tuberculous meningitis in children
Introduction
Introduction to tuberculous meningitis in children Tuberculous meningitis is caused by tuberculosis invading the meninges and inflammation caused by brain parenchyma. It is the most serious type of tuberculosis. It is more common in children under 5 years of age. The main source of infection is from adults with open tuberculosis. The respiratory tract is predominant, often occurring within 6 months to 1 year after initial infection with tuberculosis. Early symptoms are not typical, can be expressed as poor appetite, gradual weight loss, sweating after sleep, long-term irregular low fever, diagnosis and treatment is not timely, the condition gradually worsened to high fever convulsions, coma, and even death. If the disease is not treated with anti-tuberculosis drugs, the mortality rate is 100%. Since the general vaccination of BCG and the application of anti-tuberculosis drugs, the incidence and mortality of tuberculous meningitis have decreased significantly. However, the diagnosis is not timely and the treatment is not correct, and the mortality and sequelae are still high. Therefore, active prevention, early diagnosis, and early treatment are the key to reducing morbidity and mortality. basic knowledge The proportion of illness: 0.002% Susceptible people: young children Mode of infection: non-infectious Complications: hydrocephalus cerebral hemorrhage epilepsy
Cause
Causes of tuberculous meningitis in children
(1) Causes of the disease
Mycobacterium tuberculosis invades the lymphatic system and enters the local lymph nodes. The bacteremia is spread through the bloodstream into the meninges and brain parenchyma, including the subependymal and other parts, and is replicated here. When the host immune function is reduced or due to age, the tuberculosis within the lesion The bacteria activate and break into the subarachnoid space and spread with the cerebrospinal fluid, which can cause tuberculous meningitis for several days to several weeks.
Tuberculous meningitis is mostly part of systemic miliary tuberculosis. It spreads through blood. In 1180 cases of brains seen in Beijing Children's Hospital from 1964 to 1977, 44.2% of miliary tuberculosis were diagnosed. In these 14 years, From the pathological anatomy of 152 cases of brain, it was found that there were 143 cases (94%) of other organs and tuberculosis in the whole body; 142 cases (93.4%) with tuberculosis (including miliary tuberculosis in the first place); 62%, 41% of renal miliary tuberculosis, and 24% of intestinal and mesenteric lymphatic tuberculosis.
(two) pathogenesis
Tuberculosis affects the meninges mainly through the blood-cerebrospinal fluid pathway. The occurrence of brain formation is related to the high degree of hypersensitivity of the body. In addition, the brain can also be caused by the destruction of brain parenchyma or meninges, occasionally the spine, skull or middle ear The mastoid tuberculosis directly spreads to invade the meninges.
Pathogenesis
Mycobacterium tuberculosis is an aerobic bacterium. The bacterium wall is rich in a variety of lipids. Tuberculosis enters the lungs through the respiratory tract, forming a small area of infection. It does not cause an immune or inflammatory reaction because it does not secrete enzymes or toxins. The host also has no symptoms. After a few weeks, the bacillus invades the lymphatic system and enters the local lymph nodes. The bacteremia is spread through the blood into the meninges and the brain parenchyma including the subependyum and other parts, and is replicated here.
When the host immune response is caused, the T lymphocytes are sensitized, the macrophages are activated and moved to the infected foci, and the macrophages can engulf the bacilli and fuse together to form multinucleated giant cells (Langer hans giant cells), at which time most of the bacilli are This immune response is killed, a small amount can still be left in macrophages, this granulomatous lesion is surrounded by incomplete cyst wall tissue, its small size can exist in the meninges or brain parenchyma for many years or life. .
When the host immune function is reduced or due to old age, the tuberculosis in the lesion activates and breaks into the subarachnoid space, which spreads with the cerebrospinal fluid, which can cause tuberculous meningitis for several days to several weeks, and the inflammatory reaction can increase rapidly. However, the degree is related to the hypersensitivity reaction caused by the antigenic material of the bacterial wall. A large amount of exudate produced by the inflammatory process is deposited in the brain pool, which may cause arachnoiditis with the progress of time. Into the exudate, the meninges gradually proliferate and thicken, when the absorption of the meninges on the cerebrospinal fluid can cause traffic hydrocephalus, if the blockage of the fourth ventricle median and lateral holes can cause obstructive hydrocephalus.
2. Pathological changes
The brain is swollen, the pia mater is diffusely turbid, and the gray-yellow serum fibrinous exudate is scattered all over it. The bottom of the brain is the bridge pool, the chiasm and the frontal lobe are most prominent, and the inflammatory exudate invades the cerebral nerve sheath. The nerve fibers are wound and squeezed, and the diffuse inflammatory cell infiltration of the soft meninges can be seen under the microscope. The mononuclear cells and lymphocytes are mainly composed of a small number of macrophages and plasma cells. The pia mater can be found in the miliary tuberculous nodules. It consists of several multinucleated giant cells, a large number of mononuclear cells and fibroblasts, and a small amount of plasma cells. The latter is more common in the late stage. In addition, there are often caseous necrotic substances in the nodules, parenchymal edema of the brain, and sometimes tuberculosis. Tumor, but its cause is not clear, the ependymal membrane and choroid plexus can show inflammatory reaction or tuberculous nodules. The cerebral arteries and the small arteries in the brain parenchyma often have vascular inflammatory changes. The inflammatory process begins with the adventitia. Destruction of elastic fibers and inflammation of the endocarditis, further causing vascular occlusion, cerebral infarction or bleeding.
There were some autopsy cases in which tuberculous meningitis was associated with massive hemorrhage in the brain in 1986. In cases of irregular treatment or chronic processes, meningeal fibrous connective tissue hyperplasia thickened and adhesion to the brain can cause hydrocephalus, nerves. The cells were mostly acutely swollen, the gap around the cells was widened and the glial cells in the brain parenchyma increased. Domestic Ma Huaizhen and Li Wei reported a group of 65 cases of autopsy in 1988, 62 of which had extracerebral tuberculosis, more common in the lungs and bones. And lymph nodes, etc., it is considered that tuberculous meningitis is a manifestation of systemic tuberculosis.
Prevention
Prevention of tuberculous meningitis in children
Mainly seen in children aged 1 to 5 years old, with more incidence in spring and winter, measles and whooping cough are often the cause of brain disease, head trauma, surgery and overwork can be occasional incentives.
The most basic way to prevent brain infection is to prevent children from being infected with tuberculosis. The effective measures are as follows:
1. BCG primary and multiple cropping work must be done: Experience has shown that effective BCG vaccination can prevent or reduce the occurrence of brains.
2, early detection and active treatment of infectious sources: early detection of adult tuberculosis patients, especially in close contact with children such as parents, nursery nurses and kindergartens and primary school teachers, do a good job of flood prevention, strengthen adult tuberculosis Management and treatment.
3, improve the body's resistance to correct feeding, a reasonable living system and adhere to planned immunization to improve the body's resistance and reduce acute infectious diseases.
4, early detection and thorough treatment of primary tuberculosis in children: early and complete cure of primary tuberculosis in children, can greatly reduce the occurrence of brain.
Where the clinical symptoms disappear, the cerebrospinal fluid is normal, and there is no recurrence 2 years after the end of the treatment, it can be considered as a cure, but it should continue to be observed until 5 years after the treatment is stopped.
Factors affecting the condition:
1. Infection of the primary drug-resistant strain: The primary drug resistance of the children's brain has become a difficult problem in clinical treatment, which seriously affects the prognosis of the brain and increases the mortality rate.
2, treatment sooner or later: the later the treatment, the higher the mortality rate, 979 children, early cases without death, the mid-term child mortality rate of 3.3%, the late child mortality rate of 24.9%.
3, age: the younger the child, the faster the development of meningitis, the more serious, so the higher the mortality rate, the same severity, the infants under 3 years old are worse than the prognosis of those over 3 years old.
4, the disease type: severely damaged brain parenchyma, poor prognosis, serous type mortality rate is zero; cerebral meningitis type is 6.4%; meningoencephalitis type is 21.5%, accounting for 78.2% of all deaths.
5, with or without hydrocephalus: This is also related to the early and late stages of the disease, the combined mortality of children with hydrocephalus is far higher than the non-combined hydrocephalus, each accounting for 20% and 3.9%, some children can be treated In the process, anti-tuberculosis drugs have not fully functioned and died of cerebral palsy.
6, initial or re-treatment: re-treatment cases including recurrence or worsening, the prognosis is poor.
7. Treatment: In the early stage, the prognosis should be better in the early stage, the prognosis of the child may be prolonged or chronic, and the subarachnoid space may be extensively adhered to cause hydrocephalus or spinal cord disorder. Or hydronephrosis or spinal cord disorder occurs in the course of the disease, or cerebrovascular disease and cerebral infarction occur in the course of the disease, causing irreversible lesions, leading to sequelae or death.
Recurrence usually occurs within 2 years after the end of the treatment, and can occur even within 3 to 5 years. Most of the recurrences are 1 time, even multiple times. Recurrent diseases such as early detection, immediate treatment, can still be completely cured, but some relapses The efficacy of the case is not as good as the initial case, and the effect is poor.
Complication
Pediatric tuberculous meningitis complications Complications hydrocephalus cerebral hemorrhage epilepsy
The most common complications are hydrocephalus, brain parenchymal damage, cerebral hemorrhage and cranial nerve disorders. The first three are often caused by brain death. The clinical manifestations are hydrocephalus, tough brain, limb paralysis, epilepsy. Blindness, aphasia, etc.
1. Water often occurs and electrolytes are disordered:
(1) Dilute hyponatremia: also known as cerebral water poisoning, because the hypothalamic nucleus and paraventricular nucleus are stimulated by tuberculous inflammatory exudates, causing increased secretion of antidiuretic hormone (ADH) in the pituitary gland, leading to distal kidney Small tubules recover water, causing dilute hyponatremia, clinically many without obvious symptoms, called asymptomatic hyponatremia, such as excessive water retention, can cause water intoxication, oliguria, headache, frequent vomiting Even horrified coma.
(2) Cerebral salt-loss syndrome: due to damage to the midbrain or midbrain, the central failure of aldosterone is regulated, and the secretion of aldosterone from the adrenal cortex is reduced, or the sodium absorption of the renal tubule is reduced due to excessive sodium factor, and sodium is discharged from the urine. Increase, while bringing out a lot of water, causing brain salt loss syndrome.
(3) Others: may have hypokalemia, metabolic acidosis.
2. sequelae: severe sequelae are mostly hydrocephalus, limb paralysis, mental retardation, blindness, aphasia, epilepsy, diabetes insipidus, less sequelae after early brain treatment, sequelae after late brain treatment still 2/3 .
Symptom
Pediatric tuberculous meningitis symptoms Common symptoms Loss irritability, loss of appetite, hypothermia, high fever, infantile convulsions, weakness, neck, hard visceral papilledema
Clinical classification
There is no uniform classification standard for tuberculous meningitis in children. We use Baenlehnz's classification method according to pathological changes, clinical manifestations and course of disease in actual work, which is divided into 4 types, which is conducive to treatment and prognosis.
(1) Serous type: referred to as type I or reactive type, allergic type, its pathological feature is that the pulp exudate is confined to the vicinity of the vertebral column of the brain, the condition is mild, the treatment is timely, and there is no meningeal irritation and cranial nerve disorder. There are no focal symptoms, cerebrospinal fluid changes slightly, only the number of cells is slightly elevated, biochemical is normal, and few tubercle bacilli can be found. Most of them are found in acute miliary tuberculosis or primary tuberculosis during lumbar puncture. The changes in the cerebrospinal fluid quickly recovered.
(2) Meningeal meningitis type: referred to as type II, is a common type of disease, inflammatory lesions are mainly located in the skull base, fibrin exudate can be more diffuse, seen near the optic chiasm, can affect the brain stem, cerebellum, lateral cerebral palsy Surrounded by oppressive cranial nerves, meningeal diffuse congestion, miliary nodules, clinical features of obvious meningeal irritation and cranial nerve disorders, no focal symptoms, cerebrospinal fluid with typical tuberculous meningitis changes, meningeal irritation and cerebrospinal fluid The recovery is slower, the course of disease is sometimes prolonged, this type is heavier than the serous type, and the prognosis is worse than the serous type, but the adherence to treatment is better than other types.
(3) meningoencephalitis type: referred to as type III, inflammatory lesions not only in the meninges, but also spread to the brain parenchyma, visible congestive or hemorrhagic brain parenchyma, cerebral softening necrosis can be seen in vascular lesions such as occlusive endarteritis, and Caused by focal pathology, lesions in the choroid plexus or ventricle, can cause ventricular peritonitis, inflammation can spread to the diencephalon, there will be autonomic dysfunction, inflammation can occur when the medulla or medulla compression can occur vagus nerve synthesis Significant death, rapid changes in this type of cerebrospinal fluid, often the phenomenon of relative protein cell separation, long course, even if clinical recovery, often have sequelae, the prognosis is worse than the first two types.
(4) Tuberculous cerebrospinal meningococcal type: referred to as type IV, which can be transformed by the treatment of meningitis or meningoencephalitis. It can also be caused by the onset of the disease. The inflammatory lesions are not limited to the meninges. And spread to the spinal cord and spinal cord, in addition to the brain and meningitis symptoms are more obvious, common nerve root symptoms and spinal cord damage symptoms, typical cerebrospinal fluid channel obstruction and significant protein cell separation phenomenon, this type of disease is long, clinical recovery is slow, Cerebrospinal fluid recovery is slower, often with sequelae.
2. Clinical staging
From the natural process of development, it is generally slow, small babies also have more acute onset, with convulsions as the first symptom, the course can be divided into 4 phases:
(1) Early (precursor period): It is seen in the first 1-2 weeks of onset, showing personality changes, irritability and symptoms of tuberculosis. The infant's prodromal period can be short or insignificant and enter the meningeal stimulation period. Vomiting, headache.
(2) mid-term (meningeal stimulation period): about 1 to 2 weeks, from irritability, lethargy, apathy, screaming, followed by vomiting, headache with elevated body temperature, typical meningeal irritation, or cranial nerve disorders, also Spinal cord damage and neuropsychiatric disorders may occur, and the disease may develop with convulsions, and the mind is clear after the convulsion.
(3) Late stage (coma period): about 1 to 3 weeks, often after 2 weeks of onset, the above symptoms are aggravated, relaxation and high fever, confusion, convulsion, or coma after convulsion, increased intracranial pressure and brain Symptoms of stagnant water are obvious, and cerebral palsy can occur, often accompanied by cerebral hyponatremia, hypokalemia or metabolic acidosis.
(4) Chronic period: the sick child undergoes irregular treatment, or the effect of regular treatment is not significant, or some of the primary drug resistance, the disease course is delayed for more than 3 months, more fever, meningeal irritation, cranial nerve disorder and Increased intracranial pressure and hydrocephalus symptoms, protein cells are isolated from cerebrospinal fluid.
The above classification, staging has a certain significance for diagnosis, treatment and prognosis.
3. Clinical symptoms
The onset is slow, and the clinical symptoms can be divided into two categories:
(1) general symptoms of tuberculosis: fever in the afternoon, lack of energy, personality changes, anorexia, weight loss, night sweats, constipation, infants and young children can be diarrhea.
(2) Neurological symptoms:
1 meningeal irritation symptoms: headache, vomiting, neck resistance, positive Klinefelter sign, positive Brinell sign and sputum.
2 symptoms of cranial nerve damage: facial nerve palsy can appear earlier and more common, accounting for the first incidence of all cranial nerve damage, mainly as facial muscle asymmetry, one side of the nasolabial fold is shallow, followed by oculomotor disorder Can appear in the early stage, manifested as drooping eyelids, exotropia, pupils are not large, followed by nerves, optic nerve disorders, there are some children after the group of brain nerves can also be affected, but most occur in advanced diseased children.
3 symptoms of brain parenchymal damage: manifested as limb hemiplegia, sometimes the first symptoms of the nervous system, but also aphasia, hyperactivity, urine collapse, severe cases of cerebral cortical rigidity or mental disorders.
4 symptoms of increased intracranial pressure: headache, vomiting, disturbance of consciousness, severely quickly into a coma, infants and young children before the performance of fullness, cranial sutures, scalp veins anger, elderly children with head sputum smashed the sound of the pot, pupil Suddenly small and small, mouth periorbital, breathing is not complete, limb muscle tension increased or internal rotation, etc., if the disease progresses, cerebral palsy may occur.
5 spinal cord injury symptoms: as the disease progresses, the lesion can spread to the spinal cord membrane, spinal nerve roots and spinal cord, showing radiculopathy, lower limb dyskinesia with flaccid soft palate, urinary retention or urinary incontinence, constipation or incontinence If the injury is in the thoracic segment, the lower extremity is spastic paralyzed, and the knee reflex is hyperthyroidism.
Examine
Examination of tuberculous meningitis in children
1. The peripheral blood leukocyte count is normal or slightly elevated.
2. Cerebrospinal fluid examination:
(1) routine examination: cerebrospinal fluid pressure increased.
(2) Lymphocyte transformation test.
(3) Immunoglobulin assay
(4) Determination of lactate and lactate dehydrogenase, determination of lysozyme index, and examination of anti-tuberculosis antibodies to cerebrospinal fluid.
3. Basis for pathogens:
(1) The detection rate of CSF bacterial smear and bacterial culture is low.
(2) Skin tuberculin test.
(3) Early diagnosis: Polymerase chain reaction (PCR) is used to detect the DNA of tuberculosis in CSF.
In addition, enzyme-linked immunosorbent assay (ELISA) can be used to detect tuberculosis antibodies in CSF. The simultaneous application of the above two tests can improve the reliability of diagnosis, but attention should be paid to the possibility of false positives and false negatives.
4. X-ray film inspection:
The number of tuberculosis in the lungs is about 42-92%, of which 44% belong to miliary tuberculosis, and those with normal chest X-ray cannot negate the brain.
5.CT, MRI examination:
About half of the brain CT showed abnormalities. The inflammatory exudate was filled with basal pool and lateral cerebral palsy. Some patients showed tuberculoma in the brain parenchyma, 0.5 to 5 cm in diameter, single or multiple, mostly in the frontal, temporal and parietal, enhanced scanning. Shows ring enhancement or increased density.
Brain MR is enhanced by Gd-DTPA, which shows that the basal pool and other parts are strengthened, and tuberculoma and small infarcts in the brain parenchyma are easier to find.
Diagnosis
Diagnosis and diagnosis of tuberculous meningitis in children
diagnosis
1. Early diagnosis relies on detailed medical history: including close contact history and BCG vaccination history, careful clinical observation and high vigilance against the disease. Anyone with a history of tuberculosis contact, a positive reaction or tuberculosis, appears The following symptoms, such as temperament changes, mild fever, headache, convulsions, no cause of vomiting, intractable constipation or lethargy and irritability should be considered, the possibility of the disease should be considered.
2, clinical manifestations: the discovery of skin miliary rash is decisive for diagnosis, fundus examination is also helpful for diagnosis, tubercle nodules found on the choroid and miliary tuberculosis in the lung X-ray film have the same value.
3, chest X-ray photography is helpful for diagnosis According to X-ray examination of 1180 children with cerebral palsy, it shows that there are 86.9% of active tuberculosis, of which 454 are miliary tuberculosis, accounting for 44.2% of active tuberculosis, but need Note that 8.6% of the children have normal lungs, and these are older children.
4, children with suspected disease should be early to do the sputum test: positive reaction is helpful for diagnosis, but children with cerebral palsy are sometimes weak in response to sputum, so OT0.1mg or PPD5IU should not cause reaction, should be OT1 A dose of ~2mg or PPD250IU was retested.
5. Brain CT examination: Beijing Children's Hospital performed brain CT examination on 50 children with cerebral ventricle from 1986 to 1992. The abnormalities seen in the brain CT were very similar to the results of the past 152 cases in our hospital, indicating that the brain CT examination Brain diagnosis is meaningful.
6, EEG examination: the majority of children with acute electroencephalogram abnormalities in the acute phase, manifested as diffuse (3 weeks / second) and (4 ~ 7 weeks / sec) slow activity, asymmetry, visible asymmetry Occasionally pointed spines, sharp-slow, spine-slow and other current waves, visible or focal changes in patients with tuberculoma or local cerebral infarction; manifested as local delta waves, but no change in EEG Sexuality can only be used as a clinical auxiliary diagnosis, but it has little significance in the differential diagnosis of pathogens, but it is helpful for the follow-up treatment effect, prognosis and sequelae.
7. The most reliable diagnosis is based on the detection of Mycobacterium tuberculosis from cerebrospinal fluid: try to be carefully examined before treatment, and the protein membrane formed after the cerebrospinal fluid is allowed to stand on the glass for acid-fast staining. The positive rate of tuberculosis in 50 cases of cerebrospinal fluid retention was as high as 54%. In addition to direct smear examination, cerebrospinal fluid precipitation could be used for pathological biopsy for cerebrospinal fluid culture or guinea pig inoculation.
8, there are some early diagnostic methods for reference:
(1) Lymphocyte transformation test of cerebrospinal fluid: The lymphocyte transformation of cerebrospinal fluid was measured by 3H thymidine incorporation method. It was found that the lymphocyte transformation rate of cerebrospinal fluid was significantly increased under the stimulation of PPD during the brain, which has early diagnosis significance.
(2) Determination of cerebrospinal fluid lactate: It is meaningful for the identification of nodal encephalitis and viral encephalitis. Therefore, the determination of cerebrospinal fluid lactate is of great significance for the identification of brain and viral encephalitis, and also has certain value for the identification of brain and brain.
(3) Determination of the activity of adenosine deaminase in cerebrospinal fluid: Most adenosine deaminase activity in cerebrospinal fluid of patients with brain is higher than normal (normal person <9U/L), the sensitivity of the test is very high, simple and easy, As an aid for early diagnosis.
(4) Determination of cerebrospinal fluid immunoglobulin: Cerebrospinal fluid IgG was significantly elevated at the time of brain enucleation, higher than viral encephalitis and purulent meningitis; IgA and IgM were slightly higher than viral encephalitis but lower than purulent meningitis.
Differential diagnosis
There are obvious signs of meningeal irritation should be differentiated from general non-neurological diseases, including upper respiratory tract infection, pneumonia, dyspepsia, ascariasis, typhoid fever, hand and foot snoring, etc. At this time, the cerebrospinal fluid can be clearly diagnosed by lumbar puncture. After meningeal irritation and signs, even after cerebrospinal fluid examination, it needs to be differentiated from a series of central nervous system diseases.
1, purulent meningitis: the most confusing one is Haemophilus influenzae meningitis, because it is more common in children under 2 years old, the number of cerebrospinal fluid cells is sometimes not very high, followed by meningococcal meningitis and pneumococci Meningitis, identification of the history of exposure to tuberculosis, lignin response and pulmonary X-ray examination can help diagnosis, the important thing is cerebrospinal fluid examination, the number of cells is higher than 1000 × 106 / L (1000 / mm3), and in the classification When polymorphic granulocytes are predominant, suppurative meningitis should be considered; but more important is bacteriological examination.
2, viral central nervous system infections: mainly viral encephalitis, viral meningoencephalitis and viral myelitis can be confused with the brain, which emits viral encephalitis more need to identify than the epidemic.
(1) Epidemic encephalitis B: epidemic in summer and autumn, severe and frequent onset is extremely dangerous, early symptoms of encephalitis, fever, headache, lethargy, 3 to 4 days later into the extreme period, high fever, convulsions, coma and Respiratory circulatory failure, at this time, it is difficult to identify with the brain, and the mild cases are easy to be confused with the early brain. The symptoms of brain parenchymal damage in the early stage of the brain are easily misdiagnosed as encephalitis, but the history of JE has an epidemic, protein in cerebrospinal fluid. Only mild increase, sugar or chloride normal or increased are helpful to identify.
(2) Mumps meningoencephalitis: can be popular in winter and spring, can also be distributed, especially when encephalitis occurs before mumps or no mumps at all, it is easy to be confused with the brain, according to the history of mumps exposure, tuberculosis The bacteriocin test was negative, the lungs were free of tuberculosis and the onset was more acute, and the content of sugar and chloride in the cerebrospinal fluid was not reduced and the protein increase was not significant.
(3) polio: popular in summer and autumn, the onset is more urgent, there is a typical bimodal fever type, more unconscious disorder, affected limb paralysis reflex disappears, flaccid paralysis occurs faster, compared with limb paralysis Late and different for tonic paralysis.
(4) Enterovirus: such as Coxsackie virus, encephalitis caused by encephalitis or meningitis is more common in summer and autumn, the onset is more urgent, meningeal irritation is obvious, there may be rash and muscle pain, and the course of disease is shorter.
(5) lymphocytic choroidal plexus meningitis: more often occur in the winter and spring, common symptoms of cold, meningitis symptoms after fever and systemic symptoms, characterized by more acute onset, shorter duration, generally in 7 It can be recovered in ~10 days, and the prognosis is good. The characteristics of cerebrospinal fluid are the majority of lymphocytes, which can reach more than 95%, the sugar is normal, and the protein is slightly increased.
The main diagnostic points of various viral meningitis are: 1 often have a specific epidemic season, 2 each has its own special systemic manifestations, such as enterovirus can be associated with diarrhea, rash or myocarditis, 3 cerebrospinal fluid changes in addition to cell number and classification and knot The brain is not easy to identify, the biochemical changes are not the same, viral meningoencephalitis cerebrospinal fluid sugar and chloride normal or slightly higher, protein is not obvious, more than 1g / L (100mg / dl), 4 various viral encephalitis Or meningitis has its own specific laboratory diagnostic methods, such as serological tests and virus isolation.
3, cryptococcal meningoencephalitis: its clinical manifestations, chronic disease course and cerebrospinal fluid changes can be similar to the brain, but the course of disease is longer, can be accompanied by spontaneous relief, chronic progressive high intracranial pressure symptoms are more prominent, and other manifestations of meningitis are not parallel The disease is rare in children, so it is easy to be misdiagnosed as the brain, confirmed by the cerebrospinal fluid smear, stained with black ink to reflect the round, cryptococcal spores with thick capsule refraction, Shabao medium can be There is a growth of Cryptococcus neoformans. In addition, detection of cryptococcal polysaccharide antigen in blood and cerebrospinal fluid by latex agglutination or complement binding assay can aid diagnosis.
4, brain abscess: children with brain abscess have a history of otitis media or head trauma, sometimes secondary to sepsis, often accompanied by congenital heart disease, children with brain abscess in addition to meningitis and high intracranial pressure symptoms, often have a bureau Focal brain signs, cerebrospinal fluid changes in the absence of secondary purulent meningitis, the number of cells can be from normal to hundreds, most of the lymphocytes, sugar and chloride more normal, normal or increased protein, differential diagnosis can be used Ultrasound, EEG, lung CT and cerebral angiography.
5, brain tumors: brain tumors can be misdiagnosed as the brain.
(1) Common causes of misdiagnosis: 1% of pediatric brain tumors are located under the curtain, especially in the 4th ventricle and cerebellum. Because the cranial cavity under the cerebellum is small, it is easy to have high intracranial pressure, but in small infants, it is easy to split due to cranial suture. The symptoms of high intracranial pressure are not obvious, until the symptoms of high intracranial pressure are obvious, the course of the disease seems to be very short, and the history of the older children is longer; 2 pediatric brain tumors are mostly located in the midline, often lacking localization Symptoms; 3 common cerebral vascular tumors in children may have meningeal irritation; 4 common medulloblastoma in infants and young children can be transmitted through the subarachnoid space, prone to brain signs, cranial nerve disorders and cerebrospinal fluid changes, similar Brain knot.
(2) Brain tumor and knot brain identification points:
1 less fever.
2 convulsions are less common, even if there is convulsions, most of them are conscious after pumping, and children with advanced cerebral palsy are in a coma after convulsions.
3 coma is less common.
4 high intracranial pressure symptoms and brain signs are not parallel.
5 Cerebrospinal fluid changes are little or slight.
6 tuberculin test was negative and the lungs were normal.
7 for the diagnosis of brain tumors should be timely brain CT scan to assist in diagnosis.
(3) The brain must be differentiated from various encephalitis, cerebral cysticercosis and cerebral vascular malformation.
The typical diagnosis of the brain is easier, but it is more difficult to diagnose. The atypical brain is about the following: 1 Infants and young children are onset, progress is fast, and sometimes the first symptom can be convulsed. 2 early symptoms of brain parenchymal damage, manifested as chorea or mental disorders, 3 early cerebrovascular damage, manifested as limb paralysis, 4 with brain tuberculosis, can be like intracranial tumors, 5 other parts of tuberculosis Extremely serious, can mask the symptoms and signs of meningitis and can not be easily identified. 6 When meningitis occurs during anti-tuberculosis treatment, it often appears to be frustrated. For the above atypical cases, the diagnosis should be particularly careful to prevent misdiagnosis.
