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Complications after meningitis
Last reviewed: 01.04.2022
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Inflammation of the soft membranes of the brain, especially in severe form, is fraught with long-term consequences and is life-threatening, and many complications of meningitis are irreversible and lead to disability.[1]
Epidemiology
According to the WHO, based on studies, the majority of patients (70%) with bacterial meningitis have hydrocephalus, and serious disorders caused by it occur in almost 90% of patients.
It is also noted that the development of neurological complications often occurs with meningitis of bacterial etiology. When the meninges are affected by Streptococcus pneumonia bacteria and the development of pneumococcal meningitis, mortality reaches 20%, and complications such as brain damage, paralysis, and learning disabilities are observed in 25-50% of surviving patients.
In children after pneumococcal meningitis, hearing loss is a complication in 14-32% of cases. This complication is noted, on average, in 13.5% of patients with meningococcal inflammation of the meninges and in 20% of cases of meningitis caused by Haemophilus influenzae.
Causes of the complications of meningitis
Infectionists and neurologists associate the causes of the development of complications of meningitis with dysfunctions of cells (including neurons) when they are damaged by toxins and antibodies circulating in the blood of meningococci (Neisseria meningitidis), pneumococci (Streptococcus pneumoniae), streptococci Streptococcus agalactiae group B, listeria (Listeria monocytogenes ), Haemophilus influenzae, E. Coli (Escherichia coli), Picornaviridae family enteroviruses, Coxsackie and ECHO viruses, Paramyxoviridae, Herpes simplex, Varicella zoster.[2]
Overcoming the blood-brain barrier, they can penetrate not only into the membranes of the brain and the subarachnoid space, but also into its parenchyma.
In addition, in the alteration of neurons - during the invasion of infection and the inflammatory process induced by it - a more aggressive reaction of immune cells of microglia and dura mater plays a certain role: antibodies (IgG and IgM) produced to destroy bacteria or viruses can enhance humoral intrathecal (subthecal) immune response, leading to cell damage and the development of various neuropsychiatric consequences.[3]
Risk factors
There are such key risk factors for the development of serious complications of meningitis as:
- elderly and children's age (especially the first year of life);
- immunodeficiency states;
- severe form of meningitis, in particular, purulent;
- transient clinical course of the disease;
- long prodromal period of the inflammatory process;
- impaired consciousness at the first manifestations of the disease;
- late detection of the disease due to delays in seeking medical help;
- untimely or inadequate treatment of febrile-intoxication syndrome and meningitis itself - with a delayed start of antibiotic therapy.
Pathogenesis
The mechanism of damage to cerebral structures and the central nervous system, that is, the pathogenesis of the development of complications in inflammation of the soft membranes of the brain of bacterial and viral origin, is considered in publications:
- Acute bacterial meningitis
- Tuberculosis of the meninges (tuberculous meningitis)
- Viral meningitis
- Enteroviral meningitis
- Serous meningitis
- Purulent meningitis
For example, the mechanism of accumulation of cerebrospinal fluid (CSF) in the ventricles of the brain (hydrocephalus or dropsy of the brain) in bacterial - including tuberculous - meningitis is explained by the fact that the outflow of cerebrospinal fluid after it leaves the fourth cerebral ventricle is prevented by blockage of exudate of the villi of the arachnoid (arachnoid) membranes of the brain in the median and lateral foramens (foramina of Magendie and Luschka) of the subarachnoid space.
And hydrocephalus, swelling and focal purulent infiltrates of brain tissues lead to their necrosis and cause headaches, problems with vision and memory, convulsions, impaired coordination, etc.
Symptoms of the complications of meningitis
With complications of meningitis, symptoms appear due to the nature, localization and degree of damage to the cells of the membranes and the substance of the brain - after the disappearance of acute inflammation and symptoms of meningeal syndrome . Although the first signs that the disease will cause complications and long-term consequences may appear during the acute phase. This is 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, general weakness, diplopia (double vision), clouding of consciousness and can lead to the formation of cerebral hernia.[4]
Seizures are one of the clinical manifestations of bacterial meningitis, and when they occur within the first three days and are difficult to suppress, the patient is likely to fail to avoid persistent neurological complications.
In addition to hydrocephalus, numerous systemic and neurological complications of bacterial meningitis, including complications of meningococcal and pneumococcal meningitis, can manifest as:
- cerebral edema ;[5]
- impaired coordination of movements and balance - vestibulo-ataxic syndrome ;[6]
- convulsions and seizures of epilepsy ;[7]
- partial or complete neurosensory (sensoneural) hearing lossassociated 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]
- problems with memory and concentration, indicating cognitive impairment;[11]
- the formation of an effusion between the arachnoid and dura mater - subdural empyema , [12], which can lead to a brain abscess , [13]and, in fungal cryptococcal meningitis , to cryptococcus;[14]
- the 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 optic- chiasmatic arachnoiditis with convulsions and visual impairment due to damage to the optic nerve and its membranes; the formation in the brain of a tumor-like granulomatous formation - meningeal tuberculoma; arteritis (inflammation of the walls) of small or large vessels. [15]As doctors explain, extensive vascular complications in patients with meningeal lesions caused by Mycobacterium tuberculosis occur as a result of cerebral infarction (such as ischemic stroke) in the region of the middle cerebral and basilar arteries, brain stem and cerebellum. Their consequences are manifested by neurological disorders, which may decrease over time.
Although the development of cerebral hypertension in inflammation of the meninges of viral origin is less common than in bacterial infection, complications of viral meningitis in the form of hydrocephalus and cerebral edema may 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, paroxysmal headaches, sleep and memory disorders, mild cognitive impairment.
Complications and consequences
The main complications of purulent meningitis [16], [17]include:
- hydrocephalus and cerebral edema;
- damage to the 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]
- thrombosis of cerebral vessels and cerebral infarction;[19]
- empyema and abscesses of the brain;
- cerebral atrophy;
- septicemia and sepsis with the rapid development of septic shock and DIC in children (disseminated intravascular coagulation).
In addition to increased intracranial pressure, the development of hydrocephalic and convulsive syndromes, complications of serous meningitis include optic neuritis.
Describing the 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 common complications are dropsy of the brain, loss of hearing and vision, prolonged convulsions, epilepsy, inhibition of psychomotor development, and dysfunction of brain structures .
In older children, against the background of cerebral edema and hydracephaly (which can develop at the onset of the disease or a few weeks after the diagnosis of bacterial meningitis), speech apparatus dysfunctions are possible due to damage to the cranial nerves and focal neurological deficit; hemiparesis, mental changes and cognitive decline.[20]
Diagnostics of the complications of meningitis
Doctors of various specializations take part in the diagnosis of complications of meningitis, but a study of the neuropsychic sphere of each patient is mandatory.[21]
The main tests include a blood test - general, biochemical, for the level of antibodies; cerebrospinal fluid analysis .
With the help of computed and / or magnetic resonance imaging (MRI) of the brain , instrumental diagnostics of complications of meningitis of any etiology is carried out. Ultrasound echoencephalography and electroencephalography are also applied ; with hearing problems, they resort to tympanometry and electrocochleography , etc.[22]
Differential diagnosis
Differential diagnosis may be required, in particular, to identify other pathogenetic factors of existing symptoms, for example, cerebral tumors.
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Treatment of the complications of meningitis
Despite the high mortality rate, adequate management of systemic and neurological complications and aggressive antimicrobial therapy in the treatment of meningitis are essential to improve therapeutic outcomes.
So, in the treatment of cerebral edema, it is necessary: monitoring of respiratory function and the level of intracranial pressure, controlled hyperventilation of the lungs, the introduction of a solution
Osmotic diuretic (Mannitol) and intravenous injections of corticosteroids. Extensive cerebral edema can also be treated surgically by draining the cerebral ventricles (decompressive craniotomy).
Treatment of mild hydrocephalus may include medical therapy with diuretics and steroids, but in its obstructive form resort to CSF drainage, which can be performed by temporary or permanent placement of a ventricular (ventriculo-peritoneal) shunt or using endoscopic ventriculostomy of the third cerebral ventricle.
If the cavity of the brain abscess is surgically accessible, then its drainage is also performed.
With persistent convulsions, anticonvulsants are used - antiepileptic drugs (Carbamazepine, Phenytoin, Gabapentin, etc.).
Speech therapists deal with speech disorders, in addition, nootropics are used to treat bulbar dysarthria - drugs related to neurometabolic stimulants: Piracetam, Ceriton, Finlepsin, etc.
Cochlear implants are used to improve hearing.[23]
Prevention
To prevent neurological complications of bacterial meningitis, the most effective is the primary prevention of infections: epidemic surveillance and vaccination of children against meningococcus serogroups A and C, Haemophilus influenzae, vaccination against pneumococcal infection , vaccination against meningococcal infection .
Forecast
It is difficult to predict the outcome of systemic and neurological complications of meningitis of any etiology, given the rather high mortality rate of this disease - up to 30%.