosis meninges lesions arise due to brain infarction (a type of ischemic stroke) in the area of the middle cerebral and basilar arteries, brain stem and cerebellum. Their effects are manifested by neurological impairments that may diminish over time.

Although the development of cerebral hypertension is less common in viral cerebral inflammation than in bacterial infection, complications of viral meningitis in the form of hydrocephalus and cerebral edema can occur during the acute phase of the disease. But as the condition improves, the risks of long-term consequences decrease, but they still develop. And these are meningoencephalitis, stem encephalitis, inflammation of the myocardium (heart muscle), flaccid paralysis and muscle weakness, seizure headaches, sleep and memory disorders, mild cognitive impairment.

Complications and consequences

Major complications of purulent meningitis [16], [17] include:

• hydrocephalus and cerebral edema;
• lesion of cranial nerves with partial paralysis (paresis) of the limbs, speech disorder, decreased perception of visual signals;
• development of inflammation of the walls of the ventricles of the brain - ventriculitis; [18]
• cerebral thrombosis and cerebral infarction;
• empyemas and abscesses of the brain;
• cerebral atrophy;
• septicemia and sepsis with rapid development of septic shock and DIC in children (disseminated intravascular coagulation).

In addition to increased intracranial pressure and the development of hydrocephalus and seizure syndromes, complications of serous meningitis include optic neuritis.

When characterizing complications of meningitis in children, practitioners and researchers note that in newborns it leads to severe consequences in about 20-50% of cases. The most frequent complications are cerebral hydrocele, hearing and vision loss, prolonged convulsions, epilepsy, inhibition of psychomotor development, and dysfunction of brain structures.

In older children against the background of cerebral edema and hydracephaly (which may develop at the beginning of the disease or a few weeks after the diagnosis of bacterial meningitis) may be disorders of the speech apparatus - due to damage to cranial nerves and focal neurological deficits; hemiparesis, mental changes and cognitive decline. [19]

Diagnostics of the complications of meningitis

In the diagnosis of complications of meningitis involve doctors of various specializations, but it is obligatory to conduct study of the neuropsychiatric sphere of each patient. [20]

Basic tests include blood tests - general, biochemical, for antibody levels; analysis of cerebrospinal fluid.

Computerized and/or magnetic resonance imaging (MRI) of the brain is used for instrumental diagnosis of complications of meningitis of any etiology. Also used are ultrasound echoencephalography and electroencephalography; in case of hearing problems, tympanometry and electrocochleography are used, etc.

Differential diagnosis

A differential diagnosis may be required, particularly to identify other pathogenetic factors for the presenting symptomatology, such as cerebral tumors.

Treatment of the complications of meningitis

Despite the high mortality rate, adequate management of systemic and neurologic complications and aggressive antimicrobial therapy in the treatment of meningitis are essential to improve therapeutic outcomes.

Thus, in the treatment of cerebral edema it is necessary: monitoring of respiratory function and level of intracranial pressure, controlled hyperventilation of the lungs, administration of solution

Osmotic diuretic (Mannitol) and intravenous corticosteroid injections. Extensive cerebral edema can also be treated surgically by draining the cerebral ventricles (decompressive skull trepanning).

Treatment of mild hydrocephalus may include drug therapy with diuretics and steroids, but in its obstructive form, cerebrospinal fluid drainage is used, which may be performed by temporary or permanent placement of a ventricular (ventriculo-peritoneal) shunt or by endoscopic ventriculostomy of the third cerebral ventricle.

If the brain abscess cavity is surgically accessible, its drainage is also performed.

In persistent seizures, anticonvulsants - antiepileptic drugs (Carbamazepine, Phenytoin, Gabapentin, etc.) are used.

Speech disorders are dealt with by speech therapists, in addition, for the treatment of bulbar dysarthria use nootropics - drugs related to neurometabolic stimulants: Piracetam, Ceriton, Finlepsin and others.

Cochlear implants inserted into the ears are used to improve hearing. [21]

Prevention

To prevent neurological complications of bacterial meningitis, the most effective is primary infection prevention: epidemic surveillance and vaccination of children against meningococci of serogroups A and C, Haemophilus influenzae, pneumococcal vaccination, meningococcal vaccination.

Forecast

It is difficult to predict the outcome of systemic and neurologic complications of meningitis of any etiology, given the rather high mortality rate of this disease - up to 30%.