Lecture of Tuberculous Meningitis
Today, many modern medical techniques such as ELISA, PCR, CT-scanner ... have been studied to make the diagnosis of TB meningitis more accurate.
Tuberculosis meningitis, commonly known as “meningitis” is a form of primary tuberculosis (formerly known as “secondary tuberculosis”) caused by the tuberculosis bacillus (Mycobacterium tuberculosis). Clinical manifestations are tuberculosis syndrome accompanied by meningeal syndrome and often with damage to the brain base. The diagnosis is decisive when a TB bacillus or TB antigen is found in the CSF. Specific treatment with anti-tuberculosis antibiotics.
Tuberculosis meningitis has been known for a long time, but it was not until the eighteenth century that the disease was scientifically studied. In 1776, Morgani found soft membrane grey patterns at the visual interference of 13-year-olds who died of headaches, vomiting, convulsions and coma.
By 1882, Robert Koch found the tuberculosis bacillus, but it was not until 1888 that Obolenski found the tuberculosis bacillus in the cerebrospinal fluid and at the Medical Conference in Kenigsberg, October 30, 1893, Lichtgeim announced the results of the implantation. find tuberculosis bacilli in cerebrospinal fluid. This is considered a breakthrough in research on tuberculosis meningitis.
Today, many modern medical techniques such as ELISA, PCR, CT-scanner ... have been studied to make the diagnosis of TB meningitis more accurate.
The epidemiological characteristics of TB meningitis are similar to those of general tuberculosis.
Mycobacterium tuberculosis was first identified by Robert Koch in 1882. Therefore, bacillus tuberculosis is also known as BK (Bacille de Koch). This bacterium has a relatively complex and perfect structure. TB bacillus is difficult to color with conventional dyes, but must use the method of dyeing Ziehl - Neelsen. On the Ziehl - Neelsen stained specimen, the bacillus is free from alcohol and the acid reduces the red color of fucsin, so it is called "alcohol-resistant bacillus, anti-acidosis".
Bacillus tuberculosis is aerobic bacteria, not growing in a normal environment but must be cultured in the nutrient-rich environment (Lošwenstein medium). Bacteria grow slowly, so the application of bacteria culture for diagnosis makes little sense. Under natural conditions, BK can last 3-4 months. In tuberculosis, BK can persist for many years and when conditions are favourable, it develops again.
Currently, there are many reports of anti-tuberculosis drug resistance of BK. According to the World Health Organization, between 1999 and 2002, about 10% of TB cases were resistant to one or more anti-TB drugs (multi-drug resistance) and made it difficult to treat TB.
Like pulmonary tuberculosis, the source of the disease is TB patients with BK in their sputum.
Like pulmonary tuberculosis, the disease is spread by inhalation, in two ways:
Direct transmission: BK is in saliva, a small piece of sputum released by a TB patient when coughing and inhaled directly by a healthy person.
Indirect transmission: Inhalation of BK spit out by a TB patient in the dust of the air.
Sense of the body
It can be affected at any age, but it is more common in children, adolescents and middle-aged people. Currently, adults tend to be highly ill. The rate of TB meningitis in our country is approximately 0.75 / 100,000 people.
Mechanism of pathogenesis and pathology
Mechanism of pathogenesis
TB meningitis is found to be a form of tuberculosis "post-primary" (formerly known as "secondary tuberculosis"), usually due to:
"Intrinsic" reactivation: During the primary period, BK has spread to organs including meningitis, brain, but there is no clinical manifestation. Due to the body's resistance, BK is attacked but has not been completely eradicated, becoming in a state of "sleeping" in the cell, inactive. When the conditions are favourable, BK re-operates at the agency where they previously resided.
"Foreign" re-infection: This case occurs in patients with pre-infected tuberculosis who has recovered, now infected with BK for the second time, has poor body resistance, BK by blood sugar (chronic tuberculosis blood sugar) or Lymph on the meninges, brain.
Sometimes during the primary TB period, if the body's resistance is poor, BK can also spread early into the brain and meninges.
The fact that BK penetrates the meninges is still a matter of debate
Rich's View: BK follows the bloodstream into the brain causing tuberculosis in the brain (often called "tuberculosis Rich"). From there bacteria spread to the ventricles and meninges. Thus, in this view, when there is tuberculosis meningitis is accompanied by encephalitis (tuberculosis tubers).
New concept: In the first stage, BK follows the blood sugar, crosses the barrier of blood vessels - meninges. Then, BK from the blood vessels penetrates the membranes and cerebrospinal fluid.
BK can enter the meninges from nearby tuberculosis (such as spinal tuberculosis ...) or after cranial neurosurgery intervention.
Tuberculosis lesions in meningococcal tuberculosis are most common in the basal (basal) brain region, at the intersection of the vision, the Sylvius furrow and the medial region. The damage usually develops along the cranial nerves, along the blood vessels. Therefore, tuberculosis of the brain is often accompanied by tuberculosis in the brain. TB damage from the meninges can spread to the medullary membrane.
The basic microscopic lesions are tuberculosis cysts.
Clinical features of tuberculous meningitis
The onset of TB meningitis is often diverse, but has the following common features:
The disease usually starts slowly, lasting a few weeks with symptoms of tuberculosis toxicity such as low afternoon and evening fever, fatigue, poor appetite, weight loss, sweating, blue skin ...
In addition, there may be neurological signs, usually mild, transient and progressive at first: headache, nausea, insomnia, mood changes, sometimes transient palsy or local convulsions. .. Children often stop eating, play, or sleep ...
Some cases have sudden onset, atypical with manifestations: Psychosis, convulsions, persistent high fever, clear meningeal syndrome ... However, these cases are usually due to no be carefully monitored from the beginning, when detecting that the disease is in a severe stage.
Infection-poisoning syndrome: Fever is manifested, with mild afternoon fever or persistent high fever, fluctuating fever ... accompanied by manifestations of tuberculosis toxicity and body weakness, weakness. masterpiece fast.
Meningeal syndrome: Appears slowly, more and more clearly. Frequent dull headache, sometimes a severe headache. There are symptoms of increased stimulation, photophobia, increased muscle tone ... Examination of meningeal signs (+).
Symptoms of focal nerve damage: the most common is the underlying syndrome, manifested by the symptoms of damage to the basal brain nerve, especially the II, III, IV, VI, VII, VIII .... Heavier can see wire damage IX, X, XI ... or hemiplegia, quadriplegic ...
If not treated in time, there will be consciousness disorder, semi-coma, coma and death.
The changes in cerebrospinal fluid are of great diagnostic significance: typical cerebrospinal fluid is lemon yellow, comparatively, cells are several hundred (usually 200-500) cells/ml, lymphocyte predominates (70 - 90%). ). Protein increased 2-3 g / l, sugar and salt decreased moderately. In some severe cases, late treatment ... when the CSF is deposited after 24 - 48 hours, it will look dizzy. Cerebrospinal fluid culture can reveal tuberculosis bacillus ...
Classify the disease according to clinical
Basal TB meningitis: The most common form 40-70%, with manifestations of tuberculosis meningitis and the symptoms of damage to the basal brain nerve.
Meningitis - brain: 15-25%, manifesting meningitis and brain damage due to tuberculosis.
Tuberculosis meningitis alone: 10% of the cases are often diagnosed early, with changes in cerebrospinal fluid towards TB meningitis.
Meningitis - spinal cord: rare.
Septicaemia: Common in the elderly, poor resistance.
Suppose u ...
Implementing the quadrants
Onset slowly, there is tuberculosis poisoning syndrome.
Meningeal Syndrome: (+)
Often manifestations of brain nerve damage to the brain base (wires II, III, IV, VI, VII ...).
Usually have a history of or have TB.
Common tests: Peripheral leukocytes usually do not increase, the rate of lymphocytes increases, The rate of blood settling usually increases, Mantoux (+) ...
Cerebrospinal fluid: Very significant in diagnosis (as described above, 5.1.2.).
Fundoscopy: Sometimes tuberculosis (Bouchut tubers: white seeds, the average size is 1/4 of the diameter of the papillae, one or several tubers can be seen), usually seen with associated TB meningitis. according to TB millet. These are tuberculosis tubers in the papillary region, but may not be associated with meningeal tuberculosis. The presence of Bouchut tubers will be very valuable in diagnosing tuberculosis meningitis - brain if accompanied by changes in cerebrospinal fluid with increased lymphocytes.
Computer tomography: Tuberculosis is sometimes seen in the brain (with thin tomography).
Culture of tuberculosis bacillus in cerebrospinal fluid: There is the decisive diagnostic value when (+). However, the incidence of cultures of tuberculosis in the cerebrospinal fluid is usually low.
Find antibodies to tuberculosis in serum and in the cerebrospinal fluid: little value in diagnosis.
Find TB antigens in the serum and in the cerebrospinal fluid: Very valuable to diagnose if the TB antigen is found in the cerebrospinal fluid.
PCR technique to detect TB bacillus DNA in cerebrospinal fluid: Very valuable.
The classical techniques also introduce many nonspecific tests, but they are of great value to help suggest diagnosis (eg bromide test, etc.). These techniques are in little use nowadays.
Diagnosis of TB meningitis is often difficult, requires monitoring, distinguishing from:
Cryptococcal meningitis caused by the fungus Cryptococcus neoformans: Clinically and cerebrospinal fluid is difficult to distinguish, it should be based on culturing and finding fungi in cerebrospinal fluid and trial treatment.
Viral meningitis: Usually progresses acute, with no specific treatment.
Meningitis: Sometimes difficult if the clinical course is not clear, the cerebrospinal fluid has moderately increased cells and the ratio of polymorphonuclear leukocytes and lymphocytes is relatively balanced. A valuable method for differential diagnosis is a trial treatment with strong antibiotics in the direction of meningitis.
Prognosis, progression and sequelae
Age: Children under 3 years old or the elderly have a severe prognosis.
Primary TB drive: TB infiltrates, usually mild. Tuberculosis, usually severe.
Time of detection and treatment.
The disease forms meningitis - brain, meningitis - spinal cord, pseudo-tumour... often severe.
If detected early, treat in time and bacillus tuberculosis is not drug-resistant: After 2-4 weeks of treating the patient without fever, after 6-8 weeks of the meningeal syndrome, after 2-4 months of cerebrospinal fluid. back to normal.
Diagnosis, late treatment or drug-resistant tuberculosis bacillus: Increased fever, irregular pulse, respiratory failure, cerebrospinal fluid obstruction, cerebral oedema, coma and death.
Tuberculosis meningitis often causes severe complications.
Irreversible nerve damage: Causing symptoms of local paralysis, squinting, blindness, semi-fragility ...
Meningeal thickening, ventricular inflammation, cerebrospinal fluid and cerebrospinal fluid obstruction.
Mental disorder, intellectual disability.
Endocrine and nutritional disorders due to damage to the hypothalamus, pituitary gland causing pale, fat ...
Sequelae due to complications of long-term anti-TB drug treatment such as deafness, vestibular disorder ...
The principles of treatment
Early treatment, at the hospital.
Combine high-dose anti-tuberculosis antibiotics right from the beginning, with enough dose, long duration, enough regimen, monitoring the side effects of the drug.
Improve systemic resistance, combine monitoring against complications, sequelae ...
Treat anti-tuberculosis drugs
In principle, treatment is the same as for tuberculosis in general, but often strong regimens (a combination of 3 - 4 anti-TB drugs) must be used.
The four-drug regimen is usually: Streptomycin + rimifon + rifampyxin + pyrazinamide (or ethambutol). The 3-drug regimen is usually: Streptomycin + rimifon + rifampyxin or streptomycin + rimifon + ethambutol ...
The average duration of conventional attack treatment 2 - 4 months in the hospital (until the cerebrospinal fluid stabilizes, almost returns to normal).
Dosage of tuberculosis drugs:
Rifampicin: 10 mg / kg / 24 hours.
Rimifon: 5 - 10 mg / kg / 24 hours.
Pyrazinamide: 30-40 mg / kg / 24 hours.
Streptomycin: 15 mg / kg / 24 hours.
Ethambutol: 15-25 mg / kg / 24 hours.
Maintenance duration (family, unit): Similar to anti-tuberculosis regimens, but usually 2 months longer.
The problem of bringing anti-TB drugs into the cerebrospinal fluid: Currently, there are many anti-TB drugs absorbed well into the cerebrospinal fluid. Therefore, in general, there is no indication for the introduction of anti-TB drugs into the cerebrospinal fluid. However, in severe cases, late treatment, complications of meningeal thickening ... can be given a small dose (adult: 0.05 - 0.07 g / 1 time) streptomycin into the cerebrospinal fluid.
Treatment of the symptomatic mechanism
Corticoid therapy: Combining anti-tuberculosis drugs in severe cases, late treatment, complications or cerebrospinal fluid with high protein> 2 g / liter. Usually oral (Cortancyl), medium dose (the adult starting dose is usually 30-45 mg / 24 hours on the first day), gradually reduced (usually 7-14 days to 5 mg reduction) and prolonged (time average duration of treatment 1.5 - 2 months). Depending on the development of cerebrospinal fluid, the dose of corticosteroids should be reduced or maintained. When the dose of Cortancyl is 5 - 15 mg, it will be stopped for 10-15 days.
Anti-edema (as for meningitis).
Nutrition enhancement, protein, blood, vitamin ...
Prevent and monitor side effects of antituberculosis drugs: When using anti-tuberculosis drugs, often add hepatocellular protection drugs (fortec, eganin ...), vitamin B6 (for a dose equal to 1/10 of the rimifon dose), regularly monitor liver and kidney function tests and allergic reactions to tuberculosis drugs.
Personal hygiene, anti-ulcer.